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2019v1.0

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Basic
Pharmacology
for Nurses
This page intentionally left blank

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 EDITION

19
Basic
Pharmacology
for Nurses

Michelle J. Willihnganz, MS, RN, CNE

RCTC Nursing Instructor
Rochester Community and Technical College
Rochester, Minnesota

Samuel L. Gurevitz, PharmD

Associate Professor
College of Pharmacy and Health Sciences
Butler University
Indianapolis, Indiana

Bruce D. Clayton, BS Pharm, PharmD, RPh

Professor Emeritus of Pharmacy Practice
College of Pharmacy and Health Sciences
Butler University
Indianapolis, Indiana
ELSEVIER
3251 Riverport Lane
St. Louis, Missouri 63043

BASIC PHARMACOLOGY FOR NURSES, NINETEENTH EDITION ISBN: 978-0-323-79630-9

Copyright © 2022 by Elsevier, Inc. All rights reserved.

Previous editions copyrighted 2020, 2017, 2013, 2010, 2007, 2004, 2001, 1997, 1993, 1989, 1985, 1981, 1977, 1973,
1969, 1965, 1961, and 1957.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
mechanical, including photocopying, recording, or any information storage and retrieval system, without
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This book and the individual contributions contained in it are protected under copyright by the Publisher
(other than as may be noted herein).

Notices

Knowledge and best practice in this eld are constantly changing. As new research and experience broaden
our understanding, changes in research methods, professional practices, or medical treatment may become
necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and
using any information, methods, compounds or experiments described herein. Because of rapid advances
in the medical sciences, in particular, independent verication of diagnoses and drug dosages should be
made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or contribu-
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 To Kevin, the love of my life,
and to my wonderful daughters Katie and Jennifer,
who always stand beside me.

—MJW

To my wonderful wife Eileen

and to our daughter Maire.

—SLG

To Francine,
for her unfailing support and encouragement,
and to
Sarah, Nathaniel, Evelyn, and Grace
and
Beth, Clayton, and Arden,
the lights of our lives!

—BDC
Reviewers and Ancillary Contributors

REVIEWERS Molly M. Showalter, MSN Ed., RN

Interim Vocational Nursing Program Director
Alice M. Hupp, BS, RN Department of Health Professions
Lead Instructor Texas Southmost College
Vocational Nursing Brownsville, Texas
North Central Texas College
Gainesville, Texas Odelia Garcia, MS, MSN, BSN, RN
Vocational Nursing Program Instructor
Ashley R. Williams, MSN, RN, CEN Nursing
Assistant Professor of Nursing Texas State Technical College
Capito Department of Nursing Harlingen, Texas
University of Charleston
Charleston, West Virginia Grace Frankel BSc. Pharm, PharmD, BCPS
Cabell Huntington Hospital Clinical Pharmacist
Huntington, West Virginia Bethesda Regional Health Centre/Southern Health
Steinbach, Manitoba, Canada
Heather Clark, DNP, RN
Director James J Mizner Jr, MBA, BS, RPh
Penn State Practical Nursing Program Panacea Solutions Consulting-Principal
Penn State Lehigh Valley Reston, VA
Center Valley, Pennsylvania

Darla K. Shar, MSN, RN

ANCILLARY CONTRIBUTOR
Associate Director Laura Bevlock Kanavy, MSN, BSN, RN
Practical Nursing Education Director, Practical Nursing Program
Hannah E. Mullins School of Practical Nursing Career Technology Center of Lackawanna County
Salem, Ohio Scranton, Pennsylvania
Test Bank, NCLEX Review Questions
Joanna Cain, BSN, BA, RN
President & Founder
Global Academic Consultants
Boulder, Colorado

Lorraine Kelley, RN
Faculty
Department of Nursing and Emergency Medical Services
Pensacola State College
Pensacola, Florida

vi ALGrawany
LPN/LVN Advisory Board

Nancy Bohnarczyk, MA Tawnya S. Lawson, MS, RN

Adjunct Instructor Dean, Practical Nursing Program
College of Mount St. Vincent Hondros College
New York, New York Westerville, Ohio

Sharyn P. Boyle, MSN, RN-BC Kristin Madigan, MS, RN

Instructor, Associate Degree Nursing Nursing Faculty
Passaic County Technical Institute Pine Technical and Community College
Wayne, New Jersey Pine City, Minnesota

Nicola Contreras, BN, RN Hana Malik, DNP, FNP-BC

Faculty Academic Director
Galen College Illinois College of Nursing
San Antonio, Texas Lombard, Illinois

Dolores Cotton, MSN, RN Mary Lee Pollard, PhD, RN, CNE

Practical Nursing Coordinator Dean, School of Nursing
Meridian Technology Center Excelsior College
Stillwater, Oklahoma Albany, New York

Patricia Donovan, MSN, RN Barbara Ratliff, MSN, RN

Director of Practical Nursing and Curriculum Chair Program Director, Practical Nursing
Porter and Chester Institute Cincinnati State
Rocky Hill, Connecticut Cincinnati, Ohio

Nancy Haughton, MSN, RN Mary Ruiz-Nuve, MSN, RN

Practical Nursing Program Faculty Director of Practical Nursing Program
Chester County Intermediate Unit St. Louis College of Health Careers
Downingtown, Pennsylvania St. Louis, Missouri

Dawn Johnson, DNP, RN, Ed Renee Sheehan, MSN/Ed, RN

Practical Nurse Program Director Director of Nursing, Vocational Nursing
Great Lakes Institute of Technology Nursing Assistant Programs
Erie, Pennsylvania Summit College
Colton, California
Mary E. Johnson, MSN, RN
Director of Nursing Faye Silverman, MSN/ED, RN, WOCN, PHN
Dorsey Schools Nursing Education Consultant
Roseville, Michigan Online Nursing Instructor
Lancaster, California
Bonnie Kehm, PhD, RN
Faculty Program Director Fleur de Liza S. Tobias-Cuyco, BSc, CPhT
Excelsior College Dean, Director of Student Affairs, and Instructor
Albany, New York Preferred College of Nursing
Los Angeles, California

vii
Preface
The 19th edition of Basic Pharmacology for Nurses, in
the tradition of the book’s standards rst established
in 1957, advocates the administration of medication
with safety and precision while focusing on medication
safety through medication monitoring and patient edu-
cation. In the practice setting, the nurse not only must
demonstrate knowledge of the underlying disease pro-
cess but also must be able to perform an accurate assess-
ment. The nurse must also plan and implement care in a
manner that involves the patient as an active participant
in decisions affecting care. Therefore a primary concern
throughout this book is the integration of patient teach-
ing about drug therapy to enable the patient to reach
therapeutic goals and attain an optimum level of health.
The nurse must also validate patient understanding to
ensure that the individual has the ability to provide safe
self-care and monitoring of the prescribed treatment
plan. User friendly in content, structure, and layout, the
text is concise and easy to read. With its emphasis on the
seven Rights of Drug Administration (right drug, right
time, right indication, right dosage, right patient, right
route, and right documentation), Basic Pharmacology for
Nurses provides students with the information needed
to provide safe, effective nursing care for patients re-
ceiving drug therapy.
ORGANIZATION AND SPECIAL FEATURES
CONTENT THREADS
Basic Pharmacology for Nurses, 19th edition, shares
some features and design elements with other Elsevier
books that you may be using. The purpose of these
Content Threads is to make it easier for students and
instructors to use the variety of books required by a
fast-paced and demanding curriculum.
The shared features in Basic Pharmacology for Nurses,
19th edition, include the following:
• Cover and internal design similarities; the colorful,
student-friendly design encourages reading and
learning of this core content
• Numbered lists of Objectives that begin each chapter
• Key Terms with pronunciations at the beginning of
each chapter; the Key Terms are in color when they
are dened in the chapter
• Bulleted lists of Key Points at the end of each chapter
Next Generation (NG) NCLEX style questions are
at the end of each chapter. These questions use single-
episode and unfolding cases. They include the six
viii
NCSBN Clinical Judgment Measurement Model cogni-
tive processes and skills; answers are provided on the
Evolve student website.
In addition to content and design threads, these
textbooks benet from the advice and input of the El-
sevier Advisory Board.
CONTENTS
Unit I explores pharmacology foundations, principles,
life span considerations, the nursing process with
pharmacology, and patient education. Unit II contains
the unique Illustrated Atlas of Medication Administra-
tion that provides extensive step-by-step instructions
and illustrations that show primary routes of admin-
istration and proper administration techniques for all
forms of medications.
Units III through X provide an overview of each
drug class, followed by narrative discussions of the
most common individual drugs. The units and chap-
ters are organized by body system.
CHAPTER ORGANIZATION
• Each drug chapter in Units III through X begins
with an overview of a clinical problem and its
management.
• The general nursing implications section includes
clearly identied headings for Assessment, Imple-
mentation, and Patient Education. The Patient Edu-
cation section helps the nurse incorporate patient
education designed to promote health into the over-
all treatment plan.
• Drug monographs are provided for each major drug
class. These monographs describe Actions, Uses,
and Therapeutic Outcomes for each class.
• A drug class–specic nursing implications section
for each drug monograph highlights Premedication
Assessment, Product Availability, Dosing Instruc-
tions, Common Adverse Effects, Serious Adverse
Effects, and Drug Interactions.
SPECIAL FEATURES
Basic Pharmacology for Nurses includes special fea-
tures designed to foster effective learning and
comprehension.
• Chapter-opening features include lists of Objectives
and Key Terms with pronunciations.
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• Clinical Pitfall and Medication Safety Alert boxes
highlight critically important clinical considerations
to help students practice safety and reduce medica-
tion errors.
• Clinical Goldmine boxes put a spotlight on tips and
best practices for clinical procedures.
• Life Span Considerations boxes focus on the impli-
cations of drug therapy for children, pregnant and
breastfeeding women, and older adults.
• Herbal Interactions boxes discuss well-documented
interactions among drugs, herbal therapies, and di-
etary supplements.
• A handy bulleted list of Key Points at the end of
most chapters facilitates review of essential chapter
content.
NEW TO THIS EDITION
• This edition includes the latest US Food and Drug
Administration (FDA) approvals, including up-to-
date clinical drug indications, guidelines for use,
and recently released new drugs.
• Increased emphasis on medication safety that stress-
es imperative information for patient protection.
• Additional information on genetics, pharma-
cogenomics, and racial/gender factors in drug ac-
tions is included to highlight current research.
• New gures have been added to illustrate proper
medication administration.
• End-of-chapter NCLEX-style questions that in-
clude NG types such as Cloze, Grid/Matrix, Drag
and Drop, and Extended Multiple Response. These
types cover the six cognitive skills: Recognize Cues,
Analyze Cues, Prioritize Hypotheses, Generate So-
lutions, Take Action, and Evaluate Outcomes.
TEACHING AND LEARNING PACKAGE
FOR STUDENTS
• The Evolve Website provides free student resources,
including answers and rationales for in-text Review
Questions for the NCLEX® Examination, a math
PREFACE ix
review, animations, video clips, a collection of Pa-
tient Teaching handouts, fully customizable Patient
Self-Assessment Forms provided as “completable”
PDF documents, and a collection of 500 NCLEX-
style Review Questions.
• The revised Study Guide provides additional learn-
ing resources that complement those in the text-
book. Questions for each chapter follow the objec-
tives in the book for additional focus on these key
concepts. Matching starts each chapter, and patient
scenarios are included with the chapters that detail
the medications. NG NCLEX-style questions are in-
cluded, as are typical NCLEX questions. Each ques-
tion includes the correct answer, rationale, NCLEX
style used, and cognitive skill measured. Each
question has a page number identied to help the
student nd the answer in the textbook. Answers
to the Study Guide questions are available from
instructors.
FOR INSTRUCTORS
The comprehensive Evolve Resources with TEACH In-
structor Resource provides a rich array of resources that
include the following:
• Updated TEACH Lesson Plans, based on textbook
learning objectives, provide ready-to-use lesson
plans that tie together all of the text and ancillary
components provided for Basic Pharmacology for
Nurses.
• The collection of PowerPoint Lecture Slides is spe-
cic to the text.
• A Test Bank, delivered in ExamView, now provides
an expanded collection of approximately 900
multiple-choice and alternate-format NCLEX-style
questions. Each question includes the Correct
Answer, Rationale, and corresponding text page
numbers.
• The Image Collection contains every reproducible
image from the text. Images are suitable for incor-
poration into classroom lectures, PowerPoint pre-
sentations, or distance-learning applications.
• Answer keys are provided for the Study Guide.
Special Features

Basic Pharmacology for Nurses focuses on medication safety through medication

monitoring and patient education. Full-color art and design features accompany
detailed, understandable discussions of drugs organized by body system.

x ALGrawany
 SPECIAL FEATURES xi

• Patient Education and Health Promotion is emphasized in the overall treat-
ment plan.
• Life Span Considerations boxes focus on implications of drug therapy for chil-
dren, pregnant and breastfeeding women, and older adults.
• Clinical Pitfall and Medication Safety Alert boxes highlight critically impor-
tant clinical considerations.
• Herbal Interactions boxes describe possible adverse effects of alternative
therapies.
• Chapters open with Objectives and Key Terms with pronunciations and page
references.

STUDY GUIDE
Includes Practice Questions for the NCLEX® Examination for each textbook chapter.
Answers to the revised study guide are available from your instructor.
Contents

UNIT I Applying Pharmacology to Nursing
Practice, 1
1 Drug Denitions, Standards, and Information
Sources, 1
2 Basic Principles of Drug Action and Drug
Interactions, 13
3 Drug Action Across the Life Span, 22
4 The Nursing Process and Pharmacology, 38
5 Patient Education to Promote Health, 50
27 Drugs Used to Treat Heart Failure, 438
28 Drugs Used for Diuresis, 454
UNIT V Drugs Affecting the Respiratory
System, 469
29 Drugs Used to Treat Upper Respiratory
Disease, 469
30 Drugs Used to Treat Lower Respiratory
Disease, 482

UNIT II Illustrated Atlas of Medication UNIT VI Drugs Affecting the Digestive

Administration, 60 System, 507
6 Principles of Medication Administration and 31 Drugs Used to Treat Oral Disorders, 507
Medication Safety, 60 32 Drugs Used to Treat Gastroesophageal Reux and
7 Percutaneous Administration, 83 Peptic Ulcer Disease, 516
8 Enteral Administration, 103 33 Drugs Used to Treat Nausea and Vomiting, 530
9 Parenteral Administration: Safe Preparation of 34 Drugs Used to Treat Constipation and
Parenteral Medications, 119 Diarrhea, 550
10 Parenteral Administration: Intradermal,
Subcutaneous, and Intramuscular Routes, 137 UNIT VII Drugs That Affect the Endocrine
11 Parenteral Administration: Intravenous System, 561
Route, 149 35 Drugs Used to Treat Diabetes Mellitus, 561
36 Drugs Used to Treat Thyroid Disease, 596
UNIT III Drugs Affecting the Autonomic and 37 Corticosteroids, 606
Central Nervous Systems, 180 38 Gonadal Hormones, 615
12 Drugs Affecting the Autonomic Nervous
System, 180 UNIT VIII Drugs Affecting the Reproductive
13 Drugs Used for Sedation and Sleep, 192 System, 624
14 Drugs Used to Treat Neurodegenerative 39 Drugs Used in Obstetrics, 624
Disorders, 204 40 Drugs Used in Men’s and Women’s Health, 644
15 Drugs Used for Anxiety Disorders, 228
16 Drugs Used for Depressive and Bipolar UNIT IX Drugs Affecting Other Body Systems,
Disorders, 238 670
17 Drugs Used for Psychoses, 262 41 Drugs Used to Treat Disorders of the Urinary
18 Drugs Used for Seizure Disorders, 276 System, 670
19 Drugs Used for Pain Management, 300 42 Drugs Used to Treat Glaucoma and Other Eye
Disorders, 682
UNIT IV Drugs Affecting the Cardiovascular 43 Drugs Used to Treat Cancer, 699
System, 330 44 Drugs Used to Treat Musculoskeletal
20 Introduction to Cardiovascular Disease and Disorders, 711
Metabolic Syndrome, 330 45 Drugs Used to Treat Infections, 724
21 Drugs Used to Treat Dyslipidemias, 338
22 Drugs Used to Treat Hypertension, 353 UNIT X Drugs Affecting the General Health of
23 Drugs Used to Treat Dysrhythmias, 382 the Body, 771
24 Drugs Used to Treat Angina Pectoris, 397 46 Nutrition, 771
25 Drugs Used to Treat Peripheral Vascular Disease, 409 47 Herbal and Dietary Supplement Therapy, 792
26 Drugs Used to Treat Thromboembolic 48 Substance Abuse, 809
Disorders, 417

xii ALGrawany
Unit I Applying Pharmacology to Nursing Practice
Drug Denitions, Standards, and
Information Sources
Objectives
1. Differentiate between the chemical, generic, and brand
names of drugs.
2. Identify the various methods used to classify drugs.
3. Identify sources of drug information available for healthcare
providers.
Key Terms
pharmacology (făr-mă-KŎL-ŏ-jē) generic name (jĕ-NĀR-ĭk) (p. 2)
(p. 1) brand name (p. 2)
therapeutic methods (thĕr-ă-PYŪ-tĭk prescription drugs (p. 2)
MĔTH-ĕdz) (p. 1) nonprescription drugs (p. 2)
drugs (p. 1) over-the-counter (OTC) drugs (p. 2)
biologic therapies (p. 1) illegal drugs (ĭl-LĒ-gŭl) (p. 2)
chemical name (KĔM-ĭ-kŭl) (p. 2) biosimilars (p. 2)
Pharmacology (from the Greek pharmakon, meaning
“drugs,” and logos, meaning “science”) deals with the
study of drugs and their actions on living organisms.
Diseases that cause illness may be treated in several
different ways, which are referred to as therapies. The
various approaches to therapy are called therapeutic
methods Examples of therapeutic methods include the
following:
• Drug therapy: Treatment with drugs
• Diet therapy: Treatment with diet (e.g., a low-salt
diet for patients with cardiovascular disease)
• Physiotherapy: Treatment with natural physical
forces (e.g., water, light, heat)
• Psychological therapy: The identication of stress-
ors and methods that can be used to reduce or elimi-
nate stress
Most illnesses caused by diseases require a combi-
nation of therapeutic methods for successful treatment.
Drugs (from the Dutch droog, meaning “dry”) are
chemical substances that have an effect on living organ-
isms. Therapeutic drugs, which are often called medi-
cines, are those drugs that are used for the prevention
or treatment of diseases. Up until the early to mid-20th
century, dried plants were the most abundant source
of medicines, thus the word drug was applied to them.
1
https://evolve.elsevier.com/Willihnganz
4. Discuss the difference between prescription and
nonprescription drugs.
5. Describe the process of developing and bringing new
drugs to market.
6. Differentiate between the Canadian chemical names and
the proper name of a drug.
schedules (SKĔD-jūlz) (p. 5)
black box warnings (p. 8)
orphan drugs (ŌR-făn) (p. 8)
Food and Drugs Act and
Regulations (p. 9)
Controlled Drugs and Substances
Act (p. 10)
Whereas most drugs are individual chemicals that
cause a response in living tissues, a new class known
as biologic therapies have been discovered that have
transformed treatment of patients with disorders that
attack the body’s own organs, tissues, and cells (auto-
immune disorders), blood (hematologic disorders),
and cancers. Biologic agents are large, complex pro-
teins manufactured in a living system such as a micro-
organism, or within plant or animal cells. Biologics
have added major therapeutic choices for the treat-
ment of many diseases for which no effective therapies
were available or previously existing therapies were
clearly inadequate.
DRUG NAMES, STANDARDS,
LEGISLATION, AND DEVELOPMENT
IN THE UNITED STATES
DRUG NAMES
All drugs have several names, which may cause con-
fusion. When administering the prescribed drug, the
spelling on the drug package must correspond exactly
with the spelling of the drug ordered to ensure that the
proper medicine is administered.
1
2 UNIT I Applying Pharmacology to Nursing Practice
Each drug has three names: (1) a chemical name, (2)
a generic name, and (3) a brand name. The chemical
name is most meaningful to the chemist. By means of
the chemical name, the chemist understands the exact
chemical constitution of the drug and the exact place-
ment of its atoms or molecular groupings.
Before a drug becomes ofcial, it is given a generic
name or common name. The generic name is simpler
than the chemical name. It may be used in any country
and by any manufacturer. The rst letter of the generic
name is not capitalized. Students are strongly encour-
aged to learn and refer to drugs by their generic names
because formularies (i.e., lists of medicines avail-
able through a pharmacy) are maintained by generic
names. When a therapeutically equivalent drug be-
comes available in generic form, the generic medicine
is routinely substituted for the brand-name medicine.
Generic names are provided by the United States
Adopted Names Council, which is an organiza-
tion sponsored by the United States Pharmacopeial
Convention, the American Medical Association, and
the American Pharmacists Association. The ofcial
name, which is virtually always the generic name in
the United States, is the name under which the drug is
listed by the US Food and Drug Administration (FDA).
The FDA is empowered by federal law to generically
name the drugs for human use in the United States.
A trademark or brand name is followed by the symbol ®.
This symbol indicates that the name is registered and
that the use of the name is restricted to the owner of the
drug, which is usually the manufacturer. Most drug com-
panies place their products on the market under brand
names rather than generic names. The brand names are
deliberately made easier to pronounce, spell, and re-
member. The rst letter of the brand name is capitalized.
Example of Chemical, Generic, and Brand Names for
Drugs
Chemical name: [2-[4-[(4-Chlorophenyl)phenylmethyl]-
1-piperazinyl]ethoxy]acetic acid dihydrochloride
(Fig. 1.1)
Generic name: cetirizine
Brand name: Zyrtec Allergy
DRUG CLASSIFICATIONS
Drugs may be classied by a variety of methods ac-
cording to the body system that they affect (e.g., the
central nervous system, the cardiovascular system, the
O COOH
N and they are accepted worldwide. The Convention pub-
N (USP)/National Formulary (NF), which is revised annually.
Cl
Fig. 1.1 Cetirizine, an antihistamine.
gastrointestinal system); their therapeutic use or clinical
indications (e.g., antacids, antibiotics, antihypertensives,
diuretics, laxatives); and their physiologic or chemical ac-
tion (e.g., anticholinergics, beta-adrenergic blockers,
calcium channel blockers, cholinergics).
Drugs may be further classied as prescription or
nonprescription. Prescription drugs require an order by
a health professional who is licensed to prescribe drugs,
such as a primary healthcare provider, a nurse practi-
tioner, a physician assistant, a pharmacist, or a dentist.
Nonprescription drugs, or over-the-counter (OTC) drugs,
are sold without a prescription in a pharmacy or in the
health section of department or grocery stores. Illegal
drugs, sometimes referred to as recreational drugs, are
drugs or chemical substances used for nontherapeutic
purposes. These substances either are obtained illegally
or have not received approval for use by the FDA. See
Chapter 48 for further information about substance abuse.
A biosimilar is a biologic product that is close in
structure and function to an existing approved biologic
product, known as a reference product. For example, inf-
liximab-dyyb (Inectra) and iniximab-abda (Renexis)
are biosimilars for the reference product iniximab
(Remicade) used to treat rheumatoid arthritis. With many
patents for biologics expiring, biosimilar agents will be-
come available. In 2010 legislation created an abbreviated
licensure pathway for biologic products that are demon-
strated to be biosimilar. Biosimilars offer an opportunity
to increase access to biologics while lowering the cost of
therapy. However, unlike generic medicines in which
the active ingredients are identical to the reference small-
molecule drugs, biosimilars will not be identical to the
reference biologics. This is due to the inherent complexity
of biologic proteins. Biosimilars made by different manu-
facturers will differ from the reference product and from
each other, making each biosimilar a unique therapeutic
option for patients (Table 1.1). Biosimilars are not gener-
ics and are not interchangeable. These agents cannot be
substituted for the original reference molecule.
SOURCES OF DRUG STANDARDS AND DRUG
INFORMATION
Drug products made by different manufacturers or
in different batches by the same manufacturer must
be uniformly pure and potent. The United States
Pharmacopeial Convention is a nongovernment organi-
zation that promotes public health by establishing state-
of-the-art standards to ensure the quality of medicines
and other healthcare technologies. These standards are
developed by a unique process of public involvement,
lishes a single-volume text, the United States Pharmacopeia
The primary purpose of this volume is to provide stan-
dards for the identity, quality, strength, and purity of sub-
stances used in the practice of healthcare. The standards
described in the USP/NF are enforced by the FDA as the
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 Drug Denitions, Standards, and Information Sources CHAPTER 1 3

Table 1.1 Comparing and Contrasting Biosimilar and Generic Products

PROPERTIES BIOSIMILAR DRUGS (BIOLOGICS) GENERICS (SMALL-MOLECULE DRUGS)
Size Large Small
Structure Complex with potential structural variations Simple and well dened
Manufacturing Unique bank of living cells Predictable chemical reaction
Unlikely to achieve identical copy Identical copy can be made
Complexity Difcult to fully characterize Easy to fully characterize
Stability More sensitive to storage and handling Less sensitive to storage and handling
conditions conditions
Immunogenicity (promotes immune Higher potential Lower potential
response; potential for allergy)
Approval requirements Large clinical trials in patients Small clinical trials for safety in healthy
volunteers

ofcial standards for the manufacture and quality control
of medicines and nutritional supplements produced in
the United States. The USP/NF is also recognized by the
Canadian Food and Drugs Act as an authoritative source
of drug standards in Canada.
Table 1.2 lists and describes the common sources of
drug information available for the professional health-
care provider; additional resources are described in the
following sections.
PACKAGE INSERTS
Manufacturers of drugs are required to develop a
comprehensive but concise description of the drug,
indications and precautions for clinical use, recom-
mendations for dosage, known adverse reactions,
contraindications, and other pharmacologic informa-
tion relating to the drug. Federal law mandates that this
material be approved by the FDA before the product is
released for marketing and that it be presented on an
insert that accompanies each package of the product.
The FDA adopted a format for package inserts to
help reduce medication errors and to improve patient
education. The labeling reduces practitioners’ time
looking for information, decreases the number of pre-
ventable medication errors, and improves treatment
effectiveness and patient education. Because this label-
ing represents considerable effort and is most critical
for newer and less familiar drugs, the formatting ap-
plies only to relatively new prescription drug prod-
ucts, developed since 2006.
Clinical Goldmine
DailyMed (see Online Resources), which is sponsored by
the US National Library of Medicine, provides a database for
new package inserts that is searchable by product name, in-
dications, dosage and administration, warnings, description
of drug product, active and inactive ingredients, and how the
drug is supplied. See the section Electronic Databases.
NURSING JOURNALS
Many specialty journals have articles about drug
therapy as it relates to a specic eld of interest (e.g.,
Geriatric Nursing, American Journal of Critical Care).
Nursing journals such as RN and American Journal of
Nursing provide drug updates and articles that discuss
nursing considerations related to drug therapy and
drugs. Nurses must keep in mind that the purpose of
using resources such as journals is to obtain profes-
sional knowledge of current evidence-based practice
changes and they should not be used as a primary
source for drug information. Nurses must be mind-
ful of the accuracy of the information contained and
should check the dates on articles to validate the cur-
rency of the information.
ELECTRONIC DATABASES
With the exponential growth of information about
medicines and health, it is almost impossible to
make the information available without the use
of electronic databases. The National Library of
Medicine (NLM) provides Medline and other search-
able databases at no cost. Databases incorporated
into the NLM include information on drugs and
other chemicals that breastfeeding mothers may be
exposed to and the levels in breast milk and infant
blood with the possible adverse effects in the nurs-
ing infant. They also provide suggested therapeutic
alternatives to the drugs. Information regarding the
development and reproductive toxicology of drugs
covering teratology is included. Most of the drug
information sources listed in Table 1.2 are also avail-
able via electronic retrieval from libraries. Many col-
lege libraries subscribe to the Cumulative Index to
Nursing and Allied Health Literature (CINAHL).
These databases give nurses access to a wealth of
information from sources published in the United
States and other countries.
Databases for practitioners are also available by
subscription. UpToDate, Lexicomp, and ePocrates are
three vendors with several different packages of reg-
ularly updated information (see Online Resources).
Lexicomp has a particularly strong database because
the American Hospital Formulary Service is available
through its portal.
4 UNIT I Applying Pharmacology to Nursing Practice
Table 1.2 Sources of Drug Information for Healthcare Providers
SOURCES OF DRUG INFORMATION
AHFS Drug Information
Drug Facts and Comparisons
ASHP’s Handbook on Injectable Drugs
Handbook of Nonprescription Drugs:
An Interactive Approach to Self-Care
Martindale: The Complete Drug Reference
Natural Medicines Comprehensive Database
CANADIAN DRUG STANDARDS
European Pharmacopoeia
Pharmacopée Française
The International Pharmacopoeia (Ph. Int.)
British Pharmacopoeia
Canadian Formulary
The National Formulary
Pharmaceutical Codex
United States Pharmacopeia-National
Formulary
CANADIAN DRUG INFORMATION
Compendium of Pharmaceuticals and
Specialties (CPS)
Patient Self-Care: Helping Patients Make
Therapeutic Choices
Compendium of Self-Care Products (CSCP)
AHFS, American Hospital Formulary Service; ASHP, American Society of Health-System Pharmacists; USP, United States Pharmacopeia.
The DailyMed system (see Online Resources) was
developed in collaboration with federal agencies—
including the FDA, the NLM, the Agency for Healthcare
Research and Quality, the National Cancer Institute in
the US Department of Health and Human Services,
and the US Department of Veterans Affairs—to pro-
vide high-quality information about marketed drugs.
DailyMed makes available to healthcare providers
DESCRIPTION
Contains monographs about virtually every single-entity drug available in the
United States
Describes therapeutic uses of drugs, including approved and unapproved uses
Online version available
Contains drug monographs that describe all drugs in a therapeutic class
Monographs are formatted as tables to allow comparison of similar products,
brand names, manufacturers, cost indices, and available dosage forms
Online version available
Collection of monographs about 360 injectable drugs with sections on
available concentrations, compatibility with other drugs, dosage and rate of
administration, stability, pH, and other useful information
Interactive version available
Most comprehensive text available about over-the-counter medications that can
be purchased in the United States
Online version available
Considered one of the most comprehensive texts available for information
about drugs in current use throughout the world
Contains extensive referenced monographs about the international names,
pharmacologic activity, and side effects of more than 6400 drugs
Online subscription available
Scientic gold standard for evidence-based information about herbal medicines
and combination products involving herbal medicines
Only available in an online database by subscription or at libraries
All recognized by the Canadian Food and Drugs Act as authoritative sources
of drug standards
Published annually by the Canadian Pharmacists Association
Comprehensive list of the pharmaceutical products distributed in Canada,
as well as other practical information e-CPS available
Published by the Canadian Pharmacists Association
Provides comprehensive information for health professionals and consumers
about nonprescription drug products available in Canada e-Therapeutics
available
Nonprescription companion to CPS and Patient Self-Care
Offers at-a-glance comparative tables for thousands of products and
monographs about hundreds of commonly used nonprescription products
and the public a standard, comprehensive, up-to-date
resource about medicines.
UNITED STATES DRUG LEGISLATION
Drug legislation approved by Congress provides the
legal basis (Table 1.3) for drug manufacturing and pro-
tects the consumer from false claims made by a drug
ALGrawany
 Drug Denitions, Standards, and Information Sources CHAPTER 1
Table 1.3 Selected Major US Legislation Pertaining to Safety of Medicines
LEGISLATION (LAW)
Food, Drug, and Cosmetic Act of 1938
Durham-Humphrey Amendment (1951) to the Food, Drug,
and Cosmetic Act
Kefauver-Harris Amendment (1962) to the Food, Drug,
and Cosmetic Act
Comprehensive Drug Abuse Prevention and Control Act
(1970)
(Controlled Substances Act, 1970)
Dietary Supplement Health and Education Act (1994)
(DSHEA Act–1994)
manufacturer. The FDA is the administrative body that
oversees the drug evaluation process in the United
States and grants approval for or removal of drug
products from the market.
CONTROLLED SUBSTANCES ACT
The Comprehensive Drug Abuse Prevention and
Control Act, which is commonly referred to as the
Controlled Substances Act, is designed to improve the
administration and regulation of the manufacturing,
distribution, and dispensing of drugs that require tight-
er control by the government because of their higher
incidence of abuse and potential for addiction. The ba-
sic structure of the Controlled Substances Act consists
of ve classications, or schedules, of controlled sub-
stances. The degree of control, the conditions of record
keeping, the particular order forms required, and other
regulations depend on which schedule the individual
drug is assigned (Box 1.1).
Drugs that are listed as Schedule I are not avail-
able for other than highly controlled research pur-
poses because of their very high potential for abuse
and addiction. Drugs in Schedule II have a high po-
tential for abuse and addiction, but are available by
prescription only, in limited quantities, usually with
no more than a 7- to 30-day supply. The prescription
cannot be relled; a new prescription must be issued
for continued use. Drugs categorized as Schedule
III, IV, or V have a lower potential for abuse and ad-
diction and may be ordered by prescription with a
5
PURPOSE AND EFFECT
Requires that new drugs be safe, as well as pure (but did not
require proof of efcacy). Enforcement by FDA.
Gives the FDA the power to determine which products may be
sold with and without a prescription.
Requires proof of efcacy as well as safety for medicines
released since 1938; establishes guidelines for reporting
of information about adverse reactions, clinical testing, and
advertising of new drugs.
Outlines strict controls in the manufacture, distribution, and
prescribing of habit-forming drugs; establishes drug schedules
and programs to prevent and treat drug addiction. Established
the Drug Enforcement Administration (DEA).
Under this act, almost all herbal medicines, vitamins, minerals,
amino acids, and chemicals used for health are reclassied as
dietary supplements, a food category. The legislation allows
the label to include information about how these products
affect the human body. Labels must contain a statement
that the product has not been evaluated by the FDA for
treating, curing, or preventing any disease. The law does
not prevent nonlicensed personnel from making founded or
unfounded claims about the therapeutic effects of supplement
ingredients. The result is that dietary supplements are not
required to be safe and effective, and unfounded claims of
therapeutic benet abound. See Chapter 47
Box 1.1 Examples of Medicines in the Controlled
Substances Drug Schedules
SCHEDULE I DRUGS
Examples: lysergic acid diethylamide (LSD), peyote, heroin,
hashish
SCHEDULE II DRUGS
Examples: amphetamines, morphine, hydrocodone/
acetaminophen (Vicodin), hydrocodone/acetaminophen
(Lortab), hydrocodone/acetaminophen (Norco), methadone,
oxycodone/aspirin (Percodan), methylphenidate (Ritalin),
amphetamine/dextroamphetamine (Adderall)
SCHEDULE III DRUGS
Examples: aspirin/codeine (Empirin with codeine), aspirin/
butalbital/caffeine (Fiorinal), acetaminophen/codeine
(Tylenol with codeine)
SCHEDULE IV DRUGS
Examples: phenobarbital, chlordiazepoxide, diazepam,
urazepam, temazepam
SCHEDULE V DRUGS
Example: atropine/diphenoxylate (Lomotil, Virtussin AC)
maximum supply of 30 days of medicine. If so written
by the prescriber, the prescription may be relled up
to ve times but outdates at 6 months, at which time
a new prescription is required if the medicine is to be
continued. Prescription medicines that are not clas-
sied as controlled substances may be relled for up
to a period of time dened by individual state law, if
6 UNIT I Applying Pharmacology to Nursing Practice
approved by the prescriber. Most state laws mandate
that a prescription outdates in 1 year and must be re-
written if therapy is to be continued.
Drug Enforcement Administration
The US Drug Enforcement Administration (DEA) was
organized to enforce the Controlled Substances Act,
to gather intelligence, to train its ofcers, and to con-
duct research in the area of dangerous drugs and drug
abuse.
Every manufacturer, primary healthcare provider,
nurse practitioner, physician assistant, dentist, phar-
macy, and hospital that manufactures, prescribes, or
dispenses any of the drugs listed in the ve schedules
must register biannually with the DEA. A healthcare
provider’s prescription for substances named in this
law must contain the healthcare provider’s name, ad-
dress, DEA registration number, and signature; the
patient’s name and address; and the date of issue.
The pharmacist cannot ll such a prescription for a
controlled substance without this information on the
prescription.
Possession of Controlled Substances by
Individuals
Federal and state laws make the possession of con-
trolled substances without a valid prescription a
crime, except in specically exempted cases. The law
makes no distinction between professional and practi-
cal nurses with regard to the possession of controlled
drugs. Nurses may give controlled substances only
under the direction of a healthcare provider who has
been licensed to prescribe or dispense these agents.
Nurses may not have controlled substances in their
possession unless the following conditions are met: (1)
the nurse is giving them to a patient under an order
from a healthcare provider, (2) the nurse is a patient for
whom a healthcare provider has prescribed scheduled
drugs, or (3) the nurse is the ofcial custodian of a lim-
ited supply of controlled substances on a unit or for a
department of the hospital. Controlled substances that
are ordered for patients but not used must be returned
to the source from which they were obtained (i.e., the
primary healthcare provider or pharmacy). Violation
of or failure to comply with the Controlled Substances
Act is punishable by ne, imprisonment, or both and
by the possible loss of professional licensing.
EFFECTIVENESS OF DRUG LEGISLATION
The effectiveness of drug legislation depends on the
interest and determination used to enforce these laws,
the appropriation by government of adequate funds
for enforcement, and the vigor used by proper authori-
ties in enforcement. The interest and cooperation of
healthcare professionals and the public with regard
to the benets of appropriate drug use and the pos-
sible consequences of indiscriminate use of drugs
can be very benecial. Many individuals assist in this
education through support of national and state pro-
fessional organizations, consumer advocacy groups,
and local, state, and county health departments.
NEW DRUG DEVELOPMENT
It currently takes an average of 8 to 15 years and more
than $2 billion in research and development costs to
bring a single new drug to market; healthcare profes-
sionals and consumers alike often have a lack of un-
derstanding about this process. The Pharmaceutical
Research and Manufacturers of America estimates
that only 1 of 10,000 chemicals investigated is actu-
ally found to be “safe and effective” and ultimately
brought to the pharmacist’s shelf.
The Food, Drug, and Cosmetic Act of 1938 charged
the FDA with the responsibility of regulating new
drugs. Rules and regulations evolved by the FDA di-
vide new drug development into four stages: (1) pre-
clinical research and development; (2) clinical research
and development; (3) New Drug Application (NDA)
review; and (4) postmarketing surveillance (Fig. 1.2).
PRECLINICAL RESEARCH AND DEVELOPMENT
STAGE
The preclinical research phase of new drug develop-
ment begins with the discovery, synthesis, and pu-
rication of the drug. The goal at this stage is to use
laboratory studies to determine whether the experi-
mental drug has therapeutic value and whether the
drug appears to be safe in animals. Enough data must
be gained to justify testing the experimental drug in
humans.
The preclinical phase of data collection may require
1 to 3 years, although the average length of time is
18 months. Near the end of this phase, the investiga-
tor (often a pharmaceutical manufacturer) submits
an Investigational New Drug (IND) application to
the FDA; this application describes all of the studies
completed to date, discusses the expected safety of
the drug, and explains the testing that is planned for
human subjects. Within 30 days, the FDA must make
a decision on the basis of safety considerations about
whether to allow the human study to proceed. Only
about 20% of the chemicals tested in the preclinical
phase advance to the clinical testing phase.
CLINICAL RESEARCH AND DEVELOPMENT
STAGE
The stage in which humans are rst tested (i.e., the
clinical research or IND stage) is usually subdivided
into three phases. Phase 1 studies determine an experi-
mental drug’s pharmacologic properties, such as its
pharmacokinetics, metabolism, safe dosage range, po-
tential for toxicity at a certain dosage, and safe routes
of administration. The study population is composed
of normal volunteers or the intended treatment popu-
lation, such as those patients for whom the standard
ALGrawany
 Drug Denitions, Standards, and Information Sources CHAPTER 1
Preclinical Research Clinical
and Development FDA Research and Development
Discovery
PHASE 1
PHASE 2
Animal testing
PHASE 3
SHORT TERM
LONG TERM
Range: 1-3 years Range: 2-10 years
Average: 18 months Average: 5 years
FDA time: 30-day
safety review
Industry time
Fig. 1.2 The new drug review process. FDA, US Food and Drug Administration; NDA, New Drug Application.
treatments of certain cancers or dysrhythmias have
been ineffective. Phase 1 studies usually require 20 to
100 subjects who are treated for 4 to 6 weeks.
If phase 1 trials are successful, the drug is moved to
phase 2 trials, which involve a smaller population of
patients who have the condition that the drug is de-
signed to treat. Studies at various dosages are conduct-
ed to determine the success rate and safety of a drug
for its intended use. If successful, the drug is advanced
to phase 3 trials, in which larger patient populations
are used to ensure the statistical signicance of the re-
sults. Phase 3 studies also provide additional informa-
tion about proper dosing and safety.
The entire clinical research phase may require 2 to
10 years, with the average experimental drug requir-
ing 5 years. Each study completed is reviewed by the
FDA to help ensure patient safety and efcacy. Only
one of ve drugs that enter clinical trials makes it to
the marketplace. The others are eliminated because
of efcacy or safety problems or a lack of commercial
interest.
Fast Tracking
To expedite the development and approval of drugs
for the treatment of life-threatening illnesses (e.g.,
acquired immunodeciency syndrome), the FDA
has drafted rules that allow certain INDs to receive
the highest priority for review within the agency.
7
Postmarketing
NDA Review Surveillance
Adverse reaction
reporting
PHASE 4
TREATMENT–USE
Surveys/sampling
testing
Inspections
Range:
2 months to 7 years
Average: 24 months
NDA NDA
submitted approved
This procedure is sometimes known as fast tracking.
Additional rules allow INDs to be used for the treat-
ment of a life-threatening disease in a particular pa-
tient—even if the patient does not t the study proto-
col for the drug—when there is no alternative therapy.
These cases are known as treatment INDs. A potentially
lifesaving drug may be allowed for treatment IND sta-
tus during late phase 2 studies, during phase 3 studies,
or after all clinical studies have been completed but be-
fore marketing approval.
Parallel Tracking
Another mechanism to make INDs available to pa-
tients with life-threatening illnesses is known as parallel
tracking. With this procedure, an IND may be used for
patients who cannot participate in controlled clinical
trials and when there is no satisfactory standard thera-
peutic alternative. Parallel track studies are conducted
along with the principal controlled clinical trials; how-
ever, unlike a controlled study, the parallel track study
does not involve a concurrent control group.
Investigators and patients must realize that there
may be greater uncertainty regarding the risks and ben-
ets of therapy with agents that are in relatively early
stages of testing and development. Parallel tracking is
similar to the treatment IND process but allows for ac-
cess to investigational agents when there is less accumu-
lated evidence of efcacy than required for a treatment
8 UNIT I Applying Pharmacology to Nursing Practice
IND. A drug may be released through the parallel track
mechanism when phase 2 trials have been given ap-
proval to proceed but have not necessarily been started.
NEW DRUG APPLICATION REVIEW
When sufcient data have been collected to demonstrate
that the experimental drug is both safe and effective, the
investigator submits an NDA to the FDA to formally re-
quest approval to market a new drug for human use.
Thousands of pages of NDA data are reviewed by a
team of pharmacologists, toxicologists, chemists, pri-
mary healthcare providers, and others (as appropriate),
who then make a recommendation to the FDA about
whether the drug should be approved for use. The aver-
age NDA review takes 24 months. After a drug is ap-
proved by the FDA, it is the manufacturer’s decision as
to when to bring a product to the marketplace.
POSTMARKETING SURVEILLANCE STAGE
If the manufacturer decides to market the medicine,
the postmarketing surveillance stage begins; this is the
fourth stage of drug product development. This pro-
cess consists of an ongoing review of adverse effects of
the new drug and periodic inspections of the manufac-
turing facilities and the resulting products. Other stud-
ies completed during the fourth stage include identify-
ing other patient populations for whom the drug may
be useful, rening dosing recommendations, and ex-
ploring potential drug interactions.
Clinical Goldmine
Healthcare providers make a signicant contribution to the
knowledge of drug safety by reporting adverse effects to the
FDA using the MedWatch program for the voluntary report-
ing of adverse events and product problems (see Online
Resources).
BLACK BOX WARNING
Although the FDA’s drug approval process is one of
the most stringent in the world, the value of ongoing
safety review of medicines has been demonstrated
through the use of the MedWatch program. If safety
concerns are identied after a drug is approved for
marketing, the FDA can issue black box warnings to
the package insert of the product. When a medica-
tion’s risks and known dangers outweigh its benets,
the FDA and/or the manufacturer may decide that
the product should be withdrawn from the market.
The probability of a drug acquiring a new black box
warning or being withdrawn from the market within 25
years of being released is estimated at 20%. Consequently,
it is the responsibility of all healthcare professionals to
constantly monitor their patients for adverse effects of
drugs and to complete a MedWatch form when adverse
effects are suspected. More than 200,000 MedWatch
forms are led with the FDA annually. Health Canada
has a program for reporting adverse effects (Canada
Vigilance Program: https://www.canada.ca/en/health-
canada/services/drugs-health-products/medeffect-
canada/canada-vigilance-program.html).
From a safety standpoint, prescribers and patients
should be aware that recently marketed medicines
carry a risk of causing unsuspected serious adverse
effects. Even with the high probability that there will
be no serious complications, the devastating—and
sometimes fatal—consequences cannot be ignored.
When choosing medicines for treatment, it becomes
important to consider whether an equally effective
alternative drug is already available. At a minimum,
this reduces the risk of an undiscovered adverse drug
reaction, and it is often less expensive. At a maximum,
the patient, the family, and the prescriber are saved the
anguish of an avoidable adverse drug reaction.
RARE DISEASES AND THE DEVELOPMENT OF
ORPHAN DRUGS
The National Organization for Rare Disorders, which
is a coalition of 140 rare-disease groups, estimates that
more than 6000 rare health conditions exist in about 20
million Americans. Examples of these rare diseases are
cystic brosis, Hansen disease (leprosy), sickle cell ane-
mia, blepharospasm, infant botulism, and Pneumocystis
jiroveci pneumonia (see Online Resources). Historically,
pharmaceutical manufacturers have been reluctant to de-
velop products that could be used to treat these illnesses.
The medicines that are developed for these conditions are
known as orphan drugs because the manufacturers have
been unable to recover the costs of the research on ac-
count of the very limited use of the nal product. Because
no companies were willing to “adopt” the diseases to
complete extensive research to develop products for
treatment, the diseases became known as health orphans.
In 1983 Congress passed the Orphan Drug Act to
stimulate the development and market availability of
products that are used for the treatment of rare diseases.
The act denes the term rare disease as a condition that af-
fects fewer than 200,000 people in the United States. The
FDA’s Ofce of Orphan Products Development (OOPD)
promotes the development of products that demonstrate
promise for the diagnosis or treatment of rare diseases
or conditions. The OOPD interacts with medical and
research communities, professional organizations, aca-
demia, and the pharmaceutical industry, as well as with
rare-disease groups. The OOPD administers the major
provisions of the Orphan Drug Act, which provide incen-
tives for sponsors to develop products for rare diseases.
The law provides research grants, protocol devel-
opment assistance by the FDA, special tax credits for
the cost of clinical trials, and 7 years of exclusive mar-
keting rights after the product has been approved. On
average, an orphan drug receives FDA approval 10
to 11 months sooner than a nonorphan drug. The act
has been quite successful: more than 200 new drugs
have been approved by the FDA for rare diseases,
beneting several million people. Examples include
ALGrawany
 Drug Denitions, Standards, and Information Sources CHAPTER 1
pentamidine and atovaquone for Pneumocystis jiroveci
pneumonia, thalidomide for Hansen disease, zidovu-
dine for the human immunodeciency virus, dornase
alfa (Pulmozyme) for cystic brosis, and cladribine
(Leustatin) for hairy cell leukemia.
DRUG NAMES, STANDARDS, AND
LEGISLATION IN CANADA
CANADIAN DRUG NAMES
OFFICIAL DRUG
The term ofcial drug pertains to any drug for which a
standard is described specically in the Food and Drug
Regulations or in any publication named in the Food
and Drugs Act as being satisfactory for ofcially meet-
ing the standards for drugs in Canada.
CHEMICAL NAME
The chemical name is most meaningful to the chemist.
By means of the chemical name the chemist under-
stands the exact chemical constitution of the drug and
exact placing of its atoms or molecular groupings. The
chemical name is the same in both Canada and the
United States.
PROPER NAME OR GENERIC NAME
The proper name is the nonproprietary (generic) name,
which is used to identify an ofcial drug in Canada.
The generic name is the same in both Canada and the
United States.
BRAND NAME
The brand name (or proprietary name) is the name as-
signed to the drug by its manufacturer to distinguish
the drug for advertisement and sale. Brand names for
the same generic drug product are frequently different
between Canada and the United States. The following
example and Fig. 1.3 depict the application of termi-
nology to drug nomenclature.
Example of Canadian Drug Names
Chemical name: 4-dimethylamino-1,4,4a,5,5a,6,11,12a-
octahydro-3,6,10,12,12a-pentahydroxy-6-methyl-
1,11,dioxo-2-napthacene carboxamide (see Fig. 1.3)
Proper name: tetracycline
Ofcial name: Tetracycline, USP
Brand names: Apo-Tetra; Nu-Tetra
O
OH O OH O
OH
C tion is meant to ensure the following: (1) that patients
2 NH2
7 6 5 diabetes mellitus, angina); and (2) that patients are ed-
OH
H3C
OH N
H3C CH3
Fig. 1.3 Tetracycline, an antibiotic.
9
SOURCES OF CANADIAN DRUG STANDARDS
The Food and Drugs Act recognizes the standards de-
scribed by international authoritative books as being
acceptable for ofcial drugs in Canada (see Table 1.2).
CANADIAN DRUG LEGISLATION
FOOD AND DRUGS ACT AND REGULATIONS
The Food and Drugs Act (1927) and Regulations (1953,
1954, 1979) empower Health Canada to protect the pub-
lic from foreseeable risks related to the manufacture and
sale of drugs, cosmetics, food, and therapeutic devices.
The legislation provides for a review of the safety and
efcacy of drugs before their clearance for marketing
in Canada and determines whether the medicine is pre-
scription or nonprescription. Also included in this legisla-
tion are requirements for good manufacturing practices,
adequate labeling, and fair advertising.
In Canada (as in the United States), an effort has
been made to align the provincial drug schedules so
that the conditions for the sale of medicines are con-
sistent across Canada. The National Association of
Pharmacy Regulatory Authorities (NAPRA) governs
national drug schedules but each province’s regulatory
body can regulate how a particular drug can be sold-
sold/dispensed. The National Association of Pharmacy
Regulatory Authorities (NAPRA) proposed a new na-
tional drug scheduling model. This model is in various
stages of implementation across the provinces and ter-
ritories of Canada. With the use of this model, all medi-
cines in Canada are assigned to one of four categories:
Schedule I: All prescription drugs, including narcotics
Schedule II: Restricted-access nonprescription drugs
Schedule III: Pharmacy-only nonprescription drugs
Unscheduled: Drugs that are not assigned to the previ-
ous categories
Schedule II drugs are available for sale directly
from the pharmacist and are kept “behind the coun-
ter.” Examples include insulin, pseudoephedrine, glu-
cagon, loperamide (for children younger than age 12
years), and nitroglycerin sublingual spray and tablets
(other dosage forms are Schedule I). These medica-
tions are in two categories: (1) those that patients may
require urgently and cannot delay taking until after an
appointment with a prescriber (e.g., insulin, nitroglyc-
erin, glucagon); and (2) those that require appropriate
counseling to avoid improper use (e.g., loperamide,
pseudoephedrine). Placement with a pharmacist does
not allow for patient self-selection and allows for phar-
macist intervention for these medications. This restric-
are not self-diagnosing medically serious diseases (e.g.,
ucated about the proper use of these drugs through ap-
propriate counseling from the pharmacist.
Schedule III drugs are pharmacy-only non-
prescription drugs. These medicines can be sold only
10 UNIT I Applying Pharmacology to Nursing Practice
through pharmacies and include levonorgestrel emer-
gency contraception, diphenhydramine, child prepara-
tions of antihistamines, and the low-dose histamine-2
antagonists. It is expected that if patients have ques-
tions, they could easily consult with a pharmacist.
Medicines that are not categorized in Schedule I, II,
or III are considered to be “unscheduled” (e.g., nico-
tine gum and patches, acetylsalicylic acid, lower-dose
ibuprofen, some lower-dosage “cough and cold” prep-
arations) and can be sold at any retail outlet. Adequate
information is available for the patient to make a safe
and effective choice, and labeling is sufcient to ensure
the appropriate use of the drug without professional
supervision.
Drugs requiring a prescription—except for controlled
drugs—are listed on Schedule F of the Food and Drug
Regulations. Schedule F drugs may be prescribed only
by qualied healthcare providers because they would
normally be used most safely under supervision. Most
antibiotics, antineoplastics, corticosteroids, cardiovas-
cular drugs, and antipsychotics are Schedule F drugs.
CONTROLLED DRUGS AND SUBSTANCES ACT
The Controlled Drugs and Substances Act (1997) estab-
lished the requirements for the import, production,
export, distribution, and possession of substances
classied as narcotics and substances of abuse in
Canada. The Controlled Drugs and Substances Act
describes eight schedules of controlled substances.
Assignment to a schedule is based on the potential
for abuse and the ease with which illicit substances
can be manufactured in illegal laboratories. The de-
gree of control; the conditions of record keeping; as-
signment of penalties for possession, trafcking, and
manufacturing; and other regulations depend on
these classications. (Note that Schedules I, II, and
III under the US Food and Drugs Act as described
earlier are different from Schedules I through VIII of
the Canadian Controlled Drugs and Substances Act).
Examples of controlled substances schedule assign-
ment are as follows:
Schedule I: Opium poppy and its derivatives (e.g.,
heroin, morphine); coca and its derivatives (e.g., co-
caine), pethidine (meperidine), methadone, fentanyl
Schedule II: Cannabis
Schedule III: Amphetamines, methylphenidate, lyser-
gic acid diethylamide (LSD), methaqualone, psilo-
cybin, mescaline
Schedule IV: Sedative-hypnotic agents (e.g., barbi-
turates, benzodiazepines); butorphanol, anabolic
steroids
Schedule V: Propylhexedrine, phenylpropanolamine,
pyrovalerone
Schedule VI: Part I class A precursors (e.g., ephedrine,
pseudoephedrine, norephedrine [phenylpropanol-
amine], ergotamine) and part II precursors (e.g., ac-
etone, ethyl ether, hydrochloric acid, sulfuric acid,
toluene)
Schedule VII: Cannabis resin (3 kg); cannabis (mari-
juana) (3 kg) (must be read in conjunction with
Schedule II)
Schedule VIII: Cannabis resin (1 g); cannabis (mari-
juana) (30 g) (must be read in conjunction with
Schedule II)
The Controlled Drugs and Substances Act and
accompanying regulations provide for the non-
prescription sale of certain codeine preparations (e.g.,
Tylenol No. 1 with codeine, Benylin with codeine). The
content must not exceed the equivalent of 8 mg of co-
deine phosphate per solid dosage unit or 20 mg per 30
mL of a liquid preparation, and the preparation must
also contain two additional nonnarcotic medicinal in-
gredients. These preparations may not be advertised
or displayed, and they may be sold only by pharma-
cists (see previous discussion of Schedule II drugs). In
hospitals, the pharmacy usually requires strict inven-
tory control of these products and other narcotics.
Requirements for the legitimate administration of
drugs to patients by nurses are generally similar in
Canada and the United States. Individual hospital pol-
icy determines specic record-keeping requirements
on the basis of federal and provincial laws. Violations
of these laws will result in nes or imprisonment in ad-
dition to the loss of professional licensing.
NONPRESCRIPTION DRUGS
The NAPRA drug schedules list three categories of
nonprescription drugs: Schedule II, Schedule III, and
unscheduled drugs (see discussion under Food and
Drugs Act and Regulations).
 Drug Denitions, Standards, and Information Sources CHAPTER 1
Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions
Key Points
• In the classication system used in the United States, each
drug has three names: a chemical name, a generic name,
and a brand name. The chemical name is most meaningful
to the chemist. The generic name is simpler than the
chemical name. The rst letter of the generic name is
not capitalized. The brand names are selected by the
manufacturer and deliberately made easier to pronounce,
spell, and remember. A brand name is followed by the
symbol ®. The rst letter of the brand name is capitalized.
• Drugs may be classied by a variety of methods
according to the body system that they affect (e.g., the
central nervous system, the cardiovascular system, the
gastrointestinal system); their therapeutic use or clinical
indications (e.g., antacids, antibiotics, antihypertensives,
diuretics, laxatives); and their physiologic or chemical
action (e.g., anticholinergic agents, beta-adrenergic
blockers, calcium channel blockers, cholinergic agents).
• Table 1.2 lists and describes the common sources of drug
information available for the healthcare provider.
• Prescription drugs require an order by a healthcare
provider who is licensed to prescribe drugs, such as
a primary healthcare provider, a nurse practitioner,
a physician assistant, a pharmacist, or a dentist.
Nonprescription or over-the-counter (OTC) drugs are
sold without a prescription in a pharmacy or in the health
section of department or grocery stores.
• Rules and regulations evolved by the FDA divide new
drug development into four stages: (1) preclinical research
and development; (2) clinical research and development;
(3) new drug application review; and (4) postmarketing
surveillance (see Fig. 1.2).
• In Canada, the proper name is the nonproprietary (generic)
name, which is used to identify an ofcial drug. The generic
name is the same in both Canada and the United States.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Cla
yton) for additional online resources.
Online Resources
• DailyMed: https://dailymed.nlm.nih.gov/dailymed/index.
cfm
• ePocrates: http://www.epocrates.com/
• iPharmacy: https://itunes.apple.com/us/app/ipharm
acy-drug-guide-pubmed-direct/id378721295
• Lexicomp: http://www.wolterskluwercdi.com/lexic
omp-online/
• MedicinesComplete: https://about.medicinescomplete.
com/#/
ALGrawany
11
• MedWatch: https://www.fda.gov/Safety/MedWatch/default
.htm
• National Organization for Rare Disorders (NORD): https://ra
rediseases.org/
• UpToDate: https://www.uptodate.com/home
• US National Library of Medicine: https://www.nlm.nih.gov/
Online Resources for Canadian Practitioners
• Controlled Substances and Drugs Act (Justice Laws
Website): http://laws-lois.justice.gc.ca/eng/acts/c-38.8/
• Drug Product Database:
https://www.canada.ca/en/health-canada/services/drugs-
health-products/drug-products/drug-product-
database.html
• National Association of Pharmacy Regulatory Authorities
(NAPRA) proposal for drug schedule outlines:
http://napra.ca/national-drug-schedules
Clinical Judgment and Next-Generation NCLEX ®
Examination-Style Questionsn
The National Council of State Boards of Nursing (NCSBN) is
the body that develops and administers the NCLEX (National
Council Licensure Exam). Recent studies indicate that gradu-
ates need to develop the skill of clinical decision making, so
the NCLEX examination is changing with different types of
questions that are designed to develop clinical judgment in
patient situations. These type of questions are referred to as
Next Generation NCLEX or NGN. The following questions are
typical of the NCLEX examination and include both NGN (Next
Generation) and traditional questions. Within each chapter the
NCLEX section will identify the objective associated with it, the
type of NCLEX question that will be used, and the cognitive
skill associated with the item type. Six essential cognitive skills
of clinical judgment are being tested: recognize cues; analyze
cues; prioritize hypotheses; generate solutions; take action;
and evaluate outcomes. These six clinical judgment skills build
on and expand the nursing process (NCSBN, 2019).
TRADITIONAL NCLEX-TYPE NGN-TYPE QUESTIONS
QUESTIONS
Multiple Choice Test Item •  Enhanced Hot Spot Test
Item
Multiple Response Test Item •  Cloze Test Item
•  Extended Multiple
Ordering Test Item Response Test Item
•  Extended Drag and
Drop Test Item
•  Matrix Text Item
1. A patient has received a prescription from his primary care
provider for the drug metoprolol (Lopressor). He asks the nurse
why there are two names for the same drug. The nurse responds
with which statements(s)? (Select all that apply.)
1. “One of the names is the brand name of the drug, and
the other is the generic name.”
12 UNIT I Applying Pharmacology to Nursing Practice
2. “When drugs are discovered, all drugs are given a
detailed chemical name and a simple generic name. If
the company that discovered the drug brings it to the
marketplace for sale, the manufacturer will give it a
distinctive brand name.”
3. “Lopressor is the generic name, and metoprolol is the
brand name.”
4. “The two names are used to determine whether the drug
is a Schedule III or a Schedule IV drug.”
5. “Generally, the generic product of the drug is less
expensive than the brand name product.”
Objective: Differentiate between the chemical, generic, and brand
names of drugs.
NCLEX test item: Multiple response
Cognitive skill: Application
2. Drugs can be classied using various methods; identify the
different classication and examples as indicated.
Choose the most likely option for the information missing
from the statements below by selecting from the list of op-
tions provided.
Medications such as _________1_____________ are
classied by the _________2____________ method, whereas
medications such as ________1__________ are classied by
the _______2__________ method.
OPTIONS FOR 1 OPTIONS FOR 2
antacids body systems
antibiotics chemical action
calcium channel blockers clinical indication
Diuretics
Cholinergics
Objective: Identify the various methods used to classify drugs.
NGN test item: Cloze
Cognitive skill: Analyze cues
3. A young mother with a 2-month-old infant tells the nurse that she
is concerned about the use of any medications because she is
breastfeeding her baby. The nurse reviews the possible information
sources to discuss with the mother.
Indicate with an X in the “recommended by the nurse” column the
source of drug information listed in the left column the nurse can
recommend for the mother to use. Note that not all drug information
sources will be used.
DRUG INFORMATION SOURCE RECOMMENDED BY THE NURSE
Nursing journals
Electronic databases
Package inserts
Natural medicines database
Objective: Identify sources of drug information available for
healthcare providers.
NGN test item: Extended drag and drop
Cognitive skill: Take action
4. The nurse knows which of these factors are the differences
between prescription and nonprescription drugs? (Select all that
apply.)
1. Nonprescription drugs are available over-the-counter.
2. Prescription drugs are those drugs that may be
prescribed by dentists, pharmacists, nurse practitioners,
and primary healthcare providers.
3. Recreational drugs are available by prescription only.
4. Over-the-counter drugs are available at a pharmacy or
health section of grocery stores.
5. Prescription drugs have been approved for use by the
FDA.
Objective: Discuss the difference between prescription and
nonprescription drugs.
NCLEX test item: Multiple response
Cognitive skill: Application
5. During which stage of the process of new drug development does
testing on humans start?
1. The preclinical research and development stage
2. The postmarketing surveillance stage
3. The postclinical research and development stage
4. The clinical research and development stage
Objective: Describe the process of developing and bringing new
drugs to market.
NCLEX test item: Multiple choice
Cognitive skill: Knowledge
6. A nurse is teaching a patient from Canada the names of her
medications and reviews the differences between Canadian
names. Which statement indicates that the patient understands
the instructions?
1. “The proper name of the medication is the same as the
brand name in Canada.”
2. “The proper name of the medication is the same as the
generic name in Canada.”
3. “The chemical name is the one used the most when
buying medications in Canada.”
4. “The chemical names and the brand names are the only
names used in Canada.”
Objective: Differentiate between the Canadian chemical name and
the proper name of a drug.
NCLEX test item: Multiple choice
Cognitive skill: Evaluation
Basic Principles of Drug Action and Drug
Interactions
2
https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify common drug administration routes.
2. Identify the meaning and signicance of the term half-life
when used in relation to drug therapy.
3. Describe the process of how a drug is metabolized in the
body.
4. Compare and contrast the following terms that are used
in relationship to medications: desired action, common
adverse effects, serious adverse effects, allergic reactions,
and idiosyncratic reactions.
5. Identify what is meant by a drug interaction.
6. Differentiate among the terms additive effect, synergistic
effect, antagonistic effect, displacement, interference, and
incompatibility.
7. Identify one way in which alternatives in metabolism create
drug interactions.

Key Terms
receptors (rē-SĔP-tĕrz) (p. 13)
pharmacodynamics (făr-mă-kō-dī-
NĂM-ĭks) (p. 13)
agonists (ĂG-ŏ-nĭsts) (p. 13)
antagonists (ăn-TĂG-ŏ-nĭsts) (p. 13)
partial agonists (PĂR-shŭl ĂG-ŏ-nĭsts)
(p. 13)
enteral (ĔN-tĕr-ăl) (p. 14)
parenteral (pă-RĔN-tĕr-ăl) (p. 14)
percutaneous (pĕr-kū-TĀ-nē-ŭs)
(p. 14)
pharmacokinetics (făr-mă-kō-kĭ-NĔT-
ĭks) (p. 14)
absorption (ăb-SŎRP-shŭn) (p. 14)
distribution (dĭs-trĭ-BŪ-shŭn) (p. 15)
drug blood level (p. 15)
metabolism (mĕ-TĂB-ō-lĭz-ĕm)
(p. 15)
excretion (ĕks-KRĒ-shŭn) (p. 15)
half-life (p. 16)
onset of action (p. 17)
peak action (p. 17)
duration of action (p. 17)
desired action (p. 17)
side effects (p. 17)
common adverse effects (ĂD-vŭrs
ĕ-FĔKTS) (p. 17)
serious adverse effects (p. 17)
idiosyncratic reaction (ĭd-ē-ō-sĭn-
KRĂT-ĭk rē-ĂK-shŭn) (p. 18)
allergic reactions (ă-LŬR-jĭk) (p. 18)
drug interaction (p. 18)
unbound drug (ŭn-BŎWND) (p. 18)
additive effect (ĂD-ĭ-tĭv) (p. 19)
synergistic effect (sĭn-ĕr-JĬS-tĭk)
(p. 19)
antagonistic effect (ăn-tăg-ŏ-NĬST-ĭk)
(p. 19)
displacement (dĭs-PLĀS-měnt)
(p. 19)
interference (ĭn-tŭr-FĒR-ĕns) (p. 19)
incompatibility (ĭn-kŏm-păt-ĭ-BĬL-ĭ-tē)
(p. 19)

BASIC PRINCIPLES RELATED TO DRUG THERAPY
DRUG RESPONSES IN THE BODY
When administered to the body, drugs do not create
new responses but rather alter existing physiologic ac-
tivity in several different ways. Usually the drug forms
chemical bonds with specic sites, called receptors,
within the body. This bond forms only if the drug and
its receptor have similar shapes and if the drug has a
chemical afnity for the receptor. The relationship
between a drug and a receptor is similar to that seen
between a key and lock (Fig. 2.1A). The study of the
interactions between drugs and their receptors and the
series of events that result in a pharmacologic response
is called pharmacodynamics Most drugs have several
different atoms within each molecule that interlock
into various locations on a receptor. The better the t
between the receptor and the drug molecule, the better
the response from the drug. The intensity of a drug re-
sponse is related to how well the drug molecule ts
into the receptor and to the number of receptor sites
that are occupied. Drugs that interact with a receptor
to stimulate a response are known as agonists (Fig.
2.1B). Drugs that attach to a receptor but do not stimu-
late a response are called antagonists (Fig. 2.1C). Drugs
that interact with a receptor to stimulate a response but
inhibit other responses are called partial agonists (Fig.
2.1D).
Drug response must be stated in relation to the
physiologic activity expected in response to the drug
therapy (e.g., an antihypertensive agent is successful if
the patient’s blood pressure is lower after receiving the
drug than it was before the drug was started). Therefore
it is important to perform a thorough nursing assess-
ment to identify the baseline data. After that is done,
results from regular assessments can be compared
13
14 UNIT I Applying Pharmacology to Nursing Practice

Receptor characteristics. The study of the mathematical relation-

ships among the ADME features of individual medi-
cines over time is called pharmacokinetics

Liberation
Drug Regardless of the route of administration, a drug must
be released from the dosage form (i.e., liberated) and
A B C D dissolved in body uids before it can be absorbed into
Fig. 2.1 (A) Drugs act by forming chemical bonds with specic body tissues. For example, before a solid drug that is
receptor sites, similar to a key and lock. The better the t, the better taken orally can be absorbed into the bloodstream for
the response. (B) Drugs with complete attachment and response are transport to the site of action, the dosage form (usu-
called agonists. (C) Drugs that attach but do not elicit a response are
ally a capsule or tablet) must disintegrate and the ac-
called antagonists. (D) Drugs that attach and elicit a small response but
also block other responses are called partial agonists. tive drug must dissolve in the GI uids so that it can
be transported across the stomach or intestinal lining
into the blood. The process of converting the drug
into a form that will activate a response can be par-
Table 2.1 Drug Therapy Used in Disease Management a
tially controlled by the pharmaceutical dosage form
CLASSIFICATION OF THE DRUGS used (e.g., solution, suspension, capsule, tablet [with
DISEASES/ILLNESSES USED
various coatings]). This conversion process can also be
Cancer Chemotherapy, immunotherapy inuenced by administering the drug with or without
Mental illness Antidepressants and water or food in the patient’s stomach.
antipsychotic agents
Hypertension Antihypertensive agents Absorption
Diabetes Antidiabetic agents Absorption is the process whereby a drug is transferred
Infections Antimicrobial agents from its site of entry into the body to the circulating
Inammatory diseases Antiinammatory agents
uids of the body (i.e., blood and lymph) for distribu-
tion around the body. The rate at which this occurs de-
Nausea and vomiting Antiemetic agents
pends on the route of administration, the blood ow
Constipation Laxatives through the tissue where the drug is administered, and
Diarrhea Antidiarrheal agents the solubility of the drug. It is therefore important to
GERD Antacids do the following: (1) administer oral drugs with an ad-
aList
equate amount of uid (usually a large [8-ounce] glass
is not inclusive.
GERD, Gastroesophageal reux disease. of water); (2) give parenteral forms properly so that
they are deposited in the correct tissue for enhanced
with the baseline data by the primary healthcare pro- absorption; and (3) reconstitute and dilute drugs only
vider, the nurse, and the pharmacist to evaluate the ef- with the diluent recommended by the manufacturer
fectiveness of the drug therapy. Table 2.1 lists examples in the package literature so that drug solubility is not
of drug therapies and their related diseases. impaired. Equally important are nursing assessments
that reveal poor absorption (e.g., if insulin is admin-
ROUTES OF DRUG ADMINISTRATION istered subcutaneously and a lump remains at the site
The most common routes of drug administration are of injection 2 to 3 hours later, absorption from that site
the enteral, parenteral, and percutaneous routes. When may be impaired).
using the enteral route, the drug is administered direct- The rate of absorption when a drug is administered
ly into the gastrointestinal (GI) tract by the oral, rectal, by a parenteral route depends on the rate of blood ow
or nasogastric route. The parenteral route bypasses the through the tissues. Circulation or blood ow must be
GI tract with the use of subcutaneous (subcut), intra- determined before the administration of drugs by the
muscular (IM), or intravenous (IV) injection. The percu- parenteral route to identify any circulatory insufcien-
taneous route involves drugs being absorbed through cy. If any such insufciency is noted, injections will
the skin and mucous membranes. Methods of the per- not be absorbed properly, and the drug will not be ef-
cutaneous route include inhalation, sublingual (under fective. Subcut injections have the slowest absorption
the tongue), and topical (on the skin) administration. rate, especially if peripheral circulation is impaired. IM
injections are more rapidly absorbed because of greater
LIBERATION, ABSORPTION, DISTRIBUTION, blood ow per unit weight of muscle compared with
METABOLISM, AND EXCRETION subcut tissue. Cooling the area of injection slows the
After they have been administered, all drugs go through rate of absorption, whereas heat or massage hastens
ve stages: liberation, absorption, distribution, metab- the rate of absorption. Drugs are dispersed throughout
olism, and excretion (LADME). After liberation from the body most rapidly when they are administered by
the dosage form, each drug has its own unique ADME IV injection. The nurse must be thoroughly educated
 Basic Principles of Drug Action and Drug Interactions CHAPTER 2
regarding the responsibilities and techniques associ-
ated with administering IV medications. It is impor-
tant to remember that after a drug enters the patient’s
bloodstream, it cannot be retrieved.
The absorption of topical drugs that have been ap-
plied to the skin can be inuenced by the drug con-
centration, the length of contact time, the size of the
affected area, the thickness of the skin surface, the
hydration of the tissue, and the degree of skin disrup-
tion. Percutaneous (i.e., across-the-skin) absorption
is greatly increased in newborns and young infants,
who have thin, well-hydrated skin. When drugs are in-
haled, their absorption can be inuenced by the depth
of the patient’s respirations, the neness of the droplet
particles, the available surface area of the patient’s mu-
cous membranes, the contact time, the hydration state,
the blood supply to the area, and the concentration of
the drug itself.
Distribution
The term distribution refers to the ways in which a drug
is transported throughout the body by the circulating
body uids to the sites of action or to the receptors that
the drug affects. Drug distribution refers to the transport
of the drug throughout the entire body by the blood
and lymphatic systems and the transport from the cir-
culating uids into and out of the uids that bathe the
receptor sites. Organs with the most extensive blood
supplies (e.g., heart, liver, kidneys, brain) receive the
distributed drug most rapidly. Areas with less exten-
sive blood supplies (e.g., muscle, skin, fat) receive the
drug more slowly.
After a drug has been dissolved and absorbed into
the circulating blood, its distribution is determined by
the chemical properties of the drug and how it is affect-
ed by the blood and tissues that it contacts. Two factors
that inuence drug distribution are protein binding
and lipid (fat) solubility. Most drugs are transported
in combination with plasma proteins (especially al-
bumin), which act as carriers for relatively insoluble
drugs. Drugs that are bound to plasma proteins are
pharmacologically inactive because the large size of
the complex keeps them in the bloodstream and pre-
vents them from reaching the sites of action, metabo-
lism, and excretion. Only the free, or unbound, portion
of a drug is able to diffuse into tissues, interact with re-
ceptors, and produce physiologic effects; it is also only
this portion that can be metabolized and excreted. The
same proportions of bound and free drug are main-
tained in the blood at all times. Thus as the free drug
acts on receptor sites or is metabolized, the decrease in
the serum drug level causes some of the bound drug to
be released from protein to maintain the ratio between
bound and free drug.
When a drug leaves the bloodstream, it may be-
come bound to tissues other than those with active
receptor sites. The more lipid-soluble drugs have
a high afnity for adipose tissue, which serves as a
15
repository site for these agents. Because there is a
relatively low level of blood circulation to fat tissues,
the more lipid-soluble drugs tend to stay in the body
much longer. Equilibrium is established between the
repository site (i.e., lipid tissue) and the circulation so
that as the drug blood level drops as a result of bind-
ing at the sites of physiologic activity, metabolism, or
excretion, more drug is released from the lipid tissue.
By contrast, if more drug is given, a new equilibrium
is established among the blood, the receptor sites, the
lipid tissue repository sites, and the metabolic and ex-
cretory sites.
Distribution may be general or selective. Some
drugs cannot pass through certain types of cell mem-
branes, such as the blood-brain barrier (i.e., the cen-
tral nervous system) or the placental barrier (i.e., the
placenta), whereas other types of drugs readily pass
into these tissues. The distribution process is very im-
portant because the amount of drug that actually gets
to the receptor sites determines the extent of pharma-
cologic activity. If little of the drug actually reaches
and binds to the receptor sites, the response will be
minimal.
Metabolism
Metabolism is the process whereby the body inacti-
vates drugs. The enzyme systems of the liver are the
primary sites for the metabolism of drugs, but other
tissues and organs (e.g., white blood cells, GI tract,
lungs) metabolize certain drugs to a minor extent.
Genetic, environmental, and physiologic factors are
involved in the regulation of drug metabolism reac-
tions. The most important factors for the conversion
of drugs to their metabolites are genetic variations of
enzyme systems, the concurrent use of other drugs,
exposure to environmental pollutants, concur-
rent illnesses, and age. (For more information, see
Chapter 3.)
Excretion
The elimination of drug metabolites and, in some cases,
of the active drug itself from the body is called excre-
tion. The two primary routes of excretion are through
the GI tract into the feces and through the renal tubules
into the urine. Other routes of excretion include evapo-
ration through the skin, exhalation from the lungs, and
secretion into saliva and breast milk.
Because the kidneys are major organs of drug excre-
tion, the nurse should review the patient’s chart for the
results of urinalysis and renal function tests. A patient
with renal failure often has an increase in the action
and duration of a drug if the dosage and frequency of
administration are not adjusted to allow for the pa-
tient’s reduced renal function.
Fig. 2.2 shows a schematic review of the ADME pro-
cess of an oral medication. It is important to note how
little of the active ingredient actually reaches the recep-
tor sites for action.
16 UNIT I Applying Pharmacology to Nursing Practice

Capsule dissolved
by GI fluids (Some is
lost by degradation) Undissolved capsule
taken orally

Drug in solution in intestines

(Some is absorbed; some is
lost to degradation or by
binding to intestinal
contents and excreted)

Drug absorbed by
intestines and goes
to the liver (Some is
lost by secretion
into bile; some is lost
by biotransformation;
some is bound to tissue
and becomes inactive)

Drug reaches general circulation Drug is distributed to the entire body

(Some is lost by biotransformation; (Some is lost by biotransformation and excretion;
some is bound to plasma protein and some is distributed to other tissues and organs;
becomes inactive) some reaches receptor sites, triggering a
pharmacologic response)
Fig. 2.2 Factors that modify the quantity of drug that reaches a site of action after a single oral dose. GI, Gastrointestinal.

HALF-LIFE The half-life is determined by an individual’s

Drugs are eliminated from the body by means of me- ability to metabolize and excrete a particular drug.
tabolism and excretion. A measure of the time required Because most patients metabolize and excrete a par-
for elimination is the half-life. The half-life is dened as ticular drug at approximately the same rate, the ap-
the amount of time required for 50% of the drug to be proximate half-lives of most drugs are now known.
eliminated from the body. For example, if a patient is When the half-life of a drug is known, dosages and
given 100 mg of a drug that has a half-life of 12 hours, frequency of administration can be calculated. Drugs
the following would be observed: with long half-lives (e.g., digoxin, with a half-life of
36 hours) need to be administered only once daily,
DRUG REMAINING IN whereas drugs with short half-lives (e.g., aspirin, with
TIME (HOURS) HALF-LIFE BODY (%) a half-life of 5 hours) need to be administered every
0 — 100 mg (100) 4 to 6 hours to maintain therapeutic activity. For pa-
12 1 50 mg (50) tients who have impaired hepatic or renal function,
24 2 25 mg (25) the half-life may become considerably longer because
36 3 12.5 mg (12.5)
of their reduced ability to metabolize or excrete the
48 4 6.25 mg (6.25)
drug. For example, digoxin has a half-life of about 36
60 5 3.12 mg (3.12)
hours in a patient with normal renal function; how-
Note that as each 12-hour period (i.e., one half-life) ever, it has a half-life of about 105 hours in a patient
passes, the amount remaining is 50% of what was there with complete renal failure. Monitoring diagnostic
12 hours earlier. After six half-lives, more than 98% of tests that measure renal or hepatic function is impor-
the drug has been eliminated from the body. tant. Whenever laboratory data reect impairment of

ALGrawany
 Basic Principles of Drug Action and Drug Interactions CHAPTER 2
Toxicity
Supratherapeutic
Drug concentration
MDR (peak)
Desired
therapeutic range
Intensity
MEC
Duration
of action
Subtherapeutic
Onset Termination
Time
Fig. 2.3 A time-response curve, which is also known as a drug
concentration–time prole, demonstrates the relationship between
the administration of a drug and the patient’s response. If the drug
level does not reach the minimum effective concentration (MEC), there
will be no pharmacologic effect. If the peak level exceeds the toxicity
threshold, toxic effects will result. The optimal drug concentration is in
the middle of the therapeutic range. MDR, Maximum drug response
(peak effect).
either function, the nurse should notify the healthcare
provider.
DRUG ACTIONS
All drug actions have an onset, peak, and duration of
action. The onset of action is when the concentration of
a drug at the site of action is sufcient to start a physi-
ologic (pharmacologic) response. Many factors—such
as the route of administration and the rates of absorp-
tion, distribution, and binding to receptor sites—affect
the onset of action. In general, increasing the dose of the
drug hastens the onset of action by shortening the time
required to achieve the necessary concentration of drug
at the target site. Peak action is the time at which the
drug reaches the highest concentrations on the target
receptor sites, thereby inducing the maximal pharma-
cologic response for the dose given. The duration of ac-
tion is how long the drug has a pharmacologic effect.
The onset, peak, and duration of action of a drug are
often illustrated by a time-response curve, which is also
known as a drug concentration–time prole (Fig. 2.3). A
time-response curve demonstrates the relationship be-
tween the administration of a drug and the associated
response. If the drug level does not reach the minimum
effective concentration, there will be no pharmacologic
effect. If the peak level exceeds the toxicity threshold,
toxic effects will result. Generally, the drug concentra-
tion is targeted to be in the middle of this range, between
the minimum effective response and the toxic response;
this is referred to as the therapeutic range.
DRUG BLOOD LEVEL
When a drug is circulating in the blood, a blood sample
may be drawn and assayed to determine the amount of
17
drug present. This is known as a drug blood level. It is im-
portant for certain drugs (e.g., anticonvulsants, amino-
glycoside antibiotics) to be measured to ensure that the
drug blood level is within the therapeutic range. If the
drug blood level is low, the dosage must be increased,
or the medicine must be administered more frequently.
If the drug blood level is too high, the patient may de-
velop signs of toxicity; in this case, the dosage must be
reduced or the medicine administered less frequently.
ADVERSE EFFECTS OF DRUGS
No drug has a single action. When a drug enters a patient
and is then absorbed and distributed, the desired action
(i.e., the expected response) usually occurs. However, all
drugs have the potential to affect more than one body
system simultaneously, thereby producing responses
that are known as side effects or common adverse effects,
which are mild, or serious adverse effects, which can lead
to toxicity. The World Health Organization’s denition of
an adverse drug reaction (ADR) is “any noxious, unin-
tended, and undesired effect of a drug, which occurs at
dosages used in humans for prophylaxis, diagnosis, or
therapy.” A more common denition is as follows: “Right
drug, right dose, right patient, bad effect.” ADRs should
not be confused with medication errors or adverse drug
events (ADEs), which are dened as “an injury resulting
from medical intervention related to a drug.” (For more
information, see Chapter 6.)
Recent studies have indicated the following:
• ADRs may be responsible for more than 100,000
deaths among hospitalized patients per year, which
makes them one of the top six leading causes of
death in the United States.
• An average of 6% of hospitalized patients experi-
ence a signicant ADR at some point during their
hospitalizations.
• Between 5% and 9% of hospitalization costs are at-
tributable to ADRs.
• The most commonly seen ADRs are rash, nau-
sea, itching, thrombocytopenia, vomiting, hyper-
glycemia, and diarrhea.
• The classes of medicines that account for the larg-
est number of ADRs are antibiotics, cardiovascular
medicines, cancer chemotherapy agents, analgesics,
and antiinammatory agents.
Most ADEs are predictable because of the pharmaco-
logic effects of a drug, and patients should be monitored
so that dosages can be adjusted to allow for the maximum
therapeutic benets with a minimum of adverse effects.
As described in Units III through X of this text, each drug
has a series of parameters (e.g., therapeutic actions to
expect, adverse effects, probable drug interactions) that
should be monitored by the nurse, primary healthcare
provider, pharmacist, and patient to optimize therapy
while reducing the possibility of serious adverse effects.
Accurate and appropriate drug-drug interaction in-
formation must be available to prescribers, and contin-
ual attention is currently focused on this issue. Further
18 UNIT I Applying Pharmacology to Nursing Practice
population-based studies still need to be conducted to
meet federal initiatives to promote the meaningful use
of information technologies and to integrate knowl-
edge databases with clinical decision systems. Ideally,
clinical decision systems and the databases of drug in-
teractions that interface with them help the prescriber
to identify and avoid potential medication interactions.
All hospitals have internal mechanisms for report-
ing suspected ADRs, and healthcare providers should
not hesitate to report possible reactions. By monitor-
ing and tracking the occurrences of ADRs, clinical
protocols and improved patient screening will reduce
the frequency of recurrence. The US Food and Drug
Administration’s MedWatch program is also available
for the voluntary reporting of adverse events. (For
more information, see MedWatch on Evolve.)
Idiosyncratic Reaction
Two other types of drug actions are much more unpre-
dictable: idiosyncratic reactions and allergic reactions. An
idiosyncratic reaction occurs when something unusual or
abnormal happens when a drug is rst administered. The
patient usually demonstrates an unexpectedly strong re-
sponse to the action of the drug. This type of reaction is
generally the result of a patient’s inability to metabolize a
drug because of a genetic deciency of certain enzymes.
Fortunately, this type of reaction is rare.
Allergic Reaction
Allergic reactions, which are also known as hypersensitivity
reactions, occur in about 6% to 10% of patients who are
taking medications. Allergic reactions occur among pa-
tients who have previously been exposed to a drug and
whose immune systems have developed antibodies to
the drug. On reexposure to the drug, the antibodies cause
a reaction; this reaction is most commonly seen as raised,
irregularly shaped patches on the skin known as hives,
which cause severe itching, known as urticaria.
Occasionally, a patient has a severe, life-threatening re-
action that causes respiratory distress and cardiovascular
collapse; this is known as an anaphylactic reaction. This
condition is a medical emergency, and it must be treated
immediately. Fortunately, anaphylactic reactions occur
much less often than the more mild urticarial reactions.
If a patient has a mild reaction, it should be under-
stood as a warning to not take the medication again. The
patient is much more likely to have an anaphylactic re-
action during their next exposure to the drug. Patients
should receive information about the drug name and
be instructed to tell healthcare providers that they have
had such reactions and that they must not receive the
drug again. In addition, patients should wear a medical
alert bracelet or necklace that explains the allergy.
DRUG INTERACTIONS
A drug interaction is said to occur when the action of one
drug is altered or changed by the action of another drug.
Drug interactions are elicited in two ways: (1) by agents
that, when combined, increase the actions of one or both
drugs; and (2) by agents that, when combined, decrease
the effectiveness of one or both drugs. Some drug inter-
actions are benecial, such as the use of caffeine, a cen-
tral nervous system stimulant, with an antihistamine, a
central nervous system depressant. The stimulatory ef-
fects of the caffeine counteract the drowsiness caused
by the antihistamine without eliminating the anti-
histaminic effects. The mechanisms of drug interactions
can be categorized as those that change the absorption,
distribution, metabolism, or excretion of a drug and
those that enhance the pharmacologic effect of a drug.
CHANGES IN ABSORPTION
Most drug interactions that change absorption take
place in the GI tract, usually the stomach. Examples of
this type of interaction include the following:
• Antacids inhibit the dissolution of ketoconazole tab-
lets by increasing the gastric pH. The interaction is
managed by giving the antacid at least 2 hours after
ketoconazole administration.
• Aluminum-containing antacids inhibit the absorp-
tion of tetracycline. Aluminum salts form an insolu-
ble chemical complex with tetracycline. The interac-
tion is managed by separating the administration of
tetracycline and antacids by 3 to 4 hours.
CHANGES IN DISTRIBUTION
Drug interactions that cause a change in distribution
usually affect the binding of a drug to an inactive site
(e.g., circulating plasma albumin, muscle protein).
When a drug is absorbed into the blood, it is usually
transported throughout the body bound to plasma
proteins. It often binds to other proteins, such as those
in muscle. A drug that is highly bound (e.g., >90%
bound) to a protein-binding site may be displaced by
another drug that has a higher afnity for that bind-
ing site. Signicant interactions can take place this way
because little displacement is required to have a major
impact. Remember, only the unbound drug is pharma-
cologically active. If a drug is 90% bound to a protein,
then 10% of the drug is providing the physiologic ef-
fect. If another drug is administered with a stronger
afnity for the protein-binding site and it displaces just
5% of the bound drug, there is now 15% unbound for
physiologic activity; this is the equivalent of a 50% in-
crease in dosage (i.e., from 10% to 15% active drug).
For example, the anticoagulant action of warfarin is
increased by administration with furosemide, which
is a loop diuretic. Furosemide displaces warfarin from
albumin-binding sites, thereby increasing the amount
of unbound anticoagulant. This interaction is managed
by decreasing the warfarin dosage.
CHANGES IN METABOLISM
Drug interactions usually result from a change in metab-
olism that involves inhibiting or inducing (stimulating)
 Basic Principles of Drug Action and Drug Interactions CHAPTER 2 19

the enzymes that metabolize a drug. Medicines known CHANGES IN EXCRETION

to bind to enzymes and to slow the metabolism of other
drugs include verapamil, ketoconazole, amiodarone,
cimetidine, and erythromycin. Serum drug levels usu-
ally increase as a result of inhibited metabolism when
these drugs are given concurrently, and the dosages of
the inhibited drugs usually must be reduced to prevent
toxicity. For example, erythromycin inhibits the metabo-
lism of theophylline; therefore the dose of theophylline
must be reduced on the basis of theophylline serum
levels and signs of toxicity. Because erythromycin (an
antibiotic) is usually administered only in short courses,
the theophylline dosage usually needs to be increased
when the erythromycin is discontinued.
Common drugs that bind to enzymes and increase
the metabolism of other drugs (enzyme inducers) are
phenobarbital, carbamazepine, rifampin, and phenyt-
oin. Rapidly metabolized drugs include doxycycline,
warfarin, metronidazole, theophylline, and verapamil.
When administered with enzyme inducers, the dosag-
es of the more rapidly metabolized drugs should gen-
erally be increased to provide therapeutic activity. The
patient must be monitored closely for adverse effects.
For example, if a woman who is taking oral contra-
ceptives (see Chapter 40) requires a course of rifampin
antimicrobial therapy, the rifampin will induce the en-
zymes that metabolize both the progesterone and es-
trogen components of the contraceptive, thereby caus-
ing an increased incidence of menstrual abnormalities
and reduced effectiveness of conception control. This
interaction is managed by advising the patient to use
an additional form of contraception while she is receiv-
ing rifampin therapy. Adverse effects may also occur if
an enzyme inducer is discontinued. The metabolism of
the induced drug then decelerates, leading to accumu-
lation and toxicity if the dosage is not reduced.
Drug interactions that cause a change in excretion usu-
ally act in the kidney tubules by changing the pH to
enhance or inhibit excretion. The classic example of
altered urine pH is the combination of acetazolamide
(which elevates urine pH) and quinidine. The alkaline
urine produced by acetazolamide causes quinidine to
be reabsorbed in the renal tubules, which potentially
increases the physiologic and toxic effects of quinidine.
The frequent monitoring of quinidine serum levels and
assessments for signs of quinidine toxicity are used as
guides for reducing quinidine dosage.
DRUGS THAT ENHANCE THE PHARMACOLOGIC
EFFECTS OF OTHER DRUGS
Major drug interactions also occur between drugs.
This may occur when one drug enhances the physi-
ologic effects of another drug. Alcohol and sedative-
hypnotic agents both cause sedation, but when used
together can cause signicant central nervous system
depression. Another drug interaction that can have se-
rious consequences is the interaction between amino-
glycoside antibiotics (gentamicin, tobramycin) and a
neuromuscular blocking agent such as pancuronium.
When used together, the antibiotic increases the neuro-
muscular blockade, prolonging return to normal respi-
rations and recovery time. Table 2.2 denes the termi-
nology related to drug-drug interactions.
Because it is impossible to memorize all possible
drug interactions, the nurse must check for drug inter-
actions when they are suspected. The nurse must take
the time to consult drug resource books and pharma-
cists to ensure that a patient who is receiving multiple
medications does not experience unanticipated drug
interactions.

Table 2.2 Terminology Related to Drug-Drug Interactions

TERM DEFINITION EXAMPLE
Additive effect Two drugs with similar actions are taken for an increased effect. hydrocodone + acetaminophen =
added analgesic effect
Synergistic The combined effect of two drugs is greater than the sum of the aspirin + codeine = much greater
effect effect of each drug given together. analgesic effect
Antagonistic One drug interferes with the action of another. tetracycline + antacid = decreased
effect absorption of the tetracycline
Displacement The displacement of the rst drug from protein-binding sites (i.e., warfarin + valproic acid = increased
bound drugs are inactive) by a second drug increases the activity anticoagulant effect
of the rst drug because more unbound drug is available.
Interference The rst drug inhibits the metabolism or excretion of the second probenecid + ampicillin = prolonged
drug, thereby causing increased activity of the second drug. antibacterial activity of ampicillin
because probenecid blocks the
renal excretion of ampicillin
Incompatibility The rst drug is chemically incompatible with the second drug, ampicillin + gentamicin = ampicillin
thereby causing deterioration when the drugs are mixed in the inactivates gentamicin
same syringe or solution or are administered together at the
same site. Signs include haziness, formation of a precipitate, or
a change in the color of the solution when the drugs are mixed.
20 UNIT I Applying Pharmacology to Nursing Practice

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points 2. 25 mg (50%)

3. 12.5 mg (25%)
• The most common routes of drug administration are the 4. 6.25 mg (12.5%)
enteral, parenteral, and percutaneous routes.
Objective: Identify the meaning and signicance of the term half-
• The half-life of a drug is dened as the amount of time
life when used in relation to drug therapy.
required for 50% of the drug to be eliminated from the
NCLEX test item: Multiple choice
body.
Cognitive skill: Comprehension
• After administration, all drugs go through ve stages:
liberation, absorption, distribution, metabolism, and 3. The nurse reviews the patient’s charts for laboratory tests that
excretion (LADME). The enzyme systems of the liver are relate to how well the patient’s organ systems are working
the primary sites for the metabolism of drugs, but other because drug metabolism is inuenced by certain body systems.
tissues and organs (e.g., white blood cells, GI tract, lungs)
metabolize certain drugs to a minor extent. Choose the most likely options for the information missing from
the sentence below by selecting from the lists of options provided.
• When a drug enters a patient and is absorbed and
distributed, the desired action usually occurs. However, Metabolism is the process that deactivates drugs; sites
all drugs have the potential to affect more than one body for metabolism of drugs are ________ 1__________ and
system simultaneously, causing common adverse effects, ___________ 1_____________ and __________ 1________, and
which are generally mild, or serious adverse effects, which factors that inuence these drug metabolism reactions are
can be more severe and lead to toxicity. __________ 2_________ and __________2________.
• Drug interactions are elicited in two ways: (1) by agents
that, when combined, increase the actions of one or both
OPTIONS FOR 1 OPTIONS FOR 2
drugs; and (2) by agents that, when combined, decrease
the effectiveness of one or both of the drugs. kidneys exercise tolerance
• The mechanisms of drug interactions can be categorized white blood cells environmental pollutants
as those that change the absorption, distribution, GI tract repository sites
metabolism, or excretion of a drug and those that enhance liver concurrent use of other drugs
the pharmacologic effect of a drug. heart receptor sites

Additional Learning Resources Objective: Describe the process of how a drug is metabolized in
the body.
SG Go to your Study Guide for additional Review Questions NGN test item: Cloze
for the NCLEX® Examination, Critical Thinking Clinical Situa- Cognitive skill: Recognize cues
tions, and other learning activities to help you master this chap-
ter content. 4. When an antihypertensive drug causes a drop in blood pressure to
the normal range, what is this effect called?
Go to your Evolve website (https://evolve.elsevier.com/ 1. Antagonistic effect
Willihnganz) for additional online resources. 2. Desired therapeutic effect
3. Side effect
Clinical Judgment and Next-Generation NCLEX ® 4. Additive effect
Examination-Style Questions Objective: Compare and contrast the following terms that are used
in relationship to medications: desired action, common adverse
The following questions are typical of the NCLEX exam and effects, serious adverse effects, allergic reactions, and idiosyncratic
include both NGN (Next Generation) and traditional questions. reactions.
See Chapter 1 for further information regarding question types NCLEX test item: Multiple choice
and formats. Cognitive skill: Understanding
1. A nurse is reviewing the drug route for an order written to be given 5. The nurse noticed that, after administering an antibiotic ampicillin
via nasogastric tube and understands that this means that the drug in the patient’s IV line, the solution in the tubing started to turn
will be administered by which route? milky and hazy after injecting another drug in the same tubing. The
1. Enteral precipitate that was created meant the nurse needed to do what
2. Parenteral next? (Select all that apply.)
3. Percutaneous 1. Recognize that the two drugs are incompatible and notify
4. Intramuscular the healthcare providers.
Objective: Identify common drug administration routes. 2. Flush the line still connected to the patient until the
NCLEX test item: Multiple choice precipitate is gone.
Cognitive skill: Knowledge 3. Stop the infusion, disconnect the IV line, ush the
precipitate out, and reconnect the line.
2. A patient takes 50 mg of a drug that has a half-life of 12 hours. 4. Request that the drugs be placed on different schedules
What percentage of the dose remains in the body 36 hours after so that they are not administered at the same time.
the drug is administered? 5. Recognize that the two drugs are having a synergistic
1. 50 mg (100%) effect and notify the healthcare providers.
 Basic Principles of Drug Action and Drug Interactions CHAPTER 2 21

Objective: Differentiate among the terms: additive effect,

OPTIONS FOR 1 OPTIONS FOR 2
synergistic effect, antagonistic effect, displacement, interference,
and incompatibility. antacid codeine
NCLEX test item: Multiple response warfarin ampicillin
Cognitive skill: Application probenecid tetracycline
aspirin valproic acid
6. A patient is experiencing a rash over their torso and legs
accompanied by severe itching after receiving an antibiotic for an
ear infection. What does the nurse suspect is happening? Select all Objective: Differentiate among the following terms: additive effect,
that apply. synergistic effect, antagonistic effect, displacement, interference,
and incompatibility.
1. The patient is having an idiosyncratic reaction.
NGN test item: Cloze
2. The patient is having an antagonistic effect.
Cognitive skill: Analysis cues
3. The patient is having an allergic reaction.
4. The patient is having a common adverse effect. 10. The nurse is aware of enzymes that affect metabolism and
5. The patient is having the desired effect. therefore affect drug actions that are caused by alterations in
6. The patient is having a serious adverse effect. enzyme activity.
7. The patient is having an anaphylactic reaction.
Indicate with an arrow (up or down) whether the reaction by the
Objective: Compare and contrast the following terms that are used
enzyme activity will increase or decrease metabolism of a drug.
in relationship to medications: desired actions, common adverse
effects, serious adverse effects, allergic reactions, and idiosyncratic
reactions. CHANGE IN DRUG ACTION
NGN test item: Extended multiple response CAUSED BY ALTERED
Cognitive skill: Recognize cues ENZYME ACTIVITY METABOLISM
Enzyme inhibitors
7. When a patient who was prescribed warfarin and valproic acid
begins experiencing an increased effect of warfarin (bruising on Enzyme inducers
arms, bleeding gums), what is this known as? Enzyme enhancers
1. Synergistic effect Enzyme metabolizers
2. Antagonistic effect
3. Idiosyncratic effect
4. Displacement effect Objective: Identify one way in which alternatives in metabolism
create drug interactions.
Objective: Compare and contrast the following terms that are used NGN test item: Extended Drag and Drop
in relationship to medications: desired action, common adverse Cognitive skill: Recognize cues
effects, serious adverse effects, allergic reactions, and idiosyncratic
reactions. 11. The nurse reviews terms used to describe the therapeutic effects
NCLEX test item: Multiple choice of drugs and knows they include the additive effect and the
Cognitive skill: Knowledge synergistic effect.

8. The nurse is aware that a patient who has an increased metabolic Choose the most likely option for the information missing from the
rate (e.g., hyperthyroidism) generally requires what type of statements below by selecting from the list of options provided.
dosage?
An example of a synergistic effect is one that is
1. Normal dosage
caused by the combination of ________ 1_________ and
2. Lower-than-normal dosage
_________2___________, which increases the therapeutic
3. Higher-than-normal dosage
analgesic effect of the drugs.
4. A dosage that is based on the patient’s thyroid function
levels
OPTIONS FOR 1 OPTIONS FOR 2
Objective: Identify one way in which alternatives in metabolism
create drug interactions. antacid codeine
NCLEX test item: Multiple choice warfarin ampicillin
Cognitive skill: Comprehension probenecid tetracycline
aspirin valproic acid
9. The nurse studied the terms for drug interactions and recognized
that there are medications that will create an antagonistic effect
when given together. Objective: Differentiate among the following terms: additive effect,
synergistic effect, antagonistic effect, displacement, interference,
Choose the most likely option for the information missing from the and incompatibility.
statements below by selecting from the list of options provided. NGN test item: Cloze
Cognitive skill: Analysis cues
An example of the drug interaction that causes an
antagonistic effect is between _______
1___________ and
_________2________ in which there is a decrease in the
absorption of the second drug.
 3 Drug Action Across the Life Span

https://evolve.elsevier.com/Clayton

Objectives
1. Explain the impact of the placebo effect and the nocebo
effect.
2. Identify the importance of drug dependence and drug
accumulation.
3. Discuss the effects of age on drug absorption, distribution,
metabolism, and excretion.
4. Explain the gender-specic considerations of drug
absorption, distribution, metabolism, and excretion.
5. Describe where a nurse will nd new information about the
use of drugs during pregnancy and lactation.
6. Discuss the impact of pregnancy and breastfeeding on
drug absorption, distribution, metabolism, and excretion.
7. Discuss the role of genetics and its inuence on drug
action.

Key Terms
gender-specic medicine (JĔN-dŭr
spĕ-SĬ-fĭk) (p. 23)
placebo effect (plă-SĒ-bō ĕf-FĔKT)
(p. 23)
nocebo effect (nō-SĒ-bō) (p. 23)
placebo (plă-SĒ-bō) (p. 23)
tolerance (TŎL-ŭr-ŭns) (p. 24)
drug dependence (dē-PĔN-dĕns)
(p. 24)
drug accumulation (ă-kyū-mū-LĀ-
shŭn) (p. 24)
carcinogenicity (kăr-sĭn-ō-jĕn-ĬS-ǐ-tē)
(p. 24)
passive diffusion (PĂ-sǐv dǐ-FYŪ-
shŭn) (p. 25)
hydrolysis (hī-DRŎ-lǐ-sǐs) (p. 25)
intestinal transit (ǐn-TĔS-tǐ-năl TRĂN-
sǐt) (p. 25)
protein binding (PRŌ-tēn BĪN-dǐng)
(p. 26)
drug metabolism (mĕ-TĂB-ō-lĭz-ĕm)
(p. 26)
metabolites (mĕ-TĂB-ŏ-līts) (p. 27)
therapeutic drug monitoring (thĕr-
ă-PYŪ-tĭk) (p. 27)
polypharmacy (pŏl-ē-FĂR-mă-sē)
(p. 31)
teratogens (TĔR-ă-tō-jĕnz) (p. 31)
genetics (jĭ-NĔT-ĭks) (p. 35)
genome (JĒ-nōm) (p. 35)
polymorphisms (pŏl-ē-MŎR-fǐz-ǐmz)
(p. 35)
pharmacogenetics (făr-mă-kō-jĭ-NĔT-
ĭks) (p. 35)

FACTORS THAT AFFECT DRUG THERAPY signicant impact on drug therapy. When discussing
Patients often say “That drug really knocked me out!” the effect of age on drug therapy, it is helpful to subdi-
or “That drug didn’t touch the pain!” The effects vide the population into the following categories:
of drugs are unexpectedly potent in some patients,
whereas other patients show little response at the same AGE STAGE
dosage. In addition, some patients react differently to <38 wk gestation Premature
the same dosage of a drug that is administered at dif- 0–1 mo Newborn, neonate
ferent times. Because of individual patient variation, 1–24 mo Infant, toddler
exact responses to drug therapy are difcult to predict. 3–5 yr Young child
The following factors have been identied as contribu- 6–12 yr Older child
tors to the variable response to drugs. 13–18 yr Adolescent
19–54 yr Adult
AGE 55–64 yr Older adult
65–74 yr Elderly
Infants and the very old tend to be the most sensitive 75–84 yr The aged
to the effects of drugs. There are important differences 85 yr or older The very old
with regard to the absorption, distribution, metabo-
lism, and excretion of drugs in premature neonates,
full-term newborns, and children. The aging process BODY WEIGHT
brings about changes in body composition and organ Compared with the general population, patients who
function that can affect the older patient’s response to are considerably overweight may require an increase
drug therapy. Thus the age of the patient can have a in drug dosage to attain the same therapeutic response.
22

Conversely, patients who are underweight, compared
with the general population, tend to require lower dos-
ages for the same therapeutic response. It is important
to obtain an accurate height and weight on patients be-
cause dosages of medicines are often calculated with
these parameters.
Most pediatric dosages are calculated by milligrams
of drug per kilogram of body weight (mg/kg) to ad-
just for growth rate. The dosages of other medicines,
particularly chemotherapeutic agents, are ordered on
the basis of the body surface area (see Appendix A);
this calculation requires both height and weight. For
accurate measurements, the patient’s weight should be
taken at the same time of day and while the patient is
wearing similar-weight clothing.
GENDER
Gender-specic medicine is a developing science that
studies differences in the normal function of men and
women and addresses how people of each gender per-
ceive and experience disease. In almost every body
system, men and women function differently, as well
as perceive and experience disease differently. In the
case of angina (heart pain), women will present with
nausea, indigestion, and upper back and jaw pain,
whereas men will generally present with left-sided
chest pain or pressure. A study published in 2016 indi-
cated that women with type 1 diabetes have a fourfold
increased risk for cardiovascular disease compared
with nondiabetic women, contrasted with men with
diabetes who are at twice the risk over nondiabetic
men of developing cardiovascular disease. This indi-
cates that diabetes affects women differently from men
and further research is needed to fully understand
the impact. Unfortunately, few scientic data exist to
document differences in the pharmacokinetics of most
drugs in women compared with men. In 1993 the US
Food and Drug Administration (FDA) issued guide-
lines stating that drug development must evaluate the
effects on both genders. Testing is also needed to assess
differences in pharmacokinetic parameters between
women and men. In the women’s studies, the research
must distinguish between premenopausal and post-
menopausal women and among women in different
phases of the menstrual cycle.
METABOLIC RATE
Patients with a higher-than-average metabolic rate
(e.g., patients with hyperthyroidism) tend to metabo-
lize drugs more rapidly, thus requiring larger doses
or more frequent administration. The converse is true
for those patients with lower-than-average metabolic
rates (e.g., patients with hypothyroidism). Chronic
smoking enhances the metabolism of some drugs
(e.g., clozapine, olanzapine), thereby requiring larger
doses to be administered more frequently for a thera-
peutic effect.
Drug Action Across the Life Span CHAPTER 3 23
ILLNESS
Pathologic conditions may alter the rate of absorption,
distribution, metabolism, and excretion of a drug.
For example, patients who are in shock have reduced
peripheral vascular circulation and will absorb intra-
muscularly or subcutaneously injected drugs more
slowly. Patients who are vomiting may not be able to
retain a medication in the stomach long enough for dis-
solution and absorption. Patients with conditions such
as nephrotic syndrome or malnutrition may have re-
duced amounts of serum proteins in the blood that are
necessary for adequate distribution of drugs. Patients
with kidney failure generally will excrete drugs at
a slower rate and must have signicant reductions
in dosages of medications that are excreted by the
kidneys (Table 3.1).
PSYCHOLOGY
Attitudes and expectations play a major role in a pa-
tient’s response to therapy and in their willingness to
take the medication as prescribed. When the disease
state physically affects the patient’s ability to func-
tion, the treatment protocol is generally followed, as in
a patient with insulin-dependent diabetes who needs
insulin or a patient with arthritis who needs pain medi-
cation. When the disease has few symptoms (e.g., hyper-
tension, dyslipidemia), it becomes harder to follow the
treatment protocol because body cues are not present
to remind patients. Patients frequently voluntarily dis-
continue treatment because their current lifestyle is not
affected by the hypertension or dyslipidemia.
Other psychological considerations are the placebo
effect and the nocebo effect. It is well documented that
a patient’s positive expectations about treatment and
the care received can positively affect the outcome of
therapy; this is a phenomenon known as the placebo
effect (from Latin, meaning “I will please”). Although
more difcult to prove because of ethical consider-
ations, it is also believed that negative expectations
about therapy and the care received can have a noce-
bo effect (from Latin, meaning “I will harm”), which
results in less-than-optimal outcomes of therapy. It is
thought that the nocebo effect plays a major role in
psychogenic illness, especially in stress-related prob-
lems, because the patient may worry about their con-
dition or treatment. A placebo is a drug dosage form
(e.g., tablet, capsule) that has no pharmacologic activ-
ity because the dosage form has no active ingredients.
However, when the placebo is taken, the patient may
report a therapeutic response. Placebos are frequently
used in studies of new medicines to measure the phar-
macologic effects of a new medicine compared with
the inert placebo. The American Pain Society and the
Agency for Healthcare Research and Quality recom-
mend the avoidance of the deceitful use of placebos
in current clinical practice guidelines for pain manage-
ment. It is thought that the deceitful use of placebos in
24 UNIT I Applying Pharmacology to Nursing Practice
Table 3.1 Selected Medications That Require Dosage Adjustment for Renal Failure a
THERAPEUTIC CATEGORY DRUG CLASS
Antibiotics Aminoglycosides
Cephalosporins
Penicillins
Quinolones
Others
Antifungal agents — amphotericin B, uconazole
Antiviral agents — acyclovir, ganciclovir, stavudine
Cardiovascular agents Angiotensin-converting enzyme inhibitors
Antiarrhythmic agents
Beta-adrenergic blocking agents
Digitalis glycoside
Gastrointestinal agents Histamine-2 antagonists
Other — lithium, allopurinol, meperidine, methotrexate
aMedicinesare representative examples only. See the Physicians’ Desk Reference. 71st ed. Montvale, NJ: PDR Network LLC; 2020, or the AHFS Drug Information
2020. Bethesda, MD: American Society of Health-System Pharmacists; 2020, for appropriate dosing and monitoring parameters.
pain management violates a patient’s right to receive
the highest quality of care possible.
TOLERANCE
Tolerance occurs when a person begins to require a
higher dosage of a medication to produce the same ef-
fects that a lower dosage once provided. An example
is the person who is addicted to heroin. After a few
weeks of use, larger doses are required to provide the
same “high.” Tolerance can be caused by psychological
dependence, or the body may metabolize a particular
drug more rapidly than before, thereby causing the ef-
fects of the drug to diminish more rapidly.
DEPENDENCE
Drug dependence, which is also known as addiction or
habituation, occurs when a person is unable to control a
desire for ingestion of drugs. The dependence may be
physiologic, in which the person develops withdrawal
symptoms if the drug is withdrawn for a certain peri-
od, or psychological, in which the patient is emotionally
attached to the drug. Drug dependence occurs most
commonly with the use of the scheduled or controlled
medications listed in Chapter 1 (e.g., hydrocodone, di-
azepam). Many people, especially older adults, wor-
ry about becoming addicted to pain medication and
therefore may not take their pain medication, even
when it is needed. The nurse needs to assure these in-
dividuals that studies have shown that less than 1%
of patients using opioids for acute pain relief become
addicted and that it is important for their overall well-
being to be as free of pain as possible. (See Chapter 48
for more information.)
EXAMPLES
amikacin, gentamicin, tobramycin
cefotaxime, cefotetan, ceftazidime, ceftriaxone,
cefuroxime, cefpodoxime
ampicillin, piperacillin, ticarcillin
ciprooxacin, levooxacin
vancomycin, minocycline, aztreonam, imipenem,
cotrimoxazole, ethambutol
benazepril, captopril, ramipril
dofetilide
atenolol, labetalol, pindolol, metoprolol, nadolol,
propranolol
digoxin
cimetidine, ranitidine
CUMULATIVE EFFECT
A drug may accumulate in the body if the next dose is
administered before the previously administered dose
has been metabolized or excreted. Excessive drug ac-
cumulation may result in drug toxicity. An example of
drug accumulation is the excessive ingestion of alco-
holic beverages. A person becomes “drunk” or “inebri-
ated” when the rate of consumption exceeds the rate of
metabolism and excretion of the alcohol.
Carcinogenicity is the ability of a drug to induce liv-
ing cells to mutate and become cancerous. Many drugs
have this potential, so all drugs are tested in several
animal species before human investigation to elimi-
nate this potential.
FACTORS THAT INFLUENCE DRUG ACTIONS
ABSORPTION
Drug absorption refers to the process by which drugs
are absorbed in the body. This occurs by way of differ-
ent routes through which the drugs are administered.
For example, the most common way to administer a
drug is orally (by mouth), and then the drug is ab-
sorbed by the gastrointestinal (GI) tract (enterally).
Other routes include intramuscularly (in the muscle)
or intravenously (in the vein). The rate of absorption is
dependent on various factors such as blood ow to the
area in which the drug has been administered.
Age
Pediatric and geriatric patients each require spe-
cial considerations for medication administration.
Medicines given intramuscularly are usually erratically

absorbed in neonates and older adults. Differences in
muscle mass, blood ow to muscles, and muscle inac-
tivity in patients who are bedridden make absorption
unpredictable.
Topical administration with percutaneous absorp-
tion is usually effective for infants because their outer
layer of skin (the stratum corneum) is not fully devel-
oped. Because the skin is more fully hydrated at this
age, water-soluble drugs are absorbed more readily.
Infants who wear plastic-coated diapers are also more
susceptible to skin absorption because the plastic acts
as an occlusive dressing that increases the hydration of
the skin. Inammation (e.g., diaper rash) also increases
the amount of drug that is absorbed.
Transdermal administration in geriatric patients is
often difcult to predict. Although dermal thickness
decreases with aging and may enhance absorption,
factors that may diminish absorption can be seen, in-
cluding drying, wrinkling, and a decrease in the num-
ber of hair follicles. With aging, decreased cardiac out-
put and diminishing tissue perfusion may also affect
transdermal drug absorption.
In most cases, medicines are administered orally.
Infants and older adults often lack a sufcient num-
ber of teeth for chewable medicines. Chewable tablets
should not be given to children or to any patient with
loose teeth. Geriatric patients often have reduced sali-
vary ow, which makes chewing and swallowing more
difcult. However, tablet and capsule forms are often
too large for pediatric or geriatric patients to swallow
safely. It is often necessary to crush a tablet for admin-
istration with food or to use a liquid formulation for
easier and safer administration. Taste also becomes
a factor when administering oral liquids because the
liquid comes into contact with the taste buds. Timed-
release tablets, enteric-coated tablets, and sublingual
tablets should not be crushed because this will increase
their absorption rate and thus the potential for toxicity.
The GI absorption of medicines is inuenced by
various factors, including gastric pH, gastric empty-
ing time, the motility of the GI tract, enzymatic activ-
ity, the blood ow of the mucous lining of the stomach
and intestines, the permeability and maturation of the
mucosal membrane, and concurrent disease processes.
Absorption by passive diffusion across the membranes
and gastric emptying time depend on the pH of the
environment.
Newborns and geriatric patients have reduced gas-
tric acidity and prolonged transit time compared with
adults. Premature infants have a high gastric pH (6 to
8) as a result of the immature acid-secreting cells in
their stomachs. In a full-term newborn, the gastric pH
is also 6 to 8, but within 24 hours the pH decreases to 2
to 4 in response to gastric acid secretion. At 1 year old,
the child’s stomach pH approximates that of an adult
(i.e., pH of 1 to 2 when empty, up to 5 when full).
Geriatric patients often have a higher gastric pH
because of the loss of acid-secreting cells. Drugs that
Drug Action Across the Life Span CHAPTER 3 25
are destroyed by gastric acid (e.g., ampicillin, penicil-
lin) are more readily absorbed in older adults because
of the decrease in acid production, which results in
higher serum concentrations. By contrast, drugs that
depend on an acidic environment for absorption (e.g.,
phenobarbital, acetaminophen, phenytoin, aspirin) are
more poorly absorbed, thereby resulting in lower se-
rum concentrations in older adults.
Premature infants and geriatric patients also have a
slower gastric emptying time, partly because of their
reduced acid secretion. A slower gastric emptying time
may allow the drug to stay in contact with the absorp-
tive tissue longer, thereby allowing for increased ab-
sorption with a higher serum concentration. There is
also the potential for toxicity caused by extended con-
tact time in the stomach for drugs that have the po-
tential to cause gastric ulcers (e.g., nonsteroidal anti-
inammatory drugs).
Another factor that affects drug absorption in the
newborn is the absence of the enzymes needed for hy-
drolysis. Hydrolysis is the process that uses water to
initiate a chemical reaction. Infants cannot metabolize
palmitic acid from chloramphenicol palmitate (an anti-
biotic), thereby preventing the absorption of the chlor-
amphenicol. Oral phenytoin dosages are also greater
in infants who are less than 6 months old because of
poor absorption (i.e., in neonates, the dosage is 15 to 20
mg/kg/24 hr compared with infants and children, in
whom the dosage is 4 to 7 mg/kg/24 hr).
The intestinal transit refers to the speed at which the
intestine moves foods, secretions, and other ingested
matter along, and this rate varies with age. Premature
and full-term newborns have a slower transit time.
As the healthy newborn matures into infancy, the GI
transit rate increases to a relatively standard rate by
about 4 months of age. Older adults develop decreased
GI motility and intestinal blood ow. This has the po-
tential for altering the absorption of medicines and for
causing constipation or diarrhea, depending on the
medicine.
Gender
Generally, a woman’s stomach empties solids more
slowly than a man’s does, and it may have lower gas-
tric acidity causing a higher pH in the stomach (pH >
3 or 5), thus slowing the absorption of certain types
of medicines (e.g., aspirin). A slower gastric emptying
time may allow the drug to stay in contact with the
absorptive tissue longer, thereby allowing for more
absorption and a higher serum concentration. Women
also have lower gastric levels of the enzyme alcohol
dehydrogenase, which is needed to metabolize ingest-
ed alcohol. Thus larger amounts of ingested alcohol
may be absorbed instead of metabolized in the stom-
ach, thereby leading to a higher blood alcohol level in
a woman than in a man for equal amounts of ingested
alcohol. Other factors, such as body weight and drug
distribution (see the next section of this chapter), may
26 UNIT I Applying Pharmacology to Nursing Practice
Table 3.2 Proportions of Body Water a
AGE (WEIGHT) EXTRACELLULAR WATER (%)
Premature (1.5 kg) 60
Full term (3.5 kg) 56
5 mo (7 kg) 50
1 yr (10 kg) 40
Adult male 40
aDevelopmental changes from birth to adulthood. Extracellular and intracellular water values are expressed as percentages of total body weight.
Data from Friis-Hansen B. Body composition during growth. Pediatrics. 1971;47(suppl 2):264.
aggravate the higher blood alcohol level and state of
intoxication in women compared with men.
DISTRIBUTION
The term distribution refers to the ways in which drugs
are transported by the circulating body uids to the
sites of action (receptors), metabolism, and excretion.
Distribution is dependent on pH, body water concen-
trations (i.e., intracellular, extracellular, and total body
water), the presence and quantity of fat tissue, protein
binding, cardiac output, and regional blood ow.
Age and Gender
Most medicines are transported either dissolved in the
circulating water (i.e., in blood) of the body or bound
to plasma proteins within the blood. Total body water
content of a preterm infant is 83%, whereas that of an
adult man is 60%; this drops to 50% in older persons.
The signicance of this is that infants have a larger vol-
ume of distribution for water-soluble drugs and thus
require a higher dose on a milligram-per-kilogram ba-
sis than an older child or an adult (Table 3.2).
With aging, lean body mass and total body water
decrease and total fat content increases. The body
weight of a preterm infant may be composed of 1% to
2% fat, whereas a full-term newborn may have 15%
fat. Adult total body fat ranges from 18% to 36% for
men and 33% to 48% for women between the ages of
18 and 35 years. Drugs that are highly fat soluble (e.g.,
antidepressants, phenothiazines, benzodiazepines,
calcium channel blockers) require a longer onset of ac-
tion and accumulate in fat tissues, thereby prolonging
their action and increasing the potential for toxicity.
For water-soluble drugs (e.g., ethanol, aminoglycoside
antibiotics), a woman’s greater proportion of body fat
produces a higher blood level compared with that of
a man when the drug is given as an equal dose per
kilogram of body weight. In the case of ethanol, this ef-
fect tends to cause a higher level of ethanol in the brain
cells, which results in greater intoxication. Highly fat-
soluble medicines (e.g., diazepam) must be given in
smaller milligram-per-kilogram dosages to low-birth-
weight infants, because there is less fat tissue to bind
the drug, thereby leaving more drug to be active at re-
ceptor sites.
INTRACELLULAR WATER (%) TOTAL BODY WATER (%)
40 83
44 74
50 60
60 59
60 60
Drugs that are relatively insoluble are transported
in the circulation by being bound to plasma proteins
(albumin and globulins), especially albumin. Protein
binding is reduced in preterm infants because of de-
creased plasma protein concentrations, lower binding
capacity of protein, and decreased afnity of proteins
for drug binding. Drugs that are known to have lower
protein binding in neonates than in adults include phe-
nobarbital, phenytoin, theophylline, propranolol, lido-
caine, and penicillin. Because serum protein binding
is diminished, the drugs are distributed over a wider
area of the neonate’s body, and a larger loading dose
is required than is needed in older children to achieve
therapeutic serum concentrations. Several drugs that
are used to treat neonatal conditions may compete
for binding sites. Little difference exists between al-
bumin protein in men and women, although there
are some differences between the globulin proteins
(i.e., corticosteroid-binding and sex-hormone–binding
globulins). In adults who are more than 40 years old,
the composition of body proteins begins to change.
Although the total body protein concentration is unaf-
fected, albumin concentrations gradually decrease and
other protein levels (e.g., globulins) increase. As albu-
min levels diminish, the level of unbound active drug
increases. Increased levels of naproxen and valproate
have been found in older adults, presumably as a re-
sult of decreased albumin levels. Disease states such
as cirrhosis, renal failure, and malnutrition can lower
albumin levels. Initial doses of highly protein-bound
drugs (e.g., warfarin, phenytoin, propranolol, diaz-
epam) should be reduced and then increased slowly if
there is evidence of decreased serum albumin. Lower
protein binding may also lead to a greater immedi-
ate pharmacologic effect because more active drug is
available; however, the duration of action may be re-
duced because more of the unbound drug is available
for metabolism and excretion.
METABOLISM
Drug metabolism is the process whereby the body in-
activates medicines. It is controlled by factors such as
genetics, diet, age, health, and the maturity of enzyme
systems. Enzyme systems, primarily in the liver, are
the major pathways of drug metabolism.

Age
All enzyme systems are present at birth, but they ma-
ture at different rates, taking several weeks to a year to
fully develop. Liver weight, the number of function-
ing hepatic cells, and hepatic blood ow decrease with
age; this results in the slower metabolism of drugs in
older adults. Reduced metabolism can be seriously
aggravated by the presence of liver disease or heart
failure. Drugs that are extensively metabolized by the
liver (e.g., morphine, lidocaine, propranolol) can have
substantially prolonged durations of action if hepatic
blood ow is reduced. Dosages usually must be re-
duced or the time interval between doses extended to
prevent the accumulation of active medicine and po-
tential toxicity. Drug metabolism can also be affected
in all age groups by genetics, smoking, diet, gender,
other medicines, and diseases (e.g., hepatitis, cirrho-
sis). Liver enzymes are monitored to determine any
elevated levels during the course of drug therapy. No
specic laboratory tests are available for measuring
liver function that can be used to adjust drug dosages
(Table 3.3). Renal function must be assessed and dos-
ages adjusted based on creatinine clearance.
Gender
It is now recognized that males and females differ
with regard to the concentrations of enzyme systems
throughout life. The CYP3A4 component of the cyto-
chrome P450 (CYP) system of enzymes metabolizes
more than 50% of all drugs, and it is 40% more active
in women. Drugs such as erythromycin, prednisolone,
verapamil, and diazepam are metabolized faster in
women than in men.
EXCRETION
Metabolites of drugs, which are the products of me-
tabolism—and, in some cases, the active drug itself—
are eventually excreted from the body. The primary
routes are through the renal tubules into the urine and
through the GI tract into the feces. Other generally mi-
nor routes of excretion include evaporation through
the skin, exhalation from the lungs, and secretion into
the saliva and breast milk.
Age
At birth, a preterm infant has up to 15% of the renal
capacity of an adult, whereas a full-term newborn has
approximately 35% of that capacity. The ltration ca-
pacity of an infant increases to about 50% of adult ca-
pacity at 4 weeks of age and is equivalent to full adult
function at 9 to 12 months. Drugs that are excreted
primarily by the kidneys (e.g., penicillin, gentamicin,
tobramycin, vancomycin) must be administered in in-
creased dosages or given more often to maintain ad-
equate therapeutic serum concentrations as renal func-
tion matures.
As the body ages, important physiologic changes
take place in the kidneys, including decreased renal
Drug Action Across the Life Span CHAPTER 3 27
blood ow caused by atherosclerosis and reduced car-
diac output, a loss of glomeruli, and decreased tubu-
lar function and urine-concentrating ability. However,
there is a great degree of individual variation with re-
gard to changes in renal function, and no prediction
of renal function can be made solely on the basis of a
person’s age. The renal function of older adult patients
should be estimated using equations that factor in the
patient’s age. More optimally, renal function should be
calculated by measuring urine creatinine levels over
time. Serum creatinine can give a general estimate of
renal function, but in older adult patients these deter-
minations tend to exaggerate actual functional capabil-
ity. This happens because the production of creatinine
depends on muscle mass, which is diminished in older
adults. Signicant elevations occur only when there
has been major deterioration of renal function. Blood
urea nitrogen concentration is also a poor predictor of
renal function because it is signicantly altered by diet,
status of hydration, and blood loss (Table 3.4).
THERAPEUTIC DRUG MONITORING
Therapeutic drug monitoring is the measurement of a
drug’s concentration in biologic uids to correlate
the dosage administered and the level of medicine in
the body with the pharmacologic response. Assays
of blood (serum) samples for drug concentrations
are most commonly used, but assays that involve the
use of saliva are being perfected for some medicines.
Saliva samples have the advantage of the easy collec-
tion of specimens without pain or the loss of blood that
may require replacement by transfusion at a later date.
Therapeutic drug monitoring is essential for neonates,
infants, and children to ensure that drugs are within an
appropriate therapeutic range, given the major physio-
logic changes that affect drug absorption, distribution,
metabolism, and excretion.
The dosage and the frequency of administration
must often be adjusted to help maintain therapeutic
serum concentrations. Therapeutic drug monitoring
is routine for conditions such as epilepsy (e.g., phe-
nytoin, carbamazepine, valproic acid, phenobarbital),
stroke (e.g., warfarin), heart failure (e.g., digoxin), and
antimicrobial therapy (e.g., gentamicin, tobramycin,
vancomycin) to prevent toxicities and to ensure that
dosages are adequate to provide appropriate thera-
peutic levels. Blood levels of drugs can be measured if
toxicity is suspected. The extent to which a serum drug
level is elevated may dictate how the toxicity should
be treated (e.g., acetaminophen, digoxin). Blood and
urine samples can also be obtained for legal purposes if
it is suspected that drugs (e.g., ethanol, amphetamines,
marijuana, benzodiazepines, cocaine) have been con-
sumed illicitly.
The timing of the drug’s administration and the
collection of the specimen are crucial to the accurate
interpretation of the data obtained after assay. Certain
28 UNIT I Applying Pharmacology to Nursing Practice

Table 3.3 Medications That Require Hepatic Monitoring a b

GENERIC NAME BRAND NAME GENERIC NAME BRAND NAME
acetaminophen Tylenol methotrexate Rheumatrex
amiodarone Pacerone methsuximide Celontin
atorvastatin Lipitor naproxen Naprosyn
azathioprine Imuran nevirapine Viramune
carbamazepine Tegretol niacin Niaspan
diclofenac Voltaren oxcarbazepine Trileptal
efavirenz Sustiva pentamidine Pentam
ethosuximide Zarontin pioglitazone Actos
ethotoin Peganone piroxicam Feldene
felbamate Felbatol pravastatin Pravachol
fenobrate Tricor rifampin Rifadin
uvastatin Lescol ritonavir Norvir
gembrozil Lopid rosiglitazone Avandia
griseofulvin Gris-PEG rosuvastatin Crestor
indinavir Crixivan simvastatin Zocor
isoniazid Nydrazid tacrine Cognex
ketoconazole Nizoral terbinane Lamisil
lamivudine Epivir tizanidine Zanaex
leunomide Arava tolcapone Tasmar
lovastatin Mevacor valproic acid Depakote
meloxicam Mobic a

usually at the beginning of therapy and then every few weeks to months thereafter (see individual monographs).
bEnzymes that are routinely monitored for liver function are alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase. If the patient’s levels

become elevated, the primary healthcare provider should be notied for individualized treatment.
Data from Tice SA, Parry D. Medications that require hepatic monitoring. Hosp Pharm. 2001;36(4):456-464; Tice SA, Parry D. Medications that require hepatic
monitoring. Hosp Pharm. 2004;39(6):595-606; Porter RS, Kaplan JL, eds. The Merck Manual of Diagnosis and Therapy. 19th ed. Whitehouse Station, NJ: Merck;
2012; American Geriatrics Society 2015 Beers Criteria Update Expert Panel. American Geriatrics Society 2015 Updated Beers criteria for potentially inappropriate
medication use in older adults. J Am Geriatr Soc. 2015;63(11):2227-2246.

medicines (e.g., aminoglycosides, gentamicin, tobra-
mycin) require that blood be drawn before and after
the administration of the drug to assess subtherapeu-
tic levels and the potential for toxicity. One sample is
drawn immediately before the next dose is to be ad-
ministered to obtain the trough, or lowest, blood level
of medicine, and another is drawn 20 minutes after the
medicine has been administered intravenously or 60
minutes after the medicine has been administered oral-
ly to obtain the peak, or highest, blood level. All institu-
tions have policies that prescribe the best approach to
therapeutic drug monitoring with specic medicines
to ensure the accuracy and usefulness of results. To co-
ordinate blood draws with the timing of drug admin-
istration, institutional policies regarding the handling
of laboratory requests should be checked.
NURSING IMPLICATIONS WHEN MONITORING DRUG
THERAPY
Chapter 4 discusses in detail the nursing process as it
applies to pharmacology. In this chapter, which dis-
cusses drug action across the life span, it is appropriate
to discuss nursing actions that relate to high-risk popu-
lations, such as pediatric patients, older adult patients,
pregnant patients, and breastfeeding patients.
MONITORING PARAMETERS
All medicines have a number of parameters (e.g., ex-
pected therapeutic actions, common adverse effects,
serious adverse effects, and any drug interactions) that
a nurse must be knowledgeable about before taking on
the responsibility of administering medications to pa-
tients. When peak and trough blood levels for a medi-
cation have been ordered, it is important that the nurse
check the laboratory results in a timely manner and
make sure that the prescriber is notied of the labora-
tory results. The next dose of the medication should
not be given until the dosage has been claried on the
basis of the blood levels measured.
Although many of the same monitoring parameters
(e.g., vital signs, urine output, renal function tests) are
used to plan dosages and to monitor the effects of drug
therapy in patients of all ages, it is absolutely crucial
that the normal values for these monitoring param-
eters and laboratory tests be related to the age of the
 Drug Action Across the Life Span CHAPTER 3 29

Table 3.4 Overview of Factors That Inuence Drug Actions With Regard to Age and Gender
FACTOR AGE/GENDER PHYSIOLOGIC VARIABLES
Absorption Infants •  Erratic absorption for intramuscular (IM) medications resulting from underdeveloped
muscles
•  Topical medications absorbed faster because skin underdeveloped
•  Reduced gastric acidity and prolonged transit time for medications orally
Elderly •  Unpredictable absorption for IM medications; muscle mass, blood ow, and muscle
activity are factors
•  Topical medications affected by skin thickness, tissue perfusion
•  Reduced gastric acidity, slower gastric emptying time for oral medications
Gender •  Women have slower gastric emptying time
Distribution Infants •  Greater total body water content
•  Total fat content low
•  Protein binding lower, with lower circulating plasma proteins
Elderly •  Lower total body water content
•  Total fat content increases as one ages
•  Protein binding lower, albumin levels diminish after 40 yr of age
Gender •  Women have greater proportion of body fat than men
Metabolism Infants •  Liver enzyme systems are immature
Elderly •  Liver function decreases with age, slowing metabolism
Gender •  Women have more active cytochrome P450 enzymes, which metabolize drugs faster
than men
Excretion Infants •  Renal capacity is 15% of that of an adult at full-term birth; lower with preterm birth
Elderly •  Renal function based on serum creatinine; creatinine production is based on muscle
mass, which may be lower in the elderly
Gender •  Both renal blood ow and glomerular ltration rate (GFR) are higher in men than in
women
•  Women show a slower clearance of drugs that are eliminated via the kidneys
•  During pregnancy the GFR may double, requiring an increased dosage or more frequent
administration of drugs excreted by glomerular ltration to maintain a therapeutic effect

patient being monitored. For example, neonates have
higher respiratory and heart rates and lower normal
blood pressures than adults. As with all medications,
patient education is important. Involving the appro-
priate family members, caregivers, and the school
nurse in the overall health teaching plan is essential
(see Chapter 5).
Pediatric Patients
Children are not just smaller versions of adults; there-
fore the principles of drug therapy cannot be extrapo-
lated to infants and children only on the basis of size.
Infants and children are at greater risk for complica-
tions from drug therapy because their body and organ
functions are in an ongoing state of development.
General principles that a nurse can apply to the care
of a pediatric patient include the following:
• Although infants and young children have a higher
total body water content, they are more susceptible
to dehydration from fever, vomiting, or diarrhea.
• Weight variations and growth spurts are expected
in pediatric patients during normal maturation.
Dosage adjustments are frequently necessary for
patients who are taking medicine on a regular basis
(e.g., seizure medicines, allergy medicines) because
they outgrow their dosages (see Appendix A for
a nomogram for estimating body surface area).
Therefore it is important to obtain accurate height
and weight measurements on a regular basis.
• Therapeutic drug monitoring is essential for neo-
nates, infants, and children to ensure that drugs are
within an appropriate therapeutic range. The nurse
must document the precise times that blood sam-
ples are drawn and the time over which the medi-
cine was infused for accurate interpretation of the
results.
• It is often difcult to assess the therapeutic response
to the medicines administered to neonates, infants,
and young children because these patients are often
nonverbal or cannot tell us where it hurts. The nurse
must rely more on laboratory values and assessment
parameters such as temperature, pulse, respirations,
heart sounds, lung sounds, bowel sounds, intake
and output data, appetite, general appearance, and
responsiveness.
• Nurses may nd it difcult to measure and admin-
ister doses of oral medicines to pediatric patients ac-
curately. The volume delivered by a household tea-
spoon ranges from 2.5 to 7.5 mL and may vary when
the same spoon is used by different caregivers. The
30 UNIT I Applying Pharmacology to Nursing Practice
American Academy of Pediatrics recommends the
use of appropriate devices for liquid administra-
tion, such as a medication cup, an oral dropper, or
an oral syringe. Although tablets and capsules can
usually be swallowed by a child who is 5 years old
or older, the nurse should evaluate each child’s
ability to swallow a tablet before administration.
Tablets that are not sustained-release or enteric-
coated formulations may be crushed. Most capsules
may be opened and the contents sprinkled on small
amounts of food (e.g., applesauce, jelly, pudding).
Box 3.1 provides selected pediatric administration
guidelines for oral administration.
• Oral and parenteral medicines available in powder
form must be diluted properly in accordance with
the manufacturer’s directions to allow for the ac-
curate measurement of doses and to prevent hyper-
osmolar solutions from being administered. When
taken orally, hyperosmolar solutions may cause di-
arrhea and dehydration.
• Many medicines are not approved by the FDA for
use in children. Primary healthcare providers may
still legally prescribe medicines for what is termed
off-label use, but it is important for the nurse to ques-
tion a specic dose of medicine if it is not readily
available for cross-checking with reference texts or
with the drug information service in the pharma-
cy. The nurse must document in the nurses’ notes
that the drug order was veried before the pre-
scribed medicine was administered. Nurses must
be well versed in the monitoring parameters of the
drug, and report adverse effects to the healthcare
provider.
• In general, salicylates (aspirin) should not be admin-
istered to pediatric patients from infancy through
adolescence. These children are susceptible to a life-
threatening illness known as Reye syndrome if they
ingest aspirin at the time of or shortly after viral in-
fection with chickenpox or inuenza.
• Medicines that are routinely used for analgesia and
antipyresis (fever reduction) in pediatric patients
are ibuprofen and acetaminophen.
• Allergic reactions can occur rapidly in children,
particularly if the medicine is administered intra-
venously. Reactions occur most commonly to anti-
biotics, especially penicillins. The nurse needs to be
observant for responses to medication administra-
tion; if an event should occur, prompt intervention
is needed. The rst symptoms may be intense anxi-
ety, weakness, sweating, and shortness of breath.
Other symptoms may include hypotension, shock,
dysrhythmia, respiratory congestion, laryngeal ede-
ma, nausea, and defecation. The nurse should sum-
mon assistance (call a code if severity warrants),
stay with the child to provide comfort, facilitate
breathing (administer oxygen, as needed), and, if
the child stops breathing, initiate cardiopulmonary
resuscitation.
Selected Guidelines for the Administration of
Box 3.1
Oral Medicine to Pediatric Patients a
INFANTS
• Use a calibrated dropper or an oral syringe.
• Support the infant’s head while holding the infant in the
lap.
• Give small amounts of medicine to prevent choking.
• If desired, crush non–enteric-coated or slow-release
tablets into a powder and then sprinkle the powder on
small amounts of food.
• Provide physical comforting while administering
medications to help calm the infant.
TODDLERS
• Allow the toddler to choose a position in which to take
the medication.
• If necessary, disguise the taste of the medication with
a small volume of avored drink or a small amount of
food; also, a rinse with a avored drink or water will
help remove any unpleasant aftertaste.
• Use simple commands in the toddler’s jargon to obtain
cooperation.
• Allow the toddler to choose which medication to take
rst if more than one is being taken.
• Provide verbal and tactile responses to promote
cooperation.
• Allow the toddler to become familiar with the oral
dosing device.
PRESCHOOL CHILDREN
• If possible, place a tablet or capsule near the back of
the tongue, and then provide water or a avored liquid
to help with the swallowing of the medication.
• If the child’s teeth are loose, do not use chewable
tablets.
• Use a straw to administer medications that could stain
teeth.
• Use a follow-up rinse with a avored drink to help
minimize any unpleasant aftertaste.
• Allow the child to help make decisions about the
dosage formulation, the place of administration, which
medication to take rst, and the type of avored drink
to use.
aForall age groups listed, use a liquid dosage form, if available.
From Brown LM, Isetts BJ. Patient assessment and consultation. In: Krinsky
DL, Berardi RR, eds. Handbook of Nonprescription Drugs: An Interactive
Approach to Self-Care. 17th ed. Washington, DC: American Pharmacists
Association; 2012:27. Reproduced with permission from the American
Pharmacists Association.
Geriatric Patients
Geriatric patients represent an ever-increasing portion
of the population. Although people who are more than
65 years old represent about 14% of the US population,
they consume more than 25% of all prescription medi-
cines and 33% of all nonprescription medicines sold.
The prevalence of prescription medication use in the
ambulatory adult population increases with advanc-
ing age. A recent study of the US noninstitutionalized
adult population has indicated that more than 90%
of persons 65 years old or older use at least one
medication per week. More than 40% use 5 or more

medications and 12% use 10 or more different medica-
tions per week.
Life Span Considerations
Older Adults
It is important that healthcare professionals understand the
physiologic and pathologic changes that develop with ad-
vancing age and adjust drug therapy for the individual patient
accordingly. Factors that place older adults at greater risk
for drug interactions or drug toxicity include reduced renal
and hepatic function, chronic illnesses that require multi-
drug therapy (polypharmacy), and a greater likelihood of
malnourishment.
Unfortunately, a lack of complete understanding of
the effects of medicines in older adults also leads to
a problem that is the opposite of overuse: underuse.
Caregivers walk a ne line between polypharmacy and
undertreatment because of the complexity of chronic
illnesses, changes in physiology and nutrition, com-
pliance with multidrug regimens, and the pharmaco-
kinetic factors associated with drug therapy during the
later decades of a person’s life. Although medicines
may impair an older patient’s quality of life, medicines
are also the most cost-effective treatment for prevent-
ing illness and disability in the geriatric population.
When caring for a geriatric patient, it is important
to complete a thorough drug history that includes the
patient’s use of nonprescription and herbal medicines
(especially laxatives and antacids), nutritional and
herbal supplements, and alternative therapies (e.g.,
aromatherapy, heat therapy, cold therapy). Similarly,
a thorough nutrition history should be completed for
the patient. Determine whether the patient’s diet is bal-
anced with regard to carbohydrates, fats, proteins, and
vitamins. Assess whether a loss of teeth or loose-tting
dentures could interfere with chewing. A functional
health assessment that includes sight and ne-motor
control should be completed to assess the patient’s
ability to self-medicate.
When evaluating a new symptom in a geriatric pa-
tient, determine rst whether it was induced by medi-
cines that the patient is taking. The adjustment of dos-
ages or the elimination of certain medicines is often
the easiest, quickest, and most cost-effective therapy
available.
When discontinuing drug therapy, it is important to
taper the dosage when appropriate (e.g., beta blockers,
antidepressants) to prevent symptoms that could oc-
cur as a result of sudden discontinuation.
When initiating therapy with a geriatric patient, re-
member the following:
• Start at one-third to one-half of the normal adult
recommended dosage, and then gradually increase
the dosage at appropriate intervals to assess for the
therapeutic effect and the development of adverse
effects.
Drug Action Across the Life Span CHAPTER 3 31
• Keep multidrug regimens simple; use aids such as
a calendar or a pillbox with time slots to prevent
confusion.
• Use therapeutic drug monitoring when serum drug
level data are available for a particular medicine.
• Offer assistance with destroying expired prescrip-
tions to minimize confusion with the current medi-
cation regimen.
• Periodically review the regimen to see whether
any medications can be discontinued (e.g., allergy
medicines outside of allergy season). Ask whether
new prescriptions from other healthcare providers
or nonprescription or herbal medicines have been
started.
• Be alert to prescriptions for the medications listed in
Table 3.5. This list of medicines is part of the Beers
Criteria, which are used to evaluate prescription
quality and safety in nursing homes. These medi-
cines are considered to be potentially inappropriate
(but not contraindicated) for older patients. Their
use should be documented as the best alternative
for a patient’s particular needs. The Centers for
Medicare and Medicaid Services has incorporated
the Beers Criteria into federal safety regulations for
long-term care facilities.
• Geriatric patients may have difculty with swal-
lowing large tablets or capsules. Tablets may need
to be broken in half or crushed if there is a score
mark on the tablet. Remember that timed-release
tablets, enteric-coated tablets, and sublingual tab-
lets should never be crushed because of the effect
on the absorption rate and the potential for toxicity.
Applesauce, ice cream, pudding, and jelly are good
foods to use to administer crushed medications.
• It is extremely important that patients understand
the purposes of the medications that they are tak-
ing and any complications that could occur if they
discontinue their drugs.
• When handing a patient a new prescription to be
lled, inquire about their ability to pay for the new
medicine. Do not let an inability to pay be a barrier
to therapy; refer the patient to social services, as
needed.
Pregnant Patients
During pregnancy, the fetus is exposed to most medi-
cines and foreign substances that are circulating in the
mother’s blood. Fetuses are particularly sensitive to
toxic substances while in utero for the following rea-
sons: (1) they have few circulating proteins that can
bind drugs; (2) their enzyme systems, which will later
metabolize drugs, are not yet developed or are imma-
ture; and (3) their excretory systems are only minimal-
ly functioning. Some drugs known as teratogens will
cause the abnormal development of key tissues (i.e.,
birth defects) if they are taken at a certain time during
pregnancy (Table 3.6).
32 UNIT I Applying Pharmacology to Nursing Practice

Table 3.5 Potentially Inappropriate Drugs for Older Adult Patients a

GENERIC NAME BRAND NAME RATIONALE
MEDICATIONS TO AVOID
Antidepressants
amitriptyline Elavil Highly anticholinergic
doxepin greater than 6 mg Sedating and cause orthostatic hypotension
paroxetine Paxil
Antihistamines
chlorpheniramine Chlor-Trimeton Highly anticholinergic
cyproheptadine Risk of confusion, dry mouth, and constipation
Diphenhydramine used for acute treatment of severe allergic reactions
diphenhydramine Benadryl
may be appropriate
hydroxyzine Vistaril
Antiinfective
nitrofurantoin Macrobid Potential for pulmonary toxicity, hepatoxicity, and peripheral neuropathy,
especially with long-term use; safer alternatives available
Avoid in individuals with creatinine clearance of less than 30 mL/min or
for long-term suppression of bacteria
Antispasmodics
dicyclomine Bentyl Highly anticholinergic
hyoscyamine Levsin
Antipsychotics
First Generation (Typical) All increase risk of cerebrovascular accident and greater cognitive
uphenazine decline and mortality in patients with dementia
Do not use for behavior problems of dementia or delirium
haloperidol Haldol
Avoid, except for schizophrenia, bipolar disorder, or as antiemetic
Second Generation (Atypical) during chemotherapy
aripiprazole Abilify
quetiapine Seroquel
Benzodiazepines
Short and Intermediate Acting Older patients are very sensitive to benzodiazepines and have
alprazolam Xanax decreased ability to metabolize long-acting benzodiazepines
All benzodiazepines increase risk of cognitive impairment, delirium, falls,
lorazepam Ativan
and fractures
temazepam Restoril Long-acting benzodiazepines may be appropriate for seizure disorders,
Long Acting ethanol withdrawal, severe generalized anxiety disorder
clonazepam Klonopin
diazepam Valium
urazepam
Cardiovascular Drugs
Antiarrhythmics
amiodarone Pacerone Amiodarone is effective for maintaining sinus rhythm but has greater
toxicities than other antiarrhythmics; avoid as rst line unless patient
has heart failure
digoxin Lanoxin Digoxin may be associated with increased mortality in atrial brillation
and heart failure; do not use rst line and limit dose to less than
0.125 mg/day
Peripheral Alpha-1 Blockers High risk of orthostatic hypotension; avoid use to treat hypertension
doxazosin Cardura
terazosin Hytrin
Central Alpha Blockers High risk of central nervous system effects; may cause bradycardia
and orthostatic hypotension; not recommended to routinely treat
hypertension
clonidine Catapres
Continued
 Drug Action Across the Life Span CHAPTER 3 33

Table 3.5 Potentially Inappropriate Drugs for Older Adult Patients a—cont’d
GENERIC NAME BRAND NAME RATIONALE
Gastrointestinal Drugs
metoclopramide Reglan Can cause extrapyramidal effects, including tardive dyskinesia; risk may
be greater in frail older adults and with prolonged exposure
Avoid, unless for gastroparesis do not used for more than 12 wk.
Proton-pump inhibitors Risk of Clostridium difcile infection and bone loss and fractures
Do not use for >8 wk unless for high-risk patients (e.g., oral
corticosteroids or chronic NSAID use, Barret esophagitis)
Nonsteroidal Antiinammatory Drugs
aspirin greater than 325 mg Increased gastrointestinal bleeding
ibuprofen Motrin Avoid chronic use
naproxen Naprosyn
Nonbenzodiazepines
eszopiclone Lunesta Have adverse effects similar to benzodiazepines
zolpidem Ambien
aThese medicines are still approved for use; however, it is believed that the adverse effects are generally more common, and thus the medicines should be avoided in
older adult patients unless treatment has failed with other medicines.
Data from American Geriatrics Society 2019 Beers Criteria Update Expert Panel. American Geriatrics Society 2019 Updated AGS Beers Criteria for Potentially
Inappropriate Medication Use in Older Adults. J Am Geriatr Soc. 2019;67(4):674-694.

Table 3.6 Drugs Known to Be Teratogens

DRUG CLASS EXAMPLE(S)
Androgenic and estrogenic hormones oral contraceptives, diethylstilbestrol, conjugated estrogens, clomiphene,
exemestane
Angiotensin-converting enzyme inhibitors benazepril, captopril, enalapril, fosinopril, lisinopril, moexipril, perindopril, ramipril,
trandolapril
Angiotensin II receptor antagonists azilsartan, candesartan, eprosartan, irbesartan, losartan, olmesartan, telmisartan,
valsartan
Anticonvulsants carbamazepine, phenytoin, trimethadione, valproic acid
Antimanic agents lithium
Antithyroid drugs propylthiouracil, methimazole
Chemotherapeutic agents busulfan, cyclophosphamide, methotrexate
Hydroxymethylglutaryl coenzyme A atorvastatin, uvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin
reductase inhibitors (statins)
Other teratogens ambrisentan, anastrozole, azathioprine, cocaine, dronedarone, dutasteride,
ethanol (high dose, frequent use), isotretinoin, alitretinoin, ribavirin, tetracycline,
thalidomide, vitamin A (>18,000 units/day), warfarin

Because of the potential for injury to the develop-
ing fetus, drug therapy during pregnancy should be
avoided if at all possible. However, studies indicate
that about two-thirds of women take at least one
drug while pregnant and that about two-thirds of the
medicines are nonprescription self-care remedies. The
medicines that are most commonly taken include acet-
aminophen, antacids, and cold and allergy products.
Because few data are available for determining the
safety of medicines in humans during pregnancy, very
few medicines can be considered completely safe for
use during pregnancy.
In 2015 the FDA instituted new rules for drug labels
that replace the lettered categories with new categories
on pregnancy, lactation, and reproductive potential. In
addition to including information that summarizes the
risks of using a drug during pregnancy (increasing the
risk to the fetus for birth defects, called teratogenicity)
and lactation, labeling must now include relevant in-
formation about contraception, pregnancy testing, and
infertility to inform the healthcare provider prescrib-
ing drugs for females and males of reproductive poten-
tial (and for the consumer). It will be several years be-
fore the older system is completely phased out, but the
new format will allow for consistency of information
regarding risks and benets of prescription drugs used
during pregnancy and lactation and by females and
males of reproductive potential. Information regarding
drug use in pregnancy, in lactation, and in females and
males of reproductive potential is found in section 8 of
the package insert and in other online drug informa-
tion resources such as ePocrates and Lexicomp. Two
34 UNIT I Applying Pharmacology to Nursing Practice
Table 3.7 Drugs and Nursing Infants
DRUGS’ POTENTIAL ADVERSE EFFECTS
Drugs that may interfere with the
metabolism of a nursing infant
Drugs of abuse reported to have adverse
effects on nursing infants
Drugs for which effect on nursing infants
is unknown but may be of concern
Antianxiety medications
Antidepressants
Others
Drugs associated with signicant effects
on nursing infantsa
aDrugs for which the effect on nursing infants is unknown but may be of concern. Give to nursing mothers with caution.
excellent resources—LactMed and DART—are avail-
able on the National Library of Medicine’s TOXNET
website. These resources include information on non-
prescription medications, whereas the new labeling
requirements do not provide information on these
drugs. (See Online Resources for links.)
General principles that a nurse can apply to the care
of a pregnant patient include the following (see also
Chapter 39):
• When taking a history, be alert to the possibility of
pregnancy in any woman of childbearing age, es-
pecially in those showing symptoms of early preg-
nancy, including nausea, vomiting (especially in the
morning), and frequent urination.
• Complete a thorough drug history, including the
use of nonprescription and herbal medicines and
nutritional supplements.
• Complete a thorough nutrition history; assess for a
diet that is balanced with regard to carbohydrates,
fats, proteins, and vitamins. Good nutrition with
the appropriate ingestion of vitamins (especially fo-
lic acid) and minerals (calcium and phosphorus) is
particularly important for preventing birth defects.
• Instruct the patient to avoid drugs in general at any
stage of pregnancy, unless such use is recommend-
ed by the patient’s primary healthcare provider.
• Advise against the consumption of alcohol during
pregnancy. Excessive use may cause the child to be
born with fetal alcohol syndrome, which is a lifelong
condition that can be avoided by eliminating alcohol
during pregnancy. If the woman is planning to be-
come pregnant, it is recommended that she stop using
alcohol 2 to 3 months before the planned conception.
• Advise against the use of tobacco. Mothers who
smoke have a higher frequency of miscarriage,
stillbirths, premature births, and low-birth-weight
infants.
EXAMPLES
cyclophosphamide, cyclosporine, doxorubicin, methotrexate, capecitabine,
cytarabine, gemcitabine, pemetrexed
amphetamine, cocaine, heroin, marijuana, phencyclidine, ethanol
Benzodiazepines: alprazolam, diazepam, quazepam
Cyclic antidepressants: amitriptyline, clomipramine, nortriptyline, desipramine,
imipramine, doxepin, bupropion, trazodone
Serotonin reuptake inhibitors: uoxetine, uvoxamine, paroxetine, sertraline
Antipsychotic drugs: chlorpromazine, clozapine, haloperidol, mesoridazine,
triuoperazine
amiodarone, lamotrigine, metronidazole
aspirin, beta-adrenergic blocking agents (acebutolol, atenolol), clemastine, lithium,
phenobarbital, primidone
• Before they use medicines, advise pregnant women
to try nonpharmacologic treatments. For morning
sickness, the patient can try lying down when she
feels nauseated; ingesting crackers or sipping small
quantities of liquids before arising; eating small,
frequent meals that are high in carbohydrates; and
lowering fat content of meals. Pregnant women
with morning sickness should avoid spicy foods,
dairy products, and smells or situations that might
cause vomiting.
• Herbal medicines that have not been scientical-
ly tested in women during pregnancy should be
avoided.
Breastfeeding Infants
Many drugs are known to enter the breast milk of nurs-
ing mothers and have the potential to harm the infant.
The American Academy of Pediatrics provides a list of
medicines and their potential effects on nursing infants
(Table 3.7).
Nurses should keep in mind when caring for pa-
tients who are breastfeeding that although drug lev-
els in breast milk may be safe, it is always best for the
mother to discuss all medicines she uses—including
prescription, nonprescription, and herbal products—
with a healthcare provider before taking them. If med-
icine is being taken, encourage the mother to take it
immediately after the infant nishes breastfeeding or
just before the infant’s longer sleep periods. Educate
the mother about what adverse effects of the drug
might occur in the infant so that other therapy can be
considered.
GENETICS AND DRUG METABOLISM
Genetic composition serves as the basic foundation
for all drug responses and their duration of action in

the body throughout the person’s lifetime. Many other
factors have an impact on drug action and duration,
but the foundation starts with the genetic blueprint.
Genetics is the study of how living organisms inher-
it the characteristics or traits of their ancestors, such
as hair color, eye color, and skin pigmentation. Other
much less obvious—but extremely important—traits
of inheritance include the function of the metabolic
pathways and susceptibility to illnesses (e.g., heart
disease or cancer).
A genome is the complete package of genetic cod-
ing of an organism. The human genome is composed
of 23 chromosome pairs, 22 of which are known as
autosomal (i.e., not gender related) pairs; the remain-
ing pair is the X or Y chromosome that determines the
presence of male or female sex characteristics. Twenty-
three chromosomes each are donated by the biologic
mother and father. Genetic information is carried on
the chromosomes by a large molecule called deoxyri-
bonucleic acid (DNA), which is copied and passed on
to future generations. Traits are carried in DNA as
instructions for building and operating an organism.
These instructions are contained in segments of DNA
called genes. The sequence of the DNA linkages in a
gene determines what traits the gene controls. The se-
quence of DNA is similar to a sequence of words that
are linked together to form a meaningful sentence.
Several genes are frequently responsible for a specic
trait or function. The sequence of genes is known as the
genetic code. The organism reads the sequence of these
units and decodes the instructions. Polymorphisms are
naturally occurring variations in the structures of genes
and the instructions that they give to the organism.
In 1989 the National Center for Human Genome
Research was created to lead the US contribution to
the Human Genome Project, an international public
effort to sequence all 3 billion DNA base pairs of the
human genetic blueprint. The Human Genome Project
was completed in April 2003, and the database is now
available for worldwide biomedical research.
An unfolding science based on genetics is pharma-
cogenetics, which is the study of how drug response
may vary in accordance with inherited differences. As
Drug Action Across the Life Span CHAPTER 3 35
described in Chapter 2, drug action depends on ve
factors: liberation, absorption, distribution, metabo-
lism, and excretion. Each of these factors is greatly in-
uenced by genetic polymorphisms, but each also var-
ies on the basis of such factors as age, gender, organ
function, other drug therapy, and drug interactions.
Research has shown signicant differences among ra-
cial and ethnic groups with regard to the metabolism,
clinical effectiveness, and side effect proles of differ-
ent medications.
Most studies to date have concentrated on car-
diovascular and psychiatric drugs, analgesics, anti-
histamines, and ethanol. The research so far primarily
applies to African Americans, whites, and Asians, but
more research is now focusing on Hispanic Americans
because they represent the largest racial or ethnic group
after whites in the United States. It is anticipated that
discoveries in pharmacogenetics will allow a blood
sample to be analyzed for specic gene characteristics
(genotyped) that are important determinants of drug
pharmacokinetics and pharmacodynamics, thereby al-
lowing drug selection to be tailored to the individual
patient’s genetic makeup.
Monoclonal antibodies are early examples of medi-
cines that were synthesized to attack certain types of
cancers on the basis of the presence of genetically de-
termined types of cells in some cancers. Laboratory
tests are used to determine the presence of these pro-
teins in a patient’s cancer cells and whether the cancer
cells will be susceptible to the monoclonal antibody.
Another recent discovery is the potential for fatal skin
reactions (i.e., Stevens-Johnson syndrome, toxic epi-
dermal necrolysis) that can be caused by carbamaze-
pine therapy in patients with the human leukocyte an-
tigen allele HLA-B*1502. This allele is most common in
persons of Asian and South Asian Indian ancestry (see
the discussion of carbamazepine in Chapter 18). The
FDA maintains a website that lists genomic biomark-
ers that have been identied (see Online Resources).
These can be tested for before the initiation of drug
therapy to target therapy or prevent potentially fatal
drug reactions.
36 UNIT I Applying Pharmacology to Nursing Practice
Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• The placebo effect occurs when a patient believes they
had a positive response to a drug, even though the patient
did not have any chemically active drug. The nocebo effect
occurs when the patient has negative expectations about
therapy and the patient believes that a drug is not working.
• Drug dependence occurs when a patient develops physical
withdrawal symptoms if the drug is withdrawn for a certain
period, or when a patient is emotionally attached to a drug.
• The age of the patient has signicant effects on the
absorption, distribution, metabolism, and excretion of
the drug. Pediatric patients and elderly patients are more
susceptible to the effects of drugs than adult patients.
Physical changes that occur during the aging process can
alter the effect drugs will have on the elderly patient.
• Men and women often do not respond to drugs or physical
disease states in the same way, and gender differences
can alter the effect of drugs.
• Pregnant and breastfeeding women need to be aware that
any drug they take will have an effect on their unborn fetus
and/or infant.
• Pharmacogenetics currently focuses on determining the
appropriate drug to use based on the individual’s genetic
composition.
Additional Learning Resources
SG Go to your Study Guide for additional Review Ques-
tions for the NCLEX® Examination, Critical Thinking Clinical
Situations, and other learning activities to help you master this
chapter content.
Go to your Evolve website (https://evolve.elsevier
.com/Clayton) for additional online resources.
Online Resources
•  DART: https://toxnet.nlm.nih.gov/newtoxnet/dart.htm
• LactMed: https://toxnet.nlm.nih.gov/newtoxnet/lactmed.
htm
• Pharmacogenomic biomarkers: https://www.fda.gov/Drug
s/ScienceResearch/ucm572698.htm
Clinical Judgment and Next-Generation NCLEX®
Examination-Style Questions
The following questions are typical of the NCLEX examination and
include both NGN (Next Generation) and traditional questions.
See Chapter 1 for further information regarding question types.
1. A patient who has been asked to participate in a study asks
the nurse what the term placebo means. What would be an
appropriate response by the nurse?
1. “The word placebo refers to the type of abnormal
response that may occur when taking medications.”
2. “That term means the body has built up a resistance to a
drug and that more of the drug is needed to get the same
response.”
3. “The term placebo refers to a dosage form that has no
active ingredients; these are frequently used in studies to
determine the effect of a new medication.”
4. “The word placebo comes from Latin and means ‘I will
harm.’ ”
Objective: Explain the impact of the placebo effect and the nocebo
effect.
NCLEX test item: Multiple choice
Cognitive skill: Evaluation
2. Why is it important for the nurse to understand the difference
between drug dependence and drug accumulation?
1. Drug accumulation can be detected more easily than
drug dependence.
2. Drug accumulation may result in drug toxicity, and drug
dependence can result in cell mutation.
3. Drug dependence can be prevented, and drug
accumulation is inevitable.
4. Drug dependence can be the result of taking addictive
substances for a prolonged time, and drug accumulation
can result in drug overdose.
Objective: Identify the importance of drug dependence and drug
accumulation.
NCEX test item: Multiple choice
Cognitive skill: Understanding
3. The nurse knows that drug absorption in the elderly is affected by
which of these physiologic factors? (Select all that apply.)
1. Changes in albumin levels
2. Increased ltration capacity of the kidneys
3. Reduced cardiac output
4. Higher gastric pH
5. Decreased GI motility
Objective: Discuss the effects of age on drug absorption,
distribution, metabolism, and excretion.
NCLEX test item: Multiple response
Cognitive skill: Application
4. Which nursing action(s) would be essential when monitoring drug
therapy in the geriatric patient? (Select all that apply.)
1. Monitoring renal and liver function
2. Monitoring for drug interactions
3. Completing a thorough drug history, including over-the-
counter and alternative therapies
4. Inquiring about the ability to pay for medications
5. Educating the patient and caregivers about all drugs and
potential complications
Objective: Discuss the effects of age on drug absorption,
distribution, metabolism, and excretion.
NCLEX test item: Multiple response
Cognitive skill: Application
5. The nurse caring for an elderly patient understands that when
giving medications there are aging factors that affect how the drug
will work.
Indicate with an X the factors that inuence drug actions re-
lated to aging.
 Drug Action Across the Life Span CHAPTER 3 37

AGING FACTORS AND OTHER EFFECTS DRUG ABSORPTION DRUG DISTRIBUTION DRUG METABOLISM DRUG EXCRETION
Genetics, smoking, diet, gender, other
medications and diseases
Albumin levels diminish
Decreased renal blood ow
Muscle inactivity and changes in muscle mass

Objective: Discuss the effects of age on drug absorption, 8. A pregnant woman asked a nurse at the obstetrician’s clinic
distribution, metabolism, and excretion. how she could determine which drug was safe to take during
NGN test item: Matrix pregnancy. What would be an appropriate response by the nurse?
Cognitive skill: Recognize cues 1. “Because there are few studies done to determine the
6. While discussing with a mother the importance of administering safe use of drugs during pregnancy, it is okay to keep
furosemide orally to an infant with a cardiac abnormality, the nurse taking what was previously prescribed by your primary
would recognize the need for further explanation if the mother healthcare provider.”
makes which statement? 2. “Because there are few studies done to determine the
safe use of drugs during pregnancy, it is advisable to ask
1. “I know that my baby needs this drug every day at your primary healthcare provider or pharmacist regarding
approximately the same time.” taking prescription and over-the-counter drugs.”
2. “My baby will have no problem taking this tablet.” 3. “You are not to take any drugs during pregnancy.”
3. “I will check to make sure that the furosemide is working 4. “It would be ne to take over-the-counter drugs, since
by monitoring the number of wet diapers.” they never cause any issues.”
4. “I understand that my baby will continue to grow even
while taking this drug.” Objective: Describe where a nurse will nd new information about
the use of drugs during pregnancy and lactation.
Objective: Discuss the effects of age on drug absorption, NCLEX test item: Multiple choice
distribution, metabolism, and excretion. Cognitive skill: Comprehension
NCLEX test item: Multiple choice
Cognitive skill: Comprehension 9. An expecting mother asks the nurse if it would be okay for her to
take some cold medicine. What would be an appropriate response
7. The nurse recognized there are gender considerations to keep in by the nurse?
mind with regard to drug actions.
1. “There are not a lot of studies done with regard to how
Choose the most likely options for the information missing safe medications are to take during pregnancy.”
from the sentence below by selecting from the lists of op- 2. “I am sure it is safe to take, no problem.”
tions provided. 3. “I believe the cold medication is contraindicated for
The gender considerations to keep in mind with regard pregnant women.”
to drug actions are that _______1____________ 4. “Animal studies have revealed no evidence of harm to the
will affect ___________2___________ and fetus using these drugs.”
that ___________1____________ will affect Objective: Discuss the impact of pregnancy and breastfeeding on
________2_________, as well as that ______1___________ drug absorption, distribution, metabolism, and excretion.
will affect _______2___________. NCLEX test item: Multiple choice
Cognitive skill: Understanding
OPTIONS FOR 1 OPTIONS FOR 2
10. A patient was discussing with the nurse the idea that in the
women have longer life distribution future we will be able to determine which drug will be effective
spans depending on a person’s genetic makeup. Which term does this
women have greater excretion refer to?
proportion of body fat
1. Polymorphisms
women have slower gastric metabolism
2. Pharmacogenetics
emptying time
3. Genome coding
women have more active absorption
4. Pharmacokinetics
cytochrome P450 enzymes
Objective: Discuss the role of genetics and its inuence on drug
action.
Objective: Explain the gender-specic considerations of drug NCLEX test item: Multiple choice
absorption, distribution, metabolism, and excretion. Cognitive skill: Knowledge
NGN test item: Cloze
Cognitive skill: Analyze cues
 4 The Nursing Process and Pharmacology

https://evolve.elsevier.com/Willihnganz

Objectives
1. Discuss the components and purpose of the nursing
process.
2. Explain what the nurse does to collect patient information
during an assessment.
3. Discuss how nursing diagnosis statements are written.
4. Differentiate between a nursing diagnosis and a medical
diagnosis.
5. Discuss how evidence-based practice is used in planning
nursing care.
6. Differentiate between nursing interventions and outcome
statements.
7. Explain how Maslow’s hierarchy of needs is used to
prioritize patient needs.
8. Compare and contrast the differences between
dependent, interdependent, and independent nursing
actions.
9. Discuss how the nursing process applies to pharmacology.

Key Terms
nursing process (NŬR-sĭng PRŎ-sĕs)
(p. 38)
assessment (ă-SĔS-mĕnt) (p. 39)
nursing diagnosis (NŬR-sĭng dī-ăg-
NŌ-sĭs) (p. 40)
dening characteristics (dĕ-FĪN-ĭng
kăr-ăk-těr-ĬS-tĭks) (p. 41)
medical diagnosis (p. 41)
focused assessment (FŌ-kŭst ă-SĔS-
mĕnt) (p. 41)
planning (p. 41)
nursing care plan (p. 42)
critical pathways (KRĬ-tĭ-kŭl PĂTH-
wāz) (p. 42)
evidence-based practice (ĔV-ĭ-dĕns
BĀSD PRĂK-tĭs) (p. 42)
core measures (p. 42)
priority setting (prī-ŌR-ĭ-tē SĔT-tĭng)
(p. 42)
measurable outcome
statement (MĔ-zhŭr-ĕ-bŭl GŌL
STĀT-mĕnt) (p. 42)
implementation (ĭm-plĕ-mĕn-TĀ-
shŭn) (p. 44)
nursing interventions (p. 44)
nursing actions (p. 44)
dependent actions (dē-PĔN-dĕnt)
(p. 44)
interdependent actions (ĭn-tŭr-dē-
PĔN-dĕnt) (p. 44)
independent actions (ĭn-dē-PĔN-
dĕnt) (p. 44)
drug history (HĬS-tō-rē) (p. 45)
primary source (PRĪ-măr-ē SŌRS)
(p. 45)
subjective data (sŭb-JĔK-tĭv DĀ-tă)
(p. 45)
objective data (ŏb-JĚK-tĭv DĀ-tă)
(p. 45)
secondary sources (SĔK-ŏn-dār-ē
SŌR-sĕz) (p. 45)
tertiary sources (TĔR-shē-ăr-ē)
(p. 45)
drug monographs (MŎN-ō-grăfs)
(p. 45)
therapeutic intent (thěr-ă-PYŪ-tĭk)
(p. 46)

The NursiNg Process Many nursing education programs and healthcare

The practice of nursing is an art and science that uses
a systematic approach to identify and solve the po-
tential problems that individuals may experience as
they strive to maintain basic human function along
the wellness-illness continuum. The focus of all nurs-
ing care is to help individuals maximize their potential
for maintaining the highest possible level of indepen-
dence for the meeting of self-care needs.
The nursing process is the foundation for the clini-
cal practice of nursing. It provides the framework for
consistent nursing actions and involves the use of a
problem-solving approach. The nursing process also
provides a method for evaluating the outcomes of the
therapy delivered.
facilities use a ve-step nursing process model: (1) as-
sessment, (2) nursing diagnosis, (3) planning, (4) im-
plementation, and (5) evaluation. These ve steps are
actually an overlapping process (Fig. 4.1). Information
from each step is used to formulate and develop the
next step in the process. Box 4.1 illustrates the process
that is used to assemble data and organize informa-
tion into categories to identify the patient’s strengths
and problem areas. Thereafter, nursing diagnosis state-
ments can be developed and focused nursing assess-
ments can be initiated. Planning can be individualized,
and measurable goals can be identied. Individualized
nursing interventions can be developed to coincide
with the individual’s abilities and resources, as well as

38
 The Nursing Process and Pharmacology CHAPTER 4 39

Evaluation
1. Document/revise
Assessment (data collection)
outcome attainment
1. Nursing history, medical history
2. Continue care or start
2. Professional observations
referral to community-
3. Physical examination
based health agency
4. Diagnostic test results
or discharge process

Implementation Holistic Nursing diagnosis

1. Meet physical and Care 1. Identify defining
emotional needs Needs characteristics, high-risk
2. Provide for patient safety factors, or problems
3. Perform/modify nursing 2. Perform focused assessment
interventions 3. Formulate nursing
4. Monitor for potential diagnosis statements
complications 4. Identify and seek
5. Perform ongoing orders/directions from
assessments appropriate health team
6. Document care delivered members for collaborative
and patient responses problems

Planning
1. Set priorities
2. Develop written outcome
statements
3. Formulate nursing
interventions
4. Formulate anticipated
therapeutic outcomes
5. Integrate outcomes/classification
systems into critical pathways
and/or care plans

Fig. 4.1 The nursing process and the holistic needs of the patient.

the disease processes being treated. During the imple-
mentation process, the individual’s physical, psycho-
social, and cultural needs must be considered. The as-
sessment process should continue to focus not only on
the evolving changes in the presenting symptoms and
problems but also on the detection of potential compli-
cations that may occur.
Nurses should familiarize themselves with the nurse
practice act in the state in which they practice to iden-
tify the educational and experiential qualications that
are necessary for the performing of assessments and
the development of nursing diagnoses. The formula-
tion of nursing diagnoses requires a broad knowledge
base to make the discriminating judgments needed to
identify the individual patient’s care needs. All mem-
bers of the healthcare team need to contribute data re-
garding the patient’s care needs and their response to
the prescribed treatment regimen.
Just as body functions are constantly undergoing
adjustments to maintain homeostasis in the internal
and external environments, the nursing process is an
ongoing cyclic process that must respond to the chang-
ing requirements of the patient. The nurse must con-
tinually interact with people in a variety of settings
to establish and execute nursing functions creatively
and cooperatively to meet the holistic care needs of pa-
tients (see Fig. 4.1).
Assessment
Assessment is the rst phase of the ve-step nurs-
ing process. It is the problem-identifying phase of the
nursing process. The initial assessment must be per-
formed by a registered nurse with the necessary skills
to complete the physical examination. The assessment
identies patient problems based on dening charac-
teristics (i.e., signs, symptoms, and clinical evidence).
In addition, the nurse should identify risk factors that
make an individual vulnerable to developing certain
problems in response to a disease process or to its pre-
scribed therapy (e.g., adverse effects of drugs).
40 UNIT I Applying Pharmacology to Nursing Practice

Box 4.1 Principles of the Nursing Process and Their Application to Pharmacologic Needs
AssessmeNT imPlemeNTATioN
• Collect all relevant data associated with the individual • Perform the nursing intervention planned to achieve the
patient’s symptoms; their history and physical, established goals or outcomes.
laboratory, and diagnostic data; and medical diagnosis • Monitor the patient’s response to treatments,
to detect actual and risk/high-risk problems that require and monitor for complications related to existing
intervention. pathophysiology.
• Data sources can be primary, secondary, or tertiary. • Provide for patient safety.
• Specic assessments related to the patient’s • Perform ongoing assessments on a continuum.
pharmacologic needs include collecting the drug history; • Document the care given and any additional ndings on
allergies; height and weight; age and disease process; the patient’s chart.b
hepatic function results (AST, ALT, alkaline phosphatase, • Specic interventions related to the patient’s
LDH, bilirubin [total and direct]); and renal function results pharmacologic needs include administering the
(serum creatinine, creatinine clearance, BUN, urinalysis, prescribed drug using the seven rights: verifying the
protein [total and 24-hour urine]), as well as discussing right patient, the right drug, the right dose, the right
the patient’s understanding of drug therapy and the route, the right time, the right indication, and the right
treatment plan and determining their readiness to learn. documentation. The nurse also will be monitoring the
patient using diagnostic parameters; monitoring for
NursiNg DiAgNosis
adverse effects of medications; and performing and
• On the basis of the data collected, formulate a statement
documenting health teaching, which includes having the
about the behaviors or problems of concern and their
patient understand the drug name, the dose, the route of
cause.
administration, the anticipated therapeutic response, the
• Formulate nursing diagnosis statements for problems
adverse effects, what to do if a dose is missed, and how
that are amenable to nursing actions.
to ll a prescription.
• Identify and seek orders or direction from appropriate
healthcare team members for collaborative problems.a evAluATioN
• Evaluation is an ongoing process that occurs at every
PlANNiNg
phase of the nursing process. Establish target data to
• Prioritize the problems identied from the assessment
review and analyze at intervals prescribed by guidelines
data, with the most severe or life-threatening problems
in the practice setting.
addressed rst. Other problems are arranged in
• Review and analyze the data regarding the patient, and
descending order of importance. (Maslow’s hierarchy of
modify the care plan so that goals and outcomes of care,
needs is frequently used as a basis for prioritizing; other
which are used to return the patient to the highest level
approaches may be equally valid.)
of functioning, are attained.
• Develop short- and long-term patient goals and
• Evaluate outcomes with the use of the classication
outcomes in measurable statements that are appropriate
systems, critical pathways, or standardized care plans
to the clinical setting and the length of stay.
that are used in the clinical setting.
• Identify the monitoring parameters to be used to detect
• Follow a systematic approach to recording progress,
possible complications of the disease process or the
depending on the setting and charting methodology.
treatments being used.
• Continue the nursing process, initiate referral to a
• Plan nursing approaches to correlate with each identied
community-based health agency, or execute discharge
patient goal or outcome.
procedures as ordered by the healthcare provider.
• Integrate outcomes and classication systems into
• Specic evaluation criteria related to the patient’s
critical pathways or standardized care plans to be used
pharmacologic needs include evaluating the patient’s
in clinical settings.
tolerance of drug therapy and their understanding of the
• Specic planning related to the patient’s pharmacologic
treatment regimen.
needs includes examining drug monographs and
developing an individualized teaching plan.
aBecause not all patient problems are amenable to resolution by nursing actions, those complications or problems associated with medical diagnosis or that result from
treatment-related issues are placed in a category known as “Collaborative Problems,” which the nurse monitors.
bIntegrate the classication system that is currently in use in the clinical setting when charting (e.g., Nursing Minimum Data Set, Omaha System, Home Health Care

Classication System).
ALT, Alanine aminotransferase; AST, aspartate aminotransferase; BUN, blood urea nitrogen; LDH, lactate dehydrogenase.

During the assessment, the nurse collects a compre-
hensive information base about the patient from the
physical examination, the nursing history, the medica-
tion history, and professional observations. Formats
commonly used for data collection, organization, and
analysis are the head-to-toe assessment, body systems
assessment, and Gordon’s Functional Health Patterns
Model. The head-to-toe and body systems approaches
focus on the patient’s physiology, whereas the Gordon’s
Functional Health Patterns Model (Box 4.2) includes so-
ciocultural, psychological, spiritual, and developmental
factors that affect the individual’s needs.
nursing DiAgnosis
Nursing diagnosis is the second phase of the ve-step
nursing process. NANDA International (NANDA-I,
 The Nursing Process and Pharmacology CHAPTER 4
Box 4.2 Gordon’s Functional Health Patterns Model
Health Perception–Health Management Pattern
Nutrition-Metabolic Pattern
Elimination Pattern
Activity-Exercise Pattern
Cognitive-Perceptual Pattern
Sleep-Rest Pattern
Self-Perception–Self-Concept Pattern
Role-Relationship Pattern
Sexuality-Reproductive Pattern
Coping–Stress Tolerance Pattern
Value-Belief Pattern
Adapted from Gordon M. Manual of Nursing Diagnosis. 11th ed. Sudbury, MA:
Jones & Bartlett; 2007.
formerly the North American Nursing Diagnosis
Association) approved the following ofcial denition
of the term nursing diagnosis: “[a] clinical judgment
about individual, family, or community responses to
actual or potential health problems/life processes.”
Using knowledge and skills related to anatomy,
physiology, nutrition, psychology, pharmacology, mi-
crobiology, nursing practice skills, and communication
techniques, the nurse analyzes the data collected dur-
ing the assessment phase to identify whether certain
major and minor dening characteristics (i.e., manifes-
tations or signs and symptoms) relate to a particular pa-
tient problem. This analysis determines which data is
important to act on and which data is to be monitored.
The nurse may conclude that certain actual problems
are present and identies them with a nursing diagno-
sis. Nursing diagnoses provide the basis for the selec-
tion of nursing interventions or actions needed to treat
the patient. Not all patient problems identied during
an assessment are treated by the nurse alone. Many of
these problems require a multidisciplinary approach.
A medical diagnosis is a statement of the patient’s
alterations in structure and function, and this results
in the diagnosis of a disease or disorder that impairs
normal physiologic function. A nursing diagnosis usu-
ally refers to the patient’s ability to perform activities
of daily living (ADLs) in relation to the impairment
induced by the medical diagnosis; it identies the in-
dividual’s response to the illness. A medical diagnosis
also tends to remain unchanged throughout the illness,
whereas nursing diagnoses may vary, depending on
the patient’s state of recovery. Concepts that help dis-
tinguish a nursing diagnosis from a medical diagnosis
include the following:
1. Conditions described by nursing diagnoses can
be accurately identied by nursing assessment
methods.
2. Nursing treatments or methods of risk-factor reduc-
tion can resolve the condition described by a nurs-
ing diagnosis.
3. Nurses assume accountability for outcomes within
the scope of nursing practice.
41
4. Nurses assume responsibility for the research re-
quired to clearly identify the dening characteris-
tics and causative factors of conditions described by
nursing diagnoses.
5. Nurses engage in improving methods of treatment
and treatment outcomes for conditions described by
nursing diagnoses.
The wording of an actual nursing diagnosis takes
the form of a three-part statement. These statements
consist of the following: (1) a patient problem summa-
rizing the issue; (2) the contributing factors or cause,
which may include decits in ADLs or the medical di-
agnosis; and (3) the dening characteristics (i.e., mani-
festations or signs and symptoms). An example related
to pharmacology would state: Insufcient knowledge re-
lated to polypharmacy as evidenced by inability to state what
prescribed medications are used for.
The risk nursing diagnosis statement con-
sists of two parts: (1) the diagnostic label from the
NANDA-I–approved list and (2) the risk factors that
make the individual more susceptible to the develop-
ment of the problem. A risk diagnosis is validated by
the presence of risk factors that would contribute to
the individual developing the stated problem.
Further discussion of the philosophy and clinical
use of nursing diagnoses can be found in other prima-
ry texts and references, especially in those developed
solely for the purpose of explaining nursing diagnoses.
Not all patient problems identied by the nurse
can be resolved by nursing actions; many care plans
include multidisciplinary input and planning to maxi-
mize patient outcomes. However, the nurse is respon-
sible for monitoring the patient on a continuum for
potential complications that are associated with the
medical diagnosis, the diagnostic procedures, or the
treatments prescribed.
Fcd A
A focused assessment is the process of collecting addi-
tional data specic to a patient or family that validates
a suggested problem or nursing diagnosis. The ques-
tions asked or the data collected are used to conrm
or rule out the dening characteristics associated with
a specic nursing diagnosis statement. During the fo-
cused assessment, prescriptive orders can be identied
that the nurse can implement and that are within the
nurse’s scope of practice.
PlAnning
Planning is the third phase of the ve-step nursing pro-
cess. After the patient has been assessed and problems
have been diagnosed, plans should be formulated to
meet the patient’s needs. Planning usually encompass-
es four phases: (1) priority setting, (2) the development
of measurable goal and outcome statements, (3) the
formulation of nursing interventions, and (4) the for-
mulation of anticipated therapeutic outcomes that can
be used to evaluate the patient’s status. The written or
42 UNIT I Applying Pharmacology to Nursing Practice
Maslow’s hierarchy of needs
morality, creativity, spontaneity, problem solving, lack
of prejudice, acceptance of facts
self-esteem, confidence, achievement, respect of
others, respect by others
friendship, family, sexual intimacy, sense of
connection
security of body, employment, resources,
morality, family, health, property
breathing, food, sex, sleep,
homeostasis, excretion
Fig. 4.2 Maslow’s Hierarchy of Needs Pyramid. (Copyright iStock.com/PyTyCzech.)
computer-generated document that evolves from this
planning process is called the nursing care plan
Critical pathways are standardized, automated care
plans that integrate protocols, interventions, goals,
and outcomes. Critical pathways are also referred to
as integrated care plans, care maps, or clinical maps. These
documents are comprehensive standardized plans
of care that are individualized on admission by the
healthcare provider and/or the nurse case manager.
A critical pathway describes a multidisciplinary plan
that is used by all caregivers to track the patient’s prog-
ress toward expected outcomes within a specied pe-
riod. Standardized outcomes and timetables require
healthcare providers to make assessments regarding
the patient’s progress toward the goals of discharge
while maintaining quality care. Revisions are made as
necessary and communicated to all healthcare team
members so that patient care continues uninterrupted
toward the discharge goals.
edc-Bad Pacc
Evidence-based practice is the application of data
from scientic research to make clinical decisions
about the care of individual patients. Evidence-based
decision making is based on the vast array of clinical
studies that have been completed and the existence of
large databases, which can be quickly accessed and
searched for the best scientic evidence when mak-
ing healthcare decisions. An example of this concept
that is seen in today’s healthcare institutions is the
quality measures known as core measures Core mea-
sures are measures of care that are tracked to show
how often hospitals and healthcare providers use the
care recommendations identied by evidence-based
practice standards for patients who are being treat-
ed for conditions such as heart attack, heart failure,
and pneumonia or for patients who are undergoing
surgery. Hospitals voluntarily submit data from the
medical records of adults who have been treated for
these conditions to help track standards of care and
clinical outcomes.
Py s
After the nursing diagnoses have been identied, they
must be prioritized. Maslow’s hierarchy of needs is
5 Self-actualization
4 Self-esteem
Love and belonging
3
2 Safety and security
1 Physiological needs
a model that is often used for establishing priorities.
Maslow identied ve levels of needs:
1. Physiologic needs, which include eating, breathing,
sleeping, elimination, and so on
2. Safety and security needs, which include feeling
safe, being employed, and having resources
3. Love and belonging needs, which include having a
sense of connection with people
4. Self-esteem needs, which include respecting self
and others and being condent
5. Self-actualization needs, which include being spon-
taneous and creative and being able to problem
solve (Fig. 4.2)
Nurses can use Maslow’s hierarchy to perform the
priority setting of an individual patient’s needs, deter-
mining which care aspect needs to be addressed rst.
These care delivery options are often organized in re-
lation to their direct effects on the maintenance of ho-
meostasis. Thus after determining that the patient is
oxygenating appropriately by pulse oximetry (rst pri-
ority), the nurse can then increase the patient’s activity
(second priority). Box 4.3 lists the priority ranking of
subcategories of Maslow’s hierarchy of human needs.
maab oc ga sa
After the patient’s needs have been prioritized, goals
must be established and statements written. Goals are
usually divided into short-term and long-term plans,
depending on the length of stay and the clinical site.
The measurable outcome statement starts with an ac-
tion word (i.e., a verb) that is followed by the behavior
or behaviors to be performed by the patient or the pa-
tient’s family within a specic amount of time. These
outcome statements need to be Specic, Measurable,
Attainable, Realistic and Timely, using the acronym
SMART the nurse can remember the components
for making proper outcome goal statements. There
should be one outcome goal statement for each nurs-
ing diagnosis.
All outcome statements must be individualized and
based on the patient’s abilities. An example of a goal
statement that follows the nursing diagnosis of knowl-
edge decit would be: The patient will create a list of all
the medications that are currently prescribed along with the
reasons for taking them, by the end of the day. The nurse
 The Nursing Process and Pharmacology CHAPTER 4 43

Priority Ranking of Subcategories of patient to expect for the amount of time during which
Box 4.3 care will be delivered. It is sometimes difcult to accept
Maslow’s Hierarchy of Human Needs
that not everyone can return to their preillness health
Physiologic NeeDs status; therefore the nurse must be realistic when set-
• Oxygen, circulation ting a measurable goal and strive to assist the patient
• Water-salt balance with obtaining an optimal degree of functioning that is
• Food balance consistent with that patient’s abilities.
• Acid-base balance
When goals are being established, it is important to
• Waste elimination
• Normal temperature
include the patient and appropriate signicant others
• Sleep, rest, relaxation in decision making because the patient and their sup-
• Activity, exercise port systems will be responsible for accomplishing the
• Energy goals. Involvement of the patient is essential to pro-
• Comfort mote cooperation and compliance with the therapeu-
• Stimulation tic regimen and to provide the patient with a sense of
• Cleanliness control over the disease process and the course of treat-
• Sexuality ment. The goals that are established should be patient
sAfeTy NeeDs goals rather than nursing goals for the patient.
• Protection from physical harm With the advent of shorter hospital stays, most of
• Protection from psychological threat the goal statements will involve short-term goals. The
• Freedom from pain nurse must keep in mind the usual length of hospital-
• Stability ization and be realistic about the number and types
• Dependence of goals and outcomes being established. Short-term
• Predictable, orderly world goals should serve as a bridge to meet the long-term
BeloNgiNg NeeDs goals established in a care plan. Long-term goals can
• Love, affection be established with assistance from referral agencies
• Acceptance in accordance with the individual’s needs and cir-
• Warm, communicating relationship cumstances. Long-term goals are then implemented in
• Approval from others long-term care settings, rehabilitation centers, mental
• Unity with loved ones health facilities, and community-based home health-
• Group companionship
care delivery settings.
self-esTeem NeeDs Most goal statements are based on the patient’s
• Recognition need to do the following:
• Dignity 1. Reduce or resolve the symptoms (usually the chief
• Appreciation from others complaint) of the disease that caused the person to
• Importance, inuence
seek medical attention.
• Reputation of good character
2. Understand the disease process and its effect on life-
• Attention
• Status style and ADLs.
• Dominance over others 3. Gain knowledge and skills associated with the treat-
ment procedures in an effort to attain the highest
self-AcTuAlizATioN NeeDs level of functioning possible (e.g., nutrition, comfort
• Personal growth and maturity
measures, medication regimen, physical therapy).
• Awareness of potential
• Increased learning
4. Have reasonable expectations of the therapy, includ-
• Full development of potential ing understanding signs and symptoms of improve-
• Improved values ment versus complications that require consultation
• Religious, philosophic satisfaction with a healthcare provider.
• Increased creativity 5. Identify monitoring parameters that should be
• Increased reality perception and problem-solving abilities maintained on a written record that reects the re-
• Less rigid conventionality sponse to the prescribed therapy.
• Less of the familiar, more of the novel 6. Establish a schedule for follow-up evaluation.
• Greater satisfaction in beauty Outcome goal statements are measured along the
• Increased pleasantness continuum of care and include therapeutic outcome
• Less of the simple, more of the complex
statements that are developed to document the effec-
From Campbell C. Nursing Diagnosis and Intervention in Nursing Practice. New tiveness of the care delivered. In the previous example,
York: John Wiley & Sons; 1978. This material is reproduced with permission of
John Wiley & Sons. the patient will do the following:
• Improve the ability to perform coughing technique.
must also refer to critical pathways when establishing • Maintain an adequate uid intake as evidenced by
the parameters. Statements must take into consider- achieving a mutually set goal of 2000 mL within 24
ation the degree of rehabilitation that is realistic for the hours.
44 UNIT I Applying Pharmacology to Nursing Practice
• Attain a respiratory rate between 18 and 24 breaths/
min.
• Perform ADLs without feeling fatigued.
Therapeutic outcomes have been identied through-
out this book for each drug classication. These can be
used by the student to identify the outcomes that are
anticipated from the use of the drugs listed in a par-
ticular classication.
exap f a thapc oc
Using the nursing diagnosis “Anxiousness related
to hospitalization and unknown prognosis,” the pri-
mary therapeutic outcome expected from the benzo-
diazepine antianxiety agents is a decrease in the level
of anxiety to a manageable level for the patient. This
decreased anxiety may be manifested by a reduction
in physical signs of anxiety, such as a worried look or
pacing, and an improvement in coping.
imPlementAtion
Implementation of nursing interventions is the fourth
phase of the nursing process, and it consists of carry-
ing out the established plan of care. Nursing care is
directed at meeting the physical and emotional needs
of the patient, providing for patient safety, monitoring
for potential complications, and performing ongoing
assessments as part of the continual process of data
collection.
Nursing actions are suggested by the etiology of
the problems identied in the nursing diagnoses, and
they are used to implement plans. They may include
activities such as counseling, teaching, providing com-
fort measures, coordinating, referring, using commu-
nication skills, and performing the actions listed in a
healthcare provider’s orders. Documentation of all
care given, including patient education and the pa-
tient’s apparent response, should be performed regu-
larly—both to assist with evaluation and reassessment
and to make other healthcare professionals aware of
the patient’s changing needs.
Within the nursing process are three types of nurs-
ing actions: (1) dependent, (2) interdependent, and
(3) independent. Dependent actions are those per-
formed by the nurse on the basis of the healthcare
provider’s orders, such as the administration of pre-
scribed medications and treatments. It is important
to note that even though these are dependent func-
tions, the nurse is still responsible for exercising pro-
fessional judgment when performing these actions.
Interdependent actions are those nursing actions that
the nurse implements cooperatively with other mem-
bers of the healthcare team for restoring or main-
taining the patient’s health. This allows the nurse
to coordinate their interventions with those of other
healthcare professionals to maximize knowledge and
skills from various disciplines for the well-being of
the patient. Collaborative communication among
multidisciplinary team members is essential for
maximizing patient outcomes in today’s healthcare
environment. Independent actions are those nursing
actions that a nurse can provide by virtue of the edu-
cation and licensure that they have attained. These ac-
tions are usually written in the nursing care plan and
originate from the nursing diagnosis.
n Ac  i sa
Nursing action or intervention statements list in a con-
cise format exactly what the nurse will do to achieve
each goal that has been developed for each nursing di-
agnosis. A nursing action is a statement that describes
nursing interventions that are applicable to any pa-
tient (e.g., promote adequate respiratory ventilation).
Nursing orders describe how specic actions, including
time intervals, will be implemented for an individual
patient.
Example of Nursing Interventions for Patient With
Respiratory Issues
(date): Cough, turn, deep breathe: 0800, 1000, 1200,
1400, 1600, 1800, 2000, 2200
(date): Educate patient re: abdominal breathing, splint-
ing the abdomen, pursed-lip breathing, and assum-
ing correct position to facilitate breathing
(date): Auscultate breath sounds: 0800, 1200, 1600, 2000
(date): Increase patient’s uid intake to at least 2000
mL/24 hr:
0700–1500: 1000 mL
1500–2300: 800 mL
2300–0700: 200 mL
(date): Assess respiratory depth and rate: 0800, 1200,
1600, 2000, 2400
eaa
Evaluation is the fth and nal phase of the ve-step
nursing process. Evaluation involves the nurse de-
termining whether the expected outcomes were met.
Evaluation of the outcome goal statement is impor-
tant so the nurse can determine whether the inter-
ventions were effective in meeting the goal. For the
evaluation process to be successful, the participants
(i.e., the patient, the patient’s family and signicant
others, and the nurse) must be willing to receive feed-
back. Therefore plans for evaluation must involve the
patient, the family, and signicant others from the
beginning and should recognize the needs of a cul-
turally diverse population with varying beliefs about
healthcare.
Although the evaluation phase is the last step in the
nursing process, it is not an end in itself. Evaluation
recognizes the successful completion of previously es-
tablished goals, but it also provides a means for the
input of new signicant data that indicate the develop-
ment of additional problems or a lack of therapeutic
responsiveness, which may require additional nursing
diagnoses or collaboration with the healthcare pro-
vider or other professionals on the healthcare team as
plans for therapy are revised.
 The Nursing Process and Pharmacology CHAPTER 4
relATiNg The NursiNg Process To
PhArmAcology
Assessment
Assessment is an ongoing process that starts with the
admission of the patient and continues daily until the
patient no longer requires care. With regard to relat-
ing the nursing process to the nursing functions asso-
ciated with medications, assessment includes taking a
drug history, which includes current prescription and
nonprescription medications, as well as the presence of
drug allergies. The drug history is important for three
reasons: (1) to evaluate the patient’s need for medica-
tion; (2) to obtain their current and past use of over-
the-counter medications, prescription medications,
herbal products, and street drugs; and (3) to identify
problems related to drug therapy. Nurses will also
want to identify risk factors such as allergies to cer-
tain medications (e.g., penicillins) or the presence of
other diseases that may limit the use of certain types of
drugs (e.g., sympathomimetic agents in patients with
hypertension).
The nurse draws on three sources to build the
medication-related information base. Whenever the
patient is able to provide reliable information, the pa-
tient should be used as the primary source of informa-
tion. Subjective and objective data serve as the baseline
for the formulation of drug-related nursing diagnoses.
Subjective data are pieces of information provided
by the patient (e.g., “Whenever I take this medicine,
I feel sick to my stomach”). Objective data are gained
from observations that the nurse makes with the use
of physiologic parameters (e.g., “skin pale, cold, and
moist; temperature, 99.2°F orally”). Other required ob-
jective information is the patient’s height and weight,
which may be needed to select drug regimens and to
use as a monitoring parameter for drug therapy later
during the patient’s treatment.
In some cases, it is necessary to obtain information
from secondary sources (e.g., relatives, signicant oth-
ers, medical records, laboratory reports, nurses’ notes,
other healthcare professionals). Secondary sources of in-
formation are subject to interpretation by someone other
than the patient. Data collected from secondary sources
should be analyzed with the use of other portions of the
database to validate the conclusions that are reached.
Tertiary sources of information (e.g., a literature
search) provide an accurate depiction of the charac-
teristics of a disease, the nursing interventions and di-
agnostic tests used, the pharmacologic treatment pre-
scribed, the dietary interventions and physical therapy
undertaken, and other factors pertinent to the patient’s
care requirements. When using these sources, the
nurse should be aware that the patient has individual
needs and that the plan of care must be adapted to t
the patient’s identied needs.
Assessment related to drug therapy continues
throughout the hospitalization period. Examples of
45
ongoing assessment activities include visiting with
the patient, determining the need for and administer-
ing as-needed (PRN) medications, monitoring vital
signs, and observing for therapeutic effects in addi-
tion to common and adverse effects and potential drug
interactions.
In preparation for the patient’s eventual discharge
and their need for education about new health-related
responsibilities, the assessment process should include
the collection of data related to the patient’s health be-
liefs, existing health problems, prior compliance with
prescribed regimens, readiness for learning (both emo-
tionally and experientially), and ability to learn and
execute the skills required for self-care.
nursing DiAgnoses
To deal effectively with identied problems (i.e., di-
agnoses), the nurse must recognize both the causative
and contributing factors. The etiology and contribut-
ing factors are those clinical and personal situations
that can cause the problem or inuence its develop-
ment. Situations can be organized into ve categories:
(1) pathophysiologic, (2) treatment related, (3) person-
al, (4) environmental, and (5) maturational (Carpenito,
2013).
When identifying problems related to medication
therapy, the nurse should review the drug monographs
starting in Chapter 12. These are detailed explanations
of the purpose for which a drug is intended, and assist
the nurse to identify common and adverse effects and
drug interactions for patient monitoring. Several nurs-
ing diagnoses can be formulated on the basis of the
patient’s drug therapy. Although the most commonly
observed problems are those associated with the drug
treatment of a disease or the adverse effects of drug
therapy, nursing diagnoses can also originate from
pathophysiology caused by drug interactions.
Example of a Nursing Diagnosis
Drugs prescribed for Parkinson disease are adminis-
tered to provide relief of symptoms (e.g., muscle
tremors, slowness of movement, muscle weakness
with rigidity, alterations in posture and equilibrium).
An actual nursing diagnosis of Compromised mobil-
ity related to neuromuscular impairment (Parkinson
disease) would be formulated on the basis of the
dening characteristics established for this nursing
diagnosis. The evaluation of the expected outcomes
from the prescribed medications is based on the de-
gree of improvement noted in the symptoms that
are present.
A second nursing diagnosis would be Potential for in-
jury related to amantadine adverse effects (confusion,
disorientation, dizziness, lightheadedness).
In this example, common adverse effects of the drug
amantadine, which is prescribed for treatment of the
symptoms of Parkinson disease, are also the basis of
the second nursing diagnosis. The second nursing di-
agnosis requires the nurse to monitor the patient for
46 UNIT I Applying Pharmacology to Nursing Practice
the development of these adverse effects. In other
words, a patient with Parkinson disease is at risk for
developing the dening characteristics. When the de-
ning characteristics are observed, notication of these
to the healthcare provider is required, and the nurse
would need to intervene to provide for the patient’s
safety.
Two nursing diagnoses that apply to all types of
medications prescribed are as follows:
• Insufcient knowledge (actual, risk) related to the
medication regimen (patient education)
• Noncooperation (actual, risk) related to the patient’s
value system, cognitive ability, cultural factors, or
economic resources
PlAnning
Planning, with reference to the prescribed medica-
tions, must include the following steps:
1. The identication of the therapeutic intent of each
prescribed medication. Determine why the drug
was prescribed and what symptoms will be relieved.
2. Review of the drug monographs provided in this
text, starting in Chapter 12, to identify the common
and adverse effects that can be alleviated or pre-
vented by actions of the nurse or patient and that
will require immediate planning for patient educa-
tion. The nurse should continuously monitor the pa-
tient for adverse effects of drug therapy and report
these suspected adverse effects to the prescriber.
3. The identication of the recommended dosage and
route of administration. The nurse should compare
the recommended dosage with the dosage ordered
and conrm that the route of administration is cor-
rect and that the dosage form ordered can be toler-
ated by the patient.
4. The scheduling of the administration of the medi-
cation is based on the prescriber’s orders and the
policies of the healthcare facility. Medications pre-
scribed must be reviewed for drug-drug interac-
tions and drug-food interactions; laboratory tests
may also need to be scheduled if serum levels of the
drug have been ordered.
5. Teaching the patient to keep written records of their
responses to the prescribed medications using the
Patient Self-Assessment Form (see Appendix B for
more information).
6. Providing additional education as needed about
techniques of self-administration (e.g., injection, the
use of topical patches, the instillation of drops), as
well as information as needed about proper storage
and how to rell a medication. When deciding what
to teach the patient the nurse keeps in mind several
factors: (1) the patient’s concerns, their health belief
system, and the patient’s priorities; (2) the urgency
or time available for the learning to take place; (3)
a sequence that allows the patient to move from
simple to more complex concepts; and (4) a review
of the overall needs of the individual. The content
taught to the patient should be well planned and
delivered in increments that the patient is capable
of mastering.
Example of Planning Medication Education
Mr. Jones will be able to state the following for each
prescribed medication by (date) and will show re-
tention of this information by repeating it on (date):
1. Drug name
2. Dosage
3. Route and administration times
4. Anticipated therapeutic response
5. Common adverse effects
6. Serious adverse effects
7. What to do if a dose is missed
8. When, how, or whether to rell the medication
To attain this goal, the patient’s ability to name all
of these factors would need to be checked at the initial
time of exposure and on subsequent meetings to vali-
date retention. After the goals have been formulated,
they should not be considered nal but rather should
be reevaluated as needed throughout the course of
treatment.
imPlementAtion
Nursing actions applied to pharmacology may be cate-
gorized as dependent, interdependent, or independent.
Dpd n Ac
Dependent nursing actions are directly related to the
orders that are written by the healthcare provider.
These orders include diagnostic procedures and medi-
cations for the immediate well-being of the patient. The
healthcare provider reviews data on a continuing basis
to determine the risks and benets of maintaining or
modifying the medication orders. The maintenance or
modication of the medication orders is the healthcare
provider’s responsibility. The nursing action of carry-
ing out the medication orders is considered dependent
because the nurse must follow a written order.
idpd n Ac
The nurse performs baseline and subsequent focused
assessments that are valuable for establishing thera-
peutic goals, the duration of therapy, the detection of
drug toxicity, and the frequency of reevaluation.
The nurse should approach any problems related to
the medication prescribed collaboratively with appro-
priate members of the healthcare team. Whenever the
nurse is in doubt about medication calculations, moni-
toring for therapeutic efcacy and adverse effects, or the
establishment of nursing interventions or patient educa-
tion, another qualied professional should be consulted.
The pharmacist reviews all aspects of the drug or-
der, prepares the medications, and then sends them
to the unit for later administration. If any portion of
the drug order or the rationale for therapy is unclear,
the nurse and the pharmacist should consult with each
other or the healthcare provider for clarication.
ALGrawany
 The Nursing Process and Pharmacology CHAPTER 4
The frequency of medication administration is de-
ned by the healthcare provider in the original order.
The nurse and the pharmacist establish the schedule of
the medication on the basis of the standardized admin-
istration times used at the practice setting. The nurse
(and occasionally the pharmacist) also coordinates the
schedule of medication administration and the collec-
tion of blood samples with the laboratory phleboto-
mist to monitor drug serum levels.
As soon as laboratory and diagnostic test results are
available, the nurse and the pharmacist review them to
identify values that could have an inuence on drug
therapy. The results of the tests are conveyed to the
healthcare provider. The nurse should also have cur-
rent assessment data available for the collaborative
discussion of signs and symptoms that may relate to
the medications prescribed, the dosage, the therapeu-
tic efcacy, or any adverse effects.
Patient education, including discharge medications,
requires that an established plan be developed, written
in the patient’s medical record, implemented, docu-
mented, and reinforced by all those who are deliver-
ing care to the patient (see the sample teaching plan in
Chapter 5, Box 5.2).
idpd n Ac
The nurse visits with the patient and obtains the nurs-
ing history, which includes a medication history as de-
scribed earlier in the section on Relating the Nursing
Process to Pharmacology, under Assessment.
The nurse veries the drug order with the medica-
tion administration record or the electronic medical
record.
The nurse formulates appropriate nursing diagno-
ses and actions to monitor for therapeutic effects and
adverse effects of medications. To do this, the nurse
may need to review drug monographs to formulate the
diagnosis and goal statements. The criteria for thera-
peutic response should describe the improvements ex-
pected in the symptoms of the disease for which the
medication was prescribed.
The nurse prepares the prescribed medications with
the use of procedures that are meant to ensure patient
safety. As part of this process, nursing professional
judgments must include the following:
1. The selection of the correct supplies (e.g., needle
gauge and length, type of syringe) for the adminis-
tration of the medications.
2. The verication of all aspects of the medication
order before preparing the medication. The order
should be veried again immediately after prepara-
tion and again before actual patient administration
47
(patients should always be identied immediately
before the administration of the medication). One
of the National Patient Safety Goals established by
The Joint Commission is to improve the accuracy of
patient identication. It is now recommended that
two patient identiers be used when administering
medications. For example, best practice would be to
look at the patient’s name band for identity and to
request that the patient state their name and birth
date.
3. The collection of appropriate data, also known as
premedication assessment, to serve as a baseline for
later assessments of therapeutic effectiveness and to
detect adverse effects of drugs.
4. The administration of the medication by the correct
route at the correct site. The selection and rotation of
sites for medication should be based on established
practices for the rotation of sites and on principles
of drug absorption, which in turn may be affected
by the presence of pathophysiologic characteristics
(e.g., poor tissue perfusion).
5. The documentation in the chart of all aspects of
medication administration. Subsequent assess-
ments to identify the drug efcacy and the develop-
ment of any adverse effects should be documented.
6. The implementation of nursing actions to minimize
common adverse effects and to identify serious ad-
verse effects to be reported promptly.
7. The education of patients on medications and gain-
ing their cooperation. When noncompliance is iden-
tied, the nurse should attempt to ascertain the pa-
tient’s reasons, and the nurse and the patient should
collaboratively discuss approaches to the problems
viewed by the patient as hindrances. The nurse
needs to be cognizant of the belief systems of a cul-
turally diverse population regarding medications,
illness, and aging among patients and their families,
along with language and other barriers that may
impede communication with healthcare providers.
evAluAtion
Evaluation associated with drug therapy is an ongoing
process that assesses the patient’s response to the med-
ications prescribed, observes for signs and symptoms
of recurring illness, evaluates for therapeutic effects or
the development of adverse effects of the medication,
determines the patient’s ability to receive patient edu-
cation and to self-administer medications, and notes
the potential for compliance. Box 4.1 presents exam-
ples of how the nursing process is applied to the nurs-
ing responsibilities associated with drug therapy.
48 UNIT I Applying Pharmacology to Nursing Practice

Cca Jd ad nx-ga nCleX ® exaa-sy Q

K Pnt 2. Arrange the components of the nursing process in the proper
order.
• The components of the nursing process are assessment,
nursing diagnosis, planning, implementation, and 1. Implementation
evaluation, and they provide a framework for nursing 2. Assessment
actions. 3. Diagnosis
4. Evaluation
• The nurse collects assessment data by completing the
5. Planning
physical examination.
• Nursing diagnosis statements include a patient problem objt: Discuss the components and purpose of the nursing
summarizing the issue; the contributing factors or cause, process.
which may include decits in ADLs or the medical NcleX tt t: Ordering
diagnosis; and dening characteristics. cnt k: Application
• A medical diagnosis is a statement of the patient’s 3. The nurse applies the nursing process by gathering patient
alterations in structure and function, and results in the information to assess the patient using which of the following
diagnosis of a disease or disorder that impairs normal methods? (Select all that apply.)
physiologic function.
1. Body systems assessment
• The goal of evidence-based practice is to improve patient 2. Head-to-toe assessment
outcomes by implementing best practices, which have 3. Critical pathway
evolved from scientic studies. 4. Evidence-based practice
• Maslow’s hierarchy of needs is a model that is often used 5. Gordon’s Functional Health Patterns Model
for establishing patient care priorities.
objt: Explain what the nurse does to collect patient
• There are three types of nursing actions: dependent, information during an assessment.
interdependent, and independent. NcleX tt t: Multiple response
• Two nursing diagnoses apply to all types of medications cnt k: Application
prescribed:
 • Insufcient knowledge (actual, risk) related to the 4. The nurse understands that it is important to learn the nursing
medication regimen (patient education) process, which includes nursing diagnoses.
 • Noncooperation (actual, risk) related to the patient’s Choose the most likely options for the information missing from
value system, cognitive ability, cultural factors, or the sentence below by selecting from the lists of options provided.
economic resources
The nursing diagnosis “Excess uid volume” is
related to __________1_________ as evidenced by
Addtna lann r _________2___________ and ___________2___________.
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa
tions, and other learning activities to help you master this chap- oPTioN 1 oPTioN 2
ter content. (Contributing Factors) (Defining Characteristics)
increased exercise loss of 2 pounds overnight
Go to your Evolve website (https://evolve.elsevier.com/ adverse effects of new +2 edema present
Willihnganz) for additional online resources. medication bilaterally below knees
increased appetite knee pain on standing
Clinical Judgment and Next-Generation NCLEX® Exam gain of 5 pounds in the last
ination-Style Questions The following questions are typical of 24 hours
the NCLEX examination and include both NGN (Next Genera decreased peripheral
tion) and traditional questions. See Chapter 1 for further infor- pulses
mation regarding question types.
1. What is the nurse evaluating during the evaluation step of the objt: Discuss how nursing diagnosis statements are written.
nursing process? NgN tt t: Cloze
1. The nursing diagnosis cnt k: Recognize cues
2. The interventions 5. The nurse understands it is important to know the difference
3. The outcome statement between a nursing diagnosis and a medical diagnosis because of
4. The medical diagnosis which factor?
objt: Discuss the components and purpose of the nursing 1. The nursing diagnosis needs to match the medical
process. diagnosis.
NcleX tt t: Multiple choice 2. The nursing diagnosis needs to be approved by the
cnt k: Understanding primary health care provider before use.
 The Nursing Process and Pharmacology CHAPTER 4 49

3. The nursing diagnosis refers to how the patient is 9. The nurse understands that the actions the nurse takes can be
responding to an illness identied in the medical determined to be from various sources. For each nursing action
diagnosis. indicate with an X whether it is a dependent, an interdependent, or
4. The medical diagnosis refers to how the patient is an independent action.
recovering from the illness that the nursing diagnosis has
established.
objt: Differentiate between a nursing diagnosis and a medical iNTerDe- iNDePeN-
diagnosis. NursiNg AcTioN DePeNDeNT PeNDeNT DeNT
NcleX tt t: Multiple choice Administering
cnt k: Understanding medications
6. The use of evidence-based practice to guide the formulation of Educating
nursing interventions based on research and clinical expertise is a patient on
part of which component of the nursing process? discharge
1. Planning medications
2. Assessment Documenting
3. Evaluation the patient’s
4. Nursing diagnosis response to a
medication
objt: Discuss how evidence-based practice is used in
planning nursing care. Consulting the
NcleX tt t: Multiple choice pharmacist
cnt k: Comprehension about a
medication order
7. Nurses need to use the nursing process to provide quality patient
Discussing with
care. Using the parts of the nursing process of goal planning and
the healthcare
creating an outcome statement, as well as writing interventions,
provider the
mark an X under the column to identify which statement is a
request from the
nursing intervention and which is an outcome statement.
patient regarding
a change in
medications
NursiNg ouTcome
iNTerveNTioN sTATemeNT
objt: Compare and contrast the differences between
Monitoring for potential
dependent, interdependent, and independent nursing actions.
complications
NgN tt t: Matrix
Changes observed in
cnt k: Analyze cues
the patient behavior
Specic actions to be 10. Match the step of the nursing process with the actions of the
performed nurse.
Prioritized goals to be
identied
Expected responses to NursiNg Process NursiNg AcTioNs
be observed Assessment Analysis of the patient data to
determine patient need
Diagnosis Identify the therapeutic intent of the
objt: Differentiate between nursing interventions and
medication
outcome statements.
Planning Take a drug history
NgN tt t: Matrix Interventions Determine patient education
cnt k: Recognize cues needed for medication side effects
Evaluation Identify the patient and administer
8. When the nurse decides that the patient needs to rest before medications
ambulating, the decision is based on what factor?
1. The patient’s wishes
2. The family’s inuences objt: Discuss how the nursing process applies to
3. The prioritization of physiologic needs pharmacology.
4. The healthcare provider’s orders NgN tt t: Matrix
cnt k: Recognize cues
objt: Explain how Maslow’s hierarchy of needs is used to
prioritize patient needs.
NcleX tt t: Multiple choice
cnt k: Knowledge
 5 Patient Education to Promote Health
https://evolve.elsevier.com/Willihnganz
Objectives
1. Differentiate among the cognitive, affective, and
psychomotor learning domains.
2. Identify the main principles of learning that are applied
when teaching a patient, family, or group.
3. Describe the essential elements of patient education in
relation to prescribed medications.
Key Terms
cognitive domain (KŎG-nĭ-tĭv psychomotor domain (sī-kō-MŌ-tŏr)
dō-MĀN) (p. 50) (p. 51)
affective domain (ă-FĔK-tĭv) (p. 50) objectives (ŏb-JĔK-tĭvz) (p. 51)
teach-back (p. 52)
An important nursing responsibility is making cer-
tain that patients receive correct healthcare informa-
tion. Because patient education is a key component of
what nurses do, understanding the principles of how
people learn is important. Nurses need to learn how to
instruct patients correctly, making information specic
to the individual, and also determine whether the in-
formation is understood by the patient.
Three Domains of Learning
The three domains of learning that all adults use when
acquiring new knowledge are the cognitive domain,
the affective domain, and the psychomotor domain
(Fig. 5.1).
Cognitive Domain
The cognitive domain is the level at which basic
knowledge is learned and stored. It is the thinking
portion of the learning process, and it incorporates
a person’s previous experiences and perceptions.
Previous experiences with health and wellness inu-
ence the learning of new materials. Prior knowledge
and experience are the foundation of the addition
of new concepts. Thus the learning process begins
by identifying what experiences the person has had
with the subject.
However, learning involves more than the delivery
of new information or concepts. A person must build
relationships between prior experiences and new con-
cepts to formulate new meanings. At a higher level
50
4. Describe the nurse’s role in fostering patient responsibility
for maintaining well-being and for adhering to the
therapeutic regimen.
5. Identify the types of information that should be discussed
with the patient or signicant others.
health teaching (p. 52)
ethnocentrism (ĕth-nō-SĔN-trĭz-ŭm)
(p. 55)
of the learning process, the new information is used
to question something that is uncertain, to recognize
when to seek additional information, and to make de-
cisions using real-life situations.
affeCtive Domain
The affective domain is the most intangible portion of
the learning process. It refers to the feelings and beliefs
a patient has about what they understand. The affec-
tive domain includes opinions and values that the pa-
tient brings to their understanding of the world. When
a patient says, “I don’t know what meds I’m on, I let
my spouse deal with that,” they are expressing the val-
ue that learning about medications are not important
to them.
It is well known that individuals view events
from different perspectives. People often choose to
internalize feelings rather than to express them. The
nurse must be willing to approach patients in a non-
judgmental fashion, to listen to their concerns, to rec-
ognize the nonverbal messages being given, and to
assess patient needs with an open mind.
Clinical Goldmine
The development of a sense of trust and condence in
healthcare providers can have a powerful effect on the at-
titude of the patient and their family members. This can inu-
ence the patient’s response to the new information that is
being taught. The nurse should be positive and accepting,
and involve the patient in a discussion to draw out their views
regarding solutions to problems.

Cognitive Psychomotor Affective
Knowledge Observing Receiving
Comprehension Imitation Responding
Application Practicing Valuing
Analysis Adapting Organization
Synthesis Originating Characterization
Evaluation
Fig. 5.1 The Three Domains of Learning. (Redrawn from Black BP.
Professional Nursing. 7th ed. Philadelphia, PA: Saunders; 2014, and
Washington CM, Leaver DT. Principles and Practice of Radiation
Therapy. 4th ed. St. Louis, MO: Mosby; 2016.)
PsyChomotor Domain
The psychomotor domain involves the learning of a
new procedure or skill. It is often referred to as the do-
ing domain. Teaching is usually done by demonstration
of the procedure or task using a step-by-step approach.
For example, the nurse can explain how to use an in-
centive spirometer and the patient will demonstrate
their learning by doing it correctly.
PrinciPLes of Teaching anD Learning
Patient education is an important nursing responsibility
that carries legal implications if there is a failure to provide
and document all relevant patient education. Providing
information to patients so that they can understand and
manage healthcare-related situations is now considered
a basic patient right, and it has been mandated by The
Joint Commission since 1996. Patient education involves
establishing goals with the patient and family based on
the healthcare needs of the patient so the patient can learn
to manage their care at home. Principles of teaching and
learning are important to keep in mind when teaching
patients (Box 5.1).
foCus the Learning
The patient must be allowed to focus on the material or
task to be learned. The environment must be conducive
Patient Education to Promote Health CHAPTER 5 51
Box 5.1 Principles of Teaching and Learning
• Focus the learning.
• Consider learning styles.
• Organize teaching sessions and materials.
• Motivate the patient to learn.
• Determine the patient’s readiness to learn.
• Space the content.
• Use repetition to enhance learning.
• Consider the patient’s education level.
• Incorporate cultural and ethnic diversity.
• Teach appropriate use of the Internet.
• Encourage adherence.
• Use relevant content.
• Communicate goals and expectations.
to learning (i.e., quiet, well lit, and equipped for a teach-
ing session). The patient requires repetition of new in-
formation to master it. Nurses may feel obligated to
teach the patient or family members everything that
they know about a disease or procedure, thereby over-
whelming them with information. Instead, nurses
must rst glean what information is essential and then
consider what the patient wants to know.
When the patient starts to ask questions about
any medications or procedures, this is considered a
teachable moment, and it is important to recognize it
as such. By beginning with what the patient brings
up, the nurse is able to give the patient some control
over learning and increase active participation in the
process.
ConsiDer Learning styLes
Learning styles vary. Some people can read and read-
ily comprehend directions, whereas others need to see,
feel, hear, touch, and think to master a task. To be effec-
tive, the nurse must t the teaching techniques to the
learner’s style. Therefore a variety of materials should
be made available for healthcare education, which will
include all domains of learning. The nurse can select
the instructional approach to be used from written
materials such as pamphlets, photographs, and charts
for the cognitive domain. The use of video recordings,
models, and computers by the nurse to teach a task
or procedure, and evaluation of a return demonstra-
tion by the patient, can correspond to the psychomotor
domain.
organize teaChing sessions anD
materiaLs
In most clinical settings, patient education materi-
als are developed by the staff and then reviewed by
a committee for adoption. Specic objectives should
be formulated for patient education sessions. The
objectives should state the purpose of the activi-
ties and the expected outcomes. Objectives may be
developed in conjunction with a nursing diagno-
sis statement (e.g., Imbalanced nutrition: Less than
52 UNIT I Applying Pharmacology to Nursing Practice
body requirements), or they can be developed for
common conditions that require care delivery (e.g.,
care of the patient who is receiving chemotherapy).
Regardless of the format used, these instructional
materials have established content that is given
in outline form, and they are arranged so that one
nurse can initiate the teaching and document the de-
gree of understanding, and then another nurse can
continue the teaching during a different shift or on a
different day. The rst nurse should check off what
has been accomplished so that the next nurse knows
where to resume the lesson.
At the start of each subsequent teaching session, it
is important to review what has been covered previ-
ously and to afrm the retention of information from
the previous lessons. The method known as teach-
back refers to asking the patient to explain in their
own words what instruction was just received. This
is an important part of patient education that will
identify gaps in learning and help focus the nurse
on what needs to be instructed. When psychomotor
skills are being taught, return demonstrations by the
patient are key to helping the patient practice and
gain condence in performing the task. Giving the
patient immediate feedback about the skills and
then giving them time to practice the skills that are
more difcult allows the patient time to improve on
mastering the procedure. If appropriate, equipment
may be left with the patient for practice before the
next session.
Sometimes it is particularly useful to set up a video
of skill demonstrations for the patient to view alone
at a convenient time. At the next meeting, the patient
can review the video together with the nurse, and im-
portant points can be discussed and claried if the
patient expresses confusion or uncertainty. This tech-
nique reinforces what has been said, reviews what has
been learned, and provides the learner with repetition,
which is necessary for learning.
motivate the Patient to Learn
Before initiating a teaching plan, the nurse should be
certain that the patient can focus and concentrate on
the tasks and materials to be learned. The patient’s ba-
sic needs (e.g., food, oxygen, pain relief) must be met
before they can focus on learning. The nurse must rec-
ognize the individual’s health beliefs when trying to
motivate the patient. Because health teaching requires
the integration of the patient’s beliefs, attitudes, val-
ues, opinions, and needs, an individualized teaching
plan must be developed based on the patient’s beliefs
and needs (Box 5.2).
Teaching does not require a formal setting. Some
of the most effective teaching can be done while
care is being delivered. The patient can be exposed
to a skill, a treatment, or facts that must be com-
prehended in small increments. The nurse who ex-
plains a certain procedure and informs the patient
why the procedure is being performed reinforces
the need for it and motivates the patient to learn.
When the patient understands the personal benefits
of performing a task, their willingness to do it is
strengthened.
Determine reaDiness to Learn
A patient’s perception of their health and health status
may differ from the nurse’s judgment; therefore the
values of healthcare to each patient may differ greatly.
The patient may not realize that a healthy lifestyle will
provide signicant benets. A person who commonly
indulges in alcohol, smoking, or a high-fat diet and
leads a sedentary lifestyle may not consider the con-
sequences of these practices in relation to health. Not
everyone is interested in the concept of healthy living.
The nurse must respect the individuality of the patient,
family, or group being treated; the nurse should accept
that not everyone is motivated by the possibility of a
higher level of wellness.
The nurse can positively inuence the learning
process by being enthusiastic about the content to be
taught. A patient’s response to the new information
will vary and depends on several factors, including
the following: the need to know, the patient’s life ex-
periences and self-concept, the effect of the illness on
the patient’s lifestyle, the patient’s experience with
learning new materials, and the patient’s readiness
to learn. Consideration must be given to the patient’s
psychosocial adaptation to illness and their ability to
focus on learning. For example, during the denial,
anger, or bargaining stages of grieving, the patient
usually is neither prepared nor willing to accept the
limitations imposed by the disease process. During
the resolution and acceptance stages of the grieving
process, the patient moves toward accepting respon-
sibility and develops a willingness to learn what is
necessary to attain an optimal level of health. The
nurse can use encouragement and support the pa-
tient’s attempts to learn new, challenging, or difcult
procedures (Fig. 5.2).
For teaching activities that are conducted with
children, psychosocial, cognitive, and language abili-
ties must be considered. Cognitive and motor devel-
opment, as well as the patient’s language usage and
understanding, must be assessed. Age denitely in-
uences the types and amounts of self-care activities
that the child is capable of learning. The nurse should
consult a text that addresses developmental theory for
further information.
Adult education is usually oriented toward learn-
ing what is necessary to maintain a particular life-
style. In general, adults need to understand why they
must learn something before they undertake the ef-
fort to learn it. When planning the educational needs
of the patient, the nurse must assess what the patient
already knows and what additional information is
desired.
 Patient Education to Promote Health CHAPTER 5
Box 5.2 Sample Teaching Plan for a Patient With Diabetes Mellitus Taking One Type of Insulin a
UnDersTanDing of heaLTh conDiTion
• Assess the patient’s and the family’s understanding of
diabetes mellitus.
• Clarify the meaning of the disease in terms that the
patient is able to understand.
• Establish learning goals through mutual discussion.
Teach the most important information rst. Set dates for
the teaching of content after discussion with the patient.
fooD anD fLUiDs
• Arrange for the patient and their family members
and signicant others to attend nutrition lectures and
demonstrations about food preparation.
• Reinforce knowledge of dietary restrictions with the use
of tactful questioning and by giving the patient a chance
to practice food selections for daily meals from the
menus provided.
• Explain how to manage the diabetic diet during illness
(e.g., with nausea and vomiting, patient should increase
uid intake) and when to contact the healthcare provider.
• Stress the interrelationship of food with the onset, peak,
and duration of the prescribed insulin.
moniToring TesTs
• Demonstrate how to collect and test blood glucose
samples and, as appropriate, urine.
• Validate understanding by having the patient collect, test,
and record the results of the testing for the remainder of
the hospitalization.
• Stress serum glucose testing before meals and at bedtime.
• Explain the importance of regular follow-up laboratory
studies (e.g., fasting plasma glucose testing,
postprandial hemoglobin A1c) to monitor the patient’s
degree of control.
meDicaTions anD TreaTmenTs
• Teach the name, dosage, route of administration, desired
action, and storage and relling procedures for the type
of insulin prescribed.
• Explain the principles of insulin action, onset, peak, and
duration (see Chapter 35).
• Demonstrate how to prepare and administer the
prescribed dose of insulin.
• Teach site location and self-administration of insulin.
• Give specic instructions that address the reading of the
syringe to be used at home.
• Teach the patient how to obtain supplies (e.g.,
disposable syringes, needles, glucometer, glucose
monitoring strips, insulin pen).
• Discuss the usual timing of reactions, the signs and
symptoms of hypoglycemia or hyperglycemia, and the
management of each complication.
• Validate the patient’s understanding of common adverse
effects and serious adverse effects.
• Teach and validate family members’ and signicant
others’ understanding of the signs and symptoms of
hypoglycemia and hyperglycemia and the management
of each complication.
a Each item listed must be assessed for the individual’s current knowledge base and level of understanding throughout the course of teaching. The process is
reassessed and the teaching continued until the patient masters all facets of self-care needs. With the advent of shorter hospitalizations, inpatient and outpatient
teaching may be necessary, and it may include referral to community-based healthcare agencies, as needed. Discharge charting and referral should carefully
document those facets of the teaching plan that have been mastered and those that need to be taught. The healthcare provider should be notied of decits in the
patient’s learning ability or in their mastery of needed elements in the teaching plan.
53
• Teach a general approach to the management of
illnesses (e.g., the actions required if nausea and
vomiting or fever occur; stress glucose monitoring
before meals and at bedtime); discuss the situations
when there is a need to call a healthcare provider.
PersonaL hygiene
• Discuss the great importance of managing personal
hygiene, and emphasize the need to consult a healthcare
provider for guidance and discussion:
 • Regular foot care
 • Meticulous oral hygiene and dental care
 • Care of cuts, scratches, and minor and major injuries
 • Stress management and needed alterations in insulin
dosage during an illness
acTiviTies
• Help the patient develop a detailed time schedule for
usual activities of daily living. Incorporate diabetic care
needs into this schedule.
• Encourage maintaining all usual activities of daily
living. Discuss anticipated problems and possible
interventions.
• Discuss personal care needs not only at home but also
in the work setting, as appropriate. (Consider involving
the industrial nurse, if available, in the work setting.)
• Discuss the effects of an increase or decrease in activity
level on the management of diabetes mellitus.
home or foLLow-UP care
• Arrange for outpatient or healthcare provider follow-up
appointments and schedule ordered laboratory tests.
• Advise the patient to seek assistance from the healthcare
provider or from the nearest emergency department
service for problems that may develop.
• Arrange appropriate referrals to community health
agencies, if needed.
• Complete a diabetic alert card or another means (e.g., an
identication necklace or bracelet) of alerting people to
the individual’s needs in case of an emergency.
• Discuss an exercise program with the healthcare provider.
sPeciaL eqUiPmenT anD insTrUcTionaL maTeriaL
• Develop a list of equipment and supplies to be
purchased; have a family member purchase and bring
these to the hospital for use during teaching sessions
(e.g., blood glucose monitoring supplies, syringes, insulin
pen, needles, alcohol wipes).
• Show audiovisual materials that address insulin
preparation, storage, and administration, as well as
serum glucose testing.
• Develop a written record (see Chapter 35), and assist the
patient with maintaining data during hospitalization.
oTher
• Teach measures to make travel easier.
• Tell the patient about the American Diabetes Association
and about the materials available from this resource.
54 UNIT I Applying Pharmacology to Nursing Practice

Life Span Considerations

Older Adults
Teaching Older Adults
The older adult needs to be further assessed before the imple-
mentation of healthcare teaching; these assessments should
include vision, hearing, and short- and long-term memory. If
a task is to be taught, ne and gross motor abilities need to
be evaluated as well. An older patient may also have major
concerns regarding the cost of the proposed treatments in
relation to available resources. A patient will often evaluate
the benets of planned medical interventions and their overall
effect on the quality of life. Any of these situations can affect
the ability of the patient to focus on the new information to
be taught, thus inuencing their response to and the over-
all outcome of the teaching. Older adults have often expe
rienced losses and may be facing social isolation, physical
(functional) losses, and nancial constraints. Because older
adults often have more chronic health problems, a new di-
agnosis, an exacerbation of a disease, or a new crisis may
be physically and emotionally overwhelming. Therefore the
timing of patient instruction is of great signicance.
When teaching an older patient, it is prudent to slow
the pace of the presentation and to limit the length of each
session to prevent overtiring. Older adults can learn the
material, but they often process things more slowly than
younger people do because their short-term memory may
be more limited. The nurse must work with the patient to
develop ways to remember what is being taught. The more
that the older person is involved in forming the associations
that will be used to remember new ideas and to connect Fig. 5.2 A patient does a return demonstration of an insulin injection after
being taught by the nurse. (Courtesy Jim Varney, North Yorkshire, UK.)
these ideas with past experiences, the better the outcome.

Many patients are embarrassed by their inability
to master a task. Asking them if they understand is
not going to be effective because they will not admit
their embarrassment or that they do not understand.
The nurse should provide information in small incre-
ments and allow for practice, review, practice, review,
and practice until success is achieved. The nurse can
stop at appropriate intervals and reschedule sessions
to meet the patient’s learning needs. Teach-back can be
used as an important tool to help the nurse verify what
information has been understood.
When the patient becomes anxious, the presenta-
tion of new information can be slowed, repeated, or
stopped and the session rescheduled. Fear and anxiety
often impair a person’s ability to focus on the task or
content being presented, so creating an environment
that is conducive to learning is important.
When anxiety is high, the ability to focus on details
is reduced. The nurse should anticipate periods during
hospitalization when teaching can be more effective.
Some teaching is most successful when it is done spon-
taneously, such as when the patient asks direct questions
about their progress toward discharge. The nurse also
must learn to anticipate inopportune times to initiate
teaching, such as when a patient becomes withdrawn
after learning about a diagnosis with a poor prognosis.
With reduced hospital stays, the ability to time patient
education ideally and to perform actual teaching is a
challenge. It is imperative that the nurse document those
aspects of healthcare teaching that have been mastered
and—of equal importance—those that have not been;
the nurse must then request referral to an appropriate
agency for follow-up teaching and assistance.
Clinical Goldmine
Consider the lighting so that there is no glare on reading
materials, face the learner for better eye contact, and speak
directly and in a clear tone, without shouting. Be calm, use
tact and diplomacy if frustrations develop, and try to instill
condence in the learner’s ability to surmount any problems.
sPaCe the Content
Spacing or staggering the amount of material given
during one session should be considered, regardless
of the age of the person being taught. People tend to
remember what is learned rst. With this principle in
mind, the nurse can provide multiple short sessions
rather than a few longer sessions that may overwhelm
the patient.
use rePetition to enhanCe Learning
It is important for the nurse to recognize that patients
need repetition to learn new content. The nurse needs

to repeat what was previously taught to help the pa-
tient understand what is important to remember and
build on it to the next level.
ConsiDer eDuCation LeveL
An important consideration to keep in mind when teach-
ing adult patients is their literacy level. Just giving the
patient a pamphlet to read may not be appropriate if the
patient cannot read it. Instead, the nurse could review
the pamphlet with the patient and then determine the
level of the patient’s understanding of the information.
Medical terms may not be understood, and written
instructions left at the bedside may be misinterpreted or
not read at all. Some patients may be illiterate, whereas
others may read at a rst-grade, seventh-grade, or col-
legiate level. Therefore if written materials are used, it is
important to consider these wide variations in literacy.
inCorPorate CuLturaL anD ethniC
Diversity
Many healthcare providers have a limited understand-
ing of what other cultures believe and the importance
of these benets to the learning process. Ethnocentrism
is the assumption that one’s culture provides the right
way, the best way, and the only way to live. Briey,
people who believe in the theory of ethnocentrism as-
sume that their way of viewing the world is superior to
that of others (Leininger, 2002). As an understanding of
cultural diversity increases, healthcare providers must
expand their knowledge of the basic tenets of the belief
systems that they may encounter among their patients.
Because there are differing beliefs, it is important that
the nurse explore the meaning of an illness with the pa-
tient. Members of other cultures do not always express
themselves when their views are in conict with those of
another culture. Unless a careful assessment of psycho-
social needs is performed, the true meaning of an illness
or the proposed intervention may never be uncovered.
Even the assessment process has obstacles attached.
Patients in some cultures do not believe that family in-
formation should be shared outside of the family. For
example, some Eastern European cultures prefer not to
reveal any history of psychiatric illness or treatment and
are usually reluctant to share any sexual history. Others,
such as the Native American cultures, believe that only
the affected individual may reveal information.
Communication is vitally important within any
cultural group. However, verbal and nonverbal types
of communication mean different things to different
cultures. For example, whites tend to value eye con-
tact, whereas in other cultures (e.g., Native Americans,
Asians) direct eye contact is a sign of disrespect or rude-
ness. As a part of communication, knowing how to ad-
dress the patient is also important. African American
patients often prefer to have their formal names used
rather than their rst names, especially older family
members. Chinese people tend to be more formal than
Americans, and spouses do not necessarily have the
Patient Education to Promote Health CHAPTER 5 55
same last name. The simple gesture of asking the pa-
tient how they prefer to be addressed is both helpful
and respectful.
Working with an interpreter when a language bar-
rier exists presents several additional challenges to
understanding. The nurse should rst explain the
educational session to the interpreter and then discuss
the types of questions that will be asked of the patient.
Whenever a third person enters into the communica-
tion cycle, a lack of clarity and misinterpretation can
occur. The nurse should keep questions brief and ask
them one at a time to give the interpreter an opportu-
nity to rephrase the question and obtain a response.
Sometimes supplementing questions with pictures
and pantomime gestures may be helpful. When using
an interpreter, the nurse should look directly at the pa-
tient (not at the interpreter) while conversing.
The members of the healthcare team should always
try to ascertain the patient’s beliefs about illness. The
following should be taken into consideration:
• Is “good health” dened as the ability to work or to
fulll family roles, or is it a reward from God or a
balance with nature?
• Does the patient believe that healthcare can im-
prove health outcomes, or does fate determine the
outcome?
• Are any cultural or religious disease prevention ap-
proaches used in the household?
• Do family members wear talismans or charms for
protection against illness?
• Are cultural healers important (e.g., Chinese herbal-
ists, Native American medicine men)?
As part of the cultural assessment, the nurse should
determine factors that relate to the cultural beliefs of
the family. Inquire as to whether other family members
should be included in the discussion of the patient’s
medical care. Be sure to include the decision makers
in the teaching session so that the teaching will not
be wasted. Always remain sensitive to the patient’s
and family’s cultural beliefs and practices. Nurses
can demonstrate understanding, empathy, respect,
and patience for the patient’s cultural values through
their communication and actual delivery of healthcare.
Consult assessment textbooks for more extensive cov-
erage of ethnic and cultural issues.
With increasing globalization becoming more com-
mon, educational materials are being adapted to meet
a variety of cultural considerations. Unfortunately, this
does not solve all of the problems. Interpreting writ-
ten materials still leaves room for misunderstanding
because many people cannot read or do not read at the
level of the provided materials.
sTraTegies for heaLThcare Teaching
teaCh aPProPriate use of the internet
It has become common for consumers to access the
Internet for healthcare inquiries, including medical
56 UNIT I Applying Pharmacology to Nursing Practice

consultation from an online primary healthcare Table 5.1 Sources of Patient Information
provider about a particular healthcare concern.
soUrce DescriPTion
Consumers can purchase medications online and re-
search healthcare treatments. The convenience of ac- Health on the Net Leading organization that
Foundation promotes and guides the
cessing electronic healthcare information is a power-
(https://www.hon.ch) deployment of useful and
ful resource for consumers, and it is one that provides reliable online medical and
anonymity and that may serve to empower the pa- healthcare information and its
tient. Valid healthcare information can assist patients appropriate and efcient use
with the making of informed healthcare decisions Healthcare institution Data available through an
(Table 5.1). intranet institution-specic intranet
Today, many patients present to the healthcare Provides an online resource
provider’s office with some knowledge of their dis- for drug information (e.g.,
ease, treatment, and medications. This has altered Micromedex)
the nurse’s role as a provider of healthcare educa- Often includes information about
tion to resemble that of a consultant. It is the nurse’s diseases and diagnostic
role to teach patients to use the Internet effectively, testing
to evaluate websites for validity, and to assist pa- Information may be printed by
tients with understanding the information that they the nurse and used for patient
education
have accessed. The nurse should also provide pa-
tients with the tools to evaluate websites for valid- Krames Online (https:/ Patients access this site on their
ity and to tell them about reputable sites that are /dhch.kramesonline. own
com/) Includes information about
specific to their healthcare needs. With the abun-
diseases, conditions,
dance of health- and disease-related information treatments, procedures,
on the Internet, the quality of information varies. surgeries, and medications,
Therefore it is essential that the nurse maintain an including prescription
educational partnership with the patient and their medications and over-
caregivers. the-counter products
Compendium of Published by the Canadian
enCourage aDherenCe Pharmacists Association
Therapeutic
Healthcare providers and educators tend to think that Choices (CTC) Extensive handbook that
a patient should change behaviors and adhere to a new describes major diseases
therapeutic regimen simply because the nurse said so. and their treatment
However, patients do have the right to make their own Discussions of medical
life choices, and they often do. Unfortunately, there is conditions are brief
Focuses on goals of therapy,
no way to ensure adherence unless the patient recog-
management algorithms,
nizes its value.
and the discussion of
Success with a healthcare regimen is enhanced nonpharmacologic and
when the nurse conveys an enthusiastic attitude, ap- pharmacologic therapies
pears positive about the subject matter, and shows con-
dence in the abilities of the patient to understand the
lesson. Reinforcing positive accomplishments fosters • High stress or daily stresses, such as dysfunctional
successful achievement. families, difcult living situations, poverty, long
The patient’s response to the therapeutic regimen working hours in a tense environment, and prob-
(including medications) and their degree of compli- lematic parenting issues
ance are inuenced by several variables, including the • Comprehension and understanding of the health-
following: care regimen or frequent changes in the regimen;
• Beliefs about the seriousness of the illness the inability to read written instructions
• Perceptions of the benets of the proposed treat- • Multiple healthcare providers prescribing
ment plans medications
• Personal beliefs, values, and attitudes toward health, • Costs of treatment in relation to resources and pos-
the provider of the medication, and the health- sible difculty with getting prescriptions lled
care system, including prior experience with the • Support of signicant others or problems with as-
system sistance needed in the home
• Effects of the proposed changes on personal lifestyle • Amount of control that the patient experiences with
• Acceptance (or denial) of the illness and its associ- regard to the disease or condition
ated problems; other psychological issues, such as • Side effects of the treatment and the degree of incon-
anger about the illness, apathy, depression, forget- venience, annoyance, or impairment in functioning
fulness, and confusion that they produce

ALGrawany

• Degree of positive response achieved
• Physical difculties that limit access to or use of
medication, such as difculty swallowing tablets,
difculty with opening containers or handling
small tablets, or the inability to distinguish colors or
identifying markings on different medications
• Concerns about taking drugs and the fear of
addiction
Evaluating the ability of a patient to comply with a
proposed healthcare regimen is a complex process that
involves using established criteria to reach a conclu-
sion. The ultimate goal is to assist patients with achiev-
ing the greatest degree of control possible within the
context of their beliefs, values, and needs. Healthcare
professionals can offer support and encouragement,
be complimentary about positive achievements, and
encourage an examination of the available options
and the benets of a healthy lifestyle. It is vital to as-
sist patients with exploring options when a problem
or complication arises rather than giving up on the
treatment because information about alternatives is
lacking. Financial considerations may also affect the
patient’s decisions. If a problem, many manufacturers
have patient assistance plans to provide medicines at
a lower expense.
s  ic adc
The challenge for nursing is to increase the adherence
of patients to their healthcare regimen and to minimize
hospital readmission and suffering from complica-
tions. It is estimated that poor adherence to medical
therapy accounts for about $300 billion in unnecessary
healthcare expenses each year. One model that has
been used to induce behavioral change in patients is
called the Case Management Adherence Guidelines, ver-
sion 2. This project, developed by Pzer and the Case
Management Society of America, is a series of tools
that are used by case managers (many of whom are
nurses) to assess the patient’s motivation level and
their knowledge of prescribed medications and other
therapies. It also assesses a patient’s social support sys-
tem. The tools help identify those who are more at risk
for nonadherence so that interventions can be initiated
early during the care process. A key principle of this
model is that the nurse must recognize that the patient
will make the nal decisions. The nurse must negoti-
ate with (not dictate to) the patient to implement ac-
tions that may result in positive change. This approach
gives the nurse and patient ownership of the goals to
be achieved.
Another type of research technique used to study
adherence is ethnography. When a patient is not
meeting expected outcomes, an ethnographer may
visit the patient at home to observe how the patient
administers their healthcare regimen. Observations
are made with regard to how and which procedures
are accomplished and what errors are being made.
Patient Education to Promote Health CHAPTER 5 57
Industry has used these methods for many years to
help design work ow for production, and it has been
discovered that this is also a valuable tool in health-
care for improving patient outcomes. It is important
to remember that the patient may not be purpose-
fully nonadherent; rather, the home environment
may not be set up to allow the patient to follow care
instructions.
use reLevant Content
Nurses tend to think that patients will do what is
suggested simply because they have been told that
it will be benecial. In the hospital, the nurse and
other healthcare members reinforce the basic ther-
apeutic regimen; at discharge, however, the pa-
tient leaves the controlled environment and is free
to choose to follow the prescribed treatment or to
alter it as deemed appropriate on the basis of per-
sonal values and beliefs. For learning to take place,
the patient must perceive the information as be-
ing relevant. Whenever possible, the nurse should
start with simple and attainable goals to build the
patient’s condence. It is important to correlate the
teaching with the patient’s perspective of the illness
and their ability to control the signs and symptoms
or the course of the disease process.
CommuniCate goaLs anD exPeCtations of
theraPy
Before discharge, reasonable responses to the planned
therapy should be discussed. The patient should know
what signs and symptoms may be altered by the pre-
scribed medications. The precautions necessary when
taking a medication must be explained by the nurse
and understood by the patient (e.g., to use caution
when operating power equipment or a motor vehicle,
to avoid direct sunlight, to ensure that follow-up labo-
ratory studies are carried out).
C  epc
Changes in the patient’s expectations should be as-
sessed as therapy progresses and as the patient gains
understanding and skill with regard to managing the
diagnosis. The expectations of therapy for patients
with acute illnesses may vary widely from those of pa-
tients with chronic illnesses.
Cp gl s
An attitude of shared input into goals and outcomes
can encourage the patient to enter into a therapeu-
tic alliance. Therefore the patient should be taught
to help monitor the parameters that are used to
evaluate therapy. It is imperative that the nurse
nurture a cooperative environment that encourages
the patient to do the following: (1) keep records of
the essential data that are needed to evaluate the
prescribed therapy and (2) contact the healthcare
58 UNIT I Applying Pharmacology to Nursing Practice

provider for advice rather than alter the medication
regimen or discontinue the medication entirely. For
each major class of drugs in this book, written re-
cords (located on Evolve) are provided to help the
nurse identify essential data that the patient needs
to understand and record. In the event that the pa-
tient and their family or significant others do not
understand all aspects of the continuing therapy
prescribed, they may be referred to a community-
based agency for help with achieving long-term
healthcare requirements.
Dc Pl d tc
A summary statement of the patient’s unmet needs
must be written and placed in the medical chart. The
healthcare provider should be consulted about the
possibility of a referral to a community-based agency
for continued monitoring or treatment. The nurse’s
discharge notes must identify the nursing diagnoses
that have not been met and the potential problems that
require continued monitoring and intervention. All
counseling information should be carefully drafted in
a manner that the patient can read and understand.

Clcl Jd d n-g nCLex® e-sl Q

K Pt 1. Match the examples of patient behavior after the nurse has given
healthcare teaching instructions with the domain of learning.
• The three domains of learning are the cognitive, affective,
and psychomotor domains.
Domain of Learning PaTienT behavior
• The main principles of learning include the patient’s
attitudes toward learning, readiness to learn, and individual Cognitive •  Patient demonstrates
learning style. the correct way to use
• Patient education in relation to medications includes a device such as a peak
understanding the benets of the medications, the ow meter
common adverse effects, and potential drug interactions. Affective • Patient verbalizes an
understanding of the
• Nurses play an important role in teaching patients about
potential side effects
how they can maintain and improve their own well-being
Psychomotor • Patient correctly
by understanding the intent of the therapies prescribed.
demonstrates a skill such
• The types of information discussed with the patient as placing medications
and their family include the medications and treatments in the proper box when
to be continued after discharge and activities, special lling a daily drug box
equipment, and follow-up care. • Patient discussed
• Specic techniques used to facilitate patient education with spouse how the
include determining the patient’s readiness to learn, treatment proposal
repetition of information, motivating the patient, and affects their life
understanding the patient’s culture.

ojt: Differentiate among the cognitive, affective, and

addtl L ru
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa
tions, and other learning activities to help you master this chap-
2. The nurse is developing a teaching plan for a patient who will
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Wil
lihnganz) for additional online resources.
cll Judt d nxt-gt ncLeX®
ext-stl qut
The following questions are typical of the NCLEX examination
and include both NGN (Next Generation) and traditional
questions. See Chapter 1 for further information regarding
question types.
psychomotor learning domains.
ngn tt t: Drag and drop
ct kll: Recognize cues
have limited activity at home after a recent fall. What principle of
learning is involved when teaching this patient?
1. The timing of the teaching is important for learning to
take place.
2. Teaching is effective when all family members are present.
3. The affective domain is particularly useful when dealing
with patients who have limited activity.
4. Constantly reminding patients what they should do at
home is critical.
ojt: Identify the main principles of learning that are applied
when teaching a patient, family, or group.
ncLeX tt t: Multiple choice
ct kll: Comprehension

3. The nurse was reviewing the discharge medication list with a
patient who recently had been hospitalized for heart failure.
The patient states that the medications were not new and that
everything is ne. What would be appropriate responses by the
nurse? (Select all that apply.)
1. “It is important to understand all your medications, as
they are intended to keep you healthy.”
2. “The doctor wants you to remember all of your
medications so when you go back to the clinic you will
know the list.”
3. “It is important to remember to take your doses every
day.”
4. “I have to tell you all these medications before you can go
home.”
5. “I would like for you to explain them to me, so I can
determine whether I need to add any more information.”
ojt: Describe the essential elements of patient education in
relation to prescribed medications.
ncLeX tt t: Multiple response
ct kll: Application
4. Which patient is most ready to begin a patient teaching session?
1. A patient who has had nausea and vomiting for the past
24 hours
2. A patient who has just been told that he needs to have
major surgery
3. A patient who has voiced a concern about how insulin
injections will affect her lifestyle
4. A patient who is complaining bitterly about a low-fat, low-
cholesterol diet after his heart attack
ojt: Describe the essential elements of patient education in
relation to prescribed medications.
ncLeX tt t: Multiple choice
ct kll: Comprehension
5. Which of the following information about medications is important
to teach patients? (Select all that apply.)
1. The name, dosage, and route of administration of the
medication
2. The laboratory studies that need to be monitored while
on the medication
3. The common adverse effects and possible serious
adverse effects to watch for
4. The correct pharmacy to obtain the medication from
5. The correct schedule or timing of the medication to follow
ojt: Describe the nurse’s role in fostering patient
responsibility for maintaining well-being and for adhering to the
therapeutic regimen.
ncLeX tt t: Multiple response
ct kll: Application
Patient Education to Promote Health CHAPTER 5 59
6. The patient presents with educational information about
medication that has been obtained from the Internet. What does
the role of the nurse as consultant include? (Select all that apply.)
1. Evaluating websites the patient uses for validity
2. Assisting the patient with purchasing medications online
3. Assisting the patient with understanding the information
accessed
4. Providing the patient with tools to evaluate websites for
validity
5. Encouraging the use of one search engine
6. Asking the patient to demonstrate how they look up
information on the Internet
7. Discouraging the use of Google for looking up
medications
8. Discussing what to look for when determining which
websites are useful
ojt: Identify the types of information that should be
discussed with the patient or signicant others.
ngn tt t: Extended multiple response
ct kll: Recognize cues
7. Which statement is an example of an objective of healthcare
teaching that involves the affective domain of learning?
1. The patient will verbalize an understanding of the reason
for taking the medication furosemide.
2. The patient will demonstrate the correct way to use the
metered-dose inhaler.
3. The patient will discuss with the family the treatment
options proposed.
4. The patient will teach the nurse the same content just
learned in the session.
ojt: Differentiate among the cognitive, affective, and
psychomotor learning domains.
ncLeX tt t: Multiple choice
ct kll: Comprehension
Unit II Illustrated Atlas of Medication Administration

6 Principles of Medication Administration and

Medication Safety
https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the legal and ethical considerations for medication
administration.
2. Compare and contrast the various systems used to
dispense medications.
3. Identify what a narcotic control system entails.
4. Identify common types of medication errors and actions
that can be taken to prevent them.
5. Identify precautions used to ensure the right drug is
prepared and given to the right patient.
6. Identify the appropriate nursing documentation of
medications, including the effectiveness of each
medication.

Key Terms
nurse practice act (p. 60)
standards of care (p. 61)
summary section (SŬM-ă-rē) (p. 61)
consent section (kŏn-SĔNT) (p. 62)
order section (ŌR-dŭr) (p. 62)
history and physical examination
section (HĬS-tō-rē and FĬZ-ĭ-kŭl ĕgz-
ăm-ĭ-NĀ-shŭn) (p. 62)
progress notes (PRŎ-grĕs) (p. 62)
nurses’ notes (p. 62)
laboratory tests record (LĂB-ōr-ă-
tōr-ē) (p. 62)
graphic record (GRĂ-fĭk) (p. 62)
ow sheets (FLŌ SHĒTS) (p. 63)
consultation reports (kŏn-sŭl-TĀ-
shŭn) (p. 63)
medication prole (PRŌ-fīl) (p. 63)
medication administration record
(MAR) (p. 64)
PRN (p. 64)
patient education record (PĀ-shĕnt
ĕd-jū-KĀ-shŭn) (p. 64)
nursing care plan (p. 65)
Kardex (KĂR-dĕks) (p. 66)
oor or ward stock system (FLŌR or
WŌRD STŎK SĬS-tĕm) (p. 67)
individual prescription order
system (ĭn-dĭ-VĬD-jū-ăl prē-SKRĬP-
shŭn) (p. 67)
unit-dose drug distribution
system (YŪ-nĭt DŌS DRŬG dĭs-trĭ-
BYŪ-shŭn) (p. 67)
computer-controlled dispensing
system (kŏm-PYŪ-tŭr kŏn-TRŌLD
dĭ-SPĔN-sĭng) (p. 68)
bar codes (BĂR KŌDZ) (p. 68)
long-term care unit-dose
system (p. 68)
narcotic control systems (năr-KŎ-tĭk
kŏn-TRŌL) (p. 69)
disposal of unused medicines (dĭs-
PŌ-zŭl of ŭn-YŪZD MĔD-ĭ-sĕnz) (p.
71)
stat order (STĂT ŌR-dŭr) (p. 72)
single order (SĬN-gŭl) (p. 72)
standing order (STĂN-dĭng) (p. 72)
PRN order (p. 72)
computerized provider order entry
(CPOE) systems (p. 72)
medication safety (p. 72)
medication errors (ĀR-ŭrz) (p. 72)
adverse drug events (p. 72)
high-alert medications (HĪ-ă-LŬRT)
(p. 73)
medication reconciliation (rĕ-kŏn-
sĭl-ē-Ă-shĕn) (p. 73)
handoffs (HĂND-ŏfs) (p. 73)
verication (văr-ĭ-fĭ-KĀ-shĕn) (p. 74)
transcription (trăn-SKRĬP-shĕn) (p. 74)

Before edictions re dinistered, the nurse ust

understnd the professionl responsibilities ssoci-
ted with ediction dinistrtion, drug orders,
ediction delivery systes, nd the nursing process
s it reltes to drug therpy. Ignornce of the nurse’s
overll responsibilities s prt of the syste y result
in delys in the receiving nd dinistering of edi-
ctions nd serious dinistrtion errors. In either
cse, cre is coproised, nd the ptient y suffer
unnecessrily.
60
LEGAL AND ETHICAL CONSIDERATIONS
The prctice of nursing under  professionl license is
 privilege, not  right. When ccepting this privilege,
the nurse ust understnd tht this responsibility in-
cludes ccountbility for one’s ctions nd judgents
during the execution of professionl duties. An under-
stnding of the nurse practice act nd the rules nd
regultions estblished by the stte bords of nurs-
ing for the vrious levels of entry (i.e., prcticl nurse,
registered nurse, nd nurse prctitioner) is  solid
 Principles of Medication Administration and Medication Safety CHAPTER 6
foundtion for beginning prctice. Mny stte bords
hve developed specic guidelines for nurses to use
when prcticing nursing.
STANDARDS OF CARE
Standards of care re guidelines tht hve been de-
veloped for the prctice of nursing. These guidelines
re dened by the nurse prctice ct of ech stte, by
stte nd federl lws tht regulte helthcre fcili-
ties, by The Joint Coission, nd by professionl or-
gniztions such s the Aericn Nurses Assocition
nd other specilty nursing orgniztions (e.g., the
Infusion Nurses Society). Nurses ust lso be filir
with the estblished policies of the eploying helth-
cre gency. Policies developed by the helthcre
gency ust dhere to the iniu stndrds of stte
regultory uthorities; however, gency policies y
be ore stringent thn those tht re recognized by the
stte. Eployent by the gency iplies the willing-
ness of the nurse to dhere to estblished stndrds
nd to work within estblished guidelines. Exples
of policy stteents tht re relted to ediction d-
inistrtion include the following:
1. Educational requirements for professionals who are au-
thorized to administer medications. Mny helthcre
fcilities require the pssing of  written test to con-
r the knowledge nd skills needed for edic-
tion clcultion, preprtion, nd dinistrtion
before grnting pprovl to n individul to din-
ister ny edictions.
2. Approved lists of intravenous (IV) solutions and med-
ications that the nurse can start or add to an existing
infusion.
3. Lists of restricted medications (e.g., antineoplastic
agents, magnesium sulfate, allergy extracts, RhoGAM
[Rho(D) immune globulin (human)], heparin) that may
be administered only by certain staff members with spe-
cic credentials or training.
4. Lists of abbreviations that are not to be used in documen-
tation to avoid medication errors (see the pge fcing
the inside bck cover of this book).
Before dinistering ny ediction, the nurse ust
hve  current license to prctice,  cler policy stte-
ent tht uthorizes the ct, nd  ediction order
signed by  prctitioner who is licensed with prescrip-
tive privileges t tht institution. The nurse ust un-
derstnd the individul ptient’s dignosis nd syp-
tos tht correlte with the rtionle for drug use. The
nurse should lso know why  prticulr ediction is
ordered nd its expected ctions, usul dosing, proper
dilution, route nd rte of dinistrtion, dverse ef-
fects, nd the contrindictions for its use. If drugs re
to be dinistered with the use of the se syringe
or t the se IV site, drug coptibility should be
conred before dinistrtion. If the nurse is unsure
bout ny of these key ediction points, then they
ust consult n uthorittive resource or the hospitl
phrcist before dinistering  ediction. The
61
nurse ust be ccurte when clculting, prepring,
nd dinistering edictions. The nurse ust ssess
the ptient to be certin tht therpeutic nd dverse
effects ssocited with the ediction regien re
reported. Nurses ust be ble to collect ptient dt
t regulrly scheduled intervls nd to record obser-
vtions in the ptient’s chrt when evluting  tret-
ent’s effectiveness. Cliing unfilirity with ny
of these nursing responsibilities when n voidble
copliction rises is uncceptble; in fct, it is consid-
ered negligence of nursing responsibility.
Nurses ust tke n ctive role in educting the p-
tient, the fily, nd signicnt others in preprtion
for the ptient’s dischrge fro the helthcre environ-
ent. A person’s helth will iprove only to the extent
tht the ptient understnds how to perfor self-cre.
Specic teching gols should be developed nd iple-
ented. Nursing observtions nd the ptient’s prog-
ress towrd the stery of skills should be chrted to
docuent the ptient’s degree of understnding.
PATIENT CHARTS
The ptient’s chrt or the electronic edicl record
(EMR) is  priry source of infortion tht is neces-
sry for the ptient ssessent so tht the nurse cn
crete nd ipleent plns for ptient cre. It is lso
where the nurse provides the docuenttion of the
nursing ssessents perfored, the observtions re-
ported to the priry helthcre provider for further
veriction, the bsic nursing esures ipleented
(e.g., dily tretents), the ptient teching perfored,
nd the observed responses to therpy.
This record serves s the couniction link ong
ll ebers of the helthcre te regrding the p-
tient’s sttus, the cre provided, nd the ptient’s prog-
ress. The chrt is  legl docuent tht describes the
ptient’s helth, lists dignostic nd therpeutic proce-
dures initited, nd describes the ptient’s response to
these esures. The chrt ust be kept current s long
s the ptient is in the hospitl. After the ptient’s dis-
chrge, this record is intined ccording to policies
within the institution. The ptient record y be used
for reserch to copre responses to selected therpies
in  spling of ptients with siilr dignoses.
CONTENTS OF PATIENT CHARTS
Although ech helthcre fcility uses  slightly differ-
ent fort, the bsic ptient chrt consists of the fol-
lowing eleents.
Summary Section
The summary section gives the ptient’s ne, ddress,
dte of birth, ttending helthcre provider, gender,
ritl sttus, llergies, nerest reltive, occuption
nd eployer, insurnce crrier nd other pyent
infortion, religious preference, dte nd tie of d-
ission to the hospitl, previous hospitl dissions,
62 UNIT II Illustrated Atlas of Medication Administration
nd ditting proble or dignosis. The dte nd
tie of dischrge re dded when pproprite.
Consent Section
The dission consent section grnts perission to
the helthcre fcility nd the helthcre provider to
provide tretent. Other types of consent fors re
used during the course of  hospitliztion, such s
n opertive procedure perit or consent, n invsive
procedure consent,  blood-product consent, nd 
consent to bill the ptient’s insurnce crrier.
Order Section
All procedures nd tretents re ordered by the
helthcre provider in the order section. These orders
include generl cre (e.g., ctivity, diet, frequency of
recording vitl signs), lbortory tests to be copleted,
other dignostic procedures (e.g., rdiogrphy, electro-
crdiogrphy, coputed toogrphy), nd ll edi-
ctions nd tretents (e.g., physicl or occuptionl
therpy).
History and Physical Examination Section
During dission to the hospitl, the ptient is inter-
viewed by  helthcre provider nd given  physicl
exintion. The helthcre provider records the nd-
ings on the history and physical examination section
nd lists the probles to be corrected (e.g., the dig-
noses). The history nd physicl exintion for is
often referred to s “the H&P.”
Progress Notes
The ttending helthcre provider records frequent ob-
servtions of the ptient’s helth sttus in the progress
notes. The progress notes re updted dily to docu-
ent the ptient’s clinicl events, nd how well the
ptient is progressing towrd helth during their sty
in the institution. In ost hospitls, other helth pro-
fessionls (e.g., phrcists, dietitins, physicl nd
respirtory therpists) y record observtions nd
suggestions in the progress notes.
Nurses’ Notes
Although the fort vries ong institutions, the
nurses’ notes generlly strt with the nursing history.
On dission, the nurse perfors  coplete helth
ssessent of the ptient. This process includes  hed-
to-toe physicl ssessent, nd it lso incorportes 
ptient nd fily history tht provides insights into
individul nd fily needs, life ptterns, psycho-
socil nd culturl dt, nd spiritul needs. This s-
sessent will serve s the bsis for the developent of
the individulized cre pln nd s  bseline for co-
prison when ongoing ssessent dt re gthered.
Nurses record the following in their notes: ongo-
ing ssessents of the ptient’s condition; respons-
es to nursing interventions ordered by the priry
helthcre provider (e.g., tretents or edictions)
or to those initited by the nurse (e.g., skin cre, p-
tient eduction); evlutions of the effectiveness of
nursing interventions; procedures copleted by oth-
er helthcre professionls (e.g., wound clening by
 priry helthcre provider, tting for  prosthe-
sis by  prosthetist); nd other pertinent infortion
(e.g., priry helthcre provider or fily visits,
ptient’s responses fter these visits). Entries y be
de on the nurses’ notes or ow sheets throughout
 shift, but generl guidelines include the following:
(1) copleting records, including vitl signs, ie-
ditely fter ssessing the ptient upon dission,
nd following ny dignostic procedure; (2) record-
ing ll “s needed” (PRN) edictions ieditely
fter dinistrtion nd ddressing the effectiveness
of the ediction; (3) recording chnge in the p-
tient’s sttus nd who ws notied (e.g., helthcre
provider, nger, ptient’s fily); (4) discussing
the tretent of  sudden chnge in the ptient’s st-
tus; nd (5) recording infortion bout the trnsfer,
dischrge, or deth of  ptient. In ddition to the
ccurte chrting of the observtions in  cler nd
concise nner, the nurse should report signicnt
chnges in  ptient’s sttus to the chrge nurse. The
chrge nurse then kes  nursing judgent regrd-
ing the notiction of the ttending helthcre pro-
vider. Coputerized chrting ethods re coon
nd llow the nurse to docuent ndings nd b-
sic cre delivered using ultiple screens of dt nd
checklist-type forts.
Laboratory Tests Record
The laboratory tests record hs ll the lbortory test
results in one section of the chrt. Hospitls tht use
coputerized reports y list consecutive vlues
of the se test if tht test hs been repeted severl
ties (e.g., electrolytes). Coputerized lbortory
dt ccess provides online lbortory results s soon
s the tests re copleted. Other hospitls y t-
tch sll report fors to  full-sized bcking sheet s
ech report returns fro the lbortory. Becuse soe
ediction doses re bsed on dily blood studies, it
is iportnt to be ble to locte these dt within the
ptient’s chrt.
Graphic Record
The graphic record (Fig. 6.1A) is n exple of the
nul recording of teperture, pulse, respirtion,
nd blood pressure. Fig. 6.1B is n electronic dtbse–
generted exple of the vitl signs, uid intke nd
output, glucose, dietry intke, nd other infortion
to be used for the ongoing ssessent of the ptient’s
sttus.
Pin ssessent, which is considered the fth vitl
sign, cn lso be recorded in  grphic for. In ddi-
tion to the grphic recording of pin, ssessents of
pin cn be found on other ow sheets in the chrt tht
will record the detils of the pin events.
 Principles of Medication Administration and Medication Safety CHAPTER 6 63

GRAPHIC SHEET
PATIENT LABEL

A
Fig. 6.1 (A) Manual vital signs record. (Courtesy St. Mary’s Health Center, St. Louis, MO.)

Flow Sheets Other Diagnostic Reports

Flow sheets re  condensed for for recording infor-
tion for the quick coprison of dt. Exples
of ow sheets in coon use re dibetic, pin, nd
neurologic ow sheets. The grphic record tht is used
for recording vitl signs is nother type of ow sheet
(see Fig. 6.1A).
Consultation Reports
When other helthcre professionls re sked to con-
sult bout  ptient, the specilist’s sury of nd-
ings, dignoses, nd recoendtions for tretent
re recorded in the consultation reports section of the
chrt.
Reports of surgery, electroencephlogrphy, electro-
crdiogrphy, pulonry function tests, rdioctive
scns, nd rdiogrphy re usully recorded in the
other dignostic reports section of the ptient’s chrt.
Medication Profile and Medication Administration
Record
The medication prole, lso clled the ediction
worklist when in n electronic fort, lists ll edic-
tions to be dinistered. The prole is intined in
the ptient’s coputerized dtbse, ensuring tht the
phrcist nd the nurse hve identicl ediction
proles for the ptient. The edictions re usully
64 UNIT II Illustrated Atlas of Medication Administration
B
Fig. 6.1 (B) Electronic charting of vital signs and intake and output. (Courtesy Creighton University Medical Center,
Omaha, NE.)
grouped ccording to the following ctegories: edi-
ctions scheduled to be given on  regulr bsis (e.g.,
every 6 hours, twice dily), prenterl edictions, stt
edictions (fro the Ltin statim, ening “ie-
ditely”), nd preopertive orders. PRN edictions
(fro the Ltin pro re nata, ening “s circustnces
require”) re those edictions tht re given on n
“s needed” bsis nd re usully listed t the botto
of the prole, or they y be found on  seprte pge
s unscheduled ediction orders.
The medication administration record (MAR) is  re-
cord of the tie tht the ediction ws dinistered
nd identies who gve it (Fig. 6.2A). Generlly, the
nurse records nd initils the tie tht the ediction
ws given. Mediction proles re kept in  notebook
or clipbord le on the ediction crt for the 24-hour
period tht they re in use; they then becoe  per-
nent prt of the ptient’s chrt. In the cute cre set-
ting,  new prole is generted every 24 hours t the
se tie tht the unit-dose crt is relled. Fig. 6.2B is
n exple of n electronic dtbse–generted MAR
tht lists ll scheduled edictions for n 8-hour shift.
By clicking the cursor on the highlighted re (i.e.,
scheduled regulr insulin in this illustrtion),  win-
dow opens to revel detils of the order.
In the long-ter cre setting the MAR uses the se
principles; however, it generlly provides  spce for
edictions to be recorded for up to 1 onth. The
MAR lso includes the ne of the phrcy tht dis-
pensed the prescribed edictions nd the ssigned
prescription nuber. Medictions tht re prescribed
for residents in the long-ter cre setting ust be re-
viewed on  scheduled bsis; therefore the MAR iden-
ties the reviewer nd the dte of review.
PRN or Unscheduled Medication Record
PRN edictions, or those tht re given s needed,
y be recorded on  seprte ediction record
rther thn the MAR to record the dte, the tie, the
PRN ediction dinistered, the dose, the reson for
dinistering the PRN ediction, nd the ptient’s
response to the drug given. However, in ost clini-
cl settings tht involve the use of electronic fors of
chrting, the PRN edictions re recorded on the
se MAR.
Patient Education Record
The patient education record provides  ens of
docuenting the helth teching provided to the p-
tient, the fily, or signicnt others, nd it includes
stteents bout the ptient’s stery of the content
presented.
Additional Patient Chart Records
Additionl records in  ptient’s chrt y include the
following: seprte MARs; opertive nd nesthesiology
 Principles of Medication Administration and Medication Safety CHAPTER 6 65

MARTINDALE HOMETOWN HOSPITAL

MEDICATION ADMINISTRATION RECORD

NAME: Joseph Lorenzo RM-BD: 621-2 Init Signature Title
ID NO: 016-28-3978 AGE: 62
DIAGNOSIS: Myocardial Infarction SEX: M
PHYSICIAN: M. Martin, M.D. Ht: 6’ Wt: 200 lb

**SCHEDULED MEDICATIONS**
DATES: MEDICATION—STRENGTH—FORM—ROUTE 0030-0729 0730-1529 1530-0029
1/25/yr RANITIDINE 0900 1800
ZANTAC
150 MG TABLET ORAL
TWICE A DAY
1/25/yr DILTIAZEM HYDROCHLORIDE 0900 1800
CARDIZEM 1300 2100
90 MG TABLET ORAL
4 TIMES DAILY
1/25/yr WARFARIN SODIUM NOT GIVEN TODAY
COUMADIN
1 MG TABLET ORAL
EVERY OTHER DAY
**IV AND PIGGYBACK ORDERS**
1/25/yr CEFTAZIDIME (FORTAZ) 1 G IV 0200 1000 1800
SODIUM CHLORIDE 0.9% 50 ML
EVERY 8 HOURS INFUSE: 20 MIN
1/25/yr GENTAMICIN PREMIX 80 MG IV 0200 1400
ISO-OSMOTIC SOLN 100 ML
BY IV PUMP
EVERY 12 HOURS INFUSE: 30 MIN
1/25/yr BY IV PUMP 1 IV
DSW-5/0.2 NACl 1000 ML
RATE: 100 ML/HR
**PRN MEDICATIONS**
1/25/yr ACETAMINOPHEN
TYLENOL
650 MG (23325) TABLET ORAL
EVERY 4 HOURS AS NEEDED PRN
1/25/yr MAGNESIUM HYDROXIDE
MILK OF MAGNESIA
60 ML (CONC) ORAL CONC
AS NEEDED PRN
1/25/yr ALBUTEROL
PROVENTIL INHALER
90 MCG/INH AEROSOL INH
AS NEEDED PRN
SEE RESPIRATORY THERAPY NOTES
AT BEDSIDE

Age/Sex HT WT Date ALLERGIES: CODEINE

62/ M 6’0” 200 lb 1/25/yr
Room-Bd Name
621 2 Joseph Lorenzo

A
Fig. 6.2A Medication prole. Note the separation of scheduled orders, intravenous (IV), and as-needed (PRN) medications.
(Courtesy Creighton University Medical Center, Omaha, NE.)

records; recovery roo records; physicl, occuptionl,
or speech therpy records; inhltion therpy reports;
nd  person with dibetes’ dily record of insulin dos-
ge nd blood glucose (sugr) test results. Ech pge
tht is plced in the ptient’s chrt is iprinted with the
ptient’s ne, registrtion nuber, nd unit or roo
nuber. Nurses often use dt fro ll of the chrt sec-
tions to forulte  nursing cre pln.
Nursing Care Plans
After the initil dt collection, the nurse develops n
individulized nursing care plan. Cre plns incorpo-
rte nursing dignoses, criticl pthwy infortion,
nd helthcre provider–ordered nd nursing-or-
dered cre (see Nursing Cre Pln). Most cute cre
fcilities require the nurse to chrt ginst ech iden-
tied nursing dignosis stted in the cre pln every
8 hours. Cre plns re evluted nd odied on 
continuu throughout the course of tretent. The
pln should be shred with the helthcre te to
ensure n interdisciplinry pproch to cre. Mny
institutions hve developed stndrdized cre plns
for the vrious nursing dignoses. It is the nurse’s
responsibility to identify those dignoses, interven-
tions, nd outcoes tht re pproprite for the
ptient.
66 UNIT II Illustrated Atlas of Medication Administration

B
Fig. 6.2B Electronically generated medication sheet listing all scheduled medications for an 8-hour shift. By clicking the
cursor on the highlighted area (“4 UNIT SUB” in this illustration), a window opens to reveal details of the order. (Courtesy
Creighton University Medical Center, Omaha, NE.)

KARDEX RECORDS stndrds of cre. The Joint Coission requires tht

The Kardex in pper for is  lrge index-type crd
tht is usully kept in  ip le or  seprte holder
tht contins pertinent infortion such s the p-
tient’s ne, dignosis, llergies, tretents, nd
the nursing cre pln. When the unit-dose syste is
used, edictions re not listed on the Krdex; rther,
they re listed seprtely on the ediction prole.
Although the Krdex is used pririly by nurses, p-
tient dt cn be quickly ccessed by ll ebers of
the helthcre te. The Krdex is often copleted
in pencil nd updted regulrly. Becuse it is not  le-
gl docuent, it is destroyed when the ptient is dis-
chrged fro the institution. Electronic Krdex infor-
tion is prt of the electronic dtbse tht kes
up the EMR. This is used to give nurse-to-nurse shift
reports nd is continully updted throughout ech
shift.
CHARTING METHODOLOGIES
Regrdless of the ethod of chrting used, the doc-
uenttion process needs to dhere to The Joint
Coission stndrds tht incorporte estblished
ll chrting ethodologies incorporte nursing pro-
cess criteri nd evidence of teching nd dischrge
plnning. When ore thn one helthcre discipline
is providing ptient cre,  ultidisciplinry cre
pln ust be copleted. This fcilittes couni-
ction ong interdisciplinry te ebers nd
helthcre providers. Iproving ptient sfety t the
point of cre hs becoe stndrd in every helthcre
institution.
The fort nd extent of use of electronic dtbse
chrting vry widely ong institutions, but ech
ethod incorportes the stndrds of cre nd The
Joint Coission requireents. Soe clinicl sites
hve extensive online electronic chrting developed,
wheres others hve little or none. For exple, one
hospitl y elect to cobine ll of the eleents for-
erly found in the Krdex, the cre pln, the MAR,
nd the criticl pthwys into one docuent known
s  patient prole tht the nurse cn ccess during
ech shift. Regrdless of the ethodology used, the
dge “If you didn’t chrt it, it didn’t hppen” still
holds true.

ALGrawany
 Principles of Medication Administration and Medication Safety CHAPTER 6
DRUG DISTRIBUTION SYSTEMS
Before dinistering edictions, it is iportnt tht
the nurse understnd the overll ediction delivery
syste tht is used t the eploying helthcre gency.
Although no two drug distribution systes function in
exctly the se wy, the following generl types re
used.
FLOOR OR WARD STOCK SYSTEM
In the oor or ward stock system, ll but the ost dn-
gerous or rrely used edictions re stocked t the
nursing sttion in stock continers. This syste hs
generlly been used in very sll hospitls nd hospi-
tls in which there re no direct chrges to the ptient
for edictions (e.g., in soe governent hospitls).
Soe dvntges of this syste re the redy vilbil-
ity of ost drugs, fewer inptient prescription orders,
nd the inil return of edictions. The disdvn-
tges re s follows:
• Incresed potentil for ediction errors becuse of
the lrge rry of stock edictions fro which to
choose nd the lck of review by the phrcist of 
ptient’s ediction order
• Incresed dnger of the unnoticed pssing of expi-
rtion dtes nd drug deteriortion, s well s in-
cresed quntities of expired drugs to be discrded
• Econoic loss cused by isplced or forgotten
chrges nd the ispproprition of ediction by
hospitl personnel
• Need for lrger stocks nd frequent totl drug
inventories
• Storge probles on the nursing units of ny
hospitls
INDIVIDUAL PRESCRIPTION ORDER SYSTEM
With the individual prescription order system, edic-
tions re dispensed fro the phrcy with the re-
ceipt of  prescription or drug order for n individul
ptient.
The phrcist usully sends  3- to 5-dy supply
of ediction in  bottle tht is lbeled for  specif-
ic ptient. After the prescriptions re received t the
nurses’ sttion, edictions re plced in the edic-
tion cbinet in ccordnce with institutionl prctices.
Generlly, the ediction continers re rrnged l-
phbeticlly by the ptient’s ne, but they y be
rrnged nuericlly by the ptient’s roo or bed
nuber. This syste provides greter ptient sfety
becuse of the review of prescription orders by the
phrcist nd nurse before dinistrtion; it lso
involves less dnger of drug deteriortion, esier in-
ventory control, sller totl inventories, nd reduced
revenue loss becuse of iproved chrging systes
nd less pilferge. Although dispensing ediction
to individul ptients is better thn the oor or wrd
stock syste, the jor disdvntges of this syste
re the tie-consuing procedures tht re used to
67
Fig. 6.3 Unit-dose cabinet.
schedule, prepre, dinister, control, nd record the
drug distribution nd dinistrtion process.
UNIT-DOSE SYSTEM
The unit-dose drug distribution system uses single-unit
pckges of drugs tht re dispensed to ll ech dose
requireent s it is ordered. Ech pckge is lbeled
with the drug’s generic nd brnd nes, the nu-
fcturer, the lot nuber, nd the expirtion dte. When
they re dispensed by the phrcy, the individul
pckges re plced in lbeled drwers tht re s-
signed to individul ptients. The drwers re kept in
 lrge unit-dose cbinet (Fig. 6.3) tht is kept t the
nurses’ sttion; in soe institutions, individulized
continers or envelopes y be locked in  cbinet
in the ptient’s roo. With ost unit-dose systes,
 phrcist rells the drwers every 24 hours. In
long-ter cre fcilities, these drwers re usully ex-
chnged on  3- or 7-dy schedule.
Advntges of the syste include the following:
• The tie tht is norlly spent by nursing person-
nel prepring drugs for dinistrtion is drsticlly
reduced.
• The phrcist hs  prole of ll edictions for
ech ptient nd is therefore ble to nlyze the pre-
scribed edictions for drug interctions or contr-
indictions. This ethod increses the phrcist’s
involveent nd kes better use of their extensive
drug knowledge.
• Counting drugs fro ultidose pckets is no longer
necessry s  result of unit-dose pckging, there-
by reducing errors.
• It is the nurse’s responsibility to check drugs nd
clculte dosges (see the infortion under Right
Dose lter in this chpter), thereby reducing errors.
68 UNIT II Illustrated Atlas of Medication Administration

• There is less wste nd ispproprition becuse

single units re dispensed.
• Credit is given to the ptient for unused edic-
tions becuse ech dose is individully pckged.
(Under the individul prescription order syste, re-
turned bottles of unused edictions re destroyed
out of fer of contintion.)
The unit-dose ediction is prepred under rigid
controls, nd it is dispensed only fter phrcists
hve copleted qulity control procedures. Nurses
should lwys check edictions before dinistr-
tion. If there is  discrepncy between the ediction
prole nd the ediction in the crt, then the phr-
cist nd the originl prescriber’s order should be
consulted.
At the tie of dinistrtion, the nurse should
check ll spects of the ediction order s stted on
the ediction prole ginst the ediction contin-
er reoved fro the ptient’s drwer for dinistr-
tion. The nuber of doses reining in the drwer
for the shift should lso be checked. If the nuber
of reining doses is incorrect, the ediction order
should be checked before continuing with the drug
dinistrtion. It is lwys possible tht the drug hs
been discontinued or tht soeone else hs given the
dose, oitted  dose, or given the wrong ptient the
wrong ediction. If n error hs been de, it should
be reported in ccordnce with hospitl policies.

COMPUTER-CONTROLLED DISPENSING SYSTEM
A coon syste for ediction ordering nd d-
inistrtion is  computer-controlled dispensing sys-
tem, such s Pyxis (Fig. 6.4), tht uses the unit-dose
syste described erlier. It is resupplied by the phr-
cy dily nd is stocked with single-unit pckges of
edicines. When  drug order is received in the phr-
cy for  ptient, it is entered into the coputerized
syste. The nurse—who is using  security code nd
pssword nd, with newer systes,  ngerprint—
ccesses the syste nd selects the ptient’s ne, the
ediction prole, the ptient’s ediction drwer,
nd the drugs tht re due for dinistrtion. The
drug order ppers on the screen, nd  specic sec-
tion of the crt opens so tht the nurse cn tke  sin-
gle dose of edicine out of the crt (Fig. 6.5A). This
process continues until ll drugs ordered for  specic
tie of dinistrtion re retrieved. During the ctul
dinistrtion process t the bedside, the nurse uses
 hndheld scnner tht reds the bar codes on the
nurse’s identiction bdge, the ptient’s wristbnd,
nd the unit-dose ediction pcket, thereby linking
this infortion with the ptient dtbse (Fig. 6.5B).
If there is n error (e.g., wrong dose, wrong tie of
dinistrtion, wrong ptient), n lert pops up on
the coputer nd the user is unble to continue until
the error is corrected. If the process is correct nd the
edicine is dinistered, there is utotic docuen-
ttion in the ptient’s MAR of the dinistrtion.
Fig. 6.4 Electronic dispensing system: the Pyxis system. (Courtesy
and © Becton, Dickinson and Company, Franklin Lakes, NJ.)
Controlled drugs re lso kept in this utoted
dispensing crt. The syste provides  detiled record
of the controlled substnce dispensed, including the
dte, the tie, nd by who it ws ccessed. A second
qulied nurse ust witness the disposl of  portion
of  dose of  controlled substnce or the return to the
utoted dispensing crt of ny controlled substnce
tht is not used. The utoted dispensing syste
is currently the sfest nd ost econoicl ethod
of drug distribution in hospitls nd long-ter cre
fcilities.
Long-Term Care Unit-Dose System
The long-term care unit-dose system is n dpttion
of the syste tht is used in the cute cre setting. The
unit-dose crt is designed with individul drwers to
hold one resident’s ediction continers for 1 week.
The drwer is lbeled with the resident’s ne nd
roo nuber, the phrcy’s ne nd telephone
nuber, nd the ne of the helthcre fcility. The
phrcist lls the ediction continer with the pre-
scribed drug. Ech continer hs enough coprtents
to contin the prescribed nuber of doses of the drug
for ech dy of the week. The individul coprtents
y be lbeled with the dys of the week. The edi-
ction crt hs other coprtents for storing bottles
 Principles of Medication Administration and Medication Safety CHAPTER 6
A controlled substnces hve been encted in the United
B controlled substnces received. The nurse then signs
Fig. 6.5 (A) The nurse removes a single dose of medicine from the
electronic dispensing system. (B) A single-dose, bar-coded medication
package is scanned by the nurse before it is administered. (Courtesy
and © Becton, Dickinson and Company, Franklin Lakes, NJ.)
of ediction tht cnnot be plced in ptients’ drw-
ers. The crt hs  storge re for ediction cups, 
edicine crusher, drinking cups, strws, lcohol wipes,
syringes, nd other necessities for the preprtion nd
dinistrtion of the edictions prescribed. The en-
tire crt hs  locking syste tht should be secured
when the ediction crt is not in use or when it is un-
ttended while edictions re being dispensed.
At the tie of dinistrtion, the nurse or edic-
tion ide checks ll spects of the ediction order (s
stted on the ediction prole) ginst the edic-
tion continer tht hs been reoved fro one of the
drwers. The nuber of doses reining in the holder
is checked ginst the dys of the week tht rein
for the ediction to be dinistered. If the resident
refuses the ediction, it ust be chrted on the re-
cord with the reson tht the ediction ws refused.
In  long-ter cre setting,  resident seldo wers n
identiction bnd; therefore third-prty identiction
of the resident ust be relied on until the nurse or ed-
iction ide is ble to identify the resident. If pictures
of the residents re used s identiers, the institution
should hve  policy in plce to updte the photos on
69
 regulr bsis. Medictions should be chrted s soon
s they re dinistered. The ediction ide hs spe-
cic liittions on the types of edictions tht they
cn dinister; therefore nurses should be thoroughly
filir with the lws nd guidelines of their stte. The
nurse is ultitely responsible for verifying the quli-
ctions of the individul who is being supervised in
the ediction-ide cpcity nd for the edictions
tht the ediction ide is dinistering.
NARCOTIC CONTROL SYSTEMS
As described in Chpter 1, lws regulting the use of
Sttes nd Cnd nd re rigidly enforced in hospitls
nd long-ter cre fcilities with the use of narcotic
control systems. It is  stndrd policy tht controlled
substnces re issued in single-unit pckges nd kept
in  locked cbinet. If n utoted dispensing syste
is not vilble,  designted individul is responsible
for the key to the cbinet. When controlled substnces
re issued to  nursing unit, they re ccopnied by
n inventory control record (Fig. 6.6) tht lists ech
type of controlled substnce being supplied. This re-
cord is used to ccount for the disposition of ech type
of ediction issued. When the controlled substnce
supply is dispensed to the nursing unit by the phr-
cist, the nurse receiving the drug supply is responsible
for counting nd verifying the nuber nd types of
 record ttesting to the ccurcy nd receipt of the
controlled substnces nd locks the in the controlled
substnces (nrcotic) cbinet.
When  controlled substnce is ordered for  pr-
ticulr ptient, the nurse cring for the ptient uses 
key to the cbinet to obtin nd prepre the edic-
tion for dinistrtion. At the tie of reovl fro
the cbinet, the inventory control record (see Fig. 6.6)
ust be copleted; it ust indicte the tie, the p-
tient’s ne, the drug, nd the dose, nd it ust in-
clude the signture of the nurse who is responsible for
checking out the controlled substnce. If  portion of
the ediction is to be discrded becuse of  sller
prescribed dose, two nurses ust check the dose, the
preprtion, nd the portion discrded. Both nurses
ust then cosign the inventory control record to verify
the trnsction. The cbinet is relocked, the edicine
is dinistered, nd the docuenttion is copleted.
Before the dinistrtion of ny controlled sub-
stnce, the ptient’s chrt should be checked to verify
tht the tie intervl since the lst use of the drug hs
elpsed s specied in the helthcre provider’s or-
ders (see Chpter 19 for detils bout the onitoring
of pin nd the use of nlgesics). Ieditely fter
the dinistrtion of  controlled substnce, the nurse
who is dinistering the ediction should coplete
the chrting. At pproprite intervls fter the din-
istrtion of  controlled substnce, the degree nd du-
rtion of effectiveness should be recorded.
70 UNIT II Illustrated Atlas of Medication Administration
UNIT
DISCARDED (mg)
DOSE (mg)
DATE
DELIVERED BY
No
By ________________________________RN
Fig. 6.6 Controlled substances inventory control record. (Courtesy University Hospital, The University of Nebraska
Medical Center; © Board of Regents of the University of Nebraska, Lincoln, NE.)
At the end of ech shift, the contents of the con-
trolled substnces cbinet or the controlled substnces
crt re counted (inventoried) by two nurses: one fro
the shift tht is bout to end nd the other fro the
oncoing shift. Ech continer is counted, nd the
reining nubers of tblets, pules, nd prelled
syringes re dded to the ount used in ccordnce
with the inventory control record. The ount of ech
drug reining plus the ount recorded s being
dinistered to individul ptients should equl the
totl nuber issued. During the counting procedure,
pckges of unopened prelled syringes re visully
inspected to verify tht the sel nd cellophne cov-
erings re intct. If the pckge sel is broken, closer
scrutiny of the pckge is required. These observtions
should include tilting  pckge of prelled syringes
to observe the rte of ir bubble oveent inside the
brrel, the unifority of color of the solutions in ech
of the brrels, nd the siilrity in uid levels in ech
of the brrels. The se ediction in the se type
NURSE’S
SIGNATURE
By ________________________________ Pharmacist
of syringe should be the se color nd trvel through
the brrel t the se rte, nd ll uid levels should
be siilr.
Discrepncies in the nuber of reining doses re
checked with nursing personnel on the unit to see if ll
controlled substnces used hve been chrted. If this
does not revel the source of the inccurcy, ech p-
tient’s chrt is checked to be certin tht ll controlled
substnces recorded on the individul ptient’s chrt
for the shift coincide with the controlled substnces
inventory record. If the error is still not found, the
phrcy nd the nursing service ofce should be
contcted in ccordnce with institution policy. If the
count ppers to be ccurte but tpering with the
contents of the continers is suspected,  report should
be de to the phrcy nd the nursing service of-
ce. When the controlled substnces inventory is co-
plete, the two nurses who re counting sign the inven-
tory control shift record to verify tht the records nd
inventory re ccurte t tht tie. With the controlled
 Principles of Medication Administration and Medication Safety CHAPTER 6
substnce crt, the coputer genertes n end-of-shift
report tht lso identies discrepncies so tht the
stff involved cn ccount for the use of controlled
substnces.
When n utoted dispensing crt such s Pyxis
(see Fig. 6.4) is used, the shift chnge nrcotic check is
not done. At the tie of dinistrtion, the nurse will
verify the correct count of the drug desired before re-
oving the drug fro the crt. At tht tie, the syste
will be ctivted if  discrepncy occurs. Discrepncies
re trcked by nursing nd phrcy, nd they re
resolved s soon s they re discovered. The phr-
cy lso checks for discrepncies when controlled
substnces re restocked in the utoted dispensing
syste.
DISPOSAL OF UNUSED MEDICINES
In recent yers, environentl concerns hve risen
bout the proper disposal of unused medicines, be-
cuse trce levels of edicines hve been found in riv-
ers, lkes, nd counity wter supplies. Concerns
hve been expressed bout the ppropriteness of the
coon prctice of ushing unused edicines down
the toilet, becuse ny people ssue tht this is
the priry source of wter contintion. However,
the US Food nd Drug Adinistrtion’s Center for
Drug Evlution nd Reserch hs stted tht drugs
found in ground wter re pririly drugs tht hve
been incopletely bsorbed nd etbolized by the
body fter hun consuption nd tht hve entered
the environent fter pssing through wste-wter
tretent plnts. Scientists fro the Environentl
Protection Agency hve found no evidence of dverse
hun helth effects fro unetbolized drugs in the
environent.
The US Food nd Drug Adinistrtion, working in
conjunction with the White House Ofce of Ntionl
Drug Control Policy, issued the following guidelines
ddressing prescription nd nonprescription edic-
tion disposl:
• Follow specic disposl instructions on the drug l-
bel or in the ptient infortion leet tht cco-
pnies the ediction. Do not ush prescription
drugs down the toilet unless speciclly instructed
to do so by the nufcturer.
• If no instructions re given, throw the drugs in the
household trsh, but rst:
 • Epty the drugs fro the continer, nd then
ix the with n undesirble substnce, such s
used coffee grounds or kitty litter. This kes the
product considerbly less ppeling to children
nd pets nd less recognizble to people who
y intentionlly go through trsh (e.g., dup-
ster divers).
 • Put this ixture in  selble bg, n epty cn,
or nother continer to prevent the ediction
fro leking out of the grbge bg.
71
CLAYTON’S PHARMACY
213 West Third Street Grand Island, Nebraska
NAME enzo AGE Adult
ADDRESS DATE
Rx
ERYTHROMYCIN TABS 250 mg ENTERIC
#40 COATED
sig: TAB i q 6 h
DISPENSE AS WRITTEN SUBSTITUTION PERMISSIBLE
THIS PRESCRIPTION WILL BE FILLED GENERICALLY UNLESS PHYSICIAN
SIGNS ON THE LINE STATING “DISPENSE AS WRITTEN”
Fig. 6.7 Prescription showing patient name and age, patient address,
date, drug and strength, number of tablets, directions for use, and the
healthcare provider’s signature.
• Use counity drug tke-bck progrs tht l-
low the public to bring unused drugs to  centrl
loction for proper disposl. The drugs re often de-
stroyed using  biohzrd-controlled incinertor.
• Before throwing out n epty prescription bottle,
scrtch out ll identifying infortion on the lbel
to ke it unredble. This will help protect ptient
identity nd helth infortion.
• Controlled substnces (e.g., opite nlgesics)
should be ushed down the toilet to reduce the
dnger of unintentionl use or overdose nd ille-
gl buse. An exple is the fentnyl ptch, which,
even fter it hs been used by the ptient for 3 dys,
cn still contin enough edicine to cuse severe
respirtory depression in bbies, children, nd
pets. Environentlly friendly drug disposl bgs
(e.g., Deterr) tht dectivte edictions re used
to prevent drug diversion nd potentil overdose.
Additionl guidelines for the disposl of drugs
tht re clssied s hzrdous edictions (e.g.,
cheotherpeutic gents) hve lso been dened.
Refer to gency policies for proper disposl.
MEDICATION ORDERS
Medictions for ptient use ust be ordered by li-
censed priry helthcre providers, dentists, nurse
prctitioners, nd physicin ssistnts cting within
their res of professionl trining. Plcing n order for
 ediction or tretent is known s issuing a prescrip-
tion. Initilly,  prescription y be issued verblly or
in written for. Prescriptions tht re issued for non-
hospitlized ptients use  for tht is siilr to tht
shown in Fig. 6.7, wheres prescriptions for hospitl-
ized ptients re written on the institution’s ediction
order for. All prescriptions ust contin the follow-
ing eleents: the ptient’s full ne, the dte, the drug
ne, the route of dinistrtion, the dose, the dur-
tion of the order, nd the signture of the prescriber.
Additionl infortion y be required for certin
types of edictions (e.g., for IV dinistrtion, the
72 UNIT II Illustrated Atlas of Medication Administration
concentrtion, dilution, nd rte of ow should be
specied in ddition to the ethod [i.e., “IV push” or
“continuous infusion”]).
TYPES OF MEDICATION ORDERS
Mediction orders fll into four ctegories: stt, single,
stnding, nd PRN orders. The stat order is generlly
used on n eergency bsis. It ens tht the drug is
to be dinistered s soon s possible, but only once.
For exple, if  ptient is hving  seizure, the pri-
ry helthcre provider y order “dizep 10 g
IV stt,” which ens tht the drug is to be given i-
editely nd one tie only.
The single order ens dinistrtion t  certin
tie but only one tie. For exple,  one-tie order
y be written for “furoseide 20 g IV to be given
one tie t 7 am.” Furoseide would then be din-
istered t tht tie, but once only.
The standing order indictes tht  ediction is to
be given for  specied nuber of doses: for exple,
“cefzolin 1 g q6h × 4 doses.” A stnding order y
lso indicte tht  drug is to be dinistered until it
is discontinued t  lter dte: for exple, “picillin
500 g PO q6h.” In the interest of ptient sfety, how-
ever, ll ccredited helthcre gencies hve policies
tht utoticlly cncel n order fter  certin nu-
ber of doses re dinistered or fter  certin nuber
of dys of therpy hve pssed (e.g., surgery, fter 72
hours for nrcotics, fter one dose only for nticogu-
lnts, fter 7 dys for ntibiotics).
A PRN order ens “dinister if needed.” This or-
der llows  nurse to judge when  ediction should
be dinistered on the bsis of the ptient’s need nd
when it cn be sfely dinistered.
Verbal Orders
Helthcre gencies hve policies regrding who y
ccept verbl orders nd under wht circustnces
they should be ccepted, usully in eergency situ-
tions only. The prctice is strongly discourged nd
should be voided whenever possible to prevent edi-
ction errors. The prescriber ust cosign nd dte ny
verbl order, usully within 24 hours.
Electronic Transmission of Patient Orders
Mny priry helthcre providers’ ofces fx new
orders to the re where the ptient is ditted or
trnsferred. These fx trnsissions ust hve n
originl signture within  specied tie, often 24
hours. Hospitl units lso nd it useful to fx orders to
the nursing hoe where the individul is being trns-
ferred. This llows the receiving gency to prepre for
the ptient or resident, nd the originl orders, which
hve been signed by the priry helthcre provider,
then ccopny the individul t the tie of trnsfer.
Computerized provider order entry (CPOE) systems
re used to trnsit orders electroniclly. Softwre hs
been developed tht llows for the use of CPOE nd
Box 6.1 Examples of Medication Errors
PRESCRIBING ERRORS
• Suboptimal drug therapy decisions
• Drug prescribed for patient with known allergy or
intolerance
• Incorrect dose for diagnosis
• Unauthorized drug prescribed
DISPENSING
• Wrong drug or dose sent to nursing unit
• Wrong formulation or dosage form
ADMINISTRATION
• Incorrect strength (dose) given
• Extra dose given or missed dose
• Wrong administration time
• Incorrect administration technique
MONITORING
• Suboptimal monitoring
• Suboptimal assessment of drug response or revision of
regimen
• Suboptimal patient education
clinicl decision-king support systes (CDSSs).
The coputerized syste integrtes the ordering sys-
te with the phrcy, the lbortory, nd the nurses’
sttion, thereby providing ccess instntly to online in-
fortion tht y ffect  ptient’s cre needs.
MEDICATION SAFETY
Medication safety is freedo fro ccidentl injury fro
edictions. The nurse should be wre of how to prop-
erly hndle certin edictions (e.g., cheotherpy
drugs, topicl horones), which cn cuse  rection
when they coe in contct with the skin. The nurse lso
needs to be wre of how to correctly prepre nd din-
ister edictions to prevent injury (e.g.,  needlestick).
Medication errors cn be dened s the filure of
 plnned ction to be copleted s intended or the
use of  wrong pln to chieve  gol. Mediction er-
rors include prescribing errors, trnscription or order
couniction errors, dispensing errors, dinistr-
tion errors, nd errors of onitoring or eduction for
proper use (Box 6.1). Mediction errors cn result in
serious coplictions known s adverse drug events.
In 2005 the nuber of deths fro ediction errors
s reported to the US Food nd Drug Adinistrtion
ws 15,107 (Moore, 2007). The Ntionl Acdey of
Medicine, forerly clled the Institute of Medicine,
hs been working on inititives to reduce these events
nd nge the outcoes by exploring how they oc-
cur nd deterining wys to prevent the.
TECHNOLOGY AND PREVENTION OF ADVERSE
DRUG EVENTS
Adverse drug events occur ost coonly during
ordering nd t the dinistrtion stge. Therefore
 Principles of Medication Administration and Medication Safety CHAPTER 6
preventive esures re being ipleented tht in-
clude substntil chnges in the ordering syste
used for edictions nd lbortory studies. The use
of the CPOE technology checks for potentil drug in-
terctions nd the ppropriteness of drug dosges
ordered, s well s for lbortory ndings (e.g., ther-
peutic drug levels t the tie of order entry).
Autoted ordering nd dispensing systes
hve been developed to iniize ediction errors.
Autoted systes use robotics nd br-coding tech-
nology to ll the orders entered by the priry helth-
cre provider. Robotics in the phrcy cn free soe
of the phrcists for deployent to clinicl units,
where they cn ke ptient rounds, check for edi-
ction response, review current lbortory dt, nd
work with the prescriber to select, dose, nd onitor
drug therpy.
HIGH-ALERT MEDICATIONS
The Institute for Sfe Mediction Prctices (ISMP) hs
conducted  survey of severl cute cre hospitls to
deterine which edictions cuse serious ptient
hr or deth. As  result of this study, edictions
nd clssictions tht pose signicnt risk in the
cute clinicl setting were identied. These re now
known s high-alert medications, nd they include in-
sulin, heprin, opioids, injectble potssiu or pots-
siu phosphte concentrte, neurousculr blocking
gents, nd cheotherpeutic gents. Although is-
tkes y or y not be ore coon with these
edicines, the consequences of n error re uch ore
devstting to ptients. The ISMP continues to onitor
the frequency of drug errors in the clinicl literture to
updte the list of high-lert edictions.
High-lert edictions, the role they ply in edi-
ction errors, nd recoended prctices to id in
prevention include the following: (1) stndrdizing
processes within the institution; (2) developing pro-
cesses to ke errors stnd out (i.e., king stff ore
lert nd wre to ctch errors before they rech the
ptient); nd (3) developing ethods to iniize the
consequences of errors tht rech the ptient. Cohen
lso discussed severl prctices to proote ediction
sfety, including the following: (1) the use of technol-
ogy, including CPOE, br-coded drug dinistrtion,
nd srt pups for controlled dinistrtion; (2) the
restriction of high-lert edictions during the dis-
pensing process (e.g., reoving neurousculr block-
ing gents fro redily vilble oor stock); (3) the
voidnce of verbl orders for high-lert edicines; (4)
the use of checklists for high-lert drugs; (5) the use of
generic nd brnd nes on the MAR to void errors
with sound-like drugs; (6) the stndrdizing of drug
concentrtions nd dosing infusion chrts; nd (7) the
perfornce of double-checking before dinistrtion
nd ptient eduction. The Institute for Helthcre
Iproveent lso kes recoendtions for high-
lert ediction sfety prctices (http://www.ihi.org
73
/topics/highlertedictionsfety/pges/defult.s
px).
MEDICATION RECONCILIATION
Another process tht involves the gol of eliinting
ediction errors is medication reconciliation, which
involves copring  ptient’s current ediction or-
ders with ll of the edictions tht the ptient is ctu-
lly tking. This process kes use of  single, shred,
nd updted ediction nd llergy list for ptients
cross the continuu of inptient nd outptient cre
tht is to be used during handoffs, or the trnsition of
ptients during cre. Reconcilition is to prevent
oissions, duplictions, differences in dosing, nd
drug interctions. It should be copleted s prt of ev-
ery trnsition of cre during which new edictions
re ordered or existing orders re rewritten. Trnsitions
in cre include chnges in setting, service, prctitioner,
or level of cre (e.g., criticl cre to generl cre to re-
hbilittion services).
Mediction reconcilition is  ve-step process: (1)
develop  list of current edictions being dinis-
tered, (2) develop  list of edictions tht were pre-
scribed, (3) copre the edictions on the two lists, (4)
ke clinicl decisions on the bsis of this coprison,
nd (5) counicte the new list to pproprite cre-
givers nd to the ptient. Accurte nd coplete edi-
ction reconcilition cn prevent ny prescribing nd
dinistrtion errors. Filure to reconcile edictions
y be copounded by the prctice of writing blnket
orders (e.g., “resue preop edictions”), which re
known to result in dverse drug events. Such orders
re explicitly prohibited by The Joint Coission’s
ediction ngeent stndrds.
SOUND-ALIKE MEDICATIONS
The ISMP regulrly reports ediction errors tht
re the result of the siilrity of sound-like nes
(e.g., Mucoyst nd Mucinex; Evist nd Avinz).
Mnufcturers hve  responsibility to void using
brnd nes tht re siilr to those of other edi-
cines to help void errors. As recoended by the
ISMP, both the generic ne nd the brnd ne
should be included on the CPOE screen.
Most products with sound-like nes re used for
different purposes. It is iportnt for the nurse to be
filir with ptients’ dignoses nd to know wht
edicines re used for these conditions so tht they
re ble to question why  prticulr edicine y
hve been prescribed when  ptient does not hve 
dignosis tht requires tht edicine. For exple, the
generic ne for Evist is rloxifene, which is used to
prevent osteoporosis in postenopusl woen; l-
terntively, Avinz is n extended-relese for of or-
phine sulfte tht is used for severe pin. Seeing Evist
dispensed for  person who requires opioid nlgesi
should rise  question of ediction error; it should
not be dinistered until the need for the edicine
74 UNIT II Illustrated Atlas of Medication Administration
hs been clried. (Note the “do not confuse” icon
throughout this text in the pproprite drug ono-
grphs nd tbles.)
NURSE’S RESPONSIBILITIES
The iportnce of ccurcy t every step during order-
ing, trnscribing, dinistering, nd onitoring drug
therpy cnnot be overephsized.
Verification
With the nonutoted order nd distribution sys-
tes, fter  prescription order hs been written for
 hospitlized ptient, the nurse interprets it nd
kes  professionl judgent bout its cceptbil-
ity. Judgents ust be de regrding the type of
drug, the therpeutic intent, the usul dose, the s-
socited theticl clcultions, nd the physicl
preprtion of the dose. The nurse ust lso evlu-
te the ethod of dinistrtion in reltion to the
ptient’s physicl condition, s well s ny ptient
llergies nd the ptient’s bility to tolerte the
dose for. If ny prt of n order is vgue, the pre-
scriber who wrote the order should be consulted for
clriction.
Ptient sfety is of priry iportnce, nd the
nurse ssues responsibility for the verication nd
sfety of the ediction order. If, fter gthering ll
possible infortion, the nurse concludes tht it is in-
pproprite to dinister the ediction s ordered,
the prescriber should be notied ieditely. An ex-
plntion should be given s to why the order should
not be crried out. If the prescriber cnnot be contcted
or does not chnge the order, the nurse should notify
the director of nurses, the nursing supervisor on duty,
or both. The resons for the refusl to dinister the
drug should be recorded in ccordnce with the poli-
cies of the eploying institution.
Transcription
The transcription of the prescriber’s order is necessry
to put tht order into ction. After the veriction of
n order,  nurse or nother designted person trn-
scribes the order fro the priry helthcre pro-
vider’s order sheet onto the Krdex or ediction
prole. These dt y lso be entered into  co-
puterized ptient dtbse tht produces  Krdex
or ediction prole. When this process is delegted
to  wrd clerk or unit secretry, the nurse is still re-
sponsible for verifying ll spects of the ediction
order. The nurse ust sign the originl ediction
order to indicte tht the order hs been received, in-
terpreted, nd veried. The nurse then sends  copy
of the originl order to the phrcy, often by fx. A
sll supply is issued, either in  unit-dose for or
in  continer tht holds  dily supply. The contin-
er is lbeled with the dte, the ptient’s ne nd
roo nuber, nd the drug ne nd strength or
dose. When the supply rrives fro the phrcy, it
is stored in the ediction roo or in the ptient’s
ediction drwer of the ediction crt. In cses
where the order is sent electroniclly, the trnscrip-
tion phse is eliinted, s the order goes directly to
the phrcy. The phrcist reviews nd lls the
order, sending the edicine to the nurse who veries
nd then dinisters the edicine.
In the long-ter cre setting, crbon copies of new
ediction orders re sent to the locl phrcy to be
lled. If  stt dose is needed or if the ediction ust
be strted very soon, the phrcy is notied vi tele-
phone or fx nd written veriction of the edicines
ordered is lso supplied to the phrcy. Becuse the
locl phrcy genertes the ediction dinistr-
tion record only on  onthly bsis, new orders ust
be dded to the current ediction record by the nurse
who is trnscribing the order. Nurses lso send re-
quests to the phrcy vi fx for drug reorders (e.g.,
PRN orders).
Using stndrd drug dinistrtion ethodology,
the nurse prepres nd dinisters  drug by follow-
ing the order on the ediction prole in ccordnce
with the seven rights of drug dinistrtion. With
the new CPOE tht is supported by CDSSs, both the
veriction nd trnscription of the ediction orders
re built into the syste. It should be ephsized tht
br coding nd hndheld devices do not eliinte the
need for the nurse to use stndrd dinistrtion pro-
cedures for edictions (e.g., checking ll spects of
the drug order).
Reporting Variance
When  ediction error does occur, n incident re-
port—which includes the dte, the tie tht the drug
ws ordered, the drug ne nd dose, the route of d-
inistrtion, nd the therpeutic response or dverse
clinicl observtions—should be subitted. The dte
nd tie tht the prescriber is notied of the error nd
ny prescriber’s orders given should lso be recorded.
It is iportnt to be fctul nd not to stte opinions
on the incident report. Current prctices for reporting
ediction errors hve fcilities use  nonpunitive c-
tion when  ediction error occurs. It is uch ore
iportnt to deterine why the error occurred nd to
educte ll personnel regrding how to prevent repet
errors.
SEVEN RIGHTS OF DRUG ADMINISTRATION
The seven rights of drug dinistrtion re s follows:
right drug, right indiction, right tie, right dose, right
ptient, right route, nd right docuenttion.
RIGHT DRUG
The nurse needs to verify tht the drug given is the one
ordered. Triple-checking the drug ne is one of the
iportnt steps tht the nurse tkes to prevent edi-
ction errors.
 Principles of Medication Administration and Medication Safety CHAPTER 6
Clinical Pitfall
Many drugs have similarly spelled names and variable con-
centrations. A signicant number of medication errors occur
as a result of look-alike packaging and similar drug names.
Therefore before administering a medication, it is imperative
to compare the exact spelling and concentration of the pre-
scribed drug with the medication prole and the medication
container. Regardless of the drug distribution system used,
the drug label should be read at least three times: (1) before
removing the drug from the shelf or unit-dose cart; (2) before
preparing or measuring the actual prescribed dose; and (3)
before replacing the drug on the shelf or before opening a
unit-dose container (i.e., just before administering the drug
to the patient).
RIGHT INDICATION
The nurse hs the responsibility to verify the reson
tht the ptient is receiving the ediction. It is ipor-
tnt to understnd the indiction, which is relted to
the edicl dignosis. If in doubt bout the reson for
the order, the nurse ust verify the ediction order
with the prescriber before dinistrtion.
RIGHT TIME
When scheduling the dinistrtion tie of  edi-
ction, fctors such s tiing bbrevitions, stndrd-
ized ties, consistency of blood levels, bsorption, di-
gnostic testing, nd the use of PRN edictions ust
be considered.
Standard Timing Abbreviations
The drug order species the frequency of drug din-
istrtion. Stndrd bbrevitions tht re used s prt
of the drug order specify the ties of dinistrtion.
The nurse should lso check institutionl policy con-
cerning ediction dinistrtion. Hospitls often
hve stndrdized interprettions for bbrevitions
(e.g., “q6h” y en 0600, 1200, 1800, nd 2400; “qid”
y en 0800, 1200, 1600, nd 2000). The nurse ust
eorize nd use stndrd bbrevitions to interpret,
nd dinister edictions ccurtely.
Standardized Administration Times
For ptient sfety, certin edictions re dinis-
tered t specic ties. This llows lbortory work
or electrocrdiogrphy to be copleted rst so tht
ny djustent to the next dose cn be deterined.
For exple, wrfrin or digoxin y be dinis-
tered t 1300 if ordered by the prescriber. The edi-
ction dinistrtion ties need to be stndrdized
throughout  clinicl fcility, with ll units using
the se tie schedule to help prevent ediction
errors.
Maintenance of Consistent Blood Levels
The schedule for the dinistrtion of  drug should
be plnned to intin consistent blood levels of the
drug to xiize the drug’s therpeutic effectiveness.
75
If blood drws to estblish the current seru blood
level of  specic drug re ordered, the nurse should
follow the guidelines stted in the drug onogrph
for the specic tie t which the blood sple should
be drwn in reltion to the drug dose dinistrtion
schedule.
Maximum Drug Absorption
The schedule for the orl dinistrtion of drugs ust
be plnned to prevent incoptibilities nd to xi-
ize bsorption. Certin drugs require dinistrtion
on n epty stoch nd thus re given 1 hour before
or 2 hours fter  el. Other edictions should be
given with food to enhnce bsorption or reduce irri-
ttion, nd still other drugs re not given with diry
products or ntcids. It is iportnt to intin the
recoended schedule of dinistrtion for xi-
u therpeutic effectiveness.
Diagnostic Testing
It is necessry to deterine whether ny dignostic
tests hve been ordered for copletion before initi-
ting or continuing therpy. Before beginning nti-
icrobil therpy, ll culture speciens (e.g., blood,
urine, wound) need to be collected. If  helthcre
provider hs ordered seru levels of  certin drug
to be obtined, the dinistrtion tie of the edic-
tion should be coordinted with the tie t which the
phlebotoist is going to drw the blood sple. When
copleting the requisition for  seru level of  edi-
ction,  nottion should be de regrding the dte
nd tie tht the drug ws lst dinistered. Tiing
is iportnt; if tests re not conducted t the se tie
intervls for the se ptient, the dt gined re of
little vlue.
PRN Medications
Before the dinistrtion of ny PRN ediction, the
ptient’s chrt should be checked to ensure tht soe-
one else hs not dinistered the drug nd tht the
specied tie intervl hs pssed since the edic-
tion ws lst dinistered. When  PRN ediction
is given, it should be chrted ieditely, including
the reson for dinistrtion (e.g., nuse, pin). The
ptient’s response to the ediction should lso be
recorded.
RIGHT DOSE
Check the drug dosge ordered ginst the rnge spec-
ied in the reference books vilble t the nurses’ st-
tion or the institutionlly ccepted websites, nd co-
plete drug clcultions s indicted.
Abnormal Hepatic or Renal Function
The heptic nd renl function of the specific ptient
who will receive the drug should lwys be consid-
ered. Depending on the rte of drug etbolis
nd the route of excretion fro the body, certin
76 UNIT II Illustrated Atlas of Medication Administration
drugs require  reduction in dose to prevent tox-
icity. Conversely, ptients who re being dilyzed
y require higher-thn-norl doses. Whenever 
dosge is outside of the norl rnge for tht drug,
it should be verified before dinistrtion. After
verifiction hs been obtined,  brief explntion
should be recorded in the nurses’ notes or edic-
tion profile so tht others dinistering the edi-
ction will hve the infortion nd the helthcre
provider will not be repetedly contcted with the
se questions. The following lbortory tests re
used to onitor liver function: sprtte ino-
trnsferse (AST), lnine inotrnsferse (ALT),
g-glutyl-trnsferse (GGT), lkline phos-
phtse, nd lctte dehydrogense (LDH). The
blood ure nitrogen (BUN), seru cretinine (Crs),
nd cretinine clernce (Ccr) re used to onitor
renl function.
Pediatric and Older Patients
Specic dosges for soe drugs hve not yet been
rly estblished for the older dult or peditric p-
tient. The nurse should question ny order outside of
the norl rnge before dinistrtion. For peditric
ptients, the ost relible ethod is by proportionl
ount of body surfce re or body weight (see
Appendix A).
Nausea and Vomiting
If  ptient is voiting, orl edictions should be
held nd the prescriber should be contcted for l-
terntive ediction orders, becuse the prenterl
or rectl route y be preferred. Investigte the
onset of the nuse nd voiting. If it begn fter
the strt of the ediction regien, considertion
should be given to rescheduling the orl ediction.
Adinistrtion with food usully decreses gstric
irrittion.
Accurate Dose Forms
Do not brek  tblet. Consult with the phrcist
bout the need for scoring ny tblets nd hve the
phrcy prepre the ediction, or sk for other
vilble dosge fors.
Accurate Calculations
When clculting drug dosges, ccurcy is essen-
til to intin ediction sfety. Do not hesitte to
hve ny clcultions checked by nother helthcre
professionl.
Clinical Pitfall
Whenever a dosage is questionable or when fractional doses
are calculated, check the dose with another qualied indi
vidual. Most hospital policies require that certain medications
(e.g., insulin, heparin, IV digoxin) be checked by two qualied
nurses before they are administered.
Correct Measuring Devices
The ccurte esureent of the volue of edic-
tion prescribed is essentil. Frctionl doses require
the use of  tuberculin syringe, wheres insulin is gen-
erlly esured in n insulin syringe tht corresponds
with the nuber of units in 1 L (i.e., U-100 insulin is
esured in  U-100 syringe).
There re nuerous types of infusion pups vil-
ble, nd the nurse needs to be filir with the oper-
tion of the type used in the clinicl setting. If in doubt,
hve nother cre provider with expertise in the de-
vice’s use check ll settings before dinistering 
ediction.
RIGHT PATIENT
When using  unit-dose syste, the ne on the edi-
ction prole should be copred with the individu-
l’s identiction brcelet. Alwys check the brcelet
for llergies. Soe institutionl policies require tht
the individul be clled by ne s  ens of identi-
ction. This prctice ust tke into considertion the
ptient’s entl lertness nd orienttion. It is always
uch sfer to check the identiction brcelet. The
Joint Coission recoends tht t lest two p-
tient identiers be used (e.g., the ptient stting both
their ne nd birth dte).
Pediatric Patients
Children should never be sked their ne s  ens
of positive identiction. They y chnge beds, try to
void the stff, or seek ttention by identifying the-
selves s soeone else. Identiction brcelets should
be checked every time.
Older Patients
It is iportnt not only to check identiction brce-
lets, but lso to conr nes verblly. In  long-ter
cre setting, residents usully do not wer identi-
ction brcelets. In these cses, only  person who is
filir with  specic resident should conr their
identity for the purpose of dinistering ediction.
Clinical Pitfall
It is important to check the patient’s identication bracelet
every time that a medication is administered. The adverse
effects of the administration of the wrong medication to the
wrong patient and the potential for a lawsuit can thus be
avoided. Although automated technology will help reduce
the frequency of medication errors, this technology does not
eliminate the nurse’s responsibility for checking the patient’s
identity and other aspects of the drug order.
RIGHT ROUTE
The drug order should specify the route to be used
for the dinistrtion of the ediction. One dosge
for of ediction should never be substituted for
nother unless the prescriber is speciclly consulted
ALGrawany
 Principles of Medication Administration and Medication Safety CHAPTER 6
nd n order for the chnge is obtined. There cn be 
gret vrition in the bsorption rte of the ediction
through different routes of dinistrtion. The IV route
delivers the drug directly into the bloodstre. This
route provides not only the fstest onset, but lso the
gretest dnger of potentil dverse effects (e.g., tchy-
crdi, hypotension). The intrusculr (IM) route pro-
vides the next fstest bsorption rte, which is bsed on
the vilbility of the blood supply. This route cn be
pinful, s is the cse with ny ntibiotics. The subcu-
tneous (subcut) route is the next fstest, nd it is lso
bsed on blood supply. In soe cses, the orl route
y be s fst s the IM route, depending on the edi-
ction being given, the dose for (liquids re bsorbed
fster thn tblets), nd whether there is food in the
stoch. The orl route is usully sfe if the ptient is
conscious nd ble to swllow. The rectl route should
be voided, if possible, becuse of the resultnt irrittion
of ucosl tissues nd errtic bsorption rtes. In cse
of error, the orl nd rectl routes hve the dvntge of
recoverbility for  short tie fter dinistrtion. The
drug cn be reoved by gstric lvge or by inducing
voiting if tken orlly. If dinistered rectlly,  drug
cn be diluted nd rinsed out by n ene.
Clinical Pitfall
To ensure that the right drug is prepared at the right time
for the right patient using the right route, it is important to
maintain the highest standards of drug preparation and ad-
ministration. Attention should be focused on the calculation,
preparation, and administration of the ordered medication. A
drug that is reconstituted by a nurse should be clearly labeled
with the patient’s name, the dose or strength per unit of vol-
ume, the date and time that the drug was reconstituted, the
amount and type of diluent used, the expiration date or time,
and the initials or name of the nurse who prepared it. Once
a drug has been reconstituted, it should be administered as
soon as possible; if not given right away, it should be stored
in accordance with the manufacturer’s recommendations.
RIGHT DOCUMENTATION
The docuenttion of nursing ctions nd ptient
observtions hs lwys been n iportnt ethicl re-
sponsibility, but now it is becoing  jor edicolegl
considertion s well. The chrt should lwys hve the
following infortion: the dte nd tie of ediction
dinistrtion; the ne of the ediction; nd the
dose, route, nd site of dinistrtion. The docuen-
ttion of drug ction should be recorded s prt of the
regulrly scheduled ssessents for chnges in the dis-
ese syptos tht the ptient is exhibiting. Adverse
syptos observed should be proptly recorded nd
reported. Helth teching perfored should be docu-
ented, nd the degree of understnding exhibited by
the ptient should be evluted nd recorded.
• DO record when nd why  drug is not dinistered.
• Under soe circustnces,  ptient y refuse 
ediction. If this occurs, DO try to obtin infortion
77
bout the reson for the refusl nd to integrte these
resons into the cre pln. In soe cses, it y be
becuse of drug side effects nd  lck of understnd-
ing bout how to llevite the. Other cuses could
include the cost of the edicine, n inbility to self-
dinister  drug, or the belief tht the drug is inef-
fective. Helthcre providers ust be sensitive to
situtions when the cuse y involve  culturl belief.
• When  drug is refused, DO record ll infortion
pertining to the incident in the nurses’ notes, nd
notify the prescriber of the fcts involved.
• DO NOT record in the nurses’ notes tht n incident re-
port hs been copleted when  ediction error hs
occurred. However, dt regrding clinicl observ-
tions of the ptient relted to the occurrence should be
chrted to serve s  bseline for future coprisons.
Clinical Goldmine
CHECK the label of the container for the drug name,
the concentration, and the appropriate route of
administration.
CHECK the patient’s chart, Kardex, medication prole,
or identication bracelet for allergies. If no information
is found, ask the patient, before administering the
medication, if they have any allergies.
CHECK the patient’s chart, Kardex, or medication prole
for rotation schedules of injectable or topically applied
medications.
CHECK medications to be mixed in one syringe with
a list approved by the hospital or the pharmacy for
compatibility. Normally, all drugs mixed in a single syringe
should be administered within 15 minutes after mixing.
Immediately before administration, always check the
contents of the syringe for clarity and the absence of any
precipitate; if the solution is not clear or if a precipitate is
present, do not administer the contents of the syringe.
CHECK the patient’s identity using two identiers every time
a medication is administered.
Clinical Goldmine
DO approach the patient in a rm but kind manner that
conveys the feeling that cooperation is expected.
DO adjust the patient to the most appropriate position
for the route of administration. For example, for
oral medications, sit the patient upright to facilitate
swallowing. Have appropriate uids ready before
administration.
DO remain with the patient to be certain that all medications
have been swallowed.
DO use every opportunity to teach the patient and family
about the drug being administered.
DO give simple and honest answers or explanations to the
patient regarding the medication and the treatment plan.
DO use a plastic container, a medicine cup, a medicine
dropper, an oral syringe, or a nipple to administer oral
medications to an infant or small child.
DO reward the child who has been cooperative by giving
praise; comfort and hold the uncooperative child after
completing the medication administration.
78 UNIT II Illustrated Atlas of Medication Administration

Discharge Medication Teaching

Clinical Pitfall
DO NOT prepare or administer a drug from a container that
is not properly labeled or from a container on which the
label is not fully legible.
DO NOT give any medication that has been prepared by an
individual other than the pharmacist. Always check the
drug name, dose, frequency, and route of administration
against the order. Student nurses must know the
practice limitations instituted by the hospital or school
and which medications can be administered under what
level of supervision.
DO NOT return an unused portion or dose of medication to
a stock supply bottle.
DO NOT attempt to orally administer any drug to a
comatose patient.
DO NOT leave a medication at the patient’s bedside to be
taken “later”; remain with the individual until the drug is
taken and swallowed. (Note: A few exceptions to this
rule are available. One is that nitroglycerin may be left at
the bedside for the patient’s use. Second, in a long-term
care setting, certain patients are allowed to take their
own medications. In both cases, a specic healthcare
provider’s order is required for self-medication, and the
nurse must still chart the medications taken and the
therapeutic response achieved.)
DO NOT dilute a liquid medication form unless there are
specic written orders to do so.
1. Explin the proper ethod of tking prescribed
edictions to the ptient (e.g., do not crush or
chew enteric-coted tblets or ny cpsules; sublin-
gul ediction is plced under the tongue nd is
not tken with wter).
2. Stress the need for punctulity with regrd to the
dinistrtion of edictions nd wht to do if 
dose is issed.
3. Tech the ptient to store edictions seprtely
fro other continers nd personl hygiene ites.
4. Provide the ptient with written instructions tht
reiterte ediction nes, schedules, nd how
to obtin rells. Write the instructions in lnguge
tht is understood by the ptient, nd use LARGE,
BOLD LETTERS when necessry.
5. Identify the nticipted therpeutic response.
6. Instruct the ptient, the fily ebers, or signi-
cnt others regrding how to collect nd record dt
to onitor the response to drugs nd other tret-
ent odlities.
7. Give the ptient (or nother responsible individul)
 list of signs nd syptos tht should be reported
to the helthcre provider.
8. Stress esures tht cn be initited to iniize or
prevent nticipted dverse effects to the prescribed
ediction. It is iportnt to do this to further en-
courge the ptient to be coplint with the edi-
ctions prescribed.

Nursing Care Plan Risk for Infection

ASSESSMENT
Mrs. Spicer ws ditted to the edicl nursing unit 3 dys go with  dignosis of lypho. She received her rst dose
of ultigent cheotherpy yesterdy. Jess Rlston is the student nurse who is cring for Mrs. Spicer. He begins his shift by
conducting  focused ssessent.
Assessment Activities Findings/Defining Characteristics
Review the patient’s chart for laboratory data that The data show a reduction in the number of white blood cells (i.e.,
reflect immune function. leukopenia).
Ask the patient to describe her appetite and to The patient reports that she has not had an interest in eating for a
review her food intake for the last 24 hour. Weigh couple of weeks. She has lost approximately 6 pounds. Her current
the patient and measure her height. weight is 125 pounds, and her height is 5 7″. Her food intake
yesterday consisted of a small cup of applesauce, half of a bowl of
soup, some crackers, and two glasses of juice. The patient states, “I
get full easily and lose interest in food.”
Palpate the patient’s cervical and clavicular lymph Her lymph nodes are enlarged and painless.
nodes.
Review the effects of chemotherapy in a drug Multiagent chemotherapy causes drug-induced pancytopenia.
reference.

NURSING DIAGNOSIS
Risk for infection relted to cheotherpy nd reduced food intke s evidenced by leukopeni nd loss of ppetite
PLANNING
Goals
1. Ptient will rein free fro syptos of infection by the dischrge dte.
2. Ptient will becoe knowledgeble bout infection risks before dischrge.
 Principles of Medication Administration and Medication Safety CHAPTER 6 79

Nursing Care Plan Risk for Infection—cont’d

INTERVENTIONS
Nursing Actions Rationale
Monitor the patient’s body temperature routinely, Interventions are designed to prevent infection and ensure the early
inspect her oral cavity for lesions, inspect IV detection of infection in a patient who is at risk.
access site for drainage, and observe for evidence
of cough; ask about any unusual discharge or
burning on urination.
Teach the patient how to perform hand hygiene by Rigorous hand hygiene reduces bacterial counts on the hands.
handwashing or the use of alcohol-based hand
The patient can easily come in contact with infectious agents that can
rubs.
cause infection.
Consult with a dietitian about providing a high- Maintaining calorie and protein intake will prevent weight loss.
calorie, high-protein, low-bacteria diet. Minimize Foods high in bacteria should be avoided because they increase
the patient’s intake of salads, raw fruits and the risk for gastrointestinal infection.
vegetables, undercooked meat, pepper, and
paprika. Offer the patient small, frequent meals.
Instruct the patient to report any of the following to Signs of infection are indicative of local or systemic infection.
the healthcare provider:
 • A temperture of >100°F (38°C)
 • Shaking and chills
 • A persistent cough with or without sputum; pus
or foul-selling dringe fro  body site
 • The presence of an abscess
 • Urine that is cloudy or foul smelling
 • Burning during urintion
Teach the patient to do the following activities at These measures are designed to prevent infection in those patients
home: with impaired immune function.
 • Avoid crowds nd lrge gtherings of people.
 • Bathe daily.
 • Do not share personal toiletry items (e.g.,
toothbrush, wshcloth, deodornt stick) with
fily ebers.
 • Practice hand hygiene.
 • Do not drink water that has been standing for
>15 inutes.
 • Do not reuse cups or glsses without wshing
the rst.

EVALUATION
Nursing Actions
Compare the patient’s body
temperature and other physical
findings with baseline data.
Ask the patient to describe the signs
and symptoms that should be
reported to a healthcare provider.
Ask patient to explain the measures to
take at home to reduce exposure to
infectious agents.
Patient Response/Finding Achievement of Outcome
The patient remains afebrile and denies The patient has no active infection at this
having a cough or burning during time.
urination. There are no signs of
drainage or discharge from body
sites.
The patient is able to identify the The patient has a partial understanding
temperature range to report. Patient of the signs and symptoms to report.
was able to describe a cough but Additional instruction is required and
unable to identify signs of urinary an information sheet was offered.
infection or local discharge.
The patient is able to discuss the need The patient has a partial understanding
to avoid sharing personal hygiene of restrictions. The nurse will obtain
articles. Patient asked for a listing of printed guidelines to give to the
other precautions and requested that patient and include the patient’s
spouse be included in the discussion. family in a discussion.

Adapted from Ackley BJ, Ladwig GB, Makic MB. Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care. 11th ed. St. Louis: Mosby; 2017.
80 UNIT II Illustrated Atlas of Medication Administration
Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• The nurse should know why a medication is ordered
and its expected actions, usual dosing, proper dilution,
route and rate of administration, adverse effects, and the
contraindications for the use of a particular drug.
• Medications can be dispensed by use of a oor or ward
stock system, an individual prescription order system, a
unit-dose system, or a computer-controlled dispensing
system, which uses the unit-dose system.
• Narcotic control systems include the inventory control
record, a means to keep the narcotic locked separately,
and ways of verifying the correct count of the drug.
• The four categories of medication orders are stat, single,
standing, and PRN orders.
• Medication errors include prescribing errors, transcription
or order communication errors, dispensing errors,
administration errors, and errors of monitoring or education
for proper use.
• The name on the medication prole should be compared
with the individual’s identication bracelet using two patient
identiers to ensure the right drug is given to the right
patient.
• The seven rights of drug administration are as follows: right
drug, right indication, right time, right dose, right patient,
right route, and right documentation.
• Appropriate documentation should always have the
following information: the date and time of medication
administration; the name of the medication; and the dose,
route, and site of administration.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/
Willihnganz) for additional online resources.
Online Resources
• Centers for Medicare & Medicaid Services:
https://www.cms.gov
• ISMP List of High-Alert Medications in Acute Care
Settings: https://www.ismp.org/recommendations/h
igh-alert-medications-acute-list
• ISMP List of High-Alert Medications in Long-Term Care
(LTC) Settings: https://www.ismp.org/recommendations/h
igh-alert-medications-long-term-care-list
• ISMP List of High-Alert Medications in Community/
Ambulatory Settings: https://www.ismp.org/recommendati
ons/high-alert-medications-community-ambulatory-list
• The Joint Commission National Patient Safety Goals: https
://www.jointcommission.org/standards_information/npsgs.
aspx
 Principles of Medication Administration and Medication Safety CHAPTER 6 81

Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions

The following questions are typical of the NCLEX examination Objective: Identify what a narcotic control system entails.
and include both NGN (Next Generation) and traditional ques NCLEX item type: Multiple choice
tions. See Chapter 1 for further information regarding question Cognitive skill: Knowledge
types.
4. The nurse had just nished lling out the form that is used to
1. What are the legal responsibilities of the nurse for correctly report a medication error, and was recalling the ways to prevent
preparing and administering medications to patients? (Select all errors. Using an arrow, match the type of medication error with the
that apply.) action used to prevent it.
1. The nurse must ensure that the patient fully understands
all the effects of the medication.
2. The nurse must understand the patient’s diagnosis and WAYS USED TO PREVENT
symptoms correlating to the medication. TYPE OF MEDICATION ERROR ERRORS
3. The nurse must assess the patient for adverse effects of Prescribing errors • Taking the time to
the medication. carefully review drug
4. The nurse must be accurate in calculating and preparing name and dose
medications. Administration errors • Following routine
5. The nurse must administer all medication orders without procedures
question. Dispensing errors • Assessing the patient
Objective: Identify the legal and ethical considerations for before giving medications
medication administration. Monitoring errors • Being familiar with
NCLEX item type: Multiple response medications before
Cognitive skill: Application administration

2. The nurse was orienting a new nurse to the advantages and

disadvantages of the drug distribution system that the unit used Objective: Identify common types of medication errors and actions
for administering medication to patients. Using an arrow, match that can be taken to prevent them.
the drug distribution system with the advantage or disadvantage NGN item type: Drag and drop
for each system (more than one system may apply to the answer). Cognitive skill: Recognize cues
5. List in order what steps the nurse takes when preparing and
administering a patient’s morning medications.
ADVANTAGES AND
DRUG DISTRIBUTION SYSTEM DISADVANTAGES OF SYSTEMS 1. Document the administration of the medications.
2. Check the order to verify the medication is correct.
Floor or ward stock system • Requires security code 3. Obtain the medications for administration from the
and password medication room.
An individual prescription • Each drug package is 4. Identify the patient using two patient identiers before
order system labeled administration.
A unit-dose system • 3- to 5-day supply is 5. Triple-check that the correct medication was prepared.
available
Computer-controlled • Potential for medication Objective: Identify precautions used to ensure the right drug is
dispensing system errors from lack of review prepared and given to the right patient.
by pharmacists NCLEX item type: Ordering
Cognitive skill: Application
6. What process is used to eliminate medication errors in the
Objective: Compare and contrast the various systems used to
healthcare environment as patients transition from one clinical
dispense medications.
setting to another?
NGN item type: Drag and drop
Cognitive skill: Recognize cues 1. Case management
2. Triple checks
3. The nurse preparing the narcotic hydromorphone (Dilaudid) 3. Verication
injection needs to get assistance from another licensed healthcare 4. Medication reconciliation
provider when what occurs?
Objective: Identify the legal and ethical considerations for
1. The patient receives the injected medication and then medication administration.
becomes nauseated and vomits the drug. NCLEX item type: Multiple choice
2. The medication is ordered in a dose smaller than what is Cognitive skill: Understanding
available in a prelled syringe cartridge.
3. The patient states that the drug will not work and refuses
to take it.
4. The medication ordered is locked in the narcotic drawer.
82 UNIT II Illustrated Atlas of Medication Administration

7. The nurse has nished administering morning medications to a 9. Immediately after administering morning medications for a
patient and will need to document which important aspect(s) of patient, the nurse is expected to perform which action next?
medication administration? (Select all that apply.) 1. Document the medications administered.
1. All seven rights 2. Evaluate the effectiveness of the medications.
2. Dose and route of drug 3. Educate the patient on the adverse effects to expect.
3. Time and name of drug 4. Complete the nursing care plan for the day.
4. Triple checks Objective: Identify the appropriate nursing documentation of
5. Adverse effects observed medications, including the effectiveness of each medication.
6. Health teaching performed NCLEX item type: Multiple choice
Objective: Identify the appropriate nursing documentation of Cognitive skill: Knowledge
medications, including the effectiveness of each medication.
NCLEX item type: Multiple response
Cognitive skill: Application
8. A patient refuses an essential heart medication that has been
prescribed. List in order what the nurse will do next.
1. Noties the prescriber
2. Reports the refusal to the charge nurse
3. Seeks patient reasons for refusal
4. Documents refusal on the MAR
5. Explains importance of medication
Objective: Identify precautions used to ensure the right drug is
prepared and given to the right patient.
NCLEX item type: Ordering
Cognitive skill: Comprehension
Percutaneous Administration 7
https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the equipment needed and the techniques used to
apply each of the topical forms of medications to the skin.
2. Describe the purpose of and the procedure used for
performing patch testing.
3. Identify the equipment needed, the sites and techniques
used, and the patient education required when
nitroglycerin ointment is prescribed.
4. Identify the equipment needed, the sites and techniques
used, and the patient education required when
transdermal patch medication systems are prescribed.
5. Describe the dose forms, the sites and equipment used,
and the techniques for the administration of medications to
the mucous membranes.
6. Compare the technique used to administer eardrops to
patients who are less than 3 years old with that used for
patients who are 3 years and older.
7. Describe the purpose, the precautions necessary, and the
patient education required for those patients who require
medications via inhalation.
8. Identify the equipment needed, the site, and the specic
techniques required to administer vaginal medications or
douches.

Key Terms
creams (KRĒMZ) (p. 83)
lotions (LŌ-shŭnz) (p. 83)
aqueous (Ā-kwē-ŭs) (p. 83)
ointments (ŌYNT-měnts) (p. 84)
powders (p. 84)
patch testing (PĂCH) (p. 85)
allergens (ĂL-ěr-jěnz) (p. 85)
transdermal patch (ĂL-ěr-jěnz)
(p. 89)
buccal (BŬK-ăl) (p. 90)
ophthalmic (ŏf-THĂL-mĭk) (p. 91)
otic (Ō-tĭk) (p. 92)
aerosols (ĂR-ō-sŏlz) (p. 95)
metered-dose inhaler (MDI)
(MĒ-tŭrd DŌS ĭn-HĀL-ŭr) (p. 96)
dry powder inhaler (DPI) (DRĪ PŎW-
dŭr ĭn-HĀL-ŭr) (p. 96)

Th rs f drg dmsr c b clssd 
hr cgrs: rl, prrl, d prcs.
Th rm percutaneous administration rfrs  h ppl-
c f mdcs  h sk r mcs mmbrs
fr bsrp. Th bsrp f pcl mdcs
c b cd by h drg’s ccr, hw
lg h mdc s  cc wh h sk, h sz
f h ffcd r, h hckss f h sk, h hydr-
 f h sss, d h dgr f sk dsrp.
Mhds f prcs dmsr cld h
fllwg: h pcl pplc f ms, crms,
pwdrs, r ls  h sk; rsdrml pchs, h
sll f sls  h mcs mmbrs f
h mh, y, r, s, r vg; d h hl
f rslzd lqds r gss fr bsrp hrgh
h lgs. Th prmry dvg f h prcs
r s h h c f h drg,  grl, s lcl-
zd  h s f pplc, whch rdcs h c-
dc f sysmc sd ffcs. Ufrly, h md-
cs r smms mssy d dfcl  pply. I
dd, hy slly hv  shr dr f c
d hs rqr frq rpplc.
AdministrAtion of topicAl
medicAtions to the skin
Dose Forms
C
Creams r smsld mlss h c mdc-
l gs fr xrl pplc. Th crm bs s
grlly grsy, d  c b rmvd wh w-
r. My vr-h-cr crms r sd s ms-
rzg gs.
L
Lotions r aqueous (wr-bsd) prprs h
c sspdd mrls. Ls r cmmly
sd s shg gs  prc h sk d  r-
lv rshs d chg. Sm ls hv  clsg
c, whrs hrs hv  srg r drwg
ffc. Ls shld b gly b rmly pd 
h sk rhr h rbbd  h sk  prv -
crsd crcl d chg. Shk ll ls hr-
ghly mmdly bfr pplc, d s hm
sprgly  vd ws.
83
84 UNIT II Illustrated Atlas of Medication Administration
o
Ointments r smsld prprs f mdcl
sbscs   ly bs, sch s ll r prl-
m. Ths yp f prpr c b ppld drcly 
h sk r mcs mmbr, d  grlly c
b rmvd sly wh wr. Th bs hlps  kp
h mdcl sbsc  prlgd cc wh h
sk.
Pwd
Powders r ly grd prcls f mdc h
r cd   r bs pwdr. Thy grlly
prdc  clg, dryg, r prcv ffc whr
ppld. Clmpg ccrs f h pwdr lyr s 
hck, prvg cmpl cvrg. Pwdrs r s-
ly rmvd wh wshg.
Dressings
Svrl yps f drssgs r sd  r wds,
sch s dry gz spgs, dhr gz drss-
gs (.g., Tlf), slf-dhsv rspr lms h
c s  scd sk (.g., Tgdrm), d hydrclld
drssgs (.g., DDERM). Hydrgl drssgs r
sd  prl-hckss d fll-hckss wds
d  sk h hs b dmgd by brs. Thr
r ls xd bsrbrs sch s clcm lg
drssgs (.g., AlgDERM, Kls, Srbs) m-
fcrd frm swd h c b sd  fcd
wds.
Wd cr prdcs d wd cr hv bcm
 cmplx scc. (Rfr  fdmls f rs-
g, mdcl-srgcl rsg, d grrc rsg
xbks fr dscsss f h prcpls f wd
cr.) Drssg rcmmds fr rg prssr
jrs r vlbl frm h Agcy fr Hlhcr
Rsrch d Qly, h US Pblc Hlh Srvc,
d h US Dprm f Hlh d Hm Srvcs.
Clinical Goldmine
A major principle of wound healing is the need for a moist
environment to promote the epithelialization of the wound,
which is further enhanced by a diet that is high in protein,
vitamin A, vitamin C, and zinc.
ProCeDure ProtoCoL
Th rm procedure protocol wll b sd s pr f h
mdc dmsr chq fr h scs
 hs chpr. Ths rm clds h fllwg rs-
g rvs:
1. Assmbl h pprpr qpm d h pr-
frm hd hyg.
2. Us h seven rights f drg prpr d dm-
sr hrgh h prcdr: rgh p,
rgh drg, rgh dc, rgh r, rgh ds,
rgh m, d rgh dcm.
3. Prvd prvcy fr h p d gv  hrgh
xpl f h prcdr d wh  xpc.
4. Prfrm  prmdc ssssm bfr pply-
g y pcl prpr. S dvdl drg
mgrphs fr mr frm.
AdministrAtion of CreAms, Lotions,
Powders, And ointments
Tpcl prprs c b sd  d h fllwg:
• Cls d dbrd  wd
• Rhydr h sk
• Rdc mm
• Rlv lclzd sgs d sympms, sch s ch-
g d rsh
• Prvd  prcv brrr
• Rdc  hckg f h sk, sch s h -
vlvd wh clls frm
equiPment
• Prscrbd crm, l, pwdr, r m
• 2 × 2–ch gz spgs
• C-ppd pplcrs
• Tg bld
• Glvs
• Mdc dmsr rcrd (MAR) d md-
c prl
sites
Sk srfcs ffcd by h dsrdr bg rd.
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
2. Ps h p s h h srfc whr h
pcl mrls r  b ppld s xpsd.
Assss h crr ss f h p’s sympms.
Prvd fr p cmfr bfr srg hrpy.
3. Cleansing: Fllw h spcc rdrs f h hlh-
cr prvdr r clcl s plcs fr clsg
h s f pplc. Afr h r s xpsd d
clsd, prfrm  wd ssssm.
4. Application: Wr glvs drg h pplc
prcss. My f h gs sd my b bsrbd
hrgh h sk f bh h p d h prs
wh s pplyg h mdc.
 • Lotions: Shk wll l  frm pprc f
h ssps s bd. Apply l rmly
b gly by dbbg h srfc.
 • Ointments or creams: Us  g bld  rmv
h dsrd m frm  wd-mhd c-
r. Alrvly, sqz h m dd
  g bld r c-ppd pplcr
frm  b-yp cr. Apply ms d
crms wh  glvd hd sg rm b gl
srks. Crms r  b gly rbbd  h
r.
 • Powders: Cl d dry h sk. Shk h clsd
pwdr cr  brk p clmps f pw-
dr. Usg glvd hds, pply drcly  h
sk by shkg h p cr lghly vr

h rm r. Cr ms b k   l-
lw h pwdr  bcm rbr d hld.
Isrc h p  r hr hd r s 
wl s  brrr  vd hlg pwdr.
5. Dressings: Chck spcc rdrs rgrdg h yp
f drssg  b sd. If  drssg s  b ppld,
sprd h prscrbd m f m drcly
 h drssg mrl wh  g bld; h
mprgd drssg mrl c h b ppld 
h ffcd sk srfc. Scr h drssg  plc.
6. Wet dressings: Alwys cmplly rmv h prv-
s drssg. Wrg  w drssgs  prv
drppg, d pply h gz   sgl lyr d-
rcly  h wd srfc. Fr dpr wds,
pck h wd lsly wh ms gz spgs
s h ll srfcs r  cc wh h msr.
Apply  lyr f dry gz spgs d  b-
srb pd  h r. T scr  drssg h
rqrs rpd chgs, pply  bdr r s
Mgmry ps.
7. Cl h r d h qpm sd, d mk
sr h h p s cmfrbl fr h pplc-
 prcdr. (Note: Srl sppls, glvs, d
qpm r sd fr sm wds; hwvr,
cl rhr h srl ms [.g., gz, glvs]
my b sd wh pplyg ms yps f drssgs
[.g.,   prssr jry]. Alwys chck s-
l plcs d s clcl jdgm.)
8. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
9. Prfrm hd hyg.
Patient teaChing
1. If pprpr, ch h p hw  pply h
mdc d drssgs.
2. Tch prsl hyg msrs h r ppr-
pr  h drlyg cs f h sk cd
(.g., c, cc drms, fc).
3. Wh drssgs r rdrd, sggs h prchs
f gz d hr cssry sppls.
4. Srss glss d mdr wh rgrd  h
m f mdc  b ppld.
5. Emphsz h h p ms vd chg r
scrchg h ffcd r.
6. Tll h p  wsh hr hds bfr d fr
chg h ffcd r r pplyg h mdc-
. Srss h prv f h sprd f fc.
DoCumentation
Prvd h rgh dcm f h mdc d-
msrd d h p’s rsps  drg hrpy.
1. Chr h d, m, drg m, dsg, d r
f dmsr.
2. Prfrm d rcrd rglr p ssssms
fr h vl f h rm’s hrpc
ffcvss (.g., chg  sz f ffcd r,
rdcd drg, dcrsd chg, lwrd m-
prr wh  fc).
Percutaneous Administration CHAPTER 7 85
3. O h p’s rcrd, dcm y sgs d
sympms f dvrs drg ffcs, d prvd 
rrv dscrp f h r bg rd.
4. Dvlp  wr rcrd fr h p  s wh
chrg prgrss fr h vl f h ffc-
vss f h rms bg sd. Ls h p-
’s sympms (.g., rsh  h lwr lg wh
rdss d vscls prs, prssr jry  h
scrm). Ls h d  b cllcd rgrdg h
mdc prscrbd d s ffcvss (.g.,
vscls w crsd, wpg, r ppr  b dry-
g; rdss  lwr lg s lssg; msr h
r f dcbs  cmrs [cm] d dc
f h wd s xdg, rmg h sm, r
shrkg).
5. Edc h p  wh  xpc d wh 
d f dvrs sympms dvlp.
PAtCh testing for ALLergens
Patch testing s  mhd h s sd  dfy 
p’s ssvy  cc mrls (.g., sps,
plls, dys). Th sspcd allergens (gs) r
plcd  drc cc wh h sk srfc d cv-
rd wh sszg, bsrb p. Ulss
prcd rr pprs, h pch s slly lf
 plc fr 48 hrs d h rmvd. Th s s lf
p  r fr 15 ms d h “rd.” A psv
rc s d by h prsc f rdss d swll-
g, clld  wheal (Fg. 7.1), whch dcs  llrgy
 h spcc llrg. I my b cssry  rd h
rs fr 3 dys d g fr 7 dys  dc d-
lyd rcs.
Irdrml ss my ls b sd  drm h
p’s llrgy  spcc gs. S Chpr 10 fr
mr frm b h rdrml dmsr-
 f llrgs.
Prfrm prsg ssssms (s frm
prvdd wh sppld llrg sls).
Fig. 7.1 Example of a wheal for allergy testing. (From Rich RR etal.
Clinical Immunology. 5th ed.. St. Louis: Elsevier; 2019.)
86 UNIT II Illustrated Atlas of Medication Administration
equiPment
• Alchl fr clsg h r
• Sls f sspcd gs
• 1 × 1–ch gz pds
• Drpprs
• Mrl r lv l
• Wr
• Clpprs
• Hypllrgc p
• Rcrd fr chrg d b h sbscs p-
pld d h p’s rspss
• MAR, cmpr prl, r rdr sh
sites
Th bck, rms, r hghs r cmmly sd. (Do not
pply  h fc r rs h r sscpbl  frc-
 frm clhg.) Slcd rs r spcd 2  3
chs pr. Th yp f llrg ppld d h s
f pplc r dcmd  h p’s chr
(Fg. 7.2). Hr s clppd frm ss  sr h h
llrg s kp  cls cc wh h sk srfc,
hrby prvg  fls-gv rc.
teChnique
Caution: D  sr y yp f llrgy sg -
lss mrgcy qpm (cldg pphr) s
vlbl  h mmd r  cs f  phy-
lcc rsps. Nrss shld b fmlr wh h
prcdr  fllw f  mrgcy ds rs.
1. Fllw h prcdr prcl dscrbd rlr.
2. Chck wh h p bfr srg h sg 
sr h  hsms r mmry
gs (.g., spr, bprf, dphhydrm,
crcsrds) hv b k fr 24  48 hrs
bfr h s. If h p hs k  -
hsm r  mmry g, csl
h hlhcr prvdr bfr prcdg wh h
sg. Rvw h chr  sr h h p
s    mmcmprmsd s s  rsl
f dss r rms sch s chmhrpy r
rd hrpy.
3. Ps h p s h h srfc  whch
h s mrls r  b ppld s hrzl.
Prvd fr h p’s cmfr bfr bgg
h sg.
4. Cls h slcd sg r hrghly wh
h s f  lchl wp. Us crclr ms,
srg  h pld s f pplc d c-
g wrd  h prphry. Allw h r 
r-dry.
5. Prpr h dsgd sls sg spc ch-
q (hs rfrs  bg mdfl b prvg
cm f h sl by sg ly cl r
srl pplc mhds).
6. Fllw h spcc drcs f h mplyg
hlhcr gcy rgrdg h pplc f lqd
d sld frms f sspcd llrgs. A drppr s
slly sd  pply sspcd lqd cc–yp
mrls; sld mrls r ppld drcly  h
sk srfc d h msd wh mrl r l-
v l. Th fllwg mhds my b sd:
 • Dsgd ms f sdrdzd-srgh
chmcl sls r rrgd  ml rcp-
cls h r bckd wh hypllrgc d-
hsv. Ths sls r h ppld  h
slcd ss. I s mpr  dfy h c-
s f ch rcpcl crrcly.
 • Pchs h r mprgd wh dsgd l-
lrgs r vlbl fr drc pplc  h
prprd ss.
 • A pch s srs k s vlbl h cs
rrg ccrs f llrgs h r
pckgd  syrgs fr dsprsl. Alhgh
h k cs 20 llrgs, y mbr f hm
my b ppld  dvdl pchs r hldg
dvcs, whch r h ppld  h p’s
sk.
 • Afr pplc, fllw sl plcy fr
cvrg h s s.
7. Chr h ms, gs, ccrs, d ms
ppld. Mk  dgrm  h p’s chr, d
mbr ch lc (s Fg. 7.2B). Rcrd whch
g d ccr wr plcd  ch s
(s Fg. 7.2A). Sbsq rdgs f ch r r
h prfrmd d chrd  hs rcrd.
8. Fllw drcs rgrdg h m f h rdg
f h sk sg bg prfrmd. Th sg ss
shld b spcd  gd lgh. Grlly,  ps-
v rc (.., h dvlpm f  whl)  
dld srgh f  sspcd llrg s csd-
rd clclly sgc. Msr h dmr f
h whl d y ryhm (.., rdss  h s
f jc)  mllmrs, d plp d msr
h sz f y dr (.., h hrdg f 
r f h bdy  rsps mm). Th c-
rl s shld hv  rc, whch shld b
d.
9. Rcrd h frm frm h sk s rdg
 h p’s chr. Th fllwg s  ls f cm-
mly sd rdgs f rcs d hr ppr-
pr symbls:
+ (1+) No wheal, 3-mm are
++ (2+) 2- to 3-mm wheal with are
+++ (3+) 3- to 5-mm wheal with are
++++ (4+) >5-mm wheal
Patient teaChing
1. Tll h p h m, d, d plc f h rr
vs fr hvg h s ss rd.
2. Tll h p   bh r shwr l h pch-
s r rd d rmvd. Expl h d  vd
cvs h cld cs xcssv prspr.
ALGrawany
 Percutaneous Administration CHAPTER 7 87

Fig. 7.2 Patch test for contact dermatitis. (A) Reading chart for patch testing. (B) Patch testing sites.

3. If h p dvlps  r f svr brg r

chg, lf h pch d gly wsh h r. Tll
h p  rpr mmdly h dvlpm 1 2
f y brhg dfcly, svr hvs, r rshs.
Th p shld b ld  g  h rs mr- 3 4
gcy dprm f hy r bl  rch h
hlhcr prvdr wh prscrbd h sk ss.

DoCumentation
Prvd h rgh dcm f h llrg sg 5 7 8 6
ss d h p’s rspss  h llrgs h
wr ppld.
9 10
1. Chr h d, m, llrgs (cldg g,
ccr, d dsg), d s f dmsr-
 (s Fg. 7.2A).
2. Rd ch s  24, 48, d 72 hrs fr ppl-
c s drcd by h hlhcr prvdr r h
plcy f h hlhcr gcy. Addl rdgs
my b rqrd fr p  7 dys fr pplc.
Fig. 7.3 Sites for nitroglycerin application; numbering indicates rotation
3. Chr d rpr y sgs d sympms f d- schedule.
vrs llrg ffcs.
4. Prfrm d vld ssl p dc
rgrdg h sg d hr ssl spcs equiPment
f rv fr h llrgy h s ffcg h • Cl glvs
dvdl. • Nrglycr m
• Applcr ppr
AdministrAtion of nitrogLyCerin ointment • Nllrgc dhsv p
• MAR d mdc prl
Dose Form
Nrglycr m (Nr-Bd) prvds rlf f sites
gl p fr svrl hrs lgr h sblgl Ay r wh hr my b sd. Ms ppl pr-
prprs. Wh prprly ppld, rglycr fr h chs, k, r ppr rm r. Dvlp  r-
m s prclrly ffcv gs crl  schdl fr s f h m (Fg. 7.3). Do
cks f gl p. Spcc srcs fr r- not shv  r  pply h m; shvg my
glycr m r rvwd  hs x bcs  s cs sk rr.
h ly m h s crrly vlbl fr whch
dsg s crcl  h sccss f s (s Chpr 24). teChnique
Prfrm prmdc ssssm; s dvdl 1. Fllw h prcdr prcl dscrbd rlr.
drg mgrph fr dls. 2. Apply cl glvs.
88 UNIT II Illustrated Atlas of Medication Administration
1" 2"
Printed
side down
A
Printed side up
Ointment side
against skin
B 1. Hlp h p lr hw  pply h m
Fig. 7.4 Administering nitroglycerin topical ointment. (A) Lay the
applicator paper print-side down on a hard surface and measure the
ribbon of ointment. (B) Apply the applicator to the skin site, ointment-
side down. Spread the ointment in a uniform layer under the applicator,
and leave the paper in place.
3. Ps h p s h h srfc  whch h
pcl mrl s  b ppld s xpsd. Prvd
fr h p’s cmfr bfr srg hrpy.
(Note: Wh rpplyg m, rs rmv h
plsc wrp d ds-msrg pplcr ppr
frm h prvs ds, d cls h r f r-
mg m  h sk srfc. Slc  w
s fr h pplc f h mdc, d h
prcd wh sps 4 hrgh 7.)
4. Ly h ds-msrg pplcr ppr wh h
pr sd down    srfc (Fg. 7.4A). Th
m wll smr h pr.
5. Sqz  rbb f m f h prpr lgh
 h pplcr ppr.
6. Plc h msrg pplcr ppr  h sk
srfc  h s chs  h r schdl,
m sd down. Sprd   h, frm lyr
dr h pplcr. DO NOT RUB IN. Lv h
ppr  plc. Note: Us f h pplcr ppr
llws y  msr h prscrbd ds d pr-
vs bsrp hrgh h grps s y p-
ply h mdc (s Fg. 7.4B).
7. Cvr h r whr h ppr s plcd  ccr-
dc wh sl plcy (hs my cld
cvrg h ppr wh plsc wrp), d h
p h ppr  plc.
8. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
9. Prfrm hd hyg.
Clinical Pitfall
Applying Nitroglycerin Ointment
To promote personal safety, the nurse should always wear
gloves, whether applying nitroglycerin ointment paper or
handling transdermal patches. When nitroglycerin trans-
dermal patches are applied, chart the specic site of the ap-
plication. Occasionally, patients may move the transdermal
patch themselves because of convenience, skin irritation, or
confusion. If the patch is not found at the original location at
the scheduled time of removal, examine other areas of the
body to nd it; do not assume that the patch fell off or was
removed. Tolerance and loss of antianginal response could
develop if another patch is placed on the patient while the
rst patch is still on. Always dispose of used nitroglycerin
paper or transdermal patches in a receptacle in which the
patient, children, and pets will not have access. A substantial
amount of nitroglycerin remains on the patch and can be
toxic.
Patient teaChing
d sr h h p drsds h s r-
 schdl.
2. Tll h p h h mdc my dsclr
clhg. Th s f clr plsc wrp prcs
clhg.
3. Wh h dsg s rgld prprly, h -
m my b sd vry 3  4 hrs d  bdm.
Rmd h p h hr shld b  drg-fr
prd (slly 10  12 hrs) vry 24 hrs s
rcmmdd by h hlhcr prvdr.
4. Tll h p  wsh hr r hs hds fr p-
plc  rmv y rglycr h cm 
cc wh h grs.
5. Wh rmg h s f hs pcl m,
h dsg d frqcy f pplc shld b
grdlly rdcd vr  4-  6-wk prd. Tll
h p  cc h hlhcr prvdr f d-
jsm s hgh  b cssry. Ecrg h
p   dsc h mdc brply
(s Chpr 24).
DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  drg
hrpy.
1. Chr h d, m, drg m, dsg, s, d
r f dmsr.
2. Prfrm d rcrd rglr p ssssms
fr h vl f hrpc ffcvss (.g.,
bld prssr, pls, p, dgr d dr
f p rlf   scl f 0  10).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.

A B
C D
Fig. 7.5 Applying a nitroglycerin topical patch. (A) Carefully pick up
the system lengthwise, with the tab up. (B) Remove the clear plastic
backing from the system at the tab. Do not touch the inside of the
exposed system. (C) Place the exposed adhesive side of the system
on the chosen skin site. Press rmly with the palm of the hand. (D)
Circle the outside edge of the system with one or two ngers.
AdministrAtion of trAnsdermAL drug
deLivery systems
Dose Form
Th transdermal patch (ls clld  rsdrml dsk)
prvds fr h crlld rls f  prscrbd md-
c (.g., rglycr, cld, srg, c,
scplm, fyl) hrgh  smprmbl mm-
br fr svrl hrs  3 wks wh ppld  c
sk. Th ds rlsd dpds  h srfc r f
h pch  cc wh h sk srfc d h dvd-
l drg. S spcc drg mgrphs fr h s d
dr f c f drgs h s hs dlvry sysm.
Prfrm prmdc ssssm; s dvdl
drg mgrphs fr dls.
equiPment
• Cl glvs
• Trsdrml pch
• Clppg qpm s pprpr fr h s d
h p’s sk cd
• MAR d mdc prl
sites
Ay r wh hr my b sd. Ms ppl pr-
fr h chs, k, r ppr rm. Dvlp  r
schdl fr s f h pch (s Fg. 7.3 fr  xm-
pl f  rglycr r schdl). S mfc-
rr’s rcmmds fr lc d frqcy f
pplc f pchs hr h rglycr.
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
2. Lbl h pch wh h d, h m, d h
rs’s ls. If h dsg f h mdc s 
Percutaneous Administration CHAPTER 7 89
prd  h pch ppld,  s sfl  cld
h dsg s pr f h lblg prcss.
3. Apply cl glvs.
4. Ps h p s h h srfc  whch
h pcl mrls r  b ppld s xpsd.
Prvd fr h p’s cmfr. (Note: Wh r-
pplyg  rsdrml pch, rmv h ld pch
d cls h sk hrghly. Slc  w s
fr pplc. I s spclly mpr  h
ldr dl r h cfsd p  lk fr h
ld pch f  s  whr h prr pplc s
chrd. Th cfsd p my hv mvd 
lswhr  h bdy r rmvd . Th ld pch
c b csd  h glv s h rs rmvs ;
hs shld h b dspsd f ccrdg  s-
l plcy.)
5. Apply h smll dhsv pcl pch. Fg. 7.5 l-
lsrs rglycr bg ppld   f h
ss rcmmdd by h r schdl. Th
frqcy f pplc dpds  h spcc
mdc bg ppld v h rsdrml pch
d h dr f c f h prscrbd md-
c. Nrglycr s ppld c dly, whrs
fyl s rppld vry 3 dys; cld d
hyl srdl/rlgsrm (Orh Evr) r
rppld c vry 7 dys. Hrm rplcm
hrps my b ppld vry 4  7 dys.
6. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
7. Prfrm hd hyg.
Patient teaChing
1. Tch h p hw d wh  pply h
pchs. Note: Cr prdcs my b wr
whl shwrg; hrs shld b rplcd fr
bhg r shwrg. Rfr  h p dc-
 srcs fr spcc pplc drcs.
Scplm, whch s sd fr m sckss,
ms b ppld  ls 4 hrs bfr rvl; cl-
d rsdrml sysms r ppld c vry 7
dys. Orh Evr s  crcpv pch h s r-
ppld wkly fr 3 wks, wh h frh wk
bg pch fr;  w pch s h rs  hr
cycl f hr pchs srs h fllwg wk.
2. If  pch bcms prlly dsldgd, h rcm-
mds fr h prdc shld b fllwd. (If
 pch s prlly dsldgd r rmvd, rplc
 wh  w pch, rg  s f  wr h ld
, rmvg   h prvsly schdld m).
Alrvly, cld rsdrml pchs cm
wh  prcv dhsv vrly  b ppld
vr h pch  sr sk cc wh h rs-
drml sysm f h pch bcms lsd. S
Chpr 40 fr frhr frm b h Orh
Evr pch.
3. Ps wh r rcvg rglycr rs-
drmlly my rqr sblgl rglycr fr
gl cks, spclly whl h ds s bg
90 UNIT II Illustrated Atlas of Medication Administration
djsd. I grl, rglycr pchs r wr
fr 10  14 hrs; hs s fllwd by  drg-fr
prd f 10  12 hrs s h h rglycr wll
m s ffcvss.
4. Fyl (Drgsc) my k p  12 hrs fr
pplc  b ffcv fr h mgm f
sbl, chrc p. Thrfr  shld b cmbd
wh  shr-cg p mdc l  sfc
bld lvl f h fyl s chvd. Fyl
pchs r chgd vry 3 dys. Brkhrgh
p shld b prmply rprd  h hlhcr
prvdr. I my b cssry  crs h dsg
 chv  ssfcry lvl f p rlf.
DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  h drg
hrpy.
1. Chr h d, m, drg m, dsg, r f
dmsr, d lc f pch.
2. Prfrm d rcrd rglr p ssssms
fr h vl f hrpc ffcvss (.g.,
bld prssr, pls, dgr d dr f p
rlf   scl f 0  10).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc r-
grdg h drg hrpy.
AdministrAtion of medicAtions to
mucous membrAnes
Drgs r wll bsrbd crss mcsl srfcs,
d hrpc ffcs r sly bd. Hwvr,
mcs mmbrs r hghly slcv wh rgrd
 bsrpv cvy, d hy dffr  ssvy. I
grl, qs sls r qckly bsrbd frm
mcs mmbrs, whrs ly lqds r .
Drgs  sppsry frm c b sd fr lcl r sys-
mc ffcs  h mcs mmbrs f h vg,
h rhr, r h rcm. A drg my b hld d
bsrbd hrgh h mcs mmbrs f h s
d lgs. I my b dsslvd d bsrbd by h
mcs mmbrs f h mh r ppld  h ys
r rs fr lcl c. I my b pd, swbbd, r
rrgd   mcsl srfc.
AdministrAtion of subLinguAL And buCCAL
tAbLets
Dose Forms
Sblgl bls r dsgd  b plcd dr
h g fr dssl d bsrp hrgh h
vs wrk f bld vssls  hs r. Bccl b-
ls r dsgd  b hld  h buccal cvy (..,
bw h chk d h lwr mlr h) fr b-
srp frm h bld vssls f h chk. Th pr-
mry dvgs f hs rs f dmsr r
h sscd rpd bsrp d s f c:
h drg psss drcly  h sysmc crcl,
wh  mmd pss hrgh  h lvr, whr
xsv mblsm slly ks plc. As ppsd
 ms hr frms f dmsr  h mcs
mmbrs, h c frm hs ds frms s s-
lly sysmc rhr h lclzd  h mh.
Prfrm prmdc ssssm; s dvdl
drg mgrphs fr dls.
equiPment
• Prscrbd mdc (Note: Th mdcs
vlbl  b dmsrd by hs r r frms
f rglycr. Afr h slf-dmsr ch-
q s gh, h p shld crry h md-
c r kp  rdly vlbl  h bdsd fr
s s dd.)
• MAR d mdc prl
site
Admsr  h sblgl r (.., dr h
g; Fg. 7.6A) r h bccl pch (.., bw
h lwr mlr h d h chk; Fg. 7.6B).
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
2. P   cl glv, d plc h mdc dr
h p’s g (.., sblgl; s Fg. 7.6A) r
bw h p’s lwr mlr h d hr chk
(.., bccl; s Fg. 7.6B). If h mcs mmbrs
r dry ffr  sp f wr bfr dmsr. Th
bl s m  dsslv  hs lcs. Ecrg
h p  llw h drg  dsslv whr plcd
d  hld slv  h mh l h bl s ds-
slvd. Do not ffr wr fr dmsr.
3. Rmv h glv d dsps f   ccrdc
wh sl plcy.
4. Prfrm hd hyg.
Patient teaChing
Expl h xc plcm f h mdc, h ds-
g, d h frqcy f dss. Th p shld b -
frmd f dvrs ffcs, whr  crry h mdc,
hw  sr h mdc, h mdc’s xpr
d, d hw  rll h prscrp wh dd.
A B
Fig. 7.6 Placing medication in the mouth. (A) Under the tongue
(sublingual). (B) In the buccal pouch.

DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  drg
hrpy.
1. Chr h d, m, drg m, ds, s, d
r f dmsr.
2. Prfrm d rcrd rglr p ssssms
fr h vl f hrpc ffcvss (.g.,
bld prssr, pls, dgr d dr f p
rlf, mbr f dss k).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.
Note: Wh h p s slf-dmsrg  md-
c, h rs s sll rspsbl fr ll spcs f
h chrg d mrg prmrs  dcm
h drg hrpy d h rsps chvd.
AdministrAtion of eyedroPs And ointment
Dose Form
Mdcs fr s  h y r lbld ophthalmic
If  drg s  lbld s sch,  shld  b d-
msrd  h y. Ophhlmc sls r sr-
l d sly dmsrd, d hy slly d 
rfr wh vs wh hy r slld. Allw
y mdc  wrm  rm mprr bfr
dmsr.
Ophhlmc ms d cs lrs  vsl
cy. Hwvr, hy hv  lgr dr f c
h sls. Alwys s  spr bl r b f
y mdc fr ch p.
Prfrm prmdc ssssm; s dvdl
drg mgrphs fr dls.
equiPment
• Cl glvs
• Eydrps, m prscrbd (chck srgh
crflly)
• Drppr (s ly h drppr sppld by h
mfcrr)
• Tsss r srl y drssg (pd), s pprpr
• Nrml sl sl, f dd, fr clg ff
xds
• MAR d mdc prl
site
Ey(s)
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
2. Assmbl h phhlmc mdc d qp-
m. Esr h h mdc s lbld fr
“Ophhlmc” r “Ey” s.
3. Ps h p s h h bck f hr hd
s rmly spprd   pllw d s hr fc s
drcd wrd h clg. Wh  chld, rsrs
Percutaneous Administration CHAPTER 7 91
my b cssry f h chld s  yg  cpr-
 vlrly. Alwys sr p sfy.
4. Apply cl glvs.
5. Ispc h ffcd y  drm h crr s-
s. As pprpr, rmv xd frm h yld
d ylshs wh h s f srl sl sl.
A cl wshclh my b sd, wh  spr pr
f h clh sd fr ch y. Sr  h r c-
hs d wp wrd.
6. Exps h lwr cjcvl sc by pplyg g-
l rc  h lwr ld  h by rm f h
rb.
7. Apprch h y frm blw wh h mdc
drppr r b f m. (Nvr ch h y-
drppr r m p  h y r h fc.)
ill Dp
 • Hv h p lk pwrd vr yr hd
(Fg. 7.7).
 • Drp h spcd mbr f drps  h c-
jcvl sc. Nvr drp h mdc drcly
 h ybll.
 • Afr sllg h drps, pply gl prssr
sg  cl ss  h r chs f h
yld gs h b fr pprxmly 1  2
ms. Ths prvs h mdc frm -
rg h cl, whr  wld b bsrbd 
h vsclr mcs f h s d prdc sys-
mc ffcs. I ls srs  dq cc-
r f mdc  h y.
 • Wh mr h  yp f ydrp s rdrd
fr h sm y, w 1  5 ms bw
h sll f h dffr mdcs. Us
ly h drppr prvdd by h mfcrr.
Apply  srl drssg s rdrd.
apply o
 • Gly sqz h m   srp fsh 
h cjcvl sc (s Fg. 7.7), frm h r
chs  h r chs. Do not llw h p
f h mdc dspsr  ch h p.
Fig. 7.7 Administering ophthalmic ointment. To instill the ointment,
gently pull the lower lid down as the patient looks upward. Squeeze
the ophthalmic ointment into the lower sac. Avoid touching the tube
to the eyelid.
92 UNIT II Illustrated Atlas of Medication Administration
 • Tll h p  cls h ys gly d 
mv h ys wh h lds sh, s f lkg
rd h rm,  sprd h mdc.
8. A h ccls f hr prcdr, rmv
glvs d dsps f hm  ccrdc wh -
sl plcy.
9. Prfrm hd hyg.
Patient teaChing
1. Tch h p hw  pply hr w phhl-
mc mdc.
2. Tll h p  wp h ys gly frm h
s wrd  prv cm bw
h ys, s wll s h pssbl sprd f fc,
d  s  spr ss  wp ch y.
3. Hv h p wsh hr hds f d vd
chg h ys r h mmd srrdg r-
s, spclly wh  fc s prs. Dsps
f sss   mr h prvs h sprd f
fc.
4. Srss pcly wh rgrd  h dmsr
f y mdcs, spclly wh h mdc-
s r bg sd  r fcs r crsd
rclr prssr.
5. Tll h p  dscrd y mdcs h hv
chgd clr r bcm cldy r h c
prcls. (If h p’s vsl cy s rdcd,
sm ls shld chck h mdcs fr
clry.)
6. Th p ms  s vr-h-cr y-
wshs wh rs cslg h hlhcr pr-
vdr wh s mgg h y dsrdr.
7. Emphsz h d fr h crfl fllw-p x-
m f y y dsrdr l h hlhcr
prvdr rlss h p frm frhr cr.
DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  drg
hrpy.
1. Chr h d, m, drg m, dsg, s, d
r f dmsr.
2. Prfrm d rcrd rglr p ssssms fr
h vl f hrpc ffcvss (.g., rd-
ss, dscmfr, vsl cy, chgs  fc
r mmry rc, dgr d dr f
p rlf).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.
AdministrAtion of eArdroPs
Dose Form
Erdrps r  sl h cs  mdc h
s sd fr h rm f lclzd fc r -
mm f h r. Mdcs fr s  h r r
lbld otic. If  drg s  lbld s sch,  shld
 b dmsrd  h r. Erdrps shld b
wrmd  rm mprr bfr s, d  sp-
r bl f rdrps shld b sd fr ch p.
Prfrm prmdc ssssm; s dvdl
drg mgrphs fr dls.
equiPment
• Cl glvs
• Oc sl prscrbd; sr h  s lbld fr
s
• Drppr prvdd by h mfcrr
• MAR d mdc prl
site
Er(s)
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
2. Assmbl h c mdc d drppr. Esr
h h mdc s lbld fr “Oc” r “Er”
s. Allw h mdc  wrm  rm
mprr.
2. Ps h p s h h ffcd r s d-
rcd pwrd.
3. Rvw h plcy f h prcc sg d fl-
lw gdls rgrdg whhr glvs r  b
wr drg h sll f r mdcs.
Apply cl glvs  ccrdc wh s-
l plcy.
4. Assss h r cl fr wx ccml. If wx
s prs, b  rdr  rrg h cl b-
fr sllg h rdrps.
5. Shk h mdc wll d h drw  p 
h drppr.
6. Admsr h mdc.
 • Fr chldr wh r lss h 3 yrs ld, r-
sr h chld, r h chld’s hd  h
pprpr sd, d h gly pll h
lwr rlb downward d back (Fg. 7.8A) 
srgh h xrl dry cl. Isll h
prscrbd mbr f drps  h cl. D
 llw h drppr p  ch y pr f
h r. Afr dmsr, prss gly  h
rgs  hlp dsprs h mdc.
 • Fr chldr wh r mr h 3 yrs ld d
fr dls, ls cpr r rsr s c-
ssry. Tr h hd  h pprpr sd,
d h gly pll h ppr rlb vertically
d back (Fg. 7.8B)  srgh h xrl
dry cl. Isll h prscrbd mbr f
drps  h cl. D  llw h drppr
p  ch y pr f h r. Afr dmsr-
, prss gly  h rgs  hlp dsprs
h mdc.
7. Isrc h p  rm  hr sd fr 
fw ms fr sll; sr  c plg
loosely, f rdrd.

A B
Fig. 7.8 Administering eardrops. (A) Pull the lower earlobe downward and back for children who are less than 3 years
old. (B) Pull the upper earlobe upward and back for patients who are more than 3 years old.
8. If rdrps r rdrd fr bh rs, llw 5  10
ms bw dmsrs wh h r h
rcvd h mdc rs rmg “p.” Th
rp h prcdr  h hr r.
9. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
10. Prfrm hd hyg.
Clinical Goldmine
Remember, for children who are less than 3 years old, pull
the lower earlobe downward and back. For adults and chil-
dren who are 3 years old and older, pull the upper earlobe up
and back (see Fig. 7.8).
Patient teaChing
1. Expl h mprc f dmsrg h md-
c s prscrbd.
2. Tch h p slf-dmsr, r ch h
dmsr chq  hr prs, s
pprpr.
DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  drg
hrpy.
1. Chr h d, m, drg m, dsg, s, d
r f dmsr.
2. Prfrm d rcrd rglr p ssssms fr
h vl f hrpc ffcvss (.g., rd-
ss, prssr, dgr d dr f p rlf,
clr d m f drg).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
Percutaneous Administration CHAPTER 7 93
4. Prfrm d vld ssl p dc
b h drg hrpy.
AdministrAtion of nose droPs
Nsl sls r sd  r mprry dsrdrs
h ffc h sl mcs mmbrs. Alwys s
h drppr prvdd by h mfcrr, d gv
ch p  spr bl f s drps.
Prfrm prmdc ssssm; s dvdl
drg mgrphs fr dls.
equiPment
• Cl glvs
• Ns drps prscrbd
• Drppr sppld by h mfcrr
• Tss  blw h s
• Plgh
• MAR d mdc prl
site
Nsrl(s)
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
2. Rvw sl plcy d fllw h ppr-
pr gdls rgrdg whhr glvs r 
b sd drg h sll f s drps  pr-
v pssbl cc wh bdy d scrs.
Apply cl glvs  ccrdc wh sl
plcy.
3. Expl h sps  h prcdr  hlp h d-
vdl lr fr slf-dmsr.
4. Admsr h mdc (Fg. 7.9).
94 UNIT II Illustrated Atlas of Medication Administration
A B
Fig. 7.9 Administering nose drops. (A) Have the patient gently blow the nose. (B) Open the medication bottle and draw
the medication up to the calibration mark on the dropper. (C) Instill the medication. Have the patient remain in this
position for 2 to 3 minutes. Repeat in the other nostril, if necessary.
F adl d old Cld
 • Isrc h p  blw h s gly -
lss hs s crdcd (.g., sblds, rsk
f crsd rcrl prssr). Us  plgh
 ssss h rs.
 • Hv h p lie down and hang the head back-
ward vr h dg f h bd r vr  pllw
plcd dr h shldrs.
 • Drw h mdc  h drppr. Hld h
drppr js bv h srl, d sll h
mdc.
 • Afr  brf m, rp h dmsr pr-
css  h scd srl, f dd.
 • Hv h p rm  hs ps fr 2 
3 ms  llw h drps  rm  cc
wh h sl mcs.
F if d Y Cld
 • Ps h f r smll chld wh h hd
vr h dg f  bd r pllw, r s h “f-
bll” hld  mmblz h f.
 • Admsr s drps  h sm mr s s
sd fr  dl.
 • Fr  chld wh s cprv, ffr prs.
Prvd pprpr cmfrg d prsl
cc fr ll chldr d fs.
 • Hv ppr sss vlbl fr s f  s b-
slly cssry fr h p  blw hr
s.
5. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
6. Prfrm hd hyg.
Patient teaChing
Tch h p b h slf-dmsr f s
drps, f cssry. Tll h p h h vrs f
s drps c cs  rbd ffc, whch css
sympms  bcm wrs. If sympms hv  r-
slvd fr  wk f sl drp hrpy, h hlh-
cr prvdr shld b csld g.
C
DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  drg
hrpy.
1. Chr h d, m, drg m, dsg, s, d
r f dmsr.
2. Prfrm d rcrd rglr p ssssms
fr h vl f h hrpc ffcv-
ss (.g., sl cgs, dgr d dr-
 f rlf chvd, mprvm  vrll
ss), d rssss h cd f h rs
prdclly.
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.
AdministrAtion of nAsAL sPrAy
Th mcs mmbrs f h s bsrb qs
sls vry wll. Wh ppld s  spry, h smll
drpls f  sl h cs mdc c h
mmbrs d r rpdly bsrbd. Th dvg
f spry vr drps s h hr s lss ws f md-
c bcs sm f h drps f r dw h
bck f h p’s hr bfr bsrp c k
plc. Ech p shld hv  prsl cr
f spry.
Prfrm prmdc ssssm; s dvdl
drg mgrphs fr dls.
equiPment
• Cl glvs
• Nsl spry prscrbd
• Ppr sss  blw h s
• Plgh
• MAR d mdc prl
site
Nsrl(s)

A B
Fig. 7.10 Administering nasal spray. (A) Have the patient gently blow the nose. (B) Block one nostril; shake the medication
bottle. Insert the tip of the bottle into the patient’s nostril and squeeze a puff of spray while the patient inhales through
the open nostril. (C) Repeat procedure on other nostril.
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
2. Rvw sl plcy d fllw h ppr-
pr gdls rgrdg whhr glvs r  b
sd drg h sll f sl sprys. Apply
cl glvs  ccrdc wh sl plcy.
3. Isrc h p  gly blw h s (Fg.
7.10A), lss hs s crdcd (.g., s-
blds, rsk f crsd rcrl prssr).
4. Hv h p ssm h upright sitting position.
Us  plgh  spc h rs.
5. Blck  srl.
6. Shk h spry bl whl hldg  prgh.
7. Immdly fr shkg h bl, sr h p
 h srl (Fg. 7.10B). Ask h p  -
hl hrgh h p srl, d sqz  pff
f spry  h srl  h sm m.
8. Rp h dmsr prcss  h scd
srl, f dd (Fg. 7.10C).
9. Hv ppr sss vlbl fr s f  s bs-
lly cssry fr h p  blw hr s
fr s f h sl spry.
10. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
11. Prfrm hd hyg.
Patient teaChing
Tch h p h slf-dmsr f sl
spry, f cssry. Tll h p h h vrs f
sl spry c cs  rbd ffc, whch css
h sympms  bcm wrs. If sympms hv
 rslvd fr  wk f sl spry hrpy, h
hlhcr prvdr shld b csld g.
DoCumentation
Prvd h rgh dcm f h mdc d-
msr d h p’s rspss  drg hrpy.
1. Chr h d, m, drg m, dsg, s, d
r f dmsr.
Percutaneous Administration CHAPTER 7 95
C
2. Prfrm d rcrd rglr p ssssms
fr h vl f hrpc ffcvss (.g.,
sl cgs, dgr d dr f rlf
chvd, mprvm  vrll ss).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.
AdministrAtion of mediCAtions by
inhALAtion
Th rsprry mcs my b mdcd v h
hl f sprys r rsls. Aerosols s  w
f r r xyg dr prssr  dsprs h drg
hrgh h rsprry rc. Oly prprs
shld  b ppld  h rsprry mcs, b-
cs h l drpls my b crrd  h lgs d
cs lpd pm. Isl prcls shld
rc crr sdrds f vrsl prcs 
prv f rsmss f rbr phgs fr
ll ps d hlhcr prsl. Fllw hs
prcdrs fhflly  prv h rsmss f
dss. Ths mdcs r dlvrd wh h s
f  blzr (Fg. 7.11).
Prfrm prmdc ssssm; s spcc
drg mgrphs fr dls. Assss h p’s bl-
y  mpl h blzr.
equiPment
• Cl glvs
• Lqd rsl r spry frms f mdcs
• MAR d mdc prl
site
Rsprry rc
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
96 UNIT II Illustrated Atlas of Medication Administration
Fig. 7.11 Example of a nebulizer.
2. Rvw sl plcy d fllw h ppr-
pr gdls rgrdg whhr glvs r 
b sd drg h dmsr f mdc
by hl. Apply cl glvs  ccrdc
wh sl plcy.
3. Hv h p ssm  sg ps. Ths l-
lws fr mxmm lg xps.
4. Prpr h mdc ccrdg  h prscrbd
drcs, d ll h blzr wh dl. (Ths
my b d bfr sg h p p f m s
 fcr fr h p’s wll-bg.)
5. Acv h blzr wh cmprssd xyg r
r l   ms s wg; hs wll slly k
p  8  10 lrs f xyg r r.
6. Plc blzr msk vr p’s s d
mh d sk p  brh rmlly.
7. Allw gh m fr ll h mdc  h
blzr  b dmsrd; hs shld k p-
prxmly 10 ms.
8. Assss h p whl sll sg  drm
ffcvss.
9. Cl h qpm  ccrdc wh h m-
fcrr’s drcs.
10. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
11. Prfrm hd hyg.
Patient teaChing
1. As pprpr  h crcmscs, ch h p-
,  fmly mmbr, r  sgc hr hw 
pr h blzr h s  b sd  hm.
2. Expl h pr d clsg f h
qpm.
3. Bfr h p s dschrgd, hv h p, 
fmly mmbr, r  sgc hr dmsr
A B
Fig. 7.12 (A) Metered-dose inhaler (MDI). (B) Dry powder inhaler (DPI).
sg h qpm crrcly d vrblz h md-
cs h hv b prscrbd fr -hm s.
4. Srss h d  prfrm h prcdr xcly
s prscrbd d  rpr y dfcls h r
xprcd fr dschrg fr h hlhcr pr-
vdr’s vl.
DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  drg
hrpy.
1. Chr h d, m, drg m, dsg, d r
f dmsr.
2. Prfrm d rcrd rglr p ssssms
fr h vl f hrpc ffcvss (.g.,
bld prssr, pls, mprvm r qly f
brhg, cgh d prdcvy, lg sds, d-
gr d dr f p rlf, bly  pr
h blzr, cvy d xrcs rsrcs).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.
AdministrAtion of mediCAtions by orAL
inhALAtion
Dose Forms
Brchdlrs d crcsrds my b dms-
rd by hl hrgh h mh wh h s f
 rslzd, prssrzd metered-dose inhaler (MDI)
r  dry powder inhaler (DPI) (Fg. 7.12). Th dvgs
f h hlrs r h h mdcs c b ppld
drcly  h s f c (h brchl smh ms-
cl), smllr dss r sd, d h drg s rpdly
bsrbd. Th vlv f h prssrzd cr (..,
h MDI) r h dry pwdr pck f h DPI ls hlps
 sr h h sm ds f mdc s dms-
rd wh ch hl.
Apprxmly 25% f ps d  s MDIs
prprly d hrfr d  rcv h mxml
b f h mdc. Dvcs kw s extenders

r spacers (Fg. 7.13) hv b dsgd fr ps
wh c crd h rls f h mdc
wh hl. Th xdr dvcs c b dpd
 ms prssrzd csrs f MDIs. Ths dvcs
rp h rslzd mdc   chmbr hrgh
whch h p hls wh  fw scds fr
rlsg h mdc  h chmbr.
Prfrm prmdc ssssm; s dvdl
drg mgrphs fr dls.
equiPment
• Cl glvs
• Prscrbd mdc pckgd   MDI r DPI
• MAR d mdc prl
site
Rsprry rc
teChnique
alzd md-D il
1. Fllw h prcdr prcl dscrbd rlr.
2. Rvw sl plcy d fllw h pprpr-
 gdls rgrdg whhr glvs r  b
sd drg h dmsr f mdc by
rl hl. Apply cl glvs  ccrdc
wh s plcy.
3. Th fllwg prcpls pply  ll MDIs. Rd
d dp hs chqs  h drcs pr-
vdd by h mfcrr fr  spcc hlr d
xdr, f dd.
 • If h mdc s  ssps, shk h cs-
r. Ths dsprss d mxs h cv brch-
dlr d prpll.
 • Hv h p p hr mh d h
plc h csr l 2  4 chs  fr
f h mh. Ths spc llws h prpll
 vpr d prvs lrg prcls frm
slg  h mh. Wh sg  xdr,
hv h p plc  d f h xdr
 h mh d cls h lps rd . Ach
h hr d f h xdr  h hlr
dvc.
 • Acv h MDI, d src h p  -
hl dply vr 10 scds  sr h r-
wys r p d h h drg s dsprsd s
dply s pssbl.
 • Hv h p hld hr brh d h x-
hl slwly  prm h drg  sl  pl-
mry ss.
 • If prscrbd, rp  2  3 ms. Usg
smll dss wh w r hr hls hlps
h drg dsprs  h smllr prphrl r-
wys fr  lgr hrpc ffc.
 • If h hld mdc s  crcsrd, hv
h p rs h mh wh wr wh d-
msr s cmpl.
4. Cls h pprs ccrdg  h mfc-
rr’s rcmmds.
Percutaneous Administration CHAPTER 7 97
Fig. 7.13 Metered-dose inhaler with an extender or spacer. (From Lilley
LL, Collins SR, Snyder JS. Pharmacology and the Nursing Process.
7th ed. St. Louis: Mosby; 2014.)
5. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
6. Prfrm hd hyg.
Dy Pwd il
1. Fllw h prcdr prcl dscrbd rlr.
2. Rvw sl plcy d fllw h pprpr-
 gdls rgrdg whhr glvs r  b
sd drg h dmsr f mdc by
rl hl. Apply cl glvs  ccrdc
wh sl plcy.
3. Th fllwg prcpls pply  ll DPIs. Rd d
dp hs chqs  h drcs prvdd by
h mfcrr fr  spcc hlr d xdr,
f dd.
 • Rmv h cvr, d chck h h dvc d
h mhpc r cl.
 • Mk h mdc vlbl ccrdg  h
mfcrr’s srcs fr ch spcc
prdc. Kp h hlr hrzl.
 • Hv h p brh , wy frm h
dvc.
 • Plc h mhpc gly  h p’s
mh, d hv h p cls h lps rd
.
 • Hv h p brh  qckly, frcflly,
d dply l  fll brh hs b k.
 • Rmv h hlr frm h p’s mh.
 • Hv h p hld h brh fr b 10 sc-
ds bfr brhg .
 • Alwys chck h mbr  h ds cr
wdw  s hw my dss rm.
 • If h p drps h hlr r brhs  
fr h ds hs b ldd, h ds my b
ls. T sr prpr dsg, ld hr ds
 h hlr bfr sg .
4. Cl h dvc ccrdg  h mfcrr’s
srcs.
5. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
6. Prfrm hd hyg.
98 UNIT II Illustrated Atlas of Medication Administration
Health Promotion
Relling the Prescription
The patient should not wait until the canister is empty before
having the prescription relled. The last few doses in a canis-
ter are often subtherapeutic because of an imbalance in the
remaining amounts of medication and propellant. Consult
the manufacturer’s information on how to determine whether
the canister is almost empty. The commonly used oat test is
inaccurate for many aerosolized MDIs.
Patient teaChing
Expl h prcdr, d llw h p  dm-
sr h chq. Tchg ds fr MDIs d DPIs
wh cv grds r vlbl frm h phr-
mcy dprm  crg ps  prcc h
chq bfr mdc dmsr. I dd-
  chq, h p shld b frmd b
dvrs ffcs, hw  crry h mdc, hw 
sr , d hw  hv  rlld wh dd.
Hv h p prfrm h slf-dmsr f
h prscrbd m f rdrd mdc. Hv
h p dmsr h bly  rd h cs-
r cr  drm h m f mdc r-
mg  h cr.
DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  drg
hrpy.
1. Chr h d, m, drg m, ds, s, d
r f dmsr.
2. Prfrm d rcrd rglr p ssssms
fr h vl f hrpc ffcvss (.g.,
bld prssr, pls, mprvm f qly f
brhg, cgh d prdcvy, dgr d d-
r f p rlf, bly  pr h MDI r
DPI, cvy d xrcs rsrcs).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.
Life Span Considerations
Medicines Administered by Inhalation
When muscle coordination is not fully developed (e.g., in a
younger child or when dexterity has diminished in an older
adult patient), it may be benecial to use an extender or
spacer device (see Fig. 7.13) for medicines that are admin-
istered by aerosol inhalation. When administering medicines
by aerosol therapy to an older adult, make sure that the pa-
tient has the strength and dexterity to self-operate the equip-
ment before discharge.
AdministrAtion of vAginAL mediCAtions
Wm wh gyclgc dsrdrs my rqr
h dmsr f  mdc rvglly.
Vgl mdcs my b crms, jlls, bls,
fms, sppsrs, r rrgs (.., dchs; s
Admsr f  Vgl Dch lr). Th crms,
jlls, bls, d fms r srd wh h s f
spcl pplcrs h r prvdd by h mfc-
rr; sppsrs r slly srd wh  glvd
dx gr.
Prfrm prmdc ssssm; s dvdl
drg mgrphs fr dls.
equiPment
• Prscrbd mdc
• Vgl pplcr
• Prl pd
• Wr-slbl lbrc (fr sppsry)
• Cl glvs
• Ppr wls
• MAR d mdc prl
site
Vg
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
2. Hv h p vd  sr h h blddr s
mpy.
3. Apply cl glvs.
4. Fll h pplcr wh h prscrbd bl, jlly,
crm, r fm.
5. Plc h p  h lhmy ps, d l-
v hr hps wh  pllw. Drp h p 
prv cssry xpsr.
6. Admsr h mdc.
 • For tablets, creams, foams, and jellies, s h
glvd dm hd  sprd h lb
d xps h vg. Assss h ss f h
prsg sympms (.g., clr d vlm f
dschrg, dr, lvl f dscmfr). Lbrc
h pplcr. Gly sr h vgl pplc-
r s fr s pssbl  h vg, d psh
h plgr  dps h mdc (Fg. 7.14).
Rmv h pplcr, d wrp    ppr
wl fr clg lr.
 • For suppositories, wrp  vgl sppsry
h hs b wrmd  rm mprr,
d lbrc  wh  wr-slbl lbrc.
Lbrc h glvd dx gr f h dm-
 hd. Wh h glvd dm hd,
sprd h lb  xps h vg. Isr
h sppsry (rdd d rs) s fr 
h vg s pssbl wh h dm dx
gr.
7. Rmv h glv by rg  sd ; plc 
  ppr wl fr lr dspsl.
8. Apply  prl pd  prv drg  h
p’s clhg r bd.
9. Isrc h p  rm   sp ps
wh h hps lvd fr 5  10 ms  llw
fr h mlg d sprdg f h mdc.

Fig. 7.14 Applying vaginal medication. Gently insert the vaginal
applicator as far as possible into the vagina, and then push the plunger
to deposit the medication.
10. Dsps f ll ws  ccrdc wh s-
l plcy.
11. Prfrm hd hyg.
Patient teaChing
1. Tch h p hw  dmsr h mdc
crrcly.
2. Th pplcr shld b wshd  wrm spy
wr after each use.
3. Rvw prsl hyg msrs sch s wp-
g frm h fr  h bck fr vdg r
dfcg.
4. Tll h p   dch d  bs frm
sxl rcrs fr srg h mdc.
5. Wh ms yps f fcs, bh ml d fml
prrs rqr rm. T prv rfc,
ps shld bs frm sxl rcrs -
l ll prrs r crd.
DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  drg
hrpy.
1. Chr h d, m, drg m, dsg, d r
f dmsr.
2. Prfrm d rcrd rglr p ssssms fr
h vl f h hrpc ffcvss (.g.,
yp f dschrg prs, rr f lb, dscm-
fr, dgr d dr f p rlf).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.
Percutaneous Administration CHAPTER 7 99
AdministrAtion of A vAginAL douChe
Dchs (.., rrgs) r sd  wsh h vg.
Ths prcdr s  cssry fr rml fml
hyg, b  my b rqrd f  vgl fc
d dschrg r prs. I shld ls b d h
dchg s   ffcv mhd f brh crl.
Prfrm prmdc ssssm; s dvdl
drg mgrphs fr dls.
equiPment
• IV pl
• Cl glvs
• Wr-slbl lbrc
• Dch bg wh bg d zzl
• Dch sl
• MAR d mdc prl
site
Vg
teChnique
1. Fllw h prcdr prcl dscrbd rlr.
2. Ask h p  vd bfr h prcdr.
3. If h rs s chg hs prcdr   p
fr hm s, h p wld csmrly rcl
  bhb. Dpdg  h p’s cd
 h hspl, hs  cld ccr. Hwvr, 
my b cssry  plc h p   bdp
d drp fr prvcy.
4. Fll h dch bg wh dch sl d hg
h dch bg   IV pl,   lvl b 12
chs bv h vg. Apply cl glvs. Apply
wr-slbl lbrc   plsc vgl p.
5. Cls h vlv by llwg  smll m f s-
l  w vr h vlv d bw h lb.
6. Gly sr h zzl  h vg, drcg
h p bckwrd d dwwrd 2  3 chs.
7. Hld h lb ghr  fcl llg h v-
g wh sl. R h zzl prdclly
 hlp rrg ll prs f h vg.
8. Irmly rls h lb, llwg h sl-
  w .
9. Wh ll f h sl hs b sd, rmv h
zzl. Hv h p s p d l frwrd 
mpy h vg hrghly.
10. P h xrl r dry.
11. Cl ll qpm wh wrm spy wr after
every use; rs h qpm wh clr wr,
d llw   dry.
12. Thrghly cl d dsfc h bhb, f
sd.
13. Rmv glvs d dsps f hm  ccrdc
wh sl plcy.
14. Prfrm hd hyg.
Patient teaChing
1. Tch h p hw  dmsr h dch
crrcly.
100 UNIT II Illustrated Atlas of Medication Administration
2. Expl h h bg d bg shld b wshd
 wrm spy wr fr ch s s h hy d
 bcm  src f rfc.
3. Rvw prsl hyg msrs, sch s wpg
frm h fr  h bck fr vdg r dfcg.
4. Expl h dchg s  rcmmdd drg
prgcy.
5. Wh ms yps f fcs, bh ml d fml
prrs rqr rm. T prv rfc,
ps shld bs frm sxl rcrs -
l ll prrs r crd.
DoCumentation
Prvd h rgh dcm f h mdc
dmsr d h p’s rspss  drg
hrpy.
1. Chr h d, m, drg m, dsg, d r
f dmsr.
2. Prfrm d rcrd rglr p ssssms
fr h vl f hrpc ffcvss (.g.,
yp f dschrg prs, rr f lb, dscm-
fr, dgr d dr f p rlf).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.
 Percutaneous Administration CHAPTER 7 101

Clcl Jd d nx-g nclx® ex-syl q

K P ojc: Identify the equipment needed and the techniques used
to apply each of the topical forms of medications to the skin.
• Topical forms of medication include creams, lotions, ngn  : Matrix
ointments, and powders and may require the use of C kll: Recognize cues
sponges, cotton-tipped applicators, or a tongue blade to
apply. 2. When performing a patch test for allergens, the nurse will follow
• Patch testing is performed to determine the presence of the correct procedure.
allergy. Allergens are applied to the skin using a patch test Place in order the proper steps to use when performing a patch
kit, and results are read 24 to 72 hours later. test:
• Nitroglycerin ointment is applied using specic dose- 1. Have emergency equipment available in case of an
measuring ointment paper, covered with plastic, and taped anaphylactic response.
in place. Patient education includes proper application 2. Apply the designated patches to the skin.
technique and timing of the nitroglycerin ointment. 3. Recognize when a wheal has formed.
• Patient education involving the transdermal patch 4. Cleanse the area for testing with alcohol.
medications includes discussing rotating the site of 5. Ask the patient if they have taken any antihistamines or
application and emphasizing the timing of the medication. antiinammatory agents.
• Medications administered via the mucous membranes ojc: Describe the purpose of and the procedure used for
include sublingual and buccal tablets; eyedrops, eardrops, performing patch testing.
and nose drops; inhaled medications; and vaginal nCLeX  : Ordering
medications. C kll: Application
• Eardrops administered to a patient younger than 3 years
old require the lower earlobe to be pulled down and back, 3. The nurse assesses the patient for the treatment effectiveness of
compared with patients 3 years and older, where the the percutaneous medication nitroglycerin and documents which
upper earlobe is pulled upward and back. assessment ndings? (Select all that apply.)
• Patient education necessary for inhaled medications 1. Temperature
includes demonstrating the proper use of the equipment, 2. Blood pressure
including nebulizers, MDIs, and DPIs. 3. Urine output
• Vaginal medications come in the form of creams, foams, 4. Location of patch
and jellies that are applied using an applicator. 5. Anginal pain relief
ojc: Identify the equipment needed, the sites and techniques
Aal La rc used, and the patient education required when nitroglycerin
ointment is prescribed.
SG Go to your Study Guide for additional Review Questions for nCLeX  : Multiple response
the NCLEX® Examination, Critical Thinking Clinical Situations, and C kll: Application
other learning activities to help you master this chapter content.
4. Fentanyl patches do not usually achieve a sufcient blood level for
Go to your Evolve website (https://evolve.elsevier.com/Willihng pain control until how many hours after their initial application?
anz) for additional online resources. 1. 6 hours
2. 12 hours
Clinical Judgment and Next-Generation NCLEX® Exam- 3. 18 hours
ination-Style Questions The following questions are typical of 4. 24 hours
the NCLEX examination and include both NGN (Next Genera- ojc: Identify the equipment needed, the sites and techniques
tion) and traditional questions. See Chapter 1 for further infor- used, and the patient education required when transdermal patch
mation regarding question types. medication systems are prescribed.
nCLeX  : Multiple choice
1. The nurse was preparing to administer topical forms of medications C kll: Knowledge
and reviewed the various types of topical forms.
Mark an X to identify the technique and equipment used for each 5. A patient is to receive a medication via the buccal route. Which
topical dose form. action does the nurse plan to implement?
1. Place the medication inside the pouch between the
gentLy patient’s lower molar and the cheek.
smooth 2. Crush the medication before administration.
tyPes of shAKe over the CAn be neCessAry 3. Offer the patient a glass of water or juice after
toPiCAL ContAiner sKin when removed to use administration.
forms first APPLying by wAter gLoves 4. Use sterile technique to administer the medication.
Creams ojc: Describe the dose forms, the sites and equipment used,
Lotions and the techniques for the administration of medications to the
mucous membranes.
Powders
nCLeX  : Multiple choice
Ointments C kll: Comprehension
102 UNIT II Illustrated Atlas of Medication Administration

6. A nurse is preparing to administer eardrops to a 2-year-old child. 8. When administering vaginal medications, the nurse knows the
Choose the most likely options for the information missing from patient needs to be in which position?
the sentence below by selecting from the lists of options provided. 1. Left lateral recumbent position
2. Trendelenburg position
The nurse knows that the proper technique to use 3. Lithotomy position
for a 2-year-old child is to pull the lower earlobe 4. Prone position
________1___________ and ________1___________ and
the proper technique to use for an adult is to pull the upper ojc: Identify the equipment needed, the site, and the specic
earlobe ________2_______ and __________2__________. techniques required to administer vaginal medications or douches.
nCLeX  : Multiple choice
C kll: Knowledge
oPtions for 1 oPtions for 2
downward back
forward up
upward straight
inward out

ojc: Compare the technique used to administer eardrops to

patients who are less than 3 years old with that used for patients
who are 3 years and older.
ngn  : Cloze
C kll: Recognize cues
7. The nurse teaching a patient how to use an inhaler prescribed for
asthma knows that further teaching is needed after the patient
makes which statement?
1. “I will hold my breath for 10 seconds before breathing
out.”
2. “I will take a slow deep breath and let it out quickly.”
3. “I will check the number on the dose counter window to
see how many more puffs I have left.”
4. “I will notify my primary healthcare provider if I notice that
I am coughing a lot more than usual.”
ojc: Describe the purpose, the precautions necessary, and
the patient education required for those patients who require
medications via inhalation.
nCLeX  : Multiple choice
C kll: Comprehension
Enteral Administration 8
https://evolve.elsevier.com/Willihnganz

Objectives
1. Describe general principles of administering solid forms of
oral medications.
2. Compare the different techniques that are used with a
unit-dose distribution system and a computer-controlled
dispensing system.
3. Identify general principles used for liquid-form oral
medication administration.
4. Cite the equipment needed, techniques used, and
precautions necessary when administering medications via
gastrointestinal tubes.
5. Cite the equipment needed and the technique required
when administering rectal suppositories and disposable
enemas.

Key Terms
gastrointestinal tubes (p. 103)
capsules (KĂP-sŭlz) (p. 103)
lozenges (LŎ-zĕn-jĕz) (p. 104)
tablets (TĂB-lĕts) (p. 104)
caplet (KĂP-lĭt) (p. 104)
orally disintegrating tablet (ŌR-ăl-ē
dĭs-ĬN-tĕ-grāt-ĭng) (p. 104)
elixirs (ĕ-LĬK-sŭrz) (p. 105)
emulsions (ĕ-MŬL-shĕnz) (p. 105)
suspensions (sŭ-SPĔN-shĕnz) (p. 105)
syrups (SĬR-ĕps) (p. 105)
unit-dose packaging (YŪ-nĭt DŌS
PĂK-ĕj-ĭng) (p. 105)
bar code (BĂR KŌD) (p. 105)
soufé cup (sū-FLĀ KŬP) (p. 105)
medicine cup (MĔD-ĭ-sĭn KŬP) (p. 105)
medicine dropper (MĔD-ĭ-sĭn DRŎ-
pŭr) (p. 106)
oral syringe (ŌR-ăl sĭ-RĬNJ) (p. 106)
suppository (sŭ-PŎZ-ĭ-tōr-ē) (p. 114)

Th rus f drug adminisrain can b classid in
hr cagris: nral, parnral, and prcuanus.
Wih h enteral route, drugs ar adminisrd dircly
in h gasrinsinal (GI) rac by h ral, rcal, r
GI tube mhds. Th ral ru is saf, cnvnin,
and rlaivly cnmical, and ds frms ar radily
availabl fr ms mdicains. In cas f a mdica-
in rrr r an inninal drug vrds, much f h
drug can b rrivd fr a rasnabl im afr ad-
minisrain. Th majr disadvanag f h ral ru
is ha i has h slws and las dpndabl ra f
absrpin f h cmmnly usd rus f adminis-
rain bcaus f frqun changs in h GI nvirn-
mn ha ar prducd by fd, min, and physi-
cal aciviy. Anhr limiain f his ru is ha a
fw drugs (.g., insulin, gnamicin) ar dsryd by
digsiv uids and mus b givn parnrally fr
hrapuic aciviy. Th nral ru shuld n b
usd if h drug may harm r disclr h h r if
h pain is vmiing, has gasric r insinal suc-
in, is likly  aspira, r is uncnscius and unabl
 swallw.
Fr pains wh cann swallw r wh hav had
ral surgry, h GI ub mhd may b usd. Th
primary purps f GI ubs is  bypass h muh
and h pharynx. Advanags and disadvanags ar
similar  hs f h ral ru. Th irriain causd
by h ub in h nasal passag and hra mus b
wighd agains h rlaiv immbiliy assciad
wih cninuus inravnus (IV) infusins, h x-
pns, and h pain and irriain f mulipl injc-
ins. Fr pains wh rquir lng-rm drug and
fding adminisrain, GI ubs ar usd.
Th adminisrain f drugs via h rcal ru has
h advanags f bypassing h digsiv nzyms
and aviding irriain f h muh, sphagus, and
smach. I may als b an accpabl alrnaiv whn
nausa r vmiing is prsn. Absrpin via his
ru varis dpnding n h drug prduc, h abil-
iy f h pain  rain h suppsiry r nma,
and h prsnc f fcal marial.
ADMINISTRATION OF ORAL
MEDICATIONS
DOSE FORMS
Capsules
Capsules ar small, cylindrical, glain cnainrs ha
hld dry pwdr r liquid mdicinal agns (Fig. 8.1).
Thy ar availabl in a variy f sizs, and hy ar a
cnvnin way f adminisring drugs ha hav an
103
104 UNIT II Illustrated Atlas of Medication Administration
Fig. 8.1 Various sizes and numbers of gelatin capsules (actual size).
(Courtesy Oscar H. Allison, Jr.)
Fig. 8.2 Timed-release capsule.
unplasan dr r as. Thy d n rquir caings
r addiivs  imprv h as. Th clr and shap
f h capsuls, as wll as h manufacurr’s symbl
n h capsul surfac, ar mans f idnifying h
prduc.
Timed-release capsules and tablets. Timd-rlas r
susaind-rlas capsuls and abls prvid a grad-
ual bu cninuus rlas f a drug bcaus h gran-
uls in h capsul r h ingrdins f a abl dis-
slv a diffrn ras (Fig. 8.2). Th advanag f his
dlivry sysm is ha i rducs h numbr f dss
adminisrd pr day, usually  vry 12 r 24 hurs.
Medication Safety Alert
Timed-release capsules and tablets should not be crushed
or chewed or have their contents emptied into food or liquids
because this may alter the absorption rate and could result
in a drug overdose or subtherapeutic activity.
Lozenges
Lozenges ar a disks ha cnain a mdicinal agn
in a suiably avrd bas. Th bas may b a hard
sugar candy r a cmbinain f sugar wih sufcin
glainus subsancs  giv i frm. Lzngs ar
hld in h muh  disslv slwly, hrby rlasing
h hrapuic ingrdins.
Pills
Pills ar an bsl ds frm ha is n lngr manu-
facurd bcaus f h dvlpmn f capsuls and
cmprssd abls. Hwvr, h rm is sill usd 
rfr  abls and capsuls.
Tablets
Tablets ar drid pwdrd drugs ha hav bn cm-
prssd in small disks. In addiin  h drug, ab-
ls cnain n r mr f h fllwing ingrdins:
Color coat
Acid-resistant
coat
C Active ingredient
Fig. 8.3 (A) Scored tablet. (B) Layered tablet. (C) Enteric-coated
tablet.
bindrs, which ar adhsiv subsancs ha allw h
abl  hld ghr; disingrars, which ar sub-
sancs ha ncurag dissluin in bdy uids; lu-
bricans, which ar rquird fr fcin manufacur-
ing; and llrs, which ar inr ingrdins ha mak
h siz f h abl cnvnin. Tabls ar smims
scrd r grvd (Fig. 8.3A); h indnain may hn
b usd  divid h ds. Whn pssibl, i is bs 
rqus ha h xac ds b availabl rahr han 
amp  divid vn a scrd abl. Tabls can b
crushd, using a variy f mhds (i.. pill crushrs,
hn h pwdrd frm can b adminisrd in a slu-
in, if slubl, r i may b mixd wih a small amun
f fd (.g., applsauc).
A caplet is a abl shapd in h frm f a capsul.
Many prducs ha wr prviusly sld in capsul
frm hav bn rfrmulad  capls (slid dsag
frms in h shap f a capsul)  prvn h abiliy
 pn a capsul and cnamina h cnns f h
capsul. (Auhr’s n: Sarch nlin fr h Chicag
Tylnl murdrs.)
Tabls can b frmd in layrs (Fig. 8.3B). This
mhd allws hrwis incmpaibl mdicains 
b adminisrd a h sam im.
An nric-cad abl has a spcial caing ha
rsiss dissluin in h acidic pH f h smach bu
ha is radily disslvd in h alkalin pH f h ins-
ins (Fig. 8.3C). Enric-cad abls ar fn usd
fr adminisring mdicains ha ar dsryd in an
acid pH nvirnmn such as h smach.
A abl ha rapidly disslvs (usually wihin sc-
nds) whn placd n h ngu is knwn as an orally
disintegrating tablet Ths ar diffrniad frm lz-
ngs and frm sublingual and buccal abls, which
ak mr han a minu  disslv. Orally disin-
graing abls may b usd fr hir rapid ns f
acin (.g., fr h ramn f migrain hadach);
fr pains wh hav difculy swallwing (.g., pa-
ins wih parkinsnism r Alzhimr disas, r afr
 Enteral Administration CHAPTER 8 105

a srk); and fr hs fr whm adminisrain mus

b nsurd (.g., pains wih schizphrnia, wh f-
n amp  avid prscribd mdicain). An x-
ampl is h sublingual lm placd undr h ngu
fr vry rapid disingrain. This dsag frm is usd
 adminisr Subxn (buprnrphin plus nalx-
n), which is usd  manag pia addicin. Th
rapid disingrain f h lm prvns rrival f
h prduc fr lar sal n h sr.

Medication Safety Alert

Enteric-coated tablets must not be crushed or chewed be- Fig. 8.4 Unit-dose packages. (Courtesy Chuck Dresner.)
cause their active ingredients will be released prematurely
and destroyed in the stomach.

Elixirs
Elixirs ar clar liquids ha ar cmpsd f drugs ha
hav bn disslvd in alchl and war. Elixirs ar
usd primarily whn h drug will n disslv in war
aln. Afr h drug is disslvd in h lixir, war and
avring agns ar fn addd  imprv as. Th
alchl cnn f lixirs is highly variabl, dpnding
n h slubiliy f h drug. Many cugh mdicins
and muhwashs ar lixirs cnaining alchl.

Emulsions
Emulsions ar disprsins f small drpls f war
in il r small drpls f il in war. Th disprsin
is mainaind by an mulsifying agn such as sdium
lauryl sulfa, glain, r acacia. Emulsins ar usd 
mask bir ass,  mak h prduc fl br (pal-
aabl) in h muh and hra (hus imprving adhr-
nc), r  mak crain drugs mr slubl.
Suspensions
Suspensions ar liquid ds frms ha cnain slid,
inslubl drug paricls disprsd in a liquid bas.
All suspnsins shuld b shakn wll bfr admin-
israin  nsur h hrugh mixing f h par-
icls. Many ral liquid anacids [calcium carbna,
(Maalx), aluminum hydrxid, magnsium hydrx-
id, simhicn, (Mylana Classic)] and liquid anibi-
ics [amxicillin clavulana, (Augmnin), ryhr-
mycin succina (EryPd)] ar suspnsins.
Syrups
Syrups cnain mdicinal agns ha hav bn dis-
slvd in a cncnrad sluin f sugar (usually su-
crs) and war. Syrups ar paricularly ffciv fr
masking h bir as f a drug. Many prparains
fr pdiaric pains ar syrups bcaus childrn nd
 lik h swr avrd bas.
EQUIPMENT
Unit Dose or Single Dose
Unit-dose packaging, r singl-ds packaging, pr-
vids a singl ds f mdicain in n packag ha is
Fig. 8.5 Most unit-dose package labels include a bar code for the
electronic charting of medication administration and inventory control.
(Copyright 2003, McKesson Corporation, San Francisco, CA and/or
one of its subsidiaries. All rights reserved.)
rady fr dispnsing (Fig. 8.4). Th packag is labld
wih bh h gnric and brand nams, h manu-
facurr, h l numbr, and h da f xpirain.
Dpnding n h disribuin sysm, h pain’s
nam may b addd  h packag by h pharmacy.
Ms uni-ds packag labls includ a bar code fr
adminisrain, h lcrnic charing f mdicain
adminisrain, and invnry cnrl (Fig. 8.5).
Soufflé Cup
A soufé cup is a small papr cup ha is usd  ranspr
slid mdicain frms such as capsuls and abls  h
pain  prvn cnaminain by handling (Fig. 8.6).
Medicine Cup
A medicine cup is a plasic cnainr wih scals (mric,
hushld) fr masuring liquid mdicains (Fig. 8.7).
Examin h mdicin cup carfully bfr puring any
mdicain  nsur ha h prpr scal is bing usd
fr masurmn (Tabl 8.1). Th mdicin cup shuld
b placd n a hard surfac whn masuring liquid md-
icain and hn rad a y lvl. Th mdicin cup is
inaccura fr masuring dss f lss han 1 aspn,
alhugh i is rasnably accura fr largr vlums.
A syring cmparabl  h vlum  b masurd
106 UNIT II Illustrated Atlas of Medication Administration

2.0
mL
1.5
mL
Fig. 8.6 Medicine cup (left) and soufé cup (right). (Courtesy Chuck 1.0
Dresner.) mL
0.5
mL

1 oz 2 tbs 30 mL Fig. 8.8 Medicine dropper.

1/
2 oz 1 tbs 15 mL

1/
4 oz 1 tsp 5 mL

Fig. 8.7 Measuring scales on a medicine cup.

Fig. 8.9 Measuring teaspoon.

Table 8.1 Commonly Used Measurement Equivalents
HOUSEHOLD MEASUREMENTA METRIC MEASUREMENT
2 Tbsp 30 mL
1 Tbsp 15 mL
2 tsp 10 mL
1 tsp 5 mL
mL, Milliliter; oz, ounce; Tbsp, tablespoon; tsp, teaspoon.
a3 tsp = 1 Tbsp; 2 Tbsp = 30 mL = 1 oz.

shuld b usd fr smallr vlums. Fr vlums f lss

han 1 mL, a ubrculin syring shuld b usd. Fig. 8.10 Plastic oral syringes. (Courtesy Chuck Dresner.)

Medicine Dropper is n availabl, a aspn ha is usd spcically fr

Th medicine dropper may b usd  adminisr y-
drps, ardrps, and, ccasinally, pdiaric mdica-
ins (Fig. 8.8). Thr is gra variain wih rgard 
h siz f h drp frmd, s i is impran  us
nly h drppr supplid by h manufacurr fr a
spcic liquid mdicain. Bfr drawing mdicain
in a drppr, i is ncssary  bcm familiar wih
h calibrains n h barrl. Afr h mdicain is
drawn in h barrl, h drppr shuld n b ippd
upsid dwn bcaus h mdicain will run in h
bulb, hrby causing sm lss f h mdicain.
Mdicains shuld n b drawn in h drppr and
hn ransfrrd  anhr cnainr fr adminisra-
in bcaus par f h mdicain will adhr  h
scnd cnainr, hus diminishing h ds dlivrd.
Teaspoon
Dss f ms liquid mdicains ar prscribd in
rms using h aspn as h uni f masur (Fig.
8.9). Hwvr, hr is gra variain bwn h vl-
ums masurd by varius spns in h hm. In h
hspial, 1 aspn is cnvrd  5 mL (s Tabl 8.1),
and his is rad n h mric scal f h mdicin cup.
Fr hm us, an ral syring is rcmmndd. If his
baking may b usd as an accura masuring dvic.
Oral Syringe
A plasic oral syringe may b usd  masur liquid
mdicains accuraly (Fig. 8.10). Varius sizs ar
availabl  masur vlums frm 0.1  15 mL. N
ha a ndl will n  n h ip.
Nipple
An infan fding nippl may b usd fr adminisr-
ing ral mdicains  infans (Fig. 8.11). (S als
Gnral Principls f Liquid-Frm Oral Mdicain
Adminisrain—Fr an Adul r Child lar in his
chapr.)
ADMINISTRATION OF SOLID-FORM ORAL
MEDICATIONS
PROCEDURE PROTOCOL
Th rm procedure protocol will b usd as par f h
mdicain adminisrain chniqu fr h rus f
adminisrain dscribd in his chapr. This rm in-
cluds h fllwing nursing inrvnins:
ALGrawany

Fig. 8.11 Nipple. (Courtesy Chuck Dresner.)
1. Assmbl h apprpria quipmn and hn pr-
frm hand hygin.
2. Us h seven rights f mdicain prparain and
adminisrain hrughu h prcdur: righ pa-
in, righ drug, righ indicain, righ ru, righ
ds, righ im, and righ dcumnain.
3. Prvid privacy fr h pain and giv a hrugh
xplanain f h prcdur and wha  xpc.
4. Prfrm a prmdicain assssmn bfr admin-
isring any nral mdicain. S individual drug
mngraphs fr mr infrmain.
UNIT-DOSE SYSTEM
Prfrm prmdicain assssmn; s individual
drug mngraphs fr dails.
EQUIPMENT
• Mdicain car
• Mdicain prl
TECHNIQUE
1. Fllw h prcdur prcl dscribd arlir.
2. Rad h pain mdicain prl fr h pr-
scribd drugs and ims f adminisrain.
3. Obain h prscribd mdicain frm h drawr
in h mdicain car ha is assignd  h pain.
4. Cmpar h labl n h uni-ds packag wih
h pain mdicain prl. Chck h xpira-
in da n all mdicain labls.
5. Chck h numbr f dss rmaining in h draw-
r. (If h numbr f dss rmaining is n cnsis-
n, invsiga.)
6. Recheck h svn righs f mdicain adminis-
rain agains h pain mdicain prl and
h uni-ds packag as i is rmvd frm h
drawr.
7. Prcd  h pain’s bdsid.
 • Chck h pain’s idnicain bracl and
vrify i agains h mdicain prl. Hav h
pain sa hir nam and birh da r w
hr idnirs.
 • Carfully xplain  h pain h drugs bing
givn; sa hir nams and prvid ducain
abu h drugs bing adminisrd.
Enteral Administration CHAPTER 8 107
 • Chck prinn pain mniring paramrs
(.g., apical puls, rspirary ra).
8. Hand h mdicain  h pain and allw him
r hr  rad h packag labl.
9. Offr h pain a sip f war  facilia h
swallwing f h mdicain. Rriv h uni-
ds packag, pn i, and plac h cnns in h
pain’s hand r a mdicain cup fr placmn
in h muh.
10. Prfrm hand hygin.
COMPUTER-CONTROLLED DISPENSING SYSTEM
Prfrm prmdicain assssmn; s individual
drug mngraphs fr dails.
EQUIPMENT
• Cmpur-cnrlld dispnsing sysm
• Mdicain prl
TECHNIQUE
1. Fllw h prcdur prcl dscribd arlir.
2. Rad h mdicain prl fr h prscribd
drugs and ims f adminisrain.
3. Accss h cmpur-cnrlld dispnsing sysm
using h scuriy accss cd and passwrd.
4. Slc h pain’s nam frm h lis f pains
n h uni.
5. Rviw h pain’s n-scrn prl and slc
h mdicains  b adminisrd a his im.
6. Chck all aspcs f h n-scrn rdr agains h
mdicain prl.
7. Chck h labl n h uni-ds packag agains
h pain mdicain prl. Chck h xpira-
in das n all mdicain labls.
8. Recheck h svn righs f mdicain adminis-
rain agains h pain mdicain prl and
h uni-ds packag as i is rmvd frm h
drawr.
9. Prcd  h pain’s bdsid.
 • Chck h pain’s idnicain bracl and
vrify i agains h mdicain prl. Hav h
pain sa hir nam and birh da r w
hr idnirs.
 • Wih a cmpurizd scannr sysm, scan
h pain idnificain, h bar cd n
h uni-ds mdicain packag, and h
nurs’s badg, r us h prcl fr h
insiuin.
 • Carfully xplain  h pain h drugs bing
givn; sa hir nams and prvid ducain
abu h drugs bing adminisrd.
 • Chck prinn pain mniring paramrs
(.g., apical puls, rspirary ra).
10. Hand h mdicain  h pain and allw him
r hr  rad h packag labl.
11. Offr h pain a sip f war  facilia h
swallwing f h mdicain. Rriv h uni-
ds packag, pn i, and plac h cnns in h
108 UNIT II Illustrated Atlas of Medication Administration
Fig. 8.12 Tablet crusher. (From Potter PA, Perry AG. Fundamentals of
Nursing. 7th ed. St. Louis: Mosby; 2008.)
pain’s hand r a mdicain cup fr placmn
in h muh.
12. Prfrm hand hygin.
GENERAL PRINCIPLES OF SOLID-FORM
MEDICATION ADMINISTRATION
1. Allw h pain  drink a small amun f war
 misn h muh s ha swallwing h mdi-
cain is asir.
2. Hav h pain plac h mdicain wll -
ward h back f hir ngu. Offr apprpria
assisanc.
3. Giv h pain liquid  swallw h mdicain.
Encurag h pain  kp hir had frward
whil swallwing.
4. Drinking a full glass f uid shuld b ncuragd 
nsur ha h mdicain rachs h smach and
ha i is dilud  dcras h pnial fr irriain.
5. Always rmain wih h pain whil h mdi-
cain is akn. Do not lav h mdicain a h
bdsid unlss an rdr xiss  d s (.g., mdi-
cain such as nirglycrin may b rdrd fr h
bdsid).
6. Discard h mdicain cnainr (.g., a sufé cup,
a uni-ds packag).
7. If h pain has difculy swallwing and if liquid
mdicains ar n an pin, us a abl-crushing
dvic (Fig. 8.12). Ensur ha h mdicain is n
a capsul and ha i is n a imd-rlas r nric-
cad prduc. Fllw h guidlins fr using h
crushing dvic. Mix h crushd mdicain in a
small amun f sf fd such as applsauc, ic
cram, cusard, r jlly; his will hlp cunrac h
bir as and cnsisncy f h mixur.
DOCUMENTATION
Prvid h righ dcumnain f mdicain ad-
minisrain and f h pain’s rspnss  drug
hrapy. If using an cmpur-cnrlld dispnsing
sysm, h da, im, drug nam, ds, and ru
f adminisrain ar aumaically chard in h
lcrnic mdicain adminisrain rcrd whn
h nurs signs in, scans h pain’s idnicain
bracl, and h bar-cdd uni-ds mdicain
packag.
1. Char h da, im, drug nam, dsag, and ru
f adminisrain.
2. Prfrm and rcrd rgular pain assssmns fr
h valuain f h hrapuic ffcivnss (.g.,
bld prssur, puls, inak and upu, imprv-
mn r qualiy f cugh and prduciviy, dgr
and durain f pain rlif).
3. Char and rpr any signs r sympms f advrs
drug ffcs.
4. Prfrm and valida ssnial pain ducain
abu h drug hrapy.
ADMINISTRATION OF LIQUID-FORM
ORAL MEDICATIONS
UNIT-DOSE SYSTEM
Prfrm prmdicain assssmn; s individual
drug mngraphs fr dails.
EQUIPMENT
• Mdicain car
• Mdicain prl
TECHNIQUE
1. Fllw h prcdur prcl dscribd arlir.
2. Rad h pain mdicain prl fr h pr-
scribd drugs and ims f adminisrain.
3. Obain h prscribd mdicain frm h draw-
r in h mdicain car ha is assignd  h
pain.
4. Chck h labl n h uni-ds packag agains
h pain mdicain prl. Chck h xpira-
in das n all mdicain labls.
5. Chck h numbr f dss rmaining in h draw-
r. (If h numbr f dss rmaining is n cnsis-
n, invsiga.)
6. Recheck h svn righs f mdicain adminis-
rain agains h pain mdicain prl and
h uni-ds packag as i is rmvd frm h
drawr.
7. Prcd  h pain’s bdsid.
 • Chck h pain’s idnicain bracl and
vrify i agains h mdicain prl. Hav h
pain sa hir nam and birh da r w
hr idnirs.
 • Carfully xplain  h pain h drugs bing
givn; sa hir nams and prvid ducain
abu h drugs bing adminisrd.
 • Chck prinn pain mniring paramrs
(.g., apical puls, rspirary ra).
8. Hand h mdicain  h pain and allw him
r hr  rad h packag labl.
 Enteral Administration CHAPTER 8 109

mL
30

15 Meniscus

Fig. 8.13 Reading a meniscus. The meniscus is caused by the surface

tension of the solution against the walls of the container. The surface
tension causes the formation of a concave or hollowed curvature on
the surface of the solution. Read the level at the lowest point of the
concave curve.

9. Rriv h uni-ds packag, pn i, and plac

h cnainr in h pain’s hand fr h plac-
mn f h cnns in h pain’s muh.
10. Prfrm hand hygin.

LIQUID-FORM ORAL MEDICATIONS IN

MULTIDOSE CONTAINERS Fig. 8.14 Filling a syringe with medication directly from a bottle.
Sm liquid dsag frms (.g., pdiaric dsags) ar
n availabl in uni-ds packaging bcaus h vl-
um is  small. A small mulids cnainr may b
includd in h uni-ds drawr wih insrucins n
masuring h ds in a mdicin cup r an ral syring.
1. Fllw h prcdur prcl dscribd arlir.
2. Rad h pain mdicain prl fr h pr-
scribd drugs and ims f adminisrain.
3. Obain h prscribd mdicain frm h drawr
in h mdicain car ha is assignd  h pain.
4. Chck h labl n h mulids cnainr agains
h pain mdicain prl. Chck h xpirain
das n all mdicain labls.
5. Chck h numbr f dss rmaining in h cn-
ainr. (If h numbr f dss rmaining is n
cnsisn, invsiga.) Rmv h lid frm h
cnainr.

Measuring With a Medicine Cup
 • Hld h bl f liquid s ha h labl is in h
palm f h hand; his prvns h cnns frm
smaring h labl during puring.
 • Examin h mdicin cup and lca h xac
plac whr h masurd vlum shuld b
masurd.
 • Plac h mdicin cup n a hard surfac; pur
h prscribd vlum a y lvl.
 • Rad h vlum accuraly a h lvl f h
mniscus (Fig. 8.13).
Measuring With an Oral Syringe
S Chapr 9 fr mr infrmain abu rading h
calibrains f a syring.
 • Slc a syring f a siz ha is cmparabl 
h vlum  b masurd.
 • Method 1: Wih a larg-br ndl aachd 
h syring, draw up h prscribd vlum f
Fig. 8.15 Filling a syringe with medication directly from a medicine cup.
mdicain (Fig. 8.14). Th ndl is n nc-
ssary if h bl pning is larg nugh 
rciv h syring.
 • Method 2: Pur h amun f mdicain
ndd in a mdicin cup; hn us a syring
 draw up h prscribd vlum (Fig. 8.15).
6. Rplac h lid n h cnainr.
7. Recheck h svn righs f mdicain adminisrain
agains h pain mdicain prl and h muli-
ds cnainr as i is rmvd frm h drawr.
8. Rurn h mdicain cnainr  h uni-ds car.
9. Prcd  h pain’s bdsid whn all mdica-
ins ar assmbld fr adminisrain.
 • Chck h pain’s idnicain bracl and
vrify i agains h mdicain prl. Hav h
pain sa hir nam and birh da r w
hr idnirs.
110 UNIT II Illustrated Atlas of Medication Administration
Fig. 8.16 Position the infant with the head slightly elevated. Place the
nipple in the infant’s mouth. When the baby starts to suck, place the
medication in the back of the nipple, and allow the baby to suck.
 • Carfully xplain  h pain h drugs bing
givn; sa hir nams and prvid ducain
abu h drugs bing adminisrd.
 • Chck prinn pain mniring paramrs
(.g., apical puls, rspirary ra).
10. Hand h mdicain cup  h pain fr h
placmn f h cnns in hir muh, r ad-
minisr h mdicain via h ral syring.
11. Prfrm hand hygin.
GENERAL PRINCIPLES OF LIQUID-FORM ORAL
MEDICATION ADMINISTRATION
FOR AN ADULT OR CHILD
1. Nvr dilu a liquid mdicain unlss spcically
rdrd  d s.
2. Always rmain wih h pain whil h mdica-
in is akn. Do not lav h mdicain a h bd-
sid unlss an rdr xiss  d s.
FOR AN INFANT
1. Chck h infan’s idnicain bracl and vrify
i agains h mdicain card r prl.
2. B crain ha h infan is alr.
3. Psiin h infan s ha hir had is slighly l-
vad (Fig. 8.16).
4. Adminisrain:
 • Oral syringe or dropper: Plac h syring r drp-
pr bwn h pain’s chk and gums, half-
way back in h muh. This placmn will
rduc h chanc ha h infan will spi u h
mdicain wih ngu mvmns. Slwly in-
jc h mdicain and allw h infan  swal-
lw i. (Rapid adminisrain may caus chking
and aspirain.)
 • Nipple: Whn h infan is awak (and prfrably
hungry), plac h nippl in h infan’s muh.
Whn h baby sars  suck, plac h mdica-
in in h back f h nippl wih a syring r
drppr, and allw h baby  suck i in (s Fig.
8.16). Fllw h mdicain wih milk r frmu-
la, if ncssary.
5. Prfrm hand hygin.
DOCUMENTATION
Prvid h righ dcumnain f h mdicain
adminisrain and h pain’s rspnss  drug
hrapy.
1. Char h da, im, drug nam, dsag, and ru
f adminisrain.
2. Prfrm and rcrd rgular pain assssmns
fr h valuain f hrapuic ffcivnss (.g.,
bld prssur, puls, upu, imprvmn r
qualiy f cugh and prduciviy, dgr and dura-
in f pain rlif).
3. Char and rpr any signs and sympms f ad-
vrs drug ffcs.
4. Prfrm and valida ssnial pain ducain
abu h drug hrapy and hr ssnial aspcs
f inrvnin fr h disas prcss ha is affc-
ing h individual. If h mdicain is fr a child,
prvid and valida ssnial pain ducain 
h cargivr and child, kping in mind h child’s
dvlpmnal lvl. This shuld addrss h drug
hrapy and hr ssnial aspcs f inrvn-
in fr h disas prcss ha is affcing h
individual.
ADMINISTRATION OF MEDICATIONS BY
GASTROINTESTINAL TUBES
GI ubs ar usd  adminisr mdicains  pains
wh hav impaird swallwing,  hs wh ar cma-
s, r  hs wh hav a disrdr f h sphagus.
GI ubs ha ar insrd in hrugh h ns ar calld
nasgasric (NG) ub, nasdudnal (ND) ub, r nas-
jjunal (NJ) ub. GI ubs ha ar surgically insrd
hugh h abdmn in h smach ar calld gas-
rsmy ubs r G-ubs. Th rm percutaneous endo-
scopic gastrostomy (PEG) sands fr h prcdur dur-
ing which h gasrsmy ub is insrd, and shuld
n rfr  h ub islf. During h PEG prcdur a
ub may b insrd in h small insin; his ub is
calld a jjunsmy ub r J-ub. J-ubs, ND ubs,
and NJ ubs ar smims rfrrd  as small bwl
ubs (Fig. 8.17). Whnvr pssibl, h liquid frm
f a drug shuld b usd fr GI ub adminisrain.
If i is ncssary  us a abl r capsul, h abl
shuld b crushd r h capsul pulld apar and h
pwdr sprinkld in apprximaly 10  15 mL f wa-
r. (Do not crush nric-cad abls r pn imd-
rlas capsuls.) Th ub shuld b ushd wih a
las 30 mL f war bfr and afr h mdicin is

Nasogastric Nasoduodenal/nasojejunal
A B
Fig. 8.17 Types of gastrointestinal tubes. (A) Nasogastric tube is passed from the nose into the stomach. (B) Weighted
nasoduodenal/nasojejunal tube is passed through the nose into duodenum/jejunum. (C) Gastrostomy tube is introduced
through a temporary or permanent opening on the abdominal wall (stoma) into the stomach. (D) Jejunostomy tube is
passed through a stoma directly into the jejunum.
adminisrd. This clars h ub fr drug dlivry, fa-
cilias drug ranspr  h insin, and indicas
whhr h ub has bn clard. Whn mr han
n mdicain is  b adminisrd a abu h sam
im, ush 5  10 mL f war bwn ach mdica-
in. (Rmmbr  includ h war ha is usd 
ush h ubing as par f h al war rquirmns
fr h pain fr a 24-hur prid.)
Prfrm prmdicain assssmn; s individual
drug mngraphs fr dails.
EQUIPMENT
• Glass f war
• Tw 60-mL cahr ip syrings
• Masuring cnainr r graduad cylindr
• Pill crushr (as ndd whn mdicains ar n
liquid)
• Twl r small incninnc pad
• pH ap and clr vricain
• Glvs
TECHNIQUE
Rfr  h scins abu h adminisrain f slid-
frm r liquid-frm ral mdicains fr infrmain
abu h prparain f dss.
1. Fllw h prcdur prcl dscribd arlir.
2. Prcd  h pain’s bdsid whn all mdica-
ins ar assmbld fr adminisrain.
 • Chck h pain’s idnicain bracl and
vrify i agains h mdicain prl. Hav h
pain sa hir nam and birh da r w
hr idnirs.
 • Carfully xplain  h pain h prcdur
fr h adminisrain f mdicains in h GI
ub. Sa h drug nams and prvid duca-
in abu h drugs bing adminisrd.
Enteral Administration CHAPTER 8 111
Gastrostomy Jejunostomy
C D
3. Apply clan glvs.
4. Psiin h pain uprigh and chck h lca-
in f h GI ub bfr adminisring any liquid.
(Note: Radigraphic cnrmain f GI ub plac-
mn is prfrmd whn h ub is iniially insr-
d. Thrafr, pH and clr sing may b usd 
cnrm placmn.)
pH and Color Testing of Gastrointestinal Contents
to Check for Tube Placement
• Aspira par f h GI cnns using h 60-mL
cahr ip syring. If unabl  aspira h GI cn-
ns, rpsiin h pain n hir lf sid and ry
aspiraing again.
• Chck h clr f h aspirad uid. Clr vri-
cain guidlins ar as fllws:
 • Gasric uid = grn wih sdimn r ff-whi
 • Insinal uid = yllw (bil-clrd)
 • Plural uid = clar  sraw-clrd
 • Trachbrnchial uid = ff-whi r an
• Chck h pH f h GI cnns. Th smach
pH is lss han 3, h insinal fluid pH is 6 
7, and h rspirary fluid pH is grar han
7. Hisamin-2 (H2) anagniss (.g., ranii-
din, cimidin, famidin, nizaidin) affc
h pH f h aspirad fluid in h fllwing
ways:
 • Ppl n rciving H2 blckrs: gasric pH = 1
 4; insinal pH ≥ 6
 • Ppl rciving H2 blckrs: gasric pH = 1 
6; insinal pH ≥ 6; rachbrnchial r plural
aspira pH ≥ 7
• Rurn h GI cnns afr h cnrmain f cr-
rc ub placmn.
5. Afr h placmn f h GI ub in h prpr l-
cain is cnrmd, adminisr h mdicain.
112 UNIT II Illustrated Atlas of Medication Administration
Two-Syringe Technique for Medication
Administration
• Draw up 60 mL f pid war in h cahr ip
syring. This will b h ush syring.
• Plac a wl r small incninnc pad undr h
GI ub  prc h pain frm any pssibl wa-
r spills.
• Discnnc h GI ub frm sucin (if i was n
sucin) and pinch ub  prvn any backw f
liquid. Aach ush syring.
• Flush wih 30 mL f war  clar h ub. Plac
ush syring, sill cnncd  GI ub, n wl
and bain scnd syring. Fllw agncy prcl,
as vlums may vary.
• Wih scnd 60-mL syring, draw up liquid mdica-
in  b adminisrd; r (if ndd) crush abls,
suspnd in war (apprximaly 5  10 mL), and
hn draw up in syring.
 • Whn adminisring mulipl mdicains, giv
hm n a a im. D n mix h mdicains
ghr in n syring bcaus his may clg h
GI ub.
 • I is bs  hav mulipl mdicain sy-
rings laid u in rdrly fashin fr as f
adminisrain.
• Whn scnd syring is prpard, pinch h GI ub,
discnnc h ush syring, aach syring wih
mdicain, and adminisr mdicain, kping
cahr ip vrical.
• Pinch GI ub  prvn backw, swich  ush
syring, and ush ub wih 10 mL f war fllw-
ing mdicain adminisrain.
• Cninu adminisring mdicains and ush-
ing bwn hm unil all mdicains ar
adminisrd.
• Flush h GI ub wih 30 mL f war whn n-
ishd and clamp ub. Tub shuld rmain clampd
fr 30  60 minus  allw fr absrpin.
• Prvid ral hygin fr h pain, if ndd.
6. Rmv glvs and prfrm hand hygin.
DOCUMENTATION
Prvid h righ dcumnain f mdicain ad-
minisrain and h pain’s rspnss  drug
hrapy.
1. Char h vricain f h GI ub placmn.
2. Char h da, im, drug nam, dsag, and ru
f adminisrain. Includ all uids givn (includ-
ing h uid usd  ush h ub) n h inak
rcrd.
3. Prfrm and rcrd rgular assssmns fr hra-
puic ffcivnss (.g., bld prssur, puls, u-
pu, imprvmn r qualiy f cugh and prduc-
iviy, dgr and durain f pain rlif).
4. Char and rpr any signs and sympms f ad-
vrs drug ffcs.
5. Prfrm and valida ssnial pain ducain
abu h drug hrapy.
ADMINISTRATION OF ENTERAL
FEEDINGS VIA GASTROSTOMY OR
JEJUNOSTOMY TUBE
DOSE FORM
Enral frmulas ar availabl in a variy f mixurs
 m h individual pain’s nds. Th fur gn-
ral cagris ar as fllws: (1) inac nurin (ply-
mric); (2) lmnal; (3) disas r cndiin spcic;
and (4) mdular nurin. Th yp f frmula rdrd
will b slcd by h halhcar prvidr  m h
pain’s nrgy rquirmns  mainain bdy func-
ins and grwh dmands and  rpair issu ha
has bn damagd r dpld by illnss r injury (s
Chapr 46).
EQUIPMENT
• Prscribd nral frmula
• Dispsabl r rady--hang bag fr cninuus
adminisrain
• Infusin pump spcic fr nral frmulas
• Bld glucs sing marials (if bld glucs
lvls rdrd)
• 60-mL cahr ip syring
• 50 mL f war
• Masuring cnainr r graduad cylindr
• pH indicar ap
• Clamp (C clamp r smy plug)
• Twl r small incninnc pad
TECHNIQUE
Psiin h pain in h smi-Fwlr psiin wih a
30-dgr had-f-bd lvain.
1. Fllw h prcdur prcl dscribd arlir.
2. Prcd  h pain’s bdsid.
 • Chck h pain’s idnicain bracl and
vrify i agains h frmula prl. Hav h
pain sa hir nam and birh da r w
hr idnirs.
 • Carfully xplain  h pain h prcdur
usd fr adminisring nral fdings and pr-
vid ducain abu h frmula bing insilld.
3. Chck pain psiining and drap h pain
 avid unncssary xpsur. Plac a wl r
small incninnc pad undr h fding ub
ara  prc h ara in cas f accidnal
spills.
4. Apply clan glvs.
5. If h sma si nds clansing, clans h si as
pr insiuinal plicy.
6. Vrify ub placmn and iniia h fding:
 • Gastrostomy tube (Fig. 8.17C): Aach a 60-mL
cahr ip syring  h clampd ub; rlas
h clamp. Slwly wihdraw h plungr  aspi-
ra h rsidual marial. Obsrv h clr and
chck h pH f h aspirad cnns. (Us h
principls dscribd prviusly in h scin

Fig. 8.18 Example of feeding tube with Luer-Lok ends for use with
Luer-Lok syringes.
n pH and Clr Tsing f Gasric Cnns 
Chck fr Tub Placmn undr Adminisrain
f Mdicains by Nasgasric Tub  aspira
gasric cnns.) Nify h halhcar prvidr
if h rsidual is grar han 100 mL (r amun
spcid) sinc h las blus fding 4 hurs
arlir. Rinrduc h gasric cnns ha
wr aspirad.
 • Jejunostomy tube (Fig. 8.17D): Aspira h in-
sinal scrins using h sam mhd as
dscribd fr a gasrsmy ub. Obsrv h
clr and chck h pH.
7. Flush h ub wih 30 mL f war.
8. Clamp h ub (gasrsmy r jjunsmy).
9. Prcd wih n f h fllwing fding
chniqus.
Intermittent Tube Feeding
 • Using a dispsabl r rady--hang bag, ll h
bag wih h prscribd amun f frmula and
allw  infus by graviy by hanging h bag
n an IV pl. In gnral, his will infus vr
30 minus. Chck frqunly  nsur ha h
frmula is running.
 • Flush h ubing wih 50  60 mL f war afr
h bag is mpy and h frmula is gn. This
rmvs h frmula frm h ubing, mainains
h pancy f h ub, and prvns h fr-
mula ha rmains in h ub frm suppring
bacrial grwh.
 • Clamp r plug h smy ub. Tll h pain
 rmain in h smi-Fwlr psiin r urn
n hir righ sid fr 30  60 minus  hlp
wih h nrmal digsin f frmula and  pr-
vn gasric rux (wih pssibl aspirain) r
lakag.
Enteral Administration CHAPTER 8 113
 • Wash and dry all rusabl quipmn and sr
i in a clan ara in h pain’s nvirnmn
unil h nx fding. Chang h quipmn
(.g., syrings) in accrdanc wih insiuinal
plicy (fn vry 24 hurs).
Continuous Tube Feeding
 • Fill a dispsabl fding cnainr wih nugh
f h prscribd frmula fr an 8-hur prid.
Sr h rmaining frmula in h rfrigrar.
Labl h cnainr wih h da and im ha
h fding was iniiad. Th frmula mus b
a rm mpraur a h im f iniiain.
 • Fding ubs may hav Lur-Lk nds fr
asir aachmn  syrings, prvning h
syrings frm falling u afr bing cnncd
(Fig. 8.18).
 • Prlld fding frmulas ar als availabl
using spikd ubing  cnnc  h bag.
 • Hang h cnainr n an IV pl, clar air frm
h ubing, and hrad h ubing hrugh h
pump in h mannr prscribd by h pump’s
manufacurr.
 • Cnnc h ub frm h nral fding surc
 h nd f h fding ub. Rlas h clamp
frm h ub.
 • S h w ra f h nral frmula a h
prscribd ra  dlivr h frmula in h cr-
rc vlum vr h spcid im span. Whn
iniiaing ub fdings, h ra is iniially slw
and gradually incrasd a spcid inrvals.
 • Wash and dry all rusabl quipmn and sr
i in a clan ara in h pain’s nvirnmn
unil h nx fding. Chang h quipmn
vry 24 hurs.
10. Bld glucs drminain may b prfrmd and
h lvl rcrdd vry 6 hurs during h iniia-
in f ub fdings. Assssmns ar cninud un-
il glucs lvls ar mainaind wihin a spcid
rang fr a 24-hur prid afr h ra f nral
fding has rachd h prscribd maximum w.
11. Whn pains hav a GI ub, inspc h nars
a rgular inrvals  dc any prssur injury
crad by h fding ub. Inspc h issu sur-
runding a gasrsmy r jjunsmy ub fr
signs f brakdwn r infcin.
12. Bfr h nx schduld fding, a gasric r-
sidual vlum shuld b chckd wih syring fr
aspirain  nsur ha h frmula is laving h
smach and passing in h insin fr absrp-
in. Fr rsidual vlums f lss han 100 mL h
rsidual can b radminisrd and h fding can
b rsumd. If h rsidual vlum is grar han
100 mL, h halhcar prvidr shuld b ni-
d. If h rsidual is “cff-grund” in clr, h
halhcar prvidr shuld als b nid bcaus
his may b an indicain f blding dvlping.
13. Prfrm hand hygin.
114 UNIT II Illustrated Atlas of Medication Administration
Medication Safety Alert
Enteral formulas should be properly labeled with the time,
date, type of formula, and strength. Check the date and
time of preparation on a formula that is mixed in the hospital
pharmacy, and discard any unused portion after 24 hours.
Commercially prepared vacuum-sealed formulas are gener-
ally stored at room temperature until used. Check the ex-
piration date and return the product if it is outdated. If the
product has been opened, discard it in accordance with the
manufacturer’s recommendations or institutional policy.
For patients who are receiving enteral nutrition via
intermittent tube feedings (using institutional guidelines),
remember the following:
 • Check the residual volume before each feeding.
 • Check to ensure the presence of bowel sounds. The
absence of bowel sounds indicates the need to contact the
healthcare provider for orders before proceeding.
 • Check the position of the tube to ensure that it is still in
the stomach or intestine.
 • During the initiation of enteral feedings by intermittent
or continuous methods, blood glucose testing may be
ordered.
DOCUMENTATION
Prvid h righ dcumnain f h frmula ad-
minisrd, h clansing f h sma, and h pa-
in’s hrapuic rspns  h nral fdings.
1. Char h da and im; h amun, clr, and pH
f h rsidual ha is aspirad; h amun, yp,
and srngh f h frmula ha is insilld; and h
amun f war ha is usd  ush h ubing.
ADMINISTRATION OF RECTAL
SUPPOSITORIES
DOSE FORM
A suppository (Fig. 8.19) is a slid frm f mdicain ha
is dsignd fr inrducin in a bdy ric. A bdy
mpraur, h subsanc disslvs and is absrbd by
h mucus mmbrans. Suppsiris shuld b srd
in a cl plac  prvn sfning. If a suppsiry b-
cms sf and h packag has n y bn pnd,
hld h fil-wrappd suppsiry undr cld running
war r plac i in ic war fr a shr im unil i hard-
ns. Rcal suppsiris shuld gnrally n b usd fr
pains wh hav had rcn prsa r rcal surgry
r fr hs wh hav xprincd rcn rcal rauma.
Prfrm prmdicain assssmn; s individual
drug mngraphs fr dails.
Fig. 8.19 Rectal suppositories.
EQUIPMENT
• Glvs
• War-slubl lubrican
• Prscribd suppsiry
TECHNIQUE
1. Fllw h prcdur prcl dscribd arlir.
2. Prcd  h pain’s bdsid.
 • Chck h pain’s idnicain bracl and
vrify i agains h mdicain prl. Hav h
pain sa hir nam and birh da r w
hr idnirs.
 • Explain carfully  h pain h prcdur
usd fr adminisring suppsiris. Tll h
pain h drug’s nam and prvid ducain
abu h drug bing adminisrd.
 • Chck prinn pain mniring paramrs
(.g., im f las dfcain, svriy f nausa
r vmiing, rspirary ra) as apprpria 
h mdicain  b adminisrd.
3. Whnvr pssibl, hav h pain dfca b-
fr h suppsiry is adminisrd.
4. Prvid fr pain privacy; psiin and drap
h pain  avid unncssary xpsur (Fig.
8.20A). Gnrally, h pain is placd n hir lf
sid (i.., lf laral rcumbn psiin).
5. Apply clan glvs.
6. Ask h pain  bnd h upprms lg ward
h wais.
7. Unwrap h suppsiry, and apply a small amun
f war-slubl lubrican  is ip (Fig. 8.20B and
C). If lubrican is n availabl, us plain war 
misn h mdicain. Do not us prlum jlly
r minral il bcaus i may rduc h absrp-
in f h mdicin.
8. Plac h ip f h suppsiry a h rcal n-
ranc. Ask h pain  ak a dp brah and
 hn xhal hrugh h muh (many pains
will xprinc an invlunary rcal gripping
whn h suppsiry is prssd agains h rc-
um). Gnly insr h suppsiry abu an inch
bynd h ric and pas h inrnal sphincr
(Fig. 8.20D). Whn insring h suppsiry, us
h indx ngr fr an adul r h furh ngr fr
an infan.
9. Ask h pain  rmain lying n hir sid fr 15
 20 minus  allw fr h mling and absrp-
in f h mdicain.
 • Fr childrn, i is ncssary  cmprss h
bucks gnly bu firmly and  hld hm
in plac fr 15  20 minus  prvn
xpulsin.
10. Discard usd marials and rmv glvs.
11. Prfrm hand hygin.
DOCUMENTATION
Prvid h righ dcumnain f mdicain admin-
israin and h pain’s rspnss  drug hrapy.
 Enteral Administration CHAPTER 8 115

1. Char h da, im, drug nam, dsag, and ru
f adminisrain.
2. Prfrm and rcrd rgular pain assssmns
fr h valuain f hrapuic ffcivnss. Fr
xampl, whn a mdicain is givn as a laxaiv,
char h clr, amun, and cnsisncy f sl. If
a drug is givn fr pain rlif, char h dgr and
durain f pain rlif. If h suppsiry is givn
as an animic, char h dgr and durain f
rlif f nausa and vmiing.
3. Char and rpr any signs and sympms f ad-
vrs drug ffcs.
4. Prfrm and valida ssnial pain ducain
abu h drug hrapy.
ADMINISTRATION OF A DISPOSABLE
ENEMA
DOSE FORM
Th ds frm is a prpackagd, dispsabl nma s-
luin f h yp prscribd by h halhcar prvidr.
Prfrm prmdicain assssmn; s individual
drug mngraphs fr dails.
EQUIPMENT
• Til issu
• Bdpan, if pain is n ambulary
• War-slubl lubrican
• Glvs
• Prscribd dispsabl nma ki
TECHNIQUE
1. Fllw h prcdur prcl dscribd arlir.
2. Prcd  h pain’s bdsid.
 • Chck h pain’s idnicain bracl and
vrify i agains h mdicain prl. Hav h
pain sa hir nam and birh da r w
hr idnirs.
 • Explain carfully  h pain h prcdur
usd fr adminisring an nma and prvid
ducain abu h sluin bing adminis-
rd. Dpnding n h purps f h nma,
ask h pain  dfca if hr is an urg pri-
r  h prcdur.
 • Chck prinn pain mniring paramrs
(.g., h im f las dfcain).
3. Psiin h pain n hir lf sid, and drap
h pain  avid unncssary xpsur (Fig.
8.21A).
4. Apply clan glvs. Rmv prciv cvring
frm h nd f h nma and lubrica h nd
(Fig. 8.21B).
5. Insr h lubricad nd in h pain’s rcum
and hn dispns h sluin by cmprssing h
plasic cnainr (Fig. 8.21C).
6. Rplac h usd cnainr in is riginal packag
fr dispsal (Fig. 8.21D).
7. Encurag h pain  hld h sluin fr
abu 30 minus bfr dfcaing.
8. Assis h pain  a siing psiin n h bd-
pan r  h bahrm, as rdrs prmi.
9. Tll h pain not  ush h il. Th rsuls f
h nma nd  b dcumnd. Insruc h pa-
in rgarding h lcain f h call ligh in cas
assisanc is ndd.
10. Rmv and discard glvs.
11. Prfrm hand hygin.
DOCUMENTATION
Prvid h righ dcumnain f mdicain admin-
israin and h pain’s rspnss  drug hrapy.
1. Char h da, im, drug nam, dsag, and ru
f adminisrain.
2. Prfrm and rcrd rgular pain assssmns
fr h valuain f h hrapuic ffciv-
nss (.g., clr, amun, and cnsisncy f
sl).
3. Char and rpr any signs and sympms f ad-
vrs drug ffcs.
4. Prfrm and valida ssnial pain ducain
abu h drug hrapy.

A B C D
Fig. 8.20 Administering a rectal suppository. (A) Position the patient on their left side and then drape the patient. (B)
Unwrap the suppository and remove it from its package. (C) Apply water-soluble lubricant to the suppository. (D) Gently
insert the suppository about 1 inch past the internal sphincter. (Courtesy Chuck Dresner.)
116 UNIT II Illustrated Atlas of Medication Administration

A B

C D
Fig. 8.21 Administering a disposable enema (Fleet enema). (A) Place the patient in a left lateral position, unless a knee-
chest position has been specied. (B) Remove the protective covering from the end of the enema and lubricate the end.
(C) Insert the lubricated end into the patient’s rectum and dispense the solution by compressing the plastic container. (D)
Replace the used container in its original wrapping for disposal.
 Enteral Administration CHAPTER 8 117

Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions

Key Points 2. A nursing instructor reviewed the different types of techniques

used when getting medications from different systems.
• Solid dose forms of medications include capsules, timed-
release capsules, lozenges, tablets, caplets, and orally Mark an X under the correct column for the procedures used in the
disintegrating tablets and lms. unit-dose system and the computer-controlled system.
• Liquid dose forms for medications include elixirs,
emulsions, suspensions, and syrups.
COMPUTER-
• The unit-dose system uses individual packaged UNIT-DOSE CONTROLLED
medications that are distributed to each patient using PROCEDURES SYSTEM SYSTEM
a medication cart. The computer-controlled dispensing
system uses unit-dose medications distributed in a locked, Compares the label with the
password-protected medication system using a computer patient prole
and bar code scanner system. Uses bar code scanner to
• Liquid forms of medications are administered by unit-dose connect the nurse, patient,
container or oral syringe, or by GI tube. and medication
• Medications administered via GI tubes require checking Checks expiration date on
placement of the tube before administration and using label
the correct technique to ensure all medication is given Uses security access code
accurately. Tube feedings are administered via GI tubes Obtains medications from
also and proper technique for handling formulas and cart with drawer assigned
checking residuals need to be followed. to patient
• Rectal suppositories and enemas are administered with
the patient positioned on their left side and inserted with a
water-based lubricant. Objective: Compare the different techniques that are used with a
unit-dose distribution system and computer-controlled distribution
system.
Additional Learning Resources
NGN test item: Matrix
SG Go to your Study Guide for additional Review Questions for Cognitive skill: Recognize cues
the NCLEX® Examination, Critical Thinking Clinical Situations, and
3. The nurse needs to administer guaifenesin syrup to a 5-year-old.
other learning activities to help you master this chapter content.
List in order the steps the nurse will take.
Go to your Evolve website (https://evolve.elsevier.com/Willihn 1. Pour the correct volume of liquid in a medicine cup
ganz) for additional online resources. reading the meniscus at eye level.
2. Document the administration of the medicine in the
Clinical Judgment and Next-Generation NCLEX® Exam- patient’s chart.
ination-Style Questions The following questions are typical of 3. Hold the bottle containing the liquid so the label is
the NCLEX examination and include both NGN (Next Genera- covered with the palm of the hand.
tion) and traditional questions. See Chapter 1 for further infor- 4. Review the order for the number of milligrams of medicine
mation regarding question types. or the volume the liquid to be administered.
1. Choose the most likely options for the information missing from 5. Identify the patient through two identiers and hand the
the sentence below by selecting from the lists of options provided. medication to the patient for ingestion.
6. Check the expiration date on the medicine.
When administering medications via the enteral routes the nurse
7. Review the label to assure correct medicine and
uses the ___________1__________ or _______1__________
appropriate concentration of the liquid (e.g., number of
route, and the nurse may have to crush the _______2__________
mg per mL) and calculate the volume to be poured into
or ________2____________ dosage forms for easier delivery.
the cup.
Objective: Identify general principles used for liquid-form
OPTIONS FOR 1 OPTIONS FOR 2
medication administration.
intravenous tablets NCLEX test item: Ordering
gastrointestinal lozenges Cognitive skill: Application
oral caplets 4. The nurse is to administer several medications to the patient via a
rectal timed-release capsules GI tube. What is the nurse’s rst action?
1. Add the medication to the tube feeding being given.
Objective: Describe the general principles of administering solid 2. Crush all tablets and capsules before administration.
forms of oral medications. 3. Administer all of the medications mixed together.
NGN test item: Cloze 4. Check for the placement of the tube.
Cognitive skill: Recognize cues
118 UNIT II Illustrated Atlas of Medication Administration

Objective: Cite the equipment needed, techniques used, and Objective: Cite the equipment needed and the technique required
precautions necessary when administering medications via a GI tube. when administering rectal suppositories and disposable enemas.
NCLEX test item: Multiple choice NCLEX test item: Drag and drop
Cognitive skill: Knowledge Cognitive skill: Application
5. When administering an intermittent enteral feeding to an adult 7. Why is it important for the nurse to not crush medications that are
patient, the nurse nds that the residual aspirate returned is considered long-acting?
“coffee-ground” in color. What does the nurse do? 1. Medications that are crushed are harder to swallow,
1. Administer the next scheduled feeding making it harder to activate the effect.
2. Stop feeding the patient for 30 minutes 2. Medications that are crushed release the drug
3. Notify the healthcare provider immediately, stopping the long-acting effect, potentially
4. Reinstill the aspirate and start a new feeding causing an overdose.
Objective: Cite the equipment needed, techniques used, and 3. Medications that are crushed will not be absorbed
precautions necessary when administering medications via a GI properly, inactivating the long-acting effect.
tube. 4. Medications that are crushed will become powder and
NCLEX test item: Multiple choice lose all the effectiveness of the drug.
Cognitive skill: Comprehension Objective: Describe principles of administering solid forms of oral
medications.
6. The nurse received an order to administer a rectal suppository. NCLEX test item: Multiple choice
Indicate with an X the correct technique and correct equipment Cognitive skill: Understanding
necessary for proper administration.
8. The nurse is aspirating the patient’s GI tube to check the contents.
CORRECT CORRECT What can the nurse expect for results if the contents are gastric
TECHNIQUE/EQUIPMENT TECHNIQUE EQUIPMENT uid?

Gently insert suppository past 1. pH of 8, clear colored

the internal sphincter 2. pH of 3, green with sediment
3. pH of 7, yellow colored
Position the patient on their 4. pH of 4, off-white colored
left side
Objective: Cite the equipment needed, techniques used, and
Obtain a water-soluble
precaution necessary when administering medication via a GI tube.
lubricant
NCLEX test item: Multiple choice
Ask the patient to remain on Cognitive skill: Knowledge
their side for 20 minutes
Remove suppository from
unit-dose wrapper
Explain the procedure and
educate the patient on the
drug being administered
Obtain clean gloves
Parenteral Administration: Safe Preparation of
Parenteral Medications
9
https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify safe administration practices for parenteral
medications.
2. Compare and contrast the volumes of medications that
can be measured in a tuberculin syringe and those of
larger-volume syringes.
3. Describe how to select the correct needle gauge and
length.
4. Compare and contrast the advantages and disadvantages
of using prelled syringes.
5. Differentiate among ampules, vials, and Mix-O-Vials.
6. Describe the technique used to prepare two different drugs
in one syringe (e.g., insulin).

Key Terms
barrel (BĂ-rŭl) (p. 120)
plunger (PLŬN-jŭr) (p. 120)
tip (p. 120)
milliliter scale (MĬL-ĭ-lē-tŭr) (p. 120)
tuberculin syringe (tū-BĔR-kū-lĭn sĭ-
RĬNJ) (p. 120)
insulin syringe (ĬN-sŭ-lĭn) (p. 121)
prelled cartridges and syringes
(prē-FĬLD) (p. 122)
insulin pen (p. 122)
needle gauge (NĒ-dŭl GĀJ) (p. 124)
safety devices (SĀF-tē dĕ-VĪ-sĕz)
(p. 126)
ampules (ĀM-pyūlz) (p. 126)
vials (VĪ-ălz) (p. 126)
Mix-O-Vials (MĬKS Ō VĪ-ălz) (p. 128)

Th rus f drug adminisrain can b classid in
hr cagris: nral, parnral, and prcuanus.
Th rm parenteral mans adminisrain by any ru
hr han h nral—r gasrinsinal—rac. As
rdinarily usd, h rm parenteral route rfrs  inra
drmal (ID), subcuanus (subcu), inramuscular
(IM), r inravnus (IV) injcins.
Whn drugs ar givn parnrally rahr han
rally, h fllwing facrs ar invlvd: (1) h ns
f drug acin is gnrally mr rapid bu f shrr
durain; (2) h dsag is fn smallr bcaus drug
pncy nds n  b alrd immdialy by h
smach r livr; and (3) h cs f drug hrapy is f
n highr. Drugs ar adminisrd by injcin whn
all f h drug mus b absrbd as rapidly and cm
plly as pssibl, whn h drug mus b absrbd
a a sady and cnrlld ra, r whn a pain is
unabl  ak a mdicain rally bcaus f nausa
and vmiing.
Safe PreParation, adminiStration, and
diSPoSal of Parenteral medicationS and
SuPPlieS
Drug prparain and adminisrain rrrs hav bn
idnid as cnribuing facrs  h high incidnc
f advrs drug vns as discussd in Chapr 6. Th
acual ra f rrrs ha ccur during h prparain
and adminisrain f mdicains is n knwn, bu
h pnial is high. Thus h nurs mus b dilign
 prvn rrrs frm ccurring.
Th rl f h nurs in prviding accura drug
adminisrain rquirs anin  dail in all facs
f pharmachrapy. I is ssnial ha nurss wh ar
prparing and adminisring mdicains fcus n h
fllwing: (1) h basic knwldg ndd rgarding
h individual drugs bing rdrd, prpard, and ad
minisrd; (2) h sympms fr which h mdicain
is prscribd and h cllcin f baslin daa  b
usd fr h valuain f h hrapuic ucms
dsird fr h prscribd mdicin; and (3) h nurs
ing assssmns ncssary  dc, prvn, r am
lira advrs vns. Finally, h nurs mus xrcis
clinical judgmn rgarding h schduling f nw
drug rdrs, missd dss, mdid drug rdrs, h
subsiuin f hrapuically quivaln mdicins
by h pharmacy, r changs in h pain’s cndiin
ha rquir cnsulain wih a physician, halhcar
prvidr, r pharmacis.
Injcin f drugs rquirs skill and spcial car
bcaus f h rauma a h si f ndl puncur,
h pssibiliy f infcin, h chanc f allrgic rac
in, and h fac ha, afr i is injcd, h drug is
irrrivabl. Thrfr mdicains mus b prpard
and adminisrd carfully and accuraly. Aspic
chniqu is usd during injcin  avid infcin.
Crrc ra f drug adminisrain and crrc si f
injcin ar fllwd  avid injuris such as abscss
119
120 UNIT II Illustrated Atlas of Medication Administration
Tip Barrel Plunger
Fig. 9.1 Parts of a syringe.
frmain, ncrsis, skin slughing, nrv injuris, and
prlngd pain. Thus h parnral adminisrain f
mdicains rquirs spcializd knwldg and man
ual skills  nsur safy and hrapuic ffcivnss
fr pains.
Halhcar prfssinals plac h safy f hir
pains rs, bu h Occupainal Safy and Halh
Adminisrain (OSHA) has rprd ha mr
han 5 millin wrkrs in h halhcar indusry
and rlad ccupains ar a risk fr ccupainal
xpsur  bldbrn pahgns ha can caus
dvasaing disass, including human immun
dcincy virus, hpaiis B virus, and hpaiis C
virus. Sudis hav indicad ha as many as n
hird f all sharps injuris (i.., frm ndls, lan
cs, and scalpls) ar rlad  h dispsal prcss
and ha nurss susain h majriy f hs injuris.
Cnsqunly, nurss hav hr primary safy cn
crns: fr h pain, fr hmslvs, and fr hr
halhcar wrkrs. Paramun  h saf adminis
rain f mdicins is h nd fr nurss  fllw
sablishd plicis and prcdurs whil chcking
and vrifying rdrs; prparing, adminisring, r
crding, and mniring hrapuic rspnss 
drug hrapy; and prprly dispsing f parnral
supplis and quipmn.
equiPment uSed for Parenteral
adminiStration
SyringeS
Syrings ar gnrally mad f hard plasic; glass sy
rings ar rarly usd in clinical pracic. A syring has
hr pars (Fig. 9.1). Th barrel is h ur prin n
which h calibrains fr h masurmn f h drug
vlum ar lcad (Fig. 9.2). Th plunger is h innr
cylindrical prin ha s snugly in h barrl. This
prin is usd  draw up and jc h sluin frm
h syring. Th tip is h prin ha hlds h ndl.
Syrings ar cnsidrd  b sril whn h packag
is sill inac frm h manufacurr. Th nurs will r
mv h ur shah ha cvrs h syring and hn
hld h barrl; h usid f h barrl is hn cnsid
rd unsril r cnaminad, whras h insid f
h barrl rmains sril. Nurss mus kp h ip f
h syring sril whn cnncing ndls.
All syrings, rgardlss f hir manufacurr, ar
availabl wih a LurSlip r LurLk ip. Th Lur
sysm cnsiss f w pars: h mal aprd nd
(Fig. 9.3A) and h rvrsaprd fmal cnncr
wih an ur ang (Fig. 9.3B).
1
2
1
1
2
30M
1
2 2
0.5 1
mL
0.1
mL
2
3 mL 3
mL
Fig. 9.2 Reading the calibrations of a 3-mL syringe.
Th w yps f syring ips ar h LurSlip, which
has a mal aprd nd (Fig. 9.4A), and h LurLk
(Fig. 9.4B), which has a hradd lcking cllar usid
f h mal LurSlip ha will lck h ang f h
fmal cnncr scurly. Whn h fmal cnnc
r is placd n a mal LurSlip wih a lcking cllar
and givn a half wis, i is scurly lckd in plac (s
Fig. 9.3C r Fig. 9.4B). Hwvr, if a fmal adapr is
placd n a mal LurSlip wihu a cllar (s Fig.
9.4A), h cnncin is nly rlaivly scur.
S Cabat
A syring is calibrad in millilirs (mL) (s Fig.
9.2). Th ms cmmnly usd syrings ar 1, 3, and
5 mL, bu syrings f 10, 20, and 50 mL ar als avail
abl. (N: Tchnically, h millilir is a masur f
vlum.)
Reading the calibration of the syringe
m s. Th milliliter scale rprsns h unis
whrby mdicains ar ruinly rdrd. Fr vl
ums f 1 mL r lss, us a 1mL r ubrculin syring
fr h mr prcis masurmn f h drug (Fig.
9.5). Millilirs ar rad n h scal markd “mL” (s
Figs. 9.2 and 9.5). Th shrr lins rprsn 0.1 mL,
and h lngr lins ach rprsn 0.5 mL.
t sg. Th tuberculin syringe, r 1mL
syring, was riginally dsignd  adminisr ubr
culin inculains (s Fig. 9.5). Tday i is usd 
masur small vlums f mdicain accuraly. This
yp f syring hlds a al f 1 mL; ach f h lng
s lins rprsns 0.1 ({1/10}) mL, h inrmdia
 Parenteral Administration: Safe Preparation of Parenteral Medications CHAPTER 9 121

Male tapered end

Flange

3mL
11/2

21/2
2
A

1/

2
1
B Reverse-tapered
female connector
Hub
Threaded locking collar

3mL
11/2

21/2
2
1/

2
C

1
Fig. 9.3 The Luer system consists of two parts: the male tapered end (A) and the reverse-tapered female connector with
an outer ange (B). (C) When the two components are joined together, the hub of the female connector slips over the
male tapered end and is twisted so that the ange on the hub locks into the threads of the locking collar.

Measure dose here

1
5

2
A
Avoid Keep sterile
touching

Fig. 9.6 Reading the measured amount of medication in a plastic

syringe.
B
Fig. 9.4 (A) Male slip adapter tip (Luer-Slip). (B) Male slip adapter with
outer locking collar (Luer-Lok). (Courtesy and © Becton, Dickinson and
lins rprsn 0.05 ({5/100}) mL, and h shrs lins
Company, Franklin Lakes, NJ.) rprsn 0.01 ({1/100}) mL.
Vlums in dispsabl plasic syrings ar rad a
h pin whr h rubbr ang f h syring plung
r is paralll  h calibrain scal f h barrl (Fig.
9.6). In addiin, n h ara f h ndl  kp
sril and h ara n h syring plungr  avid
uching.
is sg. Th insulin syringe has a scal ha
has bn spcically calibrad fr h masurmn f
insulin. Insulin is nw manufacurd wih a U100 cn
cnrain in h Unid Sas. Th U100 syring (Fig.
9.7A) hlds 100 unis f insulin pr millilir. Variains
may b nicd in h way ha unis ar markd n
h scal, bu in gnral h shrr lins rprsn 2
unis f insulin, whras h lngr lins masur 10
unis f insulin. Lwds insulin syrings (Fig. 9.7B)
may b usd fr pains wh ar rciving 50 unis r
lss f U100 insulin. Th shrr lins n h scal f
h lwds insulin syring masur 1 uni, whras
h lngr lins ach rprsn 5 unis. Whn ravling
abrad, pains shuld b awar ha U40 cncnra
in insulin (i.., 40 unis f insulin/mL) is cmmnly
availabl. A spcic insulin syring ha has bn cali
brad fr U40 insulin shuld b usd wih h U40
insulin.
Insulin dlivry aids (.g., nnvisual insulin
masurmn dvics, syring magnirs, ndl
Fig. 9.5 Tuberculin syringe calibration. guids, vial sabilizrs) ar availabl fr ppl wih
122 UNIT II Illustrated Atlas of Medication Administration
10 Units 5 Units
2 Units 1 Unit
A B
Fig. 9.7 Calibration of insulin syringes. (A) U-100 insulin syringe. (B)
Low-dose insulin syringe. Low-dose syringes are available in 25-, 30-,
and 50-unit sizes to measure U-100 insulin more accurately.
visual impairmns. Infrmain abu hs prducs
is availabl in h Amrican Diabs Assciain’s an
nual diabs rsurc guid, which is publishd ach
January.
Life Span Considerations
Tuberculin Syringe
The tuberculin syringe (see Fig. 9.5), which makes use of
the metric system of measurement, will provide the most ac-
curate measurement for doses of parenteral medications of
1 mL or less. The practice of adding 0.2 mL of air bubbles
to thoroughly empty all of the medication contained in the
needle of a syringe can signicantly increase a drug dose,
especially when small volumes of medicine are being ad-
ministered to neonates or infants. Check institutional policy
regarding medication administration for the procedure to be
used.
P Cats a Ss
Svral manufacurrs supply a prmasurd amun
f mdicain ihr in prsald carridgndl
unis r in prlld cmpl syrings. Bh ar usd
nc and hn discardd. Advanags f h prelled
cartridges and syringes includ h im savd in pr
paring a sandard amun f mdicain fr n injc
in and h diminishd chanc f cnaminain b
wn pains and hspial prsnnl. Disadvanags
includ addiinal xpns and h limiain f h
vlum if a scnd mdicain is  b addd  h
carridg r syring.
Th prlld carridgndl unis ar markd
undr h brand nam Carpujc. Th carridg cn
ains h amun f drug fr n sandard ds f
mdicain. Th drug nam, cncnrain, and vl
um ar clarly prind n h carridg. Th Carpujc
prlld carridgs rquir a hldr ha crrspnds
wih h yp f carridg usd (Fig. 9.8). Exampls f
drugs dispnsd in prlld carridgs ar mrphin,
krlac, hydrmrphn, ndansrn, and hparin.
Ohr mdicins (.g., spcic vaccins, nxaparin,
dalparin, diclfnac, amidarn) ar shippd frm
h manufacurr in a syring fr as f us. Many
hspial pharmacis prll syrings fr spcic dss
f mdicain fr pains wih spcic cndiins.
Th syring is labld wih h drug nam and dsag,
h pain’s nam and rm numbr, and h das f
prparain and xpirain.
Insulin is als availabl in a prlld syring knwn
as an insulin pen (Fig. 9.9). Whn cappd, hs pns
lk vry much lik ink pns, which allws h pain
 carry insulin in a discr mannr. Whn ndd, h
cap is rmvd, a ndl is aachd, air bubbls ar r
mvd, h ds is diald in, h ndl is insrd in
h subcu issu, and a riggr is pushd  injc h
masurd ds. Whn nishd, h ndl is rmvd
and h cap rplacd, and h dvic again aks n
h apparanc f a pn. Ths pns ar availabl in a
variy f clrs and syls, including a prlld, dis
psabl mdl; a smallr, lwds mdl; and a rll
abl mdl in which a nw carridg can b insrd
whn ndd. Th pain shuld b insrucd rgard
ing h crrc mhd f hlding h pn and rading
h dsing dial as indicad by h manufacurr; his
will hlp prvn dsing rrrs.
Anhr yp f prlld syring is h EpiPn (Fig.
9.10). This syring is a dispsabl aumaic injcin
dvic ha has bn prlld wih pinphrin fr us
in an mrgncy, such as ha causd by an allrgic rac
in  insc sings r bis, fds, r drugs. Whn hld
prpndicularly agains h high and acivad, a n
dl pnras h skin in h muscl, and a singl ds
f pinphrin is injcd in h muscl. This prduc
is availabl in adul and pdiaric dsags fr us a
hm r whn ravling fr hs wh hav srng rac
ins whn hy ar xpsd  allrgns. I is impr
an  duca hs wh ar carrying hs prlld
syrings  mnir h xpirain da f his mdica
in n a rgular basis. Afr h pinphrin has bn
adminisrd, h prsn shuld g  a hspial mr
gncy dparmn bcaus addiinal ramn may b
ncssary. Ohr rcnly rlasd prducs f injcabl
pinphrin fr allrgis ar AuviQ and Impax.
The needle
Pats  t n
Th ndl pars ar h hub, h shaf, and h bvld
ip (Fig. 9.11). Th angl f h bvl can vary; h ln
gr h bvl, h asir h ndl pnrain.
Ndls ar sril whn hy arriv frm h man
ufacurr. Nurss mus pay carful anin  kp
h pars f h ndl sril and  avid cnamina
in. If cnaminain is suspcd during h prcss
f wihdrawing mdicains, discard h ndl in a
sharps cnainr and sar again wih a nw n.
 Parenteral Administration: Safe Preparation of Parenteral Medications CHAPTER 9 123

A B

E F
Fig. 9.8 (A) Carpuject cartridge holder and prelled sterile cartridge with needle. (B) Assemble the Carpuject by inserting
the prelled cartridge inside the Carpuject holder; lay the white ange of the syringe over one end and lock the blue end
down to keep the syringe in place. (C) Twist the white end to screw into the prelled cartridge. (D and E) Remove the
green cover from the tip of the cartridge (D); keeping this end sterile, attach the needle to the cartridge (E). (F) Needle is
now attached to the prelled cartridge in a Carpuject cartridge holder.

Fig. 9.9 An insulin pen. (Copyright Eli Lilly and Company, Indianapolis, Fig. 9.10 Prelled syringe and needle containing epinephrine for use
IN. All rights reserved. Used with permission.) during emergencies. (Courtesy Mylan Inc., Canonsburg, PA.)
124 UNIT II Illustrated Atlas of Medication Administration

Beveled tip
Table 9.1 Selection of Syringe and Needle
Volume
route (ml) GauGe lenGth
Intradermal 0.01–0.1 26–29 ⅜ to ½ inch
Shaft Subcutaneous 0.5–2 25–27 Individualized on
the basis of
the depth of
the appropriate
tissue at the site
Intramuscular 0.5–2b 20–25c Individualized on
the basis of
the depth of
Hub the appropriate
tissue at the site
aWhen judging the needle length, allow an extra ¼ to ½ inch to remain above
the skin surface when the injection is administered. In the rare event of a needle
Fig. 9.11 Parts of a needle. breaking, this allows a length of needle to protrude above the skin to grasp for
removal.
bDivided doses are generally recommended for volumes that exceed 2 to 3 mL,

particularly for medications that are irritating to the tissues.

cUse larger gauge (smaller bore) needles for thinner, more frail patients with
Gauge Length
smaller muscle mass.

15G
11 2" 2 "
ndl lngh fr h dlivry f h mdicain  h
18G crrc si (.g., ID, subcu, IM, r IV). Tabl 9.1 may b
11 2" 2 "
usd as a guid  slc h prpr vlum f syring
20G
and h lngh and gaug f ndl fr adul pains.
1" 11 2" In small childrn and ldr infans, h usual maxi
mum vlum fr an IM injcin a n si is 1 mL. In
22G
1" 11 2" small infans, h muscl mass may nly b abl  l
ra a vlum f 0.5 mL using a ½inch–lng ndl.
23G Fr ldr childrn, h vlum shuld b individual
1" 11 2 "
izd; gnrally, h largr h muscl mass, h grar
25G h similariy  h adul vlum fr n injcin si.
5 8"
Pdiaric IM injcins ruinly us a 25  27gaug
ndl ha is 1  1½ inchs lng, dpnding n h as
26G
1 2" 3 8" sssmn f h dph f h muscl mass f h child.
Als availabl fr pdiaric us ar 31gaug, ½inch
28G
1 2" 3 8" ndls.
Fig. 9.12 Needle length and gauge.
Sct  n lt
Assss h dph f h pain’s issu fr adminisra
n ga in (.g., muscl issu fr IM adminisrain, subcu
Th needle gauge is h diamr f h hl hrugh issu fr subcu injcin), and chs a ndl lngh
h ndl. Th largr h gaug numbr, h smallr ha crrspnds  h ndings.
h hl. Th gaug numbr is markd n h hub f h Example of How to Select Needle Length
ndl and n h usid f h dispsabl packag. Th Cmpar h muscl dph f a 250pund, bs,
prpr ndl gaug is usually slcd n h basis f sdnary wman wih h muscl dph f a
h viscsiy (hicknss) f h sluin  b injcd. A 105pund, dbiliad adul pain. An individual
hickr sluin rquirs a largr diamr, s a smallr wh is bs may rquir a 2½  3inch ndl, and
gaug numbr is chsn (Fig. 9.12). Finr ndls (.g., 27, h frail prsn may nd a 1  1½inch ndl. A
29, 31, and 32 gaug) ar availabl fr spcialy us. child may rquir a 1inch ndl (Fig. 9.13).

SeleCTion of The Syringe And needle PACkAging of SyringeS And needleS

Th siz f h syring usd is drmind by h vl
um f mdicain  b adminisrd, h dgr f
accuracy ndd fr h masurmn f h ds, and
h yp f mdicain  b adminisrd.
Ndl slcin shuld b basd n h crrc
gaug fr h viscsiy f h sluin and h crrc
Th sriliy f h syring and ndl  b usd shuld
always b inspcd and vrid whn prparing and
adminisring a parnral mdicain. Wrapprs
shuld b chckd fr hls, signs f misur pn
rain f h wrappr, and h xpirain da. Wih
prpackagd dispsabl ims, h cninuiy f h
 Parenteral Administration: Safe Preparation of Parenteral Medications CHAPTER 9
A Overweight adult
3"
Epidermis
Dermis
Subcutaneous
Muscle
B
Fig. 9.13 Use body size (A) to estimate needle length for an intramuscular injection (B).
wrappr, ls lids r ndl guards, and any pn
rain f h papr r plasic cnainr by h ndl
shuld als b chckd. Shuld cnaminain b sus
pcd, d n us h syring.
Safety SyStemS for Parenteral
PreParation, adminiStration, and diSPoSal
Th US Cngrss passd h Ndlsick Safy and
Prvnin Ac in 2000 in rspns  sharps injuris
frm mdical dvics, ms cmmnly ndlsicks.
This ac rquirs OSHA  upda is sandards n
bldbrn pahgns fr h clsr mniring and
rpring f ndlsick injuris and  manda h
dvlpmn f nw safy quipmn fr h halh
car indusry. On f h majr dvlpmns has bn
125
Ideal weight adult Child
11 2 "
Epidermis
Dermis
1"
Epidermis
Subcutaneous Dermis
Subcutaneous
Muscle
Muscle
h bradr us f ndllss sysms. In accrdanc
wih OSHA rgulains, ndllss sysms ar r
quird fr h fllwing: (1) fr h cllcin f bdy
uids r h wihdrawal f bdy uids afr iniial v
nus r arrial accss is sablishd; (2) fr h admin
israin f mdicain r uids; r (3) fr any hr
prcdur invlving h pnial fr ccupainal x
psur  bldbrn pahgns as a rsul f prcu
anus injuris frm cnaminad sharps. Ndllss
sysms prvid an alrnaiv  ndls fr ruin
prcdurs, hrby rducing h risk f injury invlv
ing cnaminad sharps. Anhr dlivry sysm un
dr dvlpmn is a j injcin sysm ha dlivrs
subcu injcins f liquid mdicain (.g., insulin,
vaccin) hrugh h skin wihu rquiring h us f
a ndl.
126 UNIT II Illustrated Atlas of Medication Administration
A and i has a vry lw was spac in h hub (s Fig. 9.18).
b
B c
a
Fig. 9.14 Needle-free access devices. (A) INTERLINK Vial Access
Cannula entering a universal vial adapter. (B) CLAVE Access System.
a, A needle-free multidose vial adapter. b, The device snaps onto the
top of a standard 20-mm medication vial. c, A single-dose vial adapter.
(A, Courtesy Baxter Healthcare Corporation, Mountain Home, AR. All
rights reserved. B, Courtesy ICU Medical Inc., San Clemente, CA.)
BlunT ACCeSS deviCeS
Th blun accss dvic (.g., h spik) is a safy innva
in ha was crad  rduc h frquncy f ndl in
juris (Fig. 9.14). N in ha ndllss accss dvics d
n hav a sainlss sl ndl ha is suiabl fr injcin
(Fig. 9.14A). Th spik is usd whn drawing liquid frm a
rubbr diaphragm–cvrd vial (Fig. 9.14B). Anhr yp
f blun accss dvic ha is mr cmmnly knwn as a
lter needle lks similar  hr spiks, bu i cnains an
inrnal lr. This dvic is usd  wihdraw liquid frm
a glass ampul. Th lr scrns u glass paricls ha
may hav falln in h ampul whn h p was brkn
ff (s Fig. 9.23). In addiin  prvning ndlsick
injuris, hs blun accss dvics hav h advanag
f drawing largr uid vlums frm h cnainr mr
rapidly. Afr h spik is usd  draw up a mdicain, i
is rmvd and h apprprialy sizd ndl is aachd
 h syring if h mdicain is inndd fr injcin
dircly in h pain.
SAfeTy deviCeS
Safety devices hav bn dvlpd fr syrings and
ndls. Sm prducs hav a slv ha is srd
arund h syring barrl whil h syring is bing lld
hrugh h ndl (Fig. 9.15). Afr adminisrain, h
slv is pulld frward fully  lck h shild prma
nnly in plac  cvr h ndl. Anhr yp f safy
shilding dvic aachs  h ndl hub (Fig. 9.16).
Afr h mdicin is injcd, h halhcar prvidr
pushs h hingd shild frward, hrby cvring h
ndl. Ohr safy shild dvics ar als availabl fr
shr ndls (Fig. 9.17) and fr clsur wih “hands
fr” dvics (Fig. 9.18). Th BD Ingra Syring Sysm
is a springladd syring ha rracs h ndl in h
syring afr injcin. This sysm als uss a chnlgy
calld TruLk chnlgy, which invlvs an apparaus
ha is similar  LurLk chnlgy. I allws fr h
changing f h ndl bwn aspirain and adminis
rain, i lcks h syring and ndl ghr scurly,
Lik all safydsignd syrings and ndls, i is ncs
sary  rad h accmpanying liraur fr adjusmns
ha nd  b mad whn praing hs dvics.
APProPriATe diSPoSAl
Th apprpria dispsal f usd syrings and ndls—
including hs wih ndl prcin dvics—is cru
cial  h prvnin f ndl injury and h ransfr
f bldbrn pahgns. T hlp minimiz accidnal
ndlsicks, a ndl dispsal cnainr is cmmnly
usd fr all sharps (Fig. 9.19). Whn h cnainr is full,
h lid says in plac and h nir cnainr is dispsd
f in a spcic mannr  cmply wih OSHA sandards. I
is impran  ach slfinjcing pains hw  prc
hmslvs and hrs frm accidnal ndlsick injury.
Pains ar ncuragd  purchas a Sharps Dispsal
by Mail Sysm a hir pharmacy fr h dispsal f
syrings, ndls, and lancs. I is criical ha pains
us hs sysms  prvn h accidnal xpsur f
saniain wrkrs  ndls. Th mail sysm includs
a sharps cnainr, an ur shipping bx, and a prpaid
psag labl s ha, whn h cnainr is lld, i can
b maild  an apprpria dispsal cnr. If a pain is
uncrain abu h safs prcdur fr h dispsal f
usd syrings and ndls, hy shuld cnac h lcal
saniain srvic r dparmn.
Parenteral doSe formS
All parnral drug ds frms ar packagd s ha
h drug is sril and rady fr rcnsiuin (if nd
d) and adminisrain.
AmPuleS
Ampules ar glass cnainrs ha usually cnain a sin
gl ds f a mdicain. Th cnainr may b scrd
(Fig. 9.20A) r hav a darknd ring arund h nck
(Fig. 9.20B)  indica whr h ampul shuld b
brkn pn fr wihdrawing h mdicain.
viAlS
Vials ar glass r plasic cnainrs ha cnain n r mr
dss f a sril mdicain. Th unusd vial is sald wih
 Parenteral Administration: Safe Preparation of Parenteral Medications CHAPTER 9 127

Safe lock
Flanges indicator Sleeve

B C D E
Fig. 9.15 An example of a safety syringe that includes a full protective sheath. (A) Syringe showing a sheath that covers
the needle with a safe lock indicator. (B) Assemble the device by holding the needle and the syringe by the anges (wings)
and twisting the needle until it is rmly seated. (C) During aspiration, press the index nger against the anges to prevent
sleeve movement. (Note: If it is necessary to transport a lled syringe to the point of administration, use a safe, passive,
one-handed recapping technique, per Occupational Safety and Health Administration standards, to cover the needle
before transporting it to the point of use.) (D) After injection, grasp the sleeve rmly, and twist the anges to loosen the
sleeve. (E) Fully retract the needle into the sleeve until it locks in the protected position. When the green band fully covers
the red band and an audible click is heard, the sleeve is locked into position. Place in sharps container.

A B

Bevel up = Lever arm up

A B

C D
Fig. 9.16 An example of a safety syringe that includes a shielding
mechanism. (A) Attach the needle and shield assembly to any standard
Luer-Lok or Luer-Slip syringe. Twist it until it is rmly seated, and then pull
the shield straight off of the needle to avoid damaging the needle’s point.
(B) Aspirate the medication into the syringe per the usual technique.
(Note: If it is necessary to transport a lled syringe to the point of
administration, use a safe, passive, one-handed recapping technique, C D
per Occupational Safety and Health Administration standards, to cover Fig. 9.17 Another example of a safety syringe that includes a shielding
the needle before transporting it to the point of use.) (C) Administer mechanism. (A) Aspirate the medication into the syringe per the
the injection in accordance with established technique. Note that the usual technique. The safety arm can be rotated for scale readability.
needle bevel is oriented to the lever arm. (D) After injection, immediately (B) Administer the injection. To facilitate a low angle of injection, the
apply a single nger stroke to the activation-assist lever arm to activate safety arm can be rotated so that it is oriented to the needle bevel. (C)
the shielding mechanism. Place in sharps container. (Note: Activate the After injection, apply a single nger stroke to activate the safety arm
device away from yourself and others, listen for the click, and visually by moving it completely forward. (D) The safety arm is locked and fully
conrm that the needle tip is fully covered.) extended when you hear the click and the needle tip is covered.
128 UNIT II Illustrated Atlas of Medication Administration

A B
Fig. 9.18 Hands-free safety device. (A) safety shield open with needle exposed, close needle cover by placing end on
table or hard surface and folding shield over needle (B) safety shield covering the needle

Lid
Rubber
diaphragm

Fig. 9.19 Needle disposal container, also known as a sharps

container. A B
Fig. 9.21 (A) Vial protected by metal lid. (B) Rubber diaphragm exposed
when lid is removed.

Scored Ringed

A B
Fig. 9.20 (A) Scored ampule. (B) Ringed ampule.

a mal lid  nsur sriliy (Fig. 9.21A). Th muh f

h vial is cvrd wih a hick rubbr diaphragm hrugh
which a ndl is passd  rmv h mdicain (Fig. Fig. 9.22 Mix-O-Vial.
9.21B). Th mdicain in h vial may b in sluin, r
i may b a sril pwdr  b rcnsiud jus bfr in h MixOVial. A h im f us, prssur is ap
adminisrain. Th drug als can b wihdrawn frm h plid  h p rubbr diaphragm plungr. This frcs
vial using a spik aachd  h syring (s Fig. 9.14). h slvn and h rubbr sppr  fall in h b
m chambr, whr h dilun mixs wih h pw
mix-o-viAlS dr, hrby disslving h drug.
Mix-O-Vials ar glass cnainrs wih w cmpar
mns (Fig. 9.22). Th lwr chambr cnains h drug PreParation of Parenteral medication
(slu), and h uppr chambr cnains a sril dilu
n (slvn); bwn h w aras is a rubbr sp equiPmenT
pr. A singl ds f mdicain is nrmally cnaind • Drug in a sril, sald cnainr
 Parenteral Administration: Safe Preparation of Parenteral Medications CHAPTER 9 129

A B C

D E F
Fig. 9.23 Withdrawing from an ampule with a lter needle. (A) Obtain a lter needle and displace the medication from the
top portion of the ampule. (B) Cover the ampule neck area with an antiseptic alcohol wipe remaining in its cover. (C and
D) Snap off the top of the ampule sharply in one swift motion. (E) Using a lter needle, withdraw the medication from the
ampule. (F) Note that the needle must be lowered to withdraw all of the solution from the ampule.

• Syring f h crrc vlum 5. Chck mdicain calculains. Whn in dub
• Ndls f h crrc gaug and lngh abu a ds, chck i wih anhr qualid nurs.
• Ndllss accss dvic (Ms hspial plicis rquir fracinal dss
• Anispic alchl wip f mdicains and dss f hparin and insulin
• Mdicain prl  b chckd by w qualid prsnnl bfr
adminisrain.)
ProCedure ProToCol 6. Knw h insiuinal plicy rgarding limiains
Th sandard prcdurs fr prparing all parnral n h yps f mdicains  b adminisrd by
mdicains ar as fllws: nursing prsnnl.
1. Prfrm hand hygin before prparing any mdica 7. Chck h xpirain da n h mdicain
in r handling sril supplis. During h acual cnainr.
prparain f a parnral mdicain, h primary 8. Afr cmpling h sandard prcdurs fr pr
rul  rmmbr is “sril  sril” and “unsr paring all parnral mdicains, cncnra n
il  unsril” whn handling h syring and h h prcdur a hand  nsur accuracy during
ndl. prparain.
2. Us h seven rights f mdicain prparain and 9. Prpar h drug in a clan, wllli ara and us
adminisrain hrughu h prcdur: righ pa aspic chniqu hrughu h nir prcdur.
in, righ drug, righ indicain, righ ru, righ
ds, righ im, and righ dcumnain. TeChniqueS
3. Chck ha h drug ds frm availabl is wha is Ppa a mcat f a Ap
rdrd. 1. Mv all h sluin  h bm f h ampul,
4. Chck cmpaibiliy chars r cnac h pharma and ick h sid f h glass cnainr wih h n
cis bfr mixing w mdicains r bfr adding grs  displac h mdicain frm h p prin
mdicain  an IV sluin. f h ampul (Fig. 9.23A).
130 UNIT II Illustrated Atlas of Medication Administration

B C D

F H

E G
Fig. 9.24 Removal of a volume of liquid from a vial for reconstitution of a powder. (A) Cleanse the rubber diaphragm of
the vial. (B) Pull back on the plunger of the syringe to ll with an amount of air that is equal to the volume of the solution
to be withdrawn. (C) Insert the needle through the rubber diaphragm; inject the air with the vial sitting in a downward
position. (D) Invert the syringe and vial and withdraw the volume of diluent required to reconstitute the drug. (E) Move
the needle downward within the rubber diaphragm to facilitate the removal of all of the diluent. (F) Tap the container with
the powdered drug to break up the caked powder. (G) Wipe the rubber diaphragm of the vial of the powdered drug with
a new antiseptic alcohol wipe. (H) Insert the needle of the syringe with the diluent into the rubber diaphragm, and inject
the diluent into the powdered drug. (I) Mix thoroughly to ensure that the powdered drug is dissolved before withdrawing
the prescribed dose.

2. Cvr h ampul nck ara wih an anispic alc
hl wip in is slv whil braking h p ff (Fig.
9.23B–D). Discard h wip and h ampul p in a
sharps cnainr.
3. Wih h us f a lr ndl, wihdraw all h
mdicain frm h ampul (Fig. 9.23E and F).
4. Rmv h lr ndl frm h ampul and pin
i vrically. Pull back n h plungr (his allws
air  nr h syring), and hn rplac h lr
ndl wih a nw sril ndl f h apprpria
gaug and lngh fr adminisrain.
5. Push h plungr slwly unil h mdicain ap
pars a h ip f h ndl r masur h amun
f air  b includd  allw fr h al claranc
f h mdicain frm h ndl whn injcd.
(Nvr add air  a syring ha is  b usd  ad
minisr an IV mdicain.)
Drugs in a vial may b in sluin rady fr admin
israin, r hy may b in pwdrd frm fr rcn
siuin bfr adminisrain.
Ppa a mcat f a va
Reconstitution of a sterile powder
1. Rad h accmpanying liraur frm h mdi
cain’s manufacurr, and fllw spcic insruc
ins fr rcnsiuing h drug ha has bn
rdrd. Add nly h dilun spcid by h
manufacurr.
2. Clans h rubbr diaphragm f h vial f dilu
n wih an anispic alchl wip (Fig. 9.24A).
 Parenteral Administration: Safe Preparation of Parenteral Medications CHAPTER 9
3. Pull back n h plungr f h syring  ll i
wih an amun f air qual  h vlum f slu
in  b wihdrawn (Fig. 9.24B).
4. Insr h ndl r ndllss accss dvic
hrugh h rubbr diaphragm and injc h air
(Fig. 9.24C).
5. Wihdraw h masurd vlum f dilun r
quird  rcnsiu h pwdrd drug (Fig.
9.24D and E). Rmv h ndl frm h dia
phragm f h dilun cnainr.
6. Rchck h yp and vlum f dilun  b in
jcd agains h yp and amun rquird.
7. Tap h vial cnaining h pwdrd drug 
brak up h cakd pwdr (Fig. 9.24F). Wip h
rubbr diaphragm f h vial f pwdrd drug
wih a nw alchl wip (Fig. 9.24G).
8. Insr h ndl r ndllss accss dvic in h
diaphragm and injc h dilun in h pwdr
(Fig. 9.24H).
9. Rmv h syring and ndl frm h rubbr
diaphragm.
10. Mix the powdered drug and diluent thoroughly  n
sur ha h pwdr is nirly disslvd before
wihdrawing h ds (Fig. 9.24I).
11. Labl h rcnsiud mdicain, and includ h
da and im f rcnsiuin, h vlum and yp
f dilun addd, h nam f h rcnsiud drug,
h cncnrain f h rcnsiud drug, h x
pirain da and im, and h nam f h prsn
wh rcnsiud h drug. Sr h mdicain in
accrdanc wih h manufacurr’s insrucins.
Removal of a volume of liquid from a vial (see Fig.
9.24A–E)
1. Calcula h vlum f mdicain rquird fr h
prscribd ds f mdicain  b adminisrd.
2. Clans h rubbr diaphragm f h vial f drug
wih an anispic alchl wip.
3. Pull back n h plungr f h syring  ll i wih
an amun f air qual  h vlum f sluin 
b wihdrawn.
4. Insr h ndl r ndllss accss dvic hrugh
h rubbr diaphragm and injc h air.
5. Wihdraw h vlum f drug rquird  adminis
r h prscribd ds.
6. Rchck all aspcs f h drug rdr.
7. Rmv h ndl r h ndllss accss dvic
frm h syring. Aach a nw sril ndl f h
apprpria gaug and lngh  adminisr h
mdicain  h pain.
Ppa a d f a m-o-va
1. Chck h drug rdr agains h mdicain avail
abl fr adminisrain.
2. Tap h cnainr in yur hand a fw ims  brak
up h cakd pwdr.
3. Rmv h plasic lid prcr (Fig. 9.25A)  ac
css h diaphragm plungr (Fig. 9.25B).
131
A B C
Fig. 9.25 Using a Mix-O-Vial. (A) Remove the plastic lid protector to
expose the diaphragm plunger. (B) The powdered drug is in the lower
half; the diluent is in the upper half. (C) Push rmly on the diaphragm
plunger; downward pressure dislodges the divider between the two
chambers.
4. Push dwn rmly n h diaphragm plungr. Th
dwnward prssur will disldg h dividr b
wn h w chambrs (Fig. 9.25C).
5. Mix hrughly  nsur ha h pwdr is com-
pletely dissolved bfr drawing up h mdicain
fr adminisrain.
6. Clans h rubbr diaphragm and rmv h drug
in h sam mannr as dscribd fr h rmval f
a vlum f liquid frm a vial (s Fig. 9.24A–E).
Ppa Tw mcats  o S
Occasinally, w mdicains may b drawn in h
sam syring fr a singl injcin. This is usually dn
whn prparing a prpraiv mdicain r whn
w yps f insulin ar rdrd  b adminisrd a
h sam im. Mixing insulin is a ruin prcdur,
s i will b usd  illusra his chniqu. Bfr
adminisring insulin, h nurs always valuas h
pain’s bld glucs lvl.
1. Chck h cmpaibiliy f h w yps f in
sulin  b mixd bfr saring  prpar h
mdicains.
2. Chck h labls f h insulin vials agains h in
sulin rdr. Chck h insulin rdr and h cal
culains f h prparain wih anhr qualid
nurs in accrdanc wih insiuinal plicy.
3. Chck h fllwing:
 • Type: Rgular, nural pramin Hagdrn
(NPH), hr
 • Concentration: U100 (U100 = 100 unis/mL)
 • Expiration date: D NOT us h insulin if h x
pirain da has passd.
 • Appearance: Clar? Cludy? Prcipia prsn?
Insulin suspnsins shuld b cludy. All hr
insulin sluins shuld b clar. S Tabl 35.5.
 • Temperature: Th insulin shuld b a rm
mpraur.
4. T rsuspnd insulin suspnsins (NPH, Humulin,
Nvlin, Humalg, Nvlg insulin), rll h vial
r pn bwn h palms f h hands r gnly
132 UNIT II Illustrated Atlas of Medication Administration

R N

A B C D

R
N
N

R N

E F G H

NPH Reg.
R N
10 units 15 units

Insulin
5 10 15 20 25
Reg. 15 units
NPH 10 units Total = 25 units

I
Fig. 9.26 Preparing two drugs in one syringe. (A) Check the insulin order and then cleanse the tops of both vials with
an antiseptic alcohol wipe. (B) Pull back on the plunger to an amount that is equal to the volume of the longer-acting
insulin. (C) Insert the needle through the rubber diaphragm of the longer-acting insulin and inject the air. Remove the
syringe and needle; do not remove the insulin. (D) Pull back the plunger on the syringe to a point that is equal to the
volume of the shorter-acting insulin ordered. (E) Insert the needle through the rubber diaphragm and inject the air. (F)
Invert the bottle and withdraw the volume of the rapid-acting insulin ordered. Remove the syringe and needle. Check
the amount withdrawn against the amount ordered. (G) Rewipe the top of the longer-acting insulin vial. (H) Insert the
needle; withdraw the specied amount of longer-acting insulin. (I) Remove the syringe and needle. Recheck the drug
order against the labels on the insulin containers and the amount in the syringe. R, Regular insulin; N, neutral protamine
Hagedorn (NPH) insulin.

invr h vial svral ims  mix h cnns
hrughly. S Tabl 35.6 n cmpaibiliy f
cmbining insulins.
5. Th Amrican Diabs Assciain’s 2017
guidlins rcmmnd drawing up h rapid
acing insulin in h syring hn adding h
inrmdiaacing insulin.
 • Whn aching a pain  mix insulin fr slf
adminisrain, using a cnsisn mhd f
prparing h mixur shuld b srssd s
ha his bcms a habi fr h pain. This
can hlp prvn h pain frm inadvrnly
rvrsing h ds f rapid and lngracing
insulin in h mixur.
6. Clans h ps f both vials wih spara ani
spic alchl wips (Fig. 9.26A).
7. Pull back h plungr n h syring  an amun
ha is qual  h vlum f h lngracing
insulin ha has bn rdrd (Fig. 9.26B).
8. Insr h ndl hrugh h rubbr sal f h
lngracing insulin bl, and injc h air
(Fig. 9.26C). D n bubbl air hrugh h insulin
 Parenteral Administration: Safe Preparation of Parenteral Medications CHAPTER 9
sluin, bcaus i migh brak up insulin pari
cls. Rmv h syring and ndl. D n wih
draw insulin a his im.
9. Pull back h plungr n h syring  an amun
ha is qual  h vlum f h shrracing in
sulin ha has bn rdrd (Fig. 9.26D).
10. Insr h ndl hrugh h rubbr sal f h sc
nd bl and injc h air (Fig. 9.26E).
11. Invr h bl, and wihdraw h vlum f rap
idacing insulin (Fig. 9.26F). (Note: Laving h
ndl in h bl, chck fr bubbls in h insulin
in h syring. Flick h sid f h syring wih h
ngrs  displac h bubbls, and hn rchck
h amun f insulin in h syring.) Rmv h
syring and ndl. Chck h mdicain rdr
agains h labl f h cnainr and h amun
in h syring.
12. Wip h lid f h lngracing insulin cnainr
again (Fig. 9.26G). Rchck h drug rdr agains
his cnainr.
13. Insr h ndl f h syring cnaining h
rapidacing insulin, and wihdraw h spcid
amun f lngracing insulin (Fig. 9.26H). B
carful not  injc any f h rs yp f insulin
alrady in h syring in h lngracing insu
lin vial.
14. Rmv h syring and ndl. Rchck h drug
rdr agains h labls n h insulin cnainrs
and h amun in h syring (Fig. 9.26I).
15. Draw back a small amun f air in h syring,
and hn mix h w mdicains, rlling h sy
ring bwn h palms f yur hands and gnly
invring h syring svral ims  mix h cn
ns hrughly. Rmv air carfully s ha par
f h mdicain is n displacd.
16. Adminisr h insulin  h pain by h subcu
ru.
guidelineS for PrePAring mediCATionS
for uSe in The STerile field during A
SurgiCAl ProCedure
ds us  t opat r
• All mdicains usd during an praiv prc
dur mus rmain sril.
• All mdicain cnainrs (.g., ampuls, vials,
piggyback cnainrs, bld bags) usd during
h surgical prcdur shuld rmain in h p
raing rm unil h nir prcdur is cm
pld. If a qusin ariss, h cnainr is hn
availabl.
• Do not save any unusd prin f mdicain fr
us during anhr surgical prcdur. Discard his
unusd mdicain a h nd f h surgical prc
dur, r snd h pain’s mdicain  h pain
car uni wih h pain, if apprpria (.g., ani
biic inmn fr a pain wh is having phhal
mic surgry).
133
• Adhr  hspial plicis ha addrss h han
dling and srag f mdicains in h praing
rm.
• Always ll h surgn h nam and dsag r cn
cnrain f h mdicain r sluin ha is bing
handd  him r hr.
• Always rpa h nir mdicain rdr back 
h surgn whn h rqus is mad  vrify all
aspcs f h rdr. If in dub, rpa his infrma
in again unil accuracy is crain.
ds us  t St Sca f
• Prpar h drug prscribd in accrdanc wih h
dircins.
• Always chck h accuracy f h drug rdr
agains h mdicain bing prpard a las
hr ims during h prparain phas: (1)
whn i is rs rmvd frm h drug srag
ara; (2) immdialy bfr rmving h slu
in fr us in h sril ld; and (3) immdia
ly afr cmpling h ransfr f h mdicain
r sluin  h sril ld. Always ll h sur
gn h nam and ds r cncnrain f h
mdicain r sluin whn passing i  him r
hr fr us.
• Th circulaing (nnsril) nurs rrivs h md
icain frm srag, rcnsius i as ndd, and
urns h mdicain cnainr s ha h scrubbd
(sril) prsn can rad h labl. I is bs  rad
h labl alud  nsur ha bh individuals ar
vrifying h cnns agains h vrbal rdr frm
h surgn.
• Th mdicain is ransfrrd  h sril ld by
n f w mhds.
Method 1
1. Th circulaing (nnsril) nurs clanss h p
f h vial r braks ff h p f h ampul, as
dscribd prviusly.
2. Th scrubbd (sril) prsn chss a syring f
h crrc vlum fr h mdicain  b wih
drawn and aachs a largbr ndl  facilia
h rmval f h sluin frm h cnainr.
3. Th circulaing (nnsril) nurs hlds h ampul
r vial in such a way ha h scrubbd (sril) pr
sn can asily insr h sril ndl ip in h
mdicain cnainr (Fig. 9.27A).
4. Th scrubbd prsn pulls back h plungr n h
syring unil all f h mdicain prscribd has
bn wihdrawn frm h cnainr and frm h
ndl usd  wihdraw h mdicain.
5. Th ndl is discnncd frm h syring and lf
in h vial r ampul (s Fig. 9.27B).
6. Th mdicain cnainr is again shwn  h
scrubbd prsn and rad alud  vrify all cm
pnns f h drug prpard agains h mdica
in r sluin rqusd.
134 UNIT II Illustrated Atlas of Medication Administration

Method 2
1. Th circulaing (nnsril) nurs rmvs h n
ir lid f h vial wih a bl pnr, clanss h
rim f h vial, and purs h mdicain dircly
A in a sril mdicin cup hld by h scrubbd
nurs.
2. Th scrubbd prsn cninus drug prparain n
h sril ld in accrdanc wih h inndd us
(.g., irrigain, injcin).
Rgardlss f h mhd usd  ransfr h mdi
cain  h sril ld, bh h sril scrubbd pr
sn and h nnsril circulaing nurs shuld knw
h lcain and h xac dispsiin f ach mdica
in n h sril ld.
B

Fig. 9.27 Preparing a medication in the operating room. (A) The

circulating (nonsterile) nurse holds the vial to facilitate the scrubbed
(sterile) person inserting the sterile needle tip into the medication
container. (B) The needle is disconnected from the syringe and left in
the vial.
 Parenteral Administration: Safe Preparation of Parenteral Medications CHAPTER 9 135

Cca Jt a nt-gat nClex® eaat-St qsts

k Pts 3. Administering the injection using clean technique

4. Understanding how the medication will work
• A syringe has three parts: the barrel, the plunger, and the 5. Evaluating the therapeutic outcome desired
tip that holds the needle. Types of safety syringes and 6. Exercising clinical judgment regarding changes in the
needles include the Luer-Lok and needleless systems of patient’s condition
blunt needles and shields over the needles. ojv: Identify safe administration practices for parental
• To correctly determine the gauge and length of the needle medications.
to use, the site of injection and the size of the patient are ncleX s : Extended multiple response
factored in, as well as the volume of medication to be cgv sk: Application
administered.
2. The nurse is preparing to give an injection into the patient’s
• The tuberculin syringe is used to measure volumes of less abdomen for the early morning insulin dose. Which needle length
than 1 mL; the standard syringe sizes are 1, 3, and 5 mL. and gauge is most appropriate to use?
• Prelled cartridge-needle units and syringes contain a
1. 18 gauge, 1½ inch
standard dose of a medication and are a time saver for
2. 120 gauge, 1 inch
the nurse, but more expensive than a multidose vial of
3. 22 gauge, ⅝ inch
medication. Cartridges require a special cartridge holder to
4. 25 gauge, ⅝ inch
administer the medication.
• Ampules are glass containers of medications that need to ojv: Identify the parts of a syringe and needle, as well as
be opened by snapping (breaking) the neck of the ampule examples of the safety-type syringes and needles.
before use. ncleX s : Multiple choice
cgv sk: Knowledge
• Vials have a rubber diaphragm that a needle passes
through to access the medication. 3. The nurse in the medication room preparing an injection recognized
• Mix-O-Vials are glass containers with two compartments. that the needle needed for the injection must be the correct gauge
The lower compartment contains the medicine in powder and length. Indicate with an X the correct needle to use in each
form, and the upper compartment contains the diluent situation.
needed to dissolve the medicine. The two chambers are
separated by a rubber plug. To mix the medicine, a rubber 1- to 1½- ⅝- 25- to 23- to 21- to
stopper on the top chamber is pushed, forcing the rubber 1½- to to 27- 25- 23-
stopper between the chambers to drop into the lower inch 2- 1- GauGe GauGe GauGe
chamber, along with the diluent. Shaking the container nee- inch inch nee- nee- nee-
dissolves the medicine, allowing it to be drawn up into a dle nee- nee- dle dle dle
syringe for administration. dle dle
• Insulin can be mixed in one syringe by drawing up the Insulin
short-acting insulin rst, then adding the longer-acting syringe
insulin to the same syringe using a specic method. IM
injection
a lg rss for thin,
frail adult
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa- IM
tions, and other learning activities to help you master this chap- injection
ter content. for
pediatric
Go to your Evolve website (https://evolve.elsevier.com/Willihng patient
anz) for additional online resources. IM
injection
Clinical Judgment and Next-Generation NCLEX® Exam- for obese
ination-Style Questions The following questions are typical of adult
the NCLEX examination and include both NGN (Next Genera-
tion) and traditional questions. See Chapter 1 for further infor-
mation regarding question types. ojv: Describe how to select the correct needle gauge and
length.
1. The nurse preparing an IM injection to be administered will nGn s : Matrix
provide accurate and safe medication practices by following which cgv sk: Recognize cues
principles? (Select all that apply.)
1. Performing premedication assessment
2. Being knowledgeable about the reason the medication is
given
136 UNIT II Illustrated Atlas of Medication Administration

4. The nurse discussing with an orientee the advantages of the 5. Inject the insulin in the proper subcut site.
prelled cartridge-needle units and syringes. Which statements by 6. Mix the two insulins in the syringe by rolling between the
the nurse are accurate? (Select all that apply.) palms and gently inverting the syringe several times.
1. “The prelled syringes require special cartridge holders.” ojv: Describe the technique used to prepare two different
2. “The prelled syringes diminish the chance of drugs in one syringe (e.g., insulin).
contamination of the medication.” ncleX s : Ordering
3. “The prelled syringes are cheaper than the multidose cgv sk: Application
vials.”
4. “The prelled syringes save the nurse the time it takes to 7. The nurse needs to determine which medications need to be in a
prepare the injection.” tuberculin syringe and which need to be in a larger volume syringe.
5. “The prelled syringes contain a standard volume and Indicate with an X which syringe would work.
strength of medication.”
ojv: Compare and contrast the advantages and tuberculin larGer Volume
SyrinGe SyrinGe
disadvantages of using prelled syringes.
ncleX s : Multiple response Subcutaneous injection
cgv sk: Understanding (1.5 mL)

5. The nurse needs to determine the difference between an ampule,
a vial, and a Mix-O-Vial. Indicate with an arrow the technique used
for the different parenteral dose forms.
doSaGe form technique uSed
Ampules •  Inject air equal to the volume of
medication to be removed
Vials •  Use a needleless spike for removing
the medication
Mix-O-Vial •  Use a lter needle or lter straw to
ensure that no glass particles are
drawn into the syringe
•  Depress the top rubber diaphragm
to displace the stopper
ojv: Differentiate among ampules, vials, and Mix-O-Vials.
nGn s : Drag and drop
cgv sk: Comprehension
6. The nurse is teaching the patient how to prepare 10 units of
regular insulin and 5 units of NPH insulin for injection. List in the
correct order the proper sequence for preparation that the nurse
will describe to the patient.
1. Inject appropriate volumes of air into the NPH vial and the
regular insulin vial.
2. Withdraw 10 units of regular insulin into the syringe.
3. Wipe the tops of the insulin vials with alcohol.
4. Withdraw 5 units of NPH insulin into the syringe to mix
with the regular insulin.
Subcutaneous injection
(0.5 mL)
Intradermal Mantoux
test (0.1 mL)
IM injection for nausea
(2 mL)
ojv: Compare and contrast the volumes of medications that
can be measured in a tuberculin syringe and those of larger-volume
syringes.
nGn s : Drag and drop
cgv sk: Recognize cues
7. The nurse needs to mix two medications in the same syringe so
that the patient will only have to get one shot. List in order the
steps necessary to mix two medications in one syringe.
1. Withdraw the medication from the second vial.
2. Wipe off the tops of both vials.
3. Check the compatibility of the two drugs.
4. Inject air into each vial equal to the volume to be
withdrawn.
5. Withdraw the medication from the rst vial.
6. Mix the two medicines in the syringe by rolling between
the palms and gently inverting the syringe several times.
ojv: Describe the technique used to prepare two different
drugs in one syringe (e.g., insulin).
ncleX s : Ordering
cgv sk: Application

ALGrawany
Parenteral Administration: Intradermal,
Subcutaneous, and Intramuscular Routes
Objectives
1. Describe the technique that is used to administer a
medication via the intradermal route.
2. Identify the equipment needed and describe the technique
that is used to administer medication via the subcutaneous
route.
3. Describe the techniques used to administer medications
intramuscularly.
Key Terms
intradermal (ĭn-tră-DŬR-măl) (p. 137) intramuscular (ĭn-tră-MŪS-kyū-lăr)
erythema (ĕr-ĭ-THĒ-mă) (p. 139) (p. 141)
induration (ĭn-dĕ-RĀ-shĕn) (p. 139) vastus lateralis (VĂS-tŭs lăt-ĕr-Ă-lĭs)
anergic (ăn-ĔR-jĭk) (p. 139) (p. 142)
subcutaneous (sŭb-kū-TĀ-nē-ŭs) rectus femoris (RĔK-tŭs FĔ-mŭr-ĭs)
(p. 139) (p. 142)
ADMINISTRATION OF MEDICATION BY THE
INTRADERMAL ROUTE
Intradermal jcs r md  h drml ly-
r f sk js blw h pdrms (Fg. 10.1). Smll
vlms, slly 0.1 mL, r jcd. Th bsrp
frm rdrml ss s slw, hrby mkg  h
r f chc fr llrgy ssvy ss, dssz-
 jcs, lcl shcs, d vccs.
Prfrm prmdc ssssms; s dvdl
drg mgrphs fr dls.
EQUIPMENT
• Mdc  b jcd r sls f sspcd
llrgs
• Tbrcl syrg wh 26-gg, ¼-ch, r
28-gg, ½-ch dl, r  spcl dl d sy-
rg fr llrgs
• Mrc rlr, f prfrmg sk-sg prcdr
• Glvs
• Rcrd fr chrg d b h sbscs p-
pld d h p’s rspss
• Aspc lchl wp
• Prscrbr’s rdr r mdc prl
SITES
Irdrml jcs my b md  y sk sr-
fc, b h s shld b hrlss d rcv ll
frc frm clhg. Th ppr chs, h scplr
10
https://evolve.elsevier.com/Willihnganz
4. Describe the landmarks that are used to identify the
vastus lateralis muscle, the rectus femoris muscle, the
ventrogluteal area, and the deltoid muscle sites before
medication is administered.
5. Identify suitable sites for the intramuscular administration
of medication in an infant, a child, an adult, and an older
adult.
ventrogluteal area (vĕn-trō-GLOO-tē-
ăl) (p. 142)
deltoid muscle (DĔL-tōyd MŬS-ŭl)
(p. 143)
Z-track method (ZĒ TRĂK MĔTH-ĭd)
(p. 145)
rs f h bck, d h r spc f h frrms
r h ms cmmly sd rs (Fg. 10.2A d B).
TECHNIQUE
Ths xmpl f  rdrml jc chq
vlvs llrgy ssvy sg. Tw mhds c
b sd  dmsr llrgy sg. O mhd r-
qrs h rdrml jc f h llrgs; h
hr s cmpld by sg h sk prck mhd.
Caution: D  sr y yp f llrgy sg
lss mrgcy qpm (cldg pphr)
s vlbl  h mmd r  cs f  -
phylcc rsps. Nrss shld b fmlr wh h
prcdr  fllw f  mrgcy ds rs.
1. Fllw h prcdr prcl  Chpr 9 (s
Prpr f Prrl Mdc).
2. Vrfy h dy f h p sg w
drs.
3. Chck wh h p bfr srg h sg 
sr h hy hv  k y hsms
r mmry gs (.g., spr, bprf,
crcsrds) d h hy hv  rcvd
mmspprss hrpy fr 24  48 hrs b-
fr h ss. If h p hs k hsms,
cr slp mdcs (.g., dxylm, dph-
hydrm), r mmry gs, chck wh
h hlhcr prvdr bfr prcdg wh h
sg.
137
138 UNIT II Illustrated Atlas of Medication Administration

4. Prvd fr p prvcy. cg wrd  crclr ms  h p-
5. Prfrm hd hyg d pply cl glvs. rphry. Allw h r  r-dry.
6. Cls h r slcd fr sg hrghly
wh  spc lchl wp. Us crclr m- Intradermal Injection Method
s, srg  h pld s f jc d  • Prpr h dsgd sls fr jc
sg spc chq. Usl vlms  b -
jcd rg bw 0.01 d 0.05 mL. A psv-
Epidermis crl sl h cs hsm d 
Dermis Bleb
gv-crl sl h cs sl r
15 h dl f h llrg r ls dmsrd.
degrees
 • Isr h dl   15-dgr gl wh h
dl bvl pwrd. (Note: Thr s  cr-
vrsy rgrdg whhr h dl bvl shld
b pwrd r dwwrd. Chck h prcdr
ml fr fcly plcy.) Th sl bg
jcd s dpsd  h spc mmd-
ly blw h sk; rmv h dl qckly.
Muscle A smll blb wll ppr  h srfc f h
Subcutaneous sk s h sl rs h rdrml r
Fig. 10.1 Intradermal injection technique. (s Fg. 10.1). B crfl   jc  h

1 2 3 4 5 6 7 8
43 44 45 49 50 51
9 10 11 12 13 14 15 16
46 47 48 52 53 54
17 18 19 20
21 22 23 24

25 26 31 32
27 28 33 34
29 30 35 36

37 40 55 58
38 41 56 59
39 42 57 60

A B

Reading Chart for Intradermal Testing

Patient Name:
Identification Number:
Physician Name:

Reading Time in Hours or Minutes

DATE: TIME: AGENT CONCENTRATION DOSAGE SITE NUMBERa
30 min or 24, 48, or 72 hr

a
Refer to diagram of sites (Fig.10.2A–B).
• Follow directions for the “reading” of the skin testing performed
• Inspect sites in a good light.
2+
• Record reaction in upper half of box using the following guidelines, e.g.,
+ (1+) No wheal, 3 mm flare
++ (2+) 2 to 3 mm wheal with flare
+++ (3+) 3 to 5 mm wheal with flare
++++ (4+) >5 mm wheal
• Record measurement of induration (process of hardening) in mm in lower half of box, e.g.,
5 mm
C
Fig. 10.2 Intradermal sites. (A) Posterior view. (B) Anterior view. (C) Reading chart for intradermal testing.
 Parenteral Administration: Intradermal, Subcutaneous, and Intramuscular Routes CHAPTER 10
sbcs spc d d  wp h s wh
lchl fr jc.
 • Do not rcp y dls h hv b sd.
Acv h sfy dvc f  h syrg.
Dsps f sd dls d syrgs  
pcr-rss dl dspsl cr 
ccrdc wh sl plcy.
Skin Prick Test Method
 • Mk  grd f  ls fr sqrs, mr f
dd,  h s s  2-cm rvls wh 
p.
 • Plc  drp f ch llrg   f h grd
sqrs f h sg s. A psv-crl s-
l h clds hsm d  gv-
crl sl h clds sl r h dl-
 f h llrg r ls dmsrd.
 • Usg  lc wh  1-mm p, prck h sk
hrgh h llrg drp. Wp h lc wh
dry gz bw ch prck  prv h cr-
ryvr f h llrg frm h prvs s.
 • Gly bl h xcss llrg ff f h s.
 • Th sk prck s c b rd 10  20 ms
fr dmsr, dpdg  prcl.
7. Rmv glvs d dsps f hm  ccrdc
wh sl plcy. Prfrm hd hyg.
8. Chr h ms, gs, ccrs, d
ms dmsrd (s Fg. 10.2C). Mk 
dgrm  h p’s chr, d mbr ch
lc. Rcrd wh g  wh ccr
ws jcd  ch s. (Sbsq rdgs f
ch r r h prfrmd d chrd  hs
rcrd.)
9. Fllw h drcs rgrdg h m f h
rdg f h sk sg bg prfrmd. Th -
spc f h jc ss shld b prfrmd
 gd lgh. Grlly,  psv rc (..,
h dvlpm f  whl; s Fg. 7.1)   d-
ld srgh f  sspcd llrg s csdrd
clclly sgc. Msr h dmr f h
whl d y erythema (.., rdss  h s f
jc)  mllmrs, d plp d msr
h sz f y induration (.., h hrdg f 
r f h bdy  rsps  mm). N
rc  h llrgs, spclly  h psv
crl, s kw s  anergic reaction. Argy s
sscd wh mmdccy dsrdrs.
10. Rcrd h frm frm h sk s rdg
 h p’s chr. Th fllwg s  ls f cm-
mly sd rdgs f rcs d hr ppr-
pr symbls:
+ (1+) No wheal, 3-mm are
++ (2+) 2- to 3-mm wheal with are
+++ (3+) 3- to 5-mm wheal with are
++++ (4+) >5-mm wheal
Grlly,  psv rc  dlyd hypr-
ssvy sk sg ( vl vv cll-mdd
139
mmy) rqrs  dr f  ls 5 mm 
dmr.
PATIENT TEACHING
1. Fr rdrml jcs, ll h p h m,
d, d plc  rr  hv h s ss rd.
2. Tll h p   wsh r scrb h r l
h jcs hv b rd.
3. If h p dvlps  r f svr brg r
chg, hy shld ry   scrch . Tll h p-
  rpr mmdly h dvlpm f y
brhg dfcly, svr hvs, r rshs d 
g  h rs mrgcy dprm f hy r
bl  rch h hlhcr prvdr wh pr-
scrbd h sk ss.
DOCUMENTATION
Prvd h rgh dcm f h llrg sg
ss d h p’s rspss  h llrgs h
wr jcd.
1. Chr h d, m, llrgs (cldg g,
ccr, d m), d s f dmsr-
 (s Fg. 10.2).
2. Prfrm  rdg f ch s fr h pplc
f h s s drcd by h hlhcr prvdr r
h plcy f h hlhcr gcy.
3. Chr d rpr y sgs d sympms f d-
vrs llrg ffcs.
4. Prfrm d vld ssl p dc
b h sg.
ADMINISTRATION OF MEDICATION BY THE
SUBCUTANEOUS ROUTE
Subcutaneous (sbc) jcs r md  h
ls ccv ss bw h drms d h
msclr lyr (Fg. 10.3). Absrp s slwr d
drg c s grlly lgr wh sbc jc-
s cmprd wh rmsclr (IM) r r-
vs (IV) jcs. If h p’s crcl s
dq, h h drg s cmplly bsrbd frm
h ss.
My drgs c b dmsrd by hs r
bcs rdrly  mr h 2 mL c b dps-
d   sbc s. Th drgs ms b q slbl
d p gh  b ffcv   smll vlm
wh csg sgc ss rr. Drgs
cmmly jcd  h sbc ss r hpr,
xpr, d sl.
Prfrm prmdc ssssms; s dvdl
drg mgrphs fr dls.
EQUIPMENT
• Mdc  b jcd
• Syrg f crrc vlm
• Ndl f crrc lgh d gg
• Glvs
• Aspc lchl wp
140 UNIT II Illustrated Atlas of Medication Administration
45
degrees
Epidermis
Dermis
Subcutaneous
Muscle
Fig. 10.3 Subcutaneous injection. Inject at a 45- to 90-degree angle
depending on the depth of subcutaneous tissue, the length of the
needle, and the volume to be injected.
• Prscrbr’s rdr
• Mdc prl
Syringe Size
Chs  syrg h crrspds wh h vlm f
drg  b jcd   s. Th sl m jc-
d sbcsly   s s 0.5  2 mL. Crrl
h syrg sz wh h sz f h p d h s-
s mss.
Needle Length
Assss ch p s h h dl lgh slcd
wll dps h mdc  h sbc ss rh-
r h h mscl ss. Ndl lghs f ⅜, ½, d
⅝ ch r rly sd. I s prd  lv  x-
r ¼ ch f dl xdg bv h sk srfc
 cs h dl brks.
Needle Gauge
Cmmly sd ggs fr sbc jcs r 25 
29 gg.
SITES
Cmm ss sd fr h sbc dmsr
f mdcs cld h ppr rms, h rr
hghs, d h bdm (Fg. 10.4). Lss cmm r-
s r h bcks d h ppr bck r scplr
rg.
A pl fr rg jc ss shld b dvl-
pd fr ll ps wh rqr rpd jcs (s
Fg. 10.4). Th rr vw (s Fg. 10.4B) llsrs
rs h r sly ccssbl fr slf-dmsr.
Th psrr vw (s Fg. 10.4A) llsrs lss cm-
mly sd rs h my b sd by  crgvr wh
s jcg h mdc  h p.
Wh dmsrg sl sbcsly,  s
mpr  r h jc ss  prv lphy-
prrphy r lprphy, whch slws h bsrp
1 2 7 8
3 4 9 10
5 6 11 12
19 20 13 14
21 22 15 16
23 24 17 18
A B
Fig. 10.4 Subcutaneous injection sites and rotation plan. (A) Posterior
view. (B) Anterior view illustrating commonly used subcutaneous sites
for self-administration. The anterior view also provides an example
of a numbered rotation schedule for insulin injection, using one site
systematically before proceeding to the next site of administration.
r f h sl. Th Amrc Dbs Assc
Clcl Prcc Rcmmds s h sl
jc ss shld b rd sysmclly wh
 r bfr prgrssg   w s fr jc
(s Fg. 10.4B);  s hgh h hs wll dcrs
vrs  sl bsrp. Absrp s kw
 b fss wh h sl s dmsrd  h
bdm; hs s fllwd by h rms, hghs, d b-
cks. Bcs xrcs s ls kw  ffc h r
f sl bsrp, s slc shld k hs
fcr  csdr.
TECHNIQUE
1. Fllw h prcdr prcl  Chpr 9 (s
Prpr f Prrl Mdc).
2. Vrfy h dy f h p sg w d-
rs. Esr h h p ds  hv  l-
lrgy  h mdc.
3. Chck h ccrcy f h drg rdr gs h
mdc bg prprd  ls hr ms
drg h prpr phs: (1) wh rs r-
mvg h drg frm h srg r, (2) m-
mdly fr prpr, d (3) mmdly
bfr dmsr.
4. Csl h msr r schdl fr h p-
 s h h drg s dmsrd  h crrc
s.
5. Expl crflly  h p wh  xpc.
6. Prvd fr h p’s prvcy d ps h
p pprprly.
7. Prfrm hd hyg d pply cl glvs.
8. Exps h slcd s d lc h ldmrks.
9. Cls h sk srfc wh  spc lc-
hl wp srg  h jc s d wrkg
wrd   crclr m wrd h prphry.
Allw h r  r-dry.
 Parenteral Administration: Intradermal, Subcutaneous, and Intramuscular Routes CHAPTER 10
10. Chck h s f jc d h lgh f h
dl. Assss whhr h jc s ms ppr-
prly dmsrd   45-  90-dgr gl
fr sbc dlvry.
11. Isr h dl qckly   45-  90-dgr gl;
slwly jc h mdc. Th Amrc Dbs
Assc Clcl Prcc Rcmmds
s h “h dvdls r chldr my d
 pch h sk d jc   45-dgr gl 
vd IM jc, spclly  h hgh r.”
12. Whdrw h dl. Gl prssr my b p-
pld  h s wh  spc lchl wp,
b do not rb.
13. Do not rcp y dls h hv b sd.
Acv h sfy dvc. Dsps f sd dls
d syrgs   pcr-rss dl ds-
psl cr  ccrdc wh sl
plcy.
14. Rmv glvs d dsps f hm ccrdg 
fcly plcy. Prfrm hd hyg.
PATIENT TEACHING
Prfrm pprpr p chg s dscrbd 
h rld drg mgrphs.
DOCUMENTATION
Prvd h rgh dcm f h mdc
dmsr d h p’s rsps  drg
hrpy.
1. Chr h d, m, drg m, ds, s, d
r f dmsr.
2. Prfrm d rcrd rglr p ssssms fr
h vl f h hrpc ffcvss (.g.,
bld prssr, pls, p, mprvm r
qly f cgh d prdcvy, dgr d dr-
 f p rlf).
3. Chr d rpr y sgs d sympms f d-
vrs drg ffcs.
4. Prfrm d vld ssl p dc
b h drg hrpy.
ADMINISTRATION OF MEDICATION BY THE
INTRAMUSCULAR ROUTE
Intramuscular jcs r md by prg 
dl hrgh h pdrms, drms, d sbc s-
s  h mscl lyr. Th jc dpss h
mdc dp wh h mscl mss (Fg. 10.5).
Absrp s mr rpd h h sscd wh
sbc jcs bcs mscl ss hs  grr
bld spply. S slc s spclly mpr
wh IM jcs bcs h crrc plcm f
h dl my cs dmg  rvs r bld vs-
sls. Cmplcs frm mprpr chq f IM -
jcs cld hmm (wh  v s pcrd)
d p (wh  rv s chd). A lrg, hlhy
mscl h s fr frm fcs d wds shld
b sd.
141
90
degrees
Epidermis
Dermis
Subcutaneous
Muscle
Fig. 10.5 Intramuscular injection technique.
Prfrm prmdc ssssms; s dvdl
drg mgrphs fr dls.
EQUIPMENT
• Mdc  b jcd
• Syrg f crrc vlm
• Ndl f crrc lgh d gg
• Glvs
• Aspc lchl wp
• Prscrbr’s rdr
• Mdc prl
Syringe Size
Chs  syrg h crrspds wh h vlm
f drg  b jcd   s. Th sl m
jcd rmsclrly   s s 0.5  3 mL.
I fs d chldr h m shld rg
bw 0.5 d 1 mL, d  shld  xcd 1
mL. Crrl h syrg sz wh h sz f h
p d h ss mss. I dls, dvdd dss
r grlly rcmmdd fr ms  xcss
f 3 mL; 1 mL s h mxmm m  b -
jcd  h dld r. Ohr fcrs h fl-
c syrg sz d dl gg cld h yp
f mdc, h s f dmsr, h hck-
ss f h sbc fy ss, d h g f h
dvdl.
Needle Length
Assss ch p s h h dl lgh slcd
wll dps h mdc  h msclr ss
(s Fg. 10.5). Thr s  sgc dffrc mg
h dl lghs h r pprpr fr  bs p-
,  f, r  mcd r dbld p.
Ndls h r cmmly sd r 1  1½ chs
lg, lhgh lgr lghs my b rqrd fr
bs ps.
142 UNIT II Illustrated Atlas of Medication Administration
Greater
trochanter
Femoral
artery
Femoral
vein
Sciatic
nerve
Vastus
lateralis
Patella
A B
Fig. 10.6 Vastus lateralis muscle. (A) Child or infant. (B) Adult.
Needle Gauge
Cmmly sd ggs fr IM jcs r 20  23
gg.
SITES
Vastus Lateralis Muscle
Th vastus lateralis mscl s lcd  h rr
lrl hgh, wy frm rvs d bld vssls (Fg.
10.6). Th mdpr s  hdbrdh blw h
grr rchr d  hdbrdh bv h
k (s Fg. 10.6B). Ths s grlly h prfrrd
s fr IM jcs  fs bcs  hs h lrg-
s mscl mss fr h g grp. Ths mscl s ls
 gd chc fr  jc s  hlhy, mbl-
ry dls. I ccmmds  lrg vlm f md-
c, d  llws fr gd drg bsrp. I h
ldr, dbld, r mblry dl, h mscl
shld b crflly ssssd bfr jc bcs
sgcly lss mscl mss my b prs. If ms-
cl mss s sfc,  lrv s shld b
slcd.
Rectus Femoris Muscle
Th rectus femoris mscl (Fg. 10.7) ls js mdl
 h vss lrls mscl, b  ds  crss h
mdl f h rr hgh. Th jc s s l-
cd  h sm mr s s sd fr h vss l-
rls mscl. Ths mscl my b sd  bh chldr
d dls wh hr ss r vlbl. A prmry
dvg  s s s h  my b sd mr sly
by ps fr slf-dmsr. A dsdvg s
h h mdl brdr s cls  h scc rv d
Femoral
artery
Femoral
vein
Greater
trochanter
Sciatic
nerve
Rectus
femoris
muscle
Femoral
artery
Femoral
vein
Patella
A B
Fig. 10.7 Rectus femoris muscle. (A) Child or infant. (B) Adult.
mjr bld vssls (s Fg. 10.7). If h mscl s 
wll dvlpd, jcs  hs s my ls cs
csdrbl dscmfr d pl jry.
Life Span Considerations
Injection Sites
 • The vastus lateralis site is preferred in infants. In the older,
debilitated, or nonambulatory adult, carefully assess the
sufciency of the muscle mass before using this site for
injection.
 • The ventrogluteal site is also appropriate for infants and
adults, and it may be used as often as needed.
 • The deltoid site is preferred when administering 1 mL or
less because of the convenience of the arm muscle.
Gluteal Area
Th gll r s  cmmly sd s f jc
bcs  s fr f mjr rvs d bld vssls.
Th drsgll r ms  b sd  chldr
wh r lss h 3 yrs ld bcs h mscl hs
 y b wll dvlpd frm wlkg. Th v-
rgll r s  pprpr s fr jcs 
chldr wh r lss h 3 yrs ld; hwvr, hs
s s  sd s f s h vss lrls mscl
bcs f h cvc f h hgh mscl. Th
r my b dvdd  w dsc jc ss:
(1) h vrgll r d (2) h drsgll r.
Ventrogluteal area. Th ventrogluteal area s sly c-
cssbl wh h p s   pr, sp, r sd-
lyg ps. I s lcd by plcg h plm f h
 Parenteral Administration: Intradermal, Subcutaneous, and Intramuscular Routes CHAPTER 10 143

Iliac crest

Anterior
superior
iliac spine

Gluteus
medius

Greater
trochanter

45°
70°
90°

A B
Fig. 10.8 Ventrogluteal site. (A) Child or infant. (B) Adult.

Fig. 10.9 Patient lying in the prone position. The toes are pointed Fig. 10.10 Patient lying on the side. Flexing the upper leg promotes
muscle relaxation.
inward to promote muscle relaxation.

hd  h lrl pr f h grr rchr
wh h hmb pg wrd h gr, h dx
gr  h rr sprr lc sp, d h md-
dl gr xdd  h lc crs. Th jc s
md  h cr f h “V” h s frmd bw
h dx d mddl grs, wh h dl drc-
d slghly pwrd wrd h crs f h lm (Fg.
10.8). P  jc c b mmzd f h mscl
s rlxd. Th p c hlp wh hs rlx by
pg h s wrd whl lyg   pr ps-
 (Fg. 10.9) r by xg h ppr lg f lyg 
hr sd (Fg. 10.10).
Dorsogluteal area. Th s f hs s s dscrgd
d  prccd  y gr x bcs f h
pssbl dmg  h scc rv.
Deltoid Muscle
Th deltoid muscle s f sd bcs f h s
f ccss  hs r wh h p s  h sd-
g, sg, r pr ps. Hwvr,  shld b
sd  fs ly wh h vlm  b jcd s
smll, h drg s rrg, d h ds wll b
qckly bsrbd. I dls, h vlm shld b lm-
d  1 mL r lss d h sbsc ms  cs
rr. C ms ls b xrcsd  vd h
clvcl, h hmrs, h crm, h brchl v
d rry, d h rdl rv. Th jc s (Fg.
10.11) f h dld mscl s lcd by plpg h
crm prcss r p f h shldr d msr-
g dw w  hr grbrdhs. I s dvsbl 
plp h mscl f h dld, whch s rghly r-
glr  shp,  drm h hcks pr f h
mscl, whch wll h b h r fr h jc.
SITE ROTATION
A msr pl fr s r shld b dvlpd
d sd fr ll ps wh rqr rpd jc-
s (Fg. 10.12).
TECHNIQUE
Standard Method
1. Fllw h prcdr prcl  Chpr 9 (s
Prpr f Prrl Mdc).
2. Vrfy h dy f h p sg w d-
rs. Esr h h p ds  hv  l-
lrgy  h mdc.
3. Chck h ccrcy f h drg rdr gs h
mdc bg prprd  ls hr ms
drg h prpr phs: (1) wh rs
144 UNIT II Illustrated Atlas of Medication Administration

Clavicle

Acromion
process

Scapula

Deltoid
muscle

Axilla

Radial
nerve

Brachial
artery

Humerus

A B
Fig. 10.11 Deltoid muscle site. (A) Child or infant. (B) Adult.

rmvg h drg frm h srg r, (2) m-
mdly fr prpr, d (3) mmdly
bfr dmsr.
4. Clcl d drw p h mdc. Chck
h sl plcy rgrdg whhr 0.1 r
0.2 mL f r shld b ddd  h syrg after
ccrly msrg h prscrbd vlm f
drg fr dmsr. (Note: Th rl fr
ddg h r s h  wll rsl  h dl
bg cmplly clrd f ll mdc  h
m f jc. Cvrsly, f h vlm s
cmplly drw  h syrg bfr chg-
g h dl, h drg vlm rdrd wll sll
b dmsrd s lg s h sm sz dl
s sd fr drwg p d jc. Ths h
dl shld  d  b cmplly clrd
f mdc by r drg dmsr.
Ths ss c b crcl wh smll vlms
f p drgs r rpdly dmsrd 
fs.)
5. Csl h msr r schdl fr h p-
 s h h drg s dmsrd  h crrc
s (s Fg. 10.12).
6. Expl crflly  h p wh wll b d.
7. Prvd fr h p’s prvcy; ps h p-
 pprprly (s Fgs. 10.9 d 10.10 fr r-
lx chqs).
8. Prfrm hd hyg d pply cl glvs.
9. Exps h slcd s d lc h ldmrks.
10. Cls h sk srfc wh  spc lc-
hl wp srg  h jc s d wrkg
wrd   crclr m wrd h prphry.
Allw h r  r-dry.
11. Usg h dm hd, sprd h sk d
hld dw  psh sbc ss wy d llw
grr dl pr.
12. Isr h dl   90-dgr gl sg  qck,
dr-hrwg c.
13. Ijc h mdc sg gl, sdy prssr
 h plgr d w fr  c f 3 bfr
rmvg h dl. Ths wll sr h ll h
mdc hs b dlvrd. (Note: Th d 
spr bfr jc s  lgr prccd; 
hs b fd  cs mr dmg d s c-
sdrd cssry.)
14. Afr rmvg h dl, pply gl prssr
 h s. Mssg c crs h p f h
mscl mss s srssd by h m f mdc-
 gv.
15. Do not rcp y dls h hv b sd.
Acv h sfy dvc. Dsps f sd dls
d syrgs   pcr-rss dl ds-
psl cr  ccrdc wh sl
plcy.
16. Apply  smll bdg  h s.
17. Prvd ml sppr  h p. Chldr
shld b cmfrd drg d fr h jc.
Smms lg  chld hld yr hd r sy
 Parenteral Administration: Intradermal, Subcutaneous, and Intramuscular Routes CHAPTER 10 145

1. Prvd fr h p’s prvcy; ps h p-

 pprprly.
5 6 2. Prfrm hd hyg d pply cl glvs.
Rectus Rectus 3. Exps h vrgll s r vss lrls s
femoris
3 4
femoris (Fg. 10.13A). Nvr jc  h p’s rm.
1 2 4. Clcl d drw p h mdc; dd 0.5 mL
Ventrogluteal
f r  sr h h drg wll clr h dl.
5. Cls h sk srfc wh  spc lc-
hl wp srg  h jc s d wrkg
Vastus lateralis
wrd   crclr m wrd h prphry.
Allw h r  r-dry.
6. Srch h p’s sk pprxmly 1 ch 
 sd (Fg. 10.13B).
7. Isr h dl. I s mpr  chs  -
A dl f sfc lgh  sr dp mscl
pr.
8. Gly jc h mdc d h w pprx-
mly 10 scds (Fg. 10.13C).
9. Rmv h dl d llw h sk  rr 
s rml ps (Fg. 10.13D).
10. Do not mssg h jc s.
11. If frhr jcs r  b md, lr
5 6 mg ss pr h msr r schdl.
Deltoid
12. Do not rcp y dls h hv b sd.
Dsps f sd dls d syrgs  
pcr-rss dl dspsl cr 
ccrdc wh sl plcy.
13. Rmv glvs d dsps f hm ccrdg 
fcly plcy. Prfrm hd hyg.
14. Tch h p h wlkg wll hlp wh h
1 2 mdc’s bsrp. Vgrs xrcs r
prssr  h jc s (.g., gh-g
clhg) shld b mprrly vdd.
Ventro-
3
gluteal
4
PATIENT TEACHING
Vastus Prfrm pprpr p chg s dscrbd 
lateralis rld drg mgrphs.
B
Fig. 10.12 Intramuscular master rotation plan. (A) Infant or child. Note DOCUMENTATION
that the deltoid site may also be used in an infant or child; however,
Prvd h rgh dcm f h mdc
the volume of medication must be small and the drug nonirritating. (B)
Adult. In an adult, avoid using the rectus femoris site because of the dmsr d h p’s rsps  drg
pain produced. hrpy.
1. Chr h d, m, drg m, ds, s, d
“ch” hlps. Prs h p fr hr sssc r f dmsr.
d cpr. 2. Prfrm d rcrd rglr p ssssms fr
18. Rmv glvs d prfrm hd hyg. h vl f h hrpc ffcvss (.g.,
bld prssr, pls, p, mprvm r
Z-Track Method qly f cgh d prdcvy).
Th s f  Z-track method (Fg. 10.13) my b ppr- 3. Chr d rpr y sgs d sympms f d-
pr fr mdcs h r prclrly rrg vrs drg ffcs.
r h s h ss. Chck fcly plcy rgrdg 4. Prfrm d vld ssl p dc
whch prsl my dmsr mdcs sg b h drg hrpy.
hs mhd.
146 UNIT II Illustrated Atlas of Medication Administration

Subcutaneous fat
Skin
Muscle

A B

C D
Fig. 10.13 Z-track method of intramuscular injection. (A) Alignment of layers before starting Z-tracking. (B) Stretch the
skin slightly to one side by approximately 1 inch. (C) Inject the medication and then wait approximately 10 seconds. (D)
Remove the needle and allow the skin to return to its normal position. Do not massage the injection site.
 Parenteral Administration: Intradermal, Subcutaneous, and Intramuscular Routes CHAPTER 10 147

Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions

Key Points 2. A student nurse has been practicing subcutaneous injections in the
laboratory and is about to administer her rst insulin injection. List
• Intradermal injections are made into the dermal layer just in correct order the proper sequence to follow when administering
below the epidermis and are usually 0.1 mL in volume. a subcut injection.
• Subcutaneous injections are made into the subcutaneous
1. Withdraw the needle
tissue or fatty layer between the dermis and the muscle.
2. Inject the insulin
The volume of injection should be no greater than 2 mL.
3. Explain procedure to patient
• Intramuscular injections are made into the muscle below 4. Dart the needle in at a 45- to 90-degree angle
the subcutaneous tissue. Care must be taken to ensure 5. Prepare the insulin per prescriber’s orders
that the muscle is injected. 6. Document the administration
• The sites for administration of IM injections include the 7. Cleanse the site with alcohol
vastus lateralis muscle, the rectus femoris muscle, the 8. Identify the patient using two identiers
ventrogluteal area, and the deltoid muscle. Generally, 9. Locate the appropriate site for administration
an immunization is only 0.5 mL and can be given in the
Objective: Identify the equipment needed and describe
deltoid muscle for most adults.
the technique that is used to administer medication via the
• The most suitable sites for an IM injection for children are subcutaneous route.
the vastus lateralis muscle, the rectus femoris muscle, or NGN test item: Ordering
the ventrogluteal area. In adults, the sites are the same as Cognitive skill: Application
for a child, but also include the deltoid muscle.
• The Z-track method is one way to deliver an IM injection 3. Why will a nurse who administers an IM medication of iron use the
when irritating medications need to be administered. Z-track method of administration?
1. It will provide faster absorption of the medication.
Additional Learning Resources 2. It will reduce discomfort from the needle.
3. It can provide more even absorption of the drug.
SG Go to your Study Guide for additional Review Questions 4. It will prevent the drug from staining or irritating sensitive
for the NCLEX® Examination, Critical Thinking Clinical Situa- tissue.
tions, and other learning activities to help you master this chap-
Objective: Describe the techniques used to administer medications
ter content.
intramuscularly.
NCLEX test item: Multiple choice
Go to your Evolve website (https://evolve.elsevier.com/Willihng
Cognitive skill: Comprehension
anz) for additional online resources.
4. The nurse is nding the landmark of the acromion process and
Clinical Judgment and Next-Generation NCLEX® Exam- measuring down two to three ngerbreadths to administer an IM
ination-Style Questions The following questions are typical of injection into which site?
the NCLEX examination and include both NGN (Next Genera-
1. Vastus lateralis muscle
tion) and traditional questions. See Chapter 1 for further infor-
2. Rectus femoris muscle
mation regarding question types.
3. Deltoid muscle
1. The instructor asks the student nurse to gather the equipment 4. Ventrogluteal site
needed to perform an intradermal injection. Which items are Objective: Describe the landmarks that are used to identify
appropriate? (Select all that apply.) the vastus lateralis muscle, the rectus femoris muscle, the
1. 3-mL syringe ventrogluteal area, and the deltoid muscle sites before medication
2. Tuberculin syringe is administered.
3. ¼-inch needle NCLEX test item: Multiple choice
4. 21-gauge needle Cognitive skill: Knowledge
5. 26-gauge needle
5. A student nurse reads an order to give a 69-year-old patient an IM
6. ⅝-inch needle
injection. Which muscles could be used for injection sites for an
Objective: Describe the technique that is used to administer a adult? (Select all that apply.)
medication via the intradermal route.
1. Deltoid
NCLEX test item: Extended multiple response
2. Dorsogluteal
Cognitive skill: Evaluate cues
3. Ventrogluteal
4. Vastus lateralis
5. Rectus femoris
Objective: Identify suitable sites for the intramuscular
administration of medication in an infant, a child, an adult, and an
older adult.
NCLEX test item: Multiple response
Cognitive skill: Application
148 UNIT II Illustrated Atlas of Medication Administration
6. The nurse needs to administer an IM injection and chooses the
rectus femoris muscle. What landmarks will the nurse use for the
injection?
1. Two ngerbreadths below the acromion process
2. One handbreadth below the greater trochanter and one
handbreadth above the knee
3. Between the V of the index nger and middle nger when
on the trochanter
4. Between the anterior superior iliac spine and the iliac
crest
Objective: Describe the landmarks that are used to identify
the vastus lateralis muscle, the rectus femoris muscle, the
ventrogluteal area, and the deltoid muscle sites before medication
is administered.
NCLEX test item: Multiple choice
Cognitive skill: Knowledge
7. The nurse is preparing to administer an IM injection to an elderly
patient; what considerations need to be practiced? (Select all that
apply.)
1. The muscle needs to be palpated to determine whether
the muscle mass is sufcient.
2. The length of the needle may need to be adjusted
because the patient is older and the muscle mass may
be insufcient.
3. The amount of the injection must be limited to 1 mL or
less.
4. The injection needs to be in the deltoid muscle only.
5. A site rotation plan should be consulted before
administration.
Objective: Identify suitable sites for the intramuscular
administration of medication in an infant, a child, an adult, and an
older adult.
NCLEX test item: Multiple response
Cognitive skill: Application
Parenteral Administration: Intravenous Route 11
https://evolve.elsevier.com/Willihnganz

Objectives
1. Discuss the different intravenous (IV) access devices used
for IV therapy.
2. Differentiate between isotonic, hypotonic, and hypertonic
IV solutions and explain their clinical uses.
3. Identify the general principles for administering medications
via the IV route.
4. Compare and contrast the differences between a
peripheral IV line and a central IV line.
5. Describe the correct techniques for administering
medications by means of a saline lock, an IV bag, an
infusion pump, and a secondary piggyback set.
6. Identify baseline assessments for IV therapy and proper
maintenance of patency of IV lines and implanted access
devices.
7. Explain the signs, symptoms, and treatment of the
complications associated with IV therapy (e.g., phlebitis,
thrombophlebitis, localized infection, septicemia,
inltration, extravasation, air in tubing, pulmonary edema,
catheter embolism, and “speed shock”).

Key Terms
intravenous (ĭn-tră-VĒ-nŭs) (p. 149)
intracellular (ĭn-tră-SĔL-yĕ-lĕr) (p. 150)
intravascular (ĭn-tră-VĂS-cū-lĕr)
(p. 150)
interstitial (ĭn-tĕr-STĬ-shĕl) (p. 150)
extracellular (ĕk-strĕ-SĔL-yĕ-lĕr)
(p. 150)
IV administration set (p. 150)
macrodrip (p. 150)
microdrip (p. 150)
programmable infusion
pumps (prō-GRĂM-ă-bŭl ĭn-FŪ-
zhăn PŬMPZ) (p. 152)
syringe pumps (sĭ-RĬNJ) (p. 152)
peripheral devices (pĕ-RĬF-ĕr-ăl dĕ-
VĪ-sĕz) (p. 153)
midline catheters (MĬD-līn KĂTH-ĕ-
tŭrz) (p. 153)
central devices (SĔN-trŭl dĕ-VĪ-sĕz)
(p. 153)
implantable venous infusion
ports (ĭm-PLĂNT-ă-bŭl VĒ-nŭs
ĭn-FŪ-zhăn PŌRTS) (p. 153)
winged, buttery, or scalp
needles (WĬNGD, BŬT-ŭr-ī, SKĂLP
NĒ-dŭlz) (p. 153)
over-the-needle catheters (p. 153)
saline lock or medlock (SĀ-lēn-lŏk,
MĔD-lŏk) (p. 153)
in-the-needle catheters (p. 153)
peripherally inserted central
venous catheters (PICCs) (pĕ-
RĬF-ŭr-ăl-ē ĭn-SŬR-tĕd SĔN-trŭl VĒ-
nŭs KĂTH-ĕ-tŭrz) (p. 154)
tunneled central venous
catheters (TŬN-ŭld) (p. 154)
implantable infusion ports (ĭm-
PLĂNT-ă-bŭl ĭn-FŪ-zhăn PŌRTZ)
(p. 155)
intravenous (IV) solutions (ĭn-tră-VĒ-
nŭs sŏl-Ū-shŭnz) (p. 156)
electrolytes (ĕ-LĔK-trō-līts) (p. 156)
isotonic (ī-sō-TŎN-ĭk) (p. 156)
hypotonic (hī-pō-TŎN-ĭk) (p. 156)
hypertonic (hī-pĕr-TŎN-ĭk) (p. 156)
tandem setup, piggyback, or IV
rider (TĂN-dĕm, PĬ-gē-băk, RĪ-dŭr)
(p. 157)
SASH guideline (SĂSH GĪD-līn)
(p. 160)
phlebitis (ĕ-BĪ-tĭs) (p. 174)
thrombophlebitis (thrŏm-bō-ĕ-BĪ-
tĭs) (p. 174)
Inltration Scale (ĭn-fĭl-TRĀ-shŭn
SKĀL) (p. 174)
septicemia (sĕp-tĭ-SĒ-mē-yŭ) (p. 175)
inltration (ĭn-fĭl-TRĀ-shŭn) (p. 175)
extravasation (ĕks-tră-vă-SĀ-shŭn)
(p. 175)
air embolism (ĀR ĔM-bō-lĭz-ŭm)
(p. 176)
pulmonary edema (PŬL-mō-nār-ē
ĕ-DĒ-mŭ) (p. 176)
pulmonary embolism (PŬL-mō-nār-ē
ĔM-bō-lĭz-ŭm) (p. 176)
“speed shock” (SPĒD SHŎK) (p. 176)

Th rm intravenous (IV) adminisrain rfrs  h
inrducin f uids dircly in h vnus bld-
sram. Th advanag f his chniqu is ha larg vl-
ums f uids can b rapidly adminisrd in h vin
fr vlum xpansin in cass f shck, r mr rapid
ns f mdicains adminisrd inravnusly in cas-
s f mrgncy. IV adminisrain is h ms rapid f
all parnral rus bcaus i bypasss all barrirs 
drug absrpin. Drugs may b givn by dirc injcin
wih a ndl in h vin, bu hy ar mr cmmnly
adminisrd inrminly r by cninuus infusin
hrugh an sablishd priphral r cnral IV lin.
An advanag f IV adminisrain cmpard wih
hr frms f parnral adminisrain is ha i is
149
150 UNIT II Illustrated Atlas of Medication Administration
C prcdurs f individual clinical pracic sings. Th
A nurs shuld chck wih hir paricular sa bard f
A
C
B biliis d n includ h adminisrain f IV mdica-
A C
Fig. 11.1 Fluid compartments of the body. (A) Intracellular spaces (e.g.,
the spaces within the cells). (B) Vascular spaces (e.g., within arteries,
veins, and capillaries). (C) Interstitial spaces (e.g., the spaces between
the cells). The body maintains a water and electrolyte balance among
these compartments for homeostasis.
gnrally mr cmfrabl fr h pain, spcially
whn svral dss f mdicains mus b adminis-
rd daily. Hwvr, disadvanags  h IV ru
includ nurss nding h skill  sablish and main-
ain an IV si. In addiin, h pain nds  b lss
mbil wih IV adminisrain, and hr is a grar
pssibiliy fr infcin and fr svr advrs rac-
ins  h drug.
Frm a physilgic sandpin, h war in h
bdy is disribud amng hr cmparmns: (1)
h intracellular cmparmn—wihin h clls (Fig.
11.1A); (2) h intravascular cmparmn—wihin h
vascular sysm (.g., h arris, vins, and capillar-
is) (Fig. 11.1B); and (3) h interstitial cmparmn—
wihin h spacs bwn h clls ha ar usid
f h vascular cmparmn (Fig. 11.1C). Th extra-
cellular cmparmn (h spacs usid h clls) is
cmpsd f h inravascular and inrsiial cm-
parmns, and i cnains abu n-hird f h al
bdy war, whras h inracllular cmparmn
(wihin h clls) cnains abu w-hirds f h al
bdy war.
All IV hrapy rquirs a wrin rdr frm a
halhcar prvidr ha is dad and ha spcis h
yp f sluin r mdicain  b adminisrd, h
dsag, and h ra and frquncy f adminisrain.
Sm hspials us infusin hrapy ams fr ad-
minisrain via h IV sysm, bu many nw assign
h rspnsibiliy fr infusin hrapy  nurss wih
arnd crdnials. Th nurs wh is prfrming vni-
puncur (iniiain f an IV lin) and infusin hrapy
mus b wll vrsd in h guidlins sablishd by
h Infusin Nurss Sciy.
Th Infusin Nurss Sciy, a prfssinal nurs-
ing rganizain, publishs h Infusin Nursing
Sandards f Pracic rlad  qualiy assuranc,
chnlgy and applicain, uids and lcrlys,
pharmaclgy, infcin cnrl, pdiarics, nclgy,
and parnral nuriin. Ms sa laws rcgniz
h rl f h licnsd pracical nurs/licnsd vca-
inal nurs (LPN/LVN) in IV hrapy, bu dlga
h scp f pracic  b dnd in h plicis and
nursing  drmin h currn guidlins and du-
cain rquirmns. In gnral, LPN/LVN rspnsi-
in, bld prducs, r aninplasic agns.
Bfr any nurs adminisrs IV hrapy, hy
shuld ask h fllwing qusins:
• “Ds h law in his sa dlga his funcin 
h nurs?”
• “Ds h wrin plicy f h insiuin r agncy
hrugh which I am mplyd, wih h apprval f
h mdical saff, prmi a nurs wih my lvl f d-
ucain and xprinc  adminisr IV hrapy?”
• “Ds h insiuin r agncy plicy limi h yps
f uids and mdicains ha I may adminisr?”
EquipmEnt usEd for intravEnous
thErapy
Intravenous admInIstratIon sets
An IV administration set is an apparaus ha cnncs a
larg vlum f parnral sluin wih h IV accss
dvic in h pain’s vin. All ss (Fig. 11.2) hav an in-
srin spik, a drip chambr, plasic ubing wih a ra-
cnrl clamp, a rubbr injcin pral (als rfrrd 
as a Y pr), a ndl adapr, and a prciv cap vr
h ndl adapr. Dpnding n h manufacurr, h
ss ar availabl in a variy f syls (.g., diffrn vl-
ums and sizs f drip chambr, “piggyback” prals,
lrs, and syls f cnrl clamps [Fig. 11.3]).
Th yp f sysm usd by a paricular insiuin
is usually drmind by h manufacurr f h IV
sluins usd by h insiuin. Each manufacurr
maks adaprs   a spcic yp f plasic r glass
larg-vlum sluin cnainr. A crucial pin  r-
mmbr abu adminisrain ss is ha h drps
dlivrd by drip chambrs vary amng manufacur-
rs. Macrodrip chambrs (s Fig. 11.2A and B) prvid
10, 15, r 20 drps/mL f sluin, whras micro-
drip chambrs (s Fig. 11.2C) dlivr 60 drps/mL f
sluin.
Micrdrip adminisrain ss ar usd whn a small
vlum f uid is bing adminisrd, paricularly
whn accuracy f vlum adminisrain is indica-
d (.g., wih nnaal and pdiaric ppulains; fr
hs pains wih uid vlum cncrns). Vlum-
cnrl chambrs (s Fig. 11.2A and C) ar als usd
as a safy facr  limi h vlum adminisrd. In
many clinical sings, micrdrip ss ar usd fr all
vlums f IV uid rdrd ha ar adminisrd a
lss han 100 mL/hr. I is ssnial  rad h labl n
h packag bfr pning i  nsur ha h crrc
IV adminisrain s has bn slcd.
Th nurs mus b abl  calcula h w ra
fr any IV sluin. Th w ras ha ar usd fr
 Parenteral Administration: Intravenous Route CHAPTER 11 151

Vent Vent

Plastic
Glass bag Macrodrip chamber Glass Microdrip chamber
bottle bottle

Primary
port
Slide
Insertion clamp
Roller spike
clamp

Macrodrip
chamber

Volume Volume
control control
chamber Roller chamber
clamp

Microdrip
Filter chamber

Macrodrip Needle adapter

chamber and protective cap
Secondary Roller
port clamp
Secondary
port

A B C
Fig. 11.2 (A and B), Different types of intravenous (IV) administration sets that make use of a macrodrip chamber. (C) An
IV administration set that includes a microdrip chamber.

infusin pumps ar gnrally in millilirs pr hur
(mL/hr). A ypical w ra prblm wuld b as
fllws: A wha ra will h nurs s h infusin
pump if h rdr rads, “Infus 1000 mL f D5W vr
8 hurs”? Calcula h ra f infusin using a simpl
frmula: mL dividd by hurs.
1000 mL
= 125 mL / hr
8 hr
Th nurs ss h pump ra fr 125 mL/hr, mak-
ing sur  n h im h infusin sard. This
infrmain is ky  pass n  h nx shif if h
infusin is n cmpld wihin h im fram ha
h nurs wh sard h infusin will b prsn.
Th primary pars f h IV adminisrain s nd
 b labld; h IV uid nds a labl ha indi-
cas whn i nds  b changd (usually in 24 
48 hurs), and h IV ubing nds a labl indica-
ing whn i nds  b changd (usually in 72 
96 hurs).
ei u i Cjci Wi I
t
A larg variy f cnncr and accss dvics ar
availabl fr varius cmpnns f infusin hrapy.
Th nurs mus bcm familiar wih h IV accss
sysms and h rms usd fr hs sysms a h
clinical pracic sing. Knwing which pars f h
sysm ar clan and which pars ar  rmain sril
is crucial fr h prvisin f saf IV hrapy.
types of InfusIon-Control pumps
Prcis infusin ras ar impran fr crain hra-
puic ffcs (.g., wih a cninuus hparin infusin
152 UNIT II Illustrated Atlas of Medication Administration
fr anicagulain) r whn mniring h adminis-
rain f mdicains  prvn xiciy (.g., nphr-
xiciy, xiciy). Prgrammabl infusin pumps
ar usd  nsur h saf adminisrain f IV uids
and mdicains (Fig. 11.4).
A B
Fig. 11.3 Control clamps for intravenous administration sets. (A) Roller
clamp. (B) Slide clamp. (A, From Perry AG, Potter PA, Ostendorf WR.
Clinical Nursing Skills and Techniques. 8th ed. St. Louis: Mosby; 2014.
B, From Otto SE. Pocket Guide to Intravenous Therapy. 4th ed. St.
Louis: Mosby; 2001.)
C B
Fig. 11.4 (A) Infusion controller. (B) Infusion pump. (C) Syringe pump. (A, Courtesy Hospira, Inc., Lake Forest, IL.
B, Courtesy Baxter Healthcare Corporation, Mountain Home, AR. All rights reserved. C, Courtesy Smiths Medical,
Minneapolis, MN.)
p
Th programmable infusion pumps apply xrnal prs-
sur  h adminisrain s ubing  squz h s-
luin hrugh h ubing a a spcic ra (.g., a cr-
ain numbr f mL/min r mL/hr). Ths pumps ar
prgrammd fr a spcic vlum vr im. Ths
pumps hav an alarm sysm ha sunds if hr is
rsisanc in h IV lin causd by a dvlping cclu-
sin as a rsul f hrmbus frmain r a kink in h
adminisrain s lin causd by pain mvmn.
Disadvanags f pumps ar h cs f h quipmn
and h raining f prsnnl, h cs f mainnanc,
h nd fr mr quipmn a h bdsid, and h
pnial fr srius IV inlrain.
si p
Syringe pumps hld a prlld syring and apply psi-
iv prssur  h plungr  dlivr a spcic vl-
um f mdicin vr a s im. Syring pumps ar
mr cmmnly usd whn small vlums nd  b
adminisrd (Fig. 11.4C). Exampls f small syring
pumps ar hs ha cninually infus insulin in
h subcuanus issu f pains wih diabs ml-
lius and pain-cnrlld analgsia pumps, which
allw pains wh ar rciving pain mdicains 
adminisr cninual infusins and inrmin blus-
s f h mdicin fr cmfr.
Syring pumps ar asy  us, and hir us is
augh  pains nding hm infusin hrapy,
 Parenteral Administration: Intravenous Route CHAPTER 11
whn pains slf-adminisr mdicains hrugh an
impland infusin pr. I is impran ha h nurs
bcm familiar wih h spcic dvics ha ar usd
in h clinical sing fr saf and fcin pain car.
Intravenous aCCess devICes
IV accss dvics ar fn subdividd in fur
grups n h basis f h lcain f h rminal ip
f h accss dvic: (1) peripheral devices ar fr shr-
rm us in priphral vins in h hand r frarm; (2)
midline catheters ar fr us vr 2  4 wks and ar
insrd in inrmdia-sizd vins and advancd
in largr vssls; (3) central devices ar insrd in
inrmdia-sizd vssls and advancd in cnral
vins whr h ip f h cahr ypically will b in
h suprir vna cava  allw fr maximal mixing
wih larg vlums f bld; and (4) implantable ve-
nous infusion ports, which ar surgically placd in
cnral vins fr lng-rm hrapy.
pi acc dic
All ndls—if hy ar lng nugh—may b usd
 adminisr mdicains r uids inravnusly.
Hwvr, spcial quipmn has bn dsignd fr
his purps. Winged needles, which ar als knwn
as buttery r scalp needles, ar shr, sharp-ippd
ndls (Fig. 11.5) ha wr riginally dsignd fr
vnipuncur f small vins in infans and fr gria-
ric us. Ths ndls ar availabl in sizs ha rang
frm 17  29 gaug, and hav bn dsignd  mini-
miz issu injury during insrin. Th wingd ara
is pinchd ghr  frm a handl whil h ndl
is bing insrd. Th wings ar hn laid a agains
h skin  frm a bas ha can b anchrd wih ap.
Tw yps f hs ndls ar nw availabl: n wih
a shr lngh f plasic ubing and a prmannly a-
achd rsalabl injcin pr and n wih a variabl
lngh f plasic ubing wih a fmal Lur adapr fr
h aachmn f a syring r an adminisrain s
(s Fig. 11.5). Th pancy f h ndl is mainaind
Fig. 11.5 Winged needle with a female Luer adapter. (Courtesy Narang
Medical Limited, New Delhi, India.)
153
wih h us f a hparin r salin ush ruin in ac-
crdanc wih faciliy plicy.
Over-the-needle catheters, which ar als knwn
as short peripheral venous catheters, ar rcmmndd
fr ruin priphral infusin hrapy. Th ndls
ar sainlss sl and cad wih a Tn-lik plasic
cahr (Fig. 11.6A). Afr h ndl pnras h
vin in h hand r frarm, h cahr is advancd
in h vin and h mal ndl is rmvd, hrby
laving h plasic cahr in plac. An IV adminisra-
in s is hn aachd  h cahr fr cninuus
infusin. This uni is usd whn IV hrapy is xpcd
 cninu fr a fw days. Th rainal fr h us f
h plasic cahr is ha i ds n hav a sharp ip
ha culd caus vnus irriain and xravasain.
Whn a pain n lngr rquirs IV uid hrapy
bu vnus accss is sill ndd fr mdicain ad-
minisrain, an xnsin ub wih an injcin pr
is aachd  h cahr and h IV uid is discnin-
ud. This yp f IV accss dvic is calld a saline lock
r a medlock (i.., medication lock). Nrmal salin (NS)
ushing rahr han hparin is sufcin  prvn
cling and mainain h priphral cahr ingriy.
Gnrally, priphral cahrs shuld b changd v-
ry 72  96 hurs  prvn infcin and phlbiis.
Bld sampls shuld n b drawn frm priphral
cahrs. If sis fr vnus accss ar limid and n
vidnc f infcin is prsn, priphral vnus
cahrs can rmain in plac, alhugh h pain and
h insrin si shuld b mnird clsly fr signs
and sympms f phlbiis, inlrain, and infcin.
Th Cnrs fr Disas Cnrl and Prvnin (CDC)
rcmmnds ha priphral cahrs n b changd
fr pdiaric pains unlss his is clinically indicad.
In-the-needle catheters mak us f larg-br n-
dls fr vnipuncur (Fig. 11.6B). A 4-  6-inch sr-
il, smallr-gaug, plasic cahr is hn advancd
hrugh h ndl in h vin. Th ndl is wih-
drawn, and h skin frms a sal arund h plasic
cahr. Th IV adminisrain s is aachd dircly
 h plasic cahr. In-h-ndl cahrs ar sl-
dm usd day fr priphral IVs bcaus f h risk
f sharing h hrugh-h-ndl cahr.
Midlin accss cahrs ar slcd fr us if i is
anicipad ha IV accss will b ndd fr 7 days r
mr. Ths cahrs ar fn lf in plac fr 2  4
wks. Midlin cahrs ar xibl and 3  8 inchs
lng, and ar insrd a h ancubial fssa in h
cphalic r basilic vin and advancd  h disal sub-
clavian vin. Thy d n nr h suprir vna cava.
Midlin cahrs appar  b assciad wih lwr
ras f phlbiis han shr priphral cahrs; hy
hav a lwr ra f infcin, and hy cs lss han
cnral vnus cahrs. Th CDC rcmmnds h r-
placmn f h cahr and h rain f h injc-
in si n mr frqunly han vry 72  96 hurs,
bu h CDC ds n prvid rcmmndains r-
garding h maximum lngh f im ha h cahr
154 UNIT II Illustrated Atlas of Medication Administration
Needle Needle
guard
Needle Needle
hub
Collar
Catheter
Catheter Protective
sleeve
Protective
cover
Catheter
hub Catheter
adapter
Needle
hub
Flow
Protective control
plug
A cap
B sis, hmhrax), hy cs lss han hr cnral v-
Fig. 11.6 (A) Over-the-needle catheter. This unit is the most commonly
used type of catheter when intravenous therapy is expected to
continue for several days. (B) In-the-needle catheters make use of a
large-bore needle for venipuncture. A 4- to 6-inch sterile, small-gauge,
plastic catheter is then advanced through the needle and into the vein.
The needle is withdrawn, and the skin forms a seal around the plastic
catheter. The intracatheter is infrequently used today.
may rmain in plac. Many insiuins rquir ha h
halhcar prvidr wri an rdr ha indicas ha
h IV infusin may b lf in plac fr mr han 72
hurs. Midlin cahrs ar usd fr cninuus ac-
css, rpad accss, r IV sluins wih high w
ras. This yp f cahr nds  b ushd wih
salin and hparin sluin afr ach us, r a las
nc daily if i is n in us. Bld shuld n b drawn
hrugh his cahr.
C acc dic
Cnral IV accss dvics, which ar als knwn as in-
dwelling catheters, ar usd in h fllwing siuains:
whn h purps f hrapy dicas hir us (.g.,
larg vlums f mdicain, fr irriaing mdicin
such as chmhrapy, r whn hyprnic sluins
such as al parnral nuriin [TPN] ar  b in-
fusd); whn priphral sis hav bn xhausd as
a rsul f rpad us r h cndiin f h vins
fr accss is pr; whn lng-rm r hm hrapy is
rquird; r whn mrgncy cndiins manda ad-
qua vascular accss.
Th cnral vnus sis ha ar ms cmmnly
usd fr cnral vnus cahrs ar h subclavian
and jugular vins. Whn h uppr bdy vins ar
n accpabl, h fmral vins may b accssd fr
shr-rm r mrgncy us. A primary halhcar
prvidr can als lc  prfrm a vniscin r a
cudwn  insr his yp f cahr in h basilic
r cphalic vins in h ancubial fssa. Thr yps
f dvics, basd n h placmn f h cahr’s
prximal ip, ar ruinly usd fr cnral cahrs:
priphral dvics, unnld dvics, and implanabl
dvics.
Peripherally inserted central venous catheters
(PICCs) ar insrd in h ancubial spac r frm
h uppr arm accssing h cphalic r basilar vins
nding in h suprir vna cava r jus usid h
righ arium. PICCs prvid an alrnaiv  sub-
clavian r jugular vnus cahrizain and ar usd
fr infusin hrapy and bld draws. PICCs ar avail-
abl in sizs ha rang frm 14  28 gaug, wih varius
lnghs, hrby making hm availabl fr pdiaric
us. Th cahr islf can hav an pn ip r a valvd
(Grshng) ip, and i cms wih a singl r dubl
lumn. Th PICC lin has h advanag f as f
insrin bcaus h prcdur can b prfrmd a
h bdsid by a qualid nurs. PICCs ar assciad
wih fwr mchanical cmplicains (.g., hrmb-
nus cahrs, hy ar asir  mainain han shr
priphral cahrs (bcaus hr is lss frqun in-
lrain and phlbiis), and hy rquir lss frqun
si rain. PICC lins ruinly rmain in plac fr
1  3 mnhs, bu hy can las fr 1 yar r mr if
hy ar card fr prprly. Whn h dvic is n in
us, h IV infusin is discnncd and h cahr is
ushd and cappd. Th lin shuld b ushd wih a
salin-hparin sluin afr vry us r daily, if n
usd, in accrdanc wih insiuinal plicy.
Tunneled central venous catheters ar surgically
placd during an upain prcdur wih h pa-
in undr lcal anshsia. Th rminal ip f h
cahr is insrd hrugh an incisin and in h
subclavian vin, whr i is hn advancd  h sup-
rir vna cava. Th prximal nd f h cahr is un-
nld abu 6 inchs away undr h skin n h chs
 xi mid chs. A Dacrn cuff is fn placd arund
h cahr undr h skin, which anchrs h cahr
and frms a sal arund h cahr as h skin hals,
hrby hlping  kp h unnl sril.
Thr yps f cahrs ha ar frqunly usd ar
h Hickman, Brviac, and Grshng cahrs (Fig.
11.7). Th Brviac cahr is a singl-lumn cahr
wih a largr xrnal diamr and a sandard nd
hl. Th Hickman cahr is largr in diamr han
h Brviac cahr, bu i cnains w r hr lu-
mns; i als has a sandard nd hl. Whn hy ar
n in us, bh f hs cahrs ar clampd  pr-
vn cnaminain, cling, and air mblism. Ths
cahrs mus als b ushd wih a salin-hparin
sluin afr vry mdicain adminisrain, r a
las nc daily if hy ar n in us. Th Grshng
cahr cnains n  hr lumns, and ach n
has a rundd valvd ip. Th Grshng valv pns
inward fr bld sampling and uward fr infusin,
bu i rmains clsd whn i is n in us. Bcaus
h valv rmains clsd whn i is n in us, i sals
 Parenteral Administration: Intravenous Route CHAPTER 11
A
B 1000 puncurs.
C xrcis, including swimming; hwvr, cnac sprs
Fig. 11.7 (A) Hickman catheter. (B) Broviac catheter. (C) Groshong
catheter. (Courtesy Chuck Dresner.)
h uid insid h cahr and prvns i frm cm-
ing in cnac wih h pain’s bld. Thus wkly
ushing wih salin sluin is all ha is rquird 
kp h cahr pan. Th valv als liminas h
nd fr ruin clamping f h cahr, alhugh i
shuld rmain cappd whn i is n bing usd.
Implantable infusion ports (.g., Infus-A-Pr, Pr-
A-Cah) ar usd whn lng-rm hrapy is rquird
and inrmin accssing f h cnral vin is r-
quird fr h adminisrain f IV uids, mdicains,
TPN, chmhrapy, and bld prducs. Th implan-
abl dvics ar similar  unnld dvics wih r-
gard  placmn; hwvr, h prximal nd f h
singl- r dubl-lumn cahr is aachd  a sin-
gl- r dubl-lumn accss pr (Fig. 11.8) and hn
impland and suurd in a subcuanus pck
in h chs ara r h uppr arm. Th dubl prs
ar dsignd  allw fr h adminisrain f w IV
sluins, w IV mdicains, r n f ach simul-
anusly. On pr can als b rsrvd fr drawing
bld sampls. Th prs cnain a slf-saling silicn
rubbr spum ha has bn spcically dsignd fr
rpad injcins vr an xndd prid f im.
155
Fig. 11.8 Silicone venous catheter with infusion ports. (From Potter
PA, Perry AG. Basic Nursing: Theory and Practice. 5th ed. St. Louis:
Mosby; 2001.)
A spcial nncring, 90-dgr-angl Hubr ndl is
usd  pnra h skin and h spum f h im-
pland dvic  minimiz damag  h slf-saling
spum. T prlng h lif f h spum, nly h
smalls-gaug nncring ndls shuld b usd. Th
chs pr is simad  wihsand up  2000 punc-
urs, whras h arm pr has an simad lif f
An impland cnral vnus accss cahr may
rmain in plac fr mr han 1 yar, and i rquirs
nly a salin-hparin sluin ush afr vry accss
r nc mnhly. Bcaus h nir pr and cahr
ar undr h skin, n daily mainnanc is ndd, al-
hugh h si shuld b mnird visually n a rg-
ular basis  chck fr swlling, rdnss, r drainag.
This yp f cnral vnus cahr givs h pain
h gras xibiliy in rms f daily aciviis and
shuld b avidd.
All cnral vnus accss dvics rquir ps
insrin radigraphy  vrify h lcain f h d-
vic and  chck fr h prsnc f a pnumhrax
fr cahrs ha ar unnld n h chs. Th CDC
rcmmnds ha cnral vnus cahrs n b ru-
inly rplacd  prvn cahr-rlad infcin.
intravEnous dosE forms
Rviw Chapr 9 fr infrmain abu h us f am-
puls, vials, and Mix-O-Vials. All parnral drug ds
frms ar packagd s ha h drug is sril and rady
fr rcnsiuin (if ndd) and adminisrain.
types of Intravenous solutIons
Undr nrmal and halhy cndiins, h bdy lss
war and lcrlys daily hrugh urin, prspira-
in, and fcs. Fluids ar rplnishd as a rsul f h
absrpin f war in h gasrinsinal rac frm
h liquids and fds ha ar cnsumd. Hwvr, as
a rsul f many diffrn disas sas (.g., vmi-
ing, diarrha, gasrinsinal sucining, hmrrhag,
drainag frm a wund, dcrasd inak, nausa,
anrxia, fvr, xcss lss frm disas [.g., uncn-
rlld diabs mllius, diabs insipidus]), pains
ar unabl  ings sufcin quaniis f uid and
156 UNIT II Illustrated Atlas of Medication Administration

lcrlys  ffs hs lsss. Whn his happns, addiin  nugh carbhydras (usually dxrs),
h IV infusin f sluins may b ncssary fr r- amin acids, and fay acids  susain lif.
placmn. S a mdical-surgical nursing xbk fr Th spnanus mvmn f war acrss h
mr infrmain abu pain assssmns fr d- inravascular cmparmn capillary mmbrans 
cin uid vlum. h inrsiial spacs and acrss h cll mmbrans
Intravenous (IV) solutions (Bx 11.1) cnsis f wa- and back  h inravascular capillary spac is calld
r (.g., a slvn) ha cnains n r mr yps f osmosis. Th war mvs frm an ara f high cn-
disslvd paricls (.g., slus). Th slus ha ar cnrain f war (.g., f lw lcrly cncnra-
ms cmmnly disslvd in IV sluins ar sdium in)  an ara f lw war cncnrain (.g., f
chlrid, dxrs, and passium chlrid. Th sl- high lcrly cncnrain). Th lcrly and
us ha disslv in war and disscia in in par- prin cncnrains f ach uid cmparmn ar
icls (.g., Na+, K+, Cl ) ar calld electrolytes bcaus wha draw war in h cmparmn unil hr is
hs ins giv war h abiliy  cnduc lcriciy. quilibrium bwn cmparmns. Th frc causd
TPN sluins cnain all h lcrlys ncssary in by h lcrlys and prins is calld osmotic pres-
sure. Th cncnrain f h disslvd paricls in
ach cmparmn is knwn as h osmolality. Nrmal
bld srum smlaliy is 295  310 millismls pr
Box 11.1 Types of Intravenous Solutions and Their lir (mOsm/L). Bcaus IV sluins als cnain dis-
Ingredientsa slvd paricls, hy als hav an smlaliy. If h IV
sluin and h bld hav apprximaly h sam
ElEctrolytE SolutionS
• 5% dextrose in water (D5W)
smlaliy, hn h sluin is said  b isotonic.
• 10% dextrose in water (D10W) Sluins ha hav fwr disslvd paricls han h
• 0.45% sodium chloride (0.45 NS) bld ar cnsidrd  b hypotonic, and hs wih a
• 0.9% sodium chloride (normal saline; NS) highr cncnrain f disslvd paricls ar hugh
• Lactated Ringer solution (LR) f as hypertonic. A 0.9% sluin f sdium chlrid,
• 5% dextrose in 0.2% sodium chloride (D5/0.2 NS) which is als knwn as normal saline (NS) r physiologic
• 5% dextrose in 0.45% sodium chloride (D5/0.45 NS) saline, is an isnic sluin wih an smlaliy f 308
• 5% dextrose in 0.9% sodium chloride (D5/0.9 NS) mOsm/L. Tabl 11.1 liss cmmnly usd IV sluins,
• 5% dextrose in lactated Ringer solution (D5/LR) hir lcrly cncnrains, and hir smlaliis.
• 5% dextrose in 0.2% sodium chloride with 20 mEq of
Ths sluins wih smlaliis blw 270 mOsm/L
potassium chloride (D5/0.2 NS + 20 KCl)
ar hypnic, hs wih valus frm 270  310
nutriEnt Solution mOsm/L ar isnic, and hs wih valus f mr
cabae han 310 mOsm/L ar hyprnic.
• Dextrose 5% to 25% (D5–25) Isnic sluins (.g., 0.9% sdium chlrid, lac-
A As (tae naes) ad Ringr) ar idal rplacmn uids fr h pa-
• Aminosyn
in wih an inravascular uid dci (.g., acu
• Travasol
• ProcalAmine
bld lss as a rsul f hmrrhag, gasrinsinal
• NephrAmine blding, r rauma). This yp f uid is usd fr
• TrophAmine hypvlmic, hypnsiv pains  incras vascu-
• HepatAmine lar vlum  suppr bld prssur; hwvr, hs
lps (tae nae) pains mus b mnird fr uid vrlad (pn-
• Intralipid ial pulmnary dma), spcially if h pain has
• Nutrilipid cngsiv har failur. Anhr isnic sluin,
• Omegaven dxrs 5% wih 0.2% sdium chlrid (D5/0.2 NS),
• SMOFlipid is a sandard sluin fr mainaining hydrain and
B-Ve Epaes lcrlys (.g., passium chlrid), adminisring
• Hetastarch
cninuus infusin IV mdicains, and  kp pn
• Dextran
• Albumin
(TKO) IV hrapy fr h inrmin adminisrain
• Plasma f mdicains. D5/0.2 NS sluins ar infusd as
• Tetrastarch isnic sluins, bu hy rapidly bcm hypn-
Aazg Ss ic sluins as h dxrs is mablizd. Thrfr
• Sodium bicarbonate D5/0.2 NS sluins—vn hugh hy ar iniially
• Tromethamine (tris[hydroxymethyl]aminomethane isnic—shuld n b usd  mainain vascular vl-
[THAM]) um in a pain wh is hypvlmic and hypnsiv.
• Sodium lactate Hypnic sluins (.g., 0.2% r 0.45% sdium
Ag S chlrid) hav lwr smlaliy han srum. This yp
• Ammonium chloride f sluin cnains fwr lcrlys and mr fr
a This is a representative listing; it is not intended to be complete. war, s h war is rapidly pulld frm h vascular
 Parenteral Administration: Intravenous Route CHAPTER 11 157

cmparmn in h inrsiial and inracllular u-
id cmparmns. Alhugh hs sluins ar usful
in cndiins f cllular dhydrain, adminisring
hm  rapidly may caus a suddn shif f uids b-
ing drawn frm h inravascular spac in h hr
cmparmns.
Hyprnic sluins hav an smlaliy ha is
highr han ha f h srum. Alhugh hypnic and
isnic sluins ar usd in paricular siuains b-
caus f hir niciy, hyprnic sluins ar rarly
usd in his way bcaus hy hav h pnial 
pull uid frm h inracllular and inrsiial cm-
parmns in h inravascular cmparmn, hr-
by causing cllular dhydrain and vascular vlum
vrlad. In cass f xravascular vlum vrlad,
hs sluins ar usd  diurs pains bcaus
hs sluins will draw uid in h vascular cm-
parmn, which hn can b xcrd by h kidnys,
usually wih h hlp f diurics such as fursmid.
Hyprnic sluins als hav h disadvanag f
causing phlbiis and vnus spasm, wih inlrain
and xravasain ccurring in h priphral vins. In
gnral, sluins wih smlaliis f mr han ap-
prximaly 600  700 mOsm/L shuld n b admin-
isrd in priphral vins. Hyprnic sluins (.g.,
parnral nuriin sluins) mus b adminisrd
hrugh cnral infusin lins, whr h sluin can
b rapidly dilud by larg vlums f rapidly wing
bld (.g., in h suprir vna cava nar h nranc
 h righ arium).
large-volume solutIon ContaIners
IV sluins ar availabl in bh plasic and glass cn-
ainrs in a variy f yps and cncnrains (s
Tabl 11.1 and Bx 11.1) and in vlums ha rang
frm 100  2000 mL. Bh h glass and plasic cn-
ainrs ar vacuum sald. Th glass bls ar sald
wih a hard rubbr sppr and hn a mal disk, and
his is fllwd by a mal cap. Righ bfr us, h
mal cap and disk ar rmvd, hrby xpsing h
hard rubbr sppr. Th insrin spik f h IV ad-
minisrain s is pushd in a spcically markd
ara n h rubbr sppr. Sm brands als hav an-
hr pning in h rubbr sppr ha srvs as an
air vn (s Fig. 11.2A and C). As h sluin runs u
f h cnainr, i is rplacd wih air. Ohr brands
mak us f a xibl plasic cnainr (s Fig. 11.2B).
As h sluin runs u f h bag, h xibl cn-
ainr cllapss.
Plasic bags ar smwha diffrn in ha h n-
ir bag and sluin ar sald insid anhr plasic
bag ha is rmvd jus bfr adminisrain. Whn
h insrin spik is frcd in h spcially markd
pral, an inrnal sal is brkn, which allws h s-
luin  w in h ubing.
small-volume solutIon ContaIners
Sm mdicins (.g., anibiics) ar adminisrd by
inrmin infusin hrugh an apparaus knwn as
a tandem setup, piggyback, r IV rider (Fig. 11.9). Ths
mdicins ar givn by a sup ha is hung in andm
and cnncd wih h primary sup. Th scndary
sup may cnsis f a drug infusin frm a small vl-
um f uid in a small bag r bl (≤250 mL; s Fig.
11.9) r frm a vlum cnrl s (Burrl, Vlurl;
s Fig. 11.2A and C). A vlum cnrl s is cmpsd
f a calibrad chambr ha is hung undr h primary
IV sluin cnainr and ha can prvid h ncs-
sary 50  250 mL f dilun pr ds f drug. Ms
inrmin dilud drug infusins ar infusd vr 20
 60 minus.
administration of mEdications by
thE intravEnous routE
dose forms
Mdicains fr IV adminisrain ar availabl in
ampuls, vials, prlld syrings, and larg-vlum
IV sluin bags. B crain ha h labl spcically
sas ha h mdicain is fr IV us. IV uid and
lcrly sluins cm in a variy f vlums
and cncnrains in glass and plasic cnainrs
(s Bx 11.1).
equIpment
• Mdicain prl
• Prscribr’s rdr
• Glvs
• Turniqu

Table 11.1 Intravenous Solutions, Electrolyte Concentrations, and Osmolality

Solution nA+ (mEq/l) cl− (mEq/l) GlucoSE (G/l) oSmolAlity (moSm/l)
0.45 Normal saline 77 77 0 154
0.9 Normal saline 154 154 0 308
5% Dextrose in 0.2% sodium chloride 34 34 50 320
5% Dextrose in 0.45% sodium chloride 77 77 50 405
5% Dextrose in 0.9% sodium chloride 154 154 50 560
Lactated Ringer solutiona 130 109 0 273
aAlso contains the following: K + (4 mEq/L), lactate (28 mEq/L), Ca 2+ (3 mEq/L).
158 UNIT II Illustrated Atlas of Medication Administration

Piggyback Piggyback

Full Empty
Basilic vein

Cephalic vein

Primary Primary Dorsal venous

infusion infusion network
container container Dorsal
metacarpal
Clamp Clamp veins
open open

Clamp Clamp Dorsal digital

open open veins

Check Check
valve valve

Fig. 11.10 Intravenous sites on the hand. (Redrawn from Williams PL,
Warwick R, Dyson M, Bannister LH, eds. Gray’s Anatomy. 37th ed.
New York: Churchill Livingstone; 1989.)

Fig. 11.9 Piggyback intermittent administration setup. Note that the
smaller bag is hung higher than the primary bag.
• Adminisrain s wih syring, apprpria ndl
r ndllss cnncr (if giving by blus), drip
chambr, and lr
• Mdicain
• Physilgic sluin rdrd
• Sril drssing marials
• Anispic sluin
• Salin lck adapr
• Arm bard (if indicad)
• Tap
• Sandard IV pl
• Salin sluin, piggyback, and addiinal sluins
as apprpria
Addiinal supplis may b rquird  accss,
ush, r chang IV adminisrain ss, inlin lrs,
r drssings, dpnding n h yp f priphral, cn-
ral, r implanabl dvic bing usd.
sItes
pi I acc
Whn slcing an IV si, cnsidr h fllwing: h
lngh f im ha h IV infusin will b rquird;
h cndiin and lcain f h vins; h purps f
h infusin (.g., rhydrain, dlivry f nuriinal
nds [.g., TPN], chmhrapy, and anibiics); and
h pain’s saus, cprain lvl, and prfrnc
fr and amun f slf-car ndd fr h injcin si
(if apprpria).
Priphral IV dvics includ h wing-ippd n-
dl (s Fig. 11.5), h vr-h-ndl cahr (s
Fig. 11.6A), and h in-h-ndl cahr (s Fig.
11.6B). Th vr-h-ndl cahrs ar h ms
cmmnly usd vnus accss sysms fr nring
h priphral vins.
If a prlngd curs f ramn is anicipad,
sar h rs IV infusin in h hand (Fig. 11.10). Th
macarpal vins, h drsal vin nwrk, h cphalic
vin, and h basilic vin ar cmmnly usd. T avid
irriain and lakag frm a prvius puncur si,
h subsqun vnipuncur sis shuld b mad
abv h arlir si. Fig. 11.11 shws h vins f h
frarm ara ha culd b usd fr addiinal vni-
puncur sis.
C I acc
Cnral IV accss dvics ar usd fr h fllwing
siuains: whn h purps f hrapy dicas (.g.,
larg-vlum, high-cncnrain, r hyprnic s-
luins ar  b infusd); whn priphral sis hav
bn xhausd as a rsul f rpad us r whn
h cndiin f h vins fr accss is pr; whn
lng-rm r hm hrapy is rquird; r whn an
mrgncy cndiin mandas adqua vascular
accss.
Th cnral vins ha ar ms cmmnly usd fr
cnral vnus cahrs ar h subclavian and jugular
vins. Whn uppr bdy vins ar n accpabl, h
 Parenteral Administration: Intravenous Route CHAPTER 11 159

• Glvs shuld b wrn hrughu h vni-

puncur prcdur. Car shuld b akn 
wash h skin surfac if h ara is cnaminad
In infraclavicular
fossa wih bld.
• Whn h prcdur is cmpl, rmv glvs
and disps f hm in accrdanc wih h pli-
In deltopectoral cis f h pracic sing. Prfrm hand hygin
groove
as sn as h glvs ar rmvd. Car shuld b
akn  avid cnaminaing h IV ubing and h
ra rgular.
• Any usd ndls, syrings, vnipuncur cahrs,
Cephalic vein r vascular accss dvics shuld b placd in a
Medial cutaneous puncur-rsisan ndl dispsal cnainr in h
nerve of forearm immdia viciniy fr dispsal in accrdanc wih
Median cubital vein
Basilic vein h plicis f h pracic sing. Ndl safy d-
vics shuld b acivad bfr placing in h dis-
Lateral cutaneous Medial cutaneous
nerve of forearm,
psal cnainr.
nerve of forearm
ulnar branch • Nvr rcap, bnd, r brak usd ndls bcaus
Accessory f h dangr f inadvrnly puncuring h
cephalic vein Basilic vein skin.
• Whnvr pssibl, us ndl prcr sys-
Median vein ms such as blun ndls, injcin prs, ndl
Cephalic vein of forearm shahs, r ndllss sysms  prvn inadvr-
n ndlsicks, as wll as h risk f inrducing
pahgns in nslf.
• B crain ha mdicains  b adminisrd in-
ravnusly ar hrughly disslvd in h crrc
vlum and yp f sluin. Always fllw h
manufacurr’s rcmmndains.
• Ms clinical pracic sings nw us ransparn
drssings vr h IV insrin si ha ar changd
in accrdanc wih hspial plicis, gnrally v-
ry 72  96 hurs. Sm clinical pracic sings
sill us gauz drssings. Whn gauz is usd, h
fur dgs f h drssing shuld b sald wih
ap. Always chck h spcic plicis f h m-
plying insiuin, as wll as h halhcar prvid-
Fig. 11.11 Veins in the forearm that are used as intravenous sites. r’s rdrs, wih rgard  h frquncy f drssing
(Redrawn from Williams PL, Warwick R, Dyson M, Bannister LH, eds. changs.
Gray’s Anatomy. 37th ed. New York: Churchill Livingstone; 1989.) • D n us pical anibiic inmns r crams
n insrin sis bcaus f h pnial 
fmral vins may b accssd fr shr-rm r mr- prm fungal infcins and animicrbial
gncy us. rsisanc.
• A h im f h drssing chang fr any yp f
general prInCIples of Intravenous IV si, h ara shuld b hrughly inspcd
medICatIon admInIstratIon fr any drainag, rdnss, ndrnss, irriain,
• Th nurs shall hav passd a skill cmpncy ha r swlling. Th prsnc f any f hs symp-
dmnsras hir knwldg f h IV adminisra- ms shuld b rprd  h halhcar pr-
in prcdur. vidr immdialy. (In addiin, ak h pain’s
• If i is insiuinal plicy  us a lcal anshic vial signs and rpr hs a h sam im.)
 anshiz h IV si bfr insrin, h nurs • Us inlin lrs as rcmmndd by h manufac-
mus drmin h pain’s allrgis  anshic urr f h drug  b infusd.
agns. • Do not adminisr any drug r IV sluin ha is
• Us apprpria barrir prcauins (.g., univrsal hazy r cludy r ha has frign paricls r pr-
bld and bdy uid prcauins)  prvn h cipia in i.
ransmissin f any infcius disass, as rcm- • Do not mix any hr drugs wih bld r bld
mndd by h CDC. prducs (.g., albumin).
160 UNIT II Illustrated Atlas of Medication Administration
• Do not adminisr a drug in an IV sluin if h
cmpaibiliy is n knwn.
• Us aspic chniqu, including h us f a cap,
mask, sril gwn, sril glvs, and a larg
sril sh, fr h insrin f cnral vnus
cahrs (including PICCs) and fr guidwir
xchangs.
• A drug mus b nirly infusd hrugh h IV
lin bfr adding a scnd mdicain  h IV
lin.
 • Drugs ha ar givn by IV push r blus gn-
rally ar givn in accrdanc wih h SASH
guideline—Salin ush rs; Adminisr h
prscribd drug; Salin ush afr h drug;
Hparin ush h lin (dpnding n h yp f
lin [.g., Hickman cahr]; chck insiuinal
plicy).
 • Th SAS chniqu is similar  h SASH guid-
lin bu wihu h hparin: Salin ush rs;
Adminisr h prscribd drug; Salin ush af-
r h drug.
• Afr a mdicain has bn mixd, knw h lngh
f im ha i rmains sabl; all unusd IV slu-
ins shuld b rurnd  h pharmacy if hy ar
n usd wihin 24 hurs.
• Chck h insiuinal plicy fr h dniin f
TKO I is usually inrprd as an infusin ra f
10  20 mL/hr, and lss han 500 mL/24 hr shuld
b infusd.
• Shad IV sluins ha cnain drugs ha shuld
b prcd frm ligh. All IV sluin bags r
bls shuld b changd vry 24  48 hurs
(chck insiuinal plicy)  minimiz h dvl-
pmn f nw infcins. Labl all IV sluins
wih h da and im iniiad. Do not us mark-
ing pns dircly n plasic IV cnainrs, bcaus
h ink may pnra h plasic and nr h IV
sluin.
• IV adminisrain ss ha ar usd  dlivr bld
r bld prducs shuld b changd afr h uni
is adminisrd. Ss ha hav bn usd  infus
lipids r TPN shuld b changd vry 24 hurs.
Adminisrain ss ha ar usd nly fr physi-
lgic IV uids (.g., D5/0.2 NS) may b changd
vry 72  96 hurs (chck insiuinal plicy). Th
ss r ubing mus b labld wih h da and
im iniiad, and h da upn which  chang
h s.
• Whnvr a pain is rciving IV uids, mnir
hir inak and upu accuraly. Rpr dclin-
ing hurly upus, as wll as hs f lss han
30 mL/hr.
• Nvr spd up an IV w ra  cach up whn
h vlum  b infusd has falln bhind. In cr-
ain cass his culd b dangrus. Th halhcar
prvidr shuld b cnsuld, paricularly fr pdi-
aric pains and fr hs wh hav cardiac, rnal,
r circulary impairmn.
Clinical Pitfalls
 • Note: Never start an IV infusion in an artery!
 • Whenever possible, initiate the IV infusion in accordance
with the patient’s preference or in their nondominant arm.
 • Do not initiate an IV infusion in an arm with compromised
lymphatic or venous ow (e.g., after mastectomy or
axillary node dissection) or in an extremity with a dialysis
or apheresis catheter or shunt inserted.
 • Avoid the use of blood vessels over bony prominences or
joints unless absolutely necessary.
 • In the older adult, using the veins in the hand area may be
a poor choice because of the fragility of the skin and veins
in this area.
 • Veins that are commonly used in infants and children for
IV administration are on the back of the hand, the dorsum
of the foot, or the temporal region of the scalp (Fig.
11.12). The scalp veins are to be used as a last resort for
infants.
Frontal vein
Superficial
temporal
vein
Posterior
auricular
vein
Occipital
vein
Fig. 11.12 Veins in infants and children that are used as intravenous
sites. (Redrawn from Hankins J, Lonsway RA, Hedrick C, Perdue
M, eds. Infusion Therapy in Clinical Practice. 2nd ed. Philadelphia:
Saunders; 2001.)
 • When possible, avoid using the veins of the lower
extremities because of the danger of the development of
thrombi and emboli.
PrEPArinG An intrAVEnouS Solution for
infuSion
dose form
Chck h halhcar prvidr’s rdr fr h spcic
IV sluin rdrd and fr any mdicain  b add-
d  h cnainr. If h rdr has n alrady bn
prpard by h pharmacy, chck h accuracy f h
drug rdr agains h mdicain r sluin bing
prpard a las hr ims during h prparain
phas: (1) whn rs rmving h drug r sluin
frm h srag ara; (2) immdialy afr prpara-
in; and (3) immdialy bfr adminisrain. Chck
h xpirain da n any addiivs and n h prima-
ry sluin. If an IV mdicain is  b addd, nsur
ha h drug is apprvd fr adminisrain by nurss.
Prfrm pr–IV accss assssmns (s Vnipuncur).
 Parenteral Administration: Intravenous Route CHAPTER 11
equIpment
• Prscribr’s rdr
• Adminisrain s wih apprpria ndl r
ndllss cnncr, apprpria drip chambr
(micrdrip r macrdrip; s Fig. 11.2), IV cahr,
and inlin lr (if usd); h primary lin admin-
israin s is usually labld “univrsal” r “cn-
inuus w”
• Mdicains fr IV dlivry and labls
• Physilgic sluin rdrd
• IV pl r pump
teChnIque
1. Assmbl quipmn and prfrm hand hygin.
2. Chck h pain’s vin fr h siz and yp f
ndl rquird  accss h vin slcd fr v-
nipuncur r fr h yp f ndl rquird  ac-
css an impland accss dvic fr h dlivry f
h IV sluin r mdicain.
3. Chck h halhcar prvidr’s rdr agains h
physilgic sluin chsn fr adminisrain.
4. Inspc h IV cnainr fr cludinss, disclr-
ain, and h prsnc f any prcipia. Vrify
h xpirain da n h IV uid cnainr.
5. Rmv h plasic cvr frm h IV cnainr, and
inspc h plasic IV bag  b crain ha i is inac;
squz i gnly  dc any puncurs. Inspc a
glass cnainr f IV sluin fr any cracks.
6. Chs h adminisrain s ha is apprpri-
a fr h yp f sluin rdrd, fr h ra f
dlivry rqusd (.g., micrdrip r macrdrip),
and fr h yp f IV cnainr bing usd. Plasic
bag IV cnainrs do not rquir an air vn in h
adminisrain s. Glass cnainrs fr IV dlivry
mus b vnd r hav an adminisrain s wih
an air lr vn in i. Rmv h adminisrain
s frm is packaging, and inspc i fr any fauls
r cnaminain.
7. Mv h rllr r slid clamp  h uppr prin
f h IV lin 6  8 inchs frm h drip chambr;
cls h clamp.
8. Cnnc h IV adminisrain s r ubing  h
IV sluin.
 • Plastic IV bags: Rmv h ab frm h spik
rcivr pr, rmv h ab frm h adminis-
rain s spik, and insr h spik rmly in
h bag pr. Mainain h sriliy f h pr
and spik hrughu h prcss.
 • Glass IV bottle: Pl back h mal ab and lif
h prciv mal disk frm h cnainr; r-
mv h lax-yp cvring (if prsn) frm
h p f h rubbr sppr. As h lax dia-
phragm is rmvd, a suddn nis shuld b
hard as h vacuum wihin h glass cnainr
is rlasd. If h nis is n hard, h cnns
f h IV cnainr may n b sril and shuld
b discardd. Rmv h ab frm h adminis-
rain s spik; insr h spik rmly in h
161
pr in h rubbr sppr. Mainain h sriliy
f h pr and spik hrughu h prcss.
 • Note: Whn addiiv mdicains ar rdrd,
hy shuld b addd  h larg-vlum cn-
ainr bfr ubing is aachd  hlp nsur a
unifrm mixing f h mdicain and h phys-
ilgic sluin. If mdicain is addd  an x-
ising IV sluin, clamp h lin bfr adding
h mdicain  h cnainr, and mak sur
ha adqua mixing aks plac bfr h infu-
sin is sard again. (S Adding a Mdicain
 an Inravnus Bag, Bl, r Vlum Cnrl
Dvic.)
9. Hang h sluin n an IV pl, squz h drip
chambr, and ll i halfway. Prim h IV lin by r-
mving h prciv ab r cap frm h disal nd
f h IV lin, invr h Y pr, pn h rllr r
slid clamp, and allw h sluin  run unil all
f h air is rmvd frm h lin. If using a pump,
prim h ubing in accrdanc wih insiuinal
plicy. Cvr h nd f h IV ubing wih a sril
cap. Inspc h nir lngh f ubing  b crain
ha all air is rmvd frm h lin. (Note: I may
b ncssary  add inlin lrs  h sup if his
is rcmmndd fr h adminisrain f h r-
drd mdicain. Purg air frm h lin bfr a-
aching h lr, hn run sluin hrugh h lr
 rmv air frm h lr.)
10. Labl h cnainr wih h pain’s nam alng
wih h da and im f prparain. If mdica-
in has bn addd, all dails f h mdicain
mus b markd n h cnainr’s labl: h drug
nam and ds, h ra f adminisrain rqus-
d in h halhcar prvidr’s rdr.
11. Labl h IV ubing wih h da and im ha
i is pnd and h da and im ha i is  b
changd. Th CDC rcmmnds ha IV ubing b
changd vry 72 hurs. Adminisrain ss ha
ar usd  dlivr bld r bld prducs may
b changd afr ach uni is infusd, as dnd by
insiuinal plicy, r wihin 24 hurs f iniiaing
h infusin. Lipid sluins hav spcial ubing
ha shuld b changd vry 24 hurs if hy ar
adminisrd by cninuus infusin r afr vry
uni if hy ar adminisrd inrminly. Fllw
insiuinal plicis.
12. Th IV sluin can nw b akn  h bdsid
fr aachmn afr a vnipuncur is prfrmd
r fr addiin  an xising IV sysm. Fr safy,
all aspcs f h IV rdr shuld b chckd again
immdialy bfr aaching h IV sluin fr
infusin.
intrAVEnouS fluid monitorinG
Th infusin f IV uids rquirs carful mniring
fr pains f all ags. Th micrdrip chambr, which
dlivrs 60 drps (g)/mL, is usd whnvr a small
162 UNIT II Illustrated Atlas of Medication Administration
vlum f IV sluin is rdrd  b infusd vr a
spcic im. Many clinical pracic sings inrpr
a small vlum as lss han 100 mL/hr. In pdiaric
unis, vlum cnrl chambr dvics (.g., a Burrl,
a SluS) and syring pump cnrllrs ar cmmnly
usd  rgula h vlum f uid ha is infusd.
basic GuidElinEs for thE
intravEnous administration of
mEdications
equIpment
• Mdicain prl
• Prscribr’s rdr
• Turniqu
• Clan glvs
• Drug in a sril, sald cnainr
• Syring f h crrc vlum
• Ndls f h crrc gaug and lngh
• Anispic alchl wips
• Tap
• Chang labl
• Spcial quipmn basd n h ru f adminisra-
in (.g., a radipaqu vr-h-ndl cahr fr
insrin; infusin pump)
• Transparn drssing supplis
premedICatIon assessment
1. Knw basic pain daa, h pain’s diagnsis,
h sympms f h disrdr r disas prcss fr
which h mdicain is rdrd, and h dsird ac-
in f h drug fr h paricular individual.
2. Obain baslin vial signs.
3. Chck fr any ap, lax, and drug allrgis r prir
drug racins.
4. Chck h accuracy f h drug rdr agains h
mdicain r sluin bing prpard a las hr
ims during h prparain phas: (1) whn rs
rmving h drug r sluin frm h srag
ara; (2) immdialy afr prparain; and (3) im-
mdialy bfr adminisrain.
5. Chck fr laks, clariy, and xpirain da n h
IV sluin and n h drug  b addd  h
sluin.
6. Rviw h individual drug mngraph  idnify
labrary sudis rcmmndd bfr r inrmi-
nly during hrapy, h calculain f h ds,
h advrs ffcs, h mniring paramrs rc-
mmndd fr h spcic drug prscribd, and
hr cnsidrains. (Wih crain ligh-snsiiv
mdicains [.g., amphricin B, nirprussid], i
is ncssary  shild h IV bag wih a dark plasic
bag  prvn h dgradain f h drug.)
7. Knw h yp f IV accss ha h pain has in
plac, h da and im f insrin, h yp f IV
uid r mdicain running, and h ra f w
prscribd.
proCedure protoCol
Th sandard prcdurs fr prparing all parnral
mdicains ar as fllws:
1. Prfrm hand hygin bfr prparing any mdi-
cain r handling sril supplis. During h ac-
ual prparain f a parnral mdicain, h
primary rul is “sril  sril” and “unsril 
unsril” whn handling h syring and ndl.
2. Us h seven rights f mdicain prparain and
adminisrain hrughu h prcdur: righ
pain, righ drug, righ indicain, righ ru,
righ ds, righ im, and righ dcumnain.
3. Chck h drug ds frm rdrd agains h
surc usd fr h prparain.
4. Chck cmpaibiliy chars r cnac h phar-
macis bfr mixing w mdicains r adding
mdicains  an IV sluin.
5. Chck mdicain calculains. Whn in dub
abu a ds, chck i wih anhr qualid nurs.
(Ms insiuinal plicis rquir fracinal dss
f mdicains and dss f hparin and insulin
 b chckd by w qualid individuals bfr
adminisrain.)
6. Knw h insiuinal plicy rgarding limia-
ins n h yps f mdicains  b adminis-
rd by nursing prsnnl. Bfr adminisring
an IV drug, h nurs shuld chck h lis f drugs
apprvd fr adminisrain by nurss in h clini-
cal car sing.
7. Prpar h drug in a clan, wll-lighd ara wih
h us f aspic chniqu hrughu h nir
prcdur.
8. Cncnra n h prcdur; nsur accuracy
during prparain.
9. Chck h xpirain da f h mdicain.
10. Rsarch h mdicain rdrd as an IV addiiv;
his prcdur als applis fr dirc push r blus
adminisrain.
 • Nam f drug.
 • Usual ds (ak in cnsidrain h pain’s
ag, wigh, and hydrain sa).
 • Cmpaibiliy f h drug wih xising IV drugs
ha ar currnly infusing.
 • Fr IV push r blus, ds h drug nd  b
dilud, r can i b givn undilud? If i shuld
b dilud, wha yps and amuns f dilun
can b usd? If i is bing addd  an xising
IV infusin, is h drug cmpaibl wih h pri-
mary sluin?
 • Rcmmndd ra f infusin.
VEniPuncturE
Prfrm h fllwing pr–IV accss assssmns:
• Assss h pain’s dmanr. Ds h pain
appar cpraiv, r will assisanc b ndd?
(Always hav sufcin assisanc whn wrking
wih pdiaric pains.)
 Parenteral Administration: Intravenous Route CHAPTER 11
• Chck fr and avid prviusly usd IV sis, aras
f impaird circulain, and any sulas ha may b
prsn in h xrmiis.
• Examin h xrmiis fr pnial sis and si-
ma h siz f h vins ha ar availabl fr us.
equIpment
• Mdicain prl
• Prscribr’s rdr
• IV sar s
• Anispic alchl wips
• On pair f glvs
• Si labl
• Tap
• Transparn drssing marials
• Tw gauz spngs, 2 × 2 inchs
• On rll f ransparn ap
• Lax urniqu
• On chang labl
• Arm bard (whn indicad)
• As apprpria, mdicains and physilgic sluins
rdrd fr IV dlivry and IV quipmn ndd (s
Prparing an Inravnus Sluin fr Infusin)
• Fr a salin lck r a mdlck, bain h crrc x-
nsin ubing and injcin cap, as apprpria (s
Adminisrain f Mdicain by a Salin Lck r
Mdlck lar); us salin and hparin ush slu-
ins in accrdanc wih insiuinal plicy (us 10-
mL syrings ha cnain an apprpria vlum f
sluin fr ushing)
• IV pump, if rquird
sci   C  B n
Whn slcing a cahr r bury ndl fr us,
chs h smalls siz ha is fasibl fr adminis-
ring h spcic yp f uid ha has bn rdrd.
Cahrs ar availabl in sizs ranging frm 27 gaug,
⅝ inch  14 gaug, ½ inch, and bury ndls ar
availabl in sizs 17  29 gaug. A mr viscus uid
such as bld rquirs a largr-diamr cahr. As
wih hr ndls, h lwr h numbr f h gaug,
h largr h diamr f h pning f h cahr.
During h assssmn prcss, h nurs ns h siz
f h vin  b accssd.
teChnIque for estaBlIshIng an
Intravenous lIne
1. Prfrm h prmdicain assssmn and fllw
h prcdur prcl dscribd.
2. Assmbl h ncssary quipmn and prfrm
hand hygin.
3. Chck all aspcs f h halhcar prvidr’s
rdrs.
4. Rchck h siz and yp f cahr r bury
ndl ndd  accss h vin slcd and any
xnsin ubing r injcin caps ha ar ndd
 prpar h si fr fuur inrmin r cn-
inuus us fr h prscribd IV hrapy.
163
5. If rdrd, h IV sluin and mdicain shuld
b prpard and akn  h bdsid fr aach-
mn afr a vnipuncur has bn prfrmd. Fr
safy, all aspcs f h IV hrapy rdrs shuld
b chckd again immdialy bfr iniiaing h
vnipuncur and bfr aaching h IV sluin
fr infusin. (Note: Always idnify h pain
by chcking hir ID bracl bfr iniiaing any
prcdur. Hav h pain sa his r hr nam
and birh da r hr idnirs. Explain h pr-
cdur, and prvid ducain abu h drug b-
ing adminisrd.)
6. Psiin h pain apprprialy. Immbiliz an
infan r child fr pain safy, if ncssary. (B
sur ha h pain is waring h yp f hspial
gwn ha has pnings n h shuldr sams.)
7. Cu ap fr sabilizing h IV cahr r bury
ndl bfr saring h prcdur. Turn h nds
f h ap back n hmslvs  frm a ab ha
will n adhr  a glv whn h ap is  b ap-
plid r rmvd. (Note: Th nurs mus cnsidr
hir glvs  b cnaminad whn hy cm
in cnac wih bld. If h glvs cm in
cnac wih h ap and drssing marials ha
hav bn usd a h vnipuncur si, h u-
sid f h drssings and ap ar hn pnially
cnaminad. Thrfr during h prcdur, h
nurs mus fcus n allwing cnaminain nly
f h dminan glvd hand; h nndminan
hand mus b mainaind as uncnaminad 
handl h aping and sabilizain f h priphr-
al accss dvic. Afr h ndl r cahr is sa-
bilizd, h glvs can b rmvd; prfrm hand
hygin and apply h gauz r h cclusiv yp
f drssing marials in accrdanc wih pracic
sing plicis.)
8. Whn xnsin ubing is usd wih h cahr r
h bury ndl, ll h xnsin ubing wih
salin and purg i f all air.
9. Apply h urniqu using a slipkn 2  6 inchs
abv h si chsn (his is h shadd ara in
Fig. 11.13A). Inspc h ara  idnify a vin f
sufcin siz  accmmda h cahr and
prvid adqua anchrag.
10. Pu n nnsril glvs. As h vin dilas, pal-
pa h vin  fl is dph and dircin (Fig.
11.13B and C). T dila h vin, i may b ncs-
sary  plac h xrmiy in a dpndn psiin.
Massag h vin agains h dircin f bld
w, hav h pain pn and cls h hand
rpadly, r rmv h urniqu and apply a
haing pad r warm w wls  h xrmiy
fr 15  20 minus, and hn rsar h prcss.
11. Clans h skin surfac wih h anispic alchl
wip, saring a h si f nry and wrking u-
ward in a circular min ward h priphry (Fig.
11.13D). D n ruch h ara whr h puncur
si will b mad. (Alrnaivs ar  pu a sril
164 UNIT II Illustrated Atlas of Medication Administration

A
B

C D
Blood in flashback
chamber Needle

External
catheter

10 degrees
E F

G H
Fig. 11.13 (A) Apply a tourniquet using a slipknot that is placed 2 to 6 inches above the chosen (shaded) area. (B) Allow
the veins to dilate. (C) Palpate the vein to feel its depth and direction. (D) Cleanse the skin surface with an antiseptic
alcohol wipe, starting at the anticipated site of entry and working outward in a circular motion to the periphery. (E) For
an over-the-needle catheter, hold the ashback chamber with the thumb and forenger and insert the catheter with
the needle at a 10- to 30-degree angle (or at the angle as specied in manufacturer’s directions), with the bevel up. (F)
Withdraw the needle from the catheter. (G) Apply gentle pressure over the catheter tip to prevent the excessive backow
of blood while the needle is removed and the intravenous line is attached. (H) Secure the connection of the intravenous
tubing to the hub of the catheter.

glv n n hand s ha h si can b uchd
again r  prpar h ngrip wih anispic.)
12. Allw h ara  air-dry.
13. Hld h cahr r bury ndl  b insrd
in h dminan hand, and rmv h prciv
cvr whil mainaining h sriliy f h ndl.
Apprach h vin dircly frm abv r frm
slighly  n sid f h vin. Prvid nsin n
h skin surfac  srch h skin and sabiliz h
vin.
 Parenteral Administration: Intravenous Route CHAPTER 11
pi o--n C Ii
(s fi. 11.6a)
 • Inspc h IV cahr and lsn h cahr
ndl by raing h cahr.
 • Hld h ashback chambr wih h humb and
frngr and insr h cahr wih h n-
dl a a 10-  30-dgr angl wih h bvl up
(Fig. 11.13E). Chck h manufacurr’s prduc
insrucins fr h rcmmndd angl f n-
ry and assss h dph f h vin; h dpr
h vin, h grar h angl f nry ndd 
puncur h skin and vnus wall.
 • Wach fr bld in h ashback chambr; afr
bld is sn, advanc h ndl and cahr an
addiinal {1/16}  ¼ inch in h vin.
 • Wihdraw h ndl frm h cahr (Fig.
11.13F), lwr h angl f h cahr slighly,
and advanc h cahr in h vin.
 • Hld h cahr hub in plac whil applying
gnl prssur n h cahr ip  prvn h
xcssiv backw f bld whil h ndl is
rmvd frm h cahr and h cahr and
IV sluin ar aachd (Fig. 11.13G).
B n Ii
 • Prpar h si as dscribd prviusly.
 • Hld h bury ndl by h abs and align
h ndl, bvl up, wih h vin ha has bn
slcd.
 • Puncur h skin and vin surfac as dscribd
prviusly.
 • Afr h vin is nrd, lwr h angl and ad-
vanc h ndl in h vin unil h abbd
ara f h bury is adjacn  h puncur
si.
14. Rlas h urniqu and scur h cnncin
f h IV ubing  h vr-h-ndl plasic n-
dl hub (Fig. 11.13H) r  h bury apparaus.
15. Clans h ara  limina any bld ha may
hav cnacd h skin r IV ubing. Rmv h
glvs and anchr h ndl and ubing  h
arm r hand wih ap and drssing, as prscribd
by h clinical pracic sing plicy. (Bcaus i is
difcul  handl ap wih glvs n, i is hlpful
 hav a scnd prsn  anchr h ndl and
ubing and  adjus h w ra.)
16. If n cninuusly wing IV sluin is aachd,
ush h cahr in accrdanc wih clinical prac-
ic sing plicy.
17. Th individual wh is prfrming h vni-
puncur can disps f all sild drssings and
cnaminad supplis in accrdanc wih h
clinical pracic sing’s plicy.
18. Adjus h ra f w sluin r s h ra n
h pump.
19. Rgardlss f h apparaus usd, mark h labl
wih h da and im f insrin.
165
20. In a way ha is apprpria  h ag, si, and
physical rinain f h individual, aach a
paddd arm bard  suppr and sabiliz h in-
fusin si.
patIent teaChIng
1. Tach h pain abu any sympms ha shuld
b rprd a h insrin si (.g., pain, swlling,
discmfr).
2. Srss h impranc f n rying  slf-adjus h
ra f an IV sluin r f any IV mdicains ha
ar bing adminisrd.
3. Explain h purps f h drssing ha has bn
applid  h IV si and h nd  lav h
drssing inac.
doCumentatIon
Prvid h righ dcumnain f h vnipuncur
(.g., IV sard r IV mdicain adminisrd and r-
spns  drug hrapy).
1. Char h da and im; h siz and yp f bu-
ry r IV cahr usd; h si accssd; and
h numbr f amps mad  prfrm h vni-
puncur. Mak nris n h apprpria IV si
w shs ha ar usd a h clinical pracic
sing.
2. On h pain’s mdicain adminisrain rcrd
(MAR), char h yp and amun f IV uid sar-
d r addd  an xising lin; h ra f adminis-
rain; and, if mdicain was addd, h da, h
drug nam, h amun addd (.g., h ds), and
h da and im f prparain and iniiain.
3. Prfrm and rcrd rgular pain assssmns
fr h valuain f hrapuic ffcivnss (.g.,
bld prssur, puls, upu, lung ld sunds, d-
gr and durain f pain rlif).
4. Char any signs and sympms f h advrs ffcs
f h drugs givn r prblms ncunrd during
h vnipuncur prcdur. If mr han n a-
mp was rquird  prfrm h vnipuncur,
rcrd h rlvan dails.
5. Rcrd any pain aching ha was dn.
6. If h IV accss dvic was ushd, i shuld b dcu-
mnd n h w sh and n h pain’s MAR.
AdminiStrAtion of mEdicAtion By A SAlinE
lock or A mEdlock
A salin lck r mdlck may b usd fr adminisra-
in f mdicains r wihdrawing bld sampls (Fig.
11.14). Prfrm prmdicain assssmns and fllw
prcdur prcl as dscribd arlir in his chapr.
In addiin, rfr  h individual drug mngraphs.
equIpment
• Mdicain prl
• Prscribr’s rdr
166 UNIT II Illustrated Atlas of Medication Administration

Fig. 11.14 Heparin lock/saline lock/medlock with an extension tubing

taped in place and ready for access.
Fig. 11.15 Syringe with a blunt-access cannula, attached by a Luer-
Lok, approaching a portal on an intravenous administration set.
(Courtesy Baxter Healthcare Corporation, Mountain Home, AR. All
• Mdicain fr IV dlivry and labl rights reserved.)
• Exnsin ubing and injcin cap, as apprpria
• Syrings and ndllss cnncrs
• Salin and hparin ush sluins
• Glvs
• Anispic alchl wips
• Sharps safy cnainr fr usd ndl and rcp-
acl fr ld drssing marial ha is rmvd

teChnIque for Intravenous Bolus

medICatIons WIth Capped Intravenous lIne
1. Slc a syring ha is svral millilirs largr
han rquird fr h vlum f h drug. This al-
lws rm fr h aspirain f bld  nsur h
prpr placmn f h ndl r cahr in h
vin and  allw bld  mix wih h drug s-
luin. Plac a ndllss accss dvic n h sy-
ring (Fig. 11.15) r us a syring ha is usd wih
a ndllss sysm (Fig. 11.16).
2. Rsarch and prpar h mdicain as dscribd
prviusly. Prpar h salin in syrings wih
ndllss accss dvics  ush h lin bfr
and afr mdicain adminisrain in accrdanc
wih insiuinal plicy. I is rcmmndd ha
10-mL syrings ha cnain a fw millilirs f
ush sluin b usd fr ushing  rduc h
prssur xrd in h vin r cahr.
3. Idnify h pain by chcking hir ID bracl.
Rchck h mdicain rdr, xplain h prc-
dur, and prvid ducain abu h drug bing
adminisrd. Hav h pain sa hir nam
and birh da r w hr idnirs.
4. Apply clan glvs.
5. Swab h slf-saling pral f h injcin si
wih an anispic alchl wip fr 15 scnds,
and aach h syring via h injcin cap. Sm
halhcar agncis us an anispic cap which
has bn sakd in chlrhxidin ha rmains cv-
ring h injcin si, in his cas rmv h cap
 accss h pr. N nd  swab h ara.
Fig. 11.16 The Baxter CLEARLINK Access System features an
integrated clamp to help protect patients from the effects of accidental
disconnection and ensure minimal uid displacement with proper
technique. Clear housing allows easy identication of residuals, which
may indicate need for replacement. A double seal provides effective
barrier to microbial ingress. A at septum with tight t to housing
helps reduce the risk of microbial contamination and eases cleansing.
(Courtesy Baxter Healthcare Corporation, Mountain Home, AR. All
rights reserved.)
6. Accss h injcin pral r cap wih a syring
ha cnains ush sluin and gnly pull back
n h plungr fr bld rurn. If rurn is n b-
aind r if rsisanc is fl, sp and valua h
caus. D n frc h insrin f h sluin r
a cl culd b disldgd.
7. Whn bld rurn is sablishd, injc h salin
fr h ush fllwd by h mdicain a h
ra spcid by h manufacurr. Always care-
fully check the drug order and a reliable reference for the
proper dilution and recommended rate of administra-
tion of the drug. Watch the clock and time the injection
rate as accurately as possible!
 Parenteral Administration: Intravenous Route CHAPTER 11
8. Obsrv h IV si a h cahr ip fr swll-
ing and mnir h pain fr cmplains f
discmfr.
9. Afr adminisrain, wihdraw h ndllss d-
vic frm h injcin pr and disps f i in a
sharps safy cnainr.
10. Accss h injcin cap and insr anhr sy-
ring ha cnains (usually) 1  2 mL f NS
 ush h rmaining drug frm h cahr.
Raach a nw clan anispic cap accrding 
agncy plicy.
11. Optional: In accrdanc wih insiuinal plicy, ush
h lck wih 1 mL f hparin (10  100 unis/mL).
Mainain cnsan prssur n h plungr f h sy-
ring whil simulanusly wihdrawing h ndl
frm h injcin pr  prvn h backw f
bld. Always vrify h hparin ds wih anhr
qualid nurs.
12. Clans h si f any bld r uids. Rmv
glvs and disps f hm prprly. Prfrm hand
hygin. Disps f quipmn in accrdanc wih
Occupainal Safy and Halh Adminisrain
sandards.
Th salin lck r mdlck shuld b ushd whn
i is iniially placd, afr adminisrain f mdica-
ins, afr wihdrawing bld sampls, r daily if
mdicains ar n adminisrd mr frqunly.
Chck h insiuinal plicy  drmin hw
lng a lck may rmain in plac bfr i is changd.
Mnir h vnipuncur si fr any advrs ffcs
r cmplicains.
patIent teaChIng
Explain  h pain h purps f h mdicain
adminisrd and any advrs ffcs fr ha mdica-
in ha shuld b rprd.
doCumentatIon
1. In h pain’s MAR, dcumn h da, im,
drug, and dsag; h ushing prcdur; and any
assssmn daa ha ar prinn (.g., hw wll
h prcdur was lrad, bsrvains f h v-
nipuncur si).
2. Prfrm and rcrd rgular pain assssmns fr
h valuain f hrapuic ffcivnss.
3. Char any signs and sympms f h advrs f-
fcs f h drugs givn r prblms ncunrd
during h prcdur.
4. Rcrd any pain aching ha was dn.
Life Span Considerations
Benzyl Alcohol Preservative
Do not use bacteriostatic water or saline that contains the
preservative benzyl alcohol to reconstitute or dilute medica-
tions or to ush the IV catheters of newborns because this
preservative is toxic to these patients.
167
AdminiStrAtion of mEdicAtionS into An
EStABliShEd intrAVEnouS linE
Prfrm prmdicain assssmns and fllw prc-
dur prcl as dscribd arlir. In addiin, rfr 
h individual drug mngraphs.
equIpment
• Mdicain prl
• Prscribr’s rdr
• Mdicain fr IV dlivry and labl
• Glvs
• Anispic alchl wips
• Syring and ndllss cnncr
• Salin sluin as apprpria
teChnIque for Intravenous Bolus
medICatIons WIth Intravenous solutIon
runnIng
1. Rsarch and hn prpar h mdicain as d-
scribd in h prcdur prcl arlir in his chap-
r. Ensur ha h drug  b prpard is cmpaibl
wih h IV sluin ha is currnly bing infusd.
Always carfully chck h drug rdr and a rliabl
rfrnc fr h prpr diluin and rcmmndd
ra f adminisrain f h drug. Many mdicains
rdrd as IV push r blus mus b adminisrd
slwly vr svral minus. An xcssiv ra f ad-
minisrain can rsul in shck and cardiac arrs.
2. Idnify h pain by chcking hir ID bracl.
Explain h prcdur and prvid ducain abu
h drug bing adminisrd. Hav h pain sa
hir nam and birh da r w hr idnirs.
3. Rchck h mdicain rdr.
4. Pu n glvs whn hr is a pnial fr xpsur
 bld r bdy uids. I is hlpful  kp n
glvd hand uncnaminad.
5. Swab h slf-saling pral f h injcin si wih
an anispic alchl wip fr 15 scnds and aach
a syring via h injcin cap.
6. Using a ndllss dvic n h syring, puncur
h Y pr si (s Fig. 11.15). Alrnaivly, fr an
injcin cap (s Fig. 11.16), aach h syring wih
mdicain dircly.
7. Injc h prscribd mdicain in h IV lin a
h ra rcmmndd by h manufacurr.
If the medication and the IV solution are not compatible:
 • Swab the injection port nearest the catheter
wih an alchl wip fr 15 scnds. If h
halhcar agncy uss an anispic cap, r-
mv his; n nd  swab h pr.
 • Insert a needleless device into the port; stop
h primary infusin and injc 2 mL f 0.9%
NS (.g., salin ush), in accrdanc wih in-
siuinal plicy, via IV push.
 • Swab the port with an alcohol wipe; insert the
ndllss dvic ha cnains mdicain
and adminisr h drug a h prscribd ra.
168 UNIT II Illustrated Atlas of Medication Administration
 • Remove the medication syringe, swab the port
again, and injc 2 mL f 0.9% NS (.g., salin
ush), in accrdanc wih insiuinal plicy,
via IV push. If injcing in a cnral lin, fl-
lw insiuinal plicy rgarding h nd 
irriga wih a salin and hparin sluin.
Raach a nw clan anispic cap accrding
 agncy plicy.
8. Whn all f h mdicain has bn adminis-
rd, pn h sablishd IV lin and radjus
h flw ra  crrspnd wih h halhcar
prvidr’s rdr. Rmv glvs and prfrm
hand hygin.
patIent teaChIng
Explain  h pain h purps f h mdicain
adminisrd and discuss any pnial advrs ffcs
f h mdicain.
doCumentatIon
1. In h pain’s MAR, dcumn h da, im,
drug, and dsag and any assssmn daa ha ar
prinn (.g., hw wll h prcdur was lr-
ad, bsrvains f h vnipuncur si).
2. Prfrm and rcrd rgular pain assssmns fr
h valuain f hrapuic ffcivnss.
3. Char any signs and sympms f h advrs f-
fcs f h drugs givn r prblms ncunrd
during h prcdur.
4. Rcrd any pain aching ha was dn.
Clinical Pitfall
Flushing the IV line by accelerating the IV infusion rate is not
recommended because the medication that is still in the
line will be administered too rapidly. This is contrary to the
manufacturer’s safety recommendation. Sudden boluses of
certain medications may also cause severe hypotension or
other signs of toxicity.
AdminiStrAtion of mEdicAtion throuGh An
imPlAntEd VEnouS AccESS dEVicE
Prfrm prmdicain assssmns and fllw prc-
dur prcl as dscribd n p. 14 in his chapr. In
addiin, rfr  h individual drug mngraphs.
equIpment
• Mdicain prl
• Prscribr’s rdr
• Mdicain fr IV dlivry and labl
• IV piggyback bag
• Drssing kis (a sm clinical pracic sings)
• Tw pairs f sril glvs
• Tw 10-mL syrings wih 0.9% NS, 2  10 mL; cn-
sul h insiuinal plicy manual fr h vlum
usd in h faciliy
• On 10-mL syring wih hparin (10  100 unis/mL),
usually 2.5  5 mL; cnsul h insiuinal plicy
manual fr h vlum usd in h faciliy
• Sril 10-mL syring
• Ndllss accss dvic
• 18-  22-gaug (⅝-inch) ndl
• Anispic sluin r swab sicks pr insiuinal
plicy
• Alchl swabs
• Hubr ndl
• Exnsin ubing
• Sharps safy cnainr fr usd ndl and rcp-
acl fr ld drssing marial ha is rmvd
teChnIque for Intravenous medICatIons
vIa Implanted venous aCCess devICe
1. Rsarch and prpar h mdicain as dscribd
in h prcdur prcl arlir in his chapr.
2. Prpar a syring wih h mdicain r add h
mdicain  an IV piggyback bag.
3. Insr h adminisrain s in h IV cnainr,
prim h IV lin  rmv all air, and hn cvr
h nd f h IV lin wih a sril cap. Lav h
prscribd mdicain in a sril syring.
4. Tak all supplis and h IV mdicain  h pa-
in’s bdsid.
5. Idnify h pain by chcking hir ID brac-
l. Explain h prcdur and prvid ducain
abu h drug bing adminisrd. Hav h pa-
in sa hir nam and birh da r w hr
idnirs.
6. Rchck all aspcs f h mdicain rdr.
7. Prfrm hand hygin.
8. If h impland pr is n alrady accssd, pal-
pa h si  idnify landmarks.
9. Opn h drssing ki, s up and prpar h
ushing supplis, and prim h infusin s whil
mainaining h sriliy f h Hubr ndl.
10. Apply sril glvs.
11. Us h nndminan glvd hand  clans h
skin vr h impland pr wih alchl; clans
frm h inndd si f insrin uward in wid-
ning circls. Rpa h clansing prcss w
mr ims. Allw h alchl  dry and hn r-
pa h clansing prcss wih h us f anisp-
ic swab sicks.
12. Using h sril glvd hand, grasp h Hubr
ndl by h wingd angs, aach i  h sy-
ring ha cnains salin, and insr h ndl
prpndicular  h pain’s skin unil h ndl
ip cms in cnac wih h bm f h pr.
Suppr h Hubr ndl wih fldd 2 × 2–inch
spngs.
13. Draw back n h plungr f h salin syring
slighly unil bld rurns. Injc NS ( ush h
pr f hparin, lf frm a prvius ush) and
hn aach h syring ha cnains mdicain
r h IV piggyback cnainr wih mdicin. If
 Parenteral Administration: Intravenous Route CHAPTER 11
adminisring frm h syring, us h IV blus
chniqu. If adminisring as an infusin wih h
IV piggyback cnainr (s Adding a Mdicain
Wih a Piggyback S lar in his chapr), aach
h primd adminisrain s  h Hubr n-
dl and adjus h ra f infusin. Prvid sup-
pr fr h IV lin. Apply ransparn r gauz
drssing and ap i in plac. Whn h mdica-
in adminisrain is cmpld, ush h lin
wih salin and hparin in accrdanc wih insi-
uinal plicy. Mainain sady prssur n h
plungr f h syring as h ndl is wihdrawn
frm h accss dvic  prvn h backw f
bld.
14. Labl h si wih h da f accss, h siz and
lngh f h Hubr ndl, and h da.
15. If h Hubr ndl is rmvd frm a hald si
a his im, clans h injcin si wih an alc-
hl wip and apply an adhsiv bandag.
16. Disps f usd ndls in a sharps safy cn-
ainr. Disps f usd xnsin ubing and hr
supplis in accrdanc wih insiuinal plicy.
17. Rmv and disps f glvs prprly. Prfrm
hand hygin.
patIent teaChIng
1. Explain  h pain h purps f h mdica-
in bing adminisrd and discuss h pnial
advrs ffcs f ha mdicain.
2. Srss h impranc f prvning infcin in h
pr; h pain shuld avid uching h si. If
mdicain is bing givn inrminly wih h
us f a pump, hav h pain pu h call ligh n
whn h machin alarm sunds.
doCumentatIon
1. In h pain’s MAR, dcumn h da, im,
drug, and dsag and any assssmn daa ha ar
prinn (.g., hw wll h prcdur was lr-
ad, bsrvains f h injcin si).
2. Prfrm and rcrd rgular pain assssmns fr
h valuain f hrapuic ffcivnss.
3. Char any signs and sympms f h advrs f-
fcs f h drugs givn r prblms ncunrd
during h prcdur.
4. Rcrd any pain aching ha was dn.
AddinG A mEdicAtion to An intrAVEnouS BAG,
BottlE, or VolumE-control dEVicE
Prfrm prmdicain assssmns and fllw prc-
dur prcl as dscribd arlir. In addiin, rfr 
h individual drug mngraphs.
equIpment
• Mdicain prl
• Prscribr’s rdr
• Mdicain fr IV dlivry and labl
169
• Glvs
• Anispic alchl wips
• Ndllss cnncr
teChnIque for addIng medICatIons to
Intravenous solutIons
1. Rsarch and prpar h mdicain as dscribd
in h prcdur prcl arlir in his chapr.
2. Idnify h pain by chcking hir ID bracl.
Explain h prcdur and prvid ducain abu
h drug bing adminisrd. Hav h pain sa
hir nam and birh da r w hr idnirs.
3. Rchck all aspcs f h mdicain rdr.
4. Prfrm hand hygin and apply glvs.
5. Idnify h injcin pr n h spcic yp f IV
cnainr r vlum cnrl s ha is bing usd;
clans h pral wih an anispic swab.
6. Clamp h IV ubing.
7. Insr h sril accss dvic in h pr and
slwly add h prscribd mdicain  h IV slu-
in. Always chck  b crain ha h mdicain
is bing addd  a cmpaibl sluin f sufcin
vlum  nsur h prpr diluin f h mdi-
cain as spcid by h manufacurr. Agia h
bag, bl, r vlum cnrl dvic  disprs h
mdicain in h uid hrughly.
8. Fr a vlum cnrl apparaus, ll h vlum
chambr wih h spcid amun f IV sluin
(s Fig. 11.2A and C) and hn clamp h ubing b-
wn h IV bl r bag and h vlum cnrl
chambr. Add h mdicain, as dscribd prvi-
usly, via h clansd injcin pr. B sur ha
h mdicain is disprsd in h sluin and ad-
jus h ra f h w sluin.
9. Afx a labl  h cnainr. Indica h mdica-
in’s nam and ds, h da and im, h pr-
pard ra f infusin, and h lngh f infusin
im.
Clinical Pitfall
When IV medications are administered by a volume control
apparatus, the calculation of the rate of infusion for adminis-
tering the drug over the proper time must include an allow-
ance for the volume of the uid in the IV tubing and for the
volume of medication.
patIent teaChIng
Explain  h pain h purps f h mdicain
adminisrd and advis him r hr f any advrs f-
fcs f h mdicain.
doCumentatIon
1. In h pain’s MAR, dcumn h da, im,
drug, and dsag; h ra f adminisrain if a vl-
um-cnrl apparaus is usd; and any assssmn
daa ha ar prinn (.g., hw wll h prcdur
was lrad).
170 UNIT II Illustrated Atlas of Medication Administration
2. Prfrm and rcrd rgular pain assssmns fr
h valuain f hrapuic ffcivnss.
3. Char any signs and sympms f h advrs f-
fcs f h drugs givn r prblms ncunrd
during h prcdur.
4. Rcrd any pain aching ha was dn.
AddinG A mEdicAtion with A PiGGyBAck SEt
Prfrm prmdicain assssmns and fllw prc-
dur prcl. In addiin, rfr  h individual drug
mngraphs.
equIpment
• Mdicain prl
• Prscribr’s rdr
• Mdicain fr IV dlivry and labl
• IV piggyback bag
• Adminisrain s wih ndllss cnncr
• Anispic alchl wips
tEchniquE for intrAVEnouS PiGGyBAck
mEdicAtionS
1. Rsarch and hn prpar h mdicain as d-
scribd in h prcdur prcl arlir in his
chapr and hn add i  an IV piggyback bag.
 • Rcnsiu a pwdr using a prassmbld IV
mdicain sysm such as h ADD-Vanag
Sysm (Fig. 11.17). This is a ndllss sysm
wih w disincly spara cmpnns: (1) an
ADD-Vanag dilun cnainr (.g., a plasic
piggyback bag) ha cnains 0.9% NS, D5W, r
0.45% sdium chlrid; and (2) an ADD-Vanag
drug vial ha cnains mdicain (.g., ampicil-
lin pwdr).
 • Hld h ADD-Vanag vial and plasic cnainr
in a vrical psiin by h bm f h aachd
drug vial (h vial is acually upsid dwn).
 • Rach hrugh h xibl cnainr f dilun,
grasp h innr sppr in h vial by h plasic
ring ha surrunds i, and pull sraigh dwn
n h ring; h sppr discnncs and falls
in h dilun sluin. Th drug pwdr als
falls u and, wih a fw squzs f h dilun
bag, mixs wih h dilun  rcnsiu h
drug.
 • Th ADD-Vanag cnainr is nw rady fr
h aachmn f h scndary IV ubing whn
i is akn  h bdsid.
 • Immdialy bfr us, chck all aspcs f h
drug rdr agains h drug cnainr.
2. Idnify h pain by chcking hir ID brac-
l. Explain h prcdur and prvid ducain
abu h drug bing adminisrd. Hav h pa-
in sa hir nam and birh da r w hr
idnirs.
Fig. 11.17 The ADD-Vantage drug delivery system. (Courtesy Bruce
Clayton.)
3. Drmin h cmpaibiliy f h primary IV s-
luin and is addiivs wih ha f h piggyback
mdicain r sluin.
4. Rchck all aspcs f h mdicain rdr.
5. Prfrm hand hygin.
6. Insr h adminisrain s in h piggyback
cnainr and aach a ndllss dvic.
7. Cnnc  h primary IV ubing by arranging h
piggyback cnainr s ha i is lvad highr
han h primary cnainr (s Fig. 11.9). Clans
h pral n h primary lin wih an anispic
swab fr 15 scnds and insr h ndllss d-
vic cnncr (Fig. 11.18) by aaching h piggy-
back ubing  h pr f h ubing f h prima-
ry sluin. Scur his in plac. Sm halhcar
agncis us anispic caps n hs Y prs in h
IV lins; rmv cap, n nd  swab si and a-
ach nd f piggyback ubing.
8. Lwr h piggyback cnainr blw h lvl f
h primary sluin, pn h scndary ubing
clamp, and slwly purg h scndary ubing f
air wih h us f h backw mhd; his will
allw h primary sluin  ll h scndary
ubing. Plac h piggyback sluin highr han
h primary IV sluin bfr adminisrain.
9. Chck h spcic rdrs fr h infusin ra
and h squnc f h sluin r mdicain
adminisrain.
10. Afx a labl  h cnainr. Indica h mdica-
in nam and ds, h da and im ha i was
prpard, h ra f infusin, and h lngh f in-
fusin im.
 Parenteral Administration: Intravenous Route CHAPTER 11
Fig. 11.18 A male Luer-Lok with an INTERLINK lever lock cannula
attached. This illustrates how a (needle-free) blunt plastic cannula-
tipped adapter can be used to attach a piggyback container to the
portal of a primary intravenous administration set. (Courtesy Baxter
Healthcare Corporation, Mountain Home, AR. All rights reserved.)
11. Whn h piggyback mpis, h chck valv in
h primary lin rlass and h primary infusin
rsums. If a pump is usd, h primary infusin
will rsum whn h piggyback r scndary in-
fusin is cmpl.
Clinical Pitfall
One of the most common mistakes when using pre-
assembled IV medication containers (for safety and ease
of reconstitution) is forgetting to activate the system and
mix the drug powder with the diluent before hanging it for
administration.
patIent teaChIng
Explain  h pain h purps f h mdicain
ha is bing adminisrd and discuss wih him r hr
any pnial advrs ffcs f h mdicain.
doCumentatIon
1. In h pain’s MAR, dcumn h da, im,
drug, and dsag and any assssmn daa ha
ar prinn (.g., hw wll h prcdur was
lrad).
2. Prfrm and rcrd rgular pain assssmns fr
h valuain f hrapuic ffcivnss.
3. Char any signs and sympms f h advrs f-
fcs f h drugs givn r prblms ncunrd
during h prcdur.
4. Rcrd any pain aching ha was dn.
171
chAnGinG to thE nExt contAinEr of
intrAVEnouS Solution
Prfrm prmdicain assssmns and fllw prc-
dur prcl. In addiin, rfr  h individual drug
mngraphs.
equIpment
• Mdicain prl
• Prscribr’s rdr
• IV sluin rdrd
• Adminisrain s wih apprpria ndl r
ndllss cnncr, drip chambr, and lr
• Chang labl
teChnIque for ChangIng Intravenous
solutIons
1. Mnir h ra f infusin and h IV insrin
si a las nc hurly. Whn h cnainr nars
cmplin, nify h nurs wh is rspnsibl fr
adding h nx cnainr.
2. Slw h ra  kp h vin pn if h lvl f
sluin in h cnainr is lw.
3. Chck h IV si, h das n h IV lins, and
h cmpaibiliy f h IV sluin ha is running
wih h nw cnainr f IV sluin  b addd.
(Mdicains may hav bn addd  h IV slu-
in pr h halhcar prvidr’s rdrs.)
4. Prfrm hand hygin.
5. Prpar h IV sluin as dscribd prviusly.
Hang h nw IV bag n h IV pl.
 • If the same tubing is used, clamp h ubing n h
primary IV lin. Using aspic chniqu, quickly
xchang h nw cnainr fr h mpy n.
 • If new tubing is used, aach h adminisrain
s  h sluin cnainr, ll h chambr n
h IV lin half full, prim h lin  purg h
air, and aach i  h vnus accss dvic.
Da and iniial h nw ubing wih h labl
ha is usd in h clinical pracic sing. If a
pump is usd, prim h IV ubing, cnnc h
ubing  h vnus accss dvic, and sar h
pump.
6. Unclamp h ubing and adjus h w ra as pr-
viusly dscribd; inspc h vnipuncur si.
7. Rchck all aspcs f h IV rdr.
patIent teaChIng
Explain  h pain h purps f h IV sluin.
doCumentatIon
1. In h pain’s MAR, dcumn h da and im,
h IV sluin usd, and h ra f adminisrain.
2. Rcrd h amun f uid infusd n h inak
and upu sh, as wll as n any w shs
mainaind a h clinical pracic sing.
3. Rcrd prinn assssmn daa cllcd.
172 UNIT II Illustrated Atlas of Medication Administration
Clinical Pitfalls
 • The ushing of central lines is an important aspect of
maintaining the patency of the central venous access
device. Two types of solutions are used to maintain the
patency of vascular access devices: heparin is used to
prevent clot formation, and 0.9% NS is used to clean
the interior diameter of the device of blood or particles of
medication. It is recommended that a 10-mL syringe be
used for ushing lines and medication administration to
prevent excessive pressure within the catheter that could
result in rupture. Always follow institutional guidelines for
recommended procedures to maintain line patency.
 • Preventing infection is a major concern with all IV devices.
Appropriate procedures for cleansing the area and the
access device with the recommended antiseptics are
mandatory.
 • If unable to aspirate blood when performing a ush
procedure, the catheter may be occluded. Never force the
solution into the IV line.
 • Start interventions by doing the simple things, like
checking that the clamp is open and that the catheter
and IV tubing are not kinked. Reposition the patient’s
upper body, and have the patient perform a Valsalva
maneuver.
 • It may be necessary to remove the injection cap,
attach a 20-mL syringe, and aspirate the blood clot.
(Check institutional policy regarding the removal and
replacement of the injection cap.) Immediately after
the aspiration of the blood clot, replace the injection
cap with a new sterile cap and institute 0.9% NS
and heparin (100 units/mL) ushing of the catheter in
accordance with institutional guidelines.
 • Report any malfunctioning of the catheter to the
healthcare provider. Radiographic evaluation and the
instillation of a thrombolytic agent (e.g., alteplase) may
be necessary.
diScontinuinG An intrAVEnouS infuSion
equIpment
• Turniqu (if usd in h halhcar agncy)
• Sril spngs
• Glvs
• Drssing marials
• Tap
• Sharps safy cnainr fr ndls and bury r
hr yps f IV cahrs
• Exnsin ubing wih cap and a salin ush in a 10-mL
syring if h infusin dvic is bing cnvrd  a
salin lck r a mdlck
teChnIque for removIng an Iv
If h IV si is bing discninud cmplly, h fl-
lwing shuld b dn:
1. Rviw insiuinal plicy rgarding h plac-
mn f a urniqu. (Sm halhcar agncis
sa ha a urniqu shuld b applid bfr h
rmval f h ndl r IV cahr in cas h ip
braks during rmval. Ohr agncis sa ha
h urniqu shuld b lsly aachd  h
limb bu n ighnd unlss ncssary.)
2. Chck h halhcar prvidr’s rdrs. Vrify
ha all IV sluins and mdicains hav bn
cmpld.
3. Chck h pain’s idniy using hir ID brac-
l. Carfully xplain wha is bing dn and why.
Hav h pain sa hir nam and birh da r
w hr idnirs.
4. Prfrm hand hygin.
5. Adqualy xps h IV si.
6. Clamp h IV ubing and urn ff h lcrnic
cnrllr r pump.
7. Prpar a gauz spng and ap fr us n h v-
nipuncur si.
8. Lsn h ap a h si whil simulanusly
sabilizing h ndl  prvn vnus damag.
If h IV si is cnaminad by bld r drainag,
pu n glvs bfr handling h ap.
9. Apply clan glvs.
10. Wih h us f a gauz pad, gnly apply prs-
sur wih h nndminan hand  h vni-
puncur si. Wihdraw h ndl r cahr,
pulling i u paralll  h skin surfac. Inspc
h ip f h ndl r cahr  b sur ha
i is inac. Rlas h urniqu, if n is in
plac. Plac h ndl r cahr in h sharps
safy cnainr.
11. Clans h ara if i has bn cnaminad wih
any bld r uid.
12. Cninu  hld h IV si rmly unil all bld-
ing cass. If h vnipuncur si was in h an-
cubial fssa, hav h pain x h lbw 
hld h gauz in plac.
13. Chck fr blding afr 1  2 minus. Rmv
h gauz, and discard i wih hr cnaminad
drssings. Clans h ara as apprpria.
14. Rmv and discard h glvs in accrdanc wih
insiuinal plicy, and prfrm hand hygin.
15. Apply a small drssing r adhsiv bandag as
sad by insiuinal plicy.
16. Prvid pain cmfr.
If h IV si is  b cnvrd  a salin lck whn
h larg-vlum sluin is discninud, h fllw-
ing shuld b dn:
1. Prfrm sps 1 hrugh 5 as dscribd fr discn-
inuing h IV si.
2. Prpar a salin ush, aach h syring  h
xnsin ubing, purg air frm h ubing, and
hn clamp h xnsin ubing. Lav h syring
aachd.
3. Clamp h ubing n h IV lin, and hn shu ff
h infusin quipmn, if prsn.
4. Pu n glvs and clans h cnncr si wih
anispic alchl wip. L air-dry.
5. Sabiliz h cahr hub whil discnncing h
IV primary ubing and hn quickly cnnc h x-
nsin ubing.
 Parenteral Administration: Intravenous Route CHAPTER 11
6. Unclamp h xnsin ubing and ush h cahr
wih salin in accrdanc wih insiuinal plicy;
clamp h ubing as h las 0.5 mL is injcd.
7. Tap h si scurly and labl and da h xn-
sin ubing.
doCumentatIon
Prvid h righ dcumnain f h rminain f
IV hrapy.
1. Char h da and im f h rminain f h IV
si r f h cnvrsin  a salin lck.
2. Prfrm and rcrd rgular pain assssmns
(.g., si daa, siz f si, clr f skin a vni-
puncur si).
3. Char and rpr any signs f advrs ffcs (.g.,
rdnss, warmh, swlling, pain a vnipuncur
si).
4. Rcrd h al amun infusd n h inak and
upu rcrd and n any w shs usd in h
clinical pracic sing.
5. Rcrd h salin ush n h pain’s MAR.
monitorinG intravEnous thErapy
Bfr iniiaing hrapy, prfrm baslin pain
assssmns  valua h pain’s currn saus.
Rpr a apprpria inrvals hrughu h curs
f ramn.
Immdialy afr rciving a rpr rgarding as-
signd pains, chck h MAR fr IV mdicains
and IV infusin rdrs fr hs pains. Mak runds
 prfrm a baslin assssmn. Daa ha shuld b
gahrd and analyzd wih rfrnc  IV hrapy in-
clud h fllwing:
• Chck ha h rdrd IV sluin (wih r wihu
mdicains) is bing adminisrd  h crrc
pain a h crrc ra f infusin.
• Chck h al amun infusd agains h amun
ha shuld hav bn infusd. Is h vlum f
infusd IV sluin r IV mdicain “n arg,”
“ahad,” r “bhind”?
• Calcula h drip ra  adminisr h mdicin
vr h apprpria im inrval. Wih a prgram-
mabl infusin pump, nsur ha h pump is s 
dlivr h prscribd vlum (mL) pr hur.
• Chck fr inlin lrs. If n is rcmmndd fr
h mdicin bing infusd, is i bing usd?
• Chck h da and im ha h infusing IV sluin
r IV mdicain was hung. Idnify whn h in-
fusing IV sluin, adminisrain s and ubing, IV
si, IV cahrs, and drssings ar  b changd in
accrdanc wih h plicis f h clinical pracic
sing. Th CDC rcmmnds ha vnipuncur
si drssings b changd whn hy bcm damp,
ls, r sild r whnvr h vnipuncur si is
changd.
• Chck h da and im ha prcdurs ar r-
drd  mainain h pancy f h sablishd IV
173
lins. (Fllw insiuinal plicis.) Th fllwing
ar gnral guidlins:
 • Priphral inrmin IV lins ar usually
ushd vry 8  12 hurs wih h us f 1 
2 mL f salin sluin. Us psiiv prssur
 prvn h backw f bld and pssibl
cclusin.
 • Cnral vnus IV lins ar usually ushd wih
a minimum f 10 mL f NS sluin whnvr
hy ar irrigad. Us a push-paus mhd 
irriga (rahr han cninuus prssur). T pr-
vn xcssiv prssur wihin h lin, always
us a las a syring wih a 10-mL capaciy  ir-
riga and mainain h pancy f a cnral lin.
Fllw insiuinal plicy fr h us f salin
and hparin sluins.
 • Grshng cahrs hav a w-way valv ha
prvns backw; hrfr hs cahrs
d n rquir hparin. Grshng cahrs ar
ushd wih 5 mL f NS wkly r a an inr-
val drmind by insiuinal plicy fr lumns
ha ar n in us. Afr mdicain adminisra-
in r TPN infusin, ush wih 10 mL f NS.
Afr bld sampl draws r bld prduc infu-
sin, ush wih 20 mL f sril NS.
 • Th amun f sluin usd  ush a Hickman,
Brviac, r Grshng cahr varis and mus b
sufcin  qual w ims h vlum rquird
 ll h cahr lumn plus h vlum f any
xnsin ubing ha is bing usd.
 • Implanabl vascular accss prs (.g., Pr-A-
Cah, Infus-A-Pr) rquir ha h pr b lld
wih sril hparinizd sluin, usually 100
unis/mL, afr ach us. If h pr is n ac-
cssd rgularly, ushs may nly b prfrmd
nc ach mnh r a an inrval cid by insiu-
inal plicy.
 • Prvn damag  cnral vnus cahrs by
clamping nly h cahr wih a paddd hm-
sa r a smh-dgd clamp.
 • Chang h injcin caps fr lumn hubs n cn-
ral vnus cahrs vry 72 hurs r as sad
in h insiuinal plicy.
 • Chck h IV ubing fr any bsrucins r air
in h lin. Th pain and h vnipuncur si
shuld b chckd a las vry hur fr w
ra, inlrain (.g., ndrnss, rdnss, puf-
nss), and advrs ffcs. Rpr and ak im-
mdia acin if h infusin is inlrad, if i is
imprprly infusing, r if signs f infcin xis.
If h w ra is falling bhind schdul, d h
fllwing:
1. Chck fr mchanical bsrucin f h ubing
(.g., clsd clamp, kinking) r lr, and ihr
irriga r chang h ubing.
2. Chck h drip chambr. If i is lss han half
full, squz i  ll i mr cmplly. D n
vrll.
174 UNIT II Illustrated Atlas of Medication Administration
3. Chck  mak sur ha h IV cnainr is n
mpy. Als, chck  mak sur ha h cn-
ainr is mr han 3 f abv h vnipuncur
si. Th high may b inadvrnly incrrc if
h pain is rpsiind r if h bd high is
radjusd.
4. Chck fr ubing ha has falln blw h vni-
puncur si. If a signican lngh has falln, l-
va and carfully cil h ubing nar h si f
h vnipuncur.
• War glvs  inspc h IV si. Chck h rans-
parn drssing fr h da ha h infusin dvic
was sard. Palpa gnly arund h cahr r
ndl fr dma, clnss, r pain, which indi-
ca inlrain. Chck fr any signs f rdnss r
ha, which indica ha an inammary prcss is
ccurring.
• Chck  drmin whhr h bvl f h ndl
is pushing agains h wall f h vin. D his by
cautiously raising r lwring h angl f h n-
dl slighly  s if w is rsrd. If s, rpsi-
in h ndl slighly wih h us f a gauz pad
in h ms apprpria lcain.
• Chck h mpraur f h sluin ha is b-
ing infusd. Cld sluins can caus spasms in h
vin.
• Chck  nsur ha a rsrain r bld prssur
cuff applid  h arm has n inrfrd wih h
w.
• If i appars ha h IV accss dvic is cld, do
not amp  clar h ndl by ushing i wih
uid. This will disldg h cl, which may caus
a hrmbmblism. Th aspirain f h ndl
r cahr wih a syring  disldg h cl is n
lngr rcmmndd; rahr, h si shuld b dis-
cninud and h IV infusin rsard.
• Rmain alr a all ims fr cmplicains assciad
wih IV hrapy f any yp (.g., phlbiis, infcin,
air in h ubing, circulary vrlad, pulmnary
dma, pulmnary mblism, drug racins frm
h IV mdicains).
• Dcumn all ndings and prcdurs prfrmd in
assciain wih IV hrapy.
• During shif rpr, idnify h xac vlum f IV
sluin r mdicain ha has bn infusd n h
currn shif and h vlum rmaining  b in-
fusd during h nx shif. In addiin, rpr any
IV sis ha ar funcining prly r IV lins ha
rquir frqun si changs.
ComplICatIons assoCIated WIth
Intravenous therapy
Cmplicains ha can ccur wih IV hrapy includ
phlbiis, hrmbphlbiis, lcalizd infcin, spi-
cmia, inlrain, xravasain, air in h ubing, air
mblism, circulary vrlad, pulmnary dma,
cahr mblism, and “spd shck.”
pbii, tbbii,  lciz
Ici
Phlebitis is h inammain f a vin; thrombophlebitis
is h inammain f a vin wih h frmain f a
hrmbus in h ara f inammain. Th hr pri-
mary causs f phlbiis ar as fllws:
1. Irriain f h vin by h cahr (.g., cahr
ha is  larg fr h vin, imprpr insrin, im-
prpr anchring wih xcssiv mvmn f h
cahr).
2. Chmical irriain frm mdicins (.g., sluin
infusd  rapidly r a a vlum ha was  larg
fr h vin, sluin is irriaing  h vin).
3. Infcin causd by imprpr aspic chniqu
during accssing r drssing changs, r frm lng-
rm cahr placmn.
If signs f rdnss (ryhma), warmh, ndr-
nss, swlling, and burning pain alng h curs f
h vin ar prsn, phlbiis r hrmbphlbiis and
infcin may b dvlping (Tabl 11.2). Cnrm h
prsnc f hs signs wih h suprvising nurs. Th
ramn f phlbiis dpnds n h caus f vnus
irriain. If h IV lin is priphral and hr is vi-
dnc f inlrain using h Inltration Scale (Tabl
11.3), h IV cahr is discninud and a nw IV lin
using all nw quipmn is insrd a a diffrn lca-
in. Fr ppl wih any yp f cnral cahr (.g.,
PICC), h halhcar prvidr shuld b nid. N
all cnral cahrs ar rmvd whn infcin ccurs;
sm may b rad wih anibiic hrapy. Many in-
siuins als rquir ha h infcin cnrl nurs
b nid. If puruln drainag is prsn, a sampl
f h drainag is baind fr culur and snsiiviy.
If a fvr and chills (.g., signs f spicmia) accm-
pany hs sympms, culurs f h pain’s bld
and h cahr ip may als b indicad. Chck insi-
uinal plicis rgarding whhr a halhcar pr-
vidr’s rdr is ncssary  d his r whhr sand-
ing rdrs xis as par f infcin cnrl prcdurs.
Gnrally, fllw-up ramn includs lvain and
h applicain f warm, mis cmprsss  h si.
Table 11.2 Assessing the Severity of Phlebitis
ScorE dEScriPtorS
0 No clinical symptoms
1 Erythema at access site, with or without pain
2 Pain at the access site with erythema and/or
edema
3 Pain at the access site with erythema, streak
formation, and/or palpable venous cord ±1
inch long
4 Pain at the access site with erythema, streak
formation, palpable venous cord >1 inch
long, and/or purulent drainage
From Infusion Nurses Society. Infusion nursing standards of practice. J Infus
Nurs. 2016, S45.
 Parenteral Administration: Intravenous Route CHAPTER 11 175

Dcumn h ndings, h ramn ha is adminis-
rd, and h rsuls f nging assssmns.
Clinical Pitfall
Only a Huber needle is used to access an implanted port.
sici
Whn pahgns ha ar assciad wih a lcal infc-
in invad h bldsram, ar carrid  hr pars
f h bdy, and riggr an inammary rspns
(.g., fvr, chills), h infcin is n lngr lcal; i is
nw sysmic, and his cndiin is calld septicemia
Ppl wh alrady hav an infcin r wh ar
immuncmprmisd ar a highr risk fr h
dvlpmn f spicmia. Th impranc f main-
aining aspic chniqu hrughu all aspcs f
cahr insrin and mainnanc car cann b
vrmphasizd. Th pnial fr cnaminain x-
iss during vry aspc f IV hrapy, saring a h
im f h manufacur and packaging f IV uids
and quipmn and cninuing hrughu h acual
prparain and adminisrain f h IV hrapy. Th
risk f spicmia als incrass wih h frquncy
wih which h cahr and si ar manipulad and
wih hw lng an IV cahr rmains in plac. Prfrm
cahr si inspcins in accrdanc wih insiu-
inal plicy. Suspc lcalizd infcin a h cahr
si if rdnss, dma, r puruln drainag is prsn
a h nry si r if h pain has an lvad m-
praur r an lvad whi bld cll cun. Kp
in mind ha immuncmprmisd pains r hs
wh ar rciving an anipyric (.g., acaminphn,
ibuprfn) may n dvlp a fvr.
Suspc spicmia if h pain dvlps h fl-
lwing: a suddn ns f ushing, fvr, chills, gnr-
al malais, hadach, nausa, vmiing, hypnsin,
shck, r a wak, rapid puls. Obain h pain’s vial
signs and nify h halhcar prvidr immdialy
f all ndings. Obain h halhcar prvidr’s rdrs,
which will usually includ bld culurs, h discn-
inuain f h IV cahr, and anibiic hrapy afr
culurs ar baind. Rurn h unusd prin f h
IV sluin  h pharmacy r labrary fr sing as
spcid by insiuinal plicy.
Dcumn h ndings, h ramn adminisrd,
and h nging assssmns.

Iii  exi

Table 11.3 Inltration Scale Inltration is h lakag f an IV sluin in h issu
ha surrunds h vin; extravasation is h lakag f
GrAdE clinicAl critEriA
an irrian chmical (.g., h mdicin bing infusd)
0 No symptoms in h issu ha surrunds h vin. Inlrain r
1 Skin blanched xravasain may b accmpanid by rdnss and
Edema <1 inch in any direction warmh, clnss and blanching f h skin, swlling,
Cool to touch and a dull ach  a svr pain a h vnipuncur
With or without pain si (s Tabl 11.3). Inlrain r xravasain ccurs
ms cmmnly whn a ndl ip puncurs h vin
2 Skin blanched
and h IV sluin laks in h issu ha surrunds
Edema 1–6 inches in any direction
h vin. Srius issu damag may ccur, paricu-
Cool to touch larly if h mdicin in h sluin is irriaing  h
With or without pain issu (.g., a calcium sal) r causs vascnsricin
3 Skin blanched, translucent (.g., lvarrnl)  h vasculaur in h ara.
Gross edema >6 inches in any direction Th nurs shuld always duca h pain r-
Cool to touch
garding h signs and sympms f hs cndiins s
ha h pain can rpr arly discmfr and arly
Mild to moderate pain
inrvnins can b iniiad in h vn ha inlra-
Possible numbness in r xravasain ds ccur.
4 Skin blanched, translucent Inspc h IV si a rgular inrvals fr inlra-
Skin tight, leaking in. Whnvr a chang in h limb’s clr, siz, r
Skin discolored, bruised, swollen skin ingriy is bsrvd, mak a cmparisn wih h
Gross edema >6 inches in any direction ppsi limb. Gnral guidlins ar as fllws:
• Fr inlrain, sp h infusin and lva h
Deep pitting tissue edema
affcd limb. Assss fr circulary cmprmis:
Circulatory impairment chck capillary rll and pulss prximal and disal
Moderate to severe pain  h ara f inlrain. If h inlrain is causd
Inltration of any amount of blood product, by an IV sluin, rmv h cahr as dircd
irritant, or vesicant by plicy and as dscribd arlir. Whhr cld r
From Infusion Nurses Society. Infusion nursing standards of practice. J Infus
ha is applid  h si dpnds n h spcic
Nurs. 2016, S46. yp f IV sluin and h yp f mdicain ha
176 UNIT II Illustrated Atlas of Medication Administration
has inlrad. Cnsul insiuinal guidlins and
dscrib h pain’s cndiin using h inlra-
in scal (s Tabl 11.3).
• Fr xravasain, h prcl will call fr h IV in-
fusin  b sppd, bu h cahr is lf in plac.
Wih auhrizain frm h halhcar prvidr,
amps may b mad  aspira h mdicain,
and rdrs fr ramn f phnlamin (Rgiin)
which can b injcd alng h si f h xrava-
sain  minimiz issu damag. Elva h x-
rmiy. Apply ic (pr insiuinal plicy) rahr
han ha fr 24 hurs, xcp fr ramn f vin-
crisin r vinblasin xravasain, which rquirs
ha rahr han cld. Dcumn h cndiin n
h pain’s char as 4+ inlrain, and dscrib
h visual apparanc and masurmns f h
siz f h si whr xravasain has ccurrd.
Phgraphs f h si may b par f h pr-
cl. Afr h prcl fr xravasain is cmpl,
rsar h IV sluin a a nw si prximal  h
ara f xravasain.
• Dcumn h ndings, h ramn adminisrd,
and h nging assssmns.
ai i  tbi  ai eb
If an air bubbl is fund in h IV ubing, clamp h ub-
ing immdialy. Swab h injcin si in h rubbr
hub nar h ndl r h piggyback pral—which-
vr is clsr  h air bubbl—wih an alchl wip.
Using sril chniqu, insr a ndllss accss d-
vic n a syring in h pral blw h air bubbl,
and wihdraw h air pck.
An air embolism ccurs as a rsul f an air bubbl
nring h cardivascular sysm. Sympms f an
air mblism may includ pain cmplains f palpi-
ains, chs pain, shrnss f brah, cyansis, hyp-
nsin, and a wak, hrady puls. If air has acually
nrd h pain via h IV ubing, urn h pain
n hir lf sid wih h had in a dpndn psi-
in. Adminisr xygn and nify h halhcar pr-
vidr immdialy. Mnir vial signs. B prpard
fr pssibl rdrs  draw arrial bld gass and
fr vnilary suppr, if ncssary. Air mbli can b
prvnd by clamping cahrs whn hy ar n in
us, insrucing h pain  prfrm h Valsalva ma-
nuvr during ubing and injcin cap changs, using
prpr inlin lrs, n allwing IV cnainrs  run
dry, and rmving all air frm ubing r syrings b-
fr cnncing hm  an IV accss dvic. Always
purg h ush r mdicain syring f air bfr a-
achmn and injcin.
Dcumn h ndings, h ramn adminisrd,
and h nging assssmns.
Cic o  p e
Circulary vrlad ha lads  pulmonary edema is
causd by infusing uid  rapidly r by giving 
much uid, paricularly  ldr aduls, infans, r
pains wih cardivascular disas. Signs f circula-
ry vrlad ar ngrgd nck vins, dyspna, r-
ducd urin upu, dma, bunding puls, and shal-
lw, rapid rspirains. Th signs f pulmnary dma
ar dyspna, cugh, anxiy, cars crackls, pssibl
cardiac dysrhyhmias, hrady puls, lvain r drp
in bld prssur (dpnding n svriy), and frhy
spuum. Whn hs sympms dvlp, slw h IV
infusin immdialy  a TKO ra. Plac h pain
in a high Fwlr’s psiin (had f bd 60  90 d-
grs), sar xygn, bain vial signs, and summn
h halhcar prvidr immdialy. During svr
rspirary disrss, h pain may rquir inubain
and a mchanical vnilar  imprv xygn d-
livry. Anicipa h halhcar prvidr’s rdrs fr
mdicains such as diurics, vasdilars, and mr-
phin sulfa.
Dcumn h ndings, h ramn adminisrd,
and h nging assssmns.
p ebi
A pulmonary embolism may ccur as a rsul f frign
marials bing injcd in h vin r frm a bld
cl ha braks ls and ravls  h lungs, whr
i ldgs in h arrils. Sympms includ h sud-
dn ns f apprhnsin and dyspna, pluriic pain,
swaing, achycardia, cugh, unxplaind hmpysis,
lw-grad fvr, and cyansis. Whn his cndiin
is suspcd, immdialy plac h pain in a smi-
Fwlr psiin, adminisr xygn, bain vial signs,
and nify h halhcar prvidr. Anicipa rdrs fr
h drawing f bld fr arrial bld gass, prfrm-
ing a lung scan  vrify h prsnc f h pulmnary
mblism, and drmining h baslin prhrmbin
im bfr iniiaing anicagulan hrapy.
Frign-paricl mbli can b prvnd by using
an inlin lr, using prpr diluns fr rcnsiuin,
nsuring h cmpl dissluin f any mdicains
ha ar addd  a sluin, and nsuring ha hr
ar n visibl signs f frign mar in IV sluins.
Thrmbmbli can b avidd by n using h vins
in h lwr xrmiis in aduls and by using a 10-
mL syring whn ushing all cnral lins. A 10-mL sy-
ring dcrass h prssur ha is xrd wihin h
vascular sysm. (Th smallr h syring, h grar
h prssur xrd.) Whn ushing a cahr, nvr
frc h ush sluin bcaus his may disldg a
cl.
Dcumn h ndings, h ramn adminisrd,
and h nging assssmns.
“s sck”
“Speed shock” ccurs as a sysmic racin  a fr-
ign subsanc ha is givn  rapidly in h bld-
sram. This can ccur whn an IV drug is adminis-
rd  rapidly in h circulain, ms cmmnly
by IV push. Th rapid dlivry f h IV drug cras
a cncnrad plasma lvl in h pain ha may
 Parenteral Administration: Intravenous Route CHAPTER 11
rsul in shck, syncp, and cardiac arrs. Diffrn
rsurcs (.g., AHFS Drug Information, Physicians’
Desk Reference) and packag insrs ha accmpany
mdicains sa h rcmmndd ra f injc-
in r w ra  prvn cmplicains ha may
rsul frm a rapid infusin ra. Th nurs nds 
im h adminisrain f an IV push mdicain by
bsrving h infusin im n a clck r wach di-
rcly. Th nurs als nds  frqunly chck h
w ra f IV infusins, us infusin cnrl dvics,
and rsis spding up mdicains r IV ras whn
hrapy is bhind schdul. Assss h pain bfr
iniiaing an IV drug  bain baslin daa (.g., vi-
al signs), and cninu mniring during IV hrapy
fr dizzinss; ushing; ighnss in h chs; rapid,
irrgular puls; hypnsin; and anaphylacic shck.
Whn spd shck is suspcd, immdialy sp h
infusin, mainain IV pancy a a TKO ra, bain
h pain’s vial signs, and nify h halhcar pr-
vidr. Anicipa h ramn f shck by chcking
insiuinal plicy.
patIent teaChIng
Always ach h pain and hir signican hrs
abu h signs and sympms f cmplicains ha
shuld b rprd immdialy  h halhcar pr-
vidr. Dpnding n h yp f IV dlivry sysm ha
is usd  adminisr h mdicain, insruc hs b-
ing rad n an upain basis r in a hm halh
sing whn  rurn fr h cahr  b changd
and whn  rurn fr h nx visi  h halhcar
prvidr r clinic.
177
doCumentatIon
Prvid h righ dcumnain f h mdicain ad-
minisrain, h pain’s rspnss  drug hrapy,
and any cmplicains f r unward racins  h
prscribd hrapy.
1. Char h da and im, h drug nam and dsag,
and h ru f adminisrain.
2. Prfrm and rcrd rgular pain assssmns
fr h valuain f hrapuic ffcivnss (.g.,
bld prssur, puls, inak and upu, lung ld
sunds, rspirary ra, pain a infusin si).
3. Prfrm rgular assssmns f h pain and h
IV accss sis fr cmplicains assciad wih IV
hrapy r h adminisrain f IV drug hrapy.
4. Char and rpr any signs and sympms f ad-
vrs drug ffcs rlad  hrapy. Nify h
halhcar prvidr f any cmplicains.
5. Char any drssing changs prfrmd and rcrd any
signs and sympms f cmplicains a h insrin
si (.g., rdnss, ndrnss, swlling, drainag).
6. Char any difculy wih ushing f any vnus
accss dvic and nify h halhcar prvidr as
apprpria.
7. Char h das and ims ha prcdurs ar pr-
frmd  mainain h pancy f h IV si, n-
dl, priphral r midlin cahr, cnral vnus
cahr, r pr (.g., hparinizd ush; salin ush
fr a Grshng cahr).
8. Prfrm and valida ssnial pain ducain
rgarding h drug hrapy and hr ssnial as-
pcs f inrvnin fr h disas prcss ha is
affcing h individual.
178 UNIT II Illustrated Atlas of Medication Administration

Ciic J  nx-gi nCleX ® exii-s qi

ke Ps 1. A nurse is starting a peripheral IV line for the rst time in an
extremity of an elderly patient and knows which site is the best
• Intravenous therapy involves the administration of uids location for an IV line?
and medications directly into the bloodstream. The three
intravascular compartments are veins, arteries, and 1. Near the antecubital space
capillaries. The three uid compartments are intracellular 2. In the biggest vein that is visible
spaces, intravascular spaces (e.g., arteries, veins, and 3. In the dominant hand
capillaries), and interstitial spaces. 4. In the metacarpal vein, if it is large enough
• Intravenous access devices include peripheral IV lines, objeve: Discuss the different IV access devices used for IV
central catheters, and implantable infusion ports. therapy.
• Intravenous solutions that are hypotonic are used for nclEx e pe: Multiple choice
dehydration, isotonic solutions are used to maintain cgve s: Knowledge
hydration, and hypertonic solutions may be used to draw 2. The nurse knows that IV solutions have different clinical uses.
uid into the intravascular compartment to support blood Match the IV solution with the clinical use.
pressure and promote diuresis.
• Principles of IV administration include the following:
 • Review the chart to determine the medical and nursing iV Solution tyPE clinicAl uSE
diagnosis, the patient’s history and allergies, and the
signicant presenting symptoms. Hypertonic Patient with signs of peripheral
 • Review the assessment of the patient’s baseline data, dehydration
current vital signs, laboratory and diagnostic data, Isotonic Patient with signs of uid volume
and type and use of any IV access. After the IV site is overload
Hypotonic Patient recovering from surgery
established, the IV solution or blood product is hung, or an
following trauma
IV medication is administered, an ongoing assessment is
required to monitor the patient’s condition, the IV site, and
response to the IV therapy that is being delivered. objeve: Differentiate between isotonic, hypotonic, and hypertonic
• Patient education needs to be implemented. All aspects of IV solutions and explain their clinical uses.
the patient’s care needs must be explained to the patient nGn e pe: Drag and drop
and their family. In addition, community resources must be cgve s: Recognize cues
arranged to assist with home infusion therapy.
3. After changing a primary IV bag, the nurse nds that it will not run.
• Complications of IV therapy include phlebitis,
What does the nurse do to problem-solve ? (Select all that apply.)
thrombophlebitis, localized infection, septicemia,
inltration, extravasation, air in the tubing, air embolism, 1. Determine that the correct type of IV solution was hung
circulatory overload, pulmonary edema, catheter 2. Check that the clamps are open
embolism, and “speed shock.” 3. Adjust the height of the IV solution
4. Prime a new IV tubing
5. Adjust the position of the patient’s arm
Aa leag reses
objeve: Identify the general principles of administering
SG Go to your Study Guide for additional Review Questions medications via the IV route.
for the NCLEX® Examination, Critical Thinking Clinical Situa- nclEx e pe: Multiple response
tions, and other learning activities to help you master this chap- cgve s: Application
ter content.

Go to your Evolve website (https://evolve.elsevier.com/Clayton)

for additional online resources.

Clinical Judgment and Next-Generation NCLEX® Exam-

ination-Style Questions The following questions are typical of
the NCLEX examination and include both NGN (Next Genera-
tion) and traditional questions. See Chapter 1 for further infor-
mation regarding question types.
 Parenteral Administration: Intravenous Route CHAPTER 11 179

4. Choose the most likely options for the information missing from the objeve: Explain the signs, symptoms, and treatment of
following sentence by selecting from the lists of options provided. the complications associated with IV therapy (e.g., phlebitis,
thrombophlebitis, localized infection, septicemia, inltration,
The nurse checking a patient’s IV site notes that there was extravasation, air in tubing, pulmonary edema, catheter embolism,
an area around the IV that looked ________1__________ and “speed shock”).
and felt ________1___________ and recognized these to nclEx e pe: Multiple response
be symptoms of a/an __________2___________. cgve s: Application
7. When administering a medication into a port with a Huber needle,
oPtionS for 1 oPtionS for 2 what are the steps the nurse takes? List the steps in order.
purulent drainage air in the tubing 1. Administer the medication and ush port again
swollen and puffy phlebitis 2. Use sterile technique throughout the procedure
cool to the touch inltration 3. Perform hand hygiene and apply sterile gloves
warm to the touch infection 4. Prepare a syringe with the medication
5. Flush the port with push-pause technique
6. Insert the Huber needle perpendicular to the patient’s
objeve: Explain the signs, symptoms, and treatment of skin
the complications associated with IV therapy (e.g., phlebitis, 7. Apply a transparent dressing
thrombophlebitis, localized infection, septicemia, inltration,
extravasation, air in tubing, pulmonary edema, catheter embolism, objeve: Identify baseline assessments for IV therapy and proper
and “speed shock”). maintenance of patency of IV lines and implanted access devices.
nGn e pe: Cloze nclEx e pe: Ordering
cgve s: Recognize cues cgve s: Application

5. The nurse knows that there are different techniques used to 8. The nurse knows to watch for which of the following signs and
administer medication in an IV. Indicate with an arrow which symptoms of speed shock? (Select all that apply.)
technique is associated with which IV type. 1. Complaint of dizziness and ushing
2. Engorged neck veins
tEchniquE for 3. Rapid, irregular pulse
AdminiStrAtion of 4. Complaint of tightness in the chest
mEdicAtion 5. Swollen, puffy area around the IV site
Infusion line (IV tubing) Aspirate for blood, ush objeve: Explain the signs, symptoms, and treatment of
the IV, infuse the med, ush the complications associated with IV therapy (e.g., phlebitis,
again thrombophlebitis, localized infection, septicemia, inltration,
IV bag Attach med syringe into Y extravasation, air in tubing, pulmonary edema, catheter embolism,
port, infuse the med and “speed shock”).
Secondary piggyback set Attach syringe to bag port, nclEx e pe: Multiple response
infuse into solution, agitate cgve s: Application
bag
9. The nurse has completed the administration of an IV injection of
Saline lock Connect tubing, backush
furosemide (Lasix) and will document this on the MAR by including
from primary, open clamp,
what information? (Select all that apply.)
hang bag higher than
primary, run medication 1. The IV site used
2. The time it took to infuse the drug
3. The time of administration
objeve: Describe the correct techniques for administering 4. The date of administration
medications by means of a saline lock, an IV bag, an infusion pump, 5. The dosage administered
and secondary piggyback set. 6. The drug administered
nGn e pe: Drag and drop 7. The provider who ordered the drug
cgve s: Application
objeve: Describe the correct techniques for administering
6. To minimize the risk of air embolism with IV therapy, the nurse medications by means of a saline lock, an IV bag, an infusion pump,
should routinely do which of the following? (Select all that apply.) and a secondary piggyback set.
nclEx e pe: Extended multiple response
1. Cap off the IV catheter when not in use.
cgve s: Evaluate cues
2. Instruct the patient to perform the Valsalva maneuver
during tubing and injection cap changes.
3. Always use proper inline lters.
4. Allow IV containers to run dry to ensure all uid/
medication is given.
5. Remove all air from tubing or syringes before connecting
to an IV access device.
Unit III Drugs Affecting the Autonomic and Central Nervous Systems

12 Drugs Affecting the Autonomic Nervous System

https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the most common neurotransmitters known to
affect central nervous system function.
2. Explain the actions of anticholinergic agents and beta-
adrenergic blocking agents.
3. Describe clinical uses and the predictable adverse effects
of anticholinergic agents.
4. Describe clinical uses and the predictable adverse effects
of beta-adrenergic blocking agents.
5. Describe clinical uses and the predictable adverse effects
of cholinergic agonists.
6. Describe clinical uses and the predictable adverse effects
of adrenergic agonists.

Key Terms
central nervous system (SĔN-trŭl
NŬR-vŭs SĬS-tĕm) (p. 180)
peripheral nervous system (pĕ-RĬF-
ĕr-ăl) (p. 180)
afferent nerves (ĂF-ĕ-rĕnt NŬRVZ)
(p. 180)
efferent nerves (ĔF-ĕ-rĕnt) (p. 180)
autonomic nervous system (ŏ-tō-
NŎM-ĭk) (p. 180)
neurons (NYŪR-ŏn) (p. 180)
synapse (SĬN-ăps) (p. 180)
neurotransmitters (nyūr-ō-TRĂNZ-mĭ-
tŭrz) (p. 180)
receptors (rē-SĔP-tŭrz) (p. 180)
norepinephrine (nōr-ĕp-ĭ-NĔF-rĭn)
(p. 181)
acetylcholine (ăs-ē-tĭl-KŌ-lēn) (p. 181)
cholinergic bers (kō-lĭn-ŬR-jĭk FĪ-
bŭrz) (p. 181)
adrenergic bers (ăd-rĭn-ŬR-jĭk)
(p. 181)
cholinergic agents (kō-lĭn-ŬR-jĭk
Ā-jĕnts) (p. 181)
adrenergic agents (ăd-rĭn-ŬR-jĭk)
(p. 181)
anticholinergic agents (ăn-tē-kō-lĭn-
ŬR-jĭk) (p. 181)
adrenergic blocking agents (ăd-rĭn-
ŬR-jĭk BLŎ-kĭng Ā-jĕnts) (p. 181)
catecholamines (kăt-ĕ-KŌL-ă-mēnz)
(p. 181)
alpha receptors (ĂL-fă rē-SĔP-tŭrz)
(p. 181)
beta receptors (BĀ-tă rē-SĔP-tŭrz)
(p. 181)
dopaminergic receptors (dō-pă-
mĭn-ŬR-jĭk rē-SĔP-tŭrz) (p. 181)

The CenTral and auTonomiC
nervous sysTems
The control of the human body as a living organism
comes primarily from two major systems: the nervous
system and the endocrine system. In general, the en-
docrine system controls the body’s metabolism. The
nervous system regulates the body’s ongoing activities
(e.g., heart and respiratory functions), its rapid response
to sudden changes in the environment (e.g., skeletal
muscles contracting to help an individual to avoid dan-
ger), and the rates of secretion of some glands.
The nervous system is composed of the central ner-
vous system (CNS), which consists of the brain and the
spinal cord, and the peripheral nervous system, which
includes the peripheral nerves subdivided into the
afferent and efferent nerves. The afferent nerves con-
duct signals from sensory receptors (e.g., vision, pres-
sure, pain, cold, warmth, touch, smell) throughout the
body to the CNS. The CNS processes these signals and
180
controls the body’s response by sending signals back
through the efferent nerves of the peripheral nervous
system. The peripheral nervous system is further sub-
divided into the somatic nervous system, which controls
voluntary movement (e.g., skeletal muscle contrac-
tions), and the autonomic nervous system, which, as
suggested by the name, works automatically and is not
under voluntary control.
Each nerve of the central and peripheral nervous sys-
tems is actually composed of a series of segments called
neurons The junction between one neuron and the next
is called a synapse The transmission of nerve signals
or impulses occurs because of the activity of chemical
substances called neurotransmitters (e.g., transmitters
of nerve impulses). A neurotransmitter is released into
the synapse at the end of one neuron, thereby activat-
ing receptors on the next neuron in the chain or, at the
end of the nerve chain, stimulating receptors on the
end organ (e.g., the heart, smooth muscle, or gland).
 Drugs Affecting the Autonomic Nervous System CHAPTER 12
Neurotransmitters can be excitatory, which means that
they stimulate the next neuron, or inhibitory, which
means that they inhibit electrical impulses through the
neuron. Because a single neuron releases only one type
of neurotransmitter, the CNS is composed of different
types of neurons that secrete separate neurotransmitters.
Research indicates that there are more than 30 differ-
ent types of neurotransmitters; the more common ones
throughout the CNS are acetylcholine, norepinephrine,
epinephrine, dopamine, glycine, gamma-aminobutyric
acid, and glutamic acid. Substance P and the enkepha-
lins and endorphins regulate the sensation of pain, and
serotonin and dopamine regulate mood. Other neu-
rotransmitters include prostaglandins, histamine, cyclic
adenosine monophosphate, amino acids, and peptides.
Neurotransmitter regulation by pharmacologic agents
(e.g., medicines) is a major mechanism that allows for
the control of disease processes caused by an excess or
deciency of these neurotransmitters. The use of inhibi-
tory and excitatory neurotransmitters to control illness-
es is explained in the rest of the chapters in this unit.
The auTonomiC nervous sysTem
With the exception of skeletal muscle, the autonomic
nervous system controls most tissue function. This ner-
vous system helps to control blood pressure, gastro-
intestinal (GI) secretion and motility, urinary bladder
function, sweating, and body temperature. In general,
it maintains a constant internal environment (homeo-
stasis) and responds to emergency situations.
There are two main branches of the autonomic ner-
vous system: the sympathetic branch and the parasym-
pathetic branch. The sympathetic and parasympathetic
branches typically function in opposition with each
other. However, this can be considered complementary
in nature rather than antagonistic. The sympathetic
branch speeds up normal processes, and the para-
sympathetic branch slows down these processes. The
sympathetic division typically functions in actions that
require quick responses during the “ght-or-ight”
response. The parasympathetic division functions as
part of actions that do not require immediate reaction
during the “rest-and-digest” response.
The two major neurotransmitters of the autonomic
nervous system are norepinephrine and acetylcholine. The
nerve endings that liberate acetylcholine are called cholin-
ergic bers; those that secrete norepinephrine are called
adrenergic bers Most organs are innervated by both ad-
renergic and cholinergic bers, but these bers produce
opposite responses. For example, in the heart, the stimula-
tion of adrenergic bers increases the heart rate, and the
stimulation of cholinergic bers slows the heart rate; in the
eyes, the stimulation of adrenergic bers causes pupillary
dilation, and the stimulation of cholinergic bers causes
pupillary constriction (Table 12.1).
Medications that cause effects in the body simi-
lar to those produced by acetylcholine are called
181
cholinergic agents (muscarinic agents) or parasympa-
thomimetic agents, because they mimic the action pro-
duced by the stimulation of the parasympathetic di-
vision of the autonomic nervous system. Medications
that cause effects similar to those produced by the ad-
renergic neurotransmitter are called adrenergic agents
or sympathomimetic agents. Agents that block or inhibit
cholinergic activity are called anticholinergic agents
(antimuscarinic agents), and those that inhibit the ad-
renergic system are referred to as adrenergic blocking
agents. Fig. 12.1 presents a diagram of the autonomic
nervous system and its representative stimulants and
inhibitors.
Drug Class: aDrenergiC agents
Actions
The adrenergic nervous system may be stimulated by
two broad classes of drugs: catecholamines and non-
catecholamines. The body’s naturally occurring neuro-
transmitter catecholamines are norepinephrine,
epinephrine, and dopamine. Norepinephrine is secreted
primarily from nerve terminals, epinephrine comes pri-
marily from the adrenal medulla, and dopamine is found
at selected sites in the brain, the kidneys, and the GI tract.
All three agents are also synthetically manufactured and
may be administered to produce the same effects as those
that are naturally secreted. Noncatecholamines have
actions that are somewhat similar to those of the catechol-
amines; however, they are more selective for certain types
of receptors, they are not quite as fast acting, and they
have a longer duration of action.
As illustrated in Fig. 12.1, the adrenergic side of the
autonomic nervous system can be subdivided into the
alpha receptors, beta receptors, and dopaminergic re-
ceptors. In general, the stimulation of the alpha-1 re-
ceptors causes the vasoconstriction of blood vessels.
The alpha-2 receptors appear to serve as mediators of
negative feedback, thereby preventing the further re-
lease of norepinephrine. Stimulation of beta-1 recep-
tors causes an increase in the heart rate, and stimula-
tion of beta-2 receptors causes the relaxation of smooth
muscle in the bronchi (bronchodilation), the uterus (re-
laxation), and the peripheral arterial blood vessels (va-
sodilation). Stimulation of the dopaminergic receptors
in the brain improves the symptoms associated with
Parkinson disease. Dopamine also increases urine out-
put as a result of the stimulation of specic receptors in
the kidneys that results in better renal perfusion.
Uses
As noted in Table 12.2, many drugs act on more than one
type of adrenergic receptor. Fortunately, each agent can
be used for a specic purpose without many adverse
effects. If recommended doses are exceeded, however,
certain receptors may be stimulated excessively, which
can cause serious adverse effects. An example of this is
terbutaline, which is primarily a beta stimulant. With
182 UNIT III Drugs Affecting the Autonomic and Central Nervous System

Table 12.1 Actions of Autonomic Nerve Impulses on Specic Tissues

CholinergiC reCeptors
tissue reCeptor type aDrenergiC reCeptors (sympathetiC) (parasympathetiC)
BlooD Vessels
a
Coronary α1 Constriction Dilation
β2 Dilation
Skin α1 Constriction Dilation
Renal α1 Constriction —
β1 and β2 Dilation
Skeletal muscle α1 Constriction Dilation
β2 Dilation
Veins (Systemic) α1 Constriction —
β2 Dilation
eye
Radial muscle, iris α1 Constriction (mydriasis) —
Sphincter muscle, iris — — Constriction (miosis)
Ciliary muscle β Relaxation for far vision Constriction for near vision
gastrointestinal traCt
Smooth muscle α1; β1 and β2 Relaxation Constriction
Sphincters α1 Constriction Relaxation
Heart β1 Increased heart rate, force of contraction Decreased heart rate
Kidney Dopamine Dilates renal vasculature, thereby increasing renal —
perfusion
lung
Bronchial muscle β2 Smooth muscle relaxation (opens airways) Smooth muscle constriction
(closes airways)
Bronchial glands α1 Decreased secretions; increased secretions Stimulation
β2
Metabolism β2 Glycogenolysis (increases blood glucose) —
urinary BlaDDer
Fundus (detrusor) β3 Relaxation Constriction
Trigone and sphincter α1 Constriction Relaxation
Uterus α1 Pregnancy: constriction (α); relaxation (β2) Variable
β2
α1, Alpha-1 receptor; β, beta receptor; β1, beta-1 receptor; β2, beta-2 receptor; β3, beta-3 receptor.

normal doses, terbutaline is an effective bronchodilator. Availability

However, in addition to bronchodilation, higher doses of
terbutaline cause CNS stimulation, which results in in-
somnia and wakefulness. See Table 12.2 for a list of the
clinical uses of the adrenergic agents.
Nursing Implications for Adrenergic Agents
See Chapters 29 and 30 for more information about
the nursing implications for respiratory tract disease,
bronchodilators, and decongestants.
Premedication assessment
1. Obtain baseline vital signs: heart rate and blood
pressure.
2. See Chapters 29 and 30 for the premedication assess-
ments for respiratory tract disease, bronchodilators,
and decongestants.
See Table 12.2.
Common adverse effects. Adverse effects associated
with adrenergic agents are usually dose related and
resolve when the dosage is reduced or the medication
discontinued. Patients who are potentially more sensi-
tive to adrenergic agents are those with impaired he-
patic function, thyroid disease, hypertension, and heart
disease. Patients with diabetes mellitus may also have
an increased frequency of episodes of hyperglycemia.
Cdvc
Palpitations, tachycardia, skin ushing, dizziness, trem-
ors. These adverse effects are usually mild, and they
tend to resolve with continued therapy. Encourage the
patient not to discontinue therapy without rst con-
sulting the healthcare provider.
 Drugs Affecting the Autonomic Nervous System CHAPTER 12 183

Autonomic nervous system

Adrenergic receptors Cholinergic receptors

(sympathetic) (parasympathetic)
(+) (−)
Acetylcholine Atropine

Alpha-1 Alpha-2 Beta-1 Beta-2 Beta-3 Dopaminergic

(+) (+) (+) (+) (+) (+) (−)
Norepinephrine Clonidine Dopamine Isoproterenol Mirabegron Dopamine
Dopamine Guanfacine Isoproterenol Terbutaline
Phenylephrine Methyldopa Dobutamine Albuterol
Epinephrine Epinephrine
(−) (−) (−) (−)
Phenoxybenzamine Phenoxybenzamine Acebutolol* Labetalol
Phentolamine Phentolamine Atenolol* Carvedilol
Carvedilol Betaxolol* Carteolol
Labetalol Bisoprolol* Nadolol
Prazosin Carvedilol Pindolol
Terazosin Carteolol
Doxazosin Esmolol
Tamsulosin Lebatalol
Silodosin Metoprolol*
Alfusosin Nadolol
Nebivolol*
(Doses ≤ 10 mg)
Pindolol
Propranolol
Sotalol
Timolol

Fig. 12.1 Receptors of the autonomic nervous system. (+) Stimulates receptors; (−) inhibits receptors; asterisks (*)
indicate selective beta-1 antagonists.

Orthostatic hypotension. Although this condition is Drug interactions

infrequent and generally mild, adrenergic agents may
cause some degree of orthostatic hypotension, which
is manifested by dizziness and weakness, particularly
when therapy is initiated. Monitor the blood pressure
daily with the patient in both the supine and stand-
ing positions. Anticipate the development of postural
hypotension, and take measures to prevent an occur-
rence. Teach the patient to rise slowly from a supine
or sitting position; encourage the patient to sit or lie
down if they feel faint.
Serious adverse effects
Cdvc
Dysrhythmias, chest pain, severe hypotension, hyper-
tension, anginal pain. Discontinue therapy immedi-
ately and notify the healthcare provider. Ask the
patient if there has been a recent change in their
regimen of prescription, nonprescription, or herbal
medicines.
g
Nausea, vomiting. Notify the healthcare provider. Ask
the patient if there has been a recent change in their
regimen of prescription, nonprescription, or herbal
medicines.
a   c c d xc ffc.
Monoamine oxidase inhibitors (e.g., phenelzine, tranylcy-
promine), tricyclic antidepressants (e.g., amitriptyline, imi-
pramine), atropine, and halothane anesthesia may increase
both therapeutic and toxic effects. Many over-the-counter
medications (e.g., cold remedies, appetite suppressants/
diet pills [e.g., pseudoephedrine, ephedrine, ma huang])
contain adrenergic medicines that can have an additive
effect when they are taken with a prescribed adrenergic
agent. Monitor patients for tachycardia, serious dysrhyth-
mias, hypotension, hypertension, and chest pain.
a  b c cv. The concurrent
use of beta-adrenergic blocking agents (e.g., proprano-
lol, nadolol, timolol, pindolol, atenolol, metoprolol),
and alpha-adrenergic blocking agents (e.g., phenoxy-
benzamine, phentolamine), with adrenergic agents is
not recommended.
Drug Class: alpha- anD Beta-aDrenergiC
BloCking agents
Actions
The alpha- and beta-adrenergic blocking agents act by
plugging the alpha or beta receptors, which prevents
184 UNIT III Drugs Affecting the Autonomic and Central Nervous System

Table 12.2 Adrenergic Agents

aDrenergiC
generiC name BranD name aVailaBility reCeptor aCtion CliniCal uses
albuterola Proventil HFA, Aerosol: 90 mcg/puff β2 Bronchodilator Asthma,
Ventolin Tablets: 2, 4 mg emphysema
HFA, ProAir Syrup: 2 mg/5 mL
HFA, Tablets, extended release (12
ProAir hr): 4, 8 mg
RespiClick, Nebulizer solution: 0.083%/3-
ProAir mL ampule, 0.5%/0.5-mL
Digihaler ampule and 20-mL bottle;
0.63-mg/3-mL ampule,
1.25-mg/3-mL ampule
arformoterola Brovana Nebulizer: 15 mcg/2 mL in β2 Bronchodilator Emphysema,
2-mL vials chronic bronchitis
dobutamine — IV: 1 mg/mL (250 mL); 2 mg/ β1, β2; α1 Cardiac stimulant Inotropic agent
mL (250 mL); 4 mg/mL
(250 mL); 12.5 mg/mL
in 250-mg/20-mL vial;
500-mg/40-mL vial
dopamine — IV: 40 mg/mL in 5-, 10-mL α, β1 Vasopressor Shock,
ampules; dopaminergic hypotension;
200, 400, and 800 mg in D5W inotropic agent
(various volumes available)
ephedrinea Bronkaid Max Tablets: 25 mg α, β Vasoconstrictor Anesthesia-induced
Akovaz IV: 50 mg/mL in 1 mL hypotension;
ampules; 10, 25, 50, 100, postoperative
250 mg prelled syringes nausea and
vomiting
epinephrinea Adrenalin, Epi- IV: 1 : 1000 in 1-mL ampules; α, β Allergic reactions, Anaphylaxis,
Pen 1 : 10,000 in 10-mL prelled vasoconstrictor, cardiac
syringes bronchodilator, arrest; topical
Solution Autoinjector; 03 cardiac stimulant vasoconstrictor
mg/0.3 ml and 0.15 mg/0.3
ml
formoterola Perforomist Nebulizer: 20 mcg/2 mL in β2 Bronchodilator Asthma,
Oxeze 2-mL container emphysema,
chronic bronchitis
indacaterola Onbrez Capsule for inhalation: 75 mcg β2 Bronchodilator Emphysema,
Breezhaler chronic bronchitis

isoproterenol Isuprel Subcut, IM, IV: 0.2 mg/mL β Bronchodilator, Shock, digitalis
solution; 1-, 5-mL vials cardiac stimulant toxicity,
bronchospasm
mirabegron Myrbetriq Tablets, extended release (24 B3 Bladder detrusor Overactive bladder
hr): 25, 50 mg muscle relaxant
norepinephrine Levophed IV: 1 mg/mL in 4-mL ampules; α1 Vasoconstrictor Shock, hypotension
(levarterenol) 4-, 8-, 16-mg/250 mL; 0.08
mg/10 mL prelled syringes
phenylephrineb Subcut, IM, IV: 10 mg/mL in α1 Vasoconstrictor Shock,
1-mL ampules and 5-mL hypotension,
vial nasal
Ophthalmic drops: 2.5%, 10% decongestant;
Nasal solutions: 0.25%, 0.5%, ophthalmic
1% vasoconstrictor,
Tablets: 10 mg mydriatic
Liquid: 2.5 mg/5 mL
Continued
 Drugs Affecting the Autonomic Nervous System CHAPTER 12
Table 12.2 Adrenergic Agents—cont’d
generiC name BranD name aVailaBility
salmeterol Serevent Aerosol powder: 50 mcg/dose
Diskus
terbutalinea Tablets: 2.5, 5 mg
Subcut: 1 mg/mL in 1-mL
ampules
aSee also bronchodilators (Chapter 30).
bSee also decongestants (Chapter 29).
α, Alpha; β, beta, IM, intramuscular; IV, intravenous; Subcut, subcutaneous.
Available in Canada.
High-alert medication.
other agents—usually the naturally occurring cat-
echolamines—from stimulating the specic receptors.
The beta blockers can be subdivided into non-
selective and selective beta antagonists. The nonselec-
tive blocking agents have an equal afnity for beta-1 and
beta-2 receptors, and they inhibit both. These agents are
propranolol, nadolol, pindolol, carteolol, sotalol, and
timolol. The selective beta-1 blocking agents exhibit ac-
tion against the heart’s beta-1 receptors (cardioselective)
and do not readily affect the beta-2 receptors of the bron-
chi. The selective beta-1 antagonists are esmolol, meto-
prolol, acebutolol, betaxolol, bisoprolol, and atenolol.
This selective action is benecial for patients in whom
nonselective beta blockers may induce bronchospasm
(e.g., those with asthma). However, it is important to
note that the selectivity of these agents is only relative.
In larger doses, these agents will also inhibit the beta-2
receptors. There are no selective beta-2 blockers avail-
able. Labetalol and carvedilol exhibit selective alpha-1
and nonselective beta-adrenergic blocking activity. The
alpha and beta blockers are listed in Fig. 12.1.
Uses
Because one of the primary actions of the alpha-
receptor stimulants is vasoconstriction, it would be
expected that alpha-blocking agents are indicated for
patients with diseases that are associated with vaso-
constriction. Alpha blockers (e.g., prazosin, terazosin,
doxazosin) are sometimes used to treat hypertension
(see Chapter 22). Alfuzosin, silodosin, and tamsulo-
sin are used to relax the smooth muscle of the bladder
and prostate; they are used to treat urinary obstruction
caused by benign prostatic hyperplasia (see Chapter 40).
Beta-adrenergic blocking agents (e.g., beta blockers)
are used extensively to treat post–myocardial infarc-
tion. They may also be used for hypertension, angina
pectoris, cardiac dysrhythmias, symptoms of hyper-
thyroidism, and stage fright. Nonselective beta block-
ers must be used with extreme caution in patients with
respiratory conditions such as bronchitis, emphysema,
asthma, or allergic rhinitis. A beta blockade produces
severe bronchoconstriction and may aggravate wheez-
ing, especially during pollen season.
185
aDrenergiC
reCeptor aCtion CliniCal uses
β2 Bronchodilator Asthma,
emphysema,
chronic bronchitis
β2 Bronchodilator, Emphysema,
uterine relaxant asthma
Beta blockers should be used with caution in patients
with diabetes and in those who are susceptible to hypo-
glycemia. Beta blockers further induce the hypoglycemic
effects of insulin and reduce the release of insulin in re-
sponse to hyperglycemia. All beta blockers mask most of
the signs and symptoms of acute hypoglycemia.
Beta-adrenergic blocking agents should be used only
in patients with controlled heart failure. Further hypo-
tension, bradycardia, or heart failure may develop.
Nursing Implications for Beta-Adrenergic Blocking
Agents
See also the nursing implications for patients with an-
tidysrhythmic therapy (Chapter 23) and for those with
hypertension (Chapter 22).
Premedication assessment
1. Obtain baseline vital signs: heart rate and blood
pressure.
2. See also the premedication assessments for patients
with antidysrhythmic therapy (Chapter 23) and for
those with hypertension (Chapter 22).
Availability, dosage, and administration
See Table 12.3.
idvdz f d. Although the onset of ac-
tivity is fairly rapid, it may take several days to weeks
for a patient to show optimal improvement and to be-
come stabilized on an adequate maintenance dosage.
Patients must be periodically reevaluated to determine
the lowest effective dosage that is necessary to control
the disorder.
sdd dc. Patients must be counseled
against poor adherence or the sudden discontinua-
tion of therapy without a healthcare provider’s advice.
Sudden discontinuation has resulted in an exacerba-
tion of anginal symptoms, and this has been followed
in some cases by myocardial infarction. When discon-
tinuing chronically administered beta blockers, the
dosage should be gradually reduced over 1 to 2 weeks,
with careful patient monitoring. If anginal symptoms
develop or become more frequent, beta blocker thera-
py should be restarted temporarily.
186 UNIT III Drugs Affecting the Autonomic and Central Nervous System

Table 12.3 Beta-Adrenergic Blocking Agents

generiC name BranD name aVailaBility CliniCal uses Dosage range
acebutolol Sectral Capsules: 200, 400 mg Hypertension, PO: initial, 400 mg daily;
ventricular maintenance, 600–1200 mg daily
dysrhythmias
atenolol Tenormin Tablets: 25, 50, 100 mg Hypertension, PO: initial, 50 mg daily; maintenance,
Teva-Atenolol Oral solution: 1, 2, 10 mg/mL angina pectoris, ≤200 mg daily
after myocardial
infarction
betaxolol Tablets: 10, 20 mg Hypertension PO: initial, 10 mg daily; maintenance,
20 mg daily
bisoprolol Monocor Tablets: 5, 10 mg Hypertension PO: initial, 5 mg daily; maintenance,
10–20 mg daily
carvedilol APO-Carvedilol Tablets: 3.125, 6.25, 12.5, Hypertension, heart PO: initial, 6.25 mg twice daily;
25 mg failure, myocardial maintenance, ≤50 mg daily
Capsules, extended release infarction PO: initial, 10 mg daily;
(24 hr): 10, 20, 40, 80 mg maintenance, ≤80 mg daily
Extended release: 10 mg daily
esmolol Brevibloc Injection: 10 mg/mL in 10-mL Supraventricular IV: initial, 500 mcg/kg/min for 1 min
ampules; 10 mg/mL in tachycardia, followed by 50 mcg/kg/min
250-mL bag; 20 mg/mL in hypertension for 4 min and then adjusted to
100-mL bag patient’s needs
Trandate Tablets: 100, 200, 300 mg Hypertension PO: initial, 100 mg twice daily;
Injection: 5 mg/mL in 4-, 20-, maintenance, ≤2400 mg daily
40-mL vials
metoprolol Lopressor, Tablets: 25, 37.5, 50, 100 mg Hypertension, PO: 50 mg twice daily; maintenance
Toprol-XL Tablets, extended release (24): myocardial dosing of ≤450 mg daily, divided
Betaloc, 25, 50, 100, 200 mg infarction, angina
Kapspargo Capsules, extended release pectoris, heart
Sprinkle (24 hr): 25-, 50-, 100-, 200- failure
mg sprinkles
Oral solution: 10 mg/mL in 90
mL bottle
Injection: 1 mg/mL in 5-mL
ampules, prelled syringes
nadolol Corgard Tablets: 20, 40, 80, 120, Angina pectoris, PO: initial, 40 mg daily; maintenance,
Apo-Nadol 160 mg hypertension 40–80 mg daily; maximum,
320 mg daily for hypertension;
maximum, 240 mg for angina
nebivolol Bystolic Tablets: 2.5, 5, 10, 20 mg Hypertension PO: initial, 5 mg daily; maintenance,
≤40 mg daily
pindolol Apo-Pindol Tablets: 5, 10 mg Hypertension PO: initial, 5 mg twice daily;
Visken maintenance, 10–30 mg daily;
maximum, 60 mg daily
propranolol, Tablets: 10, 20, 40, 60, 80 mg Dysrhythmias, PO, immediate release: initial, 40 mg
Inderal LA Solution: 4.28/mL, 20, 40 hypertension, twice daily; maintenance, 120–
Apo-Propranolol mg/5 mL angina pectoris, 640 mg daily in two to four divided
Capsules, sustained release myocardial doses
(24 hr): 60, 80, 120, 160 infarction, PO, sustained release: 80–160 mg
mg migraine, tremor, daily; maximum 640 mg daily
IV: 1 mg/mL in 1-mL ampules hypertrophic IV: 1–3 mg with close
subaortic stenosis electrocardiographic monitoring
sotalol Betapace, Tablets: 80, 120, 160, 240 mg Dysrhythmias PO: initial, 80 mg twice daily;
Sorine, IV: 150 mg/10 mL maintenance, ≤320 mg daily
Sotylize Oral solution: 5 mg/mL
timolol TEVA-Timolol Tablets: 5, 10, 20 mg Hypertension, PO: initial, 10 mg twice daily;
myocardial maintenance, ≤30 mg twice daily
infarction, migraine
IV, Intravenous; PO, by mouth.
Available in Canada.
High-alert medication.
 Drugs Affecting the Autonomic Nervous System CHAPTER 12
Common adverse effects. Most of the adverse effects
associated with beta-adrenergic blocking agents are
dose related. Response by individual patients is highly
variable. Many of the adverse effects that do occur may
be transient. Strongly encourage patients to see their
healthcare providers before discontinuing therapy.
Minor dosage adjustment may be all that is required to
eliminate most adverse effects.
edc
Patients with diabetes. Monitor for symptoms of hypo-
glycemia, including headache, weakness, decreased
coordination, general apprehension, diaphoresis,
hunger, or blurred or double vision. Many of these
symptoms may be masked by beta-adrenergic block-
ing agents. Notify the healthcare provider if any of the
symptoms described appear intermittently.
Serious adverse effects
Cdvc
Bradycardia, peripheral vasoconstriction (e.g., purple, mot-
tled skin). Discontinue further doses until the patient is
evaluated by a healthcare provider.
Heart failure. Monitor patients for an increase in ede-
ma, dyspnea, crackles, bradycardia, and orthopnea.
Notify the healthcare provider if these symptoms
develop.
r
Bronchospasm, wheezing. Withhold additional doses
until the patient has been evaluated by a healthcare
provider.
Drug interactions
av . All beta-blocking agents have
hypotensive properties that are additive with anti-
hypertensive agents (e.g., angiotensin-converting en-
zyme inhibitors, calcium-channel blockers, diuretics,
angiotensin receptor blockers, methyldopa, hydralazine,
and clonidine). If it is decided to discontinue therapy in
patients who are receiving beta blockers and clonidine
concurrently, the beta blocker should be withdrawn
gradually for several days and then discontinued before
gradually withdrawing the clonidine. The concern if
this order is not followed is the development of severe
hypertension resulting from unopposed alpha activity
if clonidine is stopped rst (see clonidine monograph
about “sudden discontinuation” of clonidine therapy).
B-dc . Depending on the dosage,
the beta stimulants (e.g., isoproterenol, terbutaline, al-
buterol) may inhibit the action of beta-blocking agents
and vice versa.
ldc, , dd, dx. When these
drugs are occasionally used concurrently with beta-
blocking agents, the patient must be monitored care-
fully for additional arrhythmias, bradycardia, and signs
of heart failure.
ez-dc . Enzyme-inducing agents
(e.g., phenobarbital, pentobarbital, rifampin, phenyto-
in) enhance the metabolism of propranolol, metoprolol,
pindolol, and timolol. This reaction probably does not
187
occur with nadolol or atenolol because they are not me-
tabolized but rather are excreted unchanged. The dos-
age of the beta blocker may have to be increased to pro-
vide therapeutic activity. If the enzyme-inducing agent
is discontinued, the dosage of the beta blocker will also
require reduction.
nd  . Indomethacin,
salicylates, and possibly other prostaglandin inhibi-
tors reduce the antihypertensive activity of proprano-
lol and pindolol. This results in a loss of hypertensive
control. The dose of the beta blocker may have to be in-
creased to compensate for the antihypertensive inhibi-
tory effect of indomethacin and perhaps other prosta-
glandin inhibitors.
Drug Class: CholinergiC agents
Actions
Cholinergic agents, which are also known as musca-
rinic or parasympathomimetic agents, produce effects that
are similar to those of acetylcholine. Some cholinergic
agents act by directly stimulating the parasympathetic
nervous system, whereas others inhibit acetylcholines-
terase, which is the enzyme that metabolizes acetylcho-
line after it has been released by the nerve ending. These
latter agents are known as indirect-acting cholinergic
agents. Some of the cholinergic actions are slow heart-
beat; increased GI motility and secretions; increased
contractions of the urinary bladder, with relaxation of
the muscle sphincter; increased secretions and contrac-
tility of the bronchial smooth muscle; sweating; miosis
(constriction) of the pupil, which reduces intraocular
pressure; increased force of the contraction of skeletal
muscle; and, sometimes, decreased blood pressure.
Uses
See Table 12.4.
Nursing Implications for Cholinergic Agents
See also the nursing implications for patients with dis-
orders of the eyes (Chapter 42), glaucoma (Chapter 42),
urinary system disease (Chapter 41), and respiratory
tract disease (Chapters 29 and 30).
Premedication assessment
1. Obtain baseline vital signs: heart rate and blood
pressure.
2. See also the premedication assessments for patients
with disorders of the eyes (Chapter 42), glaucoma
(Chapter 42), urinary system disease (Chapter 41),
and respiratory tract disease (Chapters 29 and 30).
Availability, dosage, and administration
See Table 12.4.
Common adverse effects. Because cholinergic bers
innervate the entire body, effects in most body systems
can be expected. Fortunately, because all receptors do
not respond to the same dosage, adverse effects are
188 UNIT III Drugs Affecting the Autonomic and Central Nervous System

Table 12.4 Cholinergic Agents

generiC name BranD name aVailaBility CliniCal uses
bethanechol Duvoid Tablets: 5, 10, 25, 50 mg Urinary retention
neostigmine Bloxiverz Injection: 1-, 2-mg/mL in various Reverse nondepolarizing muscle relaxants
Prostigmin volume vials (e.g., tubocurarine)
physostigmine — Injection: 1 mg/mL in 2-mL ampules Reverse toxicity of overdoses of
anticholinergic agents (e.g., pesticides,
insecticides)
pilocarpine Salagen Tablets Tablets: 5, 7.5 mg Treat symptoms of dry mouth due to salivary
Isopto Carpine gland hypofunction following radiation
therapy
Ophthalmic solution: 1, 2, 4% Glaucoma
pyridostigmine Mestinon Tablets: 30, 60 mg Treatment of myasthenia gravis
Regonol Solution: 60 mg/5 mL Reversal of nondepolarizing muscle relaxants
Tablets, sustained release: 180 mg
Injection: 10 mg/2 mL

Available in Canada.

not always seen. The higher the dosage, however, the
greater the likelihood of adverse effects.
g
Nausea, vomiting, diarrhea, abdominal cramping. These
symptoms are extensions of the pharmacologic effects
of the medication, and they are dose related. Reducing
the dosage may be effective for controlling these ad-
verse effects without eliminating the desired pharma-
cologic effect.
Cdvc
Dizziness, hypotension. Monitor the patient’s blood
pressure and pulse. To minimize hypotensive episodes,
instruct the patient to rise slowly from a supine or sit-
ting position, and have him or her perform exercises
to prevent blood from pooling while they are standing
or sitting in one position for a prolonged period. Teach
the patient to sit or lie down if they feel faint.
Serious adverse effects
r
Bronchospasm, wheezing. Withhold the next dose un-
til the patient is evaluated by a healthcare provider.
Cdvc
Bradycardia. Withhold the next dose until the patient
is evaluated by a healthcare provider.
D c
Atropine, antihistamines. Atropine, other anticholin-
ergic agents, and most antihistamines antagonize the
effects of cholinergic agents.
Drug Class: antiCholinergiC agents
Actions
Anticholinergic agents, which are also known as cho-
linergic blocking agents or antimuscarinic agents or para-
sympatholytic agents, block the action of acetylcholine in
the parasympathetic nervous system. These drugs act
by occupying receptor sites at parasympathetic nerve
endings, which prevent the action of acetylcholine. The
parasympathetic response is reduced, depending on
the amount of anticholinergic drug that is blocking the
receptors. The inhibition of cholinergic activity (e.g.,
anticholinergic effects) includes the following: my-
driasis (dilation) of the pupil to increase intraocular
pressure in patients with glaucoma; dry, tenacious
secretions of the mouth, nose, throat, and bronchi;
decreased secretions and motility of the GI tract; in-
creased heart rate; and decreased sweating.
Uses
See Table 12.5.
Nursing Implications for Anticholinergic Agents
See also the nursing implications for patients with
Parkinson disease (Chapter 14), disorders of the eyes
(Chapter 42), and antihistamines (Chapter 29).
Premedication assessment
1. All patients should be screened for closed-angle
glaucoma because anticholinergic agents may pre-
cipitate an acute attack. Patients with open-angle
glaucoma can safely use anticholinergic agents in
conjunction with miotic therapy.
2. Check the patient’s history for an enlarged prostate.
If this condition is present, anticholinergic agents
may cause the patient to have a temporary inability
to void.
3. Obtain baseline vital signs: heart rate and blood
pressure.
4. See also the premedication assessments for patients
with Parkinson disease (Chapter 14), disorders of the
eyes (Chapter 42), and antihistamines (Chapter 29).
 Drugs Affecting the Autonomic Nervous System CHAPTER 12 189

Table 12.5 Anticholinergic Agents

generiC name BranD name aVailaBility CliniCal uses
atropine Atropine Sulfate Injection: 0.05, 0.1, 0.4, 0.8, Presurgery: to reduce salivation and bronchial
1 mg/mL secretions; to minimize bradycardia
during intubation; adjuvant use with
anticholinesterases (e.g., neostigmine) to
decrease their adverse effects during reversal
of neuromuscular blockade
Bentyl Protylol Tablets: 20 mg Irritable bowel syndrome
dicyclomine Capsules: 10 mg
Injection: 10 mg/mL
Solution: 10 mg/5 mL
glycopyrrolate Cuvposa Tablets: 1, 2 mg Presurgery: to reduce salivation and bronchial
Oral solution: 1 mg/5 mL secretions and to minimize bradycardia during
Injection: 0.2 mg/mL intubation

Available in Canada.

Availability dosage and administration pcc

See Table 12.5.
Common adverse effects. Because cholinergic bers
innervate the entire body, effects from blocking this
system occur throughout most systems. Fortunately,
because all receptors do not respond to the same
dose, all adverse effects are not seen to the same de-
gree with all cholinergic blocking agents. The higher
the dosage, however, the greater the likelihood of
more adverse effects. The following symptoms are
the anticholinergic effects that are produced by these
agents. Patients who are taking these medications
should be monitored for the development of these
adverse effects.
s
Blurred vision. Warn the patient that blurred vision
may occur and make appropriate suggestions for the
patient’s personal safety.
g
Constipation; dryness of the mucosa of the mouth, nose, and
throat. Mucosal dryness may be alleviated by sucking
hard candy or ice chips or by chewing gum. Give the
patient stool softeners as prescribed. Encourage ade-
quate uid intake and the eating of foods that provide
sufcient bulk.
Serious adverse effects
s
Glaucoma. All patients should be screened for
closed-angle glaucoma before the initiation of therapy.
Patients with open-angle glaucoma can safely use anti-
cholinergic agents. Monitor the patient’s intraocular
pressures regularly.
Confusion, depression, nightmares, hallucinations. Perform
a baseline assessment of the patient’s degree of alert-
ness and orientation to name, place, and time before in-
itiating therapy. Make regularly scheduled subsequent
evaluations of the patient’s mental status and compare
ndings. Report the development of alterations and
provide for patient safety during these episodes. A
reduction in the daily medication dosage may control
these adverse effects.
Cdvc
Orthostatic hypotension. Although orthostatic hypo-
tension occurs infrequently and is generally mild, all
anticholinergic agents may cause some degree of this
condition, which is manifested by dizziness and weak-
ness, particularly when therapy is initiated. Monitor the
patient’s blood pressure daily in both the supine and
standing positions. Anticipate the development of pos-
tural hypotension and take measures to prevent it. Teach
the patient to rise slowly from a supine or sitting position,
and encourage the patient to sit or lie down if they feel
faint.
Palpitations, dysrhythmias. Contact the healthcare pro-
vider for further evaluation.
g
Urinary retention. If the patient develops urinary hes-
itancy, assess the bladder for distention. Contact the
healthcare provider for further evaluation.
Drug interactions
ad, ccc d, z. These
agents may potentiate anticholinergic adverse effects.
Confusion and hallucinations are characteristic of exces-
sive anticholinergic activity.
190 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions
k p
• The nervous system is one of two primary regulators of
body homeostasis and defense. The CNS is composed of
the brain and the spinal cord.
• The peripheral nervous system is subdivided into the
afferent and efferent nerve pathways. The afferent
nerves conduct signals from sensory receptors (e.g.,
vision, pressure, pain, cold, warmth, touch, smell)
throughout the body to the CNS. The CNS processes
these signals and controls the body’s response by
sending signals back through the efferent nerves of the
peripheral nervous system. The efferent nervous system
is subdivided into the somatic nervous system which
controls voluntary skeletal muscle, and the autonomic
nervous system, which regulates involuntary smooth
muscle and heart muscle and controls secretions from
certain glands.
• Nerve impulses are passed between neurons and from
neurons to end organs by neurotransmitters. The main
neurotransmitters of the autonomic nervous system are
acetylcholine and norepinephrine. Nerve endings that
liberate acetylcholine are called cholinergic bers; those
that secrete norepinephrine are called adrenergic bers.
• The CNS is composed of systems of different types of
neurons that secrete separate neurotransmitters, such
as acetylcholine, norepinephrine, epinephrine, dopamine,
serotonin, and gamma-aminobutyric acid.
• The control of neurotransmitters is a primary way to
alleviate the symptoms that are associated with many
diseases. As shown in Table 12.1, the administration of
one type of autonomic nervous system drug can affect
several organ systems, and adverse effects can be
numerous. Therefore the use of these drugs requires the
monitoring of more than just the symptoms for which the
medicine was prescribed.
add l rc
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Clay-
ton) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX examination and include both NGN (Next Genera-
tion) and traditional questions. For Chapters 12 and beyond
the use of case studies will be employed to further develop
clinical judgment.
sc
A 59-year-old patient came to see the primary healthcare pro-
vider regarding some discomfort that was being experienced
as shooting down the left arm. The patient has a history of
hypertension, asthma, and glaucoma. Currently the patient is
taking the following medications: atenolol for hypertension, al-
buterol for asthma (as needed), and pilocarpine drops for glau-
coma.
1. The nurse discussed with the patient in the scenario the effects
of the medications that they are currently taking. When explaining
this the nurse described the common neurotransmitters and how
they affect the central nervous system by stating which of the
following? (Select all that apply.)
1. “The major neurotransmitters of the autonomic nervous
system are acetylcholine and norepinephrine.”
2. “You see, the medications you take have an effect on
the neurotransmitters of the nervous system since this is
what controls your heart rate and blood pressure.”
3. “The medication that you take for glaucoma stimulates
the cholinergic receptors to decrease the intraocular
pressure.”
4. “The cholinergic side of the nervous system is subdivided
into alpha, beta, and dopamine receptors.”
5. “The two main branches of the autonomic nervous
system are complementary, since one branch speeds
processes up and the other slows things down.”
objcv: Identify the most common neurotransmitters known to
affect central nervous system function.
nCleX  : Multiple response
Cv : Application
2. A male patient was discussing with the nurse that he was
experiencing problems urinating after taking an antihistamine that
has anticholinergic properties and was wondering why this was
happening. Which statement by the nurse explains this effect?
1. “Antihistamines are used to treat allergy symptoms, and
do not affect the bladder.”
2. “This medication you are taking has the effect of causing
dry mouth and sedation, but I never heard of it causing
urinary retention.”
3. “I am sure your symptoms will get better if you wait a few
weeks and let your body adjust to the medication.”
4. “Your medication is causing your bladder to relax because
it is inhibiting the cholinergic receptors, therefore the
bladder is slower to contract to expel the urine.”
objcv: Explain the actions of anticholinergic agents and beta-
adrenergic blocking agents.
ngn  : Multiple choice
Cv : Recognize cues
 Drugs Affecting the Autonomic Nervous System CHAPTER 12 191

3. The patient in the scenario is taking a cholinergic agent. Indicate 5. The patient in the scenario who has recently been prescribed a
which medication is being used, what clinical effect the nurse can beta-adrenergic blocking agent now presents to the emergency
expect, and for what adverse effect the nurse should monitor. department with shortness of breath. Which adverse effect from
the medications is the patient likely exhibiting?
Choose the most likely option for the information missing from the 1. Pneumonia
statements below by selecting from the list of options provided. 2. Pulmonary embolism
The nurse will discuss with the patient the use of 3. Bronchoconstriction
_________1________, which is used for _______2________ 4. Bronchodilation
and will have the effect of _________2__________. objcv: Describe clinical uses and the predictable adverse
The predictable adverse effect for this medication is effects of beta-adrenergic blocking agents.
_______3____________. nCleX  : Multiple choice
Cv : Comprehension
option 1 option 2 option 3
6. The nurse reviewing a patient’s preoperative medications noted
atenolol hypertension diarrhea that atropine sulfate was listed. In which diagnoses should
albuterol to reduce heart rate increased atropine sulfate be used with caution? (Select all that apply.)
and blood pressure intraocular
pressure 1. Hypertension
pilocarpine glaucoma bradycardia 2. Asthma
reducing intraocular hypertension 3. Closed-angle glaucoma
pressure 4. Open-angle glaucoma
relaxing the tachycardia 5. Enlarged prostate
bronchioles 6. Irritable bowel syndrome
asthma objcv: Describe clinical uses and the predictable adverse
effects of anticholinergic agents.
nCleX  : Extended multiple response
objcv: Describe clinical uses and the predictable adverse Cv : Recognize cues
effects of cholinergic agonists.
nCleX  : Cloze
Cv : Analyze cues
4. The patient in the scenario is taking an adrenergic agonist. Indicate
which medication is being used, what effect the nurse can expect,
and for what adverse effect the nurse should monitor.

Choose the most likely option for the information missing from the
statements below by selecting from the list of options provided.
The nurse will discuss with the patient the use
of ________1____________, which is used for
________2___________ and will have the effect of
__________2_______. The predictable adverse effect for
this medication is ________3___________.

option 1 option 2 option 3

atenolol hypertension diarrhea
albuterol to reduce heart rate increased
and blood pressure intraocular
pressure
pilocarpine glaucoma bradycardia
reducing intraocular hypertension
pressure
relaxing the tachycardia
bronchioles
asthma

objcv: Describe clinical uses and the predictable adverse

effects of adrenergic agonists.
nCleX  : Cloze
Cv : Analyze cues
13 Drugs Used for Sedation and Sleep
https://evolve.elsevier.com/Willihnganz
Objectives
1. Differentiate among the terms sedative and hypnotic; initial,
intermittent, and terminal insomnia; transient, short-term,
and chronic insomnia; and rebound sleep.
2. Discuss nursing interventions that can be implemented
as an alternative to administering a sedative-hypnotic
medication.
Key Terms
rapid eye movement (REM) insomnia (ĭn-SŎM-nē-ă) (p. 193)
sleep (p. 192) hypnotic (hĭp-NŎT-ĭk) (p. 193)
SLEEP AND SLEEP PATTERN
DISTURBANCE
Sleep is  stte of unconsciousness fro which  p-
tient cn be roused by n pproprite stiulus. It is 
nturlly occurring phenoenon tht occupies bout
one-third of n dult’s life.
Adequte sleep tht progresses through the nor-
l stges is iportnt to intin body function,
including psychitric equilibriu nd the strengthen-
ing of the iune syste to wrd off disese. A nor-
l sleep durtion for dults of 7 to 8 hours per night
is thought to be optil for good helth. Studies lso
show tht  reduced ount of sleep is ssocited
with obesity, s well s the developent of risk fc-
tors ssocited with crdiovsculr disese nd type
2 dibetes ellitus (see Chpter 20). Obesity itself is
lso detrientl to helthy sleep ptterns, nd it cn
contribute to the developent of sleep pne. Other
studies show  strong connection between  short-
ened durtion of sleep nd crdiovsculr disese.
Individuls who sleep less thn 5 hours per night
hve  threefold incresed risk of hert ttcks. The
Ntionl Helth Interview Survey lso deonstrtes
 close reltionship between syptos of insoni
nd coon dverse physicl nd entl helth
conditions, including obesity, dibetes ellitus, hyper-
tension, hert filure, nxiety, nd depression. The
Healthy People 2030 progr hs s one of its objec-
tives the prootion of sleep helth, which includes
prooting optil sleep durtions nd reducing the
prevlence nd effect of sleep disorders.
192
3. Compare the effects of benzodiazepines and
nonbenzodiazepines on the central nervous system.
4. Identify the antidote drug used for the management of
benzodiazepine overdose.
5. Identify laboratory tests that should be monitored when
benzodiazepines are administered for an extended period.
sedative (SĔD-ă-tĭv) (p. 193)
rebound sleep (RĒ-bŏwnd SLĒP) (p. 194)
Nturl sleep rhythiclly progresses through
phses tht provide both physicl nd entl rest. On
the bsis of brin-wve ctivity, uscle ctivity, nd
eye oveent, norl sleep cn be divided into two
phses: non–rpid eye oveent (NREM) sleep nd
rapid eye movement (REM) sleep. Most dults will enter
sleep fro the drowsy stte vi NREM sleep. NREM
sleep is divided into three substges, ech of which
is chrcterized by  specic set of brin-wve ctivi-
ties: stge N1, stge N2, nd stge N3. Of note, older
rules hd four stges of NREM sleep, but the previous
NREM stge 3 nd NREM stge 4 hve been cobined
s stge N3.
Stge N1 is  trnsition phse between wkeful-
ness nd sleep tht lsts only  few inutes. Soe
people experience it s wkefulness, wheres oth-
ers feel it s drowsiness. Approxitely 2% to 5%
of sleep is stge N1 sleep. Stge N2 sleep kes up
bout 50% of norl sleep tie. People often expe-
rience  drifting or floting senstion, nd if they
re wkened during this stge, they will often
deny being sleep, responding, “I ws just resting
y eyes.” Stges N1 nd N2 re light sleep periods
fro which  person is esily roused. Stge N3 is
 trnsition fro the lighter to deeper sleep stte.
Stge N3 sleep is dreless, very restful, nd ssoci-
ted with  10% to 30% decrese in blood pressure,
respirtory rte, nd bsl etbolic rte. Stge N3
sleep is lso referred to s delta sleep on the bsis of
the pttern of brin wves tht re observed during
this stge. Stge N3 sleep kes up 10% to 15% of
sleep tie in young, helthy dults. Stge N3 sleep
 Drugs Used for Sedation and Sleep CHAPTER 13 193

diinishes in length s people ge, nd ny peo-

ple who re ore thn 75 yers old do not deon-
Stage N1
strte ny stge N3 sleep ptterns. Older dults lso (2-5% of cycle)
tke longer to cycle through the relxtion stges of transition phase
NREM sleep, with n incresed frequency nd dur- between
wakefulness
tion of wkenings. and sleep
During  norl night of sleep,  person will rhyth-
iclly cycle fro wkefulness through substges N1,
N2, nd N3; the person will then go bck to stge N2, Stage N2
then to REM sleep over the course of bout 90 in- (50% of cycle)
utes (Fig. 13.1). The erly episodes of REM sleep lst
only  few inutes. However, s sleep progresses, the
ount of REM sleep increses, with REM periods
becoing longer nd ore intense round 5 am. This
type of sleep represents 20% to 25% of sleep tie, nd Stage N3
delta sleep
it is chrcterized by REM, dreing, incresed hert
rte, irregulr brething, the secretion of stoch c-
ids, nd soe usculr ctivity. REM sleep ppers to
be n iportnt tie for the subconscious ind to re-
lese nxiety nd tension nd reestblish  psychitric
equilibriu. Stage N2
Insomnia is dened s the inbility to sleep. It is
the ost coon sleep disorder known; 95% of ll
dults experience insoni t lest once during their
lives, nd up to 35% of dults will hve insoni dur-
ing  given yer. In generl, insoni is not  disese REM
(20-25% of cycle)
but rther  sypto of physicl or entl stress. It dream stage
is usully ild nd lsts only  few nights. Coon
cuses re chnges in lifestyle or environent (e.g.,
hospitliztion), pin, illness, the excess consup-
tion of products tht contin cffeine (e.g., coffee,
energy drinks) or lcohol, eting lrge or rich els Stage N2
shortly before bedtie, nd stress. Initial insomnia is
the inbility to fll sleep when desired, intermittent
insomnia is the inbility to sty sleep, nd terminal
insomnia is chrcterized by erly wkening with the
inbility to fll sleep gin. Insoni is lso clssi-
ed in ccordnce with its durtion. A sleep distur- Stage N3
bnce tht lsts only  few nights is considered to be delta sleep
transient insomnia. A sleep disturbnce tht lsts less
thn 3 weeks is referred to s short-term insomnia, nd
it is usully ssocited with trvel cross tie zones,
illness, or nxiety (e.g., job-relted chnges, nn-
Fig. 13.1 Sleep cycle. Stage N1 starts cycle transitions from
cil stress, exintions, eotionl reltionships). wakefulness, into stage N2, light sleep; then into stage N3, deeper
Chronic insomnia requires t lest 1 onth of sleep sleep, known as delta sleep; then back to stage N2; then rapid eye
disturbnce before the individul is dignosed with  movement (REM) sleep, where dreaming occurs; then back to stage
sleep disorder. About 10% of dults nd up to 20% of N2, stage N3, stage N2, and REM sleep. These cycles last about 90
minutes and the sleep cycle occurs four to ve times per night.
older dults report hving chronic insoni. Woen
report experiencing insoni twice s frequently s
en. A higher incidence of insoni is reported by
SEDATIVE-HYPNOTIC THERAPY
older dults, the uneployed, those of lower socio-
econoic sttus, nd the recently seprted or wid- Drugs tht re used in conjunction with ltered pt-
owed. As ny s 40% of ptients with chronic in- terns of sleep re known s sedative-hypnotic agents. A
soni lso hve psychitric disorders (e.g., nxiety, hypnotic is  drug tht produces sleep;  sedative qui-
depression, substnce buse). People with chronic ets the ptient nd gives hi or her  feeling of relx-
insoni often develop ftigue or drowsiness tht tion nd rest, but this is not necessrily ccopnied
interferes with dytie functioning nd eployent by sleep. A good hypnotic should provide the follow-
responsibilities. ing ctions within  short period of tie: the onset of
194 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
restful, nturl sleep;  durtion of ction tht llows
 ptient to wken t the usul tie;  nturl wk-
ening with no “hngover” effects; nd no dnger of
hbit fortion. Unfortuntely, the idel hypnotic is not
vilble. The ost coonly used sedtive-hypnotic
gents increse totl sleeping tie, especilly the tie
spent in stge N2 sleep (i.e., light sleep); however, they
lso decrese the nuber of REM periods nd the totl
tie spent in REM sleep. REM sleep is needed to help
intin  entl blnce during dytie ctivities.
When REM sleep is decresed, there is  strong physio-
logic tendency to ke it up. Copenstory REM sleep,
or rebound sleep, sees to occur even when hypnotic
gents re used for only 3 or 4 dys. After the chronic
dinistrtion of sedtive-hypnotic gents, REM re-
bound y be severe nd ccopnied by restlessness
nd vivid nightres. Depending on the frequency of
hypnotic dinistrtion, norl sleep ptterns y not
be restored for weeks. The effects of REM rebound y
enhnce n individul’s chronic use of nd dependence
on these gents to void the unplesnt consequences of
rebound sleep. Becuse of this,  vicious cycle occurs s
the norl physiologic need for sleep is not et nd the
body ttepts to copenste.
Becuse sedtive-hypnotic gents hve ny dverse
effects, especilly with long-ter use, edictions tht
re recognized for other priry uses re being used
by helthcre providers for the tretent of insoni.
Antidepressnts such s itriptyline, trzodone, nd
irtzpine re prescribed in lower dosges for their
sedtive effects to ssist ptients with getting to sleep
(see Chpter 16). Anticonvulsnts tht re used in this
wy include gbpentin nd topirte (see Chpter
18). Antipsychotic gents such s quetipine nd oln-
zpine re prescribed for ptients with psychoses who
lso hve insoni (see Chpter 17). However, it is
iportnt to note tht no extensive studies hve been
copleted regrding the use of these ntidepressnts,
ntipsychotics, nd nticonvulsnts for insoni, so
their long-ter effects re unknown nd their use for
treting chronic insoni cnnot be recoended.
ACTIONS
Sedtives, which re used to produce relxtion nd
rest, nd hypnotics, which re used to produce sleep,
re not lwys different drugs. Their effects y de-
pend on the dosge nd the condition of the ptient. A
sll dose of  drug y ct s  sedtive, wheres 
lrger dose of the se drug y ct s  hypnotic nd
produce sleep.
Sedtive-hypnotic edictions y be clssied
into two groups: benzodizepines nd nonbenzodiz-
epine sedtive-hypnotic edictions.
USES
The priry uses of sedtive-hypnotic edictions re
s follows: (1) to iprove sleep ptterns for the te-
porry tretent of insoni; nd (2) to decrese the
level of nxiety nd increse relxtion or sleep before
dignostic or opertive procedures.
NURSING IMPLICATIONS FOR SEDATIVE-
HYPNOTIC THERAPY
Assessment
Central nervous system function. Becuse sedtive-
hypnotic drugs depress overll centrl nervous syste
(CNS) function, identify the ptient’s level of lertness
nd orienttion, s well s their bility to perfor vri-
ous otor functions.
Vital signs. Obtin the ptient’s current blood pres-
sure, pulse, nd respirtion rtes before inititing drug
therpy.
Sleep pattern. Assess the ptient’s usul pttern of
sleep, nd obtin infortion bout the pttern of
sleep disruption (e.g., difculty flling sleep, inbility
to rein sleep the entire night, wkening during
the erly orning hours nd unble to return to  rest-
ful sleep).
Ask bout the ount of sleep (i.e., nuber of
hours) tht the ptient considers norl nd how their
insoni is nged t hoe. Does the ptient hve 
regulr tie to go to bed nd wke up? If the ptient is
tking edictions, deterine the drug, dosge, nd
frequency of dinistrtion nd whether this y
be contributing to sleeplessness. (Medicines tht y
induce or ggrvte insoni include theophylline,
cffeine, pseudoephedrine, nicotine, levodop, corti-
costeroids, nd selective serotonin reuptke inhibitor
ntidepressnts.)
Ptients with persistent insoni should be creful-
ly onitored for the nuber of nps tken during the
dy. Investigte the type of ctivities tht the ptient
perfors ieditely before going to bed.
Anxiety level. Assess the ptient’s exhibited degree of
nxiety. Is it relly  sedtive-hypnotic ediction tht
the ptient needs, or does the ptient just need soe-
one to listen to the? Ask bout the stressors tht the
ptient hs been experiencing in their personl nd
work environents.
Environmental control. Obtin dt relted to possi-
ble disturbnces present in the individul’s sleeping
environent tht y interfere with sleep (e.g., roo
teperture, lights, noise, trfc, restlessness,  snor-
ing prtner).
Nutritional needs. Obtin  dietry history to iden-
tify sources of cffeinted products tht y ct s
stiulnts.
Alcohol intake. Although lcohol cuses sedtion, it
disrupts sleep ptterns nd y cuse erly-orning
wkening.

Exercise. Obtin dt relted to the ptient’s usul de-
gree of physicl ctivity nd t wht ties during the
dy tht they re ost ctive.
Respiratory status. Ptients with respirtory disorders
nd those who snore hevily y hve low respirtory
reserves nd should not receive hypnotic gents be-
cuse of their potentil to cuse respirtory depression.
Implementation
Vital signs. Obtin the ptient’s vitl signs periodiclly
s the sitution indictes.
Preoperative medication. Give the ptient pre-
opertive edictions t the specied tie.
Monitoring effects. When  ediction is dinis-
tered, crefully ssess the ptient t regulr intervls
for the drug’s therpeutic nd dverse effects.
As-needed medications. If giving the ptient s-needed
(PRN) edictions, sk the ptient bout the effective-
ness of previously dinistered therpy. It is soeties
necessry to repet  ediction if n order perits do-
ing so. This is done t the nurse’s discretion on the bsis
of the evlution of  prticulr ptient’s needs.
Patient Education: Promote Good Sleep Hygiene
Bedtime. Encourge the ptient to choose  stndrd
tie to go to bed to help the body estblish  rhyth
nd routine.
Nutrition. Tech the ptient pproprite nutri-
tion infortion concerning the US Food nd Drug
Adinistrtion (FDA)’s recoendtions of MyPlte
(see Chpter 46), dequte uid intke, nd vitin
use. Counicte the infortion t the eductionl
level of the ptient.
Avoiding heavy meals during the evening. Alcohol nd
cffeine consuption should be reduced or discontin-
ued, especilly within severl hours of bedtie. Educte
the ptient bout decffeinted or herbl products tht
cn be substituted for cffeinted foods. Help the p-
tient to void products tht contin cffeine, such s cof-
fee, te, energy drinks, soft drinks, nd chocolte. Liit
the totl dily intke of these ites, nd provide the p-
tient with wr ilk nd crckers s  bedtie snck.
Protein foods nd diry products contin n ino cid
tht synthesizes serotonin, which is  neurotrnsitter
tht hs been found to increse sleep tie nd decrese
the tie required to fll sleep.
For insoni, suggest tht the ptient drink wr
ilk bout 30 inutes before going to bed.
Personal comfort. Position the ptient for xiu
cofort, provide  bck rub, encourge the ptient to
epty the bldder, nd be certin tht the bedding is
Drugs Used for Sedation and Sleep CHAPTER 13 195
clen nd dry. Tke tie to eet the ptient’s indi-
vidul needs nd to cl their fers. Foster  trusting
reltionship.
Environmental control. Tell the ptient to sleep in n
environent tht prootes sleep, such s  quiet,
drkened roo free fro distrctions, nd to void
using the bedroo for wtching television, respond-
ing to e-ils, prepring work for the following dy,
eting, nd pying bills. Provide dequte ventiltion,
subdued lighting, nd  cofortble roo teper-
ture nd control trfc in nd out of the ptient’s roo.
For sfety, instruct the ptient to leve  night-light
on nd not soke in bed fter tking ediction.
Activity and exercise. Suggest the inclusion of exercise
in the ptient’s dily ctivities so tht the ptient ob-
tins sufcient exercise nd is tired enough to sleep.
For soe individuls, pln  quiet “unwinding” tie
before retiring for the night. For children, ssist with
sleep by providing  wr bth nd structure before
bedtie. Try  bedtie story tht is plesnt nd sooth-
ing (rther thn one tht y cuse nxiety or fer).
Stress management
• Explore personl nd work stressors tht could hve
 bering on the ptient’s insoni. Soe stressors
y exist in the work environent; therefore the in-
volveent of the occuptionl helth nurse, long
with  thorough explortion of work fctors, y be
pproprite. Stress produced within the dynics
of the fily y require professionl counseling.
• Tech the ptient relxtion techniques nd per-
sonl cofort esures (e.g.,  wr bth) to re-
lieve stress. Plying soft usic y lso proote
relxtion.
• Mke referrls for the stery of biofeedbck, ed-
ittion, or other techniques to reduce stress levels.
• Encourge the ptient to openly express feelings
bout their stress nd insoni. The djustent to
this sitution involves working through gret per-
sonl fers, frustrtions, hostilities, nd resentents.
• Explore the coping echniss tht the ptient
uses in response to stress, nd identify ethods of
chnneling these towrd positive relistic gols nd
lterntives to the use of ediction.
Fostering health maintenance. Throughout the course
of tretent, discuss ediction infortion nd how
it will benet the ptient. Stress the iportnce of
nonphrcologic interventions nd the long-ter ef-
fects tht coplince with the tretent regien cn
provide.
Provide the ptient or the ptient’s signicnt oth-
ers with iportnt infortion tht is contined in
the specic drug onogrphs for the edicines pre-
scribed. Additionl helth teching nd nursing inter-
ventions for the coon dverse effects nd serious
196 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
dverse effects tht require contct with the helthcre
provider re described in the following drug ono-
grphs (benzodizepines, nonbenzodizepine sed-
tive-hypnotic edictions).
Patient self-assessment. Enlist the ptient’s help
with developing nd intining  written record of
onitoring preters (e.g., extent nd frequency of
insoni); see the Ptient Self-Assessent For for
Sleeping Mediction on the Evolve website. Coplete
the Preediction Dt colun for use s  bseline
to trck the ptient’s response to drug therpy. Ensure
tht the ptient understnds how to use the for, nd
instruct the ptient to bring the copleted for to fol-
low-up visits. During these follow-up visits, focus on
issues tht will foster the ptient’s dherence with the
therpeutic interventions tht hve been prescribed.
DRUG THERAPY FOR SLEEP
DISTURBANCE
DRUG CLASS: BENZODIAZEPINES
Benzodizepines hve been extreely successful
products fro both the therpeutic nd sfety stnd-
points. A jor dvntge of the benzodizepine
sedtive-hypnotic gents is the wide sfety rgin
between therpeutic nd lethl doses. Intentionl nd
unintentionl overdoses well bove the norl ther-
peutic doses re well tolerted nd not ftl.
More thn 2000 benzodizepine derivtives hve
been identied, nd ore thn 100 hve been tested
for sedtive-hypnotic or other therpeutic ctivity.
Although there re ny siilrities ong the benzo-
dizepines, they re difcult to chrcterize s  clss.
Soe benzodizepines re effective nticonvulsnts,
others serve s ntinxiety nd uscle-relxnt gents,
nd others re used s sedtive-hypnotic drugs.
Actions
Benzodizepines exert their effects through stiultion of
the g-inobutyric cid (GABA)–benzodizepine
receptor coplex. GABA is n inhibitory neuro-
trnsitter tht exerts its effects t specic receptor
subtypes designted GABA-A nd GABA-B. GABA-A is
the priry receptor subtype in the CNS. The priry
subunits involved in the ctions of benzodizepines re l-
ph-1 nd lph-2 sites. Binding to lph-1 sites edites
sleep, wheres binding to lph-2 sites results in uscle
relxtion, ntinxiety effects, nd nticonvulsnt ctivity.
Benzodizepines do not bind to GABA-B receptors.
Uses
Estzol, urzep, quzep, tezep, nd
trizol re the benzodizepines tht hve been r-
keted for hypnosis. Trizol, which is  shorter-cting
hypnotic, s well s estzol nd tezep, which
re interedite-cting hypnotic gents, do not contin
ctive etbolites nd therefore do not ccuulte s
redily fter severl nights of dosing. Flurzep nd
quzep hve long hlf-lives nd ctive etbolites,
thus king ptients uch ore susceptible to hng-
overs the dy fter use. Benzodizepines tht re used s
sedtive-hypnotic gents increse stge N2 sleep nd de-
crese stge N3 sleep nd, to  lesser extent, REM sleep.
When benzodizepine therpy is strted, ptients
experience deep nd refreshing sleep. However,
benzodizepine-induced sleep vries fro norl
sleep in tht there is less REM sleep. With the chronic
dinistrtion of benzodizepines, the ount of REM
sleep grdully increses s tolernce develops to the
REM-suppressnt effects of the drugs. When benzodi-
zepines re discontinued,  rebound increse in REM
sleep y occur despite the ptient’s tolernce. During
the rebound period, the nuber of dres stys bout
the se, but ny of the dres re reported to be
bizrre. After long-ter use of ost benzodizepines,
there is lso  rebound in insoni. Consequently, it
is iportnt to use these gents only for short courses
(i.e., usully no ore thn 4 weeks) of therpy.
The short-cting benzodizepines (e.g., idzol,
lorzep) re used prenterlly s preopertive sed-
tives nd intrvenously for conscious sedtion before
short dignostic procedures or for the induction of
generl nesthesi. Midzol hs  ore rpid onset
of ction, produces  greter degree of nesi, nd
hs  uch shorter durtion copred with dizep.
Lorzep is used s n ntinxiety gent in generl,
but it is prticulrly useful before dignostic proce-
dures when  longer durtion of ction is required; 
prenterl dosge for is vilble. It lso hs no c-
tive etbolites tht y prolong sedtion.
Fluzenil is n ntidote tht is dinistered intr-
venously for the coplete or prtil reversl of the ef-
fects of benzodizepines tht re used s generl nes-
thetics or during dignostic or therpeutic procedures.
Fluzenil is lso used for the ngeent of n in-
tentionl or ccidentl overdose of benzodizepines.
The dinistrtion of uzenil hs been ssocited
with the onset of convulsions in ptients who re re-
lying on benzodizepine effects to control seizures,
re physiclly dependent on benzodizepines, or who
hve ingested lrge doses of other drugs.
Therapeutic Outcomes
The priry therpeutic outcoes sought fro benzo-
dizepine therpy re s follows:
1. To produce ild sedtion
2. For short-ter use, to produce sleep
3. Preopertive sedtion with nesi
Nursing Implications for Benzodiazepines
Premedication assessment
1. Record the ptient’s bseline vitl signs (e.g., blood
pressure, pulse, respirtions); esure the ptient’s
blood pressure in both sitting nd lying positions.
 Drugs Used for Sedation and Sleep CHAPTER 13 197

2. Check for  history of blood dyscrsis or heptic
disese, nd deterine whether the ptient is in the
rst triester of pregnncy.
3. Assess the ptient’s level of pin.
Availability, dosage, and administration. See Tble 13.1.
Use of benzodizepines y result in physicl nd
psychologicl dependence when tken stedily for sev-
erl dys to weeks, even when tken in recoended
dosges. Abuse nd isuse cn result in overdose or
deth, especilly when benzodizepines re cobined
with other edicines, such s opioid pin relievers, lco-
hol or illicit drugs, nd CNS depressnts (e.g., sedtives,
hypnotics, uscle relxnts). The rpid discontinunce

Table 13.1 Benzodiazepines Used for Sedation and Hypnosis

ADULT ORAL DOSAGE
GENERIC NAME BRAND NAME AVAILABILITY RANGE COMMENTS
Estazolam — Tablets: 1, 2 mg Hypnosis: 1–2 mg at Intermediate acting; Schedule
bedtime IV; used to treat insomnia;
tapering therapy recommended
to reduce rebound insomnia;
minimal morning hangover
urazepam Som-Pam Capsules: 15, 30 mg Hypnosis: 15–30 mg Long acting; Schedule IV; used
at bedtime for short-term treatment of
insomnia for up to 4 wk; morning
hangover may be signicant;
rebound insomnia and rapid
eye movement sleep occur less
frequently
lorazepam Ativan Tablets: 0.5, 1, 2 mg Hypnosis: 2–4 mg at Used primarily to treat insomnia
Do not Do not confuse Oral solution: 2 mg/mL bedtime but may also be used for
confuse Ativan with Ambien, Injection: 2, 4 mg/mL preoperative anxiety, status
lorazepam with or Atarax in 1-, 10-mL vials epilepticus; IM and IV
loperamide. Apo-Lorazepam administration also available
midazolam — Syrup: 2 mg/mL Preoperatively: Short acting; Schedule IV; causes
Suspension: 1 mg/mL 0.07–0.08 mg/ amnesia in most patients; lower
Injection: 1, 5 mg/mL kg IM 1 hr before dosages for patients more than
in 1-, 2-, 5-, 10-mL surgery 55 yr old
vials; 2 mg/2 mL in Induction of Onset: IM, 15 min; IV, 3–5 min
prelled syringes anesthesia: Duration: IM, 30–60 min; IV, 2–6 hr
IV: 1 mg/mL in 100 mL 0.2–0.3 mg/kg IV
container Conscious sedation:
0.5–2 mg IV
slowly over 2 min;
repeat every 2–3
min as needed
quazepam Doral Tablets: 15 mg Hypnosis: 7.5– Long acting; Schedule IV; used to
15 mg at bedtime treat insomnia; tapering therapy
recommended to reduce
rebound insomnia; morning
hangover may be signicant
temazepam Restoril Do not Capsules: 7.5, 15, Hypnosis: 15–30 mg Intermediate acting; Schedule IV;
confuse Restoril 22.5, 30 mg at bedtime used to treat insomnia; minimal
with Remeron, if any morning hangover;
Risperdal, or rebound insomnia may occur
Vistaril.
triazolam Halcion Tablets: 0.125, 0.25 mg Hypnosis: 0.125– Short acting; Schedule IV; used
Do not confuse 0.5 mg at bedtime to treat insomnia but tends to
Halcion with lose effectiveness within 2 wk;
Haldol. tapering therapy recommended
Apo-Triazo to reduce rebound insomnia;
rapid onset of action; no
morning hangover
IM, Intramuscular(ly); IV, intravenous(ly).
Available in Canada.
Do not confuse.
198 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
of benzodizepines fter long-ter use y result in
syptos tht re siilr to those of lcohol withdrw-
l, such s wekness, nxiety, deliriu, nd tonic-clonic
(grnd l) seizures. These syptos y not pper
for severl dys fter discontinution. Discontinution
of benzodizepines consists of grdul withdrwl over
2 to 4 weeks.
Pregnancy and lactation. It is generlly recoended
tht benzodizepines not be dinistered during t
lest the rst triester of pregnncy. There y be n
incresed incidence of birth defects if these drugs re
tken becuse these gents redily cross the plcent
nd enter the fetl circultion.
Mothers who re brestfeeding should not receive
benzodizepines regulrly. These gents redily cross
into brest ilk nd exert  phrcologic effect on
the infnt.
Common adverse effects
Neurologic
Drowsiness, hangover, sedation, lethargy, decreased level of
alertness. Ptients y coplin of “orning hngo-
ver” nd blurred vision. If the hngover effect contin-
ues nd becoes troublesoe, there should be  reduc-
tion in the drug dosge,  chnge in the ediction, or
both. People who work round chinery, drive  cr,
pour nd give edictions, or perfor other duties for
which they ust rein entlly lert should not tke
these edictions while working.
Cardiovascular
Transient hypotension when arising. Explin to the p-
tient the need to rst rise to  sitting position, to then
sty sitting for severl oents until ny dizziness or
lighthededness psses, nd to then stnd up slowly.
Assistnce with bultion y be required.
Serious adverse effects
Psychological. Confusion, gittion, hllucintions,
nesi.
All benzodizepines hve the potentil to cuse
these syptos, prticulrly in older ptients who
hve been tking higher doses or tking the drugs for
prolonged periods. Discuss the cse with the helth-
cre provider nd ke plns to coopertively p-
proch the grdul reduction of the ediction to pre-
vent withdrwl syptos nd rebound insoni.
Excessive use or abuse. The hbitul use of benzodi-
zepines y result in physicl dependence. Discuss
the cse with the helthcre provider nd ke plns
to coopertively pproch the grdul withdrwl of
the edictions tht re being bused. Assist the p-
tient with recognizing the buse proble. Identify the
ptient’s underlying needs nd pln for the ore p-
proprite ngeent of those needs. Provide for the
eotionl support of the individul nd disply n c-
cepting ttitude. Be kind but r.
Blood dyscrasias. Blood dyscrsis re rre but
hve been reported. Routine lbortory studies (e.g.,
red blood cell count, white blood cell [WBC] count,
differentil nd pltelet counts) should be scheduled.
Stress tht the ptient should return for these tests.
Monitor the ptient for the developent of  sore
throt, fever, purpur, jundice, or excessive nd pro-
gressive wekness.
Hepatotoxicity. The syptos of heptotoxicity re
norexi, nuse, voiting, jundice, heptoegly,
splenoegly, nd bnorl liver function tests (e.g.,
elevted levels of bilirubin, sprtte inotrnsferse
[AST], lnine inotrnsferse [ALT], g-
glutyltrnsferse [GGT], nd lkline phosphtse
[ALP]; incresed prothrobin tie [PT]).
Drug interactions
Antihistamines, alcohol, analgesics, anesthetics, tran-
quilizers, narcotics, cimetidine, disulram, isoniazid, eryth-
romycin, and other sedative-hypnotics. All of these gents
increse the toxic effects of these drugs.
Smoking and rifampin. Soking nd rifpin en-
hnce the etbolis of benzodizepines. Lrger
doses y be necessry to intin sedtive effects in
ptients who soke.
DRUG CLASS: NONBENZODIAZEPINE SEDATIVE-
HYPNOTIC AGENTS
Actions
The nonbenzodizepine sedtive-hypnotic drugs
re listed in Tble 13.2. They represent  vriety of
cheicl clsses, ll of which cuse CNS depression.
These include the histine-1 blockers diphenhydr-
ine nd doxyline (i.e., ntihistines); doxepin,
which is  tricyclic ntidepressnt; benzodizepine
receptor gonists (zleplon, zolpide, eszopiclone);
eltonin, which is  horone secreted fro the
pinel glnd (see Chpter 47); eltonin-receptor
stiulnts (relteon, tsielteon); orexin receptor
ntgonists (suvorexnt, leborexnt); nd vlerin,
which is n herbl edicine (see Chpter 47). All of
these drugs hve soewht vrible effects on REM
sleep, tolernce developent, rebound REM sleep,
nd insoni.
Uses
Antihistines—prticulrly diphenhydrine nd
doxyline—hve sedtive properties tht y be
used for the short-ter tretent of ild insoni.
These drugs re coon ingredients in over-the-coun-
ter sleep ids. Becuse tolernce develops fter only 
few nights of use, incresing the dose ctully cuses 
ore restless nd irregulr sleep pttern. Doxyline
hs  longer hlf-life of pproxitely 10 hours, which
frequently cuses  orning hngover.
Doxepin is  tricyclic ntidepressnt. At lower doses
it works on histine-1 receptors, which is thought to
proote nd intin sleep. It cn cuse dry outh
nd constiption.
Suvorexnt nd leborexnt re orexin receptor n-
tgonists. They iprove flling sleep nd intining
 Drugs Used for Sedation and Sleep CHAPTER 13 199

Table 13.2 Nonbenzodiazepine Sedative-Hypnotic Agents

ADULT ORAL
GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE COMMENTS
ANTIHISTAMINES
diphenhydramine Banophen, Diphenhist, Tablets: 12.5 mg; Sedation: Over-the-counter availability;
Do not confuse ZzzQuil Capsules: 25, 50 mg; 25–50 mg at used for mild insomnia
diphenhydramine Liquid: 6.25 mg/mL in bedtime for up to 1 wk; tolerance
with dicyclomine or Simply Sleep 30 mL bottle ; 12.5 develops, and increased
dipyridamole. mg/5 mL in various dosage causes more
volumes; adverse effects with no
50 mg/30 mL in 177 and additional efcacy
354 mL bottles
doxylamine Sleep Aid Tablets: 25 mg Sedation: 25 mg Over-the-counter availability;
Unisom 2 at bedtime morning hangover
may be signicant; see
diphenhydramine above
TRICYCLIC ANTIDEPRESSANT
doxepin Silenor Tablets: 3, 6 mg Hypnosis: Avoid doses >6 mg/day
3–6 mg once Also used in depression but
daily within in higher doses
30 min of
bedtime
MELATONIN RECEPTOR STIMULANTS
melatonin — — — See Chapter 47
ramelteon Rozerem Tablets: 8 mg Hypnosis: 8 mg Do not take with or
Do not confuse Do not confuse within 30 min immediately after a high-fat
ramelteon with Rozerem with of bedtime meal
Remeron, Remegel, Remeron, Remegel,
Reminyl, or Renagel. Reminyl, or Renagel.
tasimelteon Hetlioz Capsule: 20 mg Hypnosis: 20 mg Used to treat non–24-hr
Suspension: 4 mg/mL once daily at sleep-wake disorder in
the same time blind persons; may take
each night weeks to months to be
before bedtime effective due to variation in
circadian rhythms
OREXIN RECEPTOR INHIBITORS
lemborexant Dayvigo Tablets: 5, 10 mg Hypnosis: 5–10 Initial dose: 5 mg at bedtime
mg with at least 7 hr before
planned awakening
Maximum dose: 10 mg
suvorexant Belsomra Tablets: 5, 10, 15, 20 mg Hypnosis: 10 mg Schedule IV drug: may be
once daily benecial in patients having
within 30 min problems falling asleep and
of bedtime; staying asleep
may increase
to a maximum
of 20 mg once
daily
BENZODIAZEPINE-LIKE RECEPTOR AGONISTS
eszopiclone Lunesta Tablets: 1, 2, 3 mg Hypnosis: Onset within 45 min; duration
Imovane 2–3 mg 5–8 hr
Older adult patients should
start with 1 mg
zaleplon — Capsules: 5, 10 mg Hypnosis: 10 mg Schedule IV; short acting;
Do not confuse at bedtime; onset within 30 min,
zaleplon with Maintenance: duration 2–4 hr; older
zolpidem. 5–20 mg adults or low-weight
patients should start with
5 mg
200 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems

Table 13.2 Nonbenzodiazepine Sedative-Hypnotic Agents—cont’d

ADULT ORAL
GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE COMMENTS
zolpidem Ambien Tablets: 5, 10 mg Hypnosis: Schedule IV; short acting;
Do not confuse Do not confuse Women: 5 mg at onset within 30 min,
zolpidem with Ambien with Ativan bedtime duration 3–5 hr; older
zaleplon. or Atarax. (delete Men: 5–10 mg at adult patients should start
ML) bedtime with 5-mg immediate-
Ambien CR Tablets, controlled- Hypnosis: release tablets or 6.25-mg
release: 6.25, 12.5 mg Women: 6.25 mg controlled-release tablets;
at bedtime place a sublingual tablet
Men: 6.25–12.5 under tongue, where it will
mg at bedtime disintegrate in seconds;
do not chew, break, or
Edluar Tablets, sublingual: Hypnosis:
split the tablet; sublingual
5, 10 mg Women: 5 mg
tablets and oral spray
Zolpimist Oral spray: 5 mg/ Men: 5–10 mg
should not be administered
actuation with or immediately after
Intermezzo Tablets, sublingual 1.75, a meal
3.5 mg
HERBAL MEDICINE
valerian — — — See Chapter 47
Do not confuse
valerian with Valium.
Available in Canada.
Do not confuse.

sleep by inhibiting binding of orexins to orexin recep-
tors. Stiultion of orexin receptors prootes wke-
fulness. They re schedule IV controlled substnces.
They re both contrindicted in nrcolepsy.
Meltonin is vilble over the counter s  sleep
id. It ppers to be prticulrly useful for ptients
who hve been trveling through tie zones nd who
re experiencing jet lg. Becuse this edicine is clssi-
ed s  dietry suppleent nd thus is not regulted
by the FDA, there y be inconsistencies with regrd
to its potency (see Chpter 47).
Relteon nd tsielteon stiulte the el-
tonin receptors. Relteon is used to tret ptients
with insoni who hve difculty flling sleep.
Tsielteon is used for the tretent of non–24-hour
sleep-wke disorder tht ffects up to 70% of per-
sons who re totlly blind. It is  chronic sleep dis-
order rked by disruption of the circdin rhyth
king it difcult to intin dy-night perception
with norl sleep ptterns. Tsielteon stiultes
eltonin 1 nd 2 receptors tht re thought to in-
tin circdin rhyth with norl sleep ptterns.
Relteon nd tsielteon re not ssocited with
physicl dependence.
Vlerin, which is n herbl edicine, hs been
used for hundreds of yers s  ild sedtive. Its
echnis of ction is unknown, but it y inhibit
the enzye tht etbolizes GABA, thereby prolong-
ing the inhibitory neurotrnsitter’s durtion of c-
tion. Like eltonin, vlerin is clssied s  dietry
suppleent, nd thus it is not regulted by the FDA.
There y be differences in the strength nd potency
of this substnce ong distributors.
As  result of their effect on sleep ptterns nd
REM sleep, the use of benzodizepines is diinish-
ing in fvor of the newer benzodizepine receptor
gonists such s zleplon, zolpide, nd eszopiclone,
which bind to different GABA receptors in the CNS.
In contrst to benzodizepines, zleplon, zolpide,
nd eszopiclone hve less effect on sleep stge N3 nd
REM sleep. These gents re used s hypnotics to pro-
duce sleep. The recoended period of use for these
benzodizepine receptor gonists is 7 to 10 dys, with
reevlution of the ptient if use exceeds 2 to 3 weeks.
Dytie drowsiness is generlly not  proble with
these gents becuse of their short hlf-lives, lthough
it is ore likely with eszopiclone. The return of in-
soni hs been reported fter the discontinution of
these drugs. Zleplon hs  short onset of ction nd
durtion of 2 to 4 hours. It is used cliniclly for people
who hve difculty getting to sleep nd for those who
wken in the iddle of the night. Zolpide hs 
siilr onset of ction but durtion of 3 to 5 hours.
It is ore effective for helping ptients get to sleep
nd for prolonging sleep durtion without cusing 
orning hngover. Zolpide is vilble in different
forultions depending on ptient need. Iedite-
relese tblets (Abien), sublingul tblets (Edlur),
nd Zolpiist orl spry re prescribed for ptients
hving difculty flling sleep. The extended-relese

tblets (Abien CR) re recoended for ptients
who hve difculty flling sleep nd stying sleep
throughout the night. Interezzo sublingul tb-
lets re for ptients who hve iddle-of-the-night
wkening followed by difculty returning to sleep.
Interezzo y be tken under the tongue t tht
tie to induce sleep when the ptient hs t lest 4
hours of sleep tie reining.
Eszopiclone hs  slower onset of ction thn tht of
the other two gents, but its durtion of ction is 5 to 8
hours, thus king it ore effective for ptients who
wke up during the night or erly orning. It hs been
reported to cuse orning hngover, especilly ong
older ptients nd with higher doses.
Therapeutic Outcomes
The priry therpeutic outcoes sought fro non-
benzodizepine sedtive-hypnotic gents re s
follows:
1. To produce ild sedtion
2. For short-ter use to produce sleep
Nursing Implications of Nonbenzodiazepine
Sedative-Hypnotic Agents
Premedication assessment
1. Record the ptient’s bseline vitl signs (i.e., blood
pressure, pulse, nd respirtions); esure the
ptient’s blood pressure in both sitting nd lying
positions.
2. Check for the ptient’s history of heptic disese.
3. Ask fele ptients if they re pregnnt or brest-
feeding if ge pproprite.
Availability, dosage, and administration. See Tble 13.2.
The hbitul use of sedtive-hypnotic gents y re-
sult in physicl dependence. Rpid discontinunce
fter long-ter use y result in syptos tht re
siilr to those of lcohol withdrwl, such s wek-
ness, nxiety, deliriu, nd generlized seizures.
Discontinution consists of grdul withdrwl over
2 to 4 weeks.
Zleplon, zolpide, nd eszopiclone hve  very
rpid onset of ction. These gents should be tken
only ieditely before going to bed or fter the p-
tient hs gone to bed nd then hs difculty flling
sleep.
Medication Safety Alert
Rare but serious injuries, including death, have been asso-
ciated with common medications used to treat insomnia.
Complex abnormal sleep behaviors, including sleepwalking
and sleep driving, have been reported. They appear to be
more common with zaleplon, zolpidem, and eszopiclone.
Avoid use in patients who have previously experienced an
episode of complex sleep behavior with medicines used to
treat insomnia.
Drugs Used for Sedation and Sleep CHAPTER 13 201
Common adverse effects
Neurologic
Hangover, sedation, lethargy, decreased level of alert-
ness. Generl dverse effects include drowsiness,
lethrgy, hedche, uscle or joint pin, nd entl
depression. Soe people experience trnsient restless-
ness nd nxiety before flling sleep. Morning hngo-
ver coonly occurs fter the dinistrtion of hyp-
notic doses of doxyline, s well s the long-cting
benzodizepines quzep nd urzep, nd it
is lso being reported with eszopiclone. Ptients y
disply dulled ffect, subtle distortion of ood, nd
ipired coordintion.
Ptients y coplin of orning hngover,
blurred vision, nd trnsient hypotension on rising. If
the hngover effect becoes troublesoe, the dosge
should be reduced, the ediction should be chnged,
or both. People who work round chinery, drive 
cr, pour nd give edictions, or perfor other du-
ties for which they ust rein entlly lert should
not tke these edictions while working.
Cardiovascular
Transient hypotension when arising. Explin to the p-
tient the need to rst rise to  sitting position, to then
sty sitting for severl oents until ny dizziness or
lighthededness psses, nd to then stnd up slowly.
Assistnce with bultion y be required.
Psychological
Restlessness, anxiety. These dverse effects re usully
ild nd do not wrrnt discontinuing the ediction.
Encourge the ptient to try to relx nd to let the sed-
tive effect tke over. Older ptients nd those in severe
pin y respond prdoxiclly with exciteent, eu-
phori, restlessness, nd confusion. Sfety esures
such s the intennce of bed rest, side rils, nd ob-
servtion should be used during this period. Pin edi-
ctions y lso be dinistered, if indicted.
Drug interactions
Antihistamines, alcohol, analgesics, anesthetics, tran-
quilizers, narcotics, cimetidine, disulram, isoniazid, eryth-
romycin, ketoconazole, and other sedative-hypnotics. All
these gents increse the toxic effects of ll sedtive-
hypnotic gents.
Fluvoxamine. Fluvoxine speciclly inhibits the
etbolis of relteon nd tsielteon, thus cus-
ing excessive sedtion. Ptients who re receiving u-
voxine should not tke relteon or tsielteon.
Rifampin. Rifpin signicntly enhnces the e-
tbolis of zolpide, eszopiclone, relteon, nd t-
sielteon, thereby reducing their therpeutic effect.
Food. The presence of food—prticulrly food with
 high ft content—slows the bsorption of zolpide,
zleplon, eszopiclone, nd relteon, slowing the on-
set of ction. For  fster onset of ction, do not din-
ister these drugs with or ieditely fter  el.
202 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions
Key Points
• There are many types of sleep disorders, but the most
common is insomnia.
• Most cases of insomnia are short lived and can be
effectively treated by nonpharmacologic methods, such as
a back rub, eating a lighter meal in the evening, eliminating
naps, and reducing the use of alcohol and stimulants such
as caffeine and nicotine.
• People who have insomnia that lasts for more than 1
month and who also experience daytime impairment of
their social and employment responsibilities should be
referred to a healthcare provider for a complete history
and physical assessment. There may be other underlying
conditions that must be treated before the patient resorts
to the use of sedative-hypnotic agents.
• A variety of sedative-hypnotic drugs are available for
pharmacologic treatment; however, the drugs of choice
are the nonbenzodiazepines (e.g., zaleplon, zolpidem,
eszopiclone) because of their wide margin of safety.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Clayton)
for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX examination and include both NGN (Next Genera-
tion) and traditional questions. See Chapter 12 for further infor-
mation regarding question types.
Scenario
A patient who recently lost their job and is experiencing bouts
of insomnia called the nurse line to discuss options for better
sleep.
1. A patient was discussing a recent development of nightmares
and restlessness since the discontinuation of triazolam (Halcion)
with the nurse, who recognized the symptoms of which sleep
disorder?
1. Rebound sleep
2. Terminal insomnia
3. Transient insomnia
4. Initial insomnia
Objective: Differentiate among the terms sedative and hypnotic;
initial, intermittent, and terminal insomnia; transient, short-term,
and chronic insomnia; and rebound sleep.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
2. The nurse is reviewing an order for a sleep aid for a patient in the
scenario who is complaining of insomnia. The nurse understands
that a sedative is different from a hypnotic in which manner?
1. The sedative causes feelings of relaxation and rest, and
the hypnotic agent causes feelings of restlessness and
anxiety.
2. The sedative causes feelings of relaxation and rest, and
the hypnotic agent produces sleep.
3. The hypnotic agent produces sleep, and the sedative
causes no hangover effect.
4. The hypnotic agent causes feelings of relaxation and
rest, and the sedative produces sleep.
Objective: Differentiate among the terms sedative and hypnotic;
initial, intermittent, and terminal insomnia; transient, short-term,
and chronic insomnia; and rebound sleep.
NCLEX item type: Multiple choice
Cognitive skill: Understanding
3. A patient who has been receiving benzodiazepines for several
years was told by the nurse that this may cause which condition
as a complication?
1. Symptoms of renal impairment
2. A rush of morning energy with repeated usage
3. Withdrawal symptoms if the drug is discontinued rapidly
4. Seizures during the time that the drug is being
administered
Objective: Compare the effects of benzodiazepines and
nonbenzodiazepines on the central nervous system.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
4. The nurse is making rounds at 2 am on the unit during the night
shift and notes that one of the older patients is awake. The nurse
reviews the patient’s bedtime medication and sees that 5 mg of
zolpidem (Ambien) was administered at 9 pm. What interventions
are appropriate for the nurse to do next? (Select all that apply.)
1. Repeat the dose if ordered.
2. Provide patient comfort measures (e.g., back rub, quiet
room).
3. Determine what the patient normally does at home when
unable to sleep.
4. Keep the patient awake to prevent rebound sleep.
5. Assess for paradoxical symptoms.
6. Provide safety measures.
7. Turn all the lights on to keep the patient from falling asleep.
Objective: Discuss nursing interventions that can be implemented
as an alternative to administering a sedative-hypnotic medication.
NCLEX item type: Extended multiple response
Cognitive skill: Prioritize hypotheses
 Drugs Used for Sedation and Sleep CHAPTER 13 203

5. The nurse was discussing the difference between temazepam 8. The patient in the scenario came to the clinic complaining of not
(Restoril) and zolpidem (Ambien) with a patient requesting drug being able to get a good night’s sleep for the past month, as he
therapy for sleep disturbance. Which of the following statements nds that he frequently awakens throughout the night, then will
are appropriate? (Select all that apply.) fall asleep again. The nurse recognizes this condition as which
1. “When you take Restoril, it can cause rebound insomnia sleep disorder?
if you abruptly stop taking it without tapering the drug.” 1. Initial insomnia
2. “There is no difference between these drugs; you can 2. Intermittent insomnia
take them without any worries.” 3. Terminal insomnia
3. “Ambien is also available in a sublingual tablet form, 4. Transient insomnia
which disintegrates in seconds.” Objective: Differentiate among the terms sedative and hypnotic;
4. “The side effect of morning drowsiness is only caused by initial, intermittent, and terminal insomnia; transient, short-term,
Restoril, not Ambien.” and chronic insomnia; and rebound sleep.
5. “Ambien is used for short-term treatment of insomnia.” NCLEX item type: Multiple choice
Objective: Compare the effects of benzodiazepines and Cognitive skill: Knowledge
nonbenzodiazepines on the central nervous system.
NCLEX item type: Multiple response
Cognitive skill: Application
6. The nurse taking care of a patient who was admitted for an
overdose of lorazepam (Ativan) knows which antidote will be
used?
1. Fluvoxamine
2. Temazepam (Restoril)
3. Flumazenil
4. Selegiline (Zelapar)
Objective: Identify the antidote drug used for the management of
benzodiazepine overdose.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
7. The nurse is monitoring laboratory results for a patient who has
been taking quazepam (Doral) for several years. The following
laboratory values on the patient’s chart are considered elevated;
indicate with an X the ones that would alert the nurse to possible
hepatotoxicity or blood dyscrasias.

OF CONCERN
LABORATORY OF CONCERN FOR FOR BLOOD
VALUE HEPATOTOXICITY DYSCRASIAS
AST (aspartate
aminotransferase)
Platelets
ALP (alkaline
phosphatase)
WBC (white blood
cells)
ALT (alanine
aminotransferase)
PT/INR
(prothrombin
time/international
normalized ratio)

Objective: Identify laboratory tests that should be monitored when

benzodiazepines are administered for an extended period.
NCLEX item type: Matrix
Cognitive skill: Recognize cues
14 Drugs Used to Treat Neurodegenerative
Disorders
http://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the signs and symptoms of Parkinson disease.
2. Identify the neurotransmitter that is found in excess
and the neurotransmitter that is decient in people with
parkinsonism.
3. Discuss the action of carbidopa-levodopa and dopamine
agonists in Parkinson disease.
4. Explain the action of entacapone, opicapone, and the
monoamine oxidase inhibitors (selegiline, sanamide,
and rasagiline) as it relates to the treatment of Parkinson
disease.
5. Discuss the specic symptoms that should show
improvement when anticholinergic agents are administered
to the patient with Parkinson disease.
6. Explain the action of the agents used in the treatment of
Alzheimer disease.

Key Terms
Parkinson disease (PĂR-kĭn-sĕnz dĭ- anticholinergic agents (ĂN-tē-kō-lĭn- akinesia (ă-kĭ-NĒ-zhă) (p. 207)
ZĒZ) (p. 204) ŬR-jĭk) (p. 206) livedo reticularis (lĭ-VĒ-dō rĭ-tĭk-yĕ-
dopamine (DŌ-pă-mēn) (p. 204) tremors (TRĔ-mŭrz) (p. 207) LĀR-ĭs) (p. 214)
neurotransmitter (nyū-rō-TRĂNZ-mĭ- dyskinesia (dĭs-kĭ-NĒ-zhă) (p. 207) Alzheimer disease (ĂLZ-hī-mŭrz)
tĕr) (p. 204) propulsive, uncontrolled (p. 222)
acetylcholine (ăs-ē-tĭl-KŌ-lēn) movement (prō-PŬL-sĭv ŭn-kŏn-
(p. 204) TRŌLD MŬV-mĕnt) (p. 207)

an muscle tone, as well as for regulating voluntary

Parkinson Disease
Parkinson disease is a chronic, progressive isorer of
the central nervous system. It is the secon most com-
mon neuroegenerative isease after Alzheimer is-
ease. An estimate 1% of the US population that is more
than 50 years ol, 2% of the population that is more
than 60 years ol, an 4% to 5% of the population 85
years ol or oler have this isorer. Thirty percent of
patients report an onset of symptoms before the age of
50 years; 40% report that the onset occurre between
the ages of 50 an 60 years; an the remainer report
that their symptoms began after the age of 60 years. The
incience is slightly higher in men than women, an
all races an ethnic groups are affecte. Characteristic
motor symptoms inclue muscle tremors, slowness of
movement (i.e., braykinesia) when performing activi-
ties of aily living (ADLs), muscle weakness with rigi-
ity, an alterations in posture an equilibrium.
The symptoms associate with parkinsonism are
cause by a eterioration of the opaminergic neu-
rons in the substantia nigra pars compacta, which
results in a epletion of opamine along the nigros-
triatal pathway that extens into neurons in the auto-
nomic ganglia, the basal ganglia, an the spinal cor
an causes progressive neurologic ecits. These areas
of the brain are responsible for maintaining posture
204
smooth muscle activity an other nonmotor activities.
Normally, a balance exists between dopamine, which
is an inhibitory neurotransmitter, an acetylcholine,
which is an excitatory neurotransmitter. With a e-
ciency of opamine, a relative increase in acetylcholine
activity occurs an causes the symptoms of parkinson-
ism. About 80% of the opamine in the neurons of the
substantia nigra pars compacta of the brain must be
eplete for symptoms to evelop.
Whereas the motor symptoms associate with par-
kinsonism have been consiere to be the hallmarks
of the isease, subtle nonmotor symptoms are now be-
ing recognize as occurring as much as 10 years before
the onset of motor symptoms. Nonmotor symptoms
usually start with constipation, progressing over the
next few years with orthostatic hypotension, nocturnal
sleep isturbances with aytime somnolence, epres-
sion, an progressing ementia. It is not known yet
whether early treatment with meicines that control
the symptoms of Parkinson isease will slow the pro-
gression of the isease.
There are two types of parkinsonism. Primary or
iiopathic parkinsonism is cause by a reuction in
opamine-proucing cells in the substantia nigra pars
compacta. The causes are not yet known, but there
appear to be both genetic an environmental factors
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14 205

associate with its evelopment. Approximately 10%

to 15% of cases appear to be inherite. Seconary
parkinsonism is cause by hea trauma, intracranial
infections, tumors, an recurrent exposure to rugs
an pesticies. Meicines that eplete opamine an
thus cause seconary parkinsonism inclue opa-
mine antagonists such as haloperiol, phenothiazines,
an metoclopramie. In most cases of rug-inuce
parkinsonism, recovery is complete if the rug is
iscontinue.

Life Span Considerations

Parkinson Disease
Parkinson disease, which is most often seen in geriatric pa-
tients, causes a relative excess of acetylcholine as a result of
A B C
a deciency of dopamine. Drug therapy with dopaminergic
agents increases dopamine availability, whereas anticholin-
ergic medicines may be taken to counterbalance the excess
availability of acetylcholine. Approximately 40% of patients
with parkinsonism have some degree of clinical depression
as a result of the reduced availability of the active metabolites
of dopamine in the brain.

All rugs that are prescribe for the treatment of

Parkinson isease prouce a pharmacologic effect on
the central nervous system. An assessment of the pa-
tient’s mental status an physical functioning before
the initiation of therapy is essential to serve as a base-
line so that comparisons can be mae with subsequent
evaluations.
Parkinson isease is both progressive an incurable.
The goals of treatment are to moerate the symptoms
an to slow the progression of the isease. It is impor-
tant to encourage the patient to take the meications as
scheule an to stay as active an involve in ADLs
as possible.
Orthostatic hypotension is common with most of
the meicines that are use to treat Parkinson isease.
To provie for patient safety, teach the patient to rise
slowly from a supine or sitting position, an encourage
the patient to sit or lie own if they are feeling faint.
Constipation is a frequent problem among patients
with Parkinson isease. Instruct the patient to rink
six to eight 8-ounce glasses of liqui aily an to in-
crease bulk in the iet to prevent constipation. Bulk-
forming laxatives may also nee to be ae to the
aily regimen.
The motor symptoms of parkinsonism start insii-
ously an are almost imperceptible at rst, with weak-
ness an tremors graually progressing to involve
movement isorers throughout the boy (Fig. 14.1).
The symptoms usually begin on one sie of the boy
(i.e., asymmetric onset an progression) as a tremor of
a nger or han, an they then progress to become bi-
lateral. The upper part of the boy is usually affecte
rst. Eventually the iniviual has postural an gait
alterations that result in the nee for assistance with
total care nees. Varying egrees of epression are the
D E
Fig. 14.1 Stages of parkinsonism. (A) Flexion of the affected arm. The
patient leans toward the unaffected side. (B) Slow, shufing gait. (C)
The patient has increased difculty walking and looks for sources of
support to prevent falls. (D) Further progression of weakness. The
patient requires assistance from another person for ambulation. (E)
Profound disability. The patient may be conned to a wheelchair as a
result of increasing weakness.
most common (i.e., 40% to 50%) nonmotor symptom
associate with Parkinson isease. Most patients with
epression also evelop feelings of anxiety, an this
sometimes inclues panic attacks. Chronic fatigue,
which is another common symptom, may also contrib-
ute to epression. Dementia that resembles Alzheimer
isease occurs in a signicant number of patients, but
there is continuing ebate as to whether it is part of
the Parkinson isease process or if it is cause by con-
current rug therapy, Alzheimer isease, or other fac-
tors. Dementia is characterize by the slowing of the
thought processes, lapses in memory, an a loss of
impulse control. The iagnosis of Parkinson isease
is base on a careful history taking, a physical exami-
nation, an a positive response to opaminergic treat-
ment. There are no laboratory tests or imaging stuies
that can conrm the iagnosis.
206 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Nurses can have a major inuence in the positive
use of coping mechanisms as the patient an family ex-
press varying emotional responses. The primary goal
of nursing interventions shoul be to keep the patient
socially interactive an participating in ADLs. This can
be accomplishe through physical therapy, aherence
to the rug regimen, an management of the course of
treatment.
Drug TheraPy for Parkinson
Disease
Actions
The goal of the treatment of parkinsonism is minimiz-
ing the symptoms because there is no cure for the is-
ease. Pharmacologic goals are to relieve symptoms an
to restore opaminergic activity an neurotransmitter
function to as close to normal as possible. Treatment is
usually starte when symptoms progress to the point
that they interfere with the patient’s ability to perform
at work or to function in social situations or they im-
pair quality of life. The goal is to improve motor an
nonmotor symptoms to optimize quality of life. Drug
therapy inclues the use of the following: monoamine
oxiase type B (MAO-B) inhibitors (rasagiline, san-
amie, selegiline), which ecreases the metabolism of
opamine; opamine agonists (carbiopa-levoopa,
ropinirole, pramipexole, rotigotine, apomorphine),
amantaine (opamine reuptake inhibitor that increas-
es opamine release an may have anticholinergic
properties), or catechol-O-methyltransferase (COMT)
inhibitors (entacapone an opicapone), which reuce
metabolism of opamine) in various combinations to
enhance opaminergic activity; an anticholinergic
agents to inhibit the relative excess of cholinergic ac-
tivity (which causes tremors).
Therapy must be iniviualize, an realistic goals
must be set for each patient. It is not possible to elimi-
nate all symptoms of the isease because the meica-
tions’ averse effects woul not be tolerate. The tren
is to use the lowest possible ose of meication so that,
as the isease progresses, osages can be increase an
other meicines ae to obtain a combine effect.
Unfortunately, as the isease progresses, rug therapy
becomes more complex in terms of the number of me-
icines, osage ajustments, the frequency of osage
aministration, an the frequency of averse effects.
Therapies often have to be iscontinue because of the
impact of averse effects on the quality of life.
Uses
An MAO-B inhibitor (rasagiline, sanamie, sele-
giline) may be use as a treatment of symptoms for
people with early Parkinson isease. A opamine re-
ceptor agonist—often carbiopa-levoopa—is initi-
ate when the patient evelops functional impairment.
Carbiopa-levoopa continues to be the most effective
rug for the relief of symptoms; however, after 3 to 5
years, the rug’s effect graually wears off an the pa-
tient suffers from “on-off” uctuations in levoopa
activity. A COMT inhibitor (entacapone, opicapone) or
MAO-B inhibitor (rasagiline, sanamie, selegiline)
may be ae to carbiopa-levoopa therapy to pro-
long the activity of the opamine by slowing its rate of
metabolism. This prolonge uration of activity is use-
ful as a-on therapies to ecrease motor uctuations
(on-off perios) in patients taking carbiopa-levoopa.
For severe off perios subcutaneous apomorphine, in-
hale levoopa or an aenosine receptor antago-
nist (istraefylline) can be use. Dyskinesias, invol-
untary muscle movements, can be treate by aing
amantaine. Although selom use in oler aults,
anticholinergic agents provie symptomatic relief from
excessive acetylcholine. These agents are often use in
combination to optimize motor function (e.g., to improve
gait, posture, or speech) an to ecrease isease symp-
toms (e.g., tremors, rigiity, rooling). Fig. 14.2 presents
an algorithm for the treatment for Parkinson isease.
nUrsing implicAtions for pArkinson
DiseAse therApy
A
Unied Parkinson’s Disease Rating Scale. The Unie
Parkinson’s Disease Rating Scale (UPDRS) is often
use to ientify the baseline of Parkinson isease
symptoms at the time of iagnosis an to monitor
changes in symptoms that may require meicine os-
age ajustment. The UPDRS evaluates the following:
(1) mentation, behavior, an moo; (2) self-evaluation
of ADLs; (3) motor examination; (4) complications of
therapy; (5) moie Hoehn an Yahr staging; an (6)
the Schwab an Englan ADL Scale.
History of parkinsonism. Obtain a history of the pa-
tient’s exposure to known conitions associate with
the evelopment of parkinsonian symptoms, such as
hea trauma, encephalitis, tumors, an rug exposure
(e.g., phenothiazines, metoclopramie, pesticies). In
aition, ask if the person has a history of being ex-
pose to toxic levels of metals or carbon monoxie.
Obtain ata to classify the extent of parkinsonism
that the patient is exhibiting. A rating scale such as the
UPDRS may be use to assess the severity of Parkinson
isease on the basis of the egree of isability exhib-
ite by the patient:
• Stage 1: Involvement of one limb; slight tremor or
minor change in speech, facial expression, posture,
or movement; mil isease
• Stage 2: Involvement of two limbs; early pos-
tural changes; some social withrawal; possible
epression
• Stage 3: Signicant gait isturbances; moerate gen-
eralize isability
• Stage 4: Akinesia (i.e., an abnormal state of mo-
tor an psychic hypoactivity or muscle paralysis),
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14 207

Management of Parkinson’s Disease

Pharmacologic Therapy in Early PD: Nonpharmacologic Therapy:

Levodopa-carbidopa (Most effective) Education
Dopamine agonists (Consider in age Support services
less than 65) Exercise
MAO inhibitors Nutrition
Tremors only
Anticholinergics (Tremors only)

Choice of an adjunct to levodopa-carbidopa

for people with PD who have developed
dyskinesia or motor fluctuations despite
optimal levodopa therapy:
Catechol-O-methyltransferase inhibitors
MAO inhibitors
Dopamine agonists
Amantadine (primarily for dyskinesia)

Unacceptable Control Consider:

Enteral Levodopa-carbidopa suspension
Surgery

Fig. 14.2 Management of Parkinson disease. Monoamine oxidase (MAO) inhibitors may be considered in patients with
mild symptoms that have not yet begun to have a major impact on daily function and quality of life. Levodopa-carbidopa
is the most effective agent for control of motor symptoms of Parkinson disease but also requires the most frequent
dosing adjustment and is associated with the highest risk of motor complications. Dopamine agonists have intermediate
potency for improving motor symptoms and have a lower risk of motor complications than levodopa; however, they
carry a higher risk of somnolence, hallucinations, and impulse control disorders and are not well tolerated in older adults
and those with cognitive dysfunction. Consider catechol-O-methyltransferase (COMT) inhibitors to extend levodopa’s
duration of action. Consider enteral levodopa-carbidopa suspension or surgical intervention when Parkinson symptoms
cannot be satisfactorily controlled with medical therapies.

rigiity, an severe isability; still able to walk or
stan unassiste
• Stage 5: Unable to stan or walk or to perform all
ADLs; wheelchair boun or berien unless aie
Motor function. Patients with Parkinson isease pro-
gress through the following symptoms.
Tm. Tremors (uncontrolle shaking) are initially
so minor that they are observe only by the patient.
They occur primarily when the iniviual is at rest,
but they are more noticeable uring emotional turmoil
or perios of increase concentration. The tremors are
often observe in the hans an may involve the jaw,
lips, an tongue. A pill-rolling motion in the ngers
an thumbs is characteristic. Tremors are usually re-
uce with voluntary movement.
Assess the egree of tremor involvement an spe-
cic limitations in activities that are being affecte by
the tremors. Obtain a history of the progression of the
symptoms from the patient.
Dk. Dyskinesia is the impairment of the in-
iviual’s ability to perform voluntary movements.
This symptom commonly starts in one arm or han.
It is usually most noticeable because the patient ceases
to swing the arm on the affecte sie while walking.
Involuntary movements of muscles can cause jerking,
spastic symptoms that characterize chorea, which is of-
ten an averse response to treatment.
As yskinesia progresses, movement, especially in
the small muscle groups, becomes slow an jerky. This
motion is often referre to as cogwheel rigidity. Muscle
soreness, fatigue, an pain are associate with the
prolonge muscle contractions. The patient evelops
a shufing gait an may have ifculty with halting
steps while walking (i.e., festination). When starting
movement, there may be brief moments of immobility
calle freezing. Movements that were formerly auto-
matic, such as getting out of a chair or walking, require
a concentrate effort.
In aition to the shufing gait, the hea an spine
ex forwar, an the shoulers become roune an
stoope. As mobility eteriorates, the steps quicken
an become shorter. Propulsive, uncontrolled move-
ment forwar or backwar is evient, an patient safe-
ty becomes a primary consieration. Obtain antislip
pas for chairs an other positioning evices. Perform
a safety check of the patient’s environment to prevent
accients an falls (Table 14.1).
Bdk. Braykinesia is the extremely slow
boy movement that may eventually progress to aki-
nesia (i.e., a lack of movement).
ia
• Implement planne interventions that are consis-
tent with assessment ata; ientify the iniviual
nees of the patient.
208 UNIT III Drugs Affecting the Autonomic and Central Nervous System

Table 14.1 Additional Symptoms Involved in Parkinson Disease

Bradykinesia Bradykinesia is the extremely slow body movement that may eventually progress to aa (i.e., a lack
of movement).
Facial appearance The patient typically appears to be expressionless, as if wearing a mask. The eyes are wide open and
xed in position.
Nutrition Complete an assessment of the person’s dietary habits, any recent weight loss, and any difculties with
eating.
Salivation As the disease progresses, patients may be unable to swallow all secretions, and they will frequently
drool. If the pharyngeal muscles are involved, the patient will have difculty chewing and swallowing.
Psychological The chronic nature of the disease and its associated physical impairment produce mood swings and
serious depression. Patients commonly display a delayed reaction time.
Stress Obtain a detailed history of the manner in which the patient has controlled their physical and mental
stress.
Safety and self-care Assess the level of assistance that is needed by the patient for mobility and for the performance of
activities of daily living (ADLs) and self-care.
Family resources Determine what family resources are available, as well as the closeness of the family, during both daily
and stress-producing events.

• Monitor an recor the patient’s vital signs, espe-
cially bloo pressure, uring the course of therapy.
Report signicant changes in bloo pressure; these
are most likely to occur uring perios of osage
ajustment. Emphasize measures to prevent ortho-
static hypotension.
• Monitor the patient’s bowel function an imple-
ment measures to prevent constipation (e.g., ae-
quate ui intake, bulk in iet, exercise, use of stool
softeners).
• Support the patient’s efforts to remain mobile.
Provie a safe environment by removing clutter an
throw rugs; use correct equipment an supportive
evices.
• Minimize eformities by encouraging the patient to
maintain an erect posture. Maintain joint mobility
with the use of both active an passive range-of-
motion exercises.
• Nutritional nees must be carefully assesse, be-
cause ietary moications will be require as
the isease progresses. Be vigilant for ifculty
with swallowing an realize that the patient may
be prone to the aspiration of foo or water. Weigh
the patient weekly; evaluate an report uctua-
tions in boy weight to the ietitian or healthcare
provier.
• Provie a restful environment an attempt to keep
stressors at a minimum.
• Monitor the patient’s moo an affect an be alert
for signs of epression. Moo alterations an e-
pression are seconary to isease progression (e.g.,
lack of ability to participate in sex, immobility, in-
continence) an may be expecte, but they shoul
not be ignore.
• Provie for patient safety uring ambulation an
prevent falls.
• Stress that the effectiveness of meication therapy
may take several weeks.
pa edua
Nutrition. Teach the patient to rink at least six to eight
glasses of water or ui per ay to maintain aequate
hyration. Because constipation is often a problem, in-
struct the patient to inclue bulk in the iet an to use
stool softeners as neee. As the isease progresses,
the type an consistency of the foos eaten will nee
to be ajuste to meet the iniviual’s nees. Because
of fatigue an ifculty with eating, give assistance
that is appropriate to the patient’s egree of impair-
ment. Do not rush the iniviual when they are eating,
an cut foos into bite-size pieces. Teach swallow-
ing techniques to prevent aspiration. Plan six smaller
meals aily rather than three larger meals.
Instruct the patient to weigh himself or herself week-
ly. Ask the patient to state the guielines for weight
loss or gain that shoul be reporte to the healthcare
provier.
Stress that vitamins shoul not be taken unless
they have been prescribe by the healthcare provier.
Pyrioxine (vitamin B6) will reuce the therapeutic ef-
fect of levoopa.
Stress management. Explain to the patient an car-
egivers about the importance of maintaining an envi-
ronment that is as free from stress as possible. Explain
that symptoms such as tremors are enhance by
anxiety.
Self-reliance. Encourage patients to perform as many
ADLs as they can. Parkinson isease is a progressive
isorer; explain to caregivers that it is important not
to take over an that they shoul encourage patients’
self-maintenance, continue social involvement, an
participation in activities such as hobbies. Use aap-
tive evices to help the patient with ressing, an pur-
chase clothing with easy closures or fasteners such as
Velcro. As mobility iminishes, use a bath chair an
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14
hanhel shower nozzle to help the patient maintain
their cleanliness.
Exercise. Instruct the patient an caregiver about the
importance of maintaining correct boy alignment,
walking as erect as possible, an practicing the gait
training taught by the physical therapy epartment.
Gait training is essential if the patient is to elay the
onset of shufing an gait propulsion. Patients shoul
wear stury, supportive shoes an use a cane, walker,
or other assistive evice to maintain mobility. Exercises
to maintain the strength of facial muscles an of the
tongue help the patient to maintain speech clarity an
the ability to swallow. Active an passive range-of-
motion exercises of all joints help minimize eformi-
ties. Explain that maintaining the exercise program can
increase the patient’s long-term well-being.
Mood alterations. Explain to the patient an the
caregiver that epression an moo alterations are
seconary to isease progression (e.g., inability to
participate in sex, immobility, incontinence) an are
to be expecte. Changes in mental outlook shoul be
iscusse with the healthcare provier.
Fostering health maintenance. Provie the patient
an their signicant others with important informa-
tion containe in the specic rug monographs for the
meicines that are prescribe, incluing the name of
the meication; its osage, route, an aministration
time; potential averse effects; an rug-specic pa-
tient eucation.
Provie information to the patient, family, an
caregivers about resources, incluing the American
Parkinson Disease Association an the services an in-
formation available from this source. There are support
groups for patients an families that can serve as caring
environments for people with similar experiences an
concerns. Respite care may also be available, which pro-
vies temporary services to the epenent oler ault
either at home or in an institutional setting to give the
family relief from the emans of aily patient care.
Patient self-assessment. Enlist the patient’s help
with eveloping an maintaining a written recor of
monitoring parameters (e.g., egree of tremor relief,
stability, changes in mobility an rigiity, seation,
constipation, rowsiness, mental alertness, evia-
tions from the norm); see the Patient Self-Assessment
Form for Antiparkinson Agents on the Evolve website.
Complete the Premeication Data column for use as a
baseline to track the patient’s response to rug thera-
py. Ensure that the patient unerstans how to use the
form, an instruct the patient to bring the complete
form to follow-up visits. During follow-up visits, focus
on issues that will foster aherence with the therapeu-
tic interventions that have been prescribe.
209
Drug Class: MonoaMine oxiDase Type B
inhiBiTors
aa (ra-SA-ji-leen)
Az (az-a-LECt)
aad (sa-FIN-a-mide)
Xada (Ex-a-da-go)
 (se-LE-ji-leen)
Zaa (zel-ah-par)
A
Selegiline, sanamie, an rasagiline are potent
MAO-B inhibitors that reuce the metabolism of o-
pamine in the brain, thus allowing for greater opa-
minergic activity. Although there are reports that these
agents may be neuroprotective, there is currently no
conclusive proof of this from clinical trials.
U
A combination of carbiopa an levoopa is the current
rug of choice for the treatment of Parkinson isease.
Unfortunately, these agents lose effectiveness (i.e., the
“on-off” phenomenon) an evelop more averse ef-
fects (i.e., yskinesias) over time. It is often necessary
to a other opamine receptor agonists (e.g., prami-
pexole, ropinirole) or a COMT inhibitor (e.g., entaca-
pone) to improve the patient’s response an tolerance.
The MAO-B inhibitors have ajunctive activity similar
to carbiopa-levoopa for the treatment of Parkinson
isease.
The MAO-B inhibitors may be use early uring
the treatment of Parkinson isease to slow the pro-
gression of symptoms an to elay the initiation of
levoopa therapy. In aition, they prolong the ac-
tion of carbiopa-levoopa, thus making the MAO-B
inhibitors useful a-on therapies to ecrease motor
uctuations (e.g., on-off perios) in patients treate
with carbiopa-levoopa. Selegiline aministere by
a transermal patch is also approve for the treat-
ment of epression.
Selegiline, rasagiline, an sanamie have if-
ferent metabolic pathways an therefore somewhat
ifferent averse effect proles. Selegiline tablets
an capsules, when swallowe, are metabolize to
amphetamines that cause cariovascular an psychi-
atric averse effects. The orally isintegrating tablet
osage form allows the rug to be absorbe from the
buccal area in the mouth, thereby avoiing much of
the formation of these active metabolites. There is
a notable ifference in strength between the tablets
an the orally isintegrating tablets. A 10-mg tablet
of selegiline is approximately equal in potency to a
1.25-mg orally isintegrating tablet of selegiline.
Rasagiline an sanamie are not metabolize to
amphetamines, so cariovascular an psychiatric a-
verse effects are minimal.
210 UNIT III Drugs Affecting the Autonomic and Central Nervous System

tau ou immeiately place the orally isintegrating selegiline

The primary therapeutic outcomes sought from
MAO-B inhibitors for the treatment of parkinsonism
are as follows:
1. Slowing the evelopment of symptoms an the pro-
gression of the isease
2. Establishing a balance of opamine an acetylcho-
line in the basal ganglia of the brain by enhancing
the elivery of opamine to brain cells
tablets on top of the tongue, where they will isinte-
grate in secons. Patients shoul avoi ingesting foo
or liquis for 5 minutes before an 5 minutes after tak-
ing orally isintegrating selegiline tablets.
After 2 to 3 ays of treatment, the osage of carbiopa-
levoopa shoul start being titrate ownwar.
Carbiopa-levoopa osages may be able to be re-
uce by 10% to 30%.

nu ia  ma oxda t
B ib ta
Premedication assessment
1. Perform a baseline assessment of parkinsonism
with the use of the UPDRS.
2. Obtain a history of gastrointestinal (GI) symptoms.
3. Perform a baseline assessment of the patient’s e-
gree of alertness an orientation to name, place, an
time before the initiation of therapy.
4. Check for any antihypertensive therapy that is cur-
rently prescribe. Monitor the patient’s bloo pres-
sure aily in both the supine an staning positions.
If antihypertensive meications are being taken, re-
port this to the healthcare provier for possible os-
age ajustment.
5. Check other meications prescribe; see Drug
Interactions for MAO-B inhibitors later in this
section.
Availability, dosage, and administration. The osage
must be ajuste accoring to the patient’s response
an tolerance.
Adult: PO (Table 14.2). Selegiline orally isinte-
grating tablets shoul be taken in the morning before
breakfast, without liqui. Patients shoul not attempt
to push selegiline orally isintegrating tablets through
the foil backing. Patients shoul peel back the back-
ing off one or two blisters (as prescribe) with ry
hans an gently remove the tablets. Patients shoul
Common adverse effects. Selegiline, sanamie, an
rasagiline cause relatively few averse effects. They
may increase the averse opaminergic effects of levo-
opa (e.g., chorea, confusion, hallucinations). Dosage
reuction of levoopa is usually the optimal treatment.
gttt
Constipation, stomach upset. Both of these effects may
be minimize by a temporary reuction in osage, a-
ministration with foo, an the use of stool softeners
for constipation.
Serious adverse effects
nc
Chorea, confusion, hallucinations. Selegiline, sana-
mie, an rasagiline may increase these averse
opaminergic effects of levoopa, but these can be
controlle by reucing the osage of levoopa. Make
regularly scheule subsequent evaluations of the
patient’s mental status an compare nings. Report
alterations in moo. Provie patient safety, be emo-
tionally supportive, an assure the patient that these
averse effects usually issipate as tolerance evelops
over the next few weeks.
Cdc
Orthostatic hypotension. Monitor the patient’s bloo
pressure aily in both the supine an staning posi-
tions. Anticipate the evelopment of postural hypo-
tension an take measures to prevent such an occur-
rence. Teach the patient to rise slowly from a supine or

Table 14.2 Monoamine Oxidase Inhibitors Type B

generiC naMe BranD naMe availaBiliTy iniTial Dosage (po) MaxiMuM Daily Dosage
rasagiline Azilect Tablets: 0.5, 1 mg Monotherapy: 1 mg once daily 1 mg
Do not confuse rasagiline Adjunctive therapy: 0.5 mg once 1 mg
with repaglinide, daily
raloxifene, Risperdal, or
risperidone.
sanamide Xadago Tablets: 50, 100 mg 50 mg once daily After 2 wk may
increase to 100 mg
once daily
selegiline Tablets: 5 mg 5 mg daily 5 mg twice daily
Do not confuse selegiline Zelapar Tablets, orally 1.25 mg once daily for at least 2.5 mg before
with Serentil, sertraline, or disintegrating: 6 wk with concomitant breakfast, at least
Salagen. 1.25 mg levodopa/carbidopa dissolved 5 min before any
on the tongue; withhold food liquid or breakfast
and liquid for at least 5 min
Do not confuse.
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14
sitting position an encourage the patient to sit or lie
own if feeling faint.
Drug interactions
ld. MAO-B inhibitors an levoopa have
aitive neurologic effects. These interactions may be
benecial because they often allow for a reuction in
the osage of levoopa.
Md, tmd, mtd. Fatal rug interac-
tions have been reporte between monoamine oxiase
inhibitors (MAOIs) an these agents. Although these
interactions have not been reporte with selegiline,
sanamie, or rasagiline, it is recommene that sele-
giline, sanamie, an rasagiline not be aministere
with any of these agents.
Dtmt. Episoes of psychosis an bi-
zarre behavior have been reporte with selegiline an
extromethorphan. Do not aminister these rugs
concurrently.
Fd. Patients shoul avoi foos an beverages
with high tyramine content (e.g., Chianti wine, fava
beans, cheeses), particularly if they are receiving se-
legiline in excess of 9 mg/ay. Rare cases of hyper-
tensive reactions have been reporte.
att t. A osage ajustment of the
antihypertensive agent is often necessary in response
to excessive orthostatic hypotension.
Cc. This antibiotic inhibits the metabolism
of rasagiline, thus signicantly raising rasagiline se-
rum levels an potentially causing signicant hyper-
tension. Use the combination very cautiously. Reuce
the ose of rasagiline by half to avoi complications.
atdt (tccc tdt, ct -
t tk bt, t- -
tk bt, st. J’ Wt). Use these rugs with
extreme caution in conjunction with MAO-B inhibitor
therapy. Although rare, there is a potential for seroto-
nin synrome, which is manifeste by behavioral an
mental status changes, iaphoresis, muscular rigi-
ity, hypertension, syncope, an eath. Many patients
are receiving antiepressants for the treatment of e-
pression that frequently accompanies parkinsonism.
Closely monitor patients for these symptoms.
smtmmtc m (d, dd,
). Cases of hypertensive crisis have rarely
been reporte among patients who are concurrently
taking sympathomimetic amines an MAO-B inhibi-
tors. Concurrent therapy is not recommene.
Drug Class: DopaMine agonisTs
abda (kăr-bĭ-DŌ-pă) and
vda (lē-vō-DŌ-pă)
s (SĬN-ĕ-mĕt)
Do not confuse Sinemet with Senokot.
ra (rye-TAR-ee)
Dua (do-op-ah)
211
A
Dopamine, when aministere orally, oes not enter
the brain. However, levoopa does cross into the brain,
where it is metabolize to opamine an replaces the
opamine eciency in the basal ganglia. Dopamine
stimulates D1, D2, an D3 opamine receptors.
Carbiopa is an enzyme inhibitor that reuces the
metabolism of levoopa, thus allowing for a greater
portion of the aministere levoopa to reach the e-
sire receptor sites in the basal ganglia. Carbiopa has
no effect when it is use alone; it must be use in com-
bination with levoopa.
Sinemet an Rytary are combination proucts of car-
biopa an levoopa that are use orally for treating
the symptoms of Parkinson isease. Duopa, an enteral
suspension of carbiopa-levoopa, is use to treat mo-
tor uctuations in patients with avance Parkinson
isease. It is aministere into the jejunum through a
nasojejunal tube or percutaneous enoscopic gastros-
tomy–jejunostomy (PEG-J) tube with a portable infu-
sion pump.
U
About 75% of patients with parkinsonism respon
favorably to levoopa therapy. However, after a few
years the response iminishes an becomes more
uneven, an it is accompanie by many more averse
effects. This loss of therapeutic effect reects the pro-
gression of the unerlying isease process.
Carbiopa is use to reuce the ose of levoopa
require by approximately 75%. When aministere
with levoopa, carbiopa increases plasma levels an
the plasma half-life of levoopa.
tau ou
The primary therapeutic outcome sought from carbiopa-
levoopa for the treatment of parkinsonism is the estab-
lishment of a balance of opamine an acetylcholine in
the basal ganglia of the brain by enhancing the elivery
of opamine to brain cells.
nu ia  cabda-lvda
ta
Premedication assessment
1. Perform a baseline assessment of parkinsonism
with the use of the UPDRS.
2. Obtain a history of GI an cariovascular symp-
toms, incluing baseline vital signs (e.g., bloo
pressure, pulse).
3. Ask specically about any symptoms of hallucina-
tions, nightmares, ementia, or anxiety.
4. All patients shoul be screene for the presence of
close-angle glaucoma before initiating therapy.
Patients with open-angle glaucoma can safely use
levoopa. Do not aminister the meicine to peo-
ple with a history of glaucoma unless it has been
specically approve by the patient’s healthcare
provier.
212 UNIT III Drugs Affecting the Autonomic and Central Nervous System
5. Review the meicines that have been prescribe that
may require ose ajustments. Plan to perform fo-
cuse assessments to etect responses to therapy that
woul nee to be reporte to the healthcare provier.
Availability. PO: Sinemet is a combination prouct that
contains both carbiopa an levoopa. The combina-
tion prouct is available in ratios of 10/100, 25/100,
an 25/250 mg of carbiopa an levoopa, respective-
ly. There is also a sustaine-release tablet that contains
either 25/100 or 50/200 mg of carbiopa an levoo-
pa, respectively.
Rytary is an oral extene-release combination
prouct that contains both carbiopa an levoopa. It
is available in capsules in ratios of 23.75/95, 36.25/145,
48.75/195, an 61.25/245 mg of carbiopa an levoo-
pa, respectively.
Duopa is an enteral suspension of carbiopa 4.63
mg an levoopa 20 mg/mL in 100-mL containers.
Dosage and administration. Adult: PO: For patients
who are not receiving levoopa initially, give Sinemet
10/100 or 25/100 mg three times aily, increasing by
1 tablet every other ay, until a osage of 6 tablets
aily is attaine. As therapy progresses an patients
show inications of neeing more levoopa, substitute
Sinemet 25/250 mg, 1 tablet three or four times aily.
Increase by 1 tablet every other ay to a maximum of
8 tablets aily. See the manufacturer’s guielines for
converting a patient from the immeiate-release to the
sustaine-release formulation of Sinemet.
Aminister this meication with foo or milk to re-
uce gastric irritation. Therapy for at least 6 months
may be necessary to etermine this meication’s full
therapeutic benets.
Extended-Release Formulations: Sinemet Extene-
Release Tablets: For patients not currently receiving
levoopa initially, start with sustaine-release tablet
50 mg/200 mg twice aily at intervals of 6 hours or
more. Following an interval of at least 3 ays between
osage ajustments, increase or ecrease osage base
on response. Most patients are aequately treate with
a ose that provies 400 to 1600 mg of levoopa per
ay in ivie oses at intervals of 4 to 8 hours while
awake. If an interval of less than 4 hours is use an/
or if the ivie oses are not equal, give the smaller
oses at the en of the ay.
Rytary Extene-Release Capsules: For patients not
currently receiving levoopa initially, start with Rytary
23.75/95 mg three times aily for 3 ays; on ay 4, in-
crease to 36.25/145 mg three times aily. The ose may
be increase up to 97.5/390 mg three times aily, an
the frequency of osing may be increase to a maxi-
mum of ve times aily if neee an tolerate (maxi-
mum: 612.5/2450 mg per ay).
See the manufacturer’s guielines for converting
a patient from immeiate-release formulations to ex-
tene-release capsules.
Enteral Formulation: Duopa:
• See the manufacturer’s guielines for calculation an ti-
tration of morning ose an continuous infusion oses.
• Before initiation of therapy, convert patient from
all forms of levoopa to oral immeiate-release
carbiopa-levoopa tablets (1:4 ratio). Total aily
ose of levoopa consists of the morning ose, a
continuous ose an any extra oses.
• See manufacturer’s recommenations on frozen
storage, thawing in a refrigerator for 96 hours, pro-
tection from light, aministration by nasojejunal
tube or PEG-J tube an type of pump to be use.
• Following iscontinuation of the aily infusion, pa-
tients shoul receive their routine nighttime osage
or oral immeiate release carbiopa-levoopa.
Common adverse effects. Levoopa causes many a-
verse effects, but most are ose relate an reversible.
Averse effects vary greatly epening on the stage of
the isease.
gttt
Nausea, vomiting, anorexia. These effects can be re-
uce by slowly increasing the ose, iviing the total
aily osage into four to six oses, an aministering
the meication with foo or antacis. See manufactur-
er’s precautions pertaining to potential GI complica-
tions associate with enteral infusions.
Cdc
Orthostatic hypotension. Although the effects are
generally mil, levoopa may cause some egree of
orthostatic hypotension; this is manifeste by iz-
ziness an weakness, particularly when therapy
is initiate. Tolerance usually evelops after a few
weeks of therapy. Monitor the patient’s bloo pres-
sure aily in both the supine an staning positions.
Anticipate the evelopment of postural hypotension
an take measures to prevent such an occurrence.
Teach patients to rise slowly from a supine or sitting
position, an encourage them to sit or lie own if
feeling faint.
Serious adverse effects
nc
Chewing motions, bobbing, facial grimacing, rocking move-
ments. These involuntary movements occur in about
half of the patients who take levoopa for more than 6
months. A reuction in osage may be benecial.
pcc
Nightmares, depression, confusion, hallucina-
tions. Perform a baseline assessment of the patient’s
egree of alertness an orientation to name, place, an
time before initiating therapy. Make regularly sche-
ule subsequent evaluations of mental status, an
compare nings. Report alterations in moo. Provie
for patient safety uring these episoes. Reucing the
aily osage may control these averse effects.
Cdc
Tachycardia, palpitations. Take the patient’s pulse at
regularly scheule intervals. Report any changes for
further evaluation.
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14
Drug interactions. Sinemet an Rytary may be use to
treat parkinsonism in conjunction with opamine ago-
nists, COMT inhibitors, or anticholinergic agents. The
osages of all meications may nee to be reuce as
a result of combine therapy.
Mm d bt (z, tc-
m, cbzd, ). These MAOIs un-
preictably exaggerate the effects of levoopa. They
shoul be iscontinue at least 14 ays before the a-
ministration of levoopa.
izd. Use this rug with caution in conjunction
with levoopa. Discontinue isoniazi if patients who
are taking levoopa evelop hypertension, ushing,
palpitations, an tremor.
pd. Pyrioxine (vitamin B6) in oral oses of
5 to 10 mg may reuce the therapeutic an toxic ef-
fects of levoopa. Normal iets contain less than 1 mg
of pyrioxine, so ietary restrictions are not necessary.
However, the ingreients of multiple vitamins shoul
be consiere.
Dzm, cdzd, cd, t. These
agents appear to cause a eterioration of the therapeu-
tic effects of levoopa. Use them with caution for pa-
tients with parkinsonism, an iscontinue them if the
patient’s clinical status eteriorates.
ptz, d, d, mtc-
md. An averse effect associate with these agents is
a Parkinson-like synrome. Because this conition will
nullify the therapeutic effects of levoopa, o not use
the rugs concurrently.
e, mtm. Levoopa may increase
the therapeutic an toxic effects of these agents.
Monitor the patient for tachycaria, ysrhythmias,
an hypertension. Reuce the osage of these agents
if necessary.
att t. A osage ajustment of the
antihypertensive agent is frequently necessary in re-
sponse to excessive orthostatic hypotension.
atcc t (bzt, ddm,
td). Although these agents are use to
treat parkinsonism, they increase gastric eactivation
an ecrease the intestinal absorption of levoopa.
The aministration of oses of anticholinergic agents
an levoopa shoul be separate by 2 hours or more.
Tt bw c. The metabolites of levoopa re-
act with toilet bowl cleaners to turn the urine to shaes
of re to black. This may also occur if the urine is ex-
pose to air for long perios. Inform the patient that
there is no cause for alarm.
aaad dd (a-MAN-ta-dēn)
gv (go-cover-ee)
ox er (oz-MO’-lex ER)
Amantaine is a compoun evelope originally to
treat viral infections. It was aministere to a patient
with inuenza A who also ha parkinsonism. During
213
the course of therapy for inuenza, the patient showe
enite improvement in the parkinsonian symptoms.
A
The exact mechanism of action is unknown but ap-
pears to be unrelate to the rug’s antiviral activity.
Amantaine seems to slow the estruction of opa-
mine, thus making the small amount present more ef-
fective. It may also ai in the release of opamine from
its storage sites. Unfortunately, about half of the pa-
tients who benet from amantaine therapy begin to
notice a reuction in benet after 2 or 3 months. A os-
age increase or temporary iscontinuation followe
by a reinitiation of therapy several weeks later may
restore the therapeutic benets. When being iscontin-
ue, amantaine shoul be graually withrawn.
U
Amantaine is use for the relief of symptoms associ-
ate with Parkinson isease an for the treatment of
susceptible strains of viral inuenza A.
Amantaine is available in extene-release pro-
ucts. Gocovri (amantaine) is inicate for the treat-
ment of yskinesia in patients with Parkinson isease
receiving levoopa-base therapy, with or without con-
comitant opaminergic meications. Osmolex (aman-
taine) ER is inicate for the treatment of Parkinson
isease an for the treatment of rug-inuce extrapy-
ramial reactions in ault patients.
tau ou
The primary therapeutic outcome sought from amanta-
ine in treating parkinsonism is to establish a balance of
opamine an acetylcholine in the basal ganglia of the
brain by enhancing elivery of opamine to brain cells.
nu ia  Aaad ta
Premedication assessment
1. Perform a baseline assessment of parkinsonism us-
ing the UPDRS.
2. Amantaine shoul be use with caution in pa-
tients with a history of seizure activity, liver isease,
uncontrolle psychosis, or congestive heart failure.
Amantaine may cause an exacerbation of these
isorers.
3. Take baseline bloo pressures in supine an stan-
ing positions.
Availability. PO: 100-mg tablets; 100-mg capsules;
50 mg/5 mL syrup; 68.5, 137 mg extene-release
(24 hours) capsules (Gocovri); 129, 193, 258 mg exten-
e-release (24 hours) tablets (Osmolex ER).
Dosage and administration. Adult: PO: Amantaine
tablets, capsules, syrup: Initially 100 mg two times
aily; maximum aily ose is 400 mg. Because of the
possibility of insomnia, plan the last ose to be amin-
istere in the afternoon, not at betime.
214 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Extene-release proucts:
• Gocovri (amantaine) (capsules): Initially 137 mg;
after 1 week, increase to the recommene aily
osage of 274 mg
• Osmolex (amantaine) ER (tablets): Initially 129 mg
orally once aily in the morning; may be increase
in weekly intervals to a maximum aily ose of 322
mg once aily in the morning
Common adverse effects. Most of the averse effects
of amantaine therapy are ose relate an reversible.
nc
Confusion, disorientation, hallucinations, mental depres-
sion. Perform a baseline assessment of the patient’s e-
gree of alertness an orientation to name, place, an time
before initiating therapy. Make regularly scheule sub-
sequent evaluations of mental status an compare n-
ings. Report any alterations to the healthcare provier
Dizziness, lightheadedness. Provie patient safety ur-
ing perios of izziness or lightheaeness.
gttt
Anorexia, nausea, abdominal discomfort. These sie ef-
fects are usually mil an ten to resolve with contin-
ue therapy. Encourage the patient not to iscontinue
therapy without rst consulting the healthcare provier.
Cdc
Livedo reticularis (skin mottling). A ermatologic coni-
tion known as livedo reticularis is occasionally observe
in conjunction with amantaine therapy. It is character-
ize by iffuse rose-colore mottling of the skin, pre-
ominantly in the extremities an is often accompanie
by ankle eema. It is more noticeable when the patient
is staning or expose to col. It is reversible within 2 to
6 weeks after iscontinuation of amantaine. However,
iscontinuing therapy is generally not necessary.
These sie effects are usually mil an ten to re-
solve with continue therapy. Symptoms are enhance
by exposure to the col or by prolonge staning.
Encourage the patient not to iscontinue therapy with-
out rst consulting the healthcare provier.
Serious adverse effects
gttt
Hepatotoxicity. The symptoms of hepatotoxicity are
anorexia, nausea, vomiting, jaunice, hepatomegaly,
splenomegaly, an abnormal liver function tests (el-
evate bilirubin, aspartate aminotransferase [AST],
alanine aminotransferase [ALT], gamma-glutamyl-
transferase [GGT], alkaline phosphatase [ALP], an
prothrombin time [PT]).
nc
Seizure disorders, psychosis. Provie patient safety
uring episoes of izziness; report symptoms for fur-
ther evaluation.
Cdc
Dyspnea/edema. If amantaine is use with patients
who have a history of heart failure, assess lung souns,
aitional eema, an weight gain on a regular basis.
Drug interactions
atcc t (td, bzt, -
ccd, ddm). Amantaine may exacer-
bate the sie effects of anticholinergic agents that may
also be use to control the symptoms of parkinsonism.
Confusion an hallucinations may graually evelop.
The osage of amantaine or the anticholinergic agent
shoul be reuce.
a (ă-pō-MŎR-fēn)
Do not confuse apomorphine with morphine.
A (ă-PŌ-kĭn)
kb (Kin-moby)
A
Apomorphine is a nonergot opamine agonist. It is
thought to stimulate opamine receptors in the brain,
thereby temporarily restoring motor function. It is
chemically relate to morphine, but it oes not have
any opioi activity.
U
As Parkinson isease progresses, patients often expe-
rience episoes of lower responsiveness to levoopa,
which causes perios of hypomobility or off perios
(e.g., inability to rise from a chair, speak, or walk).
Apomorphine is use to treat the hypomobility associ-
ate with the “wearing off” of opamine agonists, ei-
ther near the en of a osage cycle or at unpreictable
times (i.e., the “on-off” phenomenon).
tau ou
The primary therapeutic outcomes sought from apo-
morphine for the treatment of parkinsonism are im-
proving motor an ADL scores an ecreasing off
time.
nu ia  A ta
Premedication assessment
1. Perform a baseline assessment of parkinsonism
with the use of the UPDRS.
2. Obtain a history of cariovascular symptoms, in-
cluing the baseline vital signs (e.g., bloo pressure,
heart rate).
3. Perform a baseline assessment of the patient’s
egree of mobility, alertness, an orientation to
name, place, an time before initiating therapy. Ask
specically whether the patient is taking any other
seating meicines. Make regularly scheule sub-
sequent evaluations of bloo pressure, pulse, men-
tal status, an mobility an compare nings.
Availability. Subcutaneous: 10 mg/mL in 3-mL cartrig-
es. Sublingual lm: 10 mg, 15 mg, 20 mg, 25 mg, 30 mg.
Dosage and administration. Apomorphine is aminis-
tere by a sublingual lm or with the use of a manual,
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14
reusable, multiose injector pen that hols a 3-mL car-
trige of meicine. To avoi potential confusion with
the use of the pen an inavertent overose, it is rec-
ommene that the ose of the rug be ientie in
milliliters rather than in milligrams. The pen is ajust-
able in 0.02-mL increments. A training pamphlet that
aresses the use of the injector pen is available for
patient use.
Medication Safety Alert
Do not administer apomorphine intravenously. This drug may
crystallize in the vein and form a thrombus or embolism.
adt
Use of an antiemetic. One of the pharmacologic actions
of apomorphine is emesis. The antiemetic trimethoben-
zamie shoul be aministere orally at a osage
of 300 mg three times aily for at least 3 ays before
the initial ose of apomorphine. Trimethobenzamie
shoul be continue as necessary to control nausea
an vomiting, but generally no longer than 2 months.
About 50% of patients are able to iscontinue the an-
tiemetic while continuing therapy with apomorphine.
Do not use prochlorperazine or onansetron (Zofran)
as antiemetics (see Drug Interactions for apomorphine
later in this section).
Subcutaneous: Initially, a test ose of 0.2 mL (2 mg)
shoul be aministere in the stomach area, upper leg,
or upper arm. Both supine an staning bloo pres-
sures shoul be etermine before aministering the
ose an again at 20, 40, an 60 minutes after aminis-
tration. If signicant orthostatic hypotension evelops,
therapy shoul be iscontinue an the patient shoul
receive no further oses of apomorphine.
If the patient tolerates the 0.2-mL ose an re-
spons, the starting ose shoul be 0.2 mL use on an
as-neee basis to treat off times. If neee, the ose
can be increase in 0.1-mL (1-mg) increments every
few ays on an outpatient basis. The maximum recom-
mene ose is 0.6 mL (6 mg).
If a patient iscontinues therapy for longer than 1
week an then wishes to go back to the use of apo-
morphine, therapy shoul be reinitiate at the start-
ing ose of 0.2 mL, with graual increases in osage to
optimal therapy.
Sublingual lm: Initial ose is 10 mg aministere
sublingually, in a setting where a healthcare provier
can monitor bloo pressure an pulse rate. If the patient
tolerates the 10 mg ose, an respons aequately, the
starting ose shoul be 10 mg, use on an as-neee
basis, up to ve times per ay, to treat “off” episoes.
The ose may be increase by 5 mg, if the response is
insufcient. The maximum single ose is 30 mg.
Common adverse effects. Most averse effects ob-
serve with apomorphine are irect extensions of its
pharmacologic properties.
215
gttt
Nausea, vomiting. These effects can be reuce by
premeicating the patient with trimethobenzamie
an then slowly increasing the osage.
Cdc
Orthostatic hypotension. Apomorphine commonly
causes orthostatic hypotension, which is manifeste
by izziness an weakness, particularly when therapy
is initiate. Patients with Parkinson isease are at risk
for falling because of the unerlying postural instabil-
ity associate with the isease; apomorphine may in-
crease the risk of falling by lowering bloo pressure
an altering mobility. Anticipate the evelopment of
postural hypotension an provie assistance when
necessary. Monitor the patient’s bloo pressure before
an uring apomorphine therapy in both the supine
an staning positions. Teach patients to rise slowly
from a supine or sitting position; encourage them to sit
or lie own if feeling faint.
Serious adverse effects
nc
Chewing motions, bobbing, facial grimacing, rocking move-
ments. These involuntary movements (yskinesias)
occur in some patients, especially if they are also tak-
ing levoopa. A reuction in the osage of the levo-
opa or apomorphine may be benecial.
Sudden sleep events. Sleep episoes have been re-
porte with the opamine agonists (e.g., apomorphine,
pergolie, pramipexole, ropinirole). These episoes
are escribe as “sleep attacks” or “sleep episoes,”
an they inclue aytime sleep. Some sleep events
have been reporte as suen an irresistible; other
sleep events have been precee by sufcient warn-
ing to prevent accients. Patients who are taking o-
pamine agonists shoul be informe about the possi-
bility of aytime sleepiness an outright sleep attacks
with these meicines an allowe to make their own
ecisions about riving on the basis of their past expe-
riences with the meicines. The assessment of patients
who are at risk for sleep attacks is possible with the
Epworth Sleepiness Scale.
pcc
Nightmares, depression, confusion, hallucinations. Perform
a baseline assessment of the patient’s egree of alertness
an orientation to name, place, an time before initiat-
ing therapy. Make regularly scheule subsequent eval-
uations of mental status, an compare nings. Report
alterations in moo. Provie for patient safety uring
these episoes. Reucing the aily meication osage
may control these averse effects.
Cdc
Tachycardia, palpitations. Take the patient’s pulse at
regularly scheule intervals. Report any changes for
further evaluation.
gt
Penile erection, priapism. Apomorphine may cause
penile erection an, rarely, priapism (i.e., prolonge,
216 UNIT III Drugs Affecting the Autonomic and Central Nervous System
painful erection). Apomorphine has been overuse
because of its ability to inuce erection an increase
libio. Inications of abuse inclue frequent erections,
atypical sexual behavior, heightene libio, yskine-
sias, agitation, confusion, an epression.
Drug interactions
st tt (dt, dt, -
t, t, t). The use of serotonin
antagonists with apomorphine is contrainicate.
Profoun hypotension an loss of consciousness have
been reporte.
ptz, cd cz, bt-
 (.., d), tt, mtc-
md. These meicines are opamine antagonists.
They will block the opaminergic effect of apomor-
phine, thereby aggravating parkinsonian symptoms.
et, tt t, dt (.., -
tt). The use of these agents concurrently with
apomorphine signicantly increases the frequency of
orthostatic hypotension. Alcohol shoul be avoie
when taking apomorphine. Dosage ajustment of the
antihypertensive agent is often necessary because of
excessive orthostatic hypotension.
ax (pră-mĭ-PĔKS-ŏl)
max (MĬR-ă-pĕks)
max er
Do not confuse Mirapex with MiraLAX.
A
Pramipexole is a nonergot opamine agonist that stim-
ulates D2 an D3 opamine receptors.
U
Pramipexole may be use alone to manage the early
signs an symptoms of parkinsonism by improving
ADLs an motor manifestations such as tremor, rigi-
ity, braykinesia, an postural stability. It may also be
use in combination with levoopa for avance par-
kinsonism to manage similar signs an symptoms of
the isease.
tau ou
The primary therapeutic outcomes sought from prami-
pexole for the treatment of parkinsonism are as follows:
1. Improve motor an ADL scores
2. Decrease off time
3. Reuce osage of levoopa
nu ia  pax ta
Premedication assessment
1. Perform a baseline assessment of parkinsonism
with the use of the UPDRS.
2. Obtain a history of GI an cariovascular symp-
toms, incluing baseline vital signs (e.g., bloo
pressure, pulse).
3. Ask specically about any symptoms of hallucina-
tions, nightmares, ementia, or anxiety.
Availability. PO: tablets: 0.125, 0.25, 0.5, 0.75, 1, an 1.5
mg; tablets, extene release (24 hours): 0.375, 0.75,
1.5, 2.25, 3, 3.75, an 4.5 mg.
Dosage and administration. Adult: PO:
NOTE: Dosage ajustment is require for patients
with a serum creatinine clearance of 30 mL/min or
lower. See manufacturer’s recommenations.
Immeiate-release tablets: Initially, give 0.125 mg
three times aily for 1 week. If tolerate, increase the
osage to 0.25 mg three times aily the secon week.
If tolerate, increase by increments of 0.25 mg three
times aily through the seventh week. The usual
maintenance osage is 0.5 to 1.5 mg three times aily,
with or without levoopa therapy. When pramipex-
ole is use with levoopa, consier reucing the le-
voopa ose.
Extene-release tablets: Initially, 0.375 mg orally
once a ay. Increase graually no more than every 5
to 7 ays. The rst ose increase shoul be to 0.75 mg
once aily, followe by incremental increases of 0.75
mg; assess therapeutic response an tolerability at a
minimum of 5 ays after each ose increase.
Aminister meication with foo or milk to reuce
gastric irritation.
If pramipexole is to be iscontinue, the osage
shoul be graually reuce over 1 week.
Common adverse effects. Pramipexole causes many
averse effects, but most are ose relate an are re-
versible. Averse effects vary greatly epening on
the stage of the isease an the concurrent use of other
meicines.
gttt
Nausea, vomiting, anorexia. These effects can be re-
uce by slowly increasing the osage, iviing the
total aily ose into three oses, an aministering the
meication with foo.
Cdc
Orthostatic hypotension. Although it is generally mil,
pramipexole may cause some egree of orthostatic
hypotension; this is manifeste by izziness an
weakness, particularly when therapy is being initi-
ate. Tolerance usually evelops after a few weeks of
therapy. Monitor the patient’s bloo pressure aily in
both the supine an staning positions. Anticipate the
evelopment of postural hypotension an take meas-
ures to prevent such an occurrence. Teach patients to
rise slowly from a supine or sitting position, an en-
courage them to sit or lie own if feeling faint.
Serious adverse effects
nc
Chewing motions, bobbing, facial grimacing, rocking move-
ments. These involuntary movements occur in some
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14
patients, especially if they are also taking levoopa. A
reuction in osage of the levoopa may be benecial.
Sudden sleep events. Sleep episoes have been re-
porte with the opamine agonists (e.g., pramipexole,
ropinirole). These episoes are escribe as “sleep
attacks” or “sleep episoes,” an they inclue ay-
time sleep. Some sleep events have been reporte as
suen an irresistible; other sleep events have been
precee by sufcient warning to prevent accients.
Patients who are taking opamine agonists shoul be
informe about the possibility of aytime sleepiness
an outright sleep attacks with these meicines an
be allowe to make their own ecisions about riving
on the basis of their past experiences with the mei-
cines. The assessment of patients who are at risk for
sleep attacks is possible with the Epworth Sleepiness
Scale.
pcc
Nightmares, depression, confusion, hallucinations.
Perform a baseline assessment of the patient’s egree
of alertness an orientation to name, place, an time
before initiating therapy. Make regularly scheule
subsequent evaluations of mental status, an compare
nings. Report alterations in moo. Provie for pa-
tient safety uring these episoes. Reucing the aily
osage may control these averse effects.
Impulse control/compulsive behaviors. While taking
pramipexole an other opamine agonists, patients
can experience an intense urge to gamble, increase
sexual urge, an intense urge to spen money uncon-
trollably, binge eating, an/or other intense urges with
the inability to control these urges. Patients may not
recognize these behaviors as abnormal. It is important
to notify healthcare proviers about the evelopment
of impulsive behaviors.
Cdc
Tachycardia, palpitations. Take the pulse at regularly
scheule intervals. Report any changes for further
evaluation.
Drug interactions
Cmtd, dtzm, m, qd, tm-
t. These agents inhibit the urinary excretion of
pramipexole. A ose reuction of pramipexole is often
require to prevent toxic effects.
Dm tt. Dopamine antagonists in-
clue phenothiazines, butyrophenones, thioxanthenes,
an metoclopramie. As opamine antagonists, these
agents will iminish the effectiveness of pramipexole,
which is a opaminergic agonist.
att t. A osage ajustment of the
antihypertensive agent is often necessary in response
to excessive orthostatic hypotension.
 (rō-PĬN-ĭ-rŏl)
Do not confuse ropinirole with raloxifene or
risperidone.
217
A
Ropinirole is a nonergot opamine agonist that stimu-
lates D2 an D3 opamine receptors.
U
Ropinirole may be use alone to manage the early
signs an symptoms of parkinsonism by improving
ADLs an motor manifestations such as tremor, rigi-
ity, braykinesia, an postural stability. It may also be
use in combination with levoopa for avance par-
kinsonism to manage similar signs an symptoms of
the isease an to reuce the egree of “on-off” uc-
tuations that are often associate with the long-term
use of levoopa.
tau ou
The primary therapeutic outcomes sought from ropini-
role for the treatment of parkinsonism are as follows:
1. Improve motor an ADL scores
2. Decrease off time
3. Reuce osage of levoopa
nu ia  r ta
Premedication assessment
1. Perform a baseline assessment of parkinsonism
with the use of the UPDRS.
2. Obtain a history of GI an cariovascular symp-
toms, incluing baseline vital signs (e.g., bloo
pressure, pulse).
3. Ask specically about any symptoms of hallucina-
tions, nightmares, ementia, or anxiety.
Availability. PO: tablets: 0.25, 0.5, 1, 2, 3, 4, an 5 mg;
tablets, extene release (24 hours): 2, 4, 6, 8, an 12 mg.
Dosage and administration. Adult: PO: Initially, give
0.25 mg three times aily for 1 week. If tolerate, in-
crease to 0.5 mg three times aily the secon week. If
tolerate, increase to 0.75 mg three times aily for the
thir week an then to 1 mg three times aily through
the fourth week. If necessary, the aily osage may
be increase by 1.5 mg/ay on a weekly basis up to
a aily osage of 9 mg/ay. Dosages may be further
ajuste at weekly intervals up to a total osage of 24
mg/ay.
Aminister meication with foo or milk to reuce
gastric irritation.
Extene-release tablet PO: Initially 2 mg once aily
for 1 to 2 weeks, followe by increases of 2 mg/ay
at weekly or longer intervals base on therapeutic re-
sponse an tolerability; there was no aitional benet
shown for oses greater than 8 mg/ay in avance
Parkinson isease or 12 mg/ay in early Parkinson
isease; maximum: 24 mg/ay.
When ropinirole is use with levoopa, consier
reucing the levoopa osage. If ropinirole is to be
iscontinue, the osage shoul be graually reuce
over the course of 1 week.
218 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Common adverse effects. Ropinirole causes many
averse effects, but most are ose relate an are re-
versible. Averse effects vary greatly epening on
the stage of the isease an the concurrent use of other
meicines.
gttt
Nausea, vomiting, anorexia. These effects can be re-
uce by slowly increasing the osage, iviing the
total aily osage into three oses, an aministering
the meication with foo.
Cdc
Orthostatic hypotension. Ropinirole may cause some
egree of orthostatic hypotension, although it is
generally mil; this is manifeste by izziness an
weakness, particularly when therapy is being initi-
ate. Tolerance usually evelops after a few weeks of
therapy.
Monitor the patient’s bloo pressure aily in
both the supine an staning positions. Anticipate
the evelopment of postural hypotension an take
measures to prevent such an occurrence. Teach pa-
tients to rise slowly from a supine or sitting posi-
tion, an encourage them to sit or lie own if feel-
ing faint.
Serious adverse effects
nc
Chewing motions, bobbing, facial grimacing, rocking move-
ments. These involuntary movements occur in some
patients, especially if they are also taking levoopa.
Reucing the osage of levoopa may be benecial.
Sudden sleep events. Sleep episoes have been
reporte with the opamine agonists (e.g., prami-
pexole, ropinirole). These episoes are escribe as
“sleep attacks” or “sleep episoes,” an they inclue
aytime sleep. Some sleep events have been report-
e as suen an irresistible, whereas other sleep
events have been precee by sufcient warning to
prevent accients. Patients who are taking opamine
agonists shoul be informe about the possibility of
aytime sleepiness an outright sleep attacks with
these meicines an be allowe to make their own
ecisions about riving on the basis of their past
experiences with the meicines. The assessment of
patients who are at risk for sleep attacks is possible
with the Epworth Sleepiness Scale.
pcc
Nightmares, depression, confusion, hallucina-
tions. Perform a baseline assessment of the patient’s
egree of alertness an orientation to name, place, an
time before initiating therapy. Make regularly sche-
ule subsequent evaluations of mental status an com-
pare nings. Report alterations in moo. Provie pa-
tient safety uring these episoes. Reucing the aily
osage may control these averse effects.
Impulse control/compulsive behaviors. Patients can ex-
perience an intense urge to gamble, increase sexual
urge, an intense urge to spen money uncontrollably,
binge eating, an/or other intense urges with the ina-
bility to control these urges while taking ropinirole an
other opamine agonists. Patients may not recognize
these behaviors as abnormal. It is important to notify
healthcare proviers about the evelopment of impul-
sive behaviors.
Cdc
Tachycardia, palpitations. Take the pulse at regularly
scheule intervals. Report any changes for further
evaluation.
Drug interactions
Cc. This antibiotic inhibits the metabolism
of ropinirole. A osage reuction of ropinirole is often
require to prevent toxic effects.
et (m t td). Estrogen inhib-
its ropinirole excretion. If estrogen therapy is starte
or stoppe uring treatment with ropinirole, it may be
necessary to ajust the osage of ropinirole.
Dm tt. Dopamine antagonists in-
clue phenothiazines, butyrophenones, thioxanthenes,
an metoclopramie. As opamine antagonists, these
agents will iminish the effectiveness of ropinirole,
which is a opaminergic agonist.
att t. A osage ajustment of the
antihypertensive agent is often necessary in response
to excessive orthostatic hypotension.
 (rō-TĬG-ō-tēen)
nu (new-PRO)
Do not confuse Neupro with Neupogen.
A
Rotigotine is a nonergot opamine agonist with speci-
city for D3, D2, an D1 opamine receptors.
U
Rotigotine is use to manage early-stage an late-stage
Parkinson isease.
tau ou
The primary therapeutic outcomes sought from roti-
gotine for the treatment of parkinsonism are improve
motor an ADL scores.
nu ia  r ta
Premedication assessment
1. Perform a baseline assessment of parkinsonism
with the use of the UPDRS.
2. Obtain a history of GI an cariovascular symp-
toms, incluing baseline vital signs (e.g., bloo
pressure, pulse).
3. Ask specically about any symptoms of hallucina-
tions, nightmares, ementia, or anxiety.
Availability. Transdermal: 1, 2, 3, 4, 6, an 8 mg/24 hr
patch.
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14
Dosage and administration. Adult, early-stage:
Transdermal: Initial: Apply 2 mg/24 hr patch once
aily; may increase by 2 mg/24 hr weekly base on
clinical response an tolerability.
Lowest effective dose: 4 mg/24 hr (manufacturer rec-
ommens a maximum ose of 6 mg/24 hr).
Adult, late-stage: Transdermal: Initial: Apply 4
mg/24 hr patch once aily; may increase by 2 mg/24
hr weekly base on clinical response an tolerability.
Recommended dose: 8 mg/24 hr; in clinical trials max-
imum oses up to 16 mg/24 hr were use.
When rotigotine is use with levoopa, consier
reucing the levoopa osage. If rotigotine is to be
iscontinue, the osage shoul be ecrease by less
than 2 mg/24 hr preferably every other ay until with-
rawal is complete.
Medication Safety Alert
The backing layer of rotigotine contains aluminum. To avoid
skin burns, the patch should be removed prior to magnetic
resonance imaging or cardioversion.
Heat application has been shown to increase absorption
severalfold with other transdermal products. Patients should
be advised to avoid exposing the rotigotine application site
to external sources of direct heat, such as heating pads or
electric blankets, heat lamps, saunas, hot tubs, heated water
beds, and prolonged direct sunlight.
Common adverse effects. Rotigotine causes many
averse effects, but most are ose relate an are re-
versible. Averse effects vary greatly epening on
the stage of the isease an the concurrent use of other
meicines.
gttt
Nausea, vomiting, anorexia. These effects can be re-
uce by slowly increasing the osage.
Cdc
Orthostatic hypotension. Although it is generally
mil, rotigotine may cause some egree of orthos-
tatic hypotension; this is manifeste by izziness an
weakness, particularly when therapy is being initi-
ate. Tolerance usually evelops after a few weeks of
therapy.
Monitor the patient’s bloo pressure aily in
both the supine an staning positions. Anticipate
the evelopment of postural hypotension an take
measures to prevent such an occurrence. Teach pa-
tients to rise slowly from a supine or sitting posi-
tion, an encourage them to sit or lie own if feeling
faint.
sk. Application site reactions may be seen with
rotigotine transermal patches. The signs an symp-
toms of these reactions generally are erythema, eema,
or pruritus limite to the patch area. Daily rotation of
rotigotine application sites has been shown to reuce
the incience. If the patient reports a persistent applica-
tion site reaction (of more than a few ays), reports an
219
increase in severity, or reports a skin reaction sprea-
ing outsie the application site, contact the healthcare
provier.
Serious adverse effects
nc
Chewing motions, bobbing, facial grimacing, rocking
movements. These involuntary movements occur
in some patients, especially if they are also taking
levoopa. Reucing the osage of levoopa may be
benecial.
Sudden sleep events. Sleep episoes have been re-
porte with the opamine agonists. These episoes
are escribe as “sleep attacks” or “sleep episoes,”
an they inclue aytime sleep. Some sleep events
have been reporte as suen an irresistible,
whereas other sleep events have been precee by
sufcient warning to prevent accients. Patients
who are taking opamine agonists shoul be in-
forme about the possibility of aytime sleepiness
an outright sleep attacks with these meicines an
be allowe to make their own ecisions about riv-
ing on the basis of their past experiences with the
meicines. The assessment of patients who are at
risk for sleep attacks is possible with the Epworth
Sleepiness Scale.
pcc
Nightmares, depression, confusion, hallucina-
tions. Perform a baseline assessment of the patient’s
egree of alertness an orientation to name, place, an
time before initiating therapy. Make regularly sche-
ule subsequent evaluations of mental status an com-
pare nings. Report alterations in moo. Provie pa-
tient safety uring these episoes. Reucing the aily
osage may control these averse effects.
Impulse control/compulsive behaviors. Patients can ex-
perience an intense urge to gamble, increase sexual
urge, an intense urge to spen money uncontrollably,
binge eating, an/or other intense urges with the ina-
bility to control these urges while taking rotigotine an
other opamine agonists. Patients may not recognize
these behaviors as abnormal. It is important to notify
healthcare proviers about the evelopment of impul-
sive behaviors.
Cdc
Tachycardia, palpitations. Take the pulse at regularly
scheule intervals. Report any changes for further
evaluation.
Drug interactions
Dm tt. Dopamine antagonists in-
clue phenothiazines, butyrophenones, thioxanthenes,
an metoclopramie. As opamine antagonists, these
agents will iminish the effectiveness of rotigotine,
which is a opaminergic agonist.
att t. A osage ajustment of the
antihypertensive agent is often necessary in response
to excessive orthostatic hypotension.
220 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Drug Class: CaTeChol-o-MeThylTransFerase
inhiBiTors
aa (ĕn-TĂK-ă-pōn)
ca (CŎM-tăn)
aa/vda/abda
sav (stă-LĒ-vō)
a (O-pica-pone)
o (on-jen-tis)
A
Entacapone an opicapone are COMT inhibitors that
reuce the estruction of opamine in the peripheral
tissues, thereby allowing signicantly more opa-
mine to reach the brain to eliminate the symptoms of
parkinsonism.
U
Carbiopa-levoopa is the current rug combination
of choice for the longer-term treatment of Parkinson
isease. Unfortunately, these agents lose effectiveness
(i.e., the “on-off” phenomenon) an result in the evel-
opment of more averse effects (i.e., yskinesias) over
time. Aing entacapone or opicapone inhibits the
metabolism of opamine, which results in more con-
stant opaminergic stimulation in the brain. This stim-
ulation reuces motor uctuations, increases on time,
reuces off time, an often results in a reuction in the
osage of levoopa. Entacapone an opicapone shoul
always be aministere with carbiopa-levoopa.
Entacapone an opicapone have no antiparkinsonian
effect when it is use alone. Stalevo is a combination
prouct that contains levoopa, carbiopa, an enta-
capone. Unlike entacapone, opicapone is aministere
at betime.
tau ou
The primary therapeutic outcomes sought from enta-
capone an opicapone for the treatment of parkinson-
ism are as follows:
1. Reuce motor uctuations
2. Increase on time an reuce off time
3. Reuce total aily osage of carbiopa-levoopa
nu ia  comt ib ta
Premedication assessment
1. Perform a baseline assessment of parkinsonism
with the use of the UPDRS.
2. Obtain a history of bowel patterns an any ongoing
GI symptoms.
3. Perform a baseline assessment of the patient’s e-
gree of alertness an orientation to name, place, an
time before initiating therapy.
4. Check for any antihypertensive therapy that is cur-
rently prescribe. Monitor the patient’s bloo pres-
sure aily in both the supine an staning positions.
If antihypertensive meications are being taken,
report this to the healthcare provier for possible
osage ajustment.
5. Check the patient’s hepatic function before the ini-
tiation of therapy an perioically throughout the
course of aministration.
Availability. PO: Entacapone (Comtan): 200-mg tablets
(o not aminister entacapone without levoopa/car-
biopa; it has no pharmacologic effect of its own).
Stalevo 50: 12.5 mg carbiopa, 50 mg levoopa, an
200 mg entacapone
Stalevo 75: 18.75 mg carbiopa, 75 mg levoopa,
an 200 mg entacapone
Stalevo 100: 25 mg carbiopa, 100 mg levoopa, an
200 mg entacapone
Stalevo 125: 31.25 mg carbiopa, 125 mg levoopa,
an 200 mg entacapone
Stalevo 150: 37.5 mg carbiopa, 150 mg levoopa,
an 200 mg entacapone
Stalevo 200: 50 mg carbiopa, 200 mg levoopa, an
200 mg entacapone
Opicapone: 25 an 50 mg capsules
Dosage and administration. Dosage must be a-
juste in accorance with the patient’s response an
tolerance.
etc. Adult: PO: Initially, start therapy by
aing entacapone to alreay existing levoopa/car-
biopa therapy: give one 200-mg tablet of Comtan
with each carbiopa-levoopa ose to a maximum of
eight times aily (1600 mg of entacapone). The osage
of carbiopa-levoopa will nee to be reuce, par-
ticularly if the levoopa ose is higher than 600 mg/
ay an if the patient has moerate or severe yskine-
sias before the entacapone is starte.
Once the patient has been stabilize on a new com-
bination of entacapone, levoopa, an carbiopa, the
patient may be switche to a Stalevo prouct that most
closely matches the osage of levoopa/carbiopa
an entacapone being taken.
oc. For patients receiving levoopa/carbi-
opa experiencing “off” episoes:
Adult: PO: 50 mg once a ay at betime. Shoul
not eat foo for 1 hour before an for at least 1 hour
after taking opicapone. Patients with moerate he-
patic impairment shoul receive 25 mg once aily
at betime; avoi use in patients with severe hepatic
impairment.
Common adverse effects. Entacapone an opicapone
may increase the averse opaminergic effects of levo-
opa (e.g., chorea, confusion, hallucinations), but these
can be controlle by reucing the osage of levoopa.
gttt. Entacapone may cause the evelop
of iarrhea 1 to 12 weeks after the initiation of thera-
py, especially when higher oses are use. These ef-
fects may be minimize by a temporary reuction in
osage.
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14
Constipation is a common sie effect of opicapone.
nc
Sedative effects. Patients may complain of rowsi-
ness an lethargy, especially uring the initiation of
therapy. People shoul not rive or operate complex
machinery or perform uties for which they must re-
main mentally alert until they have gaine enough ex-
perience with entacapone to know whether it affects
their mental or motor performance.
Patients receiving opicapone may complain of
insomnia.
gt. Urine discoloration.
Patients shoul be avise that entacapone may
change the color of their urine to a brownish orange
but that this is harmless an there is no cause for alarm.
Serious adverse effects
nc
Neurologic effects. Entacapone an opicapone may
increase the averse opaminergic effects of levoopa,
such as hallucinations, psychosis, yskinesia, impulse
control isorer (e.g., pathologic gambling, hypersexu-
ality, spening money), an suen onset of sleep. A
symptom complex resembling neuroleptic malignant
synrome (characterize by elevate temperature,
muscular rigiity, altere consciousness, an auto-
nomic instability), with no other obvious etiology, has
been reporte in association with rapi ose reuctions.
Make regularly scheule subsequent evaluations of
mental status an compare nings. Report alterations
in moo. A reuction of the carbiopa-levoopa osage
may be require to alleviate these effects. Provie for
patient safety, be emotionally supportive, an assure the
patient that these effects usually issipate as tolerance
to the rug evelops over the subsequent few weeks.
Cdc
Orthostatic hypotension. Monitor the patient’s bloo
pressure aily in both the supine an staning
positions. Anticipate the evelopment of postural
hypotension an take measures to prevent such an oc-
currence. Teach the patient to rise slowly from a supine
or sitting position, an encourage the patient to sit or
lie own if feeling faint.
Drug interactions
ld. Entacapone an opicapone an levoopa
have aitive neurologic effects. This interaction may
be benecial because it often allows for a reuction in
the osage of the levoopa.
att t. A osage ajustment of the
antihypertensive agent is often necessary in response
to excessive orthostatic hypotension.
am, t, , 
(t), dm, dbtm. These agents are
metabolize by COMTs. The concurrent aministra-
tion of entacapone an opicapone with these agents
may prolong their uration of activity. Monitor the pa-
tient’s bloo pressure an heart rate.
221
Drug Class: anTiCholinergiC agenTs
A
Parkinsonism is inuce by the imbalance of neu-
rotransmitters in the basal ganglia of the brain. The
primary imbalance appears to be a eciency of opa-
mine, which results in a relative excess of the cholin-
ergic neurotransmitter acetylcholine. Anticholinergic
agents are thus use to reuce the hyperstimulation
that is cause by excessive acetylcholine.
U
The anticholinergic agents reuce the severity of the
tremor an rooling that are associate with parkin-
sonism. Anticholinergic agents are more useful for
patients with minimal symptoms an no cognitive
impairment. Combination therapy with levoopa an
anticholinergic agents is also successful for controlling
symptoms of the isease more completely in about
half of patients who are alreay stabilize on levoopa
therapy. Anticholinergic agents have little effect on ri-
giity, braykinesia, or postural abnormalities. If anti-
cholinergic therapy is to be iscontinue, it shoul be
one so graually to avoi withrawal effects an the
acute exacerbation of parkinsonian symptoms, even
for patients in whom there appears to have been no
clinical response.
tau ou
The primary therapeutic outcome sought from anti-
cholinergic agents for the treatment of parkinsonism is
a reuction in the severity of the tremor an rooling
that are cause by a relative excess of acetylcholine in
the basal ganglia.
nu ia  A A
ta
Premedication assessment
1. Perform a baseline assessment of parkinsonism
with the use of the UPDRS.
2. Obtain baseline ata relate to patterns of urinary
an bowel elimination.
3. Perform a baseline assessment of the patient’s e-
gree of alertness an orientation to name, place, an
time before initiating therapy.
4. Take the patient’s bloo pressure in both the su-
pine an staning positions. Recor the pulse rate,
rhythm, an regularity.
5. All patients shoul be screene for the presence
of close-angle glaucoma before the initiation of
therapy. Anticholinergic agents may precipitate an
acute attack of close-angle glaucoma. Patients with
open-angle glaucoma can safely use anticholinergic
agents. Monitor intraocular pressure regularly.
Availability, dosage, and administration. Adult: PO
(Table 14.3). Aminister meication with foo or milk
to reuce gastric irritation.
222 UNIT III Drugs Affecting the Autonomic and Central Nervous System

Table 14.3 Anticholinergic Agents

iniTial Dosage MaxiMuM Daily
generiC naMe BranD naMe availaBiliTy range (po) Dosage range
benztropine mesylate Cogentin Tablets: 0.5, 1, 2 mg 0.5–1 mg at 6 mg
Do not confuse Injection: 1 mg/mL in 2-mL ampules bedtime
benztropine with
benzonatate.
diphenhydramine Tablets: 25, 50 mg 25–50 mg three PO: 300 mg
hydrochloride Do not confuse Capsules: 25, 50 mg or four times IM/IV: 400 mg
Do not confuse Benadryl Allergy with Elixir: 12.5 mg/5 mL daily
diphenhydramine benazepril. Syrup: 12.5 mg/5 mL
with dicyclomine or Injection : 50 mg/mL in 1-, 10-mL
dipyridamole. vials; 1-mL cartridges
Solution: 6.25 mg/5 mL
trihexyphenidyl PMS-trihexyphenidyl Tablets: 2, 5 mg 1–2 mg daily 12–15 mg
hydrochloride Elixir: 2 mg/5 mL
Available in Canada.
Do not confuse.

Common adverse effects may cause some egree of orthostatic hypotension,

gttt
Constipation; dryness of the mucosa of the mouth, throat,
and nose. These symptoms are the result of the anti-
cholinergic effects that are prouce by these agents.
Patients who are taking these meications shoul be
monitore for the evelopment of these averse ef-
fects. Miler averse effects (e.g., ry mouth) may sub-
sie with continue treatment.
Dryness of the mucosa may be relieve by sucking
har cany or ice chips or by chewing gum. Give stool
softeners as prescribe. Encourage aequate ui in-
take, foos that provie sufcient bulk, an exercise
as tolerate.
gt
Urinary retention. If patients evelop urinary hesi-
tancy, assess them for blaer istention. Report to the
healthcare provier any symptoms of urinary reten-
tion for further evaluation. This symptom is a result
of the anticholinergic effects prouce by these agents.
Patients who are taking these meications shoul be
monitore for the evelopment of this averse effect.
s
Blurred vision. This symptom may subsie with con-
tinue treatment. Provie for patient safety.
Serious adverse effects
pcc
Nightmares, depression, confusion, hallucinations. Make
regularly scheule subsequent evaluations of mental
status an compare nings. Report the evelopment
of alterations in moo. Provie patient safety uring
these episoes. Reucing the aily osage may control
these averse effects.
Cdc
Orthostatic hypotension. Although this conition is in-
frequent an generally mil, all anticholinergic agents
which is manifeste by izziness an weakness, par-
ticularly when therapy is being initiate.
Monitor the patient’s bloo pressure aily in both
the supine an staning positions. Anticipate the e-
velopment of postural hypotension an take measures
to prevent such an occurrence. Teach the patient to rise
slowly from a supine or sitting position an encourage
the patient to sit or lie own if feeling faint.
Palpitations, dysrhythmias. Report any changes for fur-
ther evaluation.
Drug interactions
amtd, tccc tdt, t-
z. These agents may enhance the anticholinergic
averse effects. Confusion an hallucinations are char-
acteristic of excessive anticholinergic activity. A osage
reuction may be require.
ld. Large oses of anticholinergic agents may
slow gastric emptying an inhibit the absorption of
levoopa. An increase in the osage of levoopa may
be require.
alzheimer Disease
Alzheimer disease is a progressive neuroegenerative
isease that affects oler aults. The probability of be-
ing iagnose with Alzheimer isease nearly oubles
every 5 years after age 65. Accoring to the Alzheimer’s
Association, more than 5 million Americans are living
with Alzheimer isease. It is the most common type
of ementia. Other types of ementia are ementia
with Lewy boies, vascular (multiinfarct) ementia,
Parkinson isease ementia, an frontotemporal is-
orers. Patients with Alzheimer isease will evelop
cognitive ysfunction (memory loss), psychiatric an
behavioral problems, an ifculty performing ADLs.
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14
The neuropathology appears to be an accumulation of
amyloi plaques an neurobrillary tangles that cause
neuronal injury. Inclue in this neuronal injury are
cholinergic neurons that are critical in memory, cog-
nition, an other cortical functions. Disturbances in
glutamate neurotransmission have been linke with
the pathophysiologic processes unerlying Alzheimer
isease. Elevate concentrations of glutamate have
been associate with increase sensitivity an/or ac-
tivity of the glutamatergic system, resulting in neuro-
nal ysfunction an cell eath in Alzheimer isease.
Although there is no cure for this isease, meications
can ecrease some of the symptoms by increasing ace-
tylcholine an inhibiting glutamate.
Drug TheraPy for alzheimer
Disease
Drug therapy is focuse on improving cognitive func-
tion. Two classes of rugs are currently use to treat
Alzheimer isease: acetylcholinesterase inhibitors (o-
nepezil, galantamine, rivastigmine) an an N-methyl-
d-aspartate (NDMA) inhibitor (memantine). To ate,
no rugs are available to slow the egenerative process.
nUrsing implicAtions for AlZheimer
DiseAse therApy
Patients start to have ifculty with memory, problem
solving, attention, counting, an language. As the is-
ease progresses, behavioral symptoms of Alzheimer
isease such as wanering, agitation, anxiety, sleep-
lessness, an aggression are manifeste. Families an
caregivers nee to learn effective management of these
behaviors to make patients more comfortable. The
focus of patient care is to maintain mental function,
manage behavioral symptoms, an slow or elay the
symptoms of isease. Be alert for these symptoms of
Alzheimer isease:
• Impaire memory an jugment; often these pa-
tients can no longer rive
• Confusion or isorientation; reirecting an calm-
ing the patient is an effective intervention
• Inability to recognize family or friens; remining
an calming the patient is use
• Aggressive behavior
• Depression; often accompanies anxiety
• Psychoses, incluing paranoia an elusions
• Anxiety
Because this isease is progressive an the patient
will continue to have worsening memory an cogni-
tive function changes, this takes its toll on the caregiver
of the patient. Developing goo coping skills an a
strong support system, as well as utilizing respite care,
can help caregivers hanle the stress of caring for a
love one with Alzheimer isease. Eventually, pa-
tients are care for in a memory care unit, usually a
separate section of a nursing home esigne to care for
Alzheimer isease patients exclusively.
223
A
• Obtain baseline assessments of presenting
symptoms.
• Recor baseline pulse, respirations, an bloo
pressure.
• Assess for an recor any GI symptoms present be-
fore initiation of therapy.
• Assess the patient’s ability to receive an uner-
stan instructions.
Safety and self-care. Caregivers are taught to repeat,
reassure, an reirect the patient with Alzheimer is-
ease as the cognitive ecline progresses. Safety issues
shoul always be a concern. Allowing the patient to be
as inepenent as long as possible is also consiere.
Stress. The patient with Alzheimer isease can be-
come agitate, anxious, an aggressive as the isease
progresses. Recognize the nee for calming reassur-
ance an repeating instructions. The memory loss
leas to confusion an frustration. Continue to reas-
sure an reirect behavior that can be stressful.
Family resources. Help families connect with pro-
grams esigne to teach them about the various stages
of Alzheimer isease an about ways to eal with if-
cult behaviors an other caregiving challenges.
ia
• Implement planne interventions that are consis-
tent with assessment ata, an ientify the inivi-
ual nees of the patient.
• Monitor an recor the patient’s vital signs, espe-
cially bloo pressure, uring the course of therapy.
Report signicant changes in bloo pressure; these
are most likely to occur uring perios of osage
ajustment. Emphasize measures to prevent ortho-
static hypotension.
pa edua
Eucation is focuse on the caregiver with regar to
how to manage the eclining cognitive abilities of
the patient. Caregivers shoul remember the three
Rs—repeat, reassure, an reirect; these are key con-
cepts to keep in min when ealing with patients with
Alzheimer isease. Allow the patient to continue to
perform ADLs as long as possible, an supervise all
househol ADLs such as cooking an cleaning.
Fostering health maintenance
• Throughout the course of treatment, iscuss meica-
tion information an how it will benet the patient.
• Provie the patient an signicant others with
the important information containe in the spe-
cic rug monographs for the rugs prescribe.
Aitional health teaching an nursing interven-
tions for common an serious averse effects will
be foun in each rug monograph.
224 UNIT III Drugs Affecting the Autonomic and Central Nervous System
• Seek cooperation an unerstaning of the fol-
lowing points so that meication compliance is in-
crease: name of meication; osage, routes, an
times of aministration; an common an serious
averse effects.
Patient self-assessment. Enlist the patient’s ai in e-
veloping an maintaining a written recor of monitor-
ing parameters (e.g., bloo pressures, weight, exercise;
see the Patient Self-Assessment Form for anticholinest-
erase inhibitors on the Evolve website). Complete the
Premeication Data column for use as a baseline to track
response to rug therapy. Ensure that the patient uner-
stans how to use the form, an instruct the patient to
bring the complete form to follow-up visits. During
follow-up visits, focus on issues that will foster aher-
ence with the therapeutic interventions prescribe.
Drug Class: aCeTylCholinesTerase
inhiBiTors
dz (dŏn-ĔP-ĭ-zĭl)
A (ĀR-ĭ-sĕpt)
aaa (ga-lanta-mēn)
razad er (raz-ah-dine)
va (riva-STIG-men)
ex (ex-el-on)
A
Donepezil, galantamine, an rivastigmine are acetyl-
cholinesterase inhibitors that allow acetylcholine to ac-
cumulate at cholinergic synapses, causing a prolonge
an exaggerate cholinergic effect.
U
Although the causes are unknown, Alzheimer isease is
characterize by a loss of cholinergic neurons in the cen-
tral nervous system, resulting in memory loss an cog-
nitive ecits (ementia). Donepezil an rivastigmine
(only the patch) are use in patients with mil to severe
ementia to enhance cholinergic function. Galantamine
is use in patients with mil to moerate ementia to
enhance cholinergic function. Their function iminishes
with ongoing loss of cholinergic neurons. Donepezil,
galantamine, an rivastigmine o not prevent or slow
the neuroegeneration cause by Alzheimer isease.
tau ou
The primary therapeutic outcome expecte from
onepezil, galantamine, an rivastigmine therapy
is improve cognitive skills (e.g., wor recall, object
naming, language, wor ning, task performance).
nu ia  Dz, gaaa,
ad rva ta
Premedication assessment
1. Obtain baseline assessments of presenting symptoms.
2. Recor baseline pulse, respirations, an bloo
pressure.
3. Assess for an recor any GI symptoms present be-
fore initiation of therapy.
Availability
Dz. PO: 5-, 10-, an 23-mg tablets; 5- an 10-
mg orally isintegrating tablets.
gtm. PO: 4-, 8-, 12-mg tablets; 4-mg/mL
oral solution; 8-, 16-, 24-mg extene-release 24-hour
capsules.
rtm. Transdermal: 4.6, 9.5, an 13.3 mg/24
hr patch.
Dosage and administration
Dz. PO: Initial osage is 5 mg aily at be-
time. After 4 to 6 weeks of therapy, osage may be
increase to 10 mg aily to assess therapeutic ben-
et. After 3 months, ose may be increase to 23 mg
in moerate to severe Alzheimer isease. Donepezil
may be taken with or without foo. The orally isin-
tegrating tablets may be helpful for patients who have
ifculty swallowing. Allow tablets to issolve on the
tongue an follow with a glass of water.
gtm. Adult: PO: Immeiate release initial
osage 4 mg twice a ay. After a minimum of 4 weeks,
osage may be increase to 8 mg twice a ay. Then,
after 4 weeks, ose shoul be increase to 12 mg twice
a ay.
Adult: PO: Extene release initial osage 8 mg
once aily. After a minimum of 4 weeks, osage may
be increase to 16 mg once a ay. Then after 4 weeks
ose shoul be increase to 24 mg once a ay.
rtm. Transdermal: Initial: Apply 4.6
mg/24 hr patch once aily; if well tolerate, ose
may be titrate (no sooner than every 4 weeks) to 9.5
mg/24 hr (continue as long as therapeutically ben-
ecial), an then to 13.3 mg/24 hr patch (maximum
ose).
Recommended effective dose: Apply 9.5 mg/24 hr or
13.3 mg/24 hr patch once aily; remove ol patch an
replace with a new patch every 24 hours.
Common adverse effects
gttt
Nausea, vomiting, dyspepsia, diarrhea. These are natu-
ral extensions of the pharmacologic effects of cho-
linergic agents. The osage may nee to be reuce
if the patient has ifculty with these averse ef-
fects. Symptoms are less common with lower oses
an ten to subsie after 2 to 3 weeks of therapy.
Graually increasing the ose may help avoi these
complications.
Serious adverse effects
Cdc
Bradycardia. Cholinergic agents cause a slowing of
the heart. These agents may enhance the braycariac
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14
effects of beta blockers. Notify the healthcare provier
if the heart rate is regularly less than 60 beats/min.
Drug interactions
atcc t. As a cholinergic agent, one-
pezil has the potential to reuce the activity of anti-
cholinergic agents (e.g., benztropine, iphenhyramine,
orphenarine, procycliine, trihexypheniyl).
sccc-t mc t, cc
t. As a cholinesterase inhibitor, onepezil is like-
ly to exaggerate the actions of the epolarizing muscle
relaxant (succinylcholine) uring anesthesia an en-
hance the pharmacologic activity of cholinergic agents
such as bethanechol.
Drug Class: nMDa reCepTor inhiBiTor
a (MĔM-ăn-tēn)
nada Xl (năm-ĔN-dă)
A
Memantine is an inhibitor of the NMDA receptor, a
type of glutamate receptor.
U
Although the causes are unknown, one of the neuro-
chemical characteristics of Alzheimer isease is per-
sistent activation of NMDA receptors in the central
nervous system. Memantine blocks these receptors
an is use alone or in combination with an acetyl-
cholinesterase inhibitor for the treatment of ementia
associate with moerate to severe Alzheimer isease.
Patients taking memantine show improvement in cog-
nitive function an behavioral symptoms an a slower
ecline in ADLs, but memantine oes not prevent or
slow the neuroegeneration of Alzheimer isease.
tau ou
The primary therapeutic outcome expecte from me-
mantine therapy is improve cognitive skills (e.g.,
wor recall, object naming, language, wor ning,
task performance).
nu ia  ma ta
Premedication assessment
1. Obtain baseline assessments of presenting
symptoms.
225
2. Recor baseline pulse, respirations, an bloo
pressure.
Availability. PO: 5- an 10-mg tablets; 7-, 14-, 21-, an
28-mg capsules, extene release (24 hours); 2 mg/mL
in 240 an 360-mL oral solution; 10 mg/5 mL in 5 mL
cup.
Dosage and administration. Adult: PO: 5 mg once ai-
ly. The ose shoul be increase in 5-mg increments to
10, 15, an 20 mg aily. The minimal interval between
ose increases is 1 week. Memantine can be taken with
or without foo.
The recommene starting ose of extene release
memantine is 7 mg once aily. The ose shoul be in-
crease in 7 mg increments to the recommene main-
tenance ose of 28 mg once aily. The minimum rec-
ommene interval between ose increases is 1 week.
Conversion: Patients taking 10-mg immeiate-
release tablets twice aily may switch to a 28-mg
extene-release capsule once aily the ay after the
last ose of a 10-mg immeiate-release tablet.
Reduction in dose for renal impairment: A target
ose of 10 mg/ay for the immeiate-release form
an 14 mg/ay for the extene-release form is rec-
ommene in patients with severe renal impairment
(creatinine clearance of 5 to 29 mL/min, base on the
Cockcroft-Gault equation).
Common and serious adverse effects
nc
Headache, dizziness, akathisia, insomnia, restlessness, in-
creased motor activity, excitement, agitation. Many of these
symptoms ecline with continue therapy an can be
reuce with a longer osage titration. Dosage may
nee to be reuce if the patient has ifculty with
these averse effects.
Drug interactions
actzmd, dm bcbt. Meicines that al-
kalinize the pH of the urine will reuce excretion of
memantine. Severe meical conitions such as renal
tubular aciosis an severe urinary tract infections
also may cause alkalization of the urine, with potential
toxicity of memantine.
226 UNIT III Drugs Affecting the Autonomic and Central Nervous System

ca Jud ad nx-ga ncleX ® exaa-s Qu

K pt
• Parkinson disease is a progressive neurologic disorder
that is caused by the deterioration of dopamine-producing
cells in the portion of the brain that is responsible for
the maintenance of posture and muscle tone and the
regulation of voluntary smooth muscle.
• Normally, a balance exists between dopamine, which is an
inhibitory neurotransmitter, and acetylcholine, which is an
excitatory neurotransmitter. The symptoms associated with
Parkinson disease develop because of a relative excess of
acetylcholine in the brain.
• The goal of treatment is to restore dopamine
neurotransmitter function to as close to normal as possible
and to relieve the symptoms that are caused by excessive
acetylcholine.
• Therapy must be individualized, but selegiline therapy is
often started rst to slow the development of symptoms.
As selegiline becomes less effective, levodopa is started,
with or without selegiline.
• Dopamine agonists (e.g., ropinirole, pramipexole) may be
added to directly stimulate dopamine receptors.
• Entacapone may be added to levodopa therapy to reduce
the metabolism of levodopa, thus prolonging its action.
• Anticholinergic agents may be added at any time to reduce
the effects of the “excessive” acetylcholine.
• The nonpharmacologic treatment (e.g., diet, exercise,
physical therapy) of Parkinson disease is equally important
as medication for maintaining the long-term well-being of
the patient.
• Although there is no cure for Alzheimer disease,
acetylcholinesterase inhibitors (donepezil, rivastigmine) and
memantine are used to help improve cognitive skills.
addt l rc
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Clayt
on) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX examination and include both NGN (Next Genera-
tion) and traditional questions. See Chapter 1 for further infor-
mation regarding question types.
1. The nurse suspects that the patient in the scenario is manifesting
early Parkinson disease because of the development of which of
these symptoms? (Select all that apply.)
1. Weakness involving one limb
2. Drooling and having difculty chewing and swallowing
3. Gait alterations causing moderate generalized disability
4. Expressionless facial features
5. Tremors on the ngers of one hand
objct: Identify the signs and symptoms of Parkinson disease.
nClex tm t: Multiple response
Ct k: Application
2. The nurse explained to the patient in the scenario that the symptoms
of Parkinson disease are related to the levels of neurotransmitters
in the brain and used which statement?
1. “Parkinson disease is related to an excess of serotonin
and a deciency of dopamine.”
2. “Parkinson disease is related to an excess of acetylcholine
and a deciency of dopamine.”
3. “Parkinson disease is related to an excess of dopamine
and a deciency of acetylcholine.”
4. “Parkinson disease is related to an excess of epinephrine
and a deciency of acetylcholine.”
objct: Identify the neurotransmitter that is found in excess and
the neurotransmitter that is decient in people with parkinsonism.
nClex tm t: Multiple choice
Ct k: Understanding
3. The patient in the scenario was started on selegiline (Zelapar)
therapy during the early treatment of Parkinson disease because
this drug will have which effect?
1. Reduce excessive acetylcholine
2. Decrease dopamine in the basal ganglia
3. Reduce the metabolism of dopamine
4. Reduce the metabolism of levodopa, thereby making
more available
objct: Explain the action of entacapone, opicapone, and
the monoamine oxidase inhibitors (selegiline, sanamide, and
rasagiline) as it relates to the treatment of Parkinson disease.
nClex tm t: Multiple choice
Ct k: Comprehension
4. Choose the most likely option for the information missing from the
following sentence by selecting from the list of options provided.
The nurse explains to the patient in the scenario that in the future
the healthcare provider may start _________1___________
therapy in addition to _______1___________, which is
part of the drug class __________2______________ and
__________2_____________, respectively.

sc opTion 1 opTion 2

A patient requested an appointment with their healthcare pro- rasagiline •  monoamine oxidase type
vider to discuss the possibility that they were developing Par- B inhibitors
kinson disease, which runs in the family. amantadine hydrochloride •  dopamine agonists
carbidopa-levodopa •  anticholinergic agents

objct: Discuss the action of carbidopa-levodopa and dopamine

agonists in Parkinson disease.
nClex tm t: Cloze
Ct k: Recognize cues
 Drugs Used to Treat Neurodegenerative Disorders CHAPTER 14 227

5. The patient in the scenario was started on selegiline with in the appropriate boxes to identify the therapeutic outcome for
carbidopa-levodopa to slow the progression of symptoms of these drugs.
Parkinson disease. The patient was asked to explain the different
drugs used for this condition. Using the following grid, place an X

sloW The esTaBlish a BalanCe

reDuCe MoTor reDuCe Dosage oF progression oF oF DopaMine anD
FluCTuaTions CarBiDopa-levoDopa The Disease aCeTylCholine
COMT inhibitors (entacapone,
opicapone)
Monoamine oxidase inhibitors
(selegiline, sanamide, and
rasagiline)

objct: Explain the action of entacapone, opicapone, and 7. The nurse is educating the family of an elderly patient on the
the monoamine oxidase inhibitors (selegiline, sanamide, and mechanism of action for donepezil (Aricept). Which statement by
rasagiline) as it relates to the treatment of Parkinson disease. the family indicates that further teaching is needed?
nClex tm t: Matrix 1. “As I understand it, this drug will improve the cognitive
Ct k: Evaluate cues skills of my dad.”
6. The nurse knows that when anticholinergic agents are used, which 2. “So you are saying that this drug is used in patients
of the following symptoms will show improvement? (Select all that with mild to moderate dementia caused by Alzheimer
apply.) disease.”
3. “Are you saying that the enzyme that normally breaks
1. Tremors down acetylcholine is inhibited by this medication?”
2. Drooling 4. “As I understand it, this medication will slow the progress
3. Cognition impairment of the neurodegeneration caused by Alzheimer disease.”
4. Bradykinesia
5. Rigidity objct: Explain the action of the agents used in the treatment of
Alzheimer disease.
objct: Discuss the specic symptoms that should show nClex tm t: Multiple choice
improvement when anticholinergic agents are administered to the Ct k: Comprehension
patient with Parkinson disease.
nClex tm t: Multiple response
Ct k: Application
15 Drugs Used for Anxiety Disorders

https://evolve.elsevier.com/Willihnganz

Objectives
1. Compare and contrast the differences between
generalized anxiety disorder, panic disorder, phobias, and
obsessive-compulsive disorder.
2. Describe the essential components included in a baseline
assessment of a patient’s mental status.
3. Discuss the drug therapy used to treat anxiety disorders.
4. Identify adverse effects that may result from drug therapy
used to treat anxiety.
5. Discuss psychological and physiologic drug dependence.

Key Terms
anxiety (ăng-ZĪ-ĭ-tē) (p. 228)
generalized anxiety disorder (JĔN-
ŭr-ăl-īzd ăng-ZĪ-ĭ-tē dĭs-ŌR-dŭr)
(p. 228)
panic disorder (PĂN-ĭk) (p. 228)
phobias (FŌ-bē-ăz) (p. 229)
obsessive-compulsive and related
disorders (ŏb-SĔS-ĭv kŏm-PŬL-sĭv)
(p. 229)
compulsion (kŏm-PŬL-shŭn) (p. 229)
anxiolytics (ăng-zē-ō-LĬ-tĭks) (p. 229)
tranquilizers (TRĂN-kwĕ-lī-zŭrz)
(p. 229)

ANXIETY DISORDERS
Anxiety is a normal human emotion that is similar to
fear. It is an unpleasant feeling of apprehension or ner-
vousness caused by the perception of potential or actual
danger that threatens a person’s security, whereas fear
is an emotional response to a real or perceived threat.
Mild anxiety is a state of heightened awareness of one’s
surroundings and is seen in response to day-to-day cir-
cumstances. This type of anxiety can be benecial as
a motivator for the individual to take action in a rea-
sonable and adaptive manner. It is sometimes said that
people nd the inner strength to meet their challenges
or “rise to the occasion.”
Patients are considered to have anxiety disorders
when their responses to stressful situations are abnor-
mal or irrational and impair normal daily function-
ing. The National Institute of Mental Health identies
anxiety disorders as the most commonly encountered
mental health disorders in clinical practice; 16% of the
general population will experience anxiety disorders
during their lifetime. Anxiety disorders usually be-
gin before the age of 30 years and are more common
among women than men. Anxiety is a primary symp-
tom of many psychiatric disorders, including schizo-
phrenia, mania, depression, dementia, and substance
abuse. Therefore the evaluation of the anxious patient
requires a thorough history and physical and psychi-
atric examinations to determine whether the anxiety
is a primary condition or secondary to another illness.
Patients who develop anxiety disorders often have
228
more than one. Patients may also have major depres-
sion or develop substance abuse problems. The most
common disorders are generalized anxiety disorder, panic
disorder, social phobia, simple phobia, and obsessive-
compulsive disorder (OCD).
Generalized anxiety disorder is described as ex-
cessive and unrealistic worry about two or more life
circumstances (e.g., nances, illness, misfortune) for
6 months or more. Symptoms are both psychological
(e.g., tension, fear, difculty concentrating, appre-
hension) and physical (e.g., tachycardia, palpitations,
tremor, sweating, gastrointestinal upset). The disease
has a gradual onset, usually among individuals in
the 20- to 30-year-old age group, and it has twice the
frequency among women as among men. This illness
usually follows a chronic uctuating course of exacer-
bations and remissions that are triggered by stressful
events in the person’s life. Persistent irrational anxi-
ety or episodic anxiety generally requires medical and
psychiatric treatment. Patients with generalized anxi-
ety disorder often develop other psychiatric disorders
(e.g., panic disorder, OCD, social anxiety disorder, major
depression) at some time during their lives.
Panic disorder is recognized as a separate entity
and not as a more severe form of chronic generalized
anxiety disorder. A panic attack is an abrupt surge of
intense fear or intense discomfort that reaches a peak
within minutes. During the attack, at least four of the
following symptoms arise: palpitations, tachycardia,
or pounding heart; sweating; shaking or trembling;

sensations of shortness of breath or smothering; feel-
ings of choking; chest pain or discomfort; nausea or ab-
dominal distress; feeling dizzy, unsteady, lightheaded,
or faint; chills or heat sensation; numbness or tin-
gling sensations; feelings of unreality or deperson-
alization; fear of losing control; and fear of dying.
The average age of onset is during the early 20s; the
disorder is often relapsing, and it may require life-
time treatment. Panic disorder is estimated to affect
1% to 2% of Americans at some time during their
lives. Women are affected two to three times more
frequently than men. Genetic factors appear to play a
signicant role in the disease; 15% to 20% of patients
will have a close relative with a similar illness. Panic
disorder begins as a series of acute or unprovoked
anxiety (panic) attacks that involve an intense, ter-
rifying fear. The attacks do not occur as a result of ex-
posure to anxiety-causing situations, as phobias do.
Initially the panic attacks are spontaneous, but later
during the course of the illness they may be associ-
ated with certain actions (e.g., driving a car, being in
a crowded place). Patients with panic disorder often
develop other psychiatric disorders (e.g., generalized
anxiety disorder, personality disorders, substance
abuse, OCD, social anxiety disorder, major depres-
sion) at some time during their lives.
Phobias are irrational fears of specic objects, ac-
tivities, or situations. Unlike other anxiety disorders,
the object or activity that creates the feeling of fear is
recognized by the patient, who also realizes that the
fear is unreasonable. The fear persists, however, and
the patient seeks to avoid the situation. Social phobia
is described as a fear of certain social situations in
which the person is exposed to scrutiny by others and
fears doing something embarrassing. A social phobia
involving public speaking is fairly common, and the
activity is usually avoided. If public speaking is un-
avoidable, it is done with intense anxiety. Social pho-
bias are rarely incapacitating, but they do cause some
interference with social or occupational functioning.
A simple phobia is an irrational fear of a specic object
or situation, such as heights (acrophobia), closed spaces
(claustrophobia), air travel, or driving. Phobias that
involve animals such as spiders, snakes, and mice are
particularly common. If the person with the phobia is
exposed to the object, there is an immediate feeling of
panic, sweating, and tachycardia. People are aware
of their phobias, and they simply avoid the feared
objects.
OCD is not classied under anxiety disorders
in the Diagnostic and Statistical Manual of Mental
Disorders, Fifth Edition (DSM-5). The DSM-5 added
a new category of disorders called obsessive-compulsive
and related disorders (OCRDs). The OCRDs category
includes the familiar OCD. Although anxiety remains
a key feature in OCRDs, there are enough unique dif-
ferences between anxiety disorders and OCRDs to
justify a separate category. The primary features of
Drugs Used for Anxiety Disorders CHAPTER 15 229
OCD are recurrent obsessions or compulsions that
cause signicant distress and interfere with normal
occupational responsibilities, social activities, and
relationships. The average age of onset of the symp-
toms of OCD is during late adolescence to the early
20s. The condition occurs with twice the frequency
in men as in women, and there also appears to be
a genetic component to the disease. It is estimated
that 2% to 8% of the general population suffers from
OCD, making it one of the most common personal-
ity disorders. An obsession is an unwanted thought,
idea, image, or urge that the patient recognizes as
time consuming and senseless but that repeatedly
intrudes into that patient’s consciousness, despite
their attempts to ignore, prevent, or counteract it.
Examples of obsessions are recurrent thoughts of dirt
or germ contamination, a fear of losing things, a need
to know or remember something, a need to count or
check something, blasphemous thoughts, or concerns
about something happening to the self or others. An
obsession produces a tremendous sense of anxiety
in the affected person. A compulsion is a repetitive,
intentional, purposeful behavior that must be per-
formed to decrease the anxiety associated with an ob-
session. The act is done to prevent a vague dreaded
event, but the person does not derive pleasure from
the act. Common compulsions deal with cleanliness,
grooming, and counting. When patients are prevent-
ed from performing a compulsion, there is a sense of
mounting anxiety. In some individuals the compul-
sion can become the patient’s lifetime activity. OCD is
a complex condition that requires a highly individu-
alized and integrated approach to treatment that in-
cludes pharmacologic, behavioral, and psychosocial
components.
DRUG THERAPY FOR ANXIETY
DISORDERS
A great many medications have been used over
the decades to treat anxiety. They range from the
purely sedative effects of ethanol, bromides, chloral
hydrate, and barbiturates to drugs with more specif-
ic antianxiety and less sedative activity, such as ben-
zodiazepines, buspirone, hydroxyzine, and propran-
olol (a beta-adrenergic antagonist). In recent years,
tricyclic antidepressants (e.g., imipramine), selective
serotonin reuptake inhibitors (SSRIs), and serotonin-
norepinephrine reuptake inhibitors (SNRIs) (dulox-
etine and extended-release venlafaxine) have been
studied and are now used for the treatment of anxi-
ety disorders. The treatment of anxiety disorders
usually requires a combination of pharmacologic
and nonpharmacologic therapies. When it is decided
to treat the anxiety in addition to the other medical
or psychiatric diagnoses, antianxiety medications—
also known as anxiolytics or tranquilizers—are pre-
scribed. See the individual drug monographs later
230 UNIT III Drugs Affecting the Autonomic and Central Nervous System
in this chapter for the mechanisms of action of these
agents.
USES
Generalized anxiety disorder is treated with psycho-
therapy and the short-term use of antianxiety agents.
The US Food and Drug Administration (FDA) has
approved four classes of compounds or medica-
tions for treatment: (1) specic benzodiazepines
(alprazolam, chlordiazepoxide, clonazepam, cloraz-
epate, diazepam, lorazepam, oxazepam); (2) SSRIs
(paroxetine and escitalopram); (3) duloxetine and
extended-release venlafaxine; and (4) buspirone. To
some extent, the beta-adrenergic blocking agents
(see Chapter 12) are also used. Although the anti-
histamine hydroxyzine is infrequently prescribed, it
may be an option in patients with a substance abuse
disorder. Panic disorders may be treated with a va-
riety of agents in addition to behavioral therapy.
Alprazolam and clonazepam (benzodiazepines), as
well as sertraline, paroxetine, and uoxetine (SSRIs),
are approved by the FDA for the treatment of panic
disorder. Other agents that show benet are the tri-
cyclic antidepressants desipramine and clomipramine,
as well as mirtazapine (see Chapter 16). Phobias are
treated with the use of avoidance, behavior therapy, and
benzodiazepines or beta-adrenergic blockers such as
propranolol or atenolol. Obsessive-compulsive and related
disorders are treated with behavioral and psychosocial
therapy in addition to paroxetine, sertraline, uoxetine,
or uvoxamine.
NURSING IMPLICATIONS FOR ANTIANXIETY
THERAPY
Assessment
History of behavior Obtain a history of the precipitat-
ing factors that may have triggered or contributed to
the individual’s current anxiety. Has the individual
been using alcohol or drugs? Has the patient had a
recent adverse event, such as a job or relationship
loss, the death of a loved one, or a divorce? Has the
individual witnessed or survived a traumatic event?
Does the individual have any medical problems
(e.g., hyperthyroidism) that could be related to these
symptoms? Are there symptoms present that could be
attributed to a panic attack, such as a feeling of chok-
ing, palpitations, sweating, chest pain or discomfort,
nausea, abdominal distress, or fear of losing control,
going crazy, or dying? Does the patient have symp-
toms of obsessions or compulsions? Does the individ-
ual have a history of agoraphobia (i.e., situations in
which they feel trapped or unable to escape)? Did the
attack occur in response to a social or performance
situation? Is the patient also depressed? What specic
fears does the individual have?
Take a detailed history of all medications that
the individual is taking. Is there any use of central
nervous system (CNS) stimulants (e.g., cocaine,
amphetamines) or CNS depressants (e.g., sedatives,
opioids, alcohol)? Adverse effects of medications be-
ing taken may be aggravating the patient’s anxiety
level.
Ask for details regarding how long the individual
has been exhibiting anxiety. Has the patient been treat-
ed for anxiety previously? When did the symptoms
start? Did they begin during intoxication or withdraw-
al from a substance?
Basic mental status Note the patient’s general ap-
pearance and appropriateness of attire. Is the individ-
ual clean and neat? Is the posture stooped, erect, or
slumped? Is the patient oriented to date, time, place,
and person? Determine whether the patient is at risk
for harming herself or himself or others. Are they able
to participate in self-directed activities of daily liv-
ing, including eating and providing the self-care that
is required to sustain life? These areas are regularly
assessed to determine whether acute hospitalization
is indicated. Otherwise, the outpatient setting is the
most common setting for the treatment of anxiety
disorders.
What coping mechanisms has the individual been
using to deal with the situation? Are these mechanisms
adaptive or maladaptive? Identify the individual’s
ability to understand new information, follow direc-
tions, and provide self-care.
Identify events that trigger anxiety in the indi-
vidual. Discuss the patient’s behavior and thoughts,
and foster an understanding of this with their family
members. Involve the family and signicant others
in the discussion of the anxiety-producing events
or circumstances, and explain how these individu-
als can help the patient to reduce anxiety or cope
more adaptively with stressors. Identify support
groups.
Mood and affect Is the individual tearful, excessively
excited, angry, hostile, or apathetic? Is the facial ex-
pression tense, fearful, sad, angry, or blank? Ask the
patient to describe their feelings. Is there worry about
real-life problems? Are the patient’s responses dis-
played as an intense fear, detachment, or absence of
emotions? If the patient is a child, are there episodes
of tantrums or clinging?
Patients who are experiencing altered think-
ing, behavior, or feelings require the careful evalua-
tion of their verbal and nonverbal actions. Often, the
thoughts, feelings, and behaviors that are displayed
are inconsistent with the so-called normal responses of
individuals in similar circumstances. Identify manage-
ment techniques for handling anxiety-producing situ-
ations effectively.
Assess whether the mood being described is con-
sistent with or appropriate for the circumstances be-
ing described. For example, is the patient speaking of
death while smiling?

Clarity of thought Evaluate the coherency, relevancy,
and organization of the patient’s thoughts. Ask spe-
cic questions about the individual’s ability to make
judgments and decisions. Is there any memory impair-
ment? Identify areas in which the patient is capable of
having input into setting goals and making decisions.
(This will help the patient to overcome a sense of pow-
erlessness over certain life situations.) When the pa-
tient is unable to make decisions, set goals to involve
the patient to the degree of their capability because
abilities change with treatment.
Psychomotor functions Ask specic questions regard-
ing the activity level that the patient has maintained. Is
the patient able to work or go to school? Is the patient
able to fulll responsibilities at work, socially, or within
the family? How have the patient’s normal responses
to daily activities been altered? Is the individual irri-
table, angry, easily startled, or hypervigilant? Observe
the patient for unusual gestures, hand tremors, voice
quivering, and actions such as pacing or the inability
to sit still.
Obsessions or compulsions Does the individual ex-
perience persistent thoughts, images, or ideas that are
inappropriate and cause increased anxiety? Are there
repetitive physical or mental behaviors, such as hand-
washing, needing to arrange things in perfect sym-
metric order, praying, or silently repeating words? If
obsessions or compulsions are present, how often do
these occur? Do the obsessions or compulsions impair
the patient’s social or occupational functioning?
Sleep pattern What is the patient’s normal sleep pat-
tern, and how has it varied since the onset of the symp-
toms? Ask specically whether insomnia is present.
Ask the individual to describe the amount and qual-
ity of the sleep. What is the degree of fatigue that is
present? Is the individual having recurrent stressful
dreams (e.g., after a traumatic event)? Is there difcul-
ty falling or staying asleep?
Dietary history Ask questions about the individual’s
appetite and note weight gains or losses not associated
with intentional dieting.
Implementation
• Deal with problems as they occur; practice reality
orientation.
• Identify signs of escalating anxiety; decrease the es-
calation of anxiety.
• Provide a safe, structured environment for the re-
lease of energy; set limits on aggressive or destruc-
tive behaviors.
• Establish a trusting relationship with the patient by
providing support and reassurance.
• Reduce stimulation by having interactions with
the patient in a quiet, calm environment. Provide a
Drugs Used for Anxiety Disorders CHAPTER 15 231
nonstimulating environment for patients who are
having sleeping difculties (e.g., dim lighting, quiet
area) that will encourage drowsiness and sleep.
• Provide an opportunity for the individual to express
their feelings. Use active listening and therapeutic
communication techniques. Be especially aware of
cues that would indicate that the patient may be
considering self-harm. (If suicidal ideation is sus-
pected, ask the patient directly if suicide is being
considered. If necessary, intervene to provide for
safety.)
Allow the patient to make decisions of which they
are capable, make decisions when the patient is not
capable, and provide a reward for progress when deci-
sions are initiated appropriately. Involve the patient in
self-care activities. During periods of severe anxiety or
during escalating anxiety, the individual may be un-
able to have insight or to make decisions appropriately.
Encourage the individual to develop coping skills
with the use of various techniques, such as rehears-
ing or role-playing responses to threatening stressors.
Have the individual practice problem solving, and dis-
cuss the possible consequences of the solutions that are
offered by the patient.
Assist individuals with nonpharmacologic mea-
sures, such as music therapy, relaxation techniques, or
massage therapy.
Patient Education
For those patients who are attending an outpatient
clinic or hospitalized, orient the individual to the unit
and the rules of the unit. Explain the process of privi-
leges and how they are obtained or lost. (The extent
of the orientation and explanations given will depend
on the individual’s orientation to date, time, place, and
abilities.)
Explain activity groups and resources that are
available within the community. A variety of group
process activities (e.g., social skills groups, self-
esteem groups, work-related groups, physical exer-
cise groups) exist in particular therapeutic settings.
Meditation, biofeedback, and relaxation therapy may
also be benecial.
Involve the patient and their family in goal setting,
and integrate them into the available group processes
to develop positive experiences for the individual to
enhance their coping skills.
Patient education should be individualized and
based on assessment data to provide the individual
with a structured environment in which to grow and
enhance self-esteem. Initially, the individual may not
be capable of understanding lengthy explanations;
therefore the approaches used should be based on the
patient’s capabilities.
Explore the coping mechanisms that the patient
uses in response to stressors, and identify methods of
channeling these toward positive realistic goals as an
alternative to the use of medication.
232 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Fostering health maintenance Throughout the course
of treatment, discuss medication information and how
the medication will benet the patient. Stress the im-
portance of the nonpharmacologic interventions and
the long-term effects that compliance with the treat-
ment regimen can provide. Additional health teach-
ing and nursing interventions for adverse effects are
described in the drug monographs later in this chap-
ter. Seek cooperation and understanding regarding
the following points so that medication compliance
is increased: the name of the medication; its dosage,
route, and times of administration; and its adverse ef-
fects. Instruct the patient not to suddenly discontinue
prescribed medications after having been on long-
term therapy. Withdrawal should be undertaken with
instructions from a healthcare provider, and it usually
requires 4 weeks of gradual reduction in dosage and
widening the intervals of administration.
Patient self-assessment Enlist the patient’s help with
developing and maintaining a written record of moni-
toring parameters (see the Patient Self-Assessment
Form for Antianxiety Medication on the Evolve web-
site). Complete the Premedication Data column for use
as a baseline to track patient response to drug therapy.
Ensure that the patient understands how to use the
form, and instruct the patient to bring the completed
form to follow-up visits. During follow-up visits, focus
on issues that will foster adherence with the therapeu-
tic interventions that have been prescribed.
DRUG CLASS: BENZODIAZEPINES
Benzodiazepines are most commonly used because
they are more consistently effective, are less likely to
interact with other drugs, are less likely to cause over-
dose, and have less potential for abuse than other anti-
anxiety agents. They account for perhaps 75% of the
100 million prescriptions that are written annually for
anxiety. Six benzodiazepine derivatives are used as an-
tianxiety agents (Table 15.1).
Actions
It is thought that the benzodiazepines have mecha-
nisms of action similar to CNS depressants, but indi-
vidual drugs in the benzodiazepine family act more
selectively at specic sites, which allows for a variety
of uses (e.g., sedative-hypnotic, muscle relaxant, anti-
anxiety agent, anticonvulsant). The benzodiazepines
reduce anxiety by binding to alpha-2 sites of the
GABA-A receptor to stimulate the inhibitory neu-
rotransmitter gamma-aminobutyric acid (GABA).
(See Chapter 13 for more discussion of the actions of
benzodiazepines.)
In patients with reduced hepatic function or in
older adults, lorazepam and oxazepam may be most
appropriate because they have a relatively short du-
ration of action and no active metabolites. The other
benzodiazepines all have active metabolites that sig-
nicantly prolong the duration of action and that may
accumulate to the point of excessive adverse effects
with chronic administration.
Uses
Patients with anxiety reactions to recent events and
those with treatable medical illnesses that induce anxi-
ety respond most readily to benzodiazepine therapy.
In general, benzodiazepines are equally effective for
the treatment of anxiety. Patients generally respond to
therapy within 1 week. Because all benzodiazepines
have similar mechanisms of action, the selection of
the appropriate derivative depends on how the ben-
zodiazepine is metabolized (see Actions previously).
Oxazepam, lorazepam, chlordiazepoxide, diazepam,
and clorazepate are used for the treatment of anxiety
associated with alcohol withdrawal. Oxazepam and
lorazepam are the drugs of choice in patients with
severe liver impairment because they have no active
metabolites. Sometimes a long-acting benzodiazepine
with active metabolites (e.g., diazepam or chlordiaz-
epoxide) is preferred because they seem to result in
a smoother clinical course with lower chance of re-
current withdrawal or seizures. However, their use
is somewhat limited for patients who cannot tolerate
oral administration as a result of nausea and vomiting.
Diazepam or lorazepam may be administered intra-
muscularly in this case (see Chapter 48).
Use of benzodiazepines during pregnancy, whether
for anxiety (see Table 15.1) or for sedation (see Table
13.1), should be avoided. Benzodiazepines are preg-
nancy category D and X. Animal studies indicate the
possibility of increased risk of congenital malforma-
tions if prescribed in the rst trimester of pregnancy.
Benzodiazepines are also not recommended for breast-
feeding mothers. The benzodiazepines transfer to
breast milk and can accumulate in breast-fed infants,
acting as a sedative.
Therapeutic Outcome
The primary therapeutic outcome expected from the
benzodiazepine antianxiety agents is a decrease in the
level of anxiety to a manageable level (i.e., coping is
improved; physical signs of anxiety such as a look of
anxiety, tremor, and pacing are reduced).
Nursing Implications for Benzodiazepines
Premedication assessment
1. Record baseline data regarding the level of anxiety
that is present.
2. Record the patient’s baseline vital signs, particu-
larly blood pressure in both the sitting and supine
positions.
3. Check for a history of blood dyscrasias or hepatic
disease.
4. Determine whether the individual is pregnant or
breastfeeding.
 Drugs Used for Anxiety Disorders CHAPTER 15 233

Table 15.1 Benzodiazepines Used to Treat Anxiety

INITIAL DOSAGE MAXIMUM DAILY DOSAGE
GENERIC NAME BRAND NAME AVAILABILITY RANGE (PO) RANGE
alprazolam Xanax Tablets: 0.25, 0.5, 1, 2 mg 0.25–0.5 mg three 4 mg for anxiety
Apo-Alpraz Tablets, orally disintegrating: times daily management
Do not confuse 0.25, 0.5, 1, 2 mg 10 mg for panic
Xanax with Zantac or Solution: 1 mg/mL disorder
Zyrtec.
Xanax XR Tablets, extended release, 0.5–1 mg daily 10 mg maximum for
24 hr: 0.5, 1, 2, 3 mg extended-release
tablets; usual range
is 3–6 mg daily
chlordiazepoxide Capsules: 5, 10, 25 mg 5–10 mg three or 100 mg
Do not confuse four times daily
chlordiazepoxide
with chlorpromazine.
clorazepate Tranxene T Tablets: 3.75, 7.5, 15 mg 10 mg once to 60 mg
three times daily
diazepam Valium Tablets: 2, 5, 10 mg 2–10 mg two to —
Do not confuse BIO-Diazepam Liquid: 5 mg/5 mL four times daily
diazepam with Do not confuse Concentrate: 5 mg/mL
Ditropan. Valium with valerian. Injection: 5 mg/mL in 2-mL
prelled syringe
Rectal gel: 2.5, 10, 20 mg/
rectal delivery system
lorazepam Ativan Tablets: 0.5, 1, 2 mg 2–3 mg divided 10 mg
Do not confuse Apo-Lorazepam Liquid: 2 mg/mL two or three
lorazepam with Do not confuse Injection: 2, 4 mg/mL in 1-, times daily
loperamide. Ativan with Ambien 10-mL vials
or Atarax.
oxazepam — Capsules: 10, 15, 30 mg 10–15 mg three or 120 mg
Apo-oxazepam four times daily
Available in Canada.
Do not confuse.
High-alert medication.

Availability, dosage, and administration. See Table 15.1.
Use of benzodiazepines may result in physical and
psychological dependence when taken steadily for sev-
eral days to weeks, even when taken in recommended
dosages. Abuse and misuse can result in overdose or
death, especially when benzodiazepines are combined
with other medicines, such as opioid pain relievers,
alcohol or illicit drugs, and CNS depressants (e.g., sed-
atives, hypnotics, muscle relaxants). The rapid discon-
tinuance of benzodiazepines after long-term use may
result in symptoms that are similar to those of alco-
hol withdrawal, such as weakness, anxiety, delirium,
and tonic-conic (grand mal) seizures. These symptoms
may not appear for several days after discontinuation.
Discontinuation of benzodiazepines consists of gradu-
al withdrawal over 2 to 4 weeks.
Pregnancy and lactation. It is recommended that ben-
zodiazepines not be administered during at least the
rst trimester of pregnancy. There may be an increased
incidence of birth defects because these agents readily
cross the placenta and enter the fetal circulation. If ben-
zodiazepines are taken regularly during pregnancy, the
infant should be monitored closely after delivery for
signs of withdrawal, including sedation and hypotonia.
Mothers who are breastfeeding should not receive
benzodiazepines regularly. The benzodiazepines read-
ily cross into the breast milk and exert a pharmacologic
effect on the infant.
Common adverse effects
Neurologic
Drowsiness, hangover, sedation, lethargy. Patients may
complain of morning hangover, blurred vision, and
transient hypotension on arising. Explain to the patient
the need for rising rst to a sitting position for several
moments until any dizziness or lightheadedness pass-
es and then standing slowly. Assist the individual with
ambulation, if necessary. If hangover becomes trouble-
some, the dosage should be reduced, the medication
changed, or both.
People who work around machinery, drive, admin-
ister medication, or perform other duties for which
they must remain mentally alert should not take these
medications while working.
234 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Serious adverse effects
Psychological
Excessive use or abuse. Habitual benzodiazepine use
may result in physical dependence. Discuss the case
with the healthcare provider and make plans to co-
operatively approach the gradual withdrawal of the
medications that are being abused. Assist the patient
with recognizing the abuse problem. Identify underlying
needs and plan for the more appropriate management
of those needs. Provide emotional support of the indivi-
dual, display an accepting attitude, and be kind but rm.
Hematologic
Blood dyscrasias. Routine laboratory studies (e.g.,
red blood cell and white blood cell counts, differential
counts) should be scheduled. Stress the patient’s need
to return for these tests. Monitor the patient for sore
throat, fever, purpura, jaundice, or excessive and pro-
gressive weakness.
Gastrointestinal
Hepatotoxicity. The symptoms of hepatotoxicity are
anorexia, nausea, vomiting, jaundice, hepatomegaly,
splenomegaly, and abnormal liver function tests (e.g.,
elevated bilirubin, aspartate aminotransferase [AST],
alanine aminotransferase [ALT], gamma-glutamyl-
transferase [GGT], and alkaline phosphatase [ALP]
levels; increased prothrombin time [PT]).
Drug interactions
Antihistamines, alcohol, analgesics, anesthetics,
probenecid, tranquilizers, opioids, cimetidine, other sedative-
hypnotics. All these agents increase the toxic effects of
benzodiazepines and may cause excessive sedation
and impaired psychomotor function.
Oral contraceptives, cimetidine, uoxetine, metoprolol, pro-
pranolol, isoniazid, ketoconazole, valproic acid. These agents
inhibit the metabolism of alprazolam, chlordiazepoxide,
clonazepam, and diazepam. Pharmacologic effects of
the benzodiazepines may be increased, and excessive se-
dation and impaired psychomotor function may result.
Smoking, rifampin. Smoking and rifampin enhance
the metabolism of benzodiazepines. Larger doses may
be necessary to maintain anxiolytic effects in patients
who smoke.
DRUG CLASS: AZASPIRONES
buspirone (byū-SPĪ-rōn)
Do not confuse buspirone with bupropion.
Actions
Buspirone is an antianxiety agent that comes from
the chemical class known as the azaspirones, which
are chemically unrelated to benzodiazepines or other
anxiolytic agents. The mechanism of action of buspi-
rone is not fully understood. It is a partial serotonin
and dopamine agonist, and it interacts in several ways
with nerve systems in the midbrain; therefore it is
sometimes called a midbrain modulator. It does not af-
fect GABA receptors. Its advantages over other anti-
anxiety agents are that it has lower sedative proper-
ties and it does not alter psychomotor functioning. It
requires 7 to 10 days of treatment before initial signs of
improvement are evident, and it takes 3 to 4 weeks of
therapy for optimal effects to occur.
Uses
Buspirone is approved for use in the treatment of gen-
eralized anxiety disorders and for the short-term relief
of the symptoms of anxiety. Buspirone has no anti-
psychotic activity, and it should not be used in place
of appropriate psychiatric treatment. Because there is
minimal potential for abuse with buspirone, it is not a
controlled substance.
Therapeutic Outcome
The primary therapeutic outcome expected from buspi-
rone is a decrease in the level of anxiety to a manageable
level (i.e., coping is improved; physical signs of anxiety
such as a look of anxiety, tremor, and pacing are reduced).
Nursing Implications for Buspirone Therapy
Premedication assessment. Record baseline data re-
garding the level of anxiety present.
Availability. PO: Tablets: 5, 7.5, 10, 15, and 30 mg.
Schedule assessments periodically throughout thera-
py for the development of slurred speech or dizziness,
which are signs of excessive dosing.
Dosage and administration. Adult: PO: Initially, 5 mg
two to three times daily. Doses may be increased by 5
mg every 2 to 3 days. Maintenance therapy often re-
quires 30 mg daily in divided doses. Do not exceed 60
mg daily.
Common adverse effects
Neurologic
Sedation, lethargy. The most common adverse effects
of buspirone therapy are CNS disturbances (3.4%),
which include dizziness, insomnia, nervousness,
drowsiness, and lightheadedness. People who work
around machinery or who perform other duties for
which they must remain mentally alert should not take
this medication while working. Slurred speech and
dizziness are signs of excessive dosing. Report to the
healthcare provider for further evaluation. Provide pa-
tient safety during these episodes.
Drug interactions
Itraconazole, erythromycin, clarithromycin, diltiazem, ve-
rapamil, uvoxamine, grapefruit juice. These substances
potentiate the toxicity of buspirone by inhibiting its
metabolism. If any of these are used together, the dose
of buspirone should be reduced by half for a few weeks
and then adjusted as needed.

Rifampin, phenytoin, phenobarbital, carbamazepine. These
drugs enhance the metabolism of buspirone. An in-
crease in the dose of buspirone may be needed.
Alcohol. Buspirone and alcohol generally do not
have additive CNS depressant effects, but individual
patients may be susceptible to impairment. Tell pa-
tients to use alcohol with extreme caution.
DRUG CLASS: SELECTIVE SEROTONIN REUPTAKE
INHIBITORS
uvoxamine (ū-VŎKS-ă-mēn)
Do not confuse uvoxamine with uoxetine.
Luvox
Do not confuse Luvox with Lasix, Levoxyl, or Lovenox.
Actions
Fluvoxamine inhibits the reuptake of serotonin at
nerve endings, thus prolonging serotonin activity.
Uses
Fluvoxamine is used for the treatment of OCRDs
when obsessions or compulsions cause marked
distress, are time consuming, or interfere substan-
tially with social or occupational responsibilities.
Fluvoxamine reduces the symptoms of these disor-
ders but does not prevent obsessions and compul-
sions. However, patients indicate that the obsessions
are less intrusive and that they have more control
over them.
Therapeutic Outcome
The primary therapeutic outcome expected from u-
voxamine is a decrease in the level of anxiety to a man-
ageable level (i.e., coping with obsession is improved;
frequency of compulsive activity is reduced).
Nursing Implications for Fluvoxamine Therapy
See Serotonin-Norepinephrine Reuptake Inhibitors
section in Chapter 16
DRUG CLASS: MISCELLANEOUS ANTIANXIETY
AGENTS
hydroxyzine (hī-DRŎKS-ĭ-zēn)
Do not confuse hydroxyzine with hydroxyurea.
Vistaril (VĬS-tă-rĭl)
Do not confuse Vistaril with Restoril or Zestril.
Actions
When dened strictly by chemical structure, hydroxy-
zine is considered an antihistamine. It acts within the
CNS to produce sedation and antiemetic, anticholinergic,
antihistaminic, antianxiety, and antispasmodic activity,
thus making it a somewhat multipurpose agent.
Drugs Used for Anxiety Disorders CHAPTER 15 235
Uses
Hydroxyzine is used as a mild tranquilizer for psy-
chiatric conditions that are characterized by anxi-
ety, tension, and agitation. It is also occasionally
used as a preoperative or postoperative sedative to
control vomiting, diminish anxiety, and reduce the
amount of opioids that are needed for analgesia.
Hydroxyzine may also be used as an antipruritic
agent to relieve the itching that is associated with
allergic reactions.
Therapeutic Outcomes
The primary therapeutic outcomes expected from hy-
droxyzine are as follows:
1. A decrease in the level of anxiety to a manageable level
(i.e., coping is improved; physical signs of anxiety such
as a look of anxiety, tremor, and pacing are reduced)
2. Sedation, relaxation, and reduction in analgesics be-
fore and after surgery
3. Absence of vomiting when used as an antiemetic
4. Itching controlled during allergic reactions
Nursing Implications for Hydroxyzine Therapy
Premedication assessment
1. Perform a baseline assessment of anxiety symptoms.
2. Determine the patient’s level of anxiety present be-
fore and after surgical intervention; record and in-
tervene appropriately.
3. For nausea and vomiting, administer when nausea
rst starts and determine the effectiveness of control
before giving subsequent doses.
4. For allergic reactions, perform a baseline assess-
ment of physical symptoms before administering
the dose; repeat this assessment before the adminis-
tration of subsequent doses to determine the medi-
cation’s effectiveness.
5. Monitor the patient for the level of sedation present,
slurred speech, or dizziness; report to the healthcare
provider if these symptoms are excessive before ad-
ministering repeat doses.
Availability. PO: 10-, 25-, and 50-mg tablets; 25-, 50-,
and 100-mg capsules; 10 mg/5 mL syrup.
IM: 25 and 50 mg/mL.
Dosage and administration. Adult:
• Antianxiety: PO: 25 to 100 mg three or four times
daily; IM: 50 to 100 mg every 4 to 6 hours
• Preoperatively and postoperatively: IM: 25 to 100
mg
• Antiemetic: IM: 25 to 100 mg
Common adverse effects. These symptoms are the anti-
cholinergic effects that are produced by hydroxyzine.
Patients who are taking these medications should
be monitored for the development of these adverse
effects.
236 UNIT III Drugs Affecting the Autonomic and Central Nervous System

Sensory
Blurred vision. Caution the patient that blurred vision
may occur and make appropriate suggestions for per-
sonal safety.
Gastrointestinal
Constipation; dryness of the mucosa of the mouth, throat,
and nose. Mucosal dryness may be relieved by sucking
hard candy or ice chips or by chewing gum. The use
of stool softeners (e.g., docusate) may be required for
constipation.
Neurologic
Sedation, slurred speech, dizziness. People who work
around machinery, drive, administer medication, or
perform other duties for which they must remain men-
tally alert should not take these medications while
working. Slurred speech and dizziness are signs of ex-
cessive dosing. Report to the healthcare provider for
further evaluation. Provide patient safety during these
episodes.
Drug interactions
Antihistamines, alcohol, analgesics, anesthetics, tran-
quilizers, opioids, other sedative-hypnotics. These all are
agents that can increase toxic effects. Monitor the pa-
tient for excessive sedation, and reduce the dosage of
hydroxyzine if necessary.

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points Clinical Judgment and Next-Generation NCLEX® Exam-

ination-Style Questions The following questions are typical of
• Anxiety is an unpleasant feeling of apprehension or the NCLEX examination and include both NGN (Next Genera-
nervousness that is caused by the perception of danger tion) and traditional questions. See Chapter 1 for further infor-
threatening the patient’s security. In most cases, it is a mation regarding question types.
normal human emotion.
• When a patient’s response to anxiety is irrational and Scenario
impairs their daily functioning, they are said to have an
anxiety disorder. Some 16% of the general population will A patient admitted to the mental health unit following a panic
experience an anxiety disorder during their lifetime. attack that lasted longer than 15 minutes was advised to come
• The most common types of anxiety disorders are in for medication adjustment.
generalized anxiety disorder, panic disorder, social phobia,
1. Identify the type of behavior the patient may be exhibiting with
simple phobia, and obsessive-compulsive disorder.
each cue. Indicate with an X in the box that gives an example of
• Anxiety is a component of many medical illnesses that the behavior.
involve the cardiovascular, pulmonary, digestive, and
endocrine systems. It is also a primary symptom of many
psychiatric disorders. Therefore the evaluation of the
Counts Excessive Declines Suddenly
anxious patient requires a thorough history and physical
the and getting feeling
and psychiatric examination to determine whether the
number unrealistic into the lightheaded
anxiety is the primary condition or secondary to another
of steps worry MRI and seeing
illness. Persistent irrational anxiety or episodic anxiety
that it about machine, spots, then
usually requires medical and psychiatric treatment.
takes to grades as feeling too fainting
• The treatment of anxiety disorders usually requires a
walk to a student conned during a
combination of pharmacologic and nonpharmacologic
the car course
therapies.
examination
• It is the responsibility of the nurse to educate patients
Phobic
about their therapy, to monitor for therapeutic benets and
disorder
common and serious adverse effects, and to intervene
whenever possible to optimize therapeutic outcomes. Generalized
anxiety
disorder
Additional Learning Resources
Obsessive-
SG Go to your Study Guide for additional Review Questions compulsive
for the NCLEX® Examination, Critical Thinking Clinical Situa- and related
tions, and other learning activities to help you master this chap- disorder
ter content. Panic
disorder
Go to your Evolve website (https://evolve.elsevier.com/
Willihnganz) for additional online resources.
 Drugs Used for Anxiety Disorders CHAPTER 15 237

Objective: Compare and contrast the differences between Objective: Identify adverse effects that may result from drug
generalized anxiety disorder, panic disorder, phobias, and therapy used to treat anxiety.
obsessive-compulsive disorder. NCLEX item type: Extended multiple response
NGN test item: Matrix Cognitive skill: Analyze cues
Cognitive skill: Analysis cues
5. The patient in the scenario was prescribed Ativan and is now
2. A nurse performing a baseline mental status assessment on the exhibiting possible adverse effects. The nurse evaluates these
patient in the scenario will include which of the following details? symptoms. For each symptom mark an X to indicate whether the
(Select all that apply.) nding is signicant for an adverse effect associated with Ativan
1. General appearance and appropriateness of attire or is an unrelated nding.
2. Clarity of thought
3. Mood and affect
4. Obsessions or compulsions SIGNIFICANT UNRELATED
5. Job history SYMPTOMS FINDING FINDING
Objective: Describe the essential components included in a Lightheadedness
baseline assessment of a patient’s mental status. Morning hangover
NCLEX item type: Multiple response
Blurred vision
Cognitive skill: Application
Excessive thirst
3. The nurse caring for the patient in the scenario with an anxiety
Urinary retention
disorder knows that certain drugs can be used for treatment of
anxiety disorders. Using an arrow, match the drug class used in Tired during the
the treatment of the specic anxiety disorder. day

Objective: Identify adverse effects that may result from drug

DRUG CLASS USED FOR therapy used to treat anxiety.
ANXIETY ANXIETY DISORDERS NCLEX item type: Matrix
• Azaspirones • GAD Cognitive skill: Evaluate outcomes
• Selective serotonin • Panic disorders 6. After discussing with the patient and the family the drug
reuptake inhibitors management of lorazepam (Ativan) for anxiety, the nurse knows
• Benzodiazepines • OCD further teaching is needed after the patient makes which
• Phobias
statement?
1. “I know that I need to avoid drinking any alcohol while
Objective: Discuss the drug therapy used to treat anxiety disorders. taking this Ativan.”
NCLEX item type: Drop and drag 2. “I understand that this drug may make me drowsy during
Cognitive skill: Comprehension the day and I should not work around machinery while
taking it.”
4. The nurse will monitor which of these laboratory values to
3. “I understand that I can stop the drug at any time that I
determine whether there are any adverse effects for the patient in
feel I do not need it anymore.”
the scenario who is receiving a benzodiazepine for anxiety?
4. “I know that Ativan will start to work within a week.”
1. Complete blood cell count with differential
Objective: Discuss psychological and physiologic drug
2. Thyroid function
dependence.
3. Lipid panel
NCLEX item type: Multiple choice
4. Blood glucose
Cognitive skill: Comprehension
5. Liver function
6. Renal function
7. Biochemical prole
8. Electrolytes
16 Drugs Used for Depressive and
Bipolar Disorders
https://evolve.elsevier.com/Willihnganz

Objectives
1. Describe the essential components of the baseline
assessment of a patient with depression or bipolar
disorder.
2. Identify the premedication assessments that are necessary
before the administration of monoamine oxidase inhibitors
(MAOIs), selective serotonin reuptake inhibitors (SSRIs),
serotonin-norepinephrine reuptake inhibitors (SNRIs),
tricyclic antidepressants (TCAs), and antimanic agents.
3. Describe the common adverse effects that may develop
for patients who are taking MAOIs.
4. Describe the common adverse effects that may develop
for patients who are taking SSRIs and SNRIs.
5. Describe the common adverse effects that may develop
for patients who are taking TCAs.
6. Describe the common adverse effects that may develop
for patients who are taking lithium.

Key Terms
mood (MŪD) (p. 238)
mood disorder (MŪD dĭs-ŌR-dŭr)
(p. 238)
neurotransmitters (nū-rō-TRĂNZ-mĭ-
tŭrz) (p. 239)
dysthymia (dĭs-THĬ-mē-ă) (p. 239)
depression (dē-PRĔSH-ŭn) (p. 239)
cognitive symptoms (KŎG-nĭ-tĭv) (p. 239)
psychomotor symptoms (sī-kō-MŌ-
tŭr) (p. 239)
bipolar disorder (bī-PŌ-lăr) (p. 239)
mania (MĀ-nē-ă) (p. 239)
euphoria (yū-FŎR-ē-ă) (p. 240)
labile mood (LĀ-bīl) (p. 240)
grandiose delusions (GRĂN-dē-ōs
dĕ-LŪ-zhŭnz) (p. 240)
cyclothymia (sī-klō-THĬ-mē-ă) (p. 240)
suicidal ideation (sū-ĭ-SĪ-dĕl ī-dē-Ā-
shĕn) (p. 240)
antidepressants (ăn-tī-dē-PRĔS-ăntz)
(p. 241)

DEPRESSIVE AND BIPOLAR DISORDERS

The Diagnostic and Statistical Manual of Mental Disorders,
Fifth Edition (DSM-5), recognizes ajor sychiatric is-
orers on a continuu, with eressive isorers an
sychotic sectru at the ens of the continuu an
with biolar isorers serving as a brige between
the two iagnostic classes in ters of sytoatol-
ogy, faily history, an genetics. The coon feature
aong eressive an biolar isorers is the res-
ence of sa, ety, or irritable oo, accoanie by
changes that signicantly affect the iniviual’s caac-
ity to function. Duration, tiing, an assue etiol-
ogy are what iffer between the isorers (DSM-5).
Mood is a sustaine eotional feeling erceive
along a noral continuu of sa to hay that af-
fects our ercetion of our surrounings. A mood dis
order (or affective isorer) is resent when certain
sytos iair a erson’s ability to function for a
tie. Moo isorers are characterize by abnoral
feelings of eression or euhoria. They involve the
rolonge an inaroriate exression of eotion
that goes beyon brief eotional uset fro negative
life exeriences. In severe cases, other sychotic fea-
tures ay also be resent. About 15% to 20% of the
US oulation will have a iagnosable oo isorer
uring their lifetie.
In Mental Health: A Report of the Surgeon General (U.S.
Deartent of Health an Huan Services, 1999)
it was recognize that the effect of ental illness on
health an rouctivity has been rofounly uner-
estiate. Major eression currently ranks as the sec-
on leaing cause of isease buren (i.e., years live
with the isability) in the Unite States; the leaing
cause is ischeic heart isease. Unfortunately, the a-
jority of eole with eression receive no treatent.
Unertreatent of oo isorers stes fro any
factors, incluing social stiga, nancial barriers,
unerrecognition by healthcare roviers, an uner-
areciation by the general ublic of the otential ben-
ets of treatent. The sytos of eression, such
as feelings of worthlessness, excessive guilt, an lack
of otivation, eter eole fro seeking treatent.
Mebers of racial an ethnic inority grous often
encounter aitional barriers.
The unerlying causes of oo isorers are still
unknown. They are too colex to be coletely ex-
laine by a single social, eveloental, or biologic
theory. A variety of factors aear to work together to

238
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
cause eressive isorers. It is known that atients
with eression have changes in the brain neuro
transmitters noreinehrine, serotonin, oaine, ace-
tylcholine, an gaa-ainobutyric aci, but other
unexecte negative life events (e.g., the suen
eath of a love one, uneloyent, eical illness,
other stressful events) also lay a role. Enocrine
abnoralities, such as excessive secretion of cortisol
an abnoral thyroi-stiulating horone, have
been foun in 45% to 60% of atients with eression.
Genetic factors also reisose atients to evelo-
ing eression. Deressive isorers an suicie
ten to cluster in failies, an relatives of atients
with eression are two to three ties ore likely to
evelo eression. Meicines being taken for other
iseases ay also contribute to eression, incluing
antihyertensives (e.g., ethyloa, cloniine, beta-
arenergic blocking agents), antiarkinsonian ei-
cines (e.g., levooa), an horones (e.g., estrogens,
rogestins, corticosterois).
DEPRESSIVE DISORDER
Major eressive isorer (MDD) an ysthyia are
known as unipolar disorders, anifeste by varying
egrees of eression. Patients with MDD exerience
one or ore secic eisoes of eression, whereas
atients with dysthymia suffer fro ore chronic, on-
going sytos of eression that last for at least 2
years.
The onset of a eressive isorer tens to occur
uring the late 20s, although it can occur at any age.
The lifetie frequency of eressive sytos a-
ears to be as high as 26% for woen an 12% for
en. Risk factors for eression inclue a ersonal or
faily history of eression, rior suicie attets, fe-
ale gener, lack of social suort, stressful life events,
substance abuse, an eical illness. The Aerican
Psychiatric Association classies eisoes of eres-
sion as il, oerate, an severe. Mil eression
causes only inor functional iairent. Moerate
eression involves an intereiate egree of i-
airent an affects both sytoatology an func-
tionality. Patients with severe eression have several
sytos that excee the iniu iagnostic crite-
ria an aily functioning is signicantly iaire; hos-
italization ay be require.
It is beyon the scoe of this text to iscuss oo
isorers in etail, but this iscussion escribes gen-
eral tyes of sytos associate with oo isor-
ers. Patients exeriencing depression islay varying
egrees of eotional, hysical, cognitive, an sy-
chootor sytos. Eotionally, the eression is
characterize by a ersistent, reuce ability to exeri-
ence leasure in life’s usual activities, such as hobbies,
faily, an work. Patients frequently aear sa, an
a ersonality change is coon. They ay escribe
their oo as sa, hoeless, or blue. Patients often feel
239
that they have let others own, although these feelings
of guilt are unrealistic. Anxiety sytos (see Chater
15) are resent in alost 90% of eresse atients.
Physical sytos often otivate the erson to seek
eical attention. Coon hysical sytos seen in
atients with eression inclue chronic fatigue, slee
isturbances such as frequent early orning awaken-
ing (terinal insonia), aetite isturbances (weight
loss or gain), an other sytos such as stoach
colaints or heart alitations. Cognitive symptoms,
such as the inability to concentrate, slowe thinking,
confusion, an oor eory of recent events, are ar-
ticularly coon in oler atients with eression.
Psychomotor symptoms of eression inclue slowe
or retare oveents, thought rocesses, an seech
or, conversely, agitation anifesting as uroseless,
restless otion (e.g., acing, han wringing, outbursts
of shouting). Coorbi conitions such as substance-
relate isorers, anic isorer, obsessive-coulsive
an relate isorers, an anorexia nervosa are co-
only resent in atients with MDD.
Life Span Considerations
Depression
The patient and caregivers must understand the impor-
tance of continuing to take the prescribed antidepressant
medication despite a minimal initial response. The lag time
of 1 to 4 weeks between the initiation of therapy and the
therapeutic response must be emphasized. In most cas-
es, the symptoms of depression may improve within a few
days (e.g., improved appetite, sleep, psychomotor activ-
ity). However, the depression still exists, and monitoring
should be continued for negative thoughts, feelings, and
behaviors. Suicide precautions should be maintained until
assessment indicates that suicidal ideation is no longer
present.
Suicide statistics are varied and not well documented.
Adolescents and older adults with depression are more likely
to have suicidal ideation, and older adults commit suicide
more frequently than depressed people of other age groups.
It appears that older adults are quite serious when attempting
suicide because one in two attempts is successful.
Suicide is the third leading cause of death in adolescents;
the incidence may be even higher because of underreporting.
Suicide is a call for help; however, it is permanent when
successfully completed. All comments about suicide or
suicide gestures should be taken seriously.
Bipolar disorder (forerly known as manic depression)
is characterize by istinct eisoes of mania (elation,
euhoria) an eression searate by intervals with-
out oo isturbances. The atient islays extree
changes in oo, cognition, behavior, ercetion, an
sensory exeriences. At any one tie, a atient with
biolar isorer ay be anic or eresse, exhibit
sytos of both ania an eression (ixe), or
be between eisoes.
Sytos of acute ania usually begin abrut-
ly an escalate over several ays. These sytos
240 UNIT III Drugs Affecting the Autonomic and Central Nervous System
inclue a heightene oo (euphoria), quicker
thoughts (ight of ieas), ore an faster seech (res-
sure seech), increase energy, increase hysical
an ental activities (sychootor exciteent), e-
crease nee for slee, irritability, heightene erce-
tual acuity, aranoia, increase sexual activity, an i-
ulsivity. There is often a labile mood, with rai shifts
towar anger an irritability. The attention san is
short, resulting in an inability to concentrate. Anything
in the environent ay change the toic of iscus-
sion, leaing to ight of ieas. Social inhibitions are
lost, an the atient ay becoe isrutive an lou,
earting suenly fro the social interaction an
leaving everything in isarray. As the anic hase
rogresses, aroxiately two-thirs of atients with
biolar isorer evelo sychotic sytos (see
Chater 17), riarily aranoi or grandiose delu
sions (the elusion that one has great talents or se-
cial owers), if treatent interventions have not been
initiate. Unfortunately, ost anic atients o not
recognize the sytos of illness in theselves an
ay resist treatent. Cyclothymia is a iler for of
biolar illness characterize by eisoes of eression
an hyoania that are not severe enough to eet the
full criteria for biolar isorer, but the sytos of
which last at least 2 years.
Biolar isorer occurs equally in en an woen,
with a revalence rate of 0.4% to 1.6% in the ault o-
ulation of the Unite States. The onset of biolar isor-
er is usually uring late aolescence or the early 20s.
It is rare before aolescence, an it ay occur as late as
age 50. Aroxiately 60% to 80% of atients with bi-
olar isease will begin with a anic eisoe. Without
treatent, eisoes last fro 6 onths to a year for
eression an for aroxiately 4 onths for a-
nia. Patients with biolar isorer coonly have
co-occurring conitions such as anxiety isorers (an-
ic attacks, hobias, social anxiety), attention-ecit/
hyeractivity isorer, an substance use isorer
(e.g., alcohol).
Peole with eressive an biolar isorers have
a high incience of atteting suicie. The frequency
of successful suicie is 15%, which is 30 ties higher
than that of the general oulation. All atients with
eressive sytos shoul be assesse for suicial
thoughts or suicidal ideation. Factors that increase the
risk of suicie inclue increasing age, being wiowe,
being unarrie, uneloyent, living alone, sub-
stance abuse, revious sychiatric aission, an feel-
ings of hoelessness. The resence of a etaile lan
with the intention an ability to carry it out inicate
strong intent an a high risk for suicie. Other hints of
otential suicial intent inclue changes in ersonality,
a suen ecision to ake a will or give away osses-
sions, an the recent urchase of a gun or hoaring a
large suly of eications, incluing antieressants,
tranquilizers, or other toxic substances.
The rognosis for eressive an biolar isorers
is highly variable. Of atients with ajor eression,
20% to 30% recover fully an o not exerience anoth-
er bout of eression. Another 50% have recurring ei-
soes, often with a year or ore searating the events.
The reaining 20% have a chronic course with ersis-
tent sytos an social iairent. Most treate
eisoes of eression last aroxiately 3 onths;
untreate ones last 6 to 12 onths. Patients with bio-
lar illness are ore likely to have ultile subsequent
eisoes of sytos.
TREATMENT OF DEPRESSIVE
AND BIPOLAR DISORDERS
Moo isorers are treate with nonharacologic
an haracologic theray. Cognitive behavior thera-
y, sychoynaic theray, an interersonal theray
with haracologic treatent have been ore suc-
cessful than any one treatent alone. Psychotheray
iroves sychosocial function, interersonal rela-
tionshis, an ay-to-ay coing. Patients an faily
ebers shoul be taught to recognize the signs an
sytos of ania, as well as those of eression,
an the iortance of treatent coliance to ini-
ize the recurrence of the illness shoul be stresse.
Patients shoul be encourage to target sytos
that hel the recognize oo changes an to seek
treatent as soon as ossible.
Most atients ass through three hases—acute,
continuation, an aintenance—before full function
is restore. The acute hase is the erio fro iag-
nosis to initial treatent resonse. The initial resonse
occurs when the sytos becoe so signicantly
reuce that the erson no longer ts the criteria for
the illness. Meication resonse in the acute hase
tyically takes 10 to 12 weeks, uring which tie the
atient is seen by the healthcare rovier weekly or
biweekly to onitor sytos an averse effects,
to ake osage ajustents, an to rovie su-
ort. Psychotheraies are initiate at the sae tie.
Treatent of the acute hase is often rolonge be-
cause about half of atients becoe noncoliant with
the eication an the sychotheray or abanon the
rogra. The goals of the continuation hase of thera-
y are to revent relase an to consoliate the initial
resonse into a colete recovery (ene as being
syto free for 6 onths). The continuation hase
involves 4 to 9 onths of cobine haracotheray
an sychotheray for atients with a rst eisoe of
MDD. Maintenance-hase theray is recoene
for iniviuals with a history of three or ore eres-
sive eisoes, chronic eression, or biolar isorer.
The goal of aintenance-hase theray is to revent
recurrences of the oo isorer; atients ay receive
haracologic an nonharacologic theray for this
conition for a year or ore.
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
Nonharacologic treatent for eression an bi-
olar illness is electroconvulsive theray (ECT). When
erfore uner the guielines rovie by the
Aerican Psychiatric Association, ECT is safe an ef-
fective for all subtyes of ajor eression an biolar
isorers. It is ore effective, ore rai in onset of ef-
fect, an safer for atients with cariovascular isease
than any rug theraies. A course of ECT usually
consists of 6 to 12 treatents, but the nuber is ini-
viualize to the nees of the atient. Patients are now
reeicate with anesthetics an neurouscular
blocking agents to revent any of the averse effects
reviously associate with ECT. Although it has been
isuse, ECT shoul be viewe as a treatent o-
tion that can be lifesaving for atients who otherwise
woul not recover fro eressive illness. It is usu-
ally followe by rug theray to iniize the rate of
relase.
DRUG THERAPY FOR DEPRESSIVE AND
BIPOLAR DISORDERS
ACTIONS
Pharacologic treatent of eression is recoen-
e for atients with sytos of oerate to severe e-
ression, an it shoul be consiere for atients who
o not reson well to sychotheray. Several classes of
rugs, collectively known as antidepressants, are use
for treatent. Patients iagnose with biolar isorer
showing sytos of ania ay be treate hara-
cologically with an antianic agent, lithiu (see Drug
Class: Antianic Agent), valroate, or an atyical anti-
sychotic agent (see Uses later).
Antieressants can be subivie into four
categories:
1. First-generation antieressants: onoaine oxi-
ase inhibitors (MAOIs) an tricyclic antieressants
(TCAs)
2. Secon-generation antieressants: selective se-
rotonin reutake inhibitors (SSRIs) an serotonin-
noreinehrine reutake inhibitors (SNRIs)
3. Miscellaneous agents: buroion, irtazaine, tra-
zoone, vilazoone, an vortioxetine
4. N-ethyl-d-asartate (NMDA) antagonist (esket-
aine): for use in treatent of resistant eression
an aults with MDD with suicial thoughts or
actions
The secon-generation antieressants have efcacy
siilar to an lower toxicity with overose than the
rst-generation antieressants, so they are reco-
ene as rst-line agents.
All antieressants excet esketaine have varying
egrees of effects on noreinehrine, oaine, an se-
rotonin by blocking reutake an reucing estruction
of these neurotransitters, thereby rolonging their
action. The eveloent of a clinical antieressant
resonse requires at least 2 to 4 weeks of theray at
241
aequate osages. In general, the antieressant use
for theray shoul be change if there is no clear effect
within 4 to 6 weeks. Patients not resoning after two
or ore trials of antieressant rugs are consiere
to have treatent-resistant eression. Esketaine
(Sravato), a raily acting rug, is arove for
treatent-resistant eression in conjunction with an
oral antieressant. It is also inicate for eressive
sytos in aults with MDD with suicial thoughts
or actions in conjunction with oral antieressants.
Esketaine is an NMDA recetor antagonist. It is
ainistere intranasally uner the suervision of a
healthcare rovier. It ay increase bloo ressure
an ay iair attention, jugent, an thinking.
Because of the averse effects it ust be ainistere
uner the suervision of a healthcare rovier, an it
is only available through a restricte rogra.
Although uch is known about the haracologic
actions of antieressants, the exact echanis of ac-
tion of these agents for treating eressive an biolar
isorers is still unknown. However, it is now uner-
stoo that these isorers are not sily a eciency
of neurotransitters, but very colex isorers as-
sociate with genetics, life stressors, an altere hysi-
ologic athways in the brain.
USES
Two factors are iortant when selecting an anti-
eressant rug: the atient’s history of resonse to
reviously rescribe antieressants an the oten-
tial for averse effects associate with ifferent class-
es of antieressants. Contrary to arketing clais,
there are no ifferences aong antieressant rugs
(with the excetion of the MAOIs) in relative overall
theraeutic efcacy an onset cause by full theraeu-
tic osages. However, there are substantial ifferenc-
es in the averse effects cause by ifferent agents. It
is not ossible to reict which rug will be the ost
effective for an iniviual atient, but atients o
show a better resonse to a secic rug, even within
the sae class of rugs. About 30% of atients o not
show areciable theraeutic benet with the rst
agent use, but they ay have a high egree of success
with a change in eication. The history of revious
treatent is helful uring the selection of new treat-
ent if illness returns. Aroxiately 65% to 70% of
atients reson to antieressant theray, an 30%
to 40% achieve reission. Theray is base on a a-
tient’s history of revious resonse or the successful
resonse of a rst-egree relative who resone to
antieressant theray. Concurrent eical coni-
tions such as obesity, seizure history, otential for
ysrhythias, resence of anxiety, an otential for
rug interactions ust also be consiere in theray
selection. Certain tyes of oo isorers reson
to eication ore reaily than others. Theraeutic
success with TCAs an lithiu can be irove by
onitoring an aintaining theraeutic seru levels
242 UNIT III Drugs Affecting the Autonomic and Central Nervous System
an ajusting osages as neee. Seru levels of
other classes of antieressants generally o not cor-
relate well with success in theray, but they ay be
helful to eterine whether the atient is ahering
to the osage regien or suffering fro toxicities as-
sociate with higher seru levels. Recent changes in
ractice guielines ehasize the nee for continu-
ing rug theray for all atients; lifelong aintenance
theray will be require for soe atients. The osag-
es of continuance an aintenance theray ust also
be the sae as the acute ose effective for eliinating
eressive sytos. When atients are given lower
aintenance osages, the risk of relase is signicant-
ly greater than when oses are aintaine at acute
ose levels.
Antieressants increase the risk of suicial think-
ing an behavior (suiciality) in short-ter stuies
of chilren an aolescents with MDD an other
sychiatric isorers. Anyone consiering the use of
an antieressant for a chil or an aolescent ust
balance the risk with the clinical nee. When thera-
y is starte, atients ust be closely observe for
clinical worsening, suiciality, or unusual changes in
behavior. Failies an caregivers nee to be avise
about the nee for close observation an couni-
cation with the rescriber. Poole analyses of short-
ter (4 to 16 weeks) lacebo-controlle trials of nine
antieressant rugs (SSRIs an others) in chilren
an aolescents with MDD, obsessive-coulsive
relate isorers, or other sychiatric isorers—a
total of 24 trials involving ore than 4400 atients—
have reveale a greater risk for averse reactions
reresenting suicial thinking or behavior uring the
rst few onths of treatent in those receiving anti-
eressants. The average risk of such reactions in a-
tients receiving antieressants was 4%, which was
twice the lacebo risk of 2%. No suicies occurre
uring these trials.
Patients ust be counsele about execte thera-
eutic benets an averse effects to be tolerate
because of antieressant theray. The hysiologic
anifestations of eression (e.g., slee isturbance,
change in aetite, loss of energy, fatigue, alita-
tions) begin to be alleviate within the rst week of
theray. The sychological sytos (e.g., eresse
oo, lack of interest, social withrawal) will irove
after 2 to 4 weeks of theray at an effective osage.
Therefore it ay take 4 to 6 weeks to ajust the osage
to otiize theray an to iniize averse effects.
Unfortunately, soe averse effects evelo early
in theray, an atients who are alreay essiistic
because of their illness have a tenency to becoe
noncoliant.
The haracologic treatent of biolar isorer
ust be iniviualize because the clinical resenta-
tion, severity, an frequency of eisoes vary wie-
ly aong atients. Acute ania is initially treate
with lithiu, valroate, or an atyical antisychotic
agent (e.g., olanzaine, riserione) as onotheray.
Otions with the best evience to suort use as ain-
tenance treatents inclue antisychotics, lithiu,
an valroate; ossible alternatives inclue laotrig-
ine, carbaazeine, or oxcarbazeine.
NURSING IMPLICATIONS FOR MOOD DISORDER
THERAPY
Assessment
History of mood disorder
• Obtain a history of the atient’s oo isorer.
Is it eressive only, or are there both anic an
eressive hases interserse with erios of
noralcy? What reciitating factors contribute
to the changes in oo? Is it associate with a
articular season? How often o the eressive,
noral, an anic oos ersist? Are there bet-
ter or worse ties of ay? Has the atient been
treate reviously for a oo isorer? What is
the atient’s current status? Has the iniviual
been using alcohol or rugs? Has there been a
recent loss (e.g., job loss, en of a relationshi,
eath of a love one)?
• Obtain a etaile history of all eications that
the iniviual is currently taking an those taken
within the ast 2 onths to evaluate the atient’s
aherence to the treatent regien. How co-
liant has the atient been with the treatent
regien?
Basic mental status
• Note the atient’s general aearance an aro-
riateness of attire. Is the iniviual clean an neat?
Is the osture erect, stooe, or slue? Is the in-
iviual oriente to ate, tie, lace, an erson?
• What coing echaniss have been use to eal
with the oo isorer? How aative are these
coing echaniss? If these coing echaniss
are alaative, initiate changes by guiing the
iniviual in the use of ore aative coing
strategies.
• Review stanarize instruents or tools co-
lete by the atient, such as the Beck Deression
Inventory II (Beck, Steer, an Brown, 1996), a wiely
use assessent tool when screening for eression.
Interpersonal relationships
• Assess the atient’s interersonal relationshis.
Ientify eole in the atient’s life who are
suortive.
• Ientify whether interersonal relationshis have
ecline between the atient an faily ebers,
at work, or in social settings.
Mood and affect
• Is the iniviual elate, overjoye, angry, irritable,
crying, tearful, or sa? Is the facial exression tense,
worrie, sa, angry, or blank? Ask the erson to
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
escribe their feelings. Be alert for exressions of
loneliness, aathy, worthlessness, or hoelessness.
Moos ay change suenly.
• Be brief, irect, an to the oint with atients exeri-
encing the anic hase who have becoe arguen-
tative an aggressive. Setting liits will be necessary.
Plan to aroach the iniviual in a quiet, safe envi-
ronent with other staff available in case the atient
is aggressive or threatens har to self or others.
• Patients with altere thinking, behavior, or feelings
ust be carefully evaluate for verbal an non-
verbal actions. Often the thoughts, feelings, an be-
haviors islaye by these atients are inconsistent
with the so-calle noral resonses of ersons in
siilar circustances.
• Assess whether the oo being escribe is con-
sistent with the circustances being escribe.
For exale, is the erson seaking of eath while
siling?
Clarity of thought. Evaluate the coherency, relevancy,
an organization of the atient’s thoughts; observe for
ight of ieas, hallucinations, elusions, aranoia, or
graniose ieation. Ask secic questions about the
iniviual’s ability to ake jugents an ecisions.
Is there evience of eory iairent? Ientify ar-
eas in which the atient is caable of roviing inut
to set goals an ake ecisions. (This will hel the in-
iviual overcoe a sense of owerlessness regaring
life situations.) When the atient is unable to ake e-
cisions, lan to ake the. Set goals to involve the a-
tient because abilities change with treatent. Provie
an oortunity to lan for self-care.
Suicidal ideation. If the iniviual is susecte of be-
ing suicial, ask the atient whether they have ever
ha thoughts about suicie. If the resonse is “yes,”
get ore etails. Has a secic lan been forulate?
How often o these thoughts occur? Does the atient
ake irect or inirect stateents regaring eath
(e.g., “things woul be better” if eath occurre)?
Psychomotor function. Ask secic questions about
the activity level the atient has aintaine. Is the er-
son able to work or go to school? Is the erson able
to fulll resonsibilities at work, socially, an within
the faily? How have the erson’s noral resonses
to aily activities been altere? Is the iniviual with-
rawn an isolate or still involve in social inter-
actions? Check gestures, gait, acing, resence or
absence of treors, an ability to erfor gross or
ne otor oveents. Is the atient hyeractive or
iulsive? Note the seech attern. Are there
rolonge auses before answers are given or altere
levels of volue an inection?
Sleep pattern. What is the atient’s noral slee at-
tern, an how oes it vary with oo swings? Ask
243
secically whether insonia is resent an whether
it is initial (falling aslee) or terinal (staying aslee)
in nature. Ask the iniviual to escribe the erce-
tion of the aount an quality of slee nightly. Are
nas taken regularly?
Dietary history. Ask questions about the atient’s a-
etite, an note weight gains or losses not associate
with intentional ieting. During the anic hase, the
iniviual ay becoe anorexic. Is the erson able
to sit own to eat a eal, or o they only eat sall
aounts while acing?
Nonadherence. Nonaherence is usually exresse
by the enial of the severity of the isease. In ai-
tion, listen for excuses that the atient ay ake for
not taking rescribe eicine (e.g., cannot affor it,
asytoatic, “I on’t like the way it changes e. I
want to be yself!”).
Implementation
• Nursing interventions ust be iniviualize an
base on atient assessent ata.
• Provie an environent of accetance that focus-
es on the iniviual’s strengths while iniizing
weaknesses. Soeties it is necessary to rovie a
new environent for the atient uring a erio of
eression. The iniviual ay not be able to work
an ay nee a new eer grou. The atient ay
also nee to be away fro the faily while restruc-
turing an regrouing ersonal resources, ienti-
fying strengths, an achieving a theraeutic rug
level.
• Provie an oortunity for the atient to exress
feelings. Use active listening an theraeutic co-
unication techniques. Allow the atient to exress
feelings in nonverbal ways, such as involveent in
hysical activities or occuational theray. Recognize
that atients are hyeractive an talkative uring the
anic hase; it ay be necessary to interrut talking
an give concise, sile irections.
• Reain cal, irect, an r when roviing care.
Because atients in the anic hase ten to be argu-
entative, avoi getting involve in an arguent.
State the unit rules in a atter-of-fact anner an
enforce the.
• Allow the atient to ake ecisions, if caable;
ake those ecisions that the atient is not caable
of aking. Provie a rewar for rogress when e-
cisions are initiate aroriately. Involve the a-
tient in self-care activities.
• If the atient is suicial, ask for etails about the
lan being forulate. Follow u on etails ob-
taine with aroriate faily ebers or signi-
cant others (e.g., have guns reove fro the hoe
if this is art of the suicie lan). Provie for atient
safety an suervision, an recor observations at
secie intervals consistent with the severity of
244 UNIT III Drugs Affecting the Autonomic and Central Nervous System
the suicie threat an the olicies of the ractice
site. This is the highest riority for those with severe
oo isorers.
• Manic atients ay har others; it ay be necessary
to liit their interactions with other atients. Patients
in the anic hase ay require a quiet roo.
• Stay with atients who are highly agitate.
• Ainister as-neee rugs as orere for hyer-
activity. Make necessary observations about atient
resonses to the eications ainistere.
• ECT ay be orere to treat severe eression.
Check the healthcare rovier’s orers secic to
the retreatent an osttreatent care of the a-
tient receiving ECT.
• Use hysical restraints within the guielines of the
clinical setting as aroriate to the behaviors being
exhibite. Use the least restrictive alternative ossi-
ble for the circustances. Have sufcient staff avail-
able to assist with violent behavior to eonstrate
the ability to control the situation while roviing
for the safety an well-being of the atient an fel-
low staff ebers.
• Provie for nutritional nees by having high-
rotein, high-calorie foos aroriate for the in-
iviual to eat while acing or highly active. Have
nutritious snacks that the atient is known to like
available on the unit, an offer the throughout
the ay. Give vitains an liqui suleental
feeings as orere.
• Maniulative behavior ust be hanle in a consis-
tent anner by all staff ebers. Set liits an use
consequences that are agree to by all staff e-
bers. When the atient attets to blae others, re-
focus on the atient’s resonsibilities. Give ositive
reinforceent for nonaniulative behaviors when
they occur.
• Slee erivation (i.e., issing one or ore night’s
slee) is a ossibility with anic atients an can
be life threatening. Provie a quiet, nonstiulating
environent for the atient to slee. For atients
with eression, o not allow the iniviual to
slee continually. Design activities uring the ay
that will stiulate the iniviual an roote slee
at night. Scheule secic rouns to evaluate the in-
iviual’s slee an safety.
Patient Education
• Orient the iniviual to the unit. Exlain the rules
an the rocess of rivileges an how they are ob-
taine or lost. (The extent of the orientation an
exlanations given will een on the atient’s
orientation to ate, tie, an lace, as well as their
abilities.)
• Describe the variety of grou activities (e.g., social
skills, self-estee, hysical exercise) available with-
in articular theraeutic settings.
• Involve the atient an the faily in goal setting,
an integrate the atient into the aroriate grou
rocesses to evelo ositive exeriences an en-
hance coing skills.
• Base atient eucation on the assessent ata an
iniviualize teaching to rovie the atient with
a structure environent in which to grow an en-
hance their self-estee.
• Before ischarge, ake sure the atient an the
faily unerstan the esire treatent outcoes
an the entire follow-u lan (e.g., frequency of
theray sessions, rescribe eications, riary
healthcare rovier visits, return-to-work goals).
Fostering health maintenance
• Throughout the course of treatent, iscuss ei-
cation inforation an how it will benet the a-
tient. Drug theray is not ieiately effective in
treating eression; therefore the atient an sig-
nicant others ust unerstan the iortance of
continuing to take the rescribe eications e-
site inial initial resonse. The lag tie of 2 to
4 weeks between the initiation of rug theray an
the theraeutic resonse ust be stresse.
• Encourage the atient, faily, an caregivers to be
alert to the eergence of anxiety, agitation, anic at-
tacks, insonia, irritability, hostility, aggressiveness,
iulsivity, akathisia (sychootor restlessness),
hyoania, ania, unusual changes in behavior,
worsening of eression, an suiciality, esecially
at the start of antieressant treatent an when
the osage is ajuste u or own. Avise the fa-
ily an caregivers to observe for the eergence of
such sytos on a aily basis because changes
ay be abrut. Such sytos shoul be reort-
e to the atient’s rescriber, esecially if they are
severe, are abrut in onset, or were not art of the
atient’s resenting sytos. Sytos such as
these ay be associate with an increase risk of
suicial thinking an behavior an ay inicate the
nee for very close onitoring an ossible chang-
es in the eication regien.
• Ehasize the nee for the lithiu bloo level to
be easure at secie intervals. Give the atient
etails regaring the ate, tie, an lace for the
test to be erfore.
• Stress the iortance of aequate hyration (i.e.,
six to eight 8-ounce glasses of water er ay) an
soiu intake when receiving lithiu theray.
• Instruct the atient to weigh hiself or herself aily.
• Provie the atient or signicant others with i-
ortant inforation containe in the secic rug
onograhs for the eicines rescribe. The ono-
grahs also contain health teaching an nursing inter-
ventions for coon an serious averse effects.
• Seek cooeration an unerstaning of the fol-
lowing oints so that eication aherence is in-
crease: nae of the eication; its osage, route,
an tie of ainistration; an its coon an
serious averse effects. Encourage the atient not to
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
iscontinue or ajust the rug osage without con-
sulting the healthcare rovier.
• Chilren an aolescent atients ust be closely
observe for clinical worsening, suiciality, or un-
usual changes in behavior. Failies an caregivers
nee to be avise of the nee for close observation
an counication with the rescriber.
• Provie atients an failies with inforation
about available counity resources, incluing the
National Alliance on Mental Illness.
Patient self-assessment. Enlist the atient’s hel with
eveloing an aintaining a written recor of oni-
toring araeters. See the Patient Self-Assessent
For for Antieressants on the Evolve website, an
colete the Preeication Data colun for use as a
baseline to track the atient’s resonse to rug thera-
y. Ensure that the atient unerstans how to use the
for, an instruct the atient to bring the colete
for to follow-u visits. During follow-u visits, focus
on issues that will foster aherence with the theraeu-
tic interventions rescribe.
Clinical Pitfall
Antidepressants may increase the risk of suicidal thinking
and behavior (suicidality) in patients of all ages who are expe-
riencing MDD. Patients who are started on antidepressants
should be monitored daily by family members and caregivers
for the emergence of agitation, irritability, unusual changes
in behavior, and suicidality. These symptoms should be im-
mediately reported to healthcare providers.
DRUG THERAPY FOR DEPRESSIVE
DISORDERS
DRUG CLASS: MONOAMINE OXIDASE INHIBITORS
Actions
MAOIs block the etabolic estruction of einehrine,
noreinehrine, oaine, an serotonin neurotrans-
itters by the enzye onoaine oxiase (MAO) in
the resynatic neurons of the brain. As a result, the
concentration of these central nervous syste (CNS)
neurotransitters becoes increase. Although MAO
inhibition starts within a few ays after initiating ther-
ay, the antieressant effects require 2 to 4 weeks to
becoe evient. Aroxiately 60% of the clinical
iroveent of sytos of eression occurs after
2 weeks, an axiu iroveent is usually at-
taine within 4 weeks.
Uses
The MAOIs use toay are henelzine, tranylcyro-
ine, isocarboxazi, an selegiline (Table 16.1). They
are equally effective an have siilar averse effects.
They are ost effective for atyical eression, anic
isorer, obsessive-coulsive relate isorers, an
245
soe hobic isorers. Selegiline is arove for treat-
ent of MDD. They are also use when TCA theray
is unsatisfactory an when ECT is inaroriate or
refuse. Selegiline is available as a transeral atch
that shoul be change once every 24 hours. Patients
using the lowest strength available (6 g) o not have
ietary restrictions. However, ietary restrictions are
require for those using the 9- an 12-g atches.
Therapeutic Outcomes
The riary theraeutic outcoes execte fro
MAOIs are elevate oo an the reuction of sy-
tos of eression.
Nursing Implications for Monoamine Oxidase
Inhibitors
Premedication assessment
1. Obtain the atient’s bloo ressure an ulse
rate before an at regular intervals after initiating
theray.
2. If the atient has iabetes, onitor the bloo glu-
cose level to establish baseline values an assess
this erioically uring theray. Because MAOIs
cause hyoglyceia, a osage ajustent in insu-
lin or oral hyerglyceic theray ay be require.
If the atient has a history of severe renal isease,
liver isease, cerebrovascular isease, or congestive
heart failure, o not give the eication an consult
with the rescriber.
3. Colete a iet history to ensure that the atient
has not ingeste eals with a high tyraine content
uring the ast few ays.
4. Colete a eication history to ensure that the
atient has not taken any of the following ei-
cines uring the ast few ays: SSRIs, SNRIs,
TCAs, extroethorhan, eherine, ahet-
aines, ethylheniate, levooa, traaol, St.
John’s wort, cyclobenzarine, carbaazeine, or
eeriine.
Availability. See Table 16.1
Medication Safety Alert
Monoamine Oxidase Inhibitors and Hypertension
Monoamine oxidase inhibitors, when used in conjunction
with certain foods and beverages that contain tyramine and
other medicines, may result in severe hypertension poten-
tially leading to stroke, other organ damage, and death.
Foos containing signicant quantities of tyraine
inclue well-riene cheeses (e.g., Caebert, Ea,
Roquefort, Paresan, ozzarella, chear); yeast
extract; re wines; ickle herring; sauerkraut; over-
rie bananas, gs, an avocaos; chicken liver; an
beer. Foos containing other cheicals that ay raise
bloo ressure inclue fava beans, chocolate, coffee,
tea, an colas.
246 UNIT III Drugs Affecting the Autonomic and Central Nervous System

Table 16.1 Antidepressants

DAILY
INITIAL DOSAGE MAINTENANCE
RANGE (ORAL UNLESS DOSAGE RANGE MAXIMUM DAILY
GENERIC NAME BRAND NAME AVAILABILITY OTHERWISE NOTED) (MG) DOSAGE RANGE (MG)
MONOAMINE OXIDASE INHIBITORS
isocarboxazid Marplan Tablets: 10 mg 10 mg twice daily 40 60
phenelzine Nardil Tablets: 15 mg 15 mg three times 15–60 90
daily
selegiline Emsam Patch, transdermal: 6-mg patch daily 6 12
Do not confuse 6, 9, 12 mg/24 hr
selegiline with
sertraline or
Salagen.
tranylcypromine Parnate Tablets: 10 mg 30 mg daily divided 30 60
SELECTIVE SEROTONIN REUPTAKE INHIBITORS
citalopram Celexa Tablets: 10, 20, 20 mg daily 20–40 40
Do not confuse 40 mg
Celexa with Liquid: 10 mg/5 mL
Zyprexa or
Celebrex.
Ran-Citalo
escitalopram Lexapro Tablets: 5, 10, 10 mg daily 10–20 20
Do not confuse 20 mg
Lexapro with Liquid: 1 mg/mL
loxapine.
Cipralex
uoxetine Prozac Capsules: 10, 20, 20 mg in the morning 20–60 80
Do not confuse Do not confuse 40 mg
uoxetine with Prozac with Tablets: 10, 20, 60
uphenazine, Prilosec or mg
uvoxamine, Proscar. Solution: 20 mg/5
famotidine, APO-Fluoxetine mL
uvastatin, or Capsules, delayed
paroxetine. release, weekly:
90 mg
uvoxamine — Tablets: 25, 50, 50 mg at bedtime 50–300 300
Do not confuse Riva-Fluvox 100 mg
uvoxamine with Capsules, 24 hr
uoxetine. sustained release:
100, 150 mg
paroxetine Paxil Capsules: 7.5, mg 20 mg daily 20–50 50–75
Do not confuse Do not confuse Tablets: 10, 20, 30,
paroxetine Paxil with 40 mg
with uoxetine, paclitaxel, Plavix, Suspension: 10
paclitaxel, or or Taxol. mg/5 mL
pyridoxine. Paxil CR Tablets, extended
release (24 hr):
12.5, 25, 37.5 mg
sertraline Zoloft Tablets: 25, 50, 50 mg daily 50–200 200
Do not confuse 100 mg
sertraline with Do not confuse Oral concentrate:
selegiline, Zoloft with Zocor 20 mg/mL
Seroquel, or or Zyloprim.
Singulair.
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16 247

Table 16.1 Antidepressants—cont’d

DAILY
INITIAL DOSAGE MAINTENANCE
RANGE (ORAL UNLESS DOSAGE RANGE MAXIMUM DAILY
GENERIC NAME BRAND NAME AVAILABILITY OTHERWISE NOTED) (MG) DOSAGE RANGE (MG)
SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS
desvenlafaxine Pristiq Tablets, 24 hr 50 mg daily at the 50–400 400
sustained release: same time
25, 50, 100 mg
duloxetine Cymbalta Capsules, sustained 40 mg daily 60 120
Do not confuse release: 20, 30,
Cymbalta with 40, 60 mg
Zyprexa or
Celebrex.
Drizalma Sprinkle
levomilnacipran Fetzima Capsules, extended 20 mg once daily 40–120 120
release: 20, 40, for 2 days; then
80, 120 mg 40 mg once daily
venlafaxine Effexor XR Tablets: 25, 37.5, 75 mg in two or three 75–225 225 (outpatients)
50, 75, 100 mg doses daily, taken 375 (inpatients)
Capsules, tablets, with food
sustained release:
37.5, 75, 150,
225 mg
TRICYCLIC ANTIDEPRESSANTS
amitriptyline — Tablets: 10, 25, 50, 25–75 mg daily, 75–200
Do not confuse 75, 100, 150 mg divided as needed 300 (inpatients)
amitriptyline with
aminophylline.
amoxapine — Tablets: 25, 50, 50 mg two or three 200–300 400 (outpatients)
100, 150 mg times daily 600 (inpatients)
clomipramine Anafranil Capsules: 25, 50, 25 mg once daily 100–150 250
75 mg
desipramine Norpramin Tablets: 10, 25, 50, 50–75 mg daily, 100–200 300
75, 100, 150 mg divided in one to
four doses
doxepin Silenor Capsules: 10, 25, 25 mg three times 75–150 300 (inpatients)
Do not confuse NOVO-Doxepin 50, 75, 100, daily
doxepin with 150 mg
digoxin. Tablets: 3, 6mg
Oral concentrate:
10 mg/mL
imipramine — Tablets: 10, 25, 30–75 mg daily in 50–150 200 (outpatients)
hydrochloride 50 mg one to four divided 300 (inpatients)
doses
imipramine pamoate — Capsules: 75, 100, 75–150 mg daily at 75–150 200 (outpatients)
125, 150 mg bedtime 300 (inpatients)
nortriptyline Pamelor Capsules: 10, 25, 25–50 mg in one to 50–75 150
Norventyl 50, 75 mg four divided doses
Solution: 10 mg/5
mL
protriptyline — Tablets: 5, 10 mg 5–10 mg three times 20–40 60
daily
trimipramine — Capsules: 25, 50, 25 mg three times 50–150 200 (outpatients)
Apo-Trimiprapine 100 mg daily 300 (inpatients)
Available in Canada.
Do not confuse.
248 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Meications (incluing over-the-counter ei-
cines) containing syathoietic aines whose
etabolis is blocke by MAOIs ay result in ex-
cessive accuulation of neurotransitters siilar to
noreinehrine. Exales are extroethorhan,
carbaazeine, cyclobenzarine, ethylheniate,
trytohan, ahetaines, eherine, ethyloa,
levooa, linezoli, an einehrine.
MAO inhibition of the etabolis of these neu-
rotransitters that originate fro foo, beverages,
an eicine ay result in a suen increase in bloo
ressure with systolic ressures in the range of 160 to
230  Hg an iastolic ressures of 100 to 130 
Hg, a hyertensive crisis an a eical eergency.
Acute sytos inclue severe heaache, stiff neck,
heart alitations, sweating, nausea, an voiting.
Patients ust be transorte to a eical facility for
eergency treatent to reuce bloo ressure before
signicant organ aage occurs. It is recoene
that at least 14 ays lase between the change in iet
avoiing tyraine-containing roucts an iscon-
tinuation of other aine-containing eicines before
initiating MAOI theray.
Dosage and administration
1. Instruct the atient how to liit tyraine-containing
foos, which coul cause a life-threatening hyer-
tensive crisis if they are ingeste concurrently with
MAOIs.
2. The osage shoul be taken in ivie oses, with
the last ose ainistere no later than 6 pm to re-
vent rug-inuce insonia. Caution the atient
not to iscontinue the eicine abrutly. If a ose
is isse, take it ieiately when this is realize
an then sace the reainer of the aily osage
throughout the rest of the ay.
3. Make certain that the atient is not receiving any of
the eications liste in the reeication assess-
ent shown reviously.
Common adverse effects
Cardiovascular
Orthostatic hypotension. The ost coon averse ef-
fect of MAOIs is hyotension; it is ore signicant with
henelzine than with tranylcyroine. Orthostatic
hyotension, anifeste by izziness an weakness,
is generally il an is ore coon when theray is
starte. Daily ivie oses hel iniize the hyo-
tension, an tolerance usually evelos after a few
weeks of theray. Monitor the atient’s bloo res-
sure aily in both the suine an staning ositions.
Anticiate the eveloent of ostural hyotension
an take easures to revent its occurrence. Teach the
atient to rise slowly fro a suine or sitting osition,
an encourage sitting or lying own if feeling faint.
Neurologic
Drowsiness, sedation. Phenelzine has il to oer-
ate seating effects. These sytos ten to isaear
with continue theray an with the ossible rea-
justent of the osage. Infor the atient of ossible
seative effects. The atient shoul use caution while
riving or erforing other tasks that require alert-
ness. Consult with the healthcare rovier to consier
oving the aily ose to betie if seation continues
to be a roble.
Restlessness, agitation, insomnia. These effects are
ore coon with tranylcyroine an are transient
as the osage is being ajuste. Have the atient take
the last ose before 6 pm to iniize insonia.
Sensory
Blurred vision. Caution the atient that blurre vision
ay occur an ake aroriate suggestions for the
atient’s ersonal safety.
Gastrointestinal
Constipation; dryness of mucosa of the mouth, throat,
nose. Mucosal ryness ay be relieve by sucking
har cany or ice chis or by chewing gu. Give the
atient stool softeners as rescribe. Encourage a-
equate ui intake an foos that will rovie suf-
cient bulk.
Genitourinary
Urinary retention. If the atient evelos urinary hesi-
tancy, assess for blaer istention. Reort this to the
healthcare rovier for further evaluation.
Serious adverse effects
Cardiovascular
Hypertension. Hyertensive crisis is a ajor otential
colication with MAOI theray, articularly with
tranylcyroine.
Drug interactions
Drugs that increase toxic effects. See the Meication
Safety Alert: Monoaine Oxiase Inhibitors an
Hyertension.
Tricyclic antidepressants. MAOIs an TCAs, esecial-
ly iiraine an esiraine, shoul not be ain-
istere concurrently. It is recoene that at least 14
ays lase between the iscontinuation of MAOIs an
the initiation of another antieressant.
Selective serotonin reuptake inhibitors, serotonin-
norepinephrine reuptake inhibitors. Severe reactions—
such as convulsions, hyeryrexia, an eath—have
been reorte with concurrent use of these rugs. It
is recoene that at least 14 ays lase between
iscontinuing an MAOI an starting SSRI or SNRI
theray. A 5-week interval is recoene between
iscontinuing uoxetine an starting MAOIs.
General anesthesia, diuretics, antihypertensive
agents. MAOIs ay otentiate the hyotensive effects of
general anesthesia, iuretics, an antihyertensive agents.
Insulin, oral hypoglycemic agents. MAOIs have an a-
itive hyoglyceic effect when cobine with insu-
lin an oral sulfonylureas. Monitor the atient’s bloo
glucose level an lower the hyoglyceic osage, if
necessary.
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
Meperidine, tramadol. When MAOIs are use con-
currently with eeriine or traaol, atients ay
suffer fro hyeryrexia, restlessness, hyertension,
hyotension, convulsions, an coa. The effects of
this interaction ay occur for several weeks after is-
continuing an MAOI. Morhine ight be an alterna-
tive at lower oses, but onitoring is neee.
DRUG CLASS: SELECTIVE SEROTONIN REUPTAKE
INHIBITORS
Actions
SSRIs (see Table 16.1) are a class of antieressants
cheically unrelate to other antieressants. They
inhibit the reutake of serotonin fro the synatic
cleft, thereby increasing the serotonin concentration
that enhances neurotransission.
Uses
SSRIs have becoe the ost wiely use class of anti-
eressants an have been shown to be as effective in
treating eression as TCAs. A articular avantage
of the SSRIs is that they o not have the anticholinergic
an cariovascular averse effects that often liit the
use of TCAs. As with other antieressants, it takes
2 to 4 weeks of theray to obtain the full theraeu-
tic benet when treating eression. Fluoxetine is the
only SSRI that has been arove for use in treating
eression in chilren an aolescents. The US Foo
an Drug Ainistration has recoene that
aroxetine not be given to atients younger than 18
years.
SSRIs are also being stuie for treatent of
obsessive-coulsive relate isorers, obesity, eat-
ing isorers (e.g., anorexia nervosa, buliia nervosa),
biolar isorer, anic isorer, autis, an several
other isorers. Fluvoxaine, aroxetine, sertraline,
an uoxetine are arove for use in atients with
obsessive-coulsive relate isorers. Fluoxetine is
arkete uner the bran nae Sarafe for treatent
of reenstrual yshoric isorer.
Therapeutic Outcomes
The riary theraeutic outcoes execte fro the
SSRIs are elevate oo an reuction of the sy-
tos of eression.
Nursing Implications for Selective Serotonin
Reuptake Inhibitor Therapy
Premedication assessment
1. Obtain the atient’s baseline bloo ressures in the
suine, an staning ositions; recor an reort
signicant lowering to the healthcare rovier be-
fore ainistering the rug.
2. Obtain the atient’s baseline weight an scheule
weekly weight easureents.
3. Note any gastrointestinal (GI) sytos resent
before the start of theray.
249
4. Monitor any CNS sytos resent, such as in-
sonia or nervousness.
5. Check the atient’s heatic stuies before initiat-
ing the eication an erioically throughout the
course of ainistration.
Availability, dosage, and administration. See Table 16.1
Medication Safety Alert
Serotonin Syndrome
Serotonin syndrome may develop as a result of excessive
accumulation of serotonin in nerve synapses. It is an uncom-
mon event, but may be potentially fatal. The syndrome oc-
curs if two or more drugs block the metabolism of serotonin,
leaving excessive serotonin in nerve synapses. Most case
reports have arisen from the combined use of SSRIs and
MAOIs, or not allowing a recommended 14-day washout pe-
riod before stopping one class of medicine and starting the
other class of medicine. Less frequently reported cases have
been noted with SSRIs, TCAs, SNRIs, buspirone, vortiox-
etine, vilazodone, linezolid, fentanyl, triptans, and meperidine.
Monitor for symptoms of serotonin syndrome, including
irritability, hallucinations, delirium, reduced consciousness,
increased muscle tone, myoclonus, diaphoresis, shivering,
tremor, hyperthermia, and increased or decreased blood
pressure and heart rate. Notify the healthcare provider
immediately.
Observation. Sytos of eression ay irove
(e.g., increase aetite, slee, an sychootor activ-
ity) within a few ays. However, the eression still
exists, an it usually takes several weeks of the atient
receiving theraeutic osing before iroveent is
note. Suicie recautions shoul be aintaine ur-
ing this tie.
Discontinuation syndrome. Abrut iscontinuation
or interrution of antieressant theray ay result
in a iscontinuation synroe. Sytos ay vary
with the antieressant but coonly inclue nau-
sea, voiting, iarrhea, heaaches, light-heaeness,
izziness, iinishe aetite, sweating, chills, tre-
ors, aresthesia, fatigue, sonolence, an slee is-
turbances (e.g., vivi reas, insonia). Greater
risks for eveloing a iscontinuation synroe have
been associate with antieressants with shorter
half-lives, longer urations of treatent, an abrut
iscontinuation.
Common adverse effects
Neurologic
Restlessness, agitation, anxiety, insomnia. These ef-
fects usually occur early in theray an ay require
short-ter treatent with seative-hynotic agents.
Avoiing betie oses ay also hel ecrease the
incience of insonia.
Sedative effect. Tell the atient about ossible sea-
tive effects. The atient shoul use caution while
250 UNIT III Drugs Affecting the Autonomic and Central Nervous System
riving or erforing other tasks that require alert-
ness. Consult with the healthcare rovier to consier
oving the aily ose to betie if seation continues
to be a roble.
Gastrointestinal
Nausea, anorexia. Most of these effects ay be ini-
ize by teorarily reucing the osage an tak-
ing the ose with foo. Encourage the atient not to
iscontinue theray without consulting the healthcare
rovier rst.
Serious adverse effects
Psychological
Suicidal ideation. Monitor the atient for changes in
thoughts, feelings, an behaviors uring the initial
stages of theray.
Drug interactions
Tricyclic antidepressants. The interaction between
SSRIs an TCAs is very colex. An increase toxicity
results fro TCAs. Observe the atient for signs of tox-
icity, such as ysrhythias, seizure activity, an CNS
stiulation.
Lithium. Lithiu ay enhance the serotonergic ef-
fect of SSRIs, thereby increasing the risk of serotonin
toxicity (serotonin synroe). Use the cobination of
SSRIs an lithiu very cautiously, onitoring closely
for signs of serotonin toxicity such as irritability, hallu-
cinations, eliriu, increase uscle tone, shivering,
yoclonus, an reuce consciousness.
Monoamine oxidase inhibitors. Severe reactions—
incluing exciteent, iahoresis, rigiity, convul-
sions, hyeryrexia, an eath—have been reorte
with the concurrent use of MAOIs an SSRIs. It is rec-
oene that at least 14 ays lase between iscon-
tinuing an MAOI an starting SSRI theray. A 5-week
sto interval is recoene between iscontinuing
uoxetine an starting MAOIs.
Haloperidol. Fluoxetine an uvoxaine increase
haloeriol levels an the frequency of extrayrai-
al sytos (EPSs). If use concurrently, the osage
of haloeriol ay nee to be ecrease.
Phenytoin, phenobarbital. Colex interactions oc-
cur when henobarbital an henytoin enhance the
etabolis of aroxetine, thereby requiring a os-
age increase in aroxetine for theraeutic effect. In a
siilar fashion, aroxetine increases the etabolis
of henytoin, thus requiring an increase in the os-
age of henytoin to aintain the theraeutic effect.
Conversely, uoxetine ay iinish the etabolis
of henytoin, thereby resulting in otential heny-
toin toxicity.
Carbamazepine. Fluoxetine an uvoxaine can in-
crease carbaazeine concentrations, which can result
in signs of toxicity such as vertigo, treor, heaache,
rowsiness, nausea, an voiting. The osage of car-
baazeine ay nee to be reuce. Carbaazeine
ay enhance the excretion of citalora, thereby
leaing to a ecrease theraeutic effect. The osage
of citalora ay nee to be increase.
Alprazolam. Fluoxetine, uvoxaine, an sertraline
rolong the activity of alrazola, which results in ex-
cessive seation an iaire otor skills.
Propranolol, metoprolol. Fluvoxaine an citalora
signicantly inhibit the etabolis of these beta-ar-
energic blocking agents. Monitor the atient closely
for braycaria an hyotension. Reuce the osage
of the beta blocker as neee.
Cimetidine. Cietiine inhibits the etabolis of
aroxetine an sertraline. Patients shoul be closely
onitore when cietiine is ae to aroxetine or
sertraline theray.
Warfarin. Fluoxetine, aroxetine, sertraline, citalo-
ra, an uvoxaine ay enhance the anticoagulant
effects of warfarin. Observe the atient for etechiae, ec-
chyoses, noseblees, bleeing gus, ark tarry stools,
an bright re or coffee-groun eesis. Monitor the in-
ternational noralize ratio (INR) of warfarin; reuce
the osage of warfarin if necessary.
Smoking. Cigarette soking enhances the etabo-
lis of uvoxaine. Dosages of uvoxaine ay nee
to be increase to achieve full theraeutic resonse.
Amphetamines, tryptophan, dextromethorphan, linezolid,
ephedrine, pseudoephedrine, epinephrine. All of these
agents increase serotonin levels, otentially causing
serotonin synroe when taken by a erson receiving
SSRIs.
DRUG CLASS: SEROTONIN-NOREPINEPHRINE
REUPTAKE INHIBITORS
Actions
SNRI (see Table 16.1) are a class of antieressants that
act by inhibiting the reutake of serotonin an norei-
nehrine—an, to a lesser extent, oaine—fro
the synatic cleft, thereby rolonging the action of the
neurotransitters.
Uses
SNRIs have becoe a wiely use class of anti-
eressants. As with other antieressants, it takes
2 to 4 weeks of theray to obtain the full theraeutic
benet in treating eression.
Venlafaxine is arove for treatent of eres-
sion, generalize anxiety isorer, social anxiety
isorer, an anic isorer. Duloxetine is arove
for treatent of MDD, generalize anxiety isorer,
broyalgia, chronic usculoskeletal ain, an ia-
betic eriheral neuroathic ain. Desvenlafaxine
an levoilnaciran are arove for treatent of
MDD.
Therapeutic Outcomes
The riary theraeutic outcoes execte fro the
SNRIs are elevate oo an reuction of sytos
of eression.
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
Nursing Implications for Serotonin-
Norepinephrine Reuptake Inhibitor Therapy
Premedication assessment
1. Obtain the atient’s baseline weight an bloo
ressure.
2. Note any GI sytos before starting theray.
3. Monitor any CNS sytos resent, such as in-
sonia or nervousness.
4. Reort any history of hyertension, substance
abuse, or renal or heatic isease to the healthcare
rovier.
Availability, dosage, and administration. See Table 16.1
Discontinuation of therapy. If the atient has taken the
eicine for ore than 1 week before iscontinuation,
the osage shoul be taere over the next few ays.
If venlafaxine has been taken for ore than 6 weeks,
the osage shoul graually be taere over the next
2 weeks.
Observation. Sytos of eression ay irove
(e.g., increase aetite, slee, an sychootor activity)
within a few ays. However, the eression still exists,
an it usually takes several weeks of the atient receiving
theraeutic osing before iroveent is note. Suicie
recautions shoul be aintaine uring this tie.
Common adverse effects
Neurologic
Dizziness, drowsiness. The atient shoul be warne
to not work with achinery, oerate a otor vehicle,
ainister eication, or erfor other uties that
require ental alertness until it is known whether this
averse effect iairs jugent.
Restlessness, agitation, anxiety, insomnia. These effects
usually occur early in theray, an the atient ay
require short-ter treatent with seative-hynotic
agents. Avoiing betie oses ay hel ecrease the
incience of insonia.
Gastrointestinal
Nausea, anorexia. Most of these effects ay be ini-
ize by teorarily reucing the osage an taking
the oses with foo.
Serious adverse effects
Psychological
Suicidal ideation. Monitor the atient for changes in
thoughts, feelings, an behaviors uring the initial
stages of theray.
Drug interactions
Monoamine oxidase inhibitors. Severe reactions—
incluing exciteent, iahoresis, rigiity, convulsions,
hyeryrexia, an eath—have been reorte with the
concurrent use of MAOIs an SNRIs. It is recoen-
e that at least 14 ays lase between iscontinuing an
MAOI an starting SNRI theray (an vice versa).
Cimetidine. Cietiine inhibits the etabolis of
venlafaxine an uloxetine. Patients shoul be closely
251
onitore for excessive effects of these two rugs when
cietiine is ae to the theraeutic regien.
Trazodone. Serotonin synroe ay evelo when
trazoone is use in conjunction with venlafaxine. Use
trazoone cautiously; initiate theray at a lower os-
age an closely onitor for the averse effects liste.
Haloperidol. Venlafaxine increases haloeriol levels
an increases the frequency of EPSs, such as akathisia,
ystonia, seuoarkinsonis, an yskinesia (see
Chater 17 for ore inforation). If these rugs are
use concurrently, the osage of haloeriol ay nee
to be ecrease.
DRUG CLASS: TRICYCLIC ANTIDEPRESSANTS
Actions
Until recently, TCAs (see Table 16.1) were the ost
wiely use eications for the treatent of eres-
sion. SRRIs now have that istinction, but their long-
ter effects are yet to be coletely eterine.
TCAs rolong the action of noreinehrine, oa-
ine, an serotonin to varying egrees by blocking
the reutake of these neurotransitters in the syna-
tic cleft between neurons. The exact echanis of ac-
tion when these rugs are use as antieressants is
unknown.
Uses
TCAs rouce antieressant an il tranquil-
izing effects. After 2 to 4 weeks of theray, these
rugs elevate oo, irove aetite, an increase
alertness in aroxiately 80% of atients with en-
ogenous eression. Cobination theray with
henothiazine erivatives ay be beneficial for
treating eression associate with schizohrenia
or oerate to severe anxiety an eression ob-
serve with sychosis.
All TCAs are equally effective for treating eres-
sion, assuing that aroriate osages are use for
an aequate erio. Consequently the selection of an
antieressant is base riarily on the characteris-
tics of each agent. Seation is ore notable with ai-
trityline, oxein, an triiraine. Protrityline
has no seative roerties, an it ay actually ro-
uce il stiulation in soe atients. All tricyclic
coouns islay anticholinergic activity, with
aitrityline islaying the ost an esiraine
the least. This factor shoul be consiere in atients
with cariac isease, rostatic hyerlasia, or glau-
coa. Other factors to consier are that en ten to
reson better to iiraine than woen an oler
aults ten to reson better to aitrityline than
younger atients.
Doxein is also arove for treating anxiety, an
iiraine is arove for treating enuresis in chil-
ren who are 6 years ol an oler. Cloiraine is
not use to treat eression, but is arove for treat-
ing obsessive-coulsive relate isorers.
252 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Selecte TCAs are also use to treat hanto lib ain,
chronic ain, cancer ain, eriheral neuroathy with ain,
ostheretic neuralgia, arthritic ain, eating isorers,
reenstrual sytos, an obstructive slee anea.
Therapeutic Outcomes
The riary theraeutic outcoes execte fro
TCAs are elevate oo an reuction of sytos
of eression.
Nursing Implications for Tricyclic Antidepressants
Premedication assessment
1. Note the consistency of the atient’s bowel ove-
ents; constiation is coon when taking TCAs.
2. Obtain the atient’s baseline bloo ressure in
suine an staning ositions; recor an reort
signicant hyotension to the healthcare rovier
before ainistering the rug.
3. Check the atient’s history for sytos of ys-
rhythias, tachycaria, or congestive heart failure;
if resent, consult the healthcare rovier before
starting theray (the atient ay require electro-
cariograhy before theray is starte).
4. If the atient has a history of seizures, check with
the healthcare rovier to see if the osage of
anticonvulsant theray eications nees to be
ajuste.
Availability, dosage, and administration. Adult: PO:
See Table 16.1. The eication shoul be initiate at
a low osage level an increase graually, articu-
larly for oler or ebilitate atients. Dosage increases
shoul be ae in the evening because increase sea-
tion often occurs.
Observation. Sytos of eression ay irove
(e.g., increase aetite, slee, an sychootor activity)
within a few ays. However, the eression still exists,
an it usually takes several weeks of the atient receiving
theraeutic osing before iroveent is note. Suicie
recautions shoul be aintaine uring this tie.
Common adverse effects
Cardiovascular
Orthostatic hypotension. All TCAs ay cause soe
egree of orthostatic hyotension, anifeste by iz-
ziness an weakness, articularly when theray is rst
begun. Monitor the atient’s bloo ressure aily in
both the suine an staning ositions. Anticiate the
eveloent of ostural hyotension an take eas-
ures to revent such an occurrence. Teach the atient
to rise slowly fro a suine or sitting osition an en-
courage the atient to sit or lie own if feeling faint.
Neurologic
Sedative effects. Tell the atient about ossible sea-
tive effects. These effects usually occur early in thera-
y. Taking a single ose at betie ay iinish or
relieve the seative effects.
Sensory
Blurred vision. Caution the atient that blurre vi-
sion ay occur an ake aroriate suggestions to
ensure the atient’s ersonal safety.
Gastrointestinal
Constipation; dryness of mucosa of the mouth, throat,
nose. Mucosal ryness ay be relieve by sucking
har cany or ice chis or by chewing gu. The use
of stool softeners such as ocusate or the occasional
use of a stiulant laxative such as bisacoyl ay be
require for constiation.
Serious adverse effects
Neurologic
Tremor. Aroxiately 10% of atients evelo this
averse effect. Treor can be controlle with sall
oses of roranolol.
Numbness, tingling. Reort these sytos to the
healthcare rovier for further evaluation.
Parkinsonian symptoms. If these sytos evelo,
the TCA osage ust be reuce or iscontinue.
Antiarkinsonian eications will not control sy-
tos inuce by TCAs.
Seizure activity. High oses of antieressants lower the
seizure threshol. Ajustent of anticonvulsant theray
ay be require, esecially for seizure-rone atients.
Cardiovascular
Dysrhythmias, tachycardia, heart failure. Reort these
sytos to the healthcare rovier for further
evaluation.
Psychological
Suicidal ideation. Monitor the atient for changes in
thoughts, feelings, an behaviors uring the initial
stages of theray.
Drug interactions
Enhanced anticholinergic activity. Antihistaines,
henothiazines, trihexyheniyl, an benztroine en-
hance the anticholinergic activity associate with TCA
theray. The averse effects are usually not severe
enough to warrant iscontinuing theray, but stool
softeners ay be require.
Enhanced sedative activity. Ethanol, barbiturates, nar-
cotics, tranquilizers, antihistaines, anesthetics, an
seative-hynotics enhance the seative activity as-
sociate with TCA theray. Concurrent theray is not
recoene.
Phenobarbital. Phenobarbital ay stiulate the
etabolis of TCAs. Dosage ajustents of the anti-
eressant ay be necessary.
Bupropion. Buroion ay increase seru levels of
TCAs. Dosages ay nee to be reuce.
Carbamazepine. TCAs can increase carbaazeine
concentrations, resulting in signs of toxicity such as ver-
tigo, treor, heaache, rowsiness, nausea, an voit-
ing. The osage of carbaazeine ay nee to be re-
uce. Carbaazeine ay also reuce seru levels of
TCAs. Dosages of the TCA ay nee to be increase.
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
Valproic acid, methylphenidate. These eications
ay increase the seru levels of the TCAs. This re-
action has been avantageous in attets to gain
a faster onset of antieressant activity, but an in-
crease incience of ysrhythias also has been
reorte.
Clonidine. TCAs inhibit the antihyertensive ef-
fects of cloniine an ay enhance the hyertension
seen with the abrut iscontinuation of cloniine.
Concurrent theray shoul be avoie.
Monoamine oxidase inhibitors. Severe reactions—
incluing convulsions, hyeryrexia, an eath—
have been reorte with concurrent use. It is reco-
ene that 2 weeks lase between iscontinuing an
MAOI an starting TCAs.
Selective serotonin reuptake inhibitors. The interaction
between SSRIs an TCAs is colex. The net result
is that there is an increase toxicity fro the TCAs.
Observe atients for signs of toxicity, such as ysrhyth-
ias, seizure activity, an CNS stiulation.
Amphetamines, tryptophan, dextromethorphan, linezolid,
ephedrine, pseudoephedrine, epinephrine. All of these
agents increase serotonin levels, otentially causing
serotonin synroe when taken by a erson receiving
TCAs. These eications shoul be use together only
uner the suervision of a healthcare rovier.
Cimetidine. Cietiine inhibits the etabolis of
TCAs. Patients shoul be closely onitore for a-
itional anticholinergic sytos. In general, cie-
tiine theray shoul be avoie in atients taking
TCAs. Ranitiine an faotiine ay be use without
rug interactions.
Smoking. Cigarette soking enhances the etabo-
lis of TCAs. Dosages of the TCA ay nee to be in-
crease to achieve a full theraeutic resonse.
DRUG CLASS: MISCELLANEOUS AGENTS
BUPROPION HYDROCHLORIDE
bupropion hydrochloride (byū-PRŌ-pē ŏn)
Do not confuse bupropion with buspirone.
Aplenzin (ah-plen-zin)
Forvo XL (for-ve-oh)
Wellbutrin SR and XL (wĕl-BYŪ-trĭn)
Actions
Buroion is a onocyclic antieressant. Its echa-
nis of action is not fully known. Coare with
TCAs, it is believe to be a weak inhibitor of the reu-
take of the neurotransitters noreinehrine an o-
aine. It has no onoaine oxiase inhibition or
serotonin reutake inhibition effect.
Uses
Buroion is arove for use in atients with MDD
who are unresonsive to TCAs or who cannot tolerate
253
the averse effects of TCAs. Disavantages inclue
seizure activity an the requireent of ultile oses
aily. It ust not be use in atients with sychotic
isorers because its oaine agonist activity causes
increase sychotic sytos.
Buroion is also arove as a 12-hour extene-
release tablet to suort soeone who is trying to quit
soking. Treatent shoul be initiate while the a-
tient is still soking because aroxiately 1 week of
treatent is require to achieve steay-state bloo lev-
els of buroion. Patients shoul set a target quit ate
uring the rst 2 weeks of treatent with buroion,
generally in the secon week. Treatent shoul be
continue for 7 to 12 weeks; longer treatent shoul
be guie by the relative benets an risks for inivi-
ual atients. Buroion 24-hour extene-release tab-
lets (Alenzin, Wellbutrin XL) are arove for use in
atients with a iagnosis of seasonal affective isorer.
Therapeutic Outcomes
The riary theraeutic outcoes execte fro bu-
roion theray when use for eression are elevat-
e oo an reuction of sytos of eression.
When it is use for soking cessation, the execte
outcoe is the terination of soking.
Nursing Implications for Bupropion Therapy
Premedication assessment
1. Obtain the atient’s baseline weight.
2. Use the Dyskinesia Ientication Syste: Conense
User Scale (DISCUS) or the Abnoral Involuntary
Moveent Scale (AIMS) (see Evolve website) at sec-
ie intervals to etect or check u on EPSs; recor
an reort in accorance with institutional olicy.
Availability. PO: 75- an 100-g tablets; 100-, 150-, an
200-g 12-hour extene-release tablets; 150, 174, 300,
348, 450, 522-g 24-hour extene-release tablets.
Dosage and administration for depression. Adult: PO:
Ieiate release; initially, 100 g twice aily. This
ay be increase to 100 g three ties aily after 3
ays of theray. No single ose of buroion shoul
excee 150 g; o not excee 450 g aily. Avoi tak-
ing a ose shortly before betie.
12-hour ER (sustaine release): 150 g once aily in
the orning. This ay be increase to 150 g twice a
ay after 3 ays. No single ose shoul excee 200 g
or 200 g twice aily.
24-hour ER: 150 g once aily in the orning. This
ay increase by ay 4 of osing to 300 g once aily.
Maxiu ose is 450 g once aily.
Dosage and administration for smoking cessa-
tion. Adult: PO: Dosing shoul begin at 150 g/
ay given every ay for the rst 3 ays, followe
by a osage increase for ost atients to the reco-
ene usual osage of 300 g/ay. There shoul
254 UNIT III Drugs Affecting the Autonomic and Central Nervous System
be an interval of at least 8 hours between successive
oses. Dosages above 300 g/ay shoul not be use.
Buroion shoul be swallowe whole, not crushe,
ivie, or chewe.
Treatent shoul continue for 7 to 12 weeks; lon-
ger treatent shoul be guie by the relative ben-
ets an risks for iniviual atients. If a atient has
not ae signicant rogress towar abstinence by
the seventh week of theray with buroion, it is un-
likely that they will quit uring that attet an treat-
ent shoul robably be iscontinue. Conversely, a
atient who successfully quits after 7 to 12 weeks of
treatent shoul be consiere for ongoing theray
with buroion. Dosage taering of buroion is not
require when iscontinuing treatent. The atient
shoul continue to receive counseling an suort
throughout treatent with buroion an for a erio
of tie thereafter.
Individualization of therapy. The soking cessation
atient is ore likely to quit soking an reain absti-
nent if seen frequently an receiving suort fro the
healthcare rovier. Ensure that the atient reas the
instructions rovie an has any questions answere.
The atient’s healthcare rovier shoul review the
overall soking cessation rogra, incluing treat-
ent with buroion. The atient shoul be avise
about the iortance of articiating in the behavioral
interventions, counseling, an suort services to be
use in conjunction with buroion.
Observation. In the atient with eression, sy-
tos of eression ay irove within a few ays
(e.g., irove aetite, slee, an sychootor activ-
ity). However, the eression still exists, an it usually
takes several weeks of the atient receiving theraeutic
osing before iroveent is note. Suicie recau-
tions shoul be aintaine uring this tie.
Common adverse effects
Gastrointestinal
Anorexia, constipation, diarrhea, nausea, vomiting. Most
GI effects ay be iniize by teorarily reucing
the osage, giving with foo, an using stool softeners
for constiation.
Neurologic
Restlessness, agitation, anxiety, insomnia. These effects
usually occur early in theray, an the atient ay
require short-ter treatent with seative-hynotic
agents. Avoiing betie oses ay hel ecrease the
incience of insonia.
Serious adverse effects
Neurologic
Seizures. See Assessent: History of Seizure Activity
in the Antieiletic Theray section of Chater 18
Psychological
Suicidal ideation. Monitor the atient for changes in
thoughts, feelings, an behaviors uring the initial
stages of theray.
Drug interactions
Cimetidine. Cietiine inhibits the etabolis of
buroion an increases buroion bloo levels. A
ecrease in the buroion osage ay be necessary.
Carbamazepine, phenobarbital, phenytoin. Carbaa-
zeine, henobarbital, an henytoin ay ecrease
buroion seru levels, leaing to ecrease hara-
cologic effect. It ay be necessary to ajust the osage
of buroion.
Nicotine replacement. Although buroion is use
in cobination with nicotine relaceent roucts to
hel with soking cessation, coainistration of nico-
tine relaceent roucts with buroion ay cause
hyertension. Monitor the atient’s bloo ressure
when roucts such as nicotine atches or nicotine
gu are being use.
Ritonavir. Ritonavir ay stiulate the etabolis
of buroion, causing a reuction in seru concentra-
tions of buroion. An increase in the buroion os-
age ay be necessary.
Levodopa. Buroion has soe il oainergic
activity an ay result in an increase in the averse ef-
fects cause by levooa. If buroion is to be ae to
levooa theray, it shoul be initiate at a lower os-
age with sall increases in the osage of buroion.
mirtazapine (mĭr-TĂZ-ĕ-pĕn)
Remeron (RĔ-mĕr-ŏn)
Do not confuse Remeron with Restoril.
Actions
Mirtazaine is a tetracyclic antieressant that is a
central resynatic alha-2 antagonist, which results
in increase release of noreinehrine an serotonin.
It oes not inhibit the reutake of noreinehrine or
serotonin. The echanis of action is unknown, but
the haracologic resonse is siilar to that of TCAs.
Uses
Mirtazaine is use to treat MDD.
Therapeutic Outcomes
The riary theraeutic outcoes execte fro ir-
tazaine theray are elevate oo an reuction of
sytos of eression.
Nursing Implications for Mirtazapine Therapy
Premedication assessment
1. Obtain the atient’s baseline bloo ressures in the
suine, an staning ositions; recor an reort
signicant hyotension to the healthcare rovier
before ainistering the rug.
2. Obtain the atient’s baseline weight an scheule
weekly weight easureents.
3. Check for a history of seizures. If resent, notify the
healthcare rovier before starting theray.
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
4. Check the atient’s heatic stuies before initiating
theray an erioically throughout the course of
ainistration.
5. Use the DISCUS or the AIMS (see Evolve website)
at secie intervals to etect or check u on EPSs;
recor an reort in accorance with institutional
olicy.
6. Obtain the atient’s white bloo cell count before
an at regular intervals after initiating theray be-
cause agranulocytosis has been reorte.
Availability. PO: 7.5-, 15-, 30-, an 45-g tablets; 15-,
30-, an 45-g orally isintegrating tablets (Reeron
SolTab).
Dosage and administration. Adult: PO: Initially, 15 g
aily. Every 1 to 2 weeks the osage ay be increase
u to a axiu of 45 g aily. Increases in osage
shoul be ae in the evening because increase sea-
tion is often resent.
Observation. See Tricyclic Antieressants section.
Sytos of eression ay irove (e.g., increase
aetite, slee, an sychootor activity) within a few
ays. However, the eression still exists, an it usu-
ally takes several weeks of the atient receiving thera-
eutic osing before iroveent is note. Suicie
recautions shoul be aintaine uring this tie.
Herbal Interactions
St. John’s Wort
St. John’s wort may increase the toxic effects of anti-
depressant medications. The use of St. John’s wort with
other antidepressants should be done only with close super-
vision by a healthcare provider.
trazodone hydrochloride (TRĂ-zō-dōn)
Do not confuse trazodone with amiodarone or tramadol.
Actions
Trazoone was the rst of the triazoloyriine anti-
eressants to be release for clinical use. The tri-
azoloyriines are cheically unrelate to the other
classes of antieressants. The exact echaniss of
action of trazoone are unknown, but it otentiates
serotonin activity by inhibiting reutake an estruc-
tion of serotonin. The actions are colex an in soe
ways reseble those of the TCAs, benzoiazeines,
an henothiazines; however, the overall activity of
trazoone is haracologically ifferent fro that of
each of these classes of rugs.
Uses
Trazoone has been shown to be as effective as TCAs
in treating eression; eression associate with
schizohrenia; an eression, treor, an anxiety
associate with alcohol eenence. Coare with
other antieressants, trazoone has a low incience
255
of anticholinergic averse effects, which akes it ar-
ticularly useful in atients whose antieressant os-
ages are liite by anticholinergic averse effects an
in atients with severe close-angle glaucoa, ros-
tatic hyerlasia, organic ental isorers, or cariac
ysrhythias. Trazoone is coonly use to treat
insonia in atients with substance abuse because it is
seating, iroves slee continuity, an has inial
otential for tolerance an aiction.
Therapeutic Outcomes
The riary theraeutic outcoes execte fro tra-
zoone theray are elevate oo an reuction of
sytos of MDD.
Nursing Implications for Trazodone Therapy
Premedication assessment
1. Obtain the atient’s baseline bloo ressures in the
suine, an staning ositions.
2. Recor an reort signicant hyotension to the
healthcare rovier before ainistering the rug.
Availability. PO: 50-, 100-, 150-, an 300-g tablets.
Dosage and administration. Adult: PO: Initially, 150
g in three ivie oses. Increase the osage in incre-
ents of 50 g aily every 3 to 4 ays while onitor-
ing the clinical resonse. Do not excee 400 g aily
in outatients or 600 g aily in hositalize atients.
Trazoone theray shoul be initiate at a low
osage an increase graually, articularly in oler
aults or ebilitate atients. Dosage increases shoul
be ae in the evening because increase seation of-
ten occurs. Ainister the eication shortly after a
eal or with a light snack to reuce averse effects.
Observation. Sytos of eression ay irove
(e.g., increase aetite, slee, an sychootor activ-
ity) within a few ays. However, the eression still
exists, an it usually takes several weeks of the atient
receiving theraeutic osing before iroveent is
note. Suicie recautions shoul be aintaine ur-
ing this tie.
Common adverse effects
Cardiovascular
Orthostatic hypotension. Although eisoes are infre-
quent an generally il, trazoone ay cause soe
egree of orthostatic hyotension, anifeste by iz-
ziness an weakness, articularly when theray is
initiate. Monitor the atient’s bloo ressure aily in
both the suine an staning ositions. Anticiate the
eveloent of ostural hyotension an take eas-
ures to revent an occurrence. Teach the atient to rise
slowly fro a suine or sitting osition, an encour-
age the atient to sit or lie own if feeling faint.
Neurologic
Drowsiness. The atient shoul be warne to
not work with achinery, oerate a otor vehicle,
256 UNIT III Drugs Affecting the Autonomic and Central Nervous System
ainister eication, or erfor other uties that
require ental alertness until it is known whether this
averse effect iairs jugent.
Serious adverse effects
Cardiovascular
Dysrhythmias, tachycardia. Reort these sytos to
a healthcare rovier for further evaluation.
Neurologic
Confusion. Before initiating theray, erfor a base-
line assessent of the atient’s egree of alertness
an orientation to nae, lace, an tie. Make regu-
larly scheule subsequent evaluations of the atient’s
ental status an coare nings. Reort any sig-
nicant alterations to the rescriber.
Dizziness, lightheadedness. Provie for atient safety
uring eisoes of izziness an reort these sy-
tos to the rescriber for further evaluation.
Drug interactions
Enhanced sedative activity. Ethanol, narcotics, tran-
quilizers, antihistaines, anesthetics, henothiazines,
an seative-hynotics enhance the seative effects
associate with trazoone theray. Concurrent thera-
y is not recoene.
MAOIs, SSRIs, SNRIs. Serotonin synroe ay e-
velo when trazoone is use in conjunction with
any of these agents. Use trazoone cautiously; initiate
theray at a lower osage an closely onitor for the
averse effects liste.
vilazodone (vĭl-ĂZ-zō-dōn)
Do not confuse vilazodone with trazodone or
nefazodone.
Viibryd (vī-brĭd)
Actions
Vilazoone is a eication that acts as an SSRI an
a artial agonist of serotonin (5-hyroxytrytaine)
5-HT1A recetors, thereby enhancing serotonin activity.
Uses
Vilazoone is arove to treat MDD in aults.
Therapeutic Outcomes
The riary theraeutic outcoes execte fro
vilazoone theray are elevate oo an reuction
of sytos of eression.
Nursing Implications for Vilazodone Therapy
Premedication assessment
1. Note any GI sytos resent before the start of
theray.
2. Monitor any CNS sytos resent (e.g., inso-
nia, restlessness).
Availability. PO: 10-, 20-, an 40-g tablets.
Dosage and administration. Adult: PO: Initially, 10
g once aily with foo for 7 ays, followe by 20
g once aily with foo for the next 7 ays, an then
increase to the recoene osage of 40 g once
aily. Vilazoone shoul be taken with foo for oti-
al absortion.
Observation. Sytos of eression ay irove
(e.g., increase aetite, slee, an sychootor activ-
ity) within a few ays. However, the eression still
exists, an it usually takes several weeks of the atient
receiving theraeutic osing before iroveent is
note. Suicie recautions shoul be aintaine ur-
ing this tie.
Common adverse effects
Gastrointestinal
Diarrhea, nausea, vomiting. These averse effects
shoul be il, articularly if the ose is ainistere
with foo. They shoul also resolve with continue
theray. Patients with ersistent voiting shoul be
evaluate for other causes, as well as for the evelo-
ent of electrolyte ibalance.
Neurologic
Dizziness, drowsiness. Provie for atient safety ur-
ing eisoes of izziness an reort these sytos
to the healthcare rovier for further evaluation. The
atient shoul not take these eications while work-
ing with achinery, oerating a otor vehicle, ain-
istering eication, or erforing other uties that
require ental alertness.
Serious adverse effects
Neurologic
Confusion. Before initiating theray, erfor a base-
line assessent of the atient’s egree of alertness
an orientation to nae, lace, an tie. Make regu-
larly scheule subsequent evaluations of the atient’s
ental status an coare nings. Reort any sig-
nicant alterations to the rescriber.
Dizziness, lightheadedness. Provie for atient safety
uring eisoes of izziness an reort these sy-
tos to the healthcare rovier for further evaluation.
Psychological
Suicidal ideation. Monitor the atient for changes in
thoughts, feelings, an behaviors, esecially uring
the initial stages of theray.
Drug interactions
Enhanced sedative activity. Ethanol, narcotics, tran-
quilizers, antihistaines, anesthetics, henothia-
zines, an seative-hynotics enhance the seative
effects that are associate with vilazoone theray.
Concurrent theray is not recoene.
Trazodone, MAOIs, SSRIs, SNRIs, tramadol,
triptans. Serotonin synroe ay evelo when vila-
zoone is use in conjunction with any of these agents.
See the Meication Safety Alert: Serotonin Synroe
earlier in this chater.
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
Aspirin, nonsteroidal antiinammatory drugs, warfarin.
Serotonin release by latelets lays an iortant role
in heostasis. SRRIs ay enhance the anticoagulant
effects of warfarin an enhance the otential for GI
bleeing cause by nonsteroial antiinaatory
rugs (NSAIDs) or asirin. Observe the atient for e-
techiae, ecchyoses, noseblees, bleeing gus, ark
tarry stools, an bright re or coffee-groun eesis.
Monitor rothrobin tie an the INR of warfarin,
an reuce the osage of warfarin if necessary.
Phenytoin, phenobarbital, carbamazepine. These agents
ay enhance the etabolis of vilazoone, reucing
seru levels an leaing to ecrease haracologic
effect.
Erythromycin, clarithromycin, uoxetine, grapefruit
juice. These rugs inhibit the etabolis of vilazo-
one, causing an increase in seru levels an the o-
tential for toxicity. Dosages of the antieressant ay
nee to be reuce by u to 50% to avoi toxicities.
vortioxetine (vōr-tē ŎX-ĕt-ēn)
Do not confuse vortioxetine with atomoxetine.
Trintellix (trĭn-TĔL-ĭx)
Actions
Vortioxetine is a eication that acts as an SSRI, an ag-
onist of the serotonin 5-HT1A recetors that enhances
serotonin activity an antagonizes the serotonin 5-HT3
recetors.
Uses
Vortioxetine is arove to treat MDD in aults.
Therapeutic Outcomes
The riary theraeutic outcoes execte fro vor-
tioxetine theray are elevate oo an reuction of
sytos of eression.
Nursing Implications for Vortioxetine Therapy
Premedication assessment
1. Note any GI sytos resent before the start of
theray.
2. Monitor any CNS sytos resent (e.g., inso-
nia, restlessness).
Availability. PO: 5-, 10-, an 20-g tablets.
Dosage and administration. Adult: PO: Initially, 10 g
once aily, followe by 20 g once aily as tolerate.
For those not tolerating 10 g aily, theray ay be
reuce to 5 g aily. Maxiu aily ose is 20 g.
If the rug is well tolerate, atients shoul reain on
theray for several onths.
When iscontinuation is lanne, the ose shoul
be taere to onitor closely for eveloent of with-
rawal sytos an to etect the eveloent of
eressive sytos. The anufacturer recoens
257
that oses of 15 g aily or higher shoul be reuce
to 10 g aily for 1 week before full iscontinuation to
revent withrawal sytos.
Common adverse effects
Gastrointestinal
Diarrhea, nausea, vomiting, dry mouth. These averse
effects shoul be il an shoul resolve with con-
tinue theray. Patients with ersistent voiting
shoul be evaluate for other causes, as well as for
the eveloent of electrolyte ibalance (synroe
of inaroriate secretion of antiiuretic horone or
serotonin synroe).
Neurologic
Dizziness, abnormal dreams. Provie for atient
safety uring eisoes of izziness. Provie co-
fort an atient safety in those reorting abnoral
reas. Reort these sytos to the healthcare
rovier for further evaluation. The atient shoul
not take these eications while working with a-
chinery, oerating a otor vehicle, ainistering
eication, or erforing other uties that require
ental alertness.
Serious adverse effects
Psychological
Suicidal actions, hypomania, mania, serotonin syn-
drome. Monitor the atient for changes in thoughts,
feelings, an behaviors, esecially uring the initial
stages of theray. Sytos of eression ay i-
rove (e.g., increase aetite, slee, an sychootor
activity) within a few ays. However, the eression
still exists, an it usually takes several weeks of the a-
tient receiving theraeutic osing before iroveent
is note. Suicie recautions shoul be aintaine
uring this tie.
Review atient history for a ersonal or faily
history of biolar isorer because vortioxetine ay
inuce latent biolar isorer. Vortioxetine is not a-
rove for treatent of biolar eression.
Drug interactions
Trazodone, MAOIs, SSRIs, SNRIs, tramadol, triptans,
buspirone, St. John’s wort, linezolid, fentanyl. Serotonin
synroe ay evelo when vortioxetine is use in
conjunction with any of these agents. Use these rugs
cautiously; initiate theray at a lower osage an
closely onitor for the averse effects liste.
Aspirin, nonsteroidal antiinammatory drugs, warfa-
rin. Serotonin release by latelets lays an iortant
role in heostasis. Selective serotonin reutake inhibi-
tors ay enhance the anticoagulant effects of warfarin
an enhance the otential for GI bleeing cause by
NSAIDs or asirin. Observe the atient for etechiae,
ecchyoses, noseblees, bleeing gus, ark tarry
stools, an bright re or coffee-groun eesis. Monitor
rothrobin tie an the INR of warfarin an reuce
the osage of warfarin if necessary.
258 UNIT III Drugs Affecting the Autonomic and Central Nervous System
Buspirone. Busirone inhibits the etabolis of vor-
tioxetine, causing an increase in seru levels an the
otential for toxicity. Dosages of vortioxetine shoul
be reuce by u to 50% to avoi toxicities.
DRUG CLASS: ANTIMANIC AGENT
LITHIUM CARBONATE
lithium carbonate (LĬTH-ē-um)
Actions
Lithiu is a onovalent cation that coetes with
other onovalent an ivalent cations (i.e., otassi-
u, soiu, calciu, agnesiu) at cellular bining
sites that are sensitive to changes in cation concentra-
tion. Lithiu relaces intracellular an intraneuronal
soiu, stabilizing the neuronal ebrane. It also
reuces the release of noreinehrine an increases
the utake of trytohan, the recursor to serotonin.
It also interacts with secon-essenger cellular ro-
cesses to inhibit intracellular concentrations of cyclic
aenosine onohoshate. Because of the colexity
of the CNS, the exact echaniss of action of lithiu
for treating oo isorers are unknown. It has no
seative, eressant, or euhoric roerties, which
ifferentiates it fro all other sychotroic agents.
Uses
Lithiu is use to treat acute ania an for rohy-
lactic treatent of recurrent anic an eressive
eisoes in atients with biolar isorer. In atients
with biolar isorer, it is ore effective in reventing
signs an sytos of ania than those of eres-
sion. It is also effective in soe atients for reucing
the recurrence of the eressive eisoes associate
with uniolar isorer.
Therapeutic Outcome
The riary theraeutic outcoe execte fro lith-
iu theray is aintaining the iniviual at an oti-
al level of functioning, with inial exacerbations
of oo swings.
Nursing Implications for Lithium Therapy
Premedication assessment
1. Before initiating lithiu theray, the following labo-
ratory tests shoul be colete for baseline infor-
ation: electrolytes, fasting bloo glucose, bloo
urea nitrogen (BUN), seru creatinine, creatinine
clearance, urinalysis, an thyroi function.
2. Obtain baseline bloo ressures with the atient in
the suine, an staning ositions; recor an re-
ort signicant hyotension to the healthcare ro-
vier before ainistering the rug.
3. Weigh the atient aily, check the hyration status
(e.g., oistness of ucous ebranes, skin turgor,
rness of eyeball), an onitor urine secic
gravity.
4. Lithiu ay enhance soiu eletion, which in-
creases lithiu toxicity. Assess for early signs of lith-
iu toxicity before giving the eication, incluing
nausea, voiting, aboinal ain, iarrhea, lethar-
gy, seech ifculty, il izziness, uscle twitch-
ing, an treor.
Availability. PO: Lithium carbonate: 150-, 300-, an 600-
g casules; 300-g tablets; 300- an 450-g slow-
release tablets. Lithium citrate: 8 Eq/5 L solution in
500-L bottles.
Dosage and administration. Adult: PO: 300 to 600 g
three or four ties aily. Ainister with foo or ilk.
An aequate iet is iortant to aintain noral se-
ru soiu levels an to revent toxicity. The onset
of the acute antianic effect of lithiu usually occurs
within 5 to 7 ays; the full theraeutic effect often re-
quires 10 to 21 ays.
Serum lithium levels. Lithiu levels are onitore once
or twice weekly uring the initiation of theray an
onthly while the atient is receiving a aintenance
osage. Bloo shoul be rawn aroxiately 12 hours
after the last ose was ainistere. The noral seru
level is 0.4 to 1.2 Eq/L. Protly reort seru levels
higher than these values to the healthcare rovier.
Good nutrition. Lithiu ay enhance soiu e-
letion, which increases lithiu toxicity. The atient
shoul aintain a noral ietary intake of soiu
an aequate aintenance uis (i.e., 10 to 12 eight-
ounce glasses of water aily), esecially when initiat-
ing theray, to revent toxicity.
Common adverse effects
Gastrointestinal
Nausea, vomiting, anorexia, abdominal cramps. These a-
verse effects are usually il an ten to resolve with
continue theray. Encourage the atient not to is-
continue theray without rst consulting the health-
care rovier. If gastric irritation occurs, ainister the
eication with foo or ilk. If sytos ersist or in-
crease in severity, reort the to the healthcare rovier
for evaluation. These also ay be early signs of toxicity.
Excessive thirst. This averse effect is usually il
an tens to resolve within a week with continue
theray. Encourage the atient not to iscontinue ther-
ay without rst consulting the healthcare rovier. If
excessive thirst ersists or becoes severe, the atient
shoul consult the healthcare rovier.
Neurologic
Fine hand tremor. If ne han treor ersists or be-
coes severe, the atient shoul consult the healthcare
rovier.
Genitourinary
Excessive urination. This averse effect is usually il
an tens to resolve within a week with continue
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16
theray. Encourage the atient not to iscontinue ther-
ay without rst consulting the healthcare rovier. If
excessive urination ersists or becoes severe, the a-
tient shoul consult the healthcare rovier.
Serious adverse effects
Gastrointestinal
Persistent vomiting, profuse diarrhea. These are sy-
tos of iening serious toxicity. Reort the i-
eiately an o not give the next ose of eica-
tion until ainistration has been reconre by the
healthcare rovier.
Neurologic
Hyperreexia, lethargy, weakness. These are signs of
iening serious toxicity. Reort the ieiately
an o not give the next ose of eication until a-
inistration has been reconre by the healthcare
rovier.
Endocrine, metabolic
Progressive fatigue, weight gain. These ay be early
signs of hyothyroiis. Reort these sytos to
the healthcare rovier for further evaluation.
Hyperglycemia. Reort this syto to the health-
care rovier for further evaluation.
Genitourinary
Nephrotoxicity. Monitor urinalysis an kiney func-
tion tests for abnoral results. Reort an increasing
BUN or creatinine level, increasing or ecreasing urine
outut or ecreasing secic gravity (esite aequate
ui intake), an casts or rotein in the urine.
Rare adverse effects from lithium therapy
Pruritus, ankle edema, metallic taste. Reort these sy-
tos for further evaluation by the healthcare rovier.
Drug interactions
Reduced serum sodium levels. The theraeutic activity
an toxicity of lithiu are highly eenent on soiu
concentrations. Decrease soiu levels signicantly
259
enhance the toxicity of lithiu an high soiu levels
result in low lithiu levels. Patients who are to begin
iuretic theray, a low-soiu iet, or activities that
rouce excessive an rolonge sweating shoul be
observe articularly closely.
Angiotensin-Converting Enzyme Inhibitors and
Angiotensin Receptor blockers. Angiotensin-converting
enzye inhibitors (ACEIs) an angiotensin recetor
blockers (ARBs) (see Chater 22) ay increase the
seru concentration of lithiu. Monitor atients re-
ceiving concurrent theray. Monitoring lithiu seru
levels ay be necessary.
Diuretics. Diuretics ay reuce the eliination of
lithiu, resulting in lithiu toxicity. Monitor the a-
tient’s lithiu seru levels closely. Monitor atients
receiving concurrent long-ter theray for signs of the
eveloent of lithiu toxicity (e.g., nausea, voit-
ing, aboinal ain, iarrhea, lethargy, seech if-
culty, il izziness, treor). A lithiu level ay be
necessary.
Methyldopa. Monitor atients receiving concurrent
long-ter theray for signs of the eveloent of lith-
iu toxicity (e.g., nausea, voiting, aboinal ain,
iarrhea, lethargy, seech ifculty, il izziness,
treor). A lithiu level ay be necessary.
Nonsteroidal Antiinammatory Drugs. NSAIDs (e.g.,
iburofen, naroxen; see Chater 19) ay increase
the seru concentration of lithiu. Monitor for signs
of lithiu toxicity (e.g., nausea, voiting, aboinal
ain, iarrhea, lethargy, seech ifculty, il izzi-
ness, treor). A lithiu level ay be necessary.
Selective Serotonin Reuptake Inhibitors. Lithiu ay
enhance the serotonergic effect of SSRIs, thereby in-
creasing the risk of serotonin toxicity (serotonin syn-
roe). Use the cobination of SSRIs an lithiu
very cautiously, onitoring closely for signs of sero-
tonin toxicity such as irritability, hallucinations, eliri-
u, increase uscle tone, shivering, yoclonus, an
reuce consciousness.
260 UNIT III Drugs Affecting the Autonomic and Central Nervous System

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points 5. Tattoos present

6. Oral hygiene and number of dental cavities
• The Diagnostic and Statistical Manual of Mental Disorders, 7. Clarity of thought
Fifth Edition (DSM-5), recognizes major psychiatric
Objective: Describe the essential components of the baseline
disorders on a continuum, with depressive disorders
assessment of a patient with depression or bipolar disorder.
and psychotic spectrum at the ends of the continuum
NCLEX item type: Extended multiple response
and bipolar disorders serving as a bridge between the
Cognitive skill: Analyze cues
two diagnostic classes in terms of symptomatology,
family history, and genetics. The common feature among 2. The patient in the scenario was being treated for depression
depressive and bipolar disorders is the presence of sad, and the nurse will monitor for thoughts of suicide. Indicate with
empty, or irritable mood, accompanied by changes that an X which behavior may indicate suicidal ideation and which is
signicantly affect the individual’s capacity to function. unrelated.
• Treatment of mood disorders requires both
nonpharmacologic and pharmacologic therapy. SIGNIFICANT UNRELATED
Simultaneous psychotherapy and pharmacologic SYMPTOMS FINDING FINDING
treatment are more successful than either treatment alone.
Patient remarking that the
• Antidepressant medications act on a variety of receptors in
patient had a plan and was
the CNS, as well as peripheral tissues, and are associated
intent on carrying it out
with many adverse effects and drug interactions. It is the
responsibility of the nurse to educate patients about therapy Poor hygiene
and to monitor for therapeutic benet and common and Comments from the patient
serious adverse effects, as well as to intervene whenever such as, “Things will get
possible to optimize therapeutic outcomes. better after I’m gone.”
• Be alert for serotonin syndrome with combined use of Pacing in the room
SSRIs and MAOIs, which may develop as a result of
Excessive appetite
excessive accumulation of serotonin in nerve synapses.
It is an uncommon event, but may be potentially fatal. Sleeping throughout the day
Symptoms include irritability, hallucinations, delirium, Patient’s relative indicated
reduced consciousness, increased muscle tone, that the patient has recently
myoclonus, diaphoresis, shivering, tremor, hyperthermia, given away a collection of
and increased or decreased blood pressure and heart rate. expensive dishes

Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Clayt
on) for additional online resources.
Objective: Describe the essential components of the baseline
assessment of a patient with depression or bipolar disorder.
NCLEX item type: Matrix
Cognitive skill: Evaluate outcomes
3. The nurse knows to assess for a severe drug interaction that can
occur between SSRIs and several drug classes. Indicate with an X
the drug class associated with the drug interaction (more than one
interaction will apply).

Clinical Judgment and Next-Generation NCLEX® Exam-

ination-Style Questions The following questions are typical of EXCITE- HALLUCI- DIAPHO- CONVUL-
the NCLEX examination and include both NGN (Next Genera- MENT NATIONS RESIS RIGIDITY SIONS
tion) and traditional questions. See Chapter 1 for further infor- MAOIs
mation regarding question types. Lithium
TCAs
Scenario
A patient with known bipolar disorder was admitted to the Objective: Describe the common adverse effects that may develop
mental health unit for medication adjustment. for patients who are taking SSRIs and SNRIs.
1. The nurse was assessing the patient in the scenario who came NCLEX item type: Matrix
in with increasing episodes of depression. Which components are Cognitive skill: Analyze cues
part of the baseline assessment? (Select all that apply.)
1. Dietary history
2. History of previous depression episodes and treatments
3. Sleep pattern
4. Suicidal ideation
 Drugs Used for Depressive and Bipolar Disorders CHAPTER 16 261

4. The nurse is explaining to the patient taking an MAOI of the need 7. The nurse is discussing ways to prevent lithium toxicity with the
to be aware of which condition developing? (Select all that apply.) patient in the scenario who currently is taking lithium. Which of the
1. Hyperpyrexia following indicate correct instructions? (Select all that apply.)
2. Constipation 1. Report symptoms of persistent vomiting
3. Hypotension 2. Drink 10 glasses of water (8 ounces each) daily
4. Blurred vision 3. Check lithium blood levels monthly
5. Hypertension 4. Diuretic therapy prevents lithium toxicity
Objective: Describe the common adverse effects that may develop 5. Report symptoms of lethargy and weakness
for patients who are taking MAOIs. 6. Report symptoms of perfuse diarrhea
NCLEX item type: Multiple response 7. Monitor thyroid function
Cognitive skill: Application Objective: Describe the common adverse effects that may develop
for patients who are taking lithium.
5. The nurse was instructing a patient staring on duloxetine NCLEX item type: Extended multiple response
(Cymbalta) on the adverse effects to expect and which ones to Cognitive skill: Analyze cues
report. Indicate with an X the common and serious effects from
SNRIs. 8. The nurse reviewed the preassessment expectations for the
typical medications used for patients with depression and bipolar
SYMPTOMS COMMON EFFECT SERIOUS EFFECT disorders and found that the assessment overlapped. Indicate with
an X which ones are associated with each drug class.
Anorexia
Drowsiness ANTIMANIC
Anxiety MAOIS TCAS SSRIS SNRIS AGENTS
Agitation Blood pressure
Suicidal ideation Pulse
Insomnia Glucose
Irritability and Hepatic
delirium laboratory tests
Medication
Objective: Describe the common adverse effects that may develop history
for patients who are taking SSRIs and SNRIs. Thyroid
NCLEX item type: Matrix laboratory tests
Cognitive skill: Evaluate cues Weight
6. Patients taking doxepin should be aware of which of the following History of
adverse effects common to TCAs? (Select all that apply.) seizures
1. Orthostatic hypotension
2. Diarrhea Objective: Identify the premedication assessments that are
3. Dry mouth and throat necessary before the administration of monoamine oxidase
4. Hyperglycemia inhibitors (MAOIs), selective serotonin reuptake inhibitors (SSRIs),
5. Blurred vision serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic
Objective: Describe the common adverse effects that may develop antidepressants (TCAs), and antimanic agents.
for patients who are taking TCAs. NCLEX item type: Matrix
NCLEX item type: Multiple response Cognitive skill: Take action
Cognitive skill: Application
17 Drugs Used for Psychoses

https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the signs and symptoms of psychotic behavior. 3. Discuss the antipsychotic medications that are used for
2. Describe the major indications for the use of antipsychotic the treatment of psychoses.
agents. 4. Identify the common adverse effects that are observed
with the use of antipsychotic medications.

Key Terms
psychosis (sī-KŌ-sĭs) (p. 262)
delusion (dĕ-LŪ-zhŭn) (p. 262)
hallucinations (hă-lū-sĭ-NĀ-shŭnz)
(p. 263)
disorganized thinking (dĭs-ŌR-găn-
īzd THĬN-kĭng) (p. 263)
loosening of associations (LŪ-sĕn-
ĭng ŭv ăs-sō-sē-Ā-shŭnz) (p. 263)
disorganized behavior (dĭs-ŌR-gă-
nīzd bē-HĀV-yŭr) (p. 263)
negative symptoms (NĔG-ĕ-tiv SĬMP-
tĕmz) (p. 263)
target symptoms (TĂR-gĕt SĬMP-
tĕmz) (p. 263)
typical (rst-generation)
antipsychotic agents (TĬP-ĭ-kŭl
ăn-tī-sī-KŎT-ĭk) (p. 264)
atypical (second-generation)
antipsychotic agents (ā-TĬP-ĭ-kŭl
ăn-tī-sī-KŎT-ĭk) (p. 264)
equipotent doses (ĕk-wē-PŌ-tĕnt
DŌS-ĕz) (p. 264)
extrapyramidal symptoms
(EPSs) (ĕks-tră-pĭ-RĂM-ĭ-dăl)
(p. 264)
dystonias (dĭs-TŌN-ē-ăz) (p. 268)
pseudoparkinsonian
symptoms (SŪ-dō-păr-kĭn-SŌ-nē-
ĭn) (p. 268)
akathisia (ă-kĕ-THĬ-zhă) (p. 268)
tardive dyskinesia (TĂR-dīv dĭs-kĭ-NĒ-
zē-ă) (p. 268)
Abnormal Involuntary Movement
Scale (AIMS) (ăb-NŌR-mŭl ĭn-VŎL-
ĕn-tār-ē MŌV-mĕnt SKĀL) (p. 269)
Dyskinesia Identication System;
Condensed User Scale
(DISCUS) (dĭs-kĭ-NĒ-zē-a ī-dĕn-tĭ-fĭ-
KĀ-shŭn SĬS-tĕm: kŏn-DĔNST YŪ-zŭr
SKĀL) (p. 269)
neuroleptic malignant syndrome
(NMS) (nyū-rō-LĔP-tĭk mă-LĬG-nănt
SĬN-drōm) (p. 269)
depot antipsychotic medicine
(DĔ-pō ăn-tē-sī-KŎT-ĭk) (p. 269)

PSYCHOSIS
Psychosis does not have a single denition but is a clinical
descriptor applied to someone who is out of touch with
reality. Psychotic symptoms can be associated with many
illnesses, including dementias and delirium, that may
have metabolic, infectious, or endocrinologic causes. The
underlying illness must be treated, not just the psychosis.
Psychotic symptoms are also common in patients
with mood disorders such as major depression and bi-
polar disorder and schizophrenia spectrum. Psychosis
can also be caused by many drugs (e.g., phencyclidine,
opiates, amphetamines, cocaine, hallucinogens, anti-
cholinergic agents, alcohol). Psychotic disorders are
characterized by loss of reality, perceptual decits such
as hallucinations and delusions, and deterioration of so-
cial functioning. Schizophrenia is the most common of
the several psychotic disorders dened by the American
Psychiatric Association in the Diagnostic and Statistical
Manual of Mental Disorders, Fifth Edition (DSM-5).
262
Psychotic disorders are extremely complex illness-
es that are inuenced by biologic, psychosocial, and
environmental circumstances. Some of the disorders
require several months of observation and testing be-
fore a nal diagnosis can be determined. It is beyond
the scope of this text to discuss psychotic disorders in
detail, but general types of symptoms associated with
psychotic disorders will be described.
A delusion is a false or irrational belief that is
rmly held despite obvious evidence to the contrary.
Delusions may be persecutory, grandiose, religious,
sexual, or hypochondriacal. Delusions of reference—in
which the patient attributes a special, irrational, and
usually negative signicance to other people, objects,
or events, such as song lyrics or newspaper articles,
in relation to self—are common. Delusions may be
dened as “bizarre” if they are clearly irrational and
do not derive from ordinary life experiences. A com-
mon bizarre delusion is the patient’s belief that their

thinking process, body parts, or actions or impulses
are controlled or dictated by some external force.
Hallucinations are false sensory perceptions that
are experienced without an external stimulus and
seem real to the patient. Auditory hallucinations ex-
perienced as voices that are characteristically heard
commenting negatively about the patient in the third
person are prominent among patients with schizo-
phrenia. Hallucinations of touch, sight, taste, smell,
and bodily sensation also occur.
Disorganized thinking is commonly associated with
psychoses. These thought disorders may consist of a
loosening of associations or a ight of ideas so that
the speaker jumps from one idea or topic to another
unrelated one (derailment) in an illogical, inappropri-
ate, or disorganized way. Answers to questions may be
obliquely related or completely unrelated (tangential-
ity). At its most serious, this incoherence of thought
extends into pronunciation itself and the speaker’s
words become garbled or unrecognizable. Speech may
also be overly concrete (loss of ability to think in ab-
stract terms) and inexpressive; it may be repetitive and
may convey little or no real information.
Disorganized behavior is another common charac-
teristic of psychosis. Problems may be noted with any
form of goal-directed behavior, leading to difculties
with performing activities of daily living such as or-
ganizing meals or maintaining hygiene. The patient
may appear markedly disheveled, may dress in an un-
usual manner (e.g., wearing several layers of clothing,
scarves, and gloves on a hot day), or may display clear-
ly inappropriate sexual behavior (e.g., public mastur-
bation) or unpredictable, nontriggered agitation (e.g.,
shouting, swearing).
Negative symptoms, or changes in affect, may also be
symptoms of psychosis. Emotional expressiveness is di-
minished; there is poor eye contact and reduced sponta-
neous movement. The patient appears to be withdrawn
from others, and the face appears to be immobile and un-
responsive. Speech is often minimal (alogia), with only
brief, slow, monotone replies given in response to ques-
tions. There is a withdrawal from areas of functioning
that affect interpersonal relationships, work, education,
and self-care (asociality), and anhedonia, the decreased
ability to experience pleasure from positive stimuli or
reduced pleasure from previously positive stimuli.
TREATMENT OF PSYCHOSIS
The importance of the initial assessment for an accurate
diagnosis cannot be overestimated for a patient with
acute psychosis. A thorough physical and neurologic
examination, a mental status examination, a complete
family and social history, and a laboratory workup
must be performed to exclude other causes of psycho-
ses, including substance abuse. Both drug and nondrug
therapies are critical to the treatment of most psycho-
ses. Long-term outcome is improved for patients with
an integrated drug and nondrug treatment regimen.
Drugs Used for Psychoses CHAPTER 17 263
Nonpharmacologic interventions benecial to patients
include (1) individual psychotherapy to improve insight
into the illness and help the patient cope with stress; (2)
group therapy to enhance socialization skills; (3) behav-
ioral or cognitive therapy; and (4) vocational training.
Referral to community resources such as the National
Alliance on Mental Illness (NAMI) may provide addi-
tional support for the patient and family.
Before initiating therapy, the treatment goals and
baseline level of functioning must be established and
documented. Target symptoms must also be identied
and documented. Target symptoms are critical moni-
toring parameters used to assess changes in an indi-
vidual’s clinical status and response to medications.
Examples of target symptoms include frequency and
type of agitation, degree of suspiciousness, delusions,
hallucinations, loose associations, grooming habits and
hygiene, sleep patterns, speech patterns, social skills,
and judgment. The ultimate goal is to restore behavior-
al, cognitive, and psychosocial processes and skills to as
close to baseline levels as possible so that the patient can
be reintegrated into the community. Realistically, unless
the psychosis is part of another medical diagnosis such
as substance abuse, most patients will have recurring
symptoms of the mental disorder for most of their lives.
Therefore treatment is focused on decreasing the se-
verity of the target symptoms that most interfere with
functioning. A variety of scales have been developed to
assist with the objective measurement of change in tar-
get symptoms in response to psychotherapy and phar-
macotherapy. These include the Brief Psychiatric Rating
Scale (BPRS), the Positive and Negative Syndrome
Scale for Schizophrenia (PANSS), the Clinical Global
Impression (CGI) scale, and the Rating of Aggression
Against People and/or Property (RAAPP) scale.
DRUG THERAPY FOR PSYCHOSIS
Pharmacologic treatment of psychosis includes several
classes of drugs. The most specic are the rst- and
second-generation antipsychotic agents, but benzo-
diazepines (see Chapter 15) are often used to control
acute psychotic symptoms. Beta-adrenergic blocking
agents (beta blockers; e.g., propranolol) (see Chapter
12), lithium (see Chapter 16), anticonvulsants (e.g.,
valproic acid) (see Chapter 18), carbamazepine (see
Chapter 18), antiparkinsonian agents (see Chapter 14),
and anticholinergic agents (see Chapters 12 and 14) oc-
casionally play a role in controlling the adverse effects
of medications used in antipsychotic therapy.
Antipsychotic (also known as neuroleptic) medica-
tions can be classied in several ways. Traditionally,
they have been divided into phenothiazines and non-
phenothiazines. Antipsychotic medications can also
be classied as low-potency or high-potency drugs.
The terms low potency and high potency refer only to
the milligram doses used for these medicines and
not to any difference in effectiveness (e.g., 100 mg of
chlorpromazine, a low-potency drug, is equivalent in
264 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
antipsychotic activity to 2 mg of haloperidol, a high-
potency drug). Chlorpromazine and thioridazine are
low-potency drugs, whereas triuoperazine, uphen-
azine, thiothixene, haloperidol, and loxapine are high-
potency drugs. Since 1990, antipsychotic medications
have also been classied as typical (rst-generation) anti-
psychotic agents or atypical (second-generation) anti-
psychotic agents on the basis of their mechanism of
action (see Table 17.1 later in this chapter). The atypical
antipsychotic agents are aripiprazole, asenapine, brex-
piprazole, cariprazine, clozapine, iloperidone, lumate-
perone, lurasidone, olanzapine, paliperidone, pima-
vanserin, quetiapine, risperidone, and ziprasidone. All
of the remaining antipsychotic agents listed in Table
17.1 are typical antipsychotic agents.
ACTIONS
The typical antipsychotic medications block the neu-
rotransmitter dopamine in the central nervous system
(CNS). The atypical antipsychotic agents block dopa-
mine receptors, but they also block serotonin receptors
to varying degrees. However, the exact mechanisms
whereby these actions prevent psychotic symptoms are
unknown. There is substantially more to the develop-
ment of psychotic symptoms than elevated dopamine
levels. There are at least ve known types of dopamine
receptors and several more types of serotonin recep-
tors in various areas of the CNS. Antipsychotic medi-
cations also stimulate or block cholinergic, histaminic,
nicotinic, alpha-adrenergic, and beta-adrenergic neu-
rotransmitter receptors to varying degrees, accounting
for many of the adverse effects of therapy.
Pimavanserin differs from other atypical anti-
psychotics in that it selectively blocks a serotonin
(5-hydroxytryptamine) receptor (5-HT2A) and lacks
activity at dopamine receptors. It is effective in treating
psychosis related to Parkinson disease dementia. Using
atypical antipsychotics for treatment of Parkinson dis-
ease dementia-related psychosis can worsen Parkinson
disease motor symptoms. Because of pimavanserin’s
lack of activity at dopamine receptors, it does not ag-
gravate Parkinson disease’s motor symptoms.
Medication Safety Alert
Increased Mortality in Elderly Patients With Dementia-Related
Psychosis
Antipsychotic drugs increase the all-cause risk of death in
elderly patients with dementia-related psychosis.
USES
All antipsychotic medications are equal in efcacy
when used in equipotent doses. There is some unpre-
dictable variation among patients, however, and in-
dividual patients sometimes show a better response
to particular drugs. In general, medication should be
selected on the basis of the need to avoid certain ad-
verse effects when dealing with concurrent medical or
psychiatric disorders. Despite practice trends, no proof
exists that agitation responds best to sedating drugs
or that withdrawn patients respond best to non-
sedating drugs. There are several reasons that a patient
may become agitated, such as pain, fear, and confusion.
Nonpharmacologic methods may be helpful initially
to manage agitated patients by seeking the source of
agitation and meeting their needs. This is especially
true for patients who have difculty communicating
(e.g., dementia, aphasia, or other cognitive impair-
ment). If medications are needed, a medication history
should be a major factor in drug selection. The nal
important factors in drug selection are the clinically
important differences in the frequency of adverse ef-
fects. No single drug is least likely to cause all adverse
effects; thus individual response should be the best de-
terminant of which drug is to be used. The atypical anti-
psychotic agents tend to be more effective in relieving
the negative and cognitive symptoms associated with
schizophrenia and treating refractory schizophrenia,
and they have a much lower incidence of extrapyramidal
symptoms (EPSs) and hyperprolactinemia.
The initial goals of antipsychotic therapy are calm-
ing the agitated patient, who may be a physical threat
to himself or herself or to others, and beginning the
treatment of the psychosis and thought disorder.
Combined therapy with benzodiazepines (often lo-
razepam) and antipsychotic medications allows lower
dosages of the antipsychotic medication to be used,
reducing the risk of serious adverse effects more com-
monly seen with higher-dose therapy. Some therapeu-
tic effects, such as reduced psychomotor agitation and
insomnia, are observed within 1 week of therapy, but
reductions in hallucinations, delusions, and thought
disorder often require 6 to 8 weeks of treatment to
achieve the full therapeutic effect. Rapid increases in
the dosing of antipsychotic medications will not reduce
the antipsychotic response time. Patients, families, and
the healthcare team must be informed about giving
antipsychotic agents an adequate chance to work before
unnecessarily escalating the dosage and increasing the
risk of adverse effects.
Clinical Pitfall
During episodes of acute psychosis, the patient is out of
touch with reality and often does not understand the need
to take medicines that will help stabilize their condition. The
nurse must ensure that the patient has actually swallowed the
medication when it is administered and not just “mouthed”
or “cheeked” it. Outpatients often require that medication
administration be supervised to ensure adherence to the
medication regimen. In some cases, it is necessary to inject
long-acting medicines to overcome a patient’s nonadherence
problem. After an acute psychotic episode has resolved and
the patient is free from overt psychotic symptoms, a deci-
sion must be made as to whether maintenance therapy is
necessary. This will depend on the diagnosed psychotic dis-
order and the patient’s tolerance of the adverse effects of the
medication. However, most psychotic disorders are treated
with lower maintenance dosages to minimize the risk of
recurrence of the disorder’s psychotic episodes (Box 17.1).
Table 17.1 Antipsychotic Agents
MAJOR ADVERSE EFFECTS
ADULT DOSAGE EXTRAPYRAMIDAL ANTICHOLINERGIC
GENERIC NAME BRAND NAME AVAILABILITY RANGE (MG) SEDATION SYMPTOMS HYPOTENSION EFFECTS
TYPICAL (FIRST-GENERATION) ANTIPSYCHOTIC AGENTS
Phenothiazines
chlorpromazine Tablets: 10, 25, 50, 100, 200 mg 25–2000 +++ ++ +++ ++
Do not confuse Teva-Chlorpromazine Injection: 25 mg/mL
chlorpromazine with
chlordiazepoxide,
chlorhexidine,
chlorpropamide, or
chlorthalidone.
uphenazine – Tablets: 1, 2.5, 5, 10 mg 0.5–40 + ++++ + +
PMS—Fluphenazine Elixir: 2.5 mg/5 mL
Concentrate: 5 mg/mL
Injection: 2.5 mg/mL; 25 mg/mL
perphenazine — Tablets: 2, 4, 8, 16 mg 12–64 + +++ + ++
prochlorperazine – Tablets: 5, 10 mg 15–150 + +++ + +
Prochlorazine Injection: 5 mg/mL
Suppository: 25 mg
thioridazine – Tablets: 10, 25, 50, 100 mg 200–800 +++ + +++ +++
triuoperazine – Tablets: 1, 2, 5, 10 mg 2–40 + +++ + +
Thioxanthenes

Drugs Used for Psychoses CHAPTER 17

thiothixene — Capsules: 1, 2, 5, 10 mg 6–60 + +++ + +
Nonphenothiazines
haloperidol Haldol Tablets: 0.5, 1, 2, 5, 10, 20 mg 1–100 + +++ + +
Teva-Haloperidol Concentrate: 2 mg/mL
Injection: 5 mg/mL
Injection, sustained release: 50
mg/ml and 100 mg/mL
loxapine Capsules: 5, 10, 25, 50 mg 20–250 ++ +++ ++ +
Do not confuse Xylac
loxapine with Lexapro.

265
 266
ATYPICAL (SECOND-GENERATION) ANTIPSYCHOTIC AGENTS
aripiprazole Abilify Tablets: 2, 5, 10, 15, 20, 30 mg 10–30 + + + 0
Abilify Maintena Tablets, orally disintegrating: 10,

UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
15 mg
Oral solution: 1 mg/mL
Injection, intramuscular
suspension: 300, 400 mg
Prelled syringes: 300, 400 mg
asenapine Saphris Tablets, sublingual: 2.5, 5, 10 mg 5–20 ++ ++ ++ +
Secuado Transdermal patch (24 hr): 3.8,
5.7, 7.6 mg
brexpiprazole Rexulti Tablets: 0.25, 0.5, 1, 2, 3, 4 mg 2–4 + + 0/+ 0/+
cariprazine Vraylar Capsules: 1.5, 3, 4.5, 6 mg 1.5–6 + ++ 0/+ 0/+
clozapine Clozaril Tablets: 25, 50, 100, 200 mg 300–900 +++ + +++ ++
Do not confuse Tablets, orally disintegrating: 12.5,
Clozaril with 25, 100, 150, 200 mg
Colazal. Oral suspension: 50 mg/mL in
Versacloz 100 mL bottle
iloperidone Fanapt Tablets: 1, 2, 4, 6, 8, 10, 12 mg 2–24 ++ + ++ ++
lumateperone Caplyta Capsules: 42 mg 42 ++ + ++ ++
lurasidone Latuda Tablets: 20, 40, 60, 80, 120 mg 20–160 ++ ++ ++ ++
olanzapine Zyprexa Tablets: 2.5, 5, 7.5, 10, 15, 20 mg PO: 5–20 ++ + ++ +++
Do not confuse Do not confuse IM short
olanzapine with Zyprexa with Celexa, acting: 30
oxcarbazepine. Zaroxolyn, or Zyrtec. Tablets, orally disintegrating: 5, mg
Zyprexa Zydis 10, 15, 20 mg IM sustained
Relprevv Injection: 10 mg release:
Zyprexa Injection, sustained release: 210, 300 mg q 2
300, 405 mg weeks
paliperidone Invega Tablets, extended release: 1.5, 3, 3–12 + +++ ++ 0
6, 9 mg
Invega Sustenna IM injection, suspension: 39, 78,
117, 156, 234 mg
Invega Trinza IM injection, suspension: 273,
410, 546, 819 mg
pimavanserin Nuplazid Tablets: 10 mg 34 + 0/+ ++ +
Capsules: 34 mg

Continued
Table 17.1 Antipsychotic Agents—cont’d
MAJOR ADVERSE EFFECTS
ADULT DOSAGE EXTRAPYRAMIDAL ANTICHOLINERGIC
GENERIC NAME BRAND NAME AVAILABILITY RANGE (MG) SEDATION SYMPTOMS HYPOTENSION EFFECTS
quetiapine Seroquel Tablets: 25, 50, 100, 200, 300, 50–800 ++ 0 ++ 0
Do not confuse 400 mg
Seroquel with or Tablets, 24-hr extended release:
Sertraline. Seroquel 50, 150, 200, 300, 400 mg
XR
risperidone Risperdal Tablets: 0.25, 0.5, 1, 2, 3, 4 mg 2–16 + ++ ++ +
Do not confuse Tablets, orally disintegrating: 0.25,
Risperdal with 0.5, 1, 2, 3, 4 mg
estradiol, reserpine, PO solution: 1 mg/mL
Restoril, risedronate, IM injection, suspension: 12.5, 25,
or ropinirole. 37.5, 50 mg
Risperdal Consta Prelled syringe: 90, 120 mg
Perseris
ziprasidone Geodon Capsules: 20, 40, 60, 80 mg 40–160 + ++ + ++
Do not confuse IM injection: 20 mg
ziprasidone with
zidovudine.
Available in Canada.

Do not confuse.

Drugs Used for Psychoses CHAPTER 17

267
268 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
Box 17.1 Antipsychotic Medicines: Response Times
and Adverse Effects
Patients who begin antipsychotic drug therapy can expect
some therapeutic effects, such as reduced psychomotor
agitation and insomnia, within 1 week of starting treatment.
However, reduction in hallucinations, delusions, and
thought disorders often requires 6 to 8 weeks for a full
therapeutic response to be achieved. Rapid increases in
dosages of antipsychotic medications will not reduce the
antipsychotic response time but will increase the frequency
of adverse effects.
Antipsychotic medicines may produce extrapyramidal
effects. Tardive dyskinesia may be reversible during its early
stages, but it becomes irreversible with continued use of
the antipsychotic medication. Regular assessment for tar-
dive dyskinesia should be performed for all patients receiv-
ing antipsychotic drugs. Older adult patients should be ob-
served for hypotension and tardive dyskinesia.
ADVERSE EFFECTS OF ANTIPSYCHOTIC
DRUG THERAPY
EXTRAPYRAMIDAL SYMPTOMS
Many of the serious adverse effects of antipsychotic
medications can be attributed to the pharmacologic
effect of blocking dopaminergic, cholinergic, hista-
minic, serotonergic, and adrenergic neurotransmitter
receptors. Although these agents block D2 dopamine
receptors in the mesolimbic area of the brain to stop
psychotic symptoms, blockade of D2 receptors in other
areas of the brain explains the occurrence of EPSs.
EPSs are the most troublesome adverse effects and
the most common cause of nonadherence associated
with antipsychotic therapy. There are four categories
of EPSs: dystonic reactions, pseudoparkinsonism,
akathisia, and tardive dyskinesia.
Acute dystonia has the earliest onset of all the EPSs.
Dystonias are spasmodic movements (prolonged tonic
contractions) of muscle groups such as tongue protru-
sion, rolling back of the eyes (oculogyric crisis), jaw
spasm (trismus), and neck torsion (torticollis). These
symptoms are often frightening and painful for the
patient. Approximately 90% of all dystonic reactions
occur during the rst 72 hours of therapy. Dystonic
reactions are most frequent in male patients, younger
patients, and patients receiving high-potency medica-
tions such as haloperidol. Dystonic reactions are gen-
erally brief and are the EPSs most responsive to treat-
ment. Acute dystonic reactions may be controlled by
intramuscular injections of diphenhydramine, ben-
ztropine, diazepam, or lorazepam. Rating scales for
assessing patients with different forms of dystonias
include the Toronto Western Spasmodic Torticollis
Rating Scale (TWSTRS), the Global Dystonia Scale
(GDS), the Unied Dystonia Rating Scale (UDRS),
and the Fahn-Marsden Scale.
Pseudoparkinsonian symptoms of tremor, muscular
rigidity, mask-like expression, shufing gait, and loss
or weakness of motor function typically begin after
2 to 3 weeks of antipsychotic drug therapy but may
occur up to 3 months after starting therapy. They are
more commonly seen in older adults. These symptoms
result from a relative deciency of dopamine, with
cholinergic excess, caused by antipsychotic medica-
tions and are well controlled by anticholinergic anti-
parkinsonian drugs (e.g., benztropine, diphenhydr-
amine, trihexyphenidyl).
Akathisia is a syndrome consisting of subjective feel-
ings of anxiety and restlessness and objective signs
of pacing, rocking, and inability to sit or stand in one
place for extended periods. Akathisia can increase ag-
gression and is a frequent cause of noncompliance.
It occurs more commonly when high-potency anti-
psychotic medications are used. The mechanism of
action is unknown. Reducing the dosage of the anti-
psychotic medication or switching to a lower-potency
drug should be considered. Treatment with anticholin-
ergic agents, benzodiazepines (e.g., diazepam, loraz-
epam), beta blockers (e.g., propranolol), and clonidine
has shown varying degrees of success.
Tardive dyskinesia is a syndrome of persistent and
involuntary hyperkinetic abnormal movements. It
develops in about 20% to 25% of patients receiving
typical antipsychotic medications on a long-term ba-
sis (e.g., months to years). There appears to be a lower
incidence in patients receiving atypical antipsychotic
agents, but these agents are newer, and it sometimes
takes years for tardive dyskinesia to develop. This
drug-induced, late-appearing neurologic disorder is
noted for such symptoms as buccolingual masticatory
syndrome or orofacial movements. The buccolingual
masticatory movements begin with mild forward,
backward, or lateral tongue movement. As the dis-
order progresses, more obvious movements appear,
including tongue thrusting, rolling, or “y-catching”
movements, as well as chewing or lateral jaw move-
ments that produce smacking noises. Symptoms may
interfere with the patient’s ability to chew, speak, or
swallow. Facial movements include frequent blinking,
brow arching, grimacing, and upward deviation of the
eyes. The severity of symptoms of tardive dyskinesia
can uctuate daily and symptoms often will remit dur-
ing sleep. The clinical manifestations of tardive dyski-
nesia are similar to those of dystonias, but there are
some signicant differences. Tardive dyskinesia typi-
cally appears after antipsychotic dosage reduction or
discontinuation, it improves when the antipsychotic
dosage is increased, it worsens with the administration
of anticholinergic agents, and it may persist for months
or years after antipsychotic medicines are discontin-
ued. The exact cause of tardive dyskinesia is unknown.
Early signs may be reversible but, over time, they may
become irreversible, even with discontinuation of the
antipsychotic medicine.

The best treatment approach to tardive dyskinesia
is prevention. Patients who receive maintenance anti-
psychotic drug therapy should be assessed for early signs
of tardive dyskinesia at least semiannually and prefer-
ably quarterly. Findings should be documented in pa-
tient records to ensure continuity of care and medico-
legal protection. Because of the variability in severity
and presentation, rating scales have been developed to
standardize assessments and diagnoses. The Abnormal
Involuntary Movement Scale (AIMS) rates dyskinetic
movements, but it is not exclusively diagnostic for tar-
dive dyskinesia (see Evolve website). The Dyskinesia
Identication System: Condensed User Scale (DISCUS)
rates the presence and severity of abnormal move-
ments and considers other variables when formulating
a conclusion. The DISCUS evaluation specically de-
scribes the type of tardive dyskinesia and allows diag-
noses to change over time (see Evolve website).
Treatment of tardive dyskinesia is not particularly
successful. When feasible, immediate tapering and
discontinuation of the offending antipsychotic drug
is recommended when signs of tardive dyskinesia be-
come apparent. Antipsychotic drug cessation (or dose
reduction) must be carefully considered because of the
potential for relapse or worsening of psychotic symp-
toms. If a patient receiving a typical antipsychotic
medicine develops signs of tardive dyskinesia, switch-
ing to an atypical antipsychotic may alleviate the ad-
verse effects.
If the patient is receiving an anticholinergic for tar-
dive dyskinesia the dose should be reduced, gradu-
ally discontinued, or switched to amantadine. Other
options to treat tardive dyskinesia are the vesicular
monoamine transporter 2 (VMAT2) inhibitors, val-
benazine (Ingrezza) and deutetrabenazine (Austedo).
These agents act centrally by depleting dopamine stor-
age in presynaptic vesicles.
Neuroleptic malignant syndrome (NMS) is a poten-
tially fatal adverse effect of antipsychotic therapy in
which the patient displays EPSs as part of the symp-
toms of the disorder. It occurs in 0.5% to 1.4% of pa-
tients receiving antipsychotic therapy and is reported
most often with high-potency antipsychotic agents
given intramuscularly. It typically occurs after 3 to 9
days of treatment with antipsychotic medications, and
it is not related to dosage or previous drug exposure.
Once NMS begins, symptoms rapidly progress over
24 to 72 hours. Symptoms usually last for 5 to 10 days
after discontinuation of oral medications and 13 to 30
days with depot antipsychotic medicine (depot: inject-
able, slow-release dose form). Most cases of NMS oc-
cur in patients younger than 40 years old, and it occurs
twice as often in men. The syndrome is characterized
by the following: fever, severe EPSs (e.g., lead-pipe ri-
gidity, trismus, choreiform movements, opisthotonos),
autonomic instability (e.g., tachycardia, labile hyper-
tension, diaphoresis, incontinence), and alterations in
consciousness (e.g., stupor, mutism, coma). Mortality
rates have been as high as 30%, but prompt recognition
Drugs Used for Psychoses CHAPTER 17 269
of the symptoms has reduced the mortality rate to 4%
in recent years. It is hypothesized that the cause of the
symptoms is excessive dopamine depletion. Treatment
includes bromocriptine or amantadine as dopamine
agonists and dantrolene as a muscle relaxant. Fever
is treated with cooling blankets, adequate hydration,
and antipyretics. After the patient’s condition has sta-
bilized, a thorough evaluation of the medications be-
ing prescribed must be made. Resumption of the anti-
psychotic medication may result in a recurrence of
NMS; therefore the lowest dose possible of an antipsy-
chotic agent is prescribed, and close observation of the
patient’s response is required.
SEIZURES
Antipsychotic agents may lower the seizure threshold
in patients with seizure disorders and even in those
with no previous history of seizures. The low-potency
typical agents and clozapine, an atypical agent, have a
higher incidence of inducing seizures.
WEIGHT GAIN
Antipsychotic drug therapy often causes substantial
weight gain. There is a higher prevalence of obesity as-
sociated with schizophrenia, and the weight gain often
contributes to nonadherence to therapy. Obesity leads
to an increased risk of type 2 diabetes mellitus, dys-
lipidemia, hypertension, coronary heart disease, and
stroke (see Chapter 20). The frequency and amount
of weight gain are generally greater with atypical
agents than with typical medications, although indi-
vidual atypical agents vary in the extent to which they
cause weight gain. Of the atypical agents, clozapine
and olanzapine cause the most weight gain, moderate
weight gain is reported with risperidone and quetiap-
ine, and aripiprazole and ziprasidone cause the least
weight gain.
HYPERGLYCEMIA
Hyperglycemia and the development of diabetes is re-
ported particularly with atypical antipsychotic agents.
The mechanism whereby this occurs is unknown, and
research in this area is more difcult because patients
with schizophrenia also have a twofold to threefold
higher incidence of diabetes mellitus than the general
population. Hyperglycemia occurs more frequently
with clozapine, olanzapine, and quetiapine, but de-
velopment of hyperglycemia with the other atypical
agents can occur.
DYSLIPIDEMIA
Dyslipidemia has been reported with atypical anti-
psychotic agents. The risk prole may differ between
agents.
DYSRHYTHMIAS
Thioridazine, ziprasidone, haloperidol, quetiapine,
olanzapine, asenapine, iloperidone, lurasidone, and
risperidone have rarely been associated with torsades
270 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
de pointes—a ventricular dysrhythmia associated
with prolongation of the QTc interval on the electro-
cardiogram, syncope, and sudden death. Bradycardia,
electrolyte imbalance (hypokalemia, hypomagnese-
mia), presence of congenital prolongation of the QTc
interval, and concomitant use of other medications
that may signicantly prolong the QTc interval (e.g.,
quinidine, sotalol, moxioxacin, dofetilide) can in-
crease the risk of torsades de pointes and sudden death
in patients receiving antipsychotic agents.
OTHER ADVERSE EFFECTS
Other adverse effects of antipsychotic therapy can also
be predicted on the basis of the receptor-blocking ac-
tivity of the agents:
• Blocking the cholinergic (acetylcholine) receptors
explains the anticholinergic effects (e.g., dry mouth,
constipation, sinus tachycardia, blurred vision, in-
hibition or impairment of ejaculation, urinary reten-
tion) associated with antipsychotic agents.
• Blocking histamine-1 receptors causes sedation,
drowsiness, and appetite stimulation and contrib-
utes to the hypotensive effects and potentiation
of CNS depressant drugs. Antipsychotic agents
also block alpha-1 and alpha-2 adrenergic recep-
tors, causing postural hypotension, sexual dys-
function, reex tachycardia, and potentiation of
antihypertensive agents. The most potent alpha-1
blockers are chlorpromazine and thioridazine,
whereas haloperidol has almost no effect on al-
pha-1 receptors.
Antipsychotic agents may produce many adverse
effects other than those already listed, including hepa-
totoxicity, blood dyscrasias, allergic reactions, endo-
crine disorders, skin pigmentation, and reversible
effects in the eyes. Patients receiving clozapine are par-
ticularly susceptible to developing agranulocytosis.
Regularly scheduled white blood cell (WBC) counts
are mandatory.
Clinical Pitfall
Antipsychotic medicines may have adverse effects such
as seizure activity, pseudoparkinsonian symptoms, tardive
dyskinesia, and hepatotoxicity that require management by
the prescribing healthcare provider. The patient and those
providing supervision need to understand the importance of
reporting any of these symptoms promptly for appropriate
interventions.
NURSING IMPLICATIONS FOR ANTIPSYCHOTIC
THERAPY
Assessment
History of behavior
• Gather information from the patient and other in-
dividuals relating to the onset, duration, and pro-
gression of the patient’s symptoms. Has the patient
previously been treated for this or other mental
disorders? Does the patient have any coexisting
health conditions?
• Take a detailed history of all medications that the
patient is taking or has taken during the past 3
months.
• Inquire about the use of illegal substances.
Basic mental status
• Note the patient’s general appearance and appro-
priateness of attire. Is the patient clean and neat? Is
the posture erect, stooped, or slumped? Is the pa-
tient oriented to date, time, place, and person?
• What coping mechanisms has the patient been us-
ing to deal with the situation? How adaptive are the
coping mechanisms? Initiate changes in maladap-
tive coping mechanisms by guiding the patient to-
ward the use of more adaptive coping strategies.
• Has the patient been able to carry out self-care ac-
tivities and social and work obligations?
• Are symptoms of depression present? Symptoms
may not be evident during the acute phase of
schizophrenia.
Interpersonal relationships. Assess the quality of the
relationships in which the patient is involved. Identify
people in the patient’s life who are supportive. Ask the
family and signicant others to describe the relation-
ship they have with the patient. Has there been deteri-
oration in their closeness and their ability to interrelate
effectively?
Mood and affect. Patients experiencing altered think-
ing, behavior, or feelings require careful evaluation of
their verbal and nonverbal actions. Often the thoughts,
feelings, and behaviors displayed are inconsistent with
the so-called normal responses of individuals in simi-
lar circumstances.
• Is the facial expression worried, sad, angry, or
blank?
• Is the patient displaying behaviors that are inap-
propriate or blunted? Does the patient have a at
affect?
• Is the patient apathetic to normal situations?
• Is there consistency when the patient is expressing
feelings verbally and nonverbally?
• Does the patient overreact to situations at times?
Clarity of thoughts and perception
• Does the patient suffer from delusions, dis-
organized speech pattern, ight of ideas, autism,
grandiose ideas, or mutism? Ask about the presence
of hallucinations (auditory, visual, tactile).
• Does the patient talk about unrelated topics (loose
association) as though they are connected and
related?
• Is the patient self-absorbed and not in contact with
reality?
• Does the patient display an interruption of thoughts?
• Does the patient display paranoid behavior?

Suicidal ideation. Ask the patient whether they have
ever had thoughts about suicide. If the response is
“yes,” get more details. Has a specic plan been for-
mulated? How often do these thoughts occur? Does
the patient make direct or indirect statements regard-
ing death (e.g., “things would be better” if death
occurred)?
Psychomotor function. What is the patient’s activity
level? Is the individual unable to sit still and instead
paces continually? Is the patient catatonic (i.e., immo-
bile as a result of psychological dysfunction)?
Sleep pattern. What is the patient’s normal sleep pat-
tern, and how has it varied since the onset of the psy-
chotic symptoms? Ask specically whether insomnia
is present. Ask the patient to describe their perception
of the amount and quality of sleep nightly. What is the
level of fatigue? Are naps taken regularly?
Dietary history. Ask questions about the patient’s ap-
petite and note weight gains or losses not associated
with intentional dieting.
Implementation
• Nursing interventions must be individualized and
based on patient assessment data.
• Provide the individual with a structured environ-
ment that is safe and that decreases external stimuli.
• Provide an environment of acceptance that focus-
es on the individual’s strengths while minimizing
weaknesses.
• Provide an opportunity for the patient to express
feelings. Use active listening and therapeutic com-
munication techniques. Allow the patient to express
feelings in nonverbal ways, such as involvement in
physical activities or occupational therapy.
• Allow the patient to make decisions, if capable;
make those decisions that the patient is not capable
of making. Provide a reward for progress when de-
cisions are initiated appropriately.
• Involve the patient in self-care activities. Assist with
personal grooming as needed. Ensure that the pa-
tient is dressed appropriately.
• Set limits for the patient to handle inappropriate be-
haviors and enforce them in a kind, rm manner.
• Once the content is known, do not reinforce the pa-
tient’s hallucinations or delusions.
• When the patient has altered perceptions, provide
diversionary activities and minimize interactions,
such as viewing television programs that may rein-
force the distorted perceptions.
• Be open and direct when handling a patient who is
highly suspicious. Speak distinctly to be heard; do
not whisper or laugh in circumstances that the pa-
tient could misconstrue.
• If the patient is suicidal, ask for details about
the plan being formulated. Follow up on details
Drugs Used for Psychoses CHAPTER 17 271
obtained with appropriate family members or sig-
nicant others. Provide for patient safety and super-
vision as appropriate.
• Use physical restraints within the guidelines of the
clinical setting as appropriate to the behaviors being
exhibited. Use the least restrictive alternative pos-
sible for the circumstances.
• Provide for nutritional needs by having high-protein,
high-calorie foods appropriate for the individual to
eat while pacing or highly active. Give vitamins and
liquid supplemental feedings as ordered.
• Provide an opportunity for the individual to be
involved in selecting foods appropriate to needs
(to lose or gain weight). If the person is paranoid
and suspects being poisoned, allow the individual
to self-serve food, open canned food, and perform
other activities, as appropriate within the setting.
• Manipulative behavior must be handled in a consis-
tent manner by all staff members. Set limits and use
consequences that are agreed to in advance by all
staff members. When the patient attempts to blame
others, refocus on the patient’s responsibilities. Give
positive reinforcement for nonmanipulative behav-
iors when they occur.
Patient Education
• Orient the individual to the unit. Explain the rules
and the process of privileges and how they are ob-
tained or lost. (The extent of the orientation and
explanations given will depend on the patient’s
orientation to date, time, and place, as well as their
abilities.)
• Base patient education on assessment data and in-
dividualize instruction to provide the patient with a
structured environment.
• Explain the activity groups available and how and
when the individual will participate in them.
• Involve the patient and family in establishing out-
comes and integrate the patient into the appropriate
group processes to develop positive experiences to
enhance coping skills.
• Before discharge, make sure the patient and the
family understand the desired treatment outcomes
and the entire follow-up plan (e.g., frequency of
therapy sessions, prescribed medications, primary
healthcare provider visits, return-to-work goals).
Fostering health maintenance
• Throughout the course of treatment, discuss medi-
cation information and how it will benet the
patient’s symptoms and circumstances. Drug ther-
apy is a major portion of antipsychotic therapy.
Although symptoms may improve, they may not be
totally eliminated. The onset of a drug’s effective-
ness varies widely, depending on the drug and the
route of administration.
• Nonadherence is a major problem in this group of
patients; therefore tracking the medications being
272 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
taken requires careful scrutiny. On an outpatient ba-
sis, many of these patients need their medications
administered by another responsible individual.
Nonadherence is thought to be a major cause of re-
peat hospitalization in these patients. Long-acting
injections may be used for some patients in an at-
tempt to overcome this problem. On an inpatient
basis, the nurse must always check to be sure that
the patient is actually swallowing the medication
because there is a high incidence of “cheeking” (i.e.,
hiding drugs between the teeth and gums).
• Use baseline clinical evaluation rating scales (e.g.,
BPRS, CGI, PANSS) and adverse effect scales (e.g.,
GDS, TWSTRS for dystonias, DISCUS or AIMS for
EPSs) at specied intervals; record and report nd-
ings in accordance with agency policy.
• Seek cooperation and understanding of the fol-
lowing points so that medication adherence is in-
creased: name of the medication; its dosage, route,
and time of administration; and its common and
serious adverse effects. Encourage the patient not to
discontinue or adjust the drug dosage without con-
sulting the healthcare provider. Provide the patient
and family with information about available com-
munity resources, including the NAMI.
Patient self-assessment. Enlist the patient’s help with
developing and maintaining a written record of moni-
toring parameters. See the Template for Developing
a Written Record for Patients to Monitor Their Own
Therapy on the Evolve website, and complete the
Premedication Data column for an assessment of the
patient’s physical and mental capabilities as a baseline
to track the patient’s response to drug therapy. Ensure
that the patient understands how to use the form, and
instruct the patient to bring the completed form to
follow-up visits. Because there are a number of debili-
tating adverse effects and others that are life threaten-
ing if they are not acted on correctly, it is important
to maintain open communication with healthcare pro-
viders, nurses, therapists, and pharmacists throughout
the course of therapy.
DRUG CLASS: ANTIPSYCHOTIC AGENTS
Actions
Although the antipsychotic medications are from dis-
tinctly different chemical classes, all are similar in that
they act by blocking the action of dopamine in the
brain. The exception is pimavanserin, which selective-
ly blocks the 5-HT2A serotonin receptor and lacks activ-
ity at dopamine receptors. The atypical antipsychotic
agents block serotonin receptors in addition to dopa-
mine receptors. Because all the antipsychotic agents
work at different sites in the brain, adverse effects
are observed in different body systems. Atypical anti-
psychotic agents tend to be more effective and have
fewer adverse effects than typical agents.
Uses
Antipsychotic agents are used to treat psychoses as-
sociated with mental illnesses such as schizophrenia,
mania, and psychotic depression. Medications used
to treat these disorders are grouped into two broad
categories (Table 17.1): rst-generation antipsychotic
drugs, also known as typical antipsychotic drugs, includ-
ing the phenothiazines and nonphenothiazines (e.g.,
thioxanthenes, haloperidol, loxapine); and second-
generation antipsychotic drugs, also known as atypi-
cal antipsychotic drugs (e.g., aripiprazole, olanzapine,
quetiapine, risperidone). The atypical antipsychotics
(except pimavanserin) are usually used rst line to
provide signicant relief of active psychotic symp-
toms such as hallucinations, delusions, and thought
disorganization for approximately 70% of patients
with schizophrenia. In addition, several of the atypical
antipsychotics are used for treatment of bipolar dis-
order (e.g., lurasidone) and as adjunctive treatment
to major depressive disorders (e.g., aripiprazole).
Risperidone is used to treat irritability associated
with autistic disorder in children and adolescents.
Clozapine is reserved for more resistant cases that do
not respond adequately to the other atypical agents.
All these antipsychotic medications also signicantly
reduce the risk of recurrence. Pimavanserin is used for
the treatment of hallucinations and delusions associat-
ed with Parkinson disease dementia-related psychosis.
As clinical experience is being gained with the sec-
ond-generation antipsychotic drugs, dramatic weight
gain, diabetes mellitus, electrocardiographic changes
(e.g., QT interval prolongation), and dyslipidemia
have been reported. The risk of these potentially seri-
ous adverse effects is not the same with all drugs, but
the US Food and Drug Administration has issued pre-
cautionary statements to encourage close monitoring
of body weight, blood glucose, and serum lipid levels
in all patients receiving these antipsychotic agents.
Therapeutic Outcome
The primary therapeutic outcome expected from anti-
psychotic therapy is maintaining the individual at an
optimal level of functioning, with minimal exacerba-
tions of psychotic symptoms and minimal adverse ef-
fects from medicines.
Nursing Implications for Antipsychotic Agent
Therapy
Premedication assessment
1. Obtain baseline blood pressures with the patient
supine and standing; record and report signicant
lowering to the healthcare provider before admin-
istering the medicine. Monitor on a yearly basis
thereafter.
2. Check the patient’s electrolyte levels, body weight,
waist circumference, height, blood glucose level,
lipid prole, hepatic function, cardiac function,
and thyroid function before initiating therapy and

periodically throughout the course of treatment.
Weight should be monitored every 4 weeks until
12 weeks after initiating therapy and then every 3
months. Monitor waist circumference and fasting
plasma glucose level annually and fasting lipid lev-
els every 5 years.
3. Use baseline clinical evaluation rating scales (e.g.,
BPRS, CGI, PANSS) and adverse effect scales (e.g.,
GDS, TWSTRS for dystonias, DISCUS or AIMS for
EPSs) at specied intervals; record and report nd-
ings in accordance with agency policy.
4. Use of clozapine requires a baseline WBC count
and weekly WBC counts for the rst 6 months of
treatment because of the high incidence of agranu-
locytosis. Thereafter, if WBC counts are acceptable
(i.e., ≥3500/mm3) and if the absolute neutrophil
count is more than 2000/mm3, WBC counts can be
monitored every other week. WBC counts must be
monitored weekly for at least 4 weeks after the dis-
continuation of clozapine.
Availability, dosage, and administration. See Table 17.1.
The dosage must be individualized according to the
patient’s degree of mental and emotional disturbance.
It will often take several weeks for a patient to show
optimal improvement and become stabilized on an ad-
equate maintenance dosage. As a result of the cumula-
tive effects of antipsychotic agents, the patient must be
reevaluated periodically to determine the lowest effec-
tive dosage necessary to control psychiatric symptoms.
Common adverse effects
Neurologic
Chronic fatigue, drowsiness. Chronic fatigue and
drowsiness are common problems associated with
medications used to treat psychoses. Sedative effects
associated with antipsychotic therapy can be mini-
mized by giving the dose of medication at bedtime.
The patient should not take these medications while
working with machinery, operating a motor vehicle,
administering medication, or performing other duties
that require mental alertness.
Cardiovascular
Orthostatic hypotension. All antipsychotic agents
may cause some degree of orthostatic hypotension
manifested by dizziness and weakness, particularly
when therapy is initiated. Monitor the patient’s blood
pressure daily in the supine and standing positions.
Anticipate the development of postural hypotension
and take measures to prevent an occurrence. Teach the
patient to rise slowly from a supine or sitting position
and encourage the patient to sit or lie down if feeling
faint.
Sensory
Blurred vision. Caution the patient that blurred vi-
sion may occur and make appropriate suggestions to
ensure the patient’s personal safety.
Drugs Used for Psychoses CHAPTER 17 273
Genitourinary
Urinary retention. Urinary retention may occur after
the administration of antipsychotic agents.
Gastrointestinal
Constipation; dryness of mucosa of the mouth, throat,
nose. Mucosal dryness may be relieved by sucking
hard candy or ice chips or by chewing gum. A high-
ber diet, stool softeners (e.g., docusate), or the occa-
sional use of a stimulant laxative (e.g., bisacodyl) may
be required to treat constipation.
Serious adverse effects
Neurologic
Seizure activity. Provide for patient safety during epi-
sodes of seizures; report this symptom to the health-
care provider for further evaluation. An adjustment of
anticonvulsant therapy may be required, especially for
seizure-prone patients.
Pseudoparkinsonian symptoms. Report the develop-
ment of drooling, cogwheel rigidity, shufing gait,
mask-like expression, or tremors. Anticholinergic
agents may be used to help control these symptoms.
Tardive dyskinesia. Tardive dyskinesia occurs
much more commonly with the rst-generation anti-
psychotic drugs. Report the development of ne trem-
ors of the tongue, “y-catching” tongue movements,
and lip smacking. This is particularly important for
patients who have been receiving antipsychotic drugs
and anticholinergic medications for several years.
Gastrointestinal
Hepatotoxicity. The symptoms of hepatotoxicity are
anorexia, nausea, vomiting, jaundice, hepatomegaly,
splenomegaly, and abnormal liver function test re-
sults (e.g., elevated bilirubin, aspartate aminotrans-
ferase [AST], alanine aminotransferase [ALT], gamma-
glutamyltransferase [GGT], and alkaline phosphatase
levels [ALP]; increased prothrombin time [PT]).
Hematologic
Blood dyscrasias. Routine laboratory studies (e.g.,
red blood cell, WBC, and differential counts) should be
scheduled. This is particularly important for patients
receiving clozapine. Monitor for sore throat, fever, pur-
pura, jaundice, or excessive and progressive weakness.
Hypersensitivity
Hives, pruritus, rash. Report these symptoms to the
healthcare provider for further evaluation.
Other
Photosensitivity. The patient should be cautioned to
avoid prolonged exposure to sunlight and ultraviolet
light. Suggest that the patient wear long-sleeved cloth-
ing, a hat, and sunglasses when exposed to sunlight.
Advise against using articial tanning lamps.
Drug interactions
Drugs that increase adverse effects. Antihistamines,
alcohol, analgesics, anesthetics, tranquilizers, opiates,
St. John’s wort, and sedative-hypnotics increase the
274 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
toxic effects of antipsychotic drugs. Monitor the pa-
tient for excessive sedation and reduce the dosage of
the previously mentioned drugs if necessary.
Drugs that decrease therapeutic effects
Dopamine agonists. Dopamine agonists (i.e., levo-
dopa, ropinirole, pramipexole) block the dopamine
antagonist effects of the antipsychotic agents. Avoid
concurrent use.
Carbamazepine, phenytoin, rifampin, St. John’s
wort. Carbamazepine, phenytoin, rifampin, and St.
John’s wort stimulates the metabolism of haloperidol,
brexpiprazole, cariprazine, clozapine, aripiprazole, ilo-
peridone, lurasidone, lumateperone, olanzapine, que-
tiapine, paliperidone, risperidone, and ziprasidone.
Adjustment of the dosage of the antipsychotic medi-
cine may be required.
Divalproex sodium. Divalproex sodium increases the
serum level of paliperidone. Dosage adjustments may
be needed to avoid toxicities.
Erythromycin, cimetidine, clarithromycin, uoxetine, grape-
fruit juice, ketoconazole. All of these agents inhibit the
metabolism of aripiprazole, asenapine, clozapine,
haloperidol, iloperidone, lurasidone, quetiapine, risp-
eridone (only uoxetine) and ziprasidone, causing an
increase in serum levels and potential toxicity from the
antipsychotic drug. Dosages of the antipsychotic drug
may need to be reduced to avoid toxicities.
Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• Psychoses are symptoms of psychotic disorders—that is,
illnesses in which the patient has lost touch with reality. The
underlying illness must be treated, not just the psychosis.
• A combination of nonpharmacologic and pharmacologic
therapies provides the most successful therapeutic
outcomes.
• The emphasis on community treatment has ensured that
almost all healthcare settings treat patients with psychotic
symptoms. Community hospitals and health maintenance
organizations now provide care to many psychiatric
patients, and nurses increasingly serve residential care
facilities. Many patients require years of antipsychotic drug
treatment to prevent exacerbations of their illness.
• Although antipsychotic medications cause many adverse
effects, most can be minimized by patient education,
manipulation of dosage and administration, and sometimes
adjunctive drug treatments. These patients require careful
monitoring of target symptoms to maximize response and
minimize adverse effects.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions for
the NCLEX® Examination, Critical Thinking Clinical Situations, and
other learning activities to help you master this chapter content.
Fluvoxamine, ciprooxacin. Fluvoxamine and cipro-
oxacin inhibit the metabolism of asenapine, clozap-
ine, and olanzapine. Dosage adjustments may be need-
ed to avoid toxicities.
Paroxetine. Paroxetine inhibits the metabolism of
brexpiprazole, haloperidol, iloperidone, risperidone,
and thioridazine. Dosage adjustments may be needed
to avoid toxicities.
Smoking. Cigarette smoking enhances the metabo-
lism of clozapine and olanzapine. Increased dosages
may be necessary to maintain effects in patients who
smoke.
Antihypertensive agents. Antihypertensive agents (see
Chapter 22) (e.g., beta blockers, angiotensin-convert-
ing enzyme inhibitors, angiotensin receptor blockers,
calcium channel blockers) signicantly enhance the
hypotensive effects of antipsychotic agents. Concurrent
therapy is not recommended unless it is used to treat
the adverse effects of antipsychotic agents.
Insulin, oral hypoglycemic agents. Patients with pre-
diabetes or diabetes must be monitored for the de-
velopment of hyperglycemia, particularly during the
early weeks of therapy. Assess patients regularly for
glycosuria and report it to the healthcare provider if
it occurs with any frequency. Patients receiving oral
hypoglycemic agents or insulin may require a dosage
adjustment.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX®
Examination-Style Questions
The following questions are typical of the NCLEX examination
and include both NGN (Next Generation) and traditional ques-
tions. See Chapter 1 for further information regarding question
types.
Scenario
A patient with a known diagnosis of schizophrenia was admit-
ted to the psychiatric area of the hospital after an episode of
psychotic behavior.
1. A nurse is assessing the patient in the scenario who has been
admitted to the psychiatric unit and who has been hearing voices
that told them to lock all the doors and not answer any phone
calls. The nurse recognizes which of the signs and symptoms
of psychotic behavior that may be exhibited? Indicate with an X
the signicant factors and the unrelated factors associated with
psychotic behavior.
 Drugs Used for Psychoses CHAPTER 17 275

4. The nurse is discussing with the patient in the scenario being

SIGNIFICANT UNRELATED
treated for psychoses with antipsychotic medications what to
FACTORS FACTORS
expect. Which statement by the nurse needs to be revised?
Auditory hallucinations
1. “While you take these medications they should work
Grandiose delusions within the week to reduce auditory hallucinations or
Wringing hands those voices you hear.”
Flight of ideas 2. “These medications will be effective in reducing your
feelings of agitation.”
Garbled speech
3. “While you take these medications you may nd that you
start to gain weight.”
Objective: Identify the signs and symptoms of psychotic behavior. 4. “These medications will allow you to get a good night’s
NCLEX item type: Matrix sleep.”
Cognitive skill: Analyze cues Objective: Discuss the antipsychotic medications that are used for
the treatment of psychoses.
2. A patient who is taking an antipsychotic agent develops
NCLEX item type: Multiple choice
extrapyramidal symptoms. Which of these symptoms, if observed
Cognitive skill: Comprehension
by the nurse, would indicate the presence of extrapyramidal
effects? (Select all that apply.) 5. The nurse reviewing a patient’s medication list recognized which
1. Tongue protrusion one as the antipsychotic?
2. Pressured speech 1. Lithium carbonate
3. Neck torsions 2. Sertraline (Zoloft)
4. Seizures 3. Olanzapine (Zyprexa)
5. Shufing gait 4. Amitriptyline (Elavil)
6. Pacing or rocking
Objective: Discuss the antipsychotic medications that are used for
7. Frequent blinking
the treatment of psychoses.
8. Jaw spasms
NCLEX item type: Multiple choice
9. Mask-like expression
Cognitive skill: Knowledge
Objective: Identify the common adverse effects that are observed
with the use of antipsychotic medications. 6. The nurse knows that the patient in the scenario who has
NCLEX item type: Extended multiple response schizophrenia will need to have their medication dose adjusted if
Cognitive skill: Prioritize hypothesis they develop which of the following?
1. Signicant weight gain
3. The nurse knows that extrapyramidal effects may be seen with
2. Delusions that they are perceived as being controlled by
antipsychotic medications; what other adverse effects should be
radio waves
monitored for? (Select all that apply.)
3. Loss of their sense of taste and smell
1. Seizures 4. The sense that the medications do not work anymore
2. Weight loss
Objective: Describe the major indications for the use of
3. Chronic fatigue
antipsychotic agents.
4. Dyslipidemia
NCLEX item type: Multiple choice
5. Hyperglycemia
Cognitive skill: Understanding
Objective: Identify the common adverse effects that are observed
with the use of antipsychotic medications.
NCLEX item type: Multiple response
Cognitive skill: Application
18 Drugs Used for Seizure Disorders

https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the different types of seizure disorders.
2. Identify nursing interventions during the management of
seizure activity.
3. Discuss the desired therapeutic outcomes from
antiepileptic agents used for seizure disorders.
4. Identify the drug classes used to treat seizure disorders.
5. Describe the neurologic assessment performed on
patients taking antiepileptic agents to monitor for common
and serious adverse effects.

Key Terms
seizures (SĒ-zhŭrz) (p. 276)
epilepsy (ĔP-ĭ-lĕp-sē) (p. 276)
generalized seizures (JĔN-ŭr-ăl-īzd)
(p. 276)
focal seizures (FŌ-kĕl) (p. 276)
antiepileptic drugs (ăn-tī-ĕp-ĭ-LĔP-
tĭk) (p. 276)
tonic phase (TŎN-ĭk) (p. 277)
clonic phase (KLŎN-ĭk) (p. 277)
postictal state (PŌST-ĭk-tĕl)
(p. 277)
status epilepticus (STĂ-tŭs
ĕp-ĭ-LĔP-tĭk-ŭs) (p. 277)
atonic seizure (ĕ-TŎN-ĭk) (p. 277)
myoclonic seizures (mī-ō-KLŎN-ĭk)
(p. 277)
seizure threshold (THRĔSH-hōld)
(p. 278)
treatment responsive (TRĒT-mĕnt
rē-SPŎN-sĭv) (p. 278)
treatment resistant (TRĒT-mĕnt
rē-ZĬS-tĕnt) (p. 278)
gingival hyperplasia (JĬN-jĭ-văl hī-
pŭr-PLĀ-zhă) (p. 281)
nystagmus (nĭs-TĂG-mŭs) (p. 284)

In 2017 h Inrnainal Lagu Agains Epilpsy,

SEIZURE DISORDERS
Seizures ar a sympm f an abnrmaliy in h
nrv clls f h brain. A sizur is a brif prid
f abnrmal lcrical aciviy in hs nrv cn
rs. Sizurs may b cnvulsiv (i.., accmpanid
by viln, invlunary muscl cnracins) r nn
cnvulsiv. During a sizur, hr is fn a chang
in h prsn’s cnsciusnss, snsry and mr
sysms, subjciv wllbing, and bjciv bhav
ir. Sizurs may rsul frm fvr, had injury, brain
umr, mningiis, hypglycmia, a drug vrds
r wihdrawal, r pisning. I is simad ha 8%
 10% f all ppl will hav a sizur during hir
lifims. If h sizurs ar chrnic and rcurrn,
h pain is diagnsd as having epilepsy. Epilpsy
is h ms cmmn f all nurlgic disrdrs. I is
n a singl disas bu rahr svral diffrn disr
drs ha hav n cmmn characrisic: a suddn
discharg f xcssiv lcrical nrgy frm nrv
clls in h brain. An simad 2.3 millin Amricans
hav hs disrdrs, and apprximaly 125,000 nw
cass ar diagnsd annually. Th caus f pilpsy
may b unknwn (i.., idipahic), r i may b h
rsul f a had injury, a brain umr, mningiis, r
a srk.
a wrldwid rganizain f pilpsy prfssinals,
mad rvisins  h classicain sysm f sizur
yps. Sizurs ar classid in focal (parial) ns,
generalized ns, and unknwn ns. Fcal sizurs
bgin in a lcalizd ara in n hmisphr f h brain
and ar subdividd in fcal ns awar sizurs and
fcal ns impaird awarnss sizurs. Focal onset
aware seizures (frmrly knwn as simpl parial si
zurs) ar characrizd by a prsn bing awak and
awar during sizurs. Focal onset impaired awareness
seizures (frmrly knwn as cmplx parial sizurs)
ar characrizd by a prsn bing cnfusd r hir
awarnss is affcd in sm way during a sizur.
Bh yps f fcal sizurs can vlv in gnral
izd sizurs, which is a prcss rfrrd  as second-
ary generalization.
Generalized seizures rfr  hs ha affc bh
hmisphrs f h brain, ar accmpanid by a lss f
cnsciusnss, and may b subdividd in cnvulsiv
and nncnvulsiv yps. Gnralizd pilpsis hav
a rang f sizur subyps, including absnc, my
clnic, anic, nic, and nicclnic sizurs. Epilpsy
is rad alms xclusivly wih mdicains knwn
as anticonvulsants r as antiepileptic drugs, a rm gain
ing mr widsprad us.

276

DESCRIPTIONS OF SEIZURES
GENERALIZED CONVULSIVE SEIZURES
Th ms cmmn gnralizd cnvulsiv sizurs ar
h nicclnic, anic, and myclnic sizurs.
TONIC-CLONIC SEIZURES
Tnicclnic sizurs ar h ms cmmn yp f
sizur. During h tonic phase, pains suddnly d
vlp inns muscular cnracins ha caus hm
 fall  h grund, ls cnsciusnss, and li rigid.
Th back may arch, h arms may x, h lgs may
xnd, and h h may clnch. Air is frcd up h
larynx, xruding saliva as fam and prducing an au
dibl sund lik a cry. Rspirains sp and h pain
may bcm cyanic. Th nic phas usually lass 20
 60 scnds bfr diffus rmbling ss in. Thn h
clonic phase bgins, which is manifsd by bilarally
symmric jrks alrnaing wih h rlaxain f h
xrmiis. Th clnic phas sars slighly and gradu
ally bcms mr viln, and i invlvs h whl
bdy. Pains fn bi hir ngus and bcm in
cninn f urin r fcs. Usually wihin 60 scnds,
his phas prcds  a rsing, recovery phas f ac
cid paralysis and slp ha lass 2  3 hurs, rfrrd
 as h postictal state. Th pain has n rcllcin
f h aack n awakning. Th svriy, frquncy,
and durain f aacks ar highly variabl; hy may
las frm 1  30 minus and may ccur as frqunly
as daily r as infrqunly as vry fw yars. Status
epilepticus is a rapidly rcurring gnralizd sizur
ha ds n allw h individual  rgain nrmal
funcin bwn sizurs. I is a mdical mrgncy
ha rquirs prmp ramn  minimiz prma
nn nrv damag and prvn dah.
Atonic or Akinetic Seizures
A suddn lss f muscl n is knwn as an atonic
seizure r a drop attack. This may b dscribd as a had
drp, h drpping f a limb, r h slumping f h
bdy  h grund. A suddn lss f muscl n r
suls in a dramaic fall. Sad pains may slump fr
ward vilnly. Pains usually rmain cnscius. Th
aacks ar shr, bu injury frqunly ccurs frm h
uncnrlld falls. Ths pains fn war prciv
hadgar  minimiz rauma.
Myoclonic Seizures
Myoclonic seizures invlv lighninglik rpiiv cn
racins f h vlunary muscls f h fac, runk, and
xrmiis. Th jrks may b islad vns, r hy may
b rapidly rpiiv. I is n uncmmn fr pains 
ls hir balanc and fall  h r. Ths aacks c
cur ms fn a nigh as h pain nrs slp. Thr
is n lss f cnsciusnss wih myclnic sizurs.
GENERALIZED NONCONVULSIVE SEIZURES
By far h ms cmmn gnralizd nncnvulsiv
sizur disrdr is absence sizurs. Ths sizurs
Drugs Used for Seizure Disorders CHAPTER 18 277
ccur primarily in childrn, and hy usually disap
par a pubry; hwvr, h pain may dvlp a
scnd yp f sizur aciviy. Aacks cnsis f par
xysmal pisds f alrd cnsciusnss lasing 5 
20 scnds. Thr ar n prdrmal r psical phas
s. Pains appar  b saring in spac, and hy
may xhibi a fw rhyhmic mvmns f h ys r
had, lip smacking, mumbling, chwing, r swallw
ing mvmns. Falling ds n ccur, pains d n
cnvuls, and hy will hav n mmry f h vns
ha ccur during h sizurs.
Focal (Localized) Seizures
Classicain f fcal sizurs (als knwn as parial
sizurs) is subdividd in fcal ns awar sizurs
(simpl mr sizurs) and fcal ns impaird un
awarnss (cmplx sizurs). Simple motor seizures
invlv lcalizd cnvulsins f vlunary muscls.
A singl bdy par such as a ngr r an xrmiy
may sar jrking. Turning h had, smacking h lips,
muh mvmns, drling, abnrmal numbnss, in
gling, and crawling snsains ar hr indicains f
fcal simpl mr sizurs. Th muscl spasm may
nd spnanusly, r i may sprad vr h whl
bdy. Th pain ds n ls cnsciusnss unlss
h sizur dvlps in a gnralizd cnvulsin.
Complex seizures ar manifsd by a vas array f ps
sibl sympms. Th pain’s uward apparanc
may b nrmal, r hr may b aimlss wandring,
lip smacking, unusual and rpad chwing, r swal
lwing mvmns. Th prsn is cnscius bu may
b in a cnfusd, dramlik sa. Th aacks, which
may ccur svral ims daily and las fr svral min
us, cmmnly nd during slp r wih a cludd
snsrium, and h pain usually has n rcllcin
f h vns f h aack.
ANTIEPILEPTIC THERAPY
Idnifying h caus f sizur aciviy is impran fr
drmining h yp f hrapy rquird. Cnribuing
facrs (.g., had injury, fvr, hypglycmia, drug
vrds) mus b spcically rad  crrc h
undrlying caus bfr chrnic anipilpic hrapy
is sard. Afr h undrlying caus is rad, i is
rar ha chrnic anipilpic hrapy is ndd. Whn
sizur aciviy cninus, drug hrapy is h primary
frm f ramn. Th gals f hrapy ar  imprv
h pain’s qualiy f lif, rduc h frquncy f si
zur aciviy, and minimiz h advrs ffcs f h
mdicain. Thrapuic ucms mus b individu
alizd fr ach pain. Th slcin f h mdicain
dpnds n h yp f sizur, h ag and gndr f
h pain, any hr mdical cndiins prsn, and
h pnial advrs ffcs f h individual mdica
ins. On pnial lngrm advrs ffc f sm
anipilpic dugs is sprsis. Carbamazpin,
phnbarbial, phnyin, and primidn can rduc
bn dnsiy lading  sprsis and fracurs.
278 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
ACTIONS
Unfrunaly, h mchanisms f sizur aciviy
ar xrmly cmplx and n wll undrsd. In
gnral, anipilpic mdicins ac by incrasing h
seizure threshold and rgulaing nurnal ring by in
hibiing xciary prcsss r nhancing inhibiry
prcsss. Th mdicains can als prvn h si
zur frm sprading  adjacn nurns. Dpnding
n h anipilpic mdicains, hy can shar mul
ipl mchanisms f acin (pirama, valpra,
and hrs) r xr jus n mchanism (lacsamid,
vigabarin). Anipilpic mdicain may mdula
h sdium (ms cmmn mchanism), passium,
r calcium channls, nhanc gammaaminbuyric
acid (GABA), inhibi h gluama rcpr, r bind
 h synapic vsicl prin (SV2A) (Tabl 18.1).
Phnyin, carbamazpin, lamrigin, znisamid,
and valpric acid ac n sdium and calcium chan
nls  sabiliz h nurnal mmbran and may
dcras h rlas f xciary nurransmirs.
Bnzdiazpins, phnbarbial, iagabin, gabapn
in, and prgabalin nhanc h inhibiry ffc f
GABA, an inhibiry nurransmir ha cunr
balancs h ffc f xciary nurransmirs.
GABA pns chlrid channls, rsuling in a hypr
plarizd cll mmbran ha prvns xciain f
h cll, spping furhr prpagain f h sizur.
Sizur cnrl mdicains ar smims subdivid
d in bradspcrum and narrwspcrum agns
in rlain  hir fcacy agains diffrn yps f
sizurs. Exampls f bradspcrum agns ar l
viracam, pirama, valpric acid, znisamid,
and lamrigin. Ths drugs ar fn usd fr h
iniial ramn f a pain wih a nwly diagnsd
sizur disrdr. Exampls f narrwspcrum agns
ar phnyin, carbamazpin, and xcarbazpin
(Frnch & Pdly, 2008).
Table 18.1 Common Mechanisms of Antiepileptic Drugs
ANTIEPILEPTIC DRUGS
Phenytoin, fosphenytoin carbamazepine, oxcarbazepine,
eslicarbazepine, lamotrigine, cenobamate, lacosamide
runamide, topiramate, zonisamide
Ethosuximide, levetiracetam, pregabalin, topiramate, zonisamide
Levetiracetam
Phenobarbital, primidone, benzodiazepines including diazepam,
lorazepam, and clonazepam; possibly topiramate
Tiagabine, vigabatrin
Levetiracetam, brivaracetam
Perampanel
Valproic acid, topiramate, zonisamide
AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; GABA, gamma-aminobutyric acid; SV2A, synaptic vesicle protein.
Adapted from Rogawski MA, Löscher W, Rho JM. Mechanisms of action of antiseizure drugs and the ketogenic diet. Cold Spring Harb Perspect Med.
2016;6(5):a022780; Miziak B, Konarzewska A, Ułamek-Kozioł M, Dudra-Jastrz ębska M, Pluta R, Czuczwar SJ. Anti-epileptogenic effects of antiepileptic drugs. Int J
Mol Sci. 2020;21(7):2340; Stefanovic S, Jankovic M, Milosavljevic M, etal. Pharmacodynamics and common drug-drug interactions of the third-generation antiepileptic
drugs. Expert Opin Drug Metab Toxicol. 2018;14(2):153-159.
In gnral, anipilpic hrapy shuld sar wih
h us f a singl drug slcd frm a grup f agns
basd n h yp f sizur. In chsing an iniial hr
apy, clinicians mus wigh rlaiv fcacy, pharmac
kinics, and pnial fr advrs ffcs f ach drug,
bu hr painspcic facrs nd  b cnsidrd,
including ag, sx, childbaring pnial, cmrbidiis,
and cncmian mdicains. Cmparaiv fcacy
and lrabiliy daa ar limid, hwvr, and rials
ha hav bn prfrmd hav n shwn signican
diffrncs amng varius drugs in rms f fcacy.
Wih mr han 20 anipilpic drugs and implanabl
anisizur dvics availabl  ra pilpsy in aduls,
ppruniis  ailr drug hrapy hav nvr bn
grar, bu h muliud f ramn pins fr si
zurs is a challng.
In gnral, if ramn is n succssful wih h
rs agn chsn, ha agn is discninud and an
hr agn is sard. If ramn fails wih h scnd
agn, h halhcar prvidr may dcid  discnin
u h scnd agn and sar a hird agn, r cmbi
nain hrapy may b sard by adding an alrnaiv
mdicain  n f h iniial agns. Occasinally
sm pains will rquir mulipldrug hrapy wih
a cmbinain f agns and will sill n b cmplly
fr f sizurs. Ths pains wih nwly diagnsd
pilpsy wh rspnd  ramn ar rfrrd  as
“treatment responsive,” and hs wh d n rspnd
 iniial agns ar rfrrd  as “treatment resistant.”
Abu half f pains wih nwly diagnsd pilpsy
bcm fr f sizurs whil using h rs prscribd
anipilpic drug. Alms whirds f pains b
cm fr f sizurs afr rciving h scnd r hird
agn.
Nnpharmaclgic ramn f rfracry sizurs
includs surgical inrvnin, h us f an implan
abl vagus nrv simular fr childrn wh ar 12
MECHANISM OF ACTION
Voltage-gated ion channels
Voltage-gated sodium channels
Voltage-gated calcium channels
Voltage-gated potassium channels
GABA inhibition
GABA-A receptors
Increases availability of neurotransmitter GABA
SV2A
Ionotropic glutamate receptors
AMPA receptor
Mixed/unknown

yars ld and ldr, and a kgnic di. Th kgnic
di is usd fr childrn, and i includs h rsricin
f carbhydra and prin inak; fa is h primary
ful ha prducs acidsis and ksis. Alhugh h
di has bn shwn  rduc rfracry sizurs in
childrn wh hav n achivd ffciv cnrl wih
drug hrapy, h advrs ffcs f his di includ
high bld lipid lvls wih lngrm ffcs ha ar
n knwn.
Medication Safety Alert
Antiepileptic drugs may increase the risk of suicidal thoughts
and behavior. This applies to all antiepileptic drugs, includ-
ing those used to treat psychiatric disorders, migraines, and
other conditions, as well as epilepsy.
Accrding  a rpr by h US Fd and Drug
Adminisrain (2008), pains wh wr rciving
anipilpic drugs had apprximaly wic h risk
f suicidal bhavir r idain (0.43%) cmpard
wih pains rciving placb (0.22%). Th incrasd
risk f suicidal bhavir and suicidal idain was b
srvd as arly as 1 wk afr saring h anipilpic
drug, and i cninud hrugh 24 wks f us f h
mdicain. Halhcar prfssinals shuld clsly
mnir all pains currnly rciving anipilpic
drugs fr nabl changs in bhavir ha culd indi
ca h mrgnc r wrsning f suicidal hughs
r bhavir r dprssin. Th drugs includd in h
analysis wr carbamazpin, flbama, gabapnin,
lamrigin, lviracam, xcarbazpin, prgabalin,
iagabin, pirama, valpra, and znisamid.
Life Span Considerations
Antiepileptic Therapy
In children, antiepileptic therapy may cause a change in per-
sonality and possible indifference to both school and family
activities. Behavioral differences must be discussed with the
healthcare provider, family or caregivers, and teachers. The
school nurse must be informed about the medications that
have been prescribed.
Liquid dosage forms of antiepileptic medicines must be
measured accurately to help maintain seizure control. It is
extremely important to shake the liquid rst to disperse the
medication uniformly in the suspension. The dosage should
then be measured with an oral syringe to ensure accuracy
before administration.
Medications should be taken at the same time daily to
maintain a consistent blood level. Dosages should not be self-
adjusted, and drugs should not be discontinued suddenly.
Monitoring the patient’s response to antiepileptic therapy
is essential. Dosages may need to be adjusted weekly,
especially during the initiation of therapy.
USES
Anipilpic mdicins ar usd  rduc h fr
quncy f sizurs.
Drugs Used for Seizure Disorders CHAPTER 18 279
NURSING IMPLICATIONS FOR ANTIEPILEPTIC
THERAPY
Nurss may play an impran rl in h crrc diag
nsis f sizur disrdrs. Accura sizur diagnsis
is crucial  h slcin f h ms apprpria mdi
cains fr ach pain. Bcaus halhcar prvidrs
ar n always abl  bsrv pain sizurs dircly,
nurss shuld larn  bsrv and rcrd hs vns
bjcivly.
Assessment
History of seizure activity
• Wha aciviis was h pain ngagd in immdi
aly bfr h las sizur?
• Has h pain bn ill rcnly?
• Is hr a hisry f fvr, unusual rash, r ick
infsain?
• Has h pain nicd any paricular aciviy ha
usually prcds h aacks?
• Whn was h las sizur bfr h currn n?
• Did h pain hav any changs in bhavir bfr
h ns f h sizur (.g., incrasing anxiy r
dprssin)?
• Is h pain awar f a prsizur “aura” (i.., a paric
ular fling r dr ha ccurs bfr a sizur ns)?
• Was hr an “pilpic cry”?
Seizure description
• Rcrd h xac im f sizur ns and h du
rain f ach phas, a dscripin f h spcic
bdy pars invlvd, and any prgrssin f sizur
acin in h affcd bdy pars.
• Did h pain ls cnsciusnss?
• Wr siffning and/r jrking mvmns prsn?
• Dscrib h aunmic rspnss usually sn
during h clnic phas: alrd, jrky rspirains;
frhy salivain; dilad pupils; any y mv
mns; cyansis; diaphrsis; incninnc.
Postictal behavior
• Rcrd h lvl f cnsciusnss (i.., rinain 
im, plac, and prsn).
• Assss h dgr f alrnss, faigu, r hadach
prsn.
• Evalua h dgr f waknss, any alrains in
spch, and mmry lss.
• Pains fn hav muscl srnss and an xrm
nd fr slp. Rcrd h durain f slp.
• Evalua any bdily harm ha ccurrd during h
sizur (.g., bruiss, cus, lacrains).
Implementation
Management of seizure activity. Assis h pain dur
ing a sizur by ding h fllwing:
• D n lav h pain.
• Hav drugs availabl  ra saus pilpicus r
knw h prcdur fr baining hm as quickly
as pssibl.
280 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
• Prc h pain frm furhr injury. Plac pad
ding arund r undr h pain’s had; d n ry
 rsrain h pain and lsn any igh clhing.
If h pain is in a sanding psiin iniially, lwr
 a hriznal psiin.
• Whn h pain sars  rlax afr a sizur, urn
slighly n h sid  allw scrins  drain u
f h muh.
• Rmain calm and qui, and giv rassuranc  h
pain whn h sizur is vr.
• Hav xygn availabl, as wll as mrgncy
quipmn fr sucining and/r vnilaing h
pain.
• Sucin h pain as ndd and iniia vn
ilary assisanc if brahing ds n rurn
spnanusly.
• Prvid a plac fr h pain  rs immdialy
afr a sizur. Summn apprpria assisanc af
r h sizur.
• Iniia nursing inrvnins apprpria  h
undrlying caus f h sizurs (.g., high fvr,
mablic disrdr, had rauma, drug r alchl
wihdrawal).
• If h pain has anhr sizur r if a sizur lass
fr mr han 4 minus, immdialy summn assis
anc; h pain may b ging in saus pilpicus.
• Obsrv all aspcs f h sizur fr daild r
crding: aura (if prsn), im sard and ndd,
bdy pars affcd, rdr f prgrssin f sizur
acin, aunmic signs (.g., alrd brahing, dia
phrsis, incninnc, salivain, ushing, pupil
dilain), psical prid bsrvains (.g., vial
signs; lvl f cnsciusnss; spch parn/disr
dr; muscl srnss, waknss, r paralysis), and
hw lng ach phas lasd.
Psychological implications
Lifestyle. Encurag h pain  mainain a nr
mal lifsyl. Prvid fr apprpria limiains
(.g., limis n praing pwr quipmn r m
r vhicls; swimming)  nsur pain safy.
Mak h pain awar f h Rhabiliain Ac f
1973, which was iniiad  nsur ha individuals
wih disabiliis d n xprinc discriminain
in mplymn. Cnac h Epilpsy Fundain f
Amrica and sa vcainal rhabiliain agncis
fr infrmain abu vcainal rhabiliain and
mplymn.
Expressing feelings. Allw h pain  vnila
hir flings. Sizurs may ccur in public, and hy
may b accmpanid by incninnc. Pains ar
usually mbarrassd abu having a sizur in frn
f hrs. Prvid fr h xprssin f flings abu
any discriminain ha h pain fls a h wrk
plac. Encurag h pn discussin f slfcncp
issus rlad  h disas and is ffc n daily ac
iviis, wrk, and h rspnss f hrs ward h
pain.
School-age children. Accpanc by prs can prsn
a prblm  a pain in his ag grup. Th schl
nurs can hlp achrs and hr childrn  undr
sand h pain’s sizurs.
Denial. B alr fr signs f dnial f h disas,
which ar indicad by incrasd sizur aciviy in a
prviusly wllcnrlld pain. Qusin h pa
in’s adhrnc  h drug rgimn.
Adherence. Drmin h pain’s currn mdi
cain schdul, including h nam f h mdica
in, h dsag, and h im f h las ds. Hav
any dss bn skippd? If s, hw many? If adhr
nc appars  b a prblm, ry  drmin h
rasns why s ha apprpria inrvnins can b
implmnd.
Status epilepticus
1. Prvid fr pain prcin and summn assis
anc  ranspr h pain  an mrgncy faciliy.
2. Adminisr xygn. Hav sucin and rsusciain
quipmn availabl and aach cardiac and xygn
saurain mnirs.
3. Esablish an inravnus (IV) lin and hav drugs
availabl fr ramn (.g., lrazpam, diazpam,
fsphnyin, phnyin, phnbarbial, valpric
acid, and lviracam). Whn adminisring IV
drugs, mnir h pain fr bradycardia, hyp
nsin, and rspirary dprssin.
4. Mnir h pain’s vial signs and nurlgic
saus.
5. Insr a nasgasric ub if h pain is vmiing.
Patient Education
Exercise and activity. Discuss wha aciviis r acins
riggr sizurs and hw  avid hm. Encurag h
pain  mainain a rgular lifsyl wih mdra
aciviy. Avid xcssiv xrcis ha culd lad  x
cssiv faigu.
Nutrition. Avid xcssiv us f simulans (.g.,
caffincnaining prducs). Sizurs ar als knwn
 fllw h signican inak f alchlic bvrags;
hrfr such ingsin shuld b avidd r limid.
Ask h halhcar prvidr whhr viamin suppl
mns ar ndd, bcaus sm anicnvulsans inr
fr wih viamin and minral absrpin.
Safety. Tach h pain  avid praing pwr
quipmn r machinry. Driving may b minimizd
r prhibid. Chck sa laws rgarding hw r if an
individual wih a hisry f sizur aciviy may qual
ify fr a drivr’s licns. B spcially alr  signs f
cnfusin and impaird crdinain in ldr pains.
Prvid fr h pain’s safy.
Stress. Th rducin f nsin and srss wihin h
individual’s nvirnmn may rduc sizur aciviy
in sm pains.

Oral hygiene. Encurag daily ral hygin prac
ics and schduling f rgular dnal xaminains.
Gingival hyperplasia, which is gum vrgrwh as
sciad wih hydanins (.g., phnyin, hin),
can b rducd wih gd ral hygin, frqun
gum massag, rgular brushing, and prpr dnal
car.
Medication considerations in pregnancy
• If prgnancy is suspcd, cnsul an bsrician as
sn as pssibl.
• Infrm h halhcar prvidr f sizur
mdicains.
• D n discninu mdicains unlss ld  d s
by h halhcar prvidr.
• Th pain shuld carry an idnicain card r
bracl.
Fostering health maintenance. Thrughu h
curs f ramn, discuss mdicain infrmain
and hw i will bn h pain. Rcgniz ha
nnadhrnc may b a mans f dnial. Explr un
drlying prblms rgarding h pain’s accpanc
f h disas and h nd fr sric adhrnc fr
maximum sizur cnrl. Prvid h pain and
signican hrs wih impran infrmain cn
aind in h spcic drug mngraphs fr h mdi
cains prscribd. Addiinal halh aching and
nursing inrvnins rgarding h advrs ffcs
ar dscribd in h drug mngraphs ha fllw.
Sk cprain and undrsanding f h fllw
ing pins s ha mdicain adhrnc is incrasd:
h nam f h mdicain, is dsag, is ru and
ims f adminisrain, and is cmmn and srius
advrs ffcs.
Patient self-assessment. Enlis h pain’s hlp
wih dvlping and mainaining a wrin rcrd r
sizur diary f mniring paramrs (.g., dgr
f lhargy; sdain; ral hygin fr gum disrdrs;
dgr f sizur rlif; any nausa, vmiing, r an
rxia prsn). S h Pain SlfAssssmn Frm
fr Anicnvulsans n h Evlv wbsi. Cmpl
h Prmdicain Daa clumn fr us as a bas
lin  rack h pain’s rspns  drug hrapy.
Ensur ha h pain and signican hrs undr
sand hw  us h frm. Hav hrs rcrd h
da, im, durain, and frquncy f any sizur
pisds. In addiin, rcrd h pain’s bhavir
immdialy bfr and afr sizurs. Emphasiz
aking mdicains a h sam im daily  hlp
mainain a cnsisn hrapuic drug lvl. Th pa
in shuld cnsul wih a pharmacis bfr aking
vrhcunr mdicains  prvn drug inr
acins. Hav h pain bring h cmpld frm 
fllwup visis.
Drugs Used for Seizure Disorders CHAPTER 18 281
DRUG THERAPY FOR SEIZURE
DISORDERS
DRUG CLASS: BENZODIAZEPINES
Actions
Th mchanisms f acin fr bnzdiazpins ar n
fully undrsd, bu i is hugh ha bnzdiazpins
simula BDZ2 rcprs  inhibi nurransmissin
by nhancing h ffcs f GABA in h pssynapic
clfs bwn nrv clls. Incrasd lvls f GABA
pn h chlrid channl, rsuling in a hypr
plarizd cll mmbran ha prvns furhr xci
ain f h cll, hus prvning prpagain f h
sizur aciviy. (S Chapr 13 fr mr dails n
bnzdiazpin aciviy.)
Uses
Th fur bnzdiazpins apprvd fr us as ani
pilpic hrapy ar diazpam, lrazpam, clnaz
pam, and clrazpa. Clnazpam is usful fr h
ral ramn f absnc, akinic, and myclnic
sizurs in childrn. Diazpam and lrazpam mus
b adminisrd inravnusly  cnrl sizurs;
hy ar h drugs f chic fr raing saus pi
lpicus. Clrazpa is usd wih hr anipilpic
agns  cnrl parial sizurs. Diazpam can b
adminisrd as a rcal gl  ra sizur clusrs
(acu rpiiv sizurs) ha can b usd a hm.
Diazpam (Valc) and midazlam (Nayzilam) can
als b adminisrd as a nasal spray a hm  ra
sizur clusrs. Sizur clusrs ar prids f in
crasd sizur aciviy, which is having w r mr
sizurs in a 24hur prid. Sizur clusrs ar dif
frn frm saus pilpicus. Saus pilpicus is
sizurs lasing lngr han 5 minus and rquirs
hspializain.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm h
bnzdiazpins ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Minimal advrs ffcs frm hrapy
Nursing Implications for Benzodiazepines
Premedication assessment
1. Rviw ruin bld sudis  dc bld dys
crasias and hpaxiciy.
2. Prfrm a baslin assssmn f h pain’s
spch parns, dgr f alrnss, and rina
in  nam, plac, and im bfr iniiaing hr
apy. Mnir h pain’s bhaviral rspnss 
hrapy.
3. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.
282 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems

Table 18.2 Antiepileptic Medicines

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE USE FOR SEIZURES
BENZODIAZEPINES
clobazam On Tablets: 10, 20 mg Up to 40 mg/day Adjunct treatment
Sympazan Oral suspension: 2.5 mg/mL of partial seizures
PMS-Clobazam (120 mL) in adolescents
Film: 5, 10, 20 mg older than 16, and
adults
clonazepam Klonopin Tablets: 0.5, 1, 2 mg Up to 20 mg/day Absence and
Do not confuse Tablets, orally disintegrating: myoclonic seizures
Rivitrol 0.125, 0.25, 0.5, 1, 2 mg
Klonopin with
clonidine.
clorazepate Tranxene-T Tablets: 3.75, 7.5, 15 mg Up to 90 mg/day Focal seizures
diazepam Valium Tablets: 2, 5, 10 mg Initially 5–10 mg/day; All forms of epilepsy;
Do not confuse Do not confuse Nasal liquid: 5, 10 mg/0.1 mL up to 30 mg/day used in conjunction
diazepam with Valium with valerian. Intramuscular, intravenous: 5 with other agents
Ditropan. Diastat mg/mL
Oral concentrate: 5 mg/mL
Gel, rectal: 2.5, 10, 20 mg
lorazepam Ativan Tablets: 0.5, 1, 2 mg Intravenous: 4–8 mg, Status epilepticus
Do not confuse Do not confuse Oral solution: 2 mg/mL repeated at 10- to
lorazepam with Ativan with Ambien. Intramuscular, intravenous: 2, 15-min intervals, if
loperamide. Apo-Lorazepam 4 mg/mL seizing
HYDANTOINS
fosphenytoin Cerebyx Intravenous: 100 mg Same dosage as for Status epilepticus;
Do not confuse phenytoin in 2-mL vials; phenytoin see also phenytoin
Cerebyx with Avelox, 500 mg phenytoin in 10-
Celebrex, or Celexa. mL vials (75 mg/mL of
fosphenytoin is equivalent
to 50 mg/mL of phenytoin)
phenytoin Dilantin Tablets, chewable: 50 mg 300–600 mg/day Generalized tonic-
Do not confuse Do not confuse Capsules: 30, 100, 200, 300 clonic seizures;
phenytoin with Dilantin with Diucan. mg psychomotor
phenylephrine. seizures
SUCCINIMIDES
ethosuximide Zarontin Capsules: 250 mg 1000–1500 mg/day Absence seizures
Syrup: 250 mg/5 mL
methsuximide Celontin Capsules: 300 mg 900–1200 mg/day Absence seizures
Available in Canada.
Do not confuse.

Availability, dosage, and administration. S Tabl
18.2. Us f bnzdiazpins may rsul in physical
and psychlgical dpndnc whn akn sadily
fr svral days  wks, vn whn akn in rcm
mndd dsags. Abus and misus can rsul in vr
ds r dah, spcially whn bnzdiazpins ar
cmbind wih hr mdicins, such as piid pain
rlivrs, alchl r illici drugs and cnral nrvus
sysm dprssans (.g., sdaivs, hypnics, mus
cl rlaxans). Th rapid discninuanc f bnzdi
azpins afr lngrm us may rsul in sympms
ha ar similar  hs f alchl wihdrawal, such
as waknss, anxiy, dlirium, and nicclnic (grand
mal) sizurs. Ths sympms may n appar fr
svral days afr discninuain. Discninuain f
bnzdiazpins cnsiss f gradual wihdrawal vr
2  4 wks.
Medication Safety Alert
Rapidly discontinuing benzodiazepines after long-term use
may result in symptoms similar to those of alcohol withdraw-
al. These may vary from weakness and anxiety to delirium
and generalized tonic-clonic seizures. The symptoms may
not appear for several days after discontinuation. Treatment
consists of the gradual withdrawal of benzodiazepines over
the course of 2 to 4 weeks.

Intravenous administration. D n mix parnral
diazpam r lrazpam in h sam syring wih
hr mdicains; d n add hs  hr IV s
luins bcaus f prcipia frmain. Adminisr
diazpam slwly a a ra f n mr han 5 mg/min
r lrazpam a a ra f n mr han 2 mg/min.
If a all pssibl, giv hs drugs wih h pain
undr lcrcardigram (ECG) mniring and b
srv clsly fr bradycardia. Whn bradycardia
ccurs, sp bluss unil h har ra rurns 
nrmal.
Common adverse effects
Neurologic
Sedation, drowsiness, dizziness, fatigue, lethargy. Th
mr cmmn advrs ffcs f bnzdiazpins ar
xnsins f hir pharmaclgic prpris. Ths
sympms nd  disappar wih cninud hrapy
and pssibl dsag radjusmn. Encurag h
pain n  discninu hrapy wihu rs cn
suling h halhcar prvidr. Th pain shuld b
warnd n  wrk wih machinry, pra a mr
vhicl, adminisr mdicain, r prfrm hr du
is ha rquir mnal alrnss. Prvid fr pain
safy during pisds f dizzinss and aaxia; rpr
hs changs  h halhcar prvidr fr furhr
valuain.
Clinical Pitfall
Do not mix parenteral diazepam, lorazepam, or phenytoin
with other medications in the same syringe, and do not add
either medication to other IV solutions because of precipi-
tate formation. Always check for IV incompatibility before ad-
ministering either medication through an established IV line,
and use the SAS (Saline ush rst, Administer the prescribed
drug, Saline ush after the drug) technique. Administer diaz-
epam slowly at a rate of 5 mg/min and lorazepam at a rate
of 2 mg/min. Administer phenytoin slowly at a rate of 25 to
50 mg/min, preferably through a large vein or as an IV piggy-
back. Phenytoin can be quite irritating to small veins. During
the administration of either medication, it is recommended
that an ECG monitor be used to closely observe for brady-
cardia. If bradycardia occurs, stop the bolus infusion until
the heart rate returns to normal. Observe the patient during
administration for respiratory depression and hypotension.
Sensory
Blurred vision. Cauin h pain ha blurrd visin
may ccur and mak apprpria suggsins fr h
pain’s prsnal safy.
Serious adverse effects
Psychological
Behavioral disturbances. Bhaviral disurbancs
such as aggrssivnss and agiain hav bn r
prd, spcially in pains wh ar mnally
handicappd r wh hav psychiaric disurbancs.
Prvid suppriv physical car and safy during
Drugs Used for Seizure Disorders CHAPTER 18 283
hs rspnss. Assss h lvl f h pain’s x
cimn, and dal calmly wih h individual. During
prids f xcimn, prc h pain frm harm
and prvid fr h physical channling f nrgy
(.g., walk wih hm). Sk a chang in h mdica
in rdr.
Hematologic
Blood dyscrasias. Ruin labrary sudis (i..,
rd bld cll [RBC], whi bld cll [WBC], diffr
nial, and plal cuns) may b schduld. Mnir
h pain fr sr hra, fvr, purpura, jaundic, r
xcssiv and prgrssiv waknss. Bld dyscrasias
ar a rar bu srius advrs ffc.
Gastrointestinal
Hepatotoxicity. Th sympms f hpaxiciy in
clud anrxia, nausa, vmiing, jaundic, hpa
mgaly, splnmgaly, and abnrmal livr funcin
s rsuls (.g., lvad bilirubin, aspara amin
ransfras [AST], alanin aminransfras [ALT],
gammagluamylransfras [GGT], and alkalin phs
phaas lvls [ALP]; incrasd prhrmbin im [PT]).
Drug interactions
Drugs that increase toxic effects. Anihisamins, al
chl, analgsics, anshics, ranquilizrs, narcics,
cimidin, sdaivhypnics, and hr cncurrn
anipilpic drugs incras h xic ffcs f bnz
diazpins. Mnir h pain fr xcssiv sdain
and limina hr mdicins n ndd fr ani
pilpic hrapy, if pssibl.
Smoking. Cigar smking nhancs h mab
lism f bnzdiazpins. Incrasd dsags may b
ncssary  mainain ffcs in pains wh smk.
DRUG CLASS: HYDANTOINS
Actions
Th primary si f acin f h hydanins is h m
r crx, whr hy inhibi h sprad f sizur ac
iviy. Th hydanins sabiliz h hrshld f nu
rnal cll mmbrans agains hyprxciabiliy causd
by blcking h vlaggad sdium channls. This
rsuls in a rducin in susaind highfrquncy nu
rnal dischargs. Phnyin als rducs h maximal
aciviy f brainsm cnrs rspnsibl fr h nic
phas f nicclnic sizurs.
Uses
Th hydanins (.g., phnyin, fsphnyin) ar
anicnvulsans usd  cnrl fcal sizurs and
gnralizd nicclnic sizurs. Phnyin is h
ms cmmnly usd anipilpic f h hydanins.
Fsphnyin is a prdrug ha is cnvrd  ph
nyin afr adminisrain. Fsphnyin is paricu
larly usful whn lading dss f phnyin mus
b adminisrd. Phnyin causs lss sdain han
phnbarbial. In xic cncnrains, phnyin can
induc sizurs.
284 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm h
hydanins ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Minimal advrs ffcs frm hrapy
Nursing Implications for Phenytoin
Premedication assessment
1. Rviw ruin bld sudis  dc bld dys
crasias and hpaxiciy.
2. Drmin baslin bld sugar lvls in pains
wih diabs. Mnir hs pains pridically a
spcid inrvals bcaus hyprglycmia may b
causd by hydanin hrapy.
3. Prfrm a baslin assssmn f h pain’s
spch parns, dgr f alrnss, and rina
in  nam, plac, and im bfr iniiaing hr
apy. Mnir h pain’s bhaviral rspnss 
hrapy.
4. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.
Availability, dosage, and administration. S Tabl 18.2.
Adminisr mdicain wih fd r milk  rduc
gasric irriain. If an ral suspnsin is usd, shak
i wll rs. Encurag h us f an ral syring fr
accura masurmn.
Intramuscular (IM): If a all pssibl, avid IM ad
minisrain. Absrpin is slw and painful.
IV: D n mix parnral phnyin in h sam
syring wih hr mdicains; bcaus f prcipia
frmain, d n add  hr IV sluins.
Adminisr phnyin slwly a a ra f 25  50
mg/min. Fsphnyin may b adminisrd a a ra
f 150 mg/min. If a all pssibl, giv hs drugs un
dr ECG mniring and bsrv h pain clsly fr
bradycardia. If bradycardia ccurs, sp bluss unil
h har ra rurns  nrmal. Thrapuic bld
lvls fr phnyin ar bwn 10 and 20 mg/L.
Common adverse effects
Gastrointestinal
Nausea, vomiting, indigestion. Ths ffcs ar cm
mn during h iniiain f hrapy. Gradual incrass
in dsag and adminisrain wih fd r milk will
rduc gasric irriain.
Neurologic
Sedation, drowsiness, dizziness, fatigue, lethargy. Ths
sympms nd  disappar wih cninud hrapy
and pssibl dsag adjusmn. Encurag h pain
n  discninu hrapy wihu rs cnsuling h
halhcar prvidr. Th pain shuld b warnd
n  wrk wih machinry, pra a mr vhicl,
adminisr mdicain, r prfrm hr duis ha
rquir mnal alrnss. Prvid fr pain safy
during pisds f dizzinss; rpr hs changs 
h halhcar prvidr fr furhr valuain.
Confusion. Prfrm a baslin assssmn f h pa
in’s dgr f alrnss and rinain  nam,
plac, and im bfr iniiaing hrapy. Mak rgu
larly schduld subsqun valuains f h pa
in’s mnal saus and cmpar ndings. Rpr
signican alrains in mnal saus  h halh
car prvidr.
Sensory
Blurred vision. Cauin h pain ha blurrd visin
may ccur and mak apprpria suggsins fr h
pain’s prsnal safy.
Nystagmus. Nystagmus is a backandfrh mv
mn f h yballs n h hriznal plain, paricu
larly whn lking larally (u f h crnrs f h
ys). Pains may dvlp nysagmus as highr ds
ag lvls ar rquird  cnrl sizurs r as h
drug accumulas in h bdy. Nysagmus may b
usd as an indicar f pssibl vrds. Mnir h
pain clsly fr hr signs f xiciy such as s
dain, lhargy, nausa and vmiing, and aaxia. If
nysagmus and hr signs f xiciy bcm mr
prminn, bring his  h anin f h halhcar
prvidr. Srum lvls may b rdrd and h dsag
rducd.
Dental hygiene
Gingival hyperplasia. Th frquncy f gum vr
grwh may b rducd by using gd ral hygin,
including gum massag, frqun brushing, and prp
r dnal car.
Serious adverse effects
Metabolic
Hyperglycemia. Hydanins may lva bld glu
cs lvls, spcially if highr dsags ar usd; pa
ins wih diabs mllius ar mr suscpibl 
hyprglycmia. Paricularly during h arly wks
f hrapy, pains wh ar diabic r prdiabic
mus b mnird fr h dvlpmn f hypr
glycmia. Assss h pain rgularly fr glycsuria
and rpr i  h halhcar prvidr if i ccurs
wih any frquncy. Pains wh ar rciving ral
hypglycmic agns r insulin may rquir a dsag
adjusmn.
Hematologic
Blood dyscrasias. Ruin labrary sudis (i..,
RBC, WBC, and diffrnial cuns) shuld b schd
uld. Mnir h pain fr sr hra, fvr, pur
pura, jaundic, r xcssiv and prgrssiv waknss.
Gastrointestinal
Hepatotoxicity. Th sympms f hpaxiciy in
clud anrxia, nausa, vmiing, jaundic, hpa
mgaly, splnmgaly, and abnrmal livr funcin
ss (.g., lvad bilirubin, AST, ALT, GGT, and ALP;
incrasd PT).
Integumentary
Dermatologic reactions. Rpr a rash r prurius
immdialy and wihhld addiinal dss pnding
apprval by h halhcar prvidr.

Drug interactions
Drugs that enhance therapeutic and toxic ef-
fects. Warfarin, carbamazpin, xcarbazpin (>1200
mg/day), pirama, mrnidazl, azl anifungal
agns (.g., iracnazl, vricnazl, ucnazl),
mprazl, phnhiazins, disulram, amidarn,
isniazid, chlramphnicl, cimidin, and sulfna
mids nhanc h hrapuic and xic ffcs f ph
nyin. Mnir pains wih cncurrn hrapy fr
signs f phnyin xiciy, such as nysagmus, sda
in, r lhargy. Srum lvls may b rdrd; a r
ducd dsag f phnyin may b rquird.
Drugs that decrease therapeutic effects. Lxapin,
phnbarbial, nirfuranin, hphyllin, hanl
(chrnic ingsin), rifampin, sucralfa, flic acid,
and anacids dcras h hrapuic ffcs f ph
nyin. Mnir pains wih cncurrn hrapy fr
incrasd sizur aciviy. Mniring changs in h
pain’s srum lvls shuld hlp prdic pssibl in
crasd sizur aciviy.
Disopyramide, quinidine, mexiletine. Phnyin d
crass h srum lvls f hs agns. Mnir pa
ins fr h rdvlpmn f dysrhyhmias.
Prednisolone, dexamethasone. Phnyin dcrass
h srum lvls f hs agns. Mnir pains fr
rducd aniinammary aciviy.
Estrogen-containing contraceptives. Phnyin n
hancs h mablism f srgns. Sping r bld
ing may b an indicain f rducd srgn lvls
and rducd cnracpiv aciviy wih srgn
cnaining cnracpivs. Using alrnaiv frms f
birh cnrl is rcmmndd.
Theophylline. Phnyin dcrass h srum lv
ls f hphyllin drivaivs. Mnir pains fr
a highr frquncy f rspirary difculy. Th h
phyllin dsag may nd  b incrasd by 50% 
100%  mainain h sam hrapuic rspns.
Valproic acid. This agn may incras r dcras
h aciviy f phnyin. Mnir h pain fr an
incrasd frquncy f sizur aciviy. Mniring
changs in srum lvls shuld hlp prdic pssibl
incrasd sizur aciviy. Mnir pains wih cn
currn hrapy fr signs f phnyin xiciy, includ
ing nysagmus, sdain, and lhargy. Srum lvls
may b rdrd, and a rducd dsag f phnyin
may b rquird.
Ketoconazole. Th cncurrn adminisrain wih
kcnazl may alr h mablism f n r
bh drugs. Mniring h lvls f bh drugs is
rcmmndd.
Medication Safety Alert
Phenytoin is associated with many drug interactions. Those
listed earlier are the most common drug interactions rec-
ognized, but it is only a representative list. Consult a re-
source such as Drug Interaction Facts for a more complete
description.
Drugs Used for Seizure Disorders CHAPTER 18 285
DRUG CLASS: SUCCINIMIDES
Actions
Th succinimids lva h sizur hrshld by d
prssin f nrv ransmissin in h crx by rduc
ing h currn in h Typ calcium channls fund in
primary affrn nurns.
Th hrapuic plasma lvl fr hsuximid is 40
 100 mcg/mL.
Uses
Succinimids (.g., hsuximid, mhsuximid) ar
usd  cnrl absnc sizurs.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm h
succinimids ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Minimal advrs ffcs frm hrapy
Nursing Implications for Succinimides
Premedication assessment
1. Prfrm a baslin assssmn f h pain’s
spch parns, dgr f alrnss, and rin
ain  nam, plac, and im bfr iniiaing
hrapy.
2. Mnir h pain’s bhaviral rspnss 
hrapy.
3. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.
Availability, dosage, and administration. S Tabl 18.2.
Common adverse effects
Gastrointestinal
Nausea, vomiting, indigestion. Ths ffcs ar cm
mn during h iniiain f hrapy. Gradual incrass
in dsag and adminisrain wih fd r milk will
rduc gasric irriain.
Neurologic
Sedation, drowsiness, dizziness, fatigue, lethargy. Ths
sympms nd  disappar wih cninud hrapy
and pssibl dsag adjusmn. Encurag h pa
in n  discninu hrapy wihu rs cnsul
ing h halhcar prvidr. Th pain shuld b
warnd n  wrk wih machinry, pra a m
r vhicl, adminisr mdicain, r prfrm h
r duis ha rquir mnal alrnss. Prvid fr
pain safy during pisds f dizzinss; rpr
hs changs  h halhcar prvidr fr furhr
valuain.
Drug interactions
Drugs that enhance toxic effects. Anihisamins, al
chl, analgsics, anshics, ranquilizrs, hr ani
pilpic drugs, and sdaivhypnics nhanc h
xic ffcs f succinimids.
286 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
DRUG CLASS: MISCELLANEOUS ANTIEPILEPTIC
MEDICINES
carbamazepine (kăr-bă-MĀZ-ă-pēn)
Tegretol (TĔG-rĕ-tŏl)
Do not confuse Tegretol with Toradol or Trileptal.
Actions
Carbamazpin blcks h vlaggad sdium
channls in brain clls, which rsuls in a rducin in
susaind highfrquncy nurnal dischargs. I als
blcks h rupak f nrpinphrin and dcrass
h rlas f nrpinphrin and h ra f dpamin
and GABA urnvr. Dspi knwldg f hs phar
maclgic ffcs, h mchanisms f acin as an ani
pilpic, slciv analgsic, and animanic agn ar
n fully knwn. Carbamazpin is srucurally rlad
 h ricyclic anidprssans.
Uses
Carbamazpin is an anipilpic fn usd in cm
binain wih hr anipilpic agns  cnrl
gnralizd nicclnic and fcal sizurs. I is n f
fciv fr cnrlling myclnic r absnc sizurs.
Carbamazpin has als bn usd succssfully  ra
h pain assciad wih rigminal nuralgia (ic du
lurux). I may als b usd  ra manicdprssiv
disrdrs whn lihium hrapy has n bn pimal.
Th US Fd and Drug Adminisrain issud an
alr  halhcar prfssinals abu dangrus and
pssibly faal skin racins ha may ccur wih car
bamazpin in crain pain ppulains. Ths
skin racins ar signicanly mr cmmn amng
pains wih a paricular human lukcy anign
(HLA): h HLAB*1502 alll. This alll ccurs alms
xclusivly in prsns f Asian ancsry. Pains wih
his ancsry shuld b scrnd wih availabl gnic
ss fr h alll bfr saring ramn wih carba
mazpin. If s rsuls ar psiiv, h drug shuld
n b sard unlss h xpcd bn clarly u
wighs h risk f srius skin racins. Pains wh
s psiiv fr h alll may als b a incrasd risk
frm hr anipilpic drugs ha hav causd srius
skin racins. Mr han 90% f all srius skin rac
ins ccur wihin h rs fw mnhs f ramn.
This mans ha pains wh hav bn n h drug
fr lngr prids wihu dvlping skin racins
hav a lw risk f racin in h fuur, vn if hy
hav sd psiiv fr h alll.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm car
bamazpin ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Minimal advrs ffcs frm hrapy
Nursing Implications for Carbamazepine
Premedication assessment
1. As a rsul f srius advrs racins, h manu
facurr rcmmnds ha h fllwing baslin
sudis b rpad a rgular inrvals: cmpl
bld cun, srum irn, livr funcin ss, urinal
ysis, bld ura nirgn (BUN), srum crainin,
srum sdium, and phhalmlgic xaminain.
2. Rviw h pain’s hisry  xclud Asian an
csry, including Suh Asian Indian ancsry. If
h pain ds hav his ancsry, bring i  h
prscribr’s anin s ha gnic sing may b
cmpld.
3. Prfrm a baslin assssmn f h pain’s spch
parns, dgr f alrnss, and rinain  nam,
plac, and im bfr iniiaing hrapy. Mnir h
pain’s bhaviral rspnss  hrapy.
4. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.
Availability. PO: 200mg abls; 100mg chwabl ab
ls; 100, 200, and 400mg abls, xndd rlas
(12 hurs); 100, 200, and 300mg capsuls, xndd
rlas (12 hurs); 100 mg/5 mL ral suspnsin.
Dosage and administration. Adult: PO: Iniial dsag
is 200 mg wic daily n h rs day. Dsag may b in
crasd by 200 mg/day a wkly inrvals. Maximum
dsag 1000 mg/day in adlscns 12  15 yars and
1200 mg/day in hs ldr han 15 yars.
Common adverse effects. Ths ffcs can b rducd
by slwly incrasing h dsag. Thy ar usually mild
and nd  rslv wih cninud hrapy. Encurag
h pain n  discninu hrapy wihu rs
cnsuling h halhcar prvidr.
Gastrointestinal. Gasrinsinal ffcs includ nau
sa and vmiing.
Neurologic
Drowsiness, dizziness. Prvid fr pain safy dur
ing pisds f drwsinss r dizzinss. Pains mus
b warnd n  wrk arund machinry, pra m
r vhicls, r prfrm hr duis ha rquir cn
san mnal alrnss unil i is knwn hw hy ar
affcd by his mdicain.
Serious adverse effects
Cardiovascular
Orthostatic hypotension, hypertension. Mnir h pa
in’s bld prssur daily in h supin and sanding
psiins. Anicipa h dvlpmn f psural hyp
nsin and ak masurs  prvn an ccurrnc.
Tach h pain  ris slwly frm a supin r siing
psiin, and ncurag h pain  si r li dwn
if fling fain.
 Drugs Used for Seizure Disorders CHAPTER 18 287

Dyspnea, edema. If carbamazpin is usd by a pa Doxycycline. Carbamazpin nhancs h mab
in wih a hisry f har failur, mnir daily lism f his anibiic. Mnir h pain fr signs f
wighs, lung sunds, and accumulain f dma. cninud infcin.
Neurologic Estrogen-containing contraceptives. Carbamazpin
Slurred speech, sedation, confusion. Prfrm a baslin nhancs h mablism f srgns. Sping r
assssmn f h pain’s spch parns, dgr f blding may b an indicain f rducd srgn lv
alrnss, and rinain  nam, plac, and im b ls and rducd cnracpiv aciviy. Th us f hr
fr iniiaing hrapy. Mak rgularly schduld sub frms f birh cnrl is rcmmndd.
squn valuains f h pain’s mnal saus and
cmpar ndings. Rpr any signican alrains  gabapentin (găb-ă-PĔN-tĭn)
h halhcar prvidr. Neurontin (nyŭr-ŎN-tĭn)
Genitourinary Do not confuse Neurontin with Neoral.
Nephrotoxicity. Mnir h pain’s urinalysis and
kidny funcin ss fr abnrmal rsuls. Rpr in
Actions
crasing BUN and crainin lvls, dcrasing urin
Th mchanism f acin f gabapnin is unknwn. I
upu r spcic graviy dspi h amun f uid
ds n appar  nhanc GABA.
inak, cass r prin in h urin, frank bld r
smkyclrd urin, r RBCs in xcss f 0  3 n h
Uses
urinalysis rpr.
Gabapnin is usually usd in cmbinain wih
Gastrointestinal
hr anipilpic drugs  cnrl fcal sizurs.
Hepatotoxicity. Th sympms f hpaxiciy in
Gabapnin is als apprvd fr pshrpic nural
clud anrxia, nausa, vmiing, jaundic, hpa
gia. Off labl, gabapnin is usd in hr disrdrs,
mgaly, splnmgaly, and abnrmal livr funcin
such as brmyalgia, diabic nurpahy, and vas
ss (i.., lvad bilirubin, AST, ALT, GGT, and ALP;
mr sympms assciad wih mnpaus.
incrasd PT).
Hematologic
Therapeutic Outcomes
Blood dyscrasias. Ruin labrary sudis (i..,
Th primary hrapuic ucms xpcd frm ga
RBC, WBC, and diffrnial cuns) shuld b schd
bapnin ar as fllws:
uld. Mnir h pain fr sr hra, fvr, pur
1. Rducd frquncy f sizurs and rducd injury
pura, jaundic, r xcssiv and prgrssiv waknss.
frm sizur aciviy
Integumentary
2. Sympmaic rlif frm rslss lgs syndrm and
Dermatologic reactions. Rpr a rash r prurius im
pshrpic nuralgia
mdialy and wihhld addiinal dss pnding ap
3. Minimal advrs ffcs frm hrapy
prval by h halhcar prvidr.
Nursing Implications for Gabapentin
Drug interactions
Premedication assessment
Drugs that enhance therapeutic and toxic ef-
1. Prfrm a baslin assssmn f h pain’s spch
fects. Isniazid, cimidin, uxin, uvxamin,
parns, dgr f alrnss, and rinain  nam,
kcnazl, and macrlid anibiics (.g., ryh
plac, and im bfr iniiaing hrapy. Mnir h
rmycin, clarihrmycin) inhibi h mablism f
pain’s bhaviral rspnss  hrapy.
carbamazpin. Mnir h pain fr signs f xic
2. Rviw h pain’s mdical rcrd  dcumn
iy, such as disrinain, aaxia, lhargy, hadach,
h frquncy f sizur aciviy.
drwsinss, nausa, and vmiing. Dsag rducins
3. Whn gabapnin is usd as an analgsic, prfrm a
in carbamazpin may b ncssary.
pain assssmn bfr adminisring i and a appr
Verapamil, diltiazem, lamotrigine. Ths drugs incras
pria inrvals during hrapy. Rpr pr pain cn
srum lvls f carbamazpin. Mnir h pain fr
rl, and bain a mdicain in h pain’s rdrs.
signs f xiciy (.g., disrinain, aaxia, lhargy,
hadach, drwsinss, nausa, vmiing). A 40% 
Availability. PO: 100, 300, and 400mg capsuls;
50% dcras in h carbamazpin dsag may b
300, 600, and 800mg abls; 250 mg/5 mL ral
ncssary.
sluin.
Warfarin. Carbamazpin may diminish h ani
cagulan ffcs f warfarin. Mnir h inrnainal
nrmalizd rai [INR] and incras h dsag f Medication Safety Alert
warfarin, if ncssary. Serious breathing difculties may occur in patients using ga-
Phenobarbital, phenytoin, valproic acid. Carbamazpin bapentinoids (gabapentin or pregabalin) who have respiratory
nhancs h mablism f hs agns. Mnir h risk factors. These include the use of opioid pain medicines
pain fr an incrasd frquncy f sizur aciviy. and other drugs that depress the central nervous system, and
conditions such as chronic obstructive pulmonary disease
Mniring changs in srum lvls shuld hlp pr
that reduce lung function. The elderly are also at higher risk.
dic pssibl incrasd sizur aciviy.
288 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
Dosage and administration. Adult: PO: 900  1800
mg daily. Iniially adminisr 300 mg a bdim n
day 1, 300 mg w ims n day 2, and hn 300 mg
hr ims n day 3. May incras using 300, 400,
600, r 800mg dsag frms givn hr ims pr
day. Effciv ds is 900  1800 mg/day, bu up 
2400 mg/day has bn usd lng rm. Dsags f
3600 mg/day hav bn givn  limid pains fr
a rlaivly shr durain. Th maximum im b
wn dss fr h hrimsdaily schdul shuld
n xcd 12 hurs. Note: Dsag adjusmn may b
ncssary in pains whs simad crainin clar
anc is lss han 50 mL/min. Thrapuic bld lvls
fr gabapnin ar 2  20 mg/L.
If h pain als uss anacids, adminisr gaba
pnin a las 2 hurs afr h las ds f anacid,
bcaus anacids rduc h absrpin f gabapnin.
Common adverse effects
Neurologic
Sedation, drowsiness, dizziness. Ths sympms nd
 disappar wih cninud hrapy and pssibl ds
ag adjusmn. Encurag h pain n  discn
inu hrapy wihu rs cnsuling h halhcar
prvidr. Prvid fr pain safy during pisds
f drwsinss r dizzinss. Pains mus b warnd
n  wrk arund machinry, pra mr vhicls,
r prfrm hr duis ha rquir cnsan mnal
alrnss unil i is knwn hw hy ar affcd by his
mdicain.
Sensory
Blurred vision. Cauin h pain ha blurrd visin
may ccur and mak apprpria suggsins fr h
pain’s prsnal safy.
Serious adverse effects
Neurologic
Slurred speech, lethargy, confusion. Prfrm a baslin
assssmn f h pain’s spch parns, dgr f
alrnss, and rinain  nam, plac, and im b
fr iniiaing hrapy. Mak rgularly schduld sub
squn valuains f h pain’s mnal saus and
cmpar ndings. Rpr any signican alrains.
Drug interactions
Enhanced sedation. Cnral nrvus sysm dprs
sans—including slp aids, analgsics, ranquilizrs,
and alchl—nhanc h sdaiv ffcs f gabap
nin. Pains mus b warnd n  wrk arund
machinry, pra mr vhicls, r prfrm hr
duis ha rquir cnsan mnal alrnss unil i
is knwn hw hy ar affcd by his mdicain.
Prvid fr pain safy during pisds f drwsi
nss r dizzinss.
Urine protein. Falspsiiv radings fr prin in
h urin hav bn rprd by pains wh ar ak
ing gabapnin wh us h Mulisix 10SG Ragn
dipsick s (Simns Halhcar, Erlangn, Grmany).
Th manufacurr rcmmnds ha h mr spcic
sulfsalicylic acid prcipiain prcdur b usd 
drmin h prsnc f urin prin.
lamotrigine (lă-MŎ-trĭ-gēn)
Do not confuse lamotrigine with lamivudine.
Lamictal (lă-MĬK-tăl)
Do not confuse Lamictal with labetalol, Lamisil, or
Lomotil.
Actions
Lamrigin is a nwr anipilpic f h phnyl
riazin class ha is unrlad  hr anipilpic
mdicains currnly availabl. I is hugh  ac
primarily by blcking vlagsnsiiv sdium. I may
als ac n h calcium channls in h nurnal mm
brans. This sabilizs h nurnal mmbrans and in
hibis h rlas f xciary nurransmirs (.g.,
gluama), which may induc sizur aciviy.
Uses
Lamrigin is usd in cmbinain wih hr ani
pilpic hrapy  ra fcal sizurs and h gnralizd
sizurs f LnnxGasau syndrm in pdiaric and
adul pains. Lamrigin is als apprvd fr us in
cmbinain wih hr sandard hrapis  ra bi
plar disrdr  dlay h im  h ns f md
pisds (i.., dprssin, mania, mixd pisds).
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm la
mrigin ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Tramn f biplar disrdr
3. Minimal advrs ffcs frm hrapy
Nursing Implications for Lamotrigine
Premedication assessment
1. Prfrm a baslin assssmn f h pain’s
spch parns, dgr f alrnss, and rina
in  nam, plac, and im bfr iniiaing hr
apy. Mnir h pain’s bhaviral rspnss 
hrapy.
2. Rviw h pain’s mdicain hisry  dr
min whhr h pain is alrady aking valpric
acid fr sizur cnrl.
3. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.
Availability. PO: abls: 25, 100, 150 and 200 mg; chw
abl abls: 5 and 25 mg; rally disingraing abls:
25, 50, 100, and 200 mg; abls, 24hur xndd r
las: 25, 50, 100, 200, 250, and 300 mg.
Dosage and administration
Seizure disorder. Adult: PO: If h pain is alrady
aking valpric acid fr sizur cnrl, iniia lam
rigin hrapy a 25 mg vry hr day fr 2 wks,

fllwd by 25 mg daily fr 3  4 wks; hn h ds
may b incrasd by 25  50 mg PO daily vry 1  2
wks unil h mainnanc dsag is achivd. Th
usual mainnanc ds is 100  400 mg/day PO, giv
n in n  w dividd dss. Th usual mainnanc
ds fr pains wh add lamrigin  valpric acid
aln rangs frm 100  200 mg/day.
If h pain is n alrady aking mablism
inducing mdicains (.g., valpric acid, carbamaz
pin, phnyin, phnbarbial, rifampin) fr sizur
cnrl, iniia lamrigin hrapy a 25 mg PO v
ry day fr 2 wks, hn 50 mg/day PO fr wks
3  4; hn h ds may b incrasd by 50 mg/day
PO vry 1  2 wks unil h mainnanc dsag
is achivd. Th usual mainnanc ds is 225  375
mg/day PO, givn in w dividd dss. If h pain
is alrady rciving mablisminducing mdicains
fr sizur cnrl, h dsag f lamrigin shuld b
apprximaly w ims hs dsags up  400 mg
daily in dividd dss; s h manufacurr’s rcm
mndains. Thrapuic bld lvls fr lamrigin
ar 3  15 mg/L.
Bipolar disorder. Adult: PO: Iniial dsag d
pnds n hr mdicains ha ar bing akn.
Targ dsag is 200 mg/daily f immdiarlas
mdicain.
Common adverse effects
Gastrointestinal
Nausea, vomiting, indigestion. Ths ffcs ar cm
mn during h iniiain f hrapy. Gradual incrass
in dsag and adminisrain wih fd r milk will
rduc gasric irriain.
Neurologic
Sedation, drowsiness, dizziness. Ths sympms nd
 disappar wih cninud hrapy and pssibl ds
ag adjusmn. Encurag h pain n  discn
inu hrapy wihu rs cnsuling h halhcar
prvidr. Prvid fr pain safy during pisds
f drwsinss r dizzinss. Pains mus b warnd
n  wrk arund machinry, pra mr vhicls,
r prfrm hr duis ha rquir cnsan mnal
alrnss unil i is knwn hw hy ar affcd by his
mdicain.
Sensory
Blurred vision. Cauin h pain ha blurrd visin
may ccur, and mak apprpria suggsins fr h
pain’s prsnal safy.
Serious adverse effects
Integumentary
Dermatologic reactions. Apprximaly 10% f pa
ins wh rciv lamrigin dvlp a skin rash
and uricaria during h rs 4  6 wks f hra
py. Slwr incrass in ach dsag adjusmn ar
hugh  dcras h incidnc f rash. In ms cas
s, h rash rslvs wih cninud hrapy; hwvr,
h halhcar prvidr shuld b prmply infrmd
Drugs Used for Seizure Disorders CHAPTER 18 289
bcaus h rash culd als b an arly indicar f
a mr srius cndiin. Cmbinain hrapy wih
valpric acid appars  b mr likly  prcipia
a srius rash.
Encurag h pain n  discninu h la
mrigin unil alrnaiv anipilpic hrapy can b
cnsidrd  prvn rnwd sizur aciviy.
Neurologic
Aseptic meningitis. Lamrigin may caus asp
ic mningiis. Pains shuld b advisd  cnac
hir halhcar prvidr immdialy if hy xp
rinc signs and sympms f mningiis, such as
hadach, fvr, siff nck, nausa, vmiing, rash,
and snsiiviy  ligh. Pains shuld b valuad
fr hr causs f mningiis; if n hr causs ar
fund, h discninuain f lamrigin shuld b
cnsidrd.
Drug interactions
Drugs that enhance therapeutic and toxic ef-
fects. Valpric acid rducs h mablism f lam
rigin by as much as 50%. Signican lamrigin ds
ag rducin may b rquird.
Drugs that decrease therapeutic effects. Phnbarbial,
phnyin, primidn, carbamazpin, xcarbazpin,
hsuximid, rifampin, acaminphn, srgn cn
aining ral cnracpivs, and prgsin ral cn
racpivs nhanc h mablism f lamrigin.
Mnir h pain fr h incrasd frquncy f
sizur aciviy. Mniring changs in srum lvls
shuld hlp prdic pssibl incrasd sizur aciviy.
Th wicdaily adminisrain f lamrigin may b
ncssary.
Enhanced sedation. Cnral nrvus sysm dprs
sans—including slp aids, analgsics, ranquilizrs,
and alchl—nhanc h sdaiv ffcs f lam
rigin. Pains mus b warnd n  wrk arund
machinry, pra mr vhicls, r prfrm hr
duis ha rquir cnsan mnal alrnss unil i
is knwn hw hy ar affcd by his mdicain.
Prvid fr pain safy during pisds f drwsi
nss r dizzinss.
levetiracetam (lĕ-vĕ-tĭr-ă-SĒ-tĕm)
Keppra (KĔP-ră)
Do not confuse Keppra with Kaletra.
Actions
Lviracam is classid as a pyrrlidin drivaiv
chmically unrlad  hr anipilpic drugs avail
abl. Is mchanism f acin is unknwn, bu i ap
pars  acs n vlaggad passiumchannls and
bind  h SV2A.
Uses
Lviracam is apprvd fr us in cmbinain
wih hr anipilpic hrapy  ra fcal sizurs,
290 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
myclnic sizurs, and primary gnralizd nic
clnic sizurs in aduls.
Therapeutic Outcomes
Th primary hrapuic ucms sugh frm lvi
racam ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Minimal advrs ffcs frm hrapy
Nursing Implications for Levetiracetam
Premedication assessment
1. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.
2. Prfrm a baslin assssmn f h pain’s
spch parns, dgr f alrnss, and rinain
 nam, plac, and im bfr iniiaing hrapy.
3. Rviw h pain’s labrary rprs and rpr
any abnrmal rnal funcin (.g., BUN, crainin,
crainin claranc).
Availability. PO: 250, 500, 750, and 1000mg abls;
250, 500, 750, 1000mg disingraing abls; 500
and 750, 1000, and 1500mg abls, xndd rlas
(24 hurs); 100 mg/mL ral sluin.
Injection: 100 mg/mL in 5mL vials; 500 mg/5 mL;
500 mg/100 mL; 1000 mg/100 mL; 1500 mg/100 mL.
Dosage and administration. Adult: PO: Iniial ds is
500 mg wic daily. Dsag may b incrasd vry 2
wks by 500 mg wic daily unil a maximum ds f
3000 mg/day is aaind.
Note: Dsag adjusmn is ncssary in pains
whs simad crainin claranc is lss han 80
mL/min. S h packag insr fr addiinal insruc
ins. Th hrapuic bld lvls fr lviracam
ar 12  46 mg/L.
Common adverse effects
Neurologic
Weakness, drowsiness, dizziness. Ths ffcs can b
rducd by slwly incrasing h dsag. Thy ar
usually mild, and hy nd  rslv wih cninud
hrapy. Encurag h pain n  discninu hr
apy wihu rs cnsuling h halhcar prvidr.
Prvid fr pain safy during pisds f waknss
and dizzinss. Pains mus b warnd n  wrk
arund machinry, pra mr vhicls, r prfrm
hr duis ha rquir cnsan mnal alrnss un
il i is knwn hw hy ar affcd by his mdicain.
Serious adverse effects
Neurologic
Confusion, disorientation. Mak rgularly schduld
assssmns f h pain’s spch parns, dgr
f alrnss, and rinain  nam, plac, and im,
and cmpar ndings. Rpr any signican alra
ins  h halhcar prvidr.
Drug interactions
Enhanced sedation. Cnral nrvus sysm dprs
sans—including slp aids, analgsics, ranquilizrs,
and alchl—nhanc h sdaiv ffcs f lvi
racam. Pains mus b warnd n  wrk arund
machinry, pra mr vhicls, r prfrm hr
duis ha rquir cnsan mnal alrnss unil i is
knwn hw hy ar affcd by his mdicain.
oxcarbazepine (ŏks-kăr-BĂZ-ĕ-pēn)
Do not confuse oxcarbazepine with olanzapine.
Trileptal (trī-LĔP-tŏl)
Do not confuse Trileptal with Tegretol.
Actions
Oxcarbazpin is a prdrug ha mablizs in
sm f h aciv mablis f carbamazpin.
Oxcarbazpin blcks h vlaggad sdium chan
nls, rsuling in sabilizain f hyprxcid nural
mmbrans. In addiin, i may mdula h vlag
gad passium and calcium channls, which may
cnribu  h anicnvulsan ffcs f h drug.
Uses
Oxcarbazpin is usd as mnhrapy r cmbi
nain hrapy fr h ramn f fcal sizurs in
aduls and as cmbinain hrapy fr h ramn
f fcal sizurs in childrn wh ar 4  16 yars ld.
Bcaus f h srucural similariy  carbamazpin,
bfr saring hrapy cnsidr scrning pains f
Asian dscn fr h varian HLAB*1502 alll.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm x
carbazpin ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Minimal advrs ffcs frm hrapy
Nursing Implications for Oxcarbazepine
Premedication assessment
1. Bcaus f his drug’s pnial  caus srius ad
vrs racins, h manufacurr rcmmnds ha
srum lcrly baslin lvls b drmind and
hn rpad pridically whil h pain is r
civing xcarbazpin hrapy.
2. Rviw h pain’s mdicain hisry  nsur
ha h pain ds n hav an allrgy  carbam
azpin. If hr is an allrgy, infrm h charg nurs
and h halhcar prvidr immdialy. D n ad
minisr h mdicain wihu spcic apprval.
3. Prfrm a baslin assssmn f h pain’s spch
parns, dgr f alrnss, and rinain  nam,
plac, and im bfr iniiaing hrapy. Mnir h
pain’s bhaviral rspnss  hrapy.
4. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.

Availability. PO: 150, 300, and 600mg abls; 150,
300, 600mg abls, xndd rlas (24 hurs);
300 mg/5 mL suspnsin.
Dosage and administration. Adult: PO: Iniial dsag
is 300 mg wic daily fr h rs 3 days. Th ds
ag may b incrasd by 300 mg/day vry 3 days
 1200 mg/day. Dsags f 2400 mg/day hav bn
fund  b ffciv fr pains cnvrd frm
hr anicnvulsan hrapy  mnhrapy wih
xcarbazpin.
Pediatric (4 to 16 years old): PO: Iniial dsag is 4
 5 mg/kg wic daily, n  xcd 600 mg/day. Th
dsag shuld b gradually incrasd vr h nx 2
wks  a arg mainnanc lvl basd n h pa
in’s bdy wigh:
20–24.9 kg 600–900 mg/day in two
divided doses
25–34.9 kg 900–1200 mg/day in two
divided doses
35–44.9 kg 900–1500 mg/day in two
divided doses
45–49.9 kg 1200–1500 mg/day in two
divided doses
50–59.9 kg 1200–1800 mg/day in two
divided doses
60–69.9 kg 1200–2100 mg/day in two
divided doses
>70 kg 1500–2100 mg/day in two
divided doses
Th hrapuic bld lvls fr xcarbazpin ar
3  35 mg/L.
Common adverse effects
Neurologic
Confusion, poor coordination, drowsiness, dizzi-
ness. Ths ffcs can b rducd by slwly incras
ing h dsag; hy ar usually mild and nd  r
slv wih cninud hrapy. Encurag h pain
n  discninu hrapy wihu rs cnsuling h
halhcar prvidr. Prfrm a baslin assssmn f
h pain’s spch parns, dgr f alrnss, and
rinain  nam, plac, and im bfr iniiaing
hrapy. Mak rgularly schduld subsqun valu
ains f h pain’s mnal saus, and cmpar
ndings; rpr any signican alrains. Prvid
fr pain safy during pisds f drwsinss, cn
fusin, r dizzinss. Pains mus b warnd n 
wrk arund machinry, pra mr vhicls, r
prfrm hr duis ha rquir cnsan mnal
alrnss unil i is knwn hw hy ar affcd by
his mdicain.
Serious adverse effects
Hematologic
Blood dyscrasias. Ruin labrary sudis (i..,
RBC, WBC, and diffrnial cuns) shuld b
Drugs Used for Seizure Disorders CHAPTER 18 291
schduld. Mnir h pain fr sr hra, f
vr, purpura, jaundic, r xcssiv and prgrssiv
waknss.
Nausea, headache, lethargy, confusion, obtundation, ma-
laise. Ths ar sympms f hypnarmia. I is x
rmly impran  nify h halhcar prvidr
if h pain is xhibiing any f hs cndiins.
Wihhld addiinal dss f h drug unil spcic r
drs  adminisr h mdicain hav bn rcivd.
Drug interactions
Drugs that decrease therapeutic effects. Phnbarbial,
primidn, phnyin, valpric acid, carbamazpin,
and vrapamil may nhanc h mablism f x
carbazpin. Mnir h pain fr an incrasd fr
quncy f sizur aciviy. Dsags f xcarbazpin
may nd  b incrasd.
Estrogen- and progestin-containing contracep-
tives. Oxcarbazpin nhancs h mablism f
srgns and prgsins. Sping r blding may
b an indicain f rducd cnracpiv aciviy.
Rcmmnd ha h pain us hr frms f birh
cnrl whil aking xcarbazpin.
phenobarbital (fē-nō-BĂR-bĭ-tŏl)
Actions
Phnbarbial, a lngacing barbiura, lvas h
sizur hrshld and prvns h sprad f lcrical
sizur aciviy by nhancing h inhibiry ffc f
GABA. Th xac mchanism is unknwn.
Uses
Phnbarbial is an ffciv anipilpic agn.
Bcaus f is sdaiv ffcs, hwvr, i is nw usd
primarily as an alrnaiv whn singl nnsdaing
anipilpic drugs ar unsuccssful fr h cnrl f
sizurs. Phnbarbial is ms usful fr raing fcal
and gnralizd nicclnic sizurs and gnralizd
myclnic sizurs, usually in cmbinain wih hr
anipilpic drugs. Th hrapuic bld lvls fr
phnbarbial ar 15  45 mg/L.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm ph
nbarbial ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Minimal advrs ffcs frm hrapy
Nursing Implications for Phenobarbital
Premedication assessment
1. Prfrm a baslin assssmn f h pain’s
spch parns, dgr f alrnss, and rina
in  nam, plac, and im bfr iniiaing hr
apy. Mnir h pain’s bhaviral rspnss 
hrapy.
292 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
2. Obain h pain’s vial signs (.g., bld prssur,
puls, rspirains).
Availability. PO: abls: 15, 16.2, 30, 32.4, 60, 64.8, 97.2,
and 100 mg; lixir and sluin: 20 mg/5 mL.
IV: 65 and 130 mg/mL.
Dosage and administration
Seizure control. Adult: PO: 60  200 mg/day r 50 
100 mg w  hr ims daily.
Status epilepticus. IV: 15 mg/kg as a singl ds.
Note: Rapidly discninuing phnbarbial afr h
lngrm us f high dsags may rsul in sympms
ha ar similar  hs f alchl wihdrawal. Ths
may vary frm waknss and anxiy  dlirium and
gnralizd sizurs. Discninuain f phnbarbial
cnsiss f cauius and gradual wihdrawal vr 2 
4 wks.
Common adverse effects. Gnral advrs f
fcs f phnbarbial includ drwsinss, lh
argy, hadach, muscl r jin pain, and mnal
dprssin.
Neurologic
Hangover, sedation, lethargy, diminished alert-
ness. Pains may cmplain f “mrning hangvr,”
blurrd visin, and ransin hypnsin n arising.
Explain  h pain h nd  rs ris  a siing
psiin, say siing fr svral mmns unil any
dizzinss r lighhaddnss passs, and hn sand
slwly. Assisanc wih ambulain may b rquird.
If h hangvr ffc bcms rublsm, hr
shuld b a rducin in h dsag, a chang in h
mdicain, r bh.
Ppl wh wrk arund machinry, driv, admin
isr mdicains, r prfrm hr duis fr which
hy mus rmain mnally alr shuld n ak his
mdicain whil wrking.
Serious adverse effects
Psychological
Excessive use or abuse. Th habiual us f phn
barbial may rsul in physical dpndnc. Discuss
h issu wih h halhcar prvidr and mak plans
 cpraivly apprach h gradual wihdrawal
f h mdicains bing abusd if sizur cnrl is
mainaind.
Paradoxical response. Oldr pains may rspnd
paradxically  phnbarbial by dmnsraing
xcimn, uphria, rslssnss, and cnfusin.
Prvid suppriv physical car and safy during
hs rspnss.
Integumentary
Hypersensitivity. Racins  phnbarbial ar infr
qun bu may b srius. Rpr sympms f hivs,
prurius, rash, high fvr, r h inammain f h
mucus mmbrans fr valuain by a halhcar
prvidr.
Hematologic
Blood dyscrasias. Bld dyscrasias ar rar; hwvr,
labrary sudis (.g., RBC, WBC, diffrnial, and
plal cuns) shuld b schduld whn sympms
warran. Srss h impranc f h pain rurning
fr his labrary wrk. Mnir h pain fr h
dvlpmn f sr hra, fvr, purpura, jaundic,
r xcssiv and prgrssiv waknss.
Drug interactions
Drugs that increase toxic effects. Anihisamins, alc
hl, analgsics, anshics, ranquilizrs, valpric acid,
mnamin xidas inhibirs, and hr sdaiv
hypnics incras h xic ffcs f phnbarbial.
Mnir h pain fr xcssiv sdain, and rduc
h dsag f phnbarbial r anhr mdicin if
ncssary.
Phenytoin. Th ffcs f phnbarbial n ph
nyin ar variabl. Srum lvls may b rdrd,
and a chang in phnyin dsag may b rquird.
Obsrv pains fr incrasd sizur aciviy and fr
signs f phnyin xiciy (.g., nysagmus, sdain,
lhargy).
Reduced therapeutic effects. Phnbarbial rducs
h ffcs f h fllwing mdicins:
• Warfarin: Mnir h pain’s inrnainal nr
malizd rai (INR) and incras h dsag f war
farin, if ncssary.
• Estrogens: This drug inracin may b criical
in pains wh ar rciving cnracpivs ha
cnain srgn. If pains dvlp sping and
brakhrugh blding, a chang in cnracpivs
and h us f alrnaiv frms f cnracpin
shuld b cnsidrd.
• Corticosteroids, beta-adrenergic blockers, metronida-
zole, doxycycline, antidepressants, quinidine, and chlor-
promazine: Th pain shuld b mnird fr
signs f incrasd aciviy f h illnss fr which
h mdicain was prscribd. Dsag incrass
may b ncssary, r phnbarbial may hav  b
discninud.
pregabalin (prĕ-GĂB-ă-lĭn)
Lyrica (LĬR-ĭ-kă)
Actions
Prgabalin wrks by blcking h vlaggad cal
cium channls. I is chmically rlad  gabapnin.
I ds n appar  nhanc GABA.
Uses
Prgabalin is an anipilpic usd in cmbinain wih
hr anipilpic agns  cnrl fcal sizurs.
Prgabalin is als apprvd fr h ramn f pain as
sciad wih brmyalgia, diabic nurpahy, nu
rpahic pain assciad wih spinal crd injury, and
pshrpic nuralgia (a cmplicain f acu hrps

zsr acivain, which is fn dscribd as unbar
abl iching, lcric shck–lik pain, r burning).
Prgabalin has h pnial fr abus and dpn
dnc, and i has bn dsignad as a Schdul V cn
rlld subsanc. Sympms suggsiv f physical
dpndnc (insmnia, nausa, hadach, diarrha)
hav bn bsrvd in sm pains in clinical sudis
afr h drug’s abrup discninuain.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm pr
gabalin ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Sympmaic rlif frm pain assciad wih 
brmyalgia, diabic nurpahy, and pshrpic
nuralgia
3. Minimal advrs ffcs frm hrapy
Nursing Implications for Pregabalin
Premedication assessment
1. Prfrm a baslin assssmn f h pain’s
spch parns, dgr f alrnss, and rina
in  nam, plac, and im bfr iniiaing hr
apy. Mnir h pain’s bhaviral rspnss 
hrapy.
2. Obain a baslin masurmn f h pain’s cr
ainin claranc fr pnial dsag adjusmn.
3. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.
4. Rviw h pain’s mdical rcrd fr indicains
f a hisry f subsanc abus.
5. Whn prgabalin is usd as an analgsic, prfrm a
pain assssmn wih h pain bfr adminisr
ing i and a apprpria inrvals during hrapy.
Rpr pr pain cnrl and bain a mdicain
in h pain’s rdrs.
Availability. PO: capsuls: 25, 50, 75, 100, 150, 200, 225,
and 300 mg; abls, 24hur xndd rlas: 82.5,
165, 330 mg; ral sluin: 20 mg/mL.
Dosage and administration. Dsags shuld b ad
jusd fr pains wih a crainin claranc blw 60
mL/min.
Seizure control. Adult: PO: 150  600 mg daily.
Iniially adminisr 50 mg hr ims daily r 75 mg
wic daily. Th daily dsag can b incrasd  a
maximum f 600 mg daily in dividd dss, dpnd
ing n h pain’s rspns and h dvlpmn f
any advrs ffcs.
Fibromyalgia. Adult: PO: 300  450 mg daily. Iniially
adminisr 75 mg wic daily and incras  150 mg
wic daily wihin 1 wk. If hr is a hrapuic bn
 and h advrs ffcs ar accpabl, h dsag
may b incrasd  225 mg wic daily fr a al f
Drugs Used for Seizure Disorders CHAPTER 18 293
450 mg daily. Th hrapuic bld lvls fr prgaba
lin hav n bn sablishd.
Neuropathic pain associated with diabetic peripheral
neuropathy. Adult: PO: Up  300 mg daily. Iniially
adminisr 50 mg hr ims daily and incras  100
mg hr ims daily wihin 1 wk n h basis f h
pain’s lranc.
Spinal cord injury-associated neuropathic pain. Adult:
PO: Up  600 mg daily. Iniially adminisr 75 mg
wic daily and incras  150 mg wic daily wihin 1
wk basd n rspns and lrabiliy.
Postherpetic neuralgia. Adult: PO: 150  600 mg dai
ly. Iniially adminisr 50 mg hr ims daily r 75 mg
wic daily. Fr pains wh d n xprinc suf
cin pain rlif afr 2  4 wks f ramn wih
300 mg daily and wh can lra advrs ffcs, h
daily dsag can b incrasd  a maximum f 600 mg
daily (i.., 200 mg hr ims daily r 300 mg wic
daily).
Medication Safety Alerts
Patients should be monitored for signs of pregabalin abuse,
including dosage escalation, tolerance, and drug-seeking
behavior. When discontinuing therapy, taper over at least 1
week to minimize the potential for withdrawal symptoms.
Serious breathing difculties may occur in patients
using gabapentinoids (gabapentin or pregabalin) who have
respiratory risk factors. These include the use of opioid
pain medicines and other drugs that depress the central
nervous system, and conditions such as chronic obstructive
pulmonary disease that reduce lung function. The elderly are
also at higher risk.
Common adverse effects
Neurologic
Sedation, drowsiness, dizziness. Ths sympms nd 
disappar wih cninud hrapy and pssibl dsag
adjusmn. Encurag h pain n  discninu
hrapy wihu rs cnsuling h halhcar prvid
r. Prvid fr pain safy during pisds f drwsi
nss r dizzinss. Pains mus b warnd n  wrk
arund machinry, pra mr vhicls, r prfrm
hr duis ha rquir cnsan mnal alrnss unil
i is knwn hw hy ar affcd by his mdicain.
Sensory
Blurred vision. Cauin h pain ha blurrd visin
may ccur, and mak apprpria suggsins fr h
pain’s prsnal safy.
Serious adverse effects
Neurologic
Confusion, disorientation. Mak rgularly schduld
assssmns f h pain’s spch parns, dgr
f alrnss, and rinain  nam, plac, and im,
294 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
and cmpar ndings. Rpr any signican alra
ins  h halhcar prvidr.
Psychological
Excessive use or abuse. Evalua h pain’s r
spns  prgabalin as an analgsic. Idnify hir
undrlying nds and plan fr h mr apprpria
managmn f hs nds. Discuss h pain’s cas
wih h halhcar prvidr and mak plans  c
praivly apprach h gradual wihdrawal f h
mdicains ha ar bing abusd. Suggs a chang
 a mildr analgsic whn indicad.
Pains d n hav  undrg h sympms f wih
drawal  b rad fr addicin. Thy may b rad
wih h gradual rducin f daily pia agnis dss.
If wihdrawal sympms bcm svr, h pain may
rciv mhadn. Th mprary adminisrain f
ranquilizrs and sdaivs may hlp rduc bh pain
anxiy and h craving fr h pia agnis.
Drug interactions
Enhanced sedation. Cnral nrvus sysm dprs
sans—including slp aids, analgsics, ranquilizrs,
bnzdiazpins, xycdn, and alchl—nhanc
h sdaiv ffcs f prgabalin. Pains mus b
warnd n  wrk arund machinry, pra m
r vhicls, r prfrm hr duis ha rquir cn
san mnal alrnss unil i is knwn hw hy ar
affcd by his mdicain. Prvid fr pain safy
during pisds f drwsinss r dizzinss.
topiramate (tō-PĬR-ă-māt)
Do not confuse topiramate with torsemide.
Topamax (TŌ-pă-măks)
Actions
Th mchanism f acin f pirama as an ani
pilpic agn is unknwn. Thr pnial mchanisms
may suppr anipilpic aciviy: (1) h prlngd
blckad f sdium channls in h nurnal mm
bran, (2) h pniain f h aciviy f h inhibi
ry nurransmir GABA, and (3) h anagnism
f crain rcprs f h xciary nurransmir.
Uses
Tpirama is an anipilpic usd in cmbinain
wih hr anipilpic agns  cnrl fcal and
gnralizd nicclnic sizurs. I is als usd fr pa
ins 2 yars ld and ldr wh hav sizurs assci
ad wih LnnxGasau syndrm.
Tpirama has als bn apprvd fr aduls fr h
prvnin (bu n ramn) f migrain hadachs.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm pi
rama ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Prvnin f migrains
3. Minimal advrs ffcs frm hrapy
Nursing Implications for Topiramate
Premedication assessment
1. Prfrm a baslin assssmn f h pain’s
spch parns and dgr f alrnss, as wll as
rinain  nam, plac, and im, bfr inii
aing hrapy. Mnir h pain’s bhaviral r
spnss  hrapy.
2. Obain h pain’s baslin wigh fr fuur rfr
nc. Wigh lss may b an advrs ffc f pira
ma hrapy.
3. Assss h pain’s baslin sa f hydrain. Rar
cass f lighidrsis (dcrasd swaing) and
hyprhrmia hav bn rprd, paricularly in
childrn and in hs pains wh ar aking hr
mdicains wih anichlinrgic aciviy. Prpr hy
drain bfr and during aciviis such as xrcis
r xpsur  warm mpraurs is rcmmndd.
4. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.
5. If his drug is usd fr migrain prvnin, rviw
h pain’s mdical rcrd  dcumn h fr
quncy f migrain hadachs.
6. Ask fmal pains if hr is a pssibiliy f prg
nancy a his im. If s, nify h halhcar pr
vidr f his pssibiliy bfr saring hrapy.
Availability. PO: 25, 50, 100, and 200mg abls; 25,
50, 100, 200mg capsuls, xndd rlas (24 hurs);
15 and 25mg sprinkl capsuls; 25, 50, 100, 150, and
200mg sprinkl capsuls, xndd rlas (24 hurs).
Dosage and administration
Antiepileptic. Adult: PO: Iniially 25 mg wic daily.
Incras h daily dsag by 50 mg a wkly inrvals un
il a clinical rspns is achivd. Th usual rcmmndd
daily dsag is 400 mg in w dividd dss. Tpirama
may b akn wih r wihu fd. Th abls shuld n
b brkn bcaus hy as bir. Th sprinkl capsuls
may b swallwd whl r adminisrd by carfully
pning h capsul and sprinkling h nir cnns n
a small amun (.g., 1aspn) f sf fd. Swallw his
drugfd mixur immdialy; d n chw. Th hra
puic bld lvls fr pirama ar 5  25 mg/L.
Migraine prevention. Adult: PO: Us h abls r
sprinkl capsuls. Dsag incras is as fllws: wk
1, 25 mg daily in h vning; wk 2, 25 mg in h
mrning and 25 mg in h vning; wk 3, 25 mg in h
mrning and 50 mg in h vning; wk 4 and hraf
r, 50 mg in h mrning and 50 mg in h vning. D
n us pirama  ra migrain hadachs.
Common adverse effects
Neurologic
Sedation, drowsiness, dizziness. Ths sympms nd
 disappar wih cninud hrapy and pssibl

dsag adjusmn. Encurag h pain n  dis
cninu hrapy wihu rs cnsuling h halh
car prvidr. Ppl wh wrk arund machinry,
pra mr vhicls, r prfrm hr duis ha
rquir cnsan mnal alrnss shuld b paricu
larly cauius unil hy knw hw h mdicain af
fcs hm. Prvid fr pain safy during pisds
f dizzinss and rpr hs pains  h halhcar
prvidr fr furhr valuain.
Serious adverse effects
Neurologic
Confusion, disorientation. Mak rgularly schduld
assssmns f h pain’s spch parns, dgr
f alrnss, and rinain  nam, plac, and im,
and cmpar ndings. Rpr any signican alra
ins  h halhcar prvidr.
Cleft palate in newborns. Tpirama incrass h risk
f dvlpmn f clf lip r clf pala in infans
brn  wmn bing rad wih pirama. Thr is
psiiv vidnc f human fal risk basd n human
daa, bu h pnial bns frm h us f h drug
in prgnan wmn may b accpabl in crain siua
ins dspi is risks.
Wmn aking pirama shuld ll hir halh
car prvidrs immdialy if hy ar planning  r
hav bcm prgnan. Pains shuld n sp ak
ing pirama unlss ld  d s by hir halhcar
prvidr.
Metabolic
Hydration status. Dcrasd swaing and vr
haing hav bn rprd wih h us f pirama,
primarily in childrn. Ms cass ccur in assciain
wih xpsur  lvad nvirnmnal mpra
urs, vigrus aciviy, r bh. Prpr hydrain b
fr and during aciviis such as xrcis r xpsur
 warm mpraurs is rcmmndd.
Drug interactions
Drugs that decrease therapeutic effects. Phnbarbial,
primidn, phnyin, valpric acid, and carbamazpin
may nhanc h mablism f pirama. Mnir h
pain fr incrasd frquncy f sizur aciviy.
Enhanced sedation. Cnral nrvus sysm dprs
sans—including slp aids, analgsics, ranquilizrs,
and alchl—nhanc h sdaiv ffcs f pira
ma. Pains mus b warnd n  wrk arund
machinry, pra mr vhicls, r prfrm hr
duis ha rquir cnsan mnal alrnss unil i
is knwn hw hy ar affcd by his mdicain.
Prvid fr pain safy during pisds f drwsi
nss r dizzinss.
Estrogen-containing contraceptives. Tpirama n
hancs h mablism f srgns. Sping r bld
ing may b an indicain f rducd srgn lvls
and rducd cnracpiv aciviy. Rcmmnd ha
h pain us alrnaiv frms f birh cnrl whil
aking his mdicain.
Drugs Used for Seizure Disorders CHAPTER 18 295
valproic acid (văl-PRŌ-ĭk Ă-sĭd)
Depakene (DĔP-ă-kēn)
Actions
Valpric acid is an anipilpic agn srucurally un
rlad  any hr agn currnly usd  ra si
zur disrdrs. Is mchanism f acin is unknwn;
hwvr, i appars  suppr GABA aciviy as an
inhibiry nurransmir.
Uses
Valpric acid has brad aciviy agains fcal sizurs
and gnralizd nicclnic sizurs. I is h nly
availabl agn ha can b usd as singldrug hrapy
fr raing pains wih a cmbinain f gnralizd
nicclnic, absnc, r myclnic sizurs. Valpric
acid is als bing sd fr us ihr aln r in cm
binain wih lihium r carbamazpin fr raing
acu mania assciad wih biplar disrdr in pa
ins wh d n rspnd  lihium hrapy aln. I
is als apprvd fr h prvnin f migrain had
achs; i is n ffciv fr h ramn f migrain
hadachs.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm val
pric acid ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Tramn f acu mania in biplar disrdr
3. Prvnin f migrains
4. Minimal advrs ffcs frm hrapy
Nursing Implications for Valproic Acid
Premedication assessment
1. Th manufacurr rcmmnds ha h fllwing
baslin sudis b cmpld bfr hrapy is inii
ad and a rgular inrvals hrafr: livr funcin
ss, srum ammnia lvls in pains xprincing
sympms f lhargy r chang in mnal saus,
blding im drminain, and plal cun.
2. Rviw h pain’s ruin bld sudis  dc
bld dyscrasias and hpaxiciy.
3. Prfrm a baslin assssmn f h pain’s spch
parns, dgr f alrnss, and rinain  nam,
plac, and im bfr saring hrapy. Mnir h
pain’s bhaviral rspnss  hrapy.
4. Ask fmal pains abu h pssibiliy f
prgnancy.
Availability. PO: 250mg capsuls; 125mg capsuls
cnaining cad paricls (sprinkls); 250, and 500
mg abls, susaind rlas (24 hurs); 250 mg/5 mL
sluin.
Injection: 100 mg/mL in 5mL vials.
296 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
Dosage and administration. Adult: PO: 10  15 mg/
kg daily, dividd in w  hr dss. Adminisr
mdicain wih fd r milk  rduc gasric irria
in. Incras by 5  10 mg/kg/day a wkly inr
vals. Th maximum daily dsag is 60 mg/kg. Th
hrapuic bld lvls ar 50  100 mg/L. A capsul
cnaining nriccad paricls is availabl fr pa
ins wh hav prsisn nausa and vmiing.
Common adverse effects
Gastrointestinal
Nausea, vomiting, indigestion. Ths ffcs ar cm
mn during iniiain f hrapy. Gradual incrass in
dsag and adminisrain wih fd r milk rduc
gasric irriain.
Neurologic
Sedation, drowsiness, dizziness. Ths sympms nd
 disappar wih cninud hrapy and pssibl ds
ag adjusmn. Encurag h pain n  discn
inu hrapy wihu rs cnsuling h halhcar
prvidr. Ppl wh wrk arund machinry, pr
a mr vhicls, r prfrm hr duis ha rquir
cnsan mnal alrnss shuld n ak hs mdi
cains whil wrking. Prvid fr pain safy dur
ing pisds f dizzinss and rpr hs pains 
h halhcar prvidr fr furhr valuain.
Sensory
Blurred vision. Cauin h pain ha blurrd visin
may ccur, and mak apprpria suggsins fr h
pain’s prsnal safy.
Serious adverse effects
Hematologic
Blood dyscrasias. Ruin labrary ss (.g., RBC,
WBC, diffrnial, and plal cuns) shuld b schd
uld. Mnir h pain fr sr hra, fvr, purpu
ra, jaundic, r xcssiv and prgrssiv waknss.
Neurologic
Birth defects. Thr is an incrasd risk f nural ub
dfcs, cranifacial dfcs, and cardivascular mal
frmains in infans xpsd  valpric acid during
gsain. Wmn f childbaring ag shuld us val
pric acid nly if i is ssnial  manag hir mdical
cndiins. Wmn wh ar n planning a prgnancy
shuld us ffciv cnracpin. Wmn wh b
cm prgnan whil aking valpric acid shuld n
discninu hrapy wihu discussing i rs wih
hir halhcar prvidrs.
Gastrointestinal
Hepatotoxicity. Th sympms f hpaxiciy ar
anrxia, nausa, vmiing, jaundic, hpamgaly,
splnmgaly, and abnrmal livr funcin s rsuls
(.g., lvad bilirubin, AST, ALT, GGT, and ALP; in
crasd PT).
Pancreatitis. Th sympms f pancraiis ar ab
dminal pain, nausa, vmiing, and anrxia. Rpr
sympms  h halhcar prvidr bcaus f h
pnial fr lifhraning cmplicains.
Drug interactions
Drugs that decrease therapeutic effects. Phnbarbial,
primidn, phnyin, pirama, and carbamazpin
may nhanc h mablism f valpric acid and hus
dcras is hrapuic ffc. Mnir h pain fr
h incrasd frquncy f sizur aciviy. Mniring
changs in srum lvls shuld hlp prdic h pn
ial fr incrasd sizur aciviy.
Enhanced sedation. Cnral nrvus sysm dprs
sans—including slp aids, analgsics, ranquilizrs,
and alchl—nhanc h sdaiv ffcs f valpric
acid. Pains mus b warnd n  wrk arund
machinry, pra mr vhicls, r prfrm hr
duis ha rquir cnsan mnal alrnss unil i
is knwn hw hy ar affcd by his mdicain.
Prvid fr pain safy during pisds f drwsi
nss r dizzinss.
zonisamide (zō-NĬS-ă-mīd)
Zonegran (Zō-nĕ-grăn)
Actions
Znisamid is classid as a sulfnamid, and i is
chmically unrlad  hr anipilpic agns. I
acs by blcking sdium and calcium channls  sa
biliz h nurnal mmbrans, prvning prpaga
in f a sizur simulus. I ds n affc GABA
aciviy.
Uses
Znisamid is apprvd fr us in cnjuncin wih
hr anipilpic hrapy fr h ramn f fcal
sizurs in aduls.
Therapeutic Outcomes
Th primary hrapuic ucms sugh frm
znisamid ar as fllws:
1. Rducd frquncy f sizurs and rducd injury
frm sizur aciviy
2. Minimal advrs ffcs frm hrapy
Nursing Implications for Zonisamide
Premedication assessment
1. Rviw h pain’s mdicain hisry  nsur
ha h pain ds n hav an allrgy  sulfn
amid mdicains (.g., Bacrim, Spra). If h pa
in ds hav such an allrgy, infrm h charg
nurs and h halhcar prvidr immdialy.
D n adminisr h mdicain wihu spcic
apprval.
2. Rviw h pain’s mdical rcrd fr a hisry f
skin rashs. If h pain dvlps a rash, infrm
h charg nurs and h halhcar prvidr imm
dialy. D n adminisr h mdicain wihu
spcic apprval.
3. Rviw h pain’s mdical rcrd  dcumn
h frquncy f sizur aciviy.
 Drugs Used for Seizure Disorders CHAPTER 18 297

4. As a rsul f h pnial fr srius advrs rac
ins, h fllwing baslin sudis shuld b r
pad a rgular inrvals: cmpl bld cun,
livr funcin ss, BUN, and srum crainin.
5. Prfrm a baslin assssmn f h pain’s
spch parns, dgr f alrnss, and rinain
 nam, plac, and im bfr saring hrapy.
6. Obain h pain’s baslin vial signs.
Availability. PO: 25, 50, and 100mg capsuls.
Dosage and administration. Adult: PO: Iniial dsag
is 100 mg daily, akn wih r wihu fd. Bcaus
f sdaiv ffcs, h drug may b akn a bdim.
Afr 2 wks, h dsag may b incrasd  200 mg/
day fr a las 2 wks. Bh capsuls may b akn a
h sam im. Th dsag can b incrasd up  600
mg/day, wih a las 2 wks bwn dsag chang
s  assss h hrapuic ffcs f hrapy and 
mnir fr advrs ffcs. Encurag h pain 
drink six  igh 8unc glasss f war daily whil
aking his mdicain. Th hrapuic bld lvls
fr znisamid ar 10  40 mg/L.
Common adverse effects
Neurologic
Drowsiness, dizziness. Ths ffcs ar usually mild
and nd  rslv wih cninud hrapy; hy can
b rducd by slwly incrasing h dsag. Encurag
h pain n  discninu hrapy wihu rs
cnsuling h halhcar prvidr. Prvid fr pain
safy during pisds f dizzinss. Pains mus b
warnd n  wrk arund machinry, pra mr
vhicls, r prfrm hr duis ha rquir cnsan
mnal alrnss unil i is knwn hw hy ar affc
d by his mdicain.
Serious adverse effects
Neurologic
Confusion, disorientation. Mak rgularly schduld
assssmns f h pain’s spch parns, dgr
f alrnss, and rinain  nam, plac, and im,
and cmpar ndings. Rpr any signican alra
ins  h halhcar prvidr.
Genitourinary
Nephrotoxicity. Mnir h pain’s kidny func
in s rsuls fr abnrmal ndings. Rpr in
crasing BUN and crainin lvls; frank bld r
smkyclrd urin; RBCs in xcss f 0  3 n h
urinalysis rpr; r back pain, abdminal pain, r
pain n urinain.
Hematologic
Blood dyscrasias. Ruin labrary sudis (.g.,
RBC, WBC, and diffrnial cuns) shuld b schd
uld. Mnir h pain fr sr hra, fvr, pur
pura, jaundic, r xcssiv and prgrssiv waknss.
Integumentary
Dermatologic reactions. Rpr a pain’s rash r pru
rius, wih r wihu fvr, immdialy and wihhld
addiinal dss f h mdicain unil apprvd by
h halhcar prvidr.
Drug interactions
Enhanced sedation. Cnral nrvus sysm dprs
sans—including slp aids, analgsics, ranquiliz
rs, and alchl—nhanc h sdaiv ffcs f
znisamid. Pains mus b warnd n  wrk
arund machinry, pra mr vhicls, r pr
frm hr duis ha rquir cnsan mnal alr
nss unil i is knwn hw hy ar affcd by his
mdicain.
S Tabl 18.3 fr a lising f hr anipilpic
mdicains.

Table 18.3 Other Antiepileptic Drugs

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE USE FOR SEIZURE
brivaracetam Briviact Intravenous: 50 mg/5 mL 50–200 mg/day Focal-onset seizures
Brivlera Oral solution: 10 mg/mL (adjunct)
(300 mL)
Tablets: 10, 25, 50, 75,
100 mg
cannabidiol Epidiolex Oral liquid: 100 mg/mL in 2.5–10 mg/kg/day twice Lennox-Gastaut
100-mL bottles daily syndrome; Dravet
syndrome
cenobamate Xcopri Tablets: 50, 100, 150, Up to 400 mg/day Focal-onset seizures
200 mg
eslicarbazepine Aptiom Tablets: 200, 400, 600, Up to 1600 mg/day Focal-onset seizures
800 mg (adjunct)
lacosamide Vimpat Intravenous: 200–400 mg/day Simple or complex focal
200 mg/20 mL seizures
Oral solution: 10 mg/mL
(200, 465 mL)
Tablets: 50, 100, 150,
200 mg
298 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems

Table 18.3 Other Antiepileptic Drugs—cont’d

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE USE FOR SEIZURE
perampanel Fycompa Oral suspension: 0.5 mg/ 2–12 mg/day Focal onset seizures with
mL (340 mL) or without secondary
Tablets: 2, 4, 6, 8, 10, generalization
12 mg (adjunct); primary
generalized tonic-
clonic seizures
(adjunct)
primidone Mysoline Tablets: 50, 250 mg 750–1500 mg; do not Focalized seizures;
exceed 2000 mg/day generalized tonic-
clonic seizures
runamide Banzel Oral suspension: 40 mg/ 400–3200 mg/day Lennox-Gastaut
mL (460 mL) syndrome (adjunct)
Tablets: 200, 400 mg
tiagabine Gabitril Tablets: 2, 4, 12 16 mg 32–56 mg in 2–4 divided Focal seizures (adjunct)
Do not confuse Do not confuse doses
tiagabine with Gabitril with
tizanidine gabapentin
vigabatrin Sabril, Tablets: 500 mg 1.5 g two times daily Refractory focal onset
Vigadrone Powder packets: 500 mg impaired awareness
seizures
Available in Canada.
Do not confuse.

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points Go to your Evolve website (https://evolve.elsevier.com/Willihng

• Seizures are the result of the sudden excessive ring of
a small number of neurons and the spread of electrical
activity to adjacent neurons.
• There are several types and many causes of seizures. If the
seizures are chronic and recurrent, the patient is diagnosed
as having epilepsy.
• Epilepsy is treated almost exclusively with antiepileptic
medications.
• The effective treatment of epilepsy requires the cooperation
of the patient and the healthcare provider.
• The desired therapeutic outcome of seizure treatment is
to reduce the frequency of seizures while minimizing the
adverse effects of drug therapy. To attain this, therapy
must be individualized to consider the type of seizure
activity and the age, gender, and concurrent medical
conditions of the patient.
• Patients, as well as their families and caregivers, require
education and support regarding their responsibilities with
respect to the management of epilepsy.
Additional Learning Resources
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX examination and include both NGN (Next Genera-
tion) and traditional questions. See Chapter 1 for further infor-
mation regarding question types.
Scenario
A patient was recently diagnosed with epilepsy by a healthcare
provider after having experienced multiple episodes of convul-
sions accompanied by loss of consciousness.
1. The nurse witnesses the patient from the scenario with epilepsy as
the patient suddenly had spasms of his arms and legs, falling to the
oor. The patient initially lost consciousness and was quite groggy
when he woke up. Which type of seizure will be documented by the
nurse?
1. Tonic-clonic seizure
2. Atonic seizure
3. Focal simple motor seizure
4. Absence seizure

SG Go to your Study Guide for additional Review Questions Objective: Identify the different types of seizure disorders.
for the NCLEX® Examination, Critical Thinking Clinical Situa- NCLEX item type: Multiple choice
tions, and other learning activities to help you master this chap- Cognitive skill: Understanding
ter content.
 Drugs Used for Seizure Disorders CHAPTER 18 299

2. An infant is brought to the emergency department with observable NCLEX item type: Multiple response
twitching of the extremities and a temperature of 104.2°F as Cognitive skill: Application
reported by his parents. The nurse will need to attend the infant.
Use an X for the appropriate (necessary) action to take, or the not 4. The patient in the scenario asked the nurse what to expect when
appropriate action (could be harmful). taking the antiepileptic valproic acid (Depakene), which was
recently initiated. What are appropriate responses by the nurse?
(Select all that apply.)
NURSING ACTION APPROPRIATE NOT APPROPRIATE
1. “You should notice a decrease in the frequency of your
Take the infant’s seizures.”
vital signs. 2. “You will not need any laboratory tests to check for the
Administer drug level.”
antiepileptic drugs 3. “Common side effects from this drug are nausea and
as ordered. gastrointestinal upset; this will decrease if you take the
Leave the infant drug with food and as your body gets used to it.”
and mother for a 4. “You may feel drowsy or dizzy at rst; these symptoms
brief time to allow tend to disappear with continued therapy.”
privacy. 5. “The drug dosage will need to be increased over several
weeks before we get to the maintenance dose.”
Assess the
infant’s airway. Objective: Discuss the desired therapeutic outcomes from
antiepileptic agents used for seizure disorders.
Monitor the
NCLEX item type: Multiple response
response to
Cognitive skill: Application
antiepileptic
therapy. 5. From the following medications ordered by the healthcare provider
Restrain the infant for patients with known seizure disorders, the nurse knows which
and swaddle in medications are for the seizures? (Select all that apply.)
blankets. 1. Levetiracetam (Keppra) 500 mg PO
Protect the infant 2. Carbamazepine (Tegretol) 200 mg PO
from injury. 3. Terbinane (Lamisil) 250 mg PO
Ensure 4. Gabapentin (Neurontin) 300 mg PO
emergency 5. Phenytoin (Dilantin) 100 mg PO
equipment is Objective: Identify the drug classes used to treat seizure disorders.
available. NCLEX item type: Multiple response
Cognitive skill: Comprehension
Objective: Identify nursing interventions during the management of 6. The nurse monitoring a patient recently started on pregabalin
seizure activity. (Lyrica) for peripheral neuropathy for any adverse effects. The
NCLEX item type: Matrix nurse knows that the healthcare provider needs to be notied after
Cognitive skill: Taking action the patient makes which statements? (Select all that apply.)
3. When caring for a patient with epilepsy who is hospitalized and is 1. “I keep having blurred vision, especially in the morning.”
recovering from a seizure, what are the expected assessments/ 2. “I seem to be slurring my words and I am having trouble
interventions by the nurse during the postictal time? (Select all concentrating.”
that apply.) 3. “I nd myself needing to take a nap after breakfast, I’m so
sleepy.”
1. Place oxygen and suction equipment at the bedside. 4. “I have a better appetite now since I have been started on
2. Determine whether any bodily harm occurred during the this drug.”
seizure. 5. “I feel like my pain has not really improved at all with this
3. Evaluate the degree of weakness, speech pattern med.”
changes, and memory loss.
4. Encourage oral hygiene and ask the patient to brush their Objective: Describe the neurologic assessment performed on
teeth. patients taking antiepileptic agents to monitor for common and
5. Turn the patient on their side to allow secretions to drain serious adverse effects.
out of the mouth. NCLEX item type: Multiple response
Cognitive skill: Application
Objective: Identify nursing interventions during the management of
seizure activity.
19 Drugs Used for Pain Management

https://evolve.elsevier.com/Willihnganz

Objectives
1. Describe the pain assessment used for patients receiving
opiate agonists.
2. Differentiate among the properties of opiate agonists,
opiate partial agonists, and opiate antagonists.
3. Discuss the common adverse effects of opiate agonists.
4. Identify opiate antagonists and expected therapeutic
outcomes to monitor.
5. Describe the three pharmacologic effects of salicylates.
6. Compare the common and serious adverse effects and
drug interactions associated with salicylates.

Key Terms
pain experience (PĀN ĕks-PĒR-ē-ĕns)
(p. 300)
pain perception (pŭr-SĔP-shŭn)
(p. 300)
pain threshold (THRĔSH-hōld) (p. 300)
pain tolerance (TŎL-ŭr-ĕns) (p. 300)
nociception (nō-sē-SĔP-shŭn) (p. 300)
acute pain (ă-KYŪT) (p. 300)
chronic pain (KRŎN-ĭk) (p. 301)
nociceptive pain (nō-sē-SĔP-tĭv)
(p. 301)
somatic pain (sō-MĂ-tĭk) (p. 301)
visceral pain (VĬS-ŭr-ăl) (p. 301)
neuropathic pain (nyŭr-ō-PĂTH-ĭk)
(p. 301)
idiopathic pain (ĭd-ē-ō-PĂTH-ĭk)
(p. 301)
analgesics (ăn-ăl-JĒ-zĭks) (p. 301)
opiate agonists (Ō-pē-ăt ĂG-ŏ-nĭsts)
(p. 301)
opiate partial agonists (Ō-pē-ăt PĂR-
shŭl ĂG-ŏ-nĭsts) (p. 301)
opiate antagonists (Ō-pē-ăt ăn-TĂG-
ŏ-nĭsts) (p. 301)
prostaglandin inhibitors (prŏs-tă-
GLĂN-dĭn ĭn-HĬ-bĭ-tŭrz) (p. 301)
salicylates (săl-ĭ-SĬL-āts) (p. 301)
nonsteroidal antiinammatory
drugs (nŏn-stĕ-RŌY-dăl ĂN-tī-ĭn-
FLĂ-mă-tō-rē) (p. 301)
nociceptors (nō-sē-SĔP-tŭrz) (p. 301)
opiate receptors (Ō-pē-ăt rē-SĔP-
tŭrz) (p. 301)
range orders (RĀNJ ŌR-dŭrz) (p. 309)
drug tolerance (DRŬG TŎL-ŭr-ĕns)
(p. 310)
ceiling effect (SĒ-lĭng ĕ-FĔKT) (p. 316)

PAIN
The International Association for the Study of Pain
denes pain as “an unpleasant sensory and emo-
tional experience associated with actual or potential
tissue damage or described in terms of such dam-
age.” An unpleasant sensation that is part of a larger
situation is called a pain experience The pain experi-
ence is highly subjective and inuenced by behav-
ioral, physiologic, sensory, emotional (e.g., attention,
anxiety, fatigue, suggestion, prior conditioning), and
cultural factors for a particular person under a cer-
tain set of circumstances. This accounts for the wide
variation in individual responses to the sensation of
pain.
The three terms used in relationship to the pain ex-
perience are pain perception, pain threshold, and pain
tolerance. Pain perception (also known as nociception) is
an individual’s awareness of the feeling or sensation of
pain. Pain threshold is the point at which an individual
rst acknowledges or interprets a sensation as being
painful. Pain tolerance is the individual’s ability to en-
dure pain.
300
Pain has physical and emotional components.
Factors that decrease an individual’s tolerance to pain
include prolonged pain that is insufciently relieved,
fatigue accompanied by the inability to sleep, an in-
crease in anxiety or fear, unresolved anger, depression,
and isolation. Patients with severe intractable pain fear
that the pain cannot be relieved, and patients with can-
cer fear that new or increasing pain means that the can-
cer is spreading or recurring.
Pain is usually described as acute or short term and
as chronic or long term. Acute pain arises from sudden
injury to the structures of the body (e.g., skin, muscles,
viscera). The intensity of pain is usually proportional
to the extent of tissue damage. The sympathetic ner-
vous system is activated, resulting in an increase in the
heart rate, pulse, respirations, and blood pressure. This
sympathetic nervous system stimulation also causes
nausea, diaphoresis, dilated pupils, and an elevated
glucose level. Continuing or persistent pain results
from ongoing tissue damage or from chemicals re-
leased by the surrounding cells during the initial trau-
ma (e.g., a crushing injury). The intensity diminishes

as the stimulus is removed or tissue repair and healing
take place. Acute pain serves an important protective
physiologic purpose that warns of potential or actual
tissue damage.
Chronic pain has a slower onset and lasts longer than
3 months beyond the healing process. Chronic pain
does not relate to an injury or provide physiologic val-
ue. Depending on the underlying cause, it is often sub-
divided into chronic cancer or noncancer pain (persis-
tent noncancer pain). It may arise from visceral organs,
muscular and connective tissue, or neurologic factors
such as diabetic neuropathy, trigeminal neuralgia, or
amputation. As chronic pain progresses, especially
poorly treated pain, other physical and emotional fac-
tors come into play, affecting almost every aspect of a
patient’s life—physical, mental, social, nancial, and
spiritual—and causing additional stress, anger, chron-
ic fatigue, and depression. Although pain has always
been viewed as a symptom of a disease or a condition,
chronic pain and its harmful physiologic effects are
now regarded as a disease itself.
Pain may also be classied by pathophysiology.
Nociceptive pain is the result of a stimulus (e.g., chemi-
cal, thermal, mechanical) to pain receptors. Nociceptive
pain is usually described by patients as dull and ach-
ing. It is called somatic pain if it originates from the
skin, bones, joints, muscles, or connective tissue (e.g.,
arthritis pain) and visceral pain if it originates from
the abdominal and thoracic organs. Nociception is the
process whereby a person becomes aware of the pres-
ence of pain. There are four steps in nociception: (1)
transduction, (2) transmission, (3) perception, and (4)
modulation (Fig. 19.1).
Neuropathic pain results from injury to the periph-
eral or central nervous system (CNS) (e.g., trigeminal
neuralgia). Patients describe neuropathic pain as stab-
bing and burning. Phantom limb pain is a neuropathic
pain experienced by amputees in a body part that is
no longer there. Idiopathic pain is a nonspecic pain of
unknown origin. Anxiety, depression, and stress are
often associated with this type of pain. Common areas
associated with idiopathic pain are the pelvis, neck,
shoulders, abdomen, and head.
PAIN MANAGEMENT
Analgesics are drugs that relieve pain without pro-
ducing loss of consciousness or loss of reexes. The
search for an ideal analgesic continues. It is difcult to
nd one that meets this denition: it should be potent
enough to provide maximum relief of pain; it should
not cause dependence; it should cause a minimum of
adverse effects (e.g., constipation, hallucinations, re-
spiratory depression, nausea, vomiting); it should not
cause tolerance; it should act promptly and over a long
period with a minimum amount of sedation so that the
patient is able to remain conscious and responsive; and
it should be relatively inexpensive.
Drugs Used for Pain Management CHAPTER 19 301
At present, no completely satisfactory classica-
tion of analgesics is available. Historically they have
been categorized based on potency (mild, moderate,
strong), origin (opium, synthetic, coal-tar derivative),
or addictive properties (narcotic, nonnarcotic).
Research into the control of pain has recently given
new insight into pathways of pain within the nervous
system and a better understanding of precise mecha-
nisms of action of analgesic agents. The current no-
menclature for analgesics stems from these recent
discoveries. In this chapter the medications have been
divided into opiate (opioid) agonists, opiate (opioid)
partial agonists, opiate (opioid) antagonists, and pros-
taglandin inhibitors (acetaminophen, salicylates, and
nonsteroidal antiinammatory drugs [NSAIDs]). The
commonly used term “opioid” refers broadly to all
substances that bind to opiate (opioid) receptors in the
brain, including opiate agonists, opiate partial ago-
nists, and opiate antagonists. Opioids, in general, are
drugs from a variety of origins, opium (heroin, mor-
phine, codeine) or synthetic (meperidine, fentanyl),
with varying degrees of analgesic potency, euphoric
effect, and addictive properties.
ACTIONS
The pathways of the pain transmission signal from
the site of injury to the brain for processing and re-
exive action have not been fully identied. The rst
step leading to the sensation of pain is the stimula-
tion of receptors known as nociceptors (see Fig.
19.1). These nerve endings are found in skin, blood
vessels, joints, subcutaneous tissues, periosteum,
viscera, and other tissues. The nociceptors are clas-
sied as thermal, chemical, and mechanical-thermal,
based on the types of sensations that they transmit.
The exact mechanism that causes stimulation of no-
ciceptors is not fully understood; however, brady-
kinins, prostaglandins, leukotrienes, histamine, and
serotonin sensitize these receptors. Receptor activa-
tion leads to action potentials that are transmitted
along afferent nerve bers to the spinal cord. A series
of neurotransmitters (somatostatin, cholecystokinin,
substance P) play roles in the transmission of nerve
impulses from the site of damage to the spinal cord.
Within the CNS, there may be at least four pain-trans-
mitting pathways up the spinal cord to various areas
of the brain for response.
The CNS contains a series of receptors that control
pain. These are known as opiate receptors because
stimulation of these receptors by the opiates blocks
the pain sensation. These receptors are subdivided
into four types: mu (μ), delta (δ), kappa (κ), and epsi-
lon (ε) receptors. Sigma (σ) receptors are another type
that react to opioid agonists and partial agonists. The
receptors are located in different areas of the CNS.
The κ receptors are found in greatest concentration in
the cerebral cortex and in the substantia gelatinosa of
the dorsal horn of the spinal cord. They are responsible
302 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems

1 Transduction
1. Noxious stimuli causes cell damage with
the release of sensitizing chemicals
• Prostaglandins
• Bradykinin
• Serotonin
• Substance P
• Histamine
2. These substances activate nociceptors 3 3 Perception
and lead to generation of action potential
Conscious experience of pain

Mod
1 Site of pain

ulati
2

on
Transmission 4

2 Transmission 4 Modulation
Action potential continues from • Neurons originating in the brainstem
• Site of injury to spinal cord descend to the spinal cord and release
• Spinal cord to brainstem and thalamus substances (e.g., endogenous opioids)
• Thalamus to cortex for processing that inhibit nociceptive impulses

Fig. 19.1 Nociceptive pain originates when the tissue is injured. 1, Transduction occurs when there is release of chemical
mediators. 2, Transmission involves the conduction of the action potential from the periphery (injury site) to the spinal
cord and then to the brainstem, thalamus, and cerebral cortex. 3, Perception is the conscious awareness of pain. 4,
Modulation involves signals from the brain going back down the spinal cord to modify incoming impulses. (Developed
by M. McCaffery, C. Pasero, and J. A. Paice. From McCaffery M, Pasero C. Pain: Clinical Manual. 2nd ed. St. Louis:
Mosby; 1999.)

for analgesia at the levels of the spinal cord and brain.
Stimulation of κ receptors also produces sedation and
dysphoria. The μ receptors are located in the pain-
modulating centers of the CNS and induce central an-
algesia, euphoria, physical dependence, miosis, and
respiratory depression. The σ receptors are located
in the limbic area of the brain and in the spinal cord
and may play a role in the euphoria produced by se-
lected opiates. The σ receptors are thought to produce
the autonomic stimulation and psychotomimetic (e.g.,
hallucinations) and dysphoric effects of some opiate
agonists and partial agonists. The functions of the σ
receptors are under investigation. Research is focusing
on developing synthetic chemicals that target specic
receptors to maximize analgesia but minimize the po-
tential for adverse effects, such as addiction.
As described, other chemicals—histamine, pros-
taglandins, serotonin, leukotrienes, substance P, and
bradykinins—released during trauma also contribute
to pain. Developing pharmaceuticals that block these
chemicals is another effective way of stopping pain.
Antihistamines (e.g., diphenhydramine), prostaglan-
din inhibitors (e.g., NSAIDs), substance P antagonists
(e.g., capsaicin), and antidepressants that prolong nor-
epinephrine and serotonin activity (e.g., tricyclic anti-
depressants, selective serotonin reuptake inhibitors)
have analgesic properties.
Other pharmacologic agents can suppress pain by
a variety of mechanisms. Adrenergic agents, such as
norepinephrine and clonidine, and gamma-amino-
butyric acid receptor stimulants (e.g., baclofen, ga-
bapentin) produce signicant analgesia by blocking
nociceptor activity. Gabapentin, pregabalin, and car-
bamazepine act as analgesics by suppressing spon-
taneous neuronal ring, as occurs in trigeminal neu-
ralgia. Tricyclic antidepressants inhibit the reuptake
of serotonin and norepinephrine, causing the onset of
analgesia to be more rapid, as well as improving the
outlook of the person with chronic pain and depres-
sion. Some antidepressants (e.g., amitriptyline) also
block pain by antihistaminic and anticholinergic ac-
tivity. Bisphosphonates (e.g., zoledronic acid) may be
effective in treating cancer pain associated with bony
metastases.
USES
The World Health Organization recommends a step-
wise approach to pain management in relation to
cancer pain (Fig. 19.2). Mild acute pain is effectively
treated with analgesics such as aspirin, NSAIDs, or
acetaminophen. Pain associated with inammation
responds well to NSAIDs. Unrelieved or moderate
pain is generally treated with a moderate-potency
opiate such as codeine or oxycodone, which is often
used in combination with acetaminophen or aspirin
(Tylenol with Codeine No. 3 and Percodan, respective-
ly). Severe acute pain is treated with opiate agonists
(e.g., morphine, hydromorphone). Morphine sulfate is

Freedom from
cancer pain
Opioid for moderate 3 risks to health and wellness through debilitation and
to severe pain
Nonopioid
 Adjuvant
Pain persisting or
increasing 2 2018 (69.5% of all drug overdose deaths). Two out of
Opioid for mild to moderate pain
 Nonopioid
 Adjuvant
Pain persisting or 1
increasing
Nonopioid
 Adjuvant
Fig. 19.2 World Health Organization’s Pain Relief Ladder. (Adapted
from World Health Organization, 2005. Retrieved from http://www.who
.int/cancer/palliative/painladder/en.)
usually the drug of choice for the treatment of severe
chronic pain. Other agents such as antidepressants or
anticonvulsants may be used as adjunctive therapy
with analgesics, depending on the causes of pain.
The healthcare delivery system in the United States
has an unfortunate, long-standing history of inade-
quate pain management. The Joint Commission’s cur-
rent standards for pain management therapy include
the following primary therapeutic outcomes:
1. Relief of pain intensity and duration of pain
complaint
2. Prevention of the conversion of persistent pain to
chronic pain
3. Prevention of suffering and disability associated
with pain
4. Prevention of psychological and socioeconomic
consequences associated with inadequate pain
management
5. Control of adverse effects associated with pain
management
6. Optimization of the ability to perform activities of
daily living (ADLs)
Although considered acceptable at one time, pla-
cebo therapy should never be used with pain man-
agement. One premise of pain management is that
the patient should be believed when describing the
presence of pain. The use of placebos implies a lack
of belief in the patient’s description and can seri-
ously damage the patient-provider relationship. The
American Pain Society has declared that the use of
placebos is unethical and should be avoided.
A Note About Opioid Abuse
Opioids are commonly prescribed for pain. Evidence
supports short-term efcacy (12 weeks or less) of opi-
oid treatment for pain management. However, few
studies have been conducted to assess the long-term
Drugs Used for Pain Management CHAPTER 19 303
benets of opioids for chronic pain (pain lasting great-
er than 12 weeks) with outcomes examined at least 1
year later. Opioid pain medications present serious
the potential for death from overdose. The Centers for
Disease Control and Prevention (CDC) reported that
opioids were involved in 46,802 overdose deaths in
three (67.0%) opioid-involved overdose deaths involve
synthetic opioids (fentanyl or fentanyl analogs).
The CDC (Dowell etal, 2016) and Canada health au-
thorities (Busse et al, 2017) have published guidelines
for prescribing opioids for chronic noncancer pain. Both
recommend nonpharmacologic therapy and nonopioid
pharmacologic therapy for chronic pain. Opioids should
only be considered if expected benets for pain manage-
ment and function are anticipated to outweigh risks to
the health of the patient. If opioids are prescribed, they
should be combined with nonpharmacologic therapy
and nonopioid pharmacologic therapy (see Chapter 48).
NURSING IMPLICATIONS FOR PAIN
MANAGEMENT
The management of all types of pain is a major health-
care concern. Rating pain as the fth vital sign means
that the patient’s pain should be assessed every time vi-
tal signs are taken and recorded. Taking the pain rating
only when doing vital signs, however, is not sufcient.
The nurse should also evaluate the pain level immedi-
ately before and after pain medications are given; at 1-,
2-, and 3-hour intervals for oral medications; and at 15-
to 30-minute intervals after parenteral administration.
Most assessment data sheets have a section on pain
management that contains the following elements: rat-
ing before and after medication, nonpharmacologic
measures initiated, patient teaching performed, and
breakthrough pain measures implemented. The pain
ow sheet provides the healthcare team members with
a quick visual reference to evaluate the overall effec-
tiveness of the pain management prescribed.
The American Pain Foundation (now defunct) de-
veloped the Pain Care Bill of Rights, which explains to
the patient exactly what to expect and/or demand in
the way of pain management (Box 19.1).
Nurses must assist the patient in managing pain.
The rst important step in this process is to believe
the patient’s description of the pain. Pain brings with
it a variety of feelings, such as anxiety, anger, loneli-
ness, frustration, and depression. Part of the patient’s
response is tied to past experiences, sociocultural fac-
tors, current emotional state, and beliefs regarding
pain.
Psychological, physical, and environmental fac-
tors all must be considered in managing pain. Never
overlook the value of general comfort measures such
as a back rub, repositioning, and the use of hot or
cold applications. A variety of relaxation techniques
and diversional activities may prove psychologically
304 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
Box 19.1 Pain Care Bill of Rights
As a person with pain, you have the right to:
• Have your pain taken seriously and to be treated with
dignity and respect by doctors, nurses, pharmacists,
and other healthcare professionals.
• Have your pain thoroughly assessed and promptly
treated.
• Be informed by your healthcare provider about the
possible causes of your pain, and possible treatments,
including the benets, risks, and costs of each.
• Participate actively in decisions about how to manage
your pain.
• Have your pain reassessed regularly and your
treatment adjusted if your pain has not been eased.
• Be referred to a pain specialist if your pain persists.
• Get clear and prompt answers to your questions, take
time to make decisions, and refuse a particular type of
treatment if you choose.
Created by the American Pain Foundation (now defunct). Retrieved from
https://masspaininitiative.org/
benecial. Decreasing environmental stimuli to ensure
the patient gets successful periods of rest is essential.
The patient’s pain must be evaluated in a consistent
manner. A wide variety of assessment tools have been
developed to enable healthcare providers to gain some
degree of uniformity in interpreting and recording the
patient’s description of pain. Some of the pain assess-
ment tools for use with infants and young children in-
clude the following:
• Riley Infant Pain Scale (RIPS) Assessment Tool
• Face, Legs, Activity, Cry, Consolability (FLACC)
Scale, for use in nonverbal patients
• Pain Observation Scale for Young Children (POCIS),
intended for children 1 to 4 years of age
• Modied Objective Pain Score (MOPS), intended
for children 1 to 4 years of age after ear, nose, and
throat surgery
• Toddler-Preschooler Postoperative Pain Scale
(TPPPS), for use in evaluating pain in smaller chil-
dren during and after medical or surgical procedures
• Postoperative Pain Score (POPS), for infants having
surgical procedures
• Neonatal Infant Pain Scale (NIPS), for pain in pre-
term and full-term neonates; used to monitor pain
before, during, and after a painful procedure
The list of tools available is extensive, and the preced-
ing is only a partial listing. For further information on
pain scales and details of each, search the Internet to
nd the data needed.
The Wong-Baker FACES pain rating scale (Fig. 19.3)
has widespread use for patients 3 years of age and
older and is particularly useful for adults who have
language barriers or who do not read because they can
select the face that best describes their pain.
The McGill-Melzack Pain Questionnaire provides
descriptive words and phrases that may be used to
help the patient communicate the subjective pain
experience (Fig. 19.4). It is especially useful for individ-
uals who have chronic pain. When possible, chart the
description in the patient’s exact words. It may be nec-
essary to seek additional data from signicant others.
Scales such as the ones shown in Fig. 19.5 are often
used to assess acute pain. The most common scale used
asks the patient to rate the pain being experienced on a
scale of 0 (no pain) to 10 (intense or excruciating). The
degree of relief for the pain after an analgesic is given
is again rated using the same 0-to-10 scale. When dif-
ferent potencies of analgesic agents are ordered for the
same patient, the nurse can use these numerical rating
data in combination with the other data gathered to de-
termine whether a more or less potent analgesic agent
should be administered. The color scale is similar to a
slide rule. The patient selects the hue or depth of color
that corresponds with the pain being experienced. The
nurse turns the slide rule scale over, and a numerical
value is identied that can be used to consistently re-
cord the patient’s response.
Effective pain control depends on the degree of pain
experienced. The previously described 0-to-10 scale is
a useful way to determine the patient’s level of pain.
For a patient with mild to moderate acute pain, a non-
narcotic agent may be successful, but a patient with
severe chronic pain may need a potent analgesic such
as morphine. The route of administration is chosen on
the basis of several factors. One major consideration is
how soon the action of the drug is needed. The oral and
rectal routes have a longer onset of action than the par-
enteral route. It is sometimes erroneously believed that
oral medications are inadequate to treat pain, but they
can provide excellent pain relief if appropriate doses
are provided. Generally the oral route is used initially
to treat pain if no nausea and vomiting are present. The
patient may initially be treated effectively with oral
medications; however, the rectal, transdermal, subcu-
taneous, intramuscular, intraspinal, epidural, and in-
travenous (IV) routes may be required, depending on
the patient and the course of the underlying disease.
Clinical Pitfall
All patients have a right to adequate management of pain.
To help ensure appropriate analgesia, the rating of pain has
been designated “the fth vital sign.” From a nursing stand-
point, this means that pain should be assessed every time
the vital signs are taken and recorded. Nurses should also
evaluate the pain level immediately before administering a
pain medication and afterward at 1-, 2-, and 3-hour inter-
vals for oral medications and at 15- to 30-minute intervals
after parenteral administration. Although pain assessment
forms vary, the elements contained in each collect similar
information about pain: rating before and after medication,
nonpharmacologic measures initiated, patient teaching per-
formed, and breakthrough pain measures implemented. The
pain ow sheet provides the healthcare team members with
a quick visual reference to evaluate the overall effectiveness
of the pain management prescribed.

0 1 2 3
No hurt Hurts Hurts
little bit little more
Fig. 19.3 Wong-Baker FACES pain rating scale. (From Hockenberry MJ, Wilson D. Wong’s Nursing Care of Infants and
Children. 10th ed. St. Louis: Mosby; 2015.)
Life Span Considerations
Analgesics
Maintaining a relatively steady blood level of analgesic is the
best way to control pain. However, drug absorption, me-
tabolism, and excretion are affected by the patient’s age.
Dosages and frequency of administration of analgesics may
have to be increased in children, especially teenagers, be-
cause many medicines are more rapidly metabolized and
excreted by patients in this age group. Conversely, an older
adult may need a somewhat smaller dose of an analgesic
given less frequently because of slower metabolism and
excretion. In either situation, it is imperative that the nurse
regularly assess the patient’s pain level and contact the
healthcare provider for adjustments in dosages and frequen-
cy based on the response to the analgesic.
Before initiating a pain assessment, assess the pa-
tient for hearing and visual impairment. If the person
is unable to hear the questions or see the visual aids
used to assess pain, any data collected may be invalid.
Nurses must evaluate and document the effective-
ness of the pain medications given in the patient’s
medical record. Record and report all complaints of
pain for analysis by the healthcare provider. The pat-
tern of pain, particularly an increase in frequency or
severity, may indicate new causes of pain. The main
reasons for increased frequency or intensity of pain are
pain from long-term immobility; pain from the treat-
ment modalities used (e.g., surgery, chemotherapy,
or radiation therapy); pain from direct extension of a
tumor or metastasis into bone, nerve, or viscera; and
pain unrelated to the original cause or the therapeutic
treatments used.
Assessment
History of pain experience
• Medication history: What medications are being
prescribed, and how effective have they been?
What dosage has been required to achieve ad-
equate comfort? Has the patient had any adverse
effects to the medications? If yes, get details of the
adverse effects and the measures taken for man-
agement. What is the patient’s attitude toward the
use of pain medications (e.g., opioids, anxiolyt-
ics)? What are the family’s or signicant other’s
attitudes toward the use of medications to control
the pain? Does the patient have any history of sub-
stance abuse?
Drugs Used for Pain Management CHAPTER 19 305
4 5
Hurts Hurts Hurts
even more whole lot worst
• Patient’s perception of pain: To identify the causes of
the pain, have the patient describe their perception
of it. What does the patient feel is the cause of the
pain? In the older adult, multiple chronic and acute
pain problems may be present, making it difcult
to determine which problem is the most urgent or
causing the most pain. Multiple pain complaints,
combined with impaired hearing, vision, memory,
and cognition, must be taken into consideration
during the pain assessment. Evaluate the pain ac-
cording to location, depth, quality, duration, and
severity.
• Obtain baseline vital signs at least every shift or
more often as dictated by the patient’s condition
and type of medications administered.
• Listen to the patient and believe the pain experience
being described, regardless of whether the physi-
cal data substantiate the degree of discomfort de-
scribed. Do not let personal biases or values interfere
with establishing interventions that provide maxi-
mum pain relief for the individual. The myths that
pain decreases with aging and that pain is expected
with aging are incorrect!
• Onset: When was the pain rst noticed? When was
the most recent attack? Is the onset slow or abrupt?
Is there any particular activity that starts the pain?
Does the pain occur in response to eating certain
foods?
• Location: What is the exact location of the pain? It may
help to have the patient mark on a drawing of a hu-
man gure the areas where the pain is felt; this may
be especially useful with pediatric patients, who can
be given crayons to help identify different intensities
in addition to the location. With acute pain, the site
of the pain can be more easily identied; however,
with chronic pain, this may be more difcult because
the normal physiologic responses of the sympathetic
nervous system are no longer present.
• Depth: What is the depth of the pain? Does it radi-
ate, having the sensation of spreading out or diffus-
ing over an area, or is it localized in a specic site?
The lack of physical symptoms comparable with the
pain described does not mean that the patient’s com-
plaints should be ignored.
• Quality: What is the actual sensation felt when the
pain is present: stabbing, dull, cramping, sore, burn-
ing, or other? Is the pain always in the same place
and of the same intensity?
306 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems

McGill-Melzack Part 2. What Does Your Pain Feel Like?

Pain Questionnaire Some of the words below describe your present pain. Circle
Patient’s name __________________ Age ___________________ ONLY those words that best describe it. Leave out any category
File No. ________________________ Date __________________ that is not suitable. Use only a single word in each appropriate
Clinical category (e.g., cardiac, neurologic) category—the one that best applies.
Diagnosis: ______________
________________ 1 6 11 16
________________ Flickering Tugging Tiring Annoying
Analgesic (if already administered): Quivering Pulling Exhausting Troublesome
1. Type _____________________________________________ Pulsing Wrenching 12 Miserable
2. Dosage __________________________________________ Throbbing 7 Sickening Intense
3. Time given in relation to this test ___________________ Beating Hot Suffocating Unbearable
Patient’s intelligence: circle number that represents best Pounding Burning 13 17
estimate. 2 Scalding Fearful Spreading
Jumping Searing Frightful Radiating
1 (low) 2 3 4 5 (high) Flashing 8 Terrifying Penetrating
Shooting Tingling 14 Piercing
This questionnaire has been designed to tell us more about 3 Itchy Punishing 18
your pain. Four major questions we ask are: Pricking Smarting Grueling Tight
Boring Stinging Cruel Numb
1. Where is your pain? Drilling 9 Vicious Drawing
2. What does it feel like? Stabbing Dull Killing Squeezing
3. How does it change with time? Lancinating Sore 15 Tearing
4. How strong is it? 4 Hurting Wretched 19
It is important that you tell us how your pain feels now. Please Sharp Aching Blinding Cool
follow the instructions at the beginning of each part. Cutting Heavy Cold
Lacerating 10 Freezing
5 Tender 20
Pinching Taut Nagging
Part 1. Where Is Your Pain? Pressing Rasping Nauseating
Please mark on the drawing below the areas where you feel Gnawing Splitting Agonizing
pain. Put E if external, or I if internal, near the areas you mark. Cramping Dreadful
Put EI if both external and internal. Crushing Torturing

Part 3. How Does Your Pain Change with Time?

1. Which word or words would you use to describe the
pattern of your pain?
1 2 3
Continuous Rhythmic Brief
Steady Periodic Momentary
Constant Intermittent Transient
2. What kind of things relieve your pain?

3. What kind of things increase your pain?

Part 4. How Strong Is Your Pain?

People agree that the following 5 words represent pain of in-
creasing intensity. They are:
1 2 3 4 5
Mild Discomforting Distressing Horrible Excruciating
To answer each question below, write the number of the
most appropriate word in the space beside the question.
1. Which word describes your pain right now? ______
2. Which word describes it at its worst? ______
3. Which word describes it when it is least? ______
4. Which word describes the worst toothache you
ever had? ______
5. Which word describes the worst headache you
ever had? ______
6. Which word describes the worst stomachache
you ever had? ______

Fig. 19.4 McGill-Melzack Pain Questionnaire. (Copyright R. Melzack, 1970, 1975. Reprinted with permission from Dr.
Melzack and Mapi Trust.)
 Drugs Used for Pain Management CHAPTER 19 307

A PAIN INTENSITY SCALES

Simple Descriptive Pain Distress Scale1

None Annoying Uncomfortable Dreadful Horrible Agonizing

0-10 Numeric Pain Distress Scale1

Distressing
No pain pain Unbearable pain
0 1 2 3 4 5 6 7 8 9 10

Visual Analog Scale (VAS)2

No Unbearable
distress distress

B PAIN RELIEF SCALES

Pain Relief Visual Analog Scale

No relief Complete
relief
C Percent Relief Scale

0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%
No relief Complete
relief

1If used as a graphic rating scale, a 10-cm baseline is recommended.

2A 10-cm baseline is recommended for VAS scales.
Fig. 19.5 Pain rating scales. (A) Pain intensity scales. (B and C) Pain relief scales. (From Ignatavicius DD. Pain: the fth
vital sign. In Ignatavicius DD, Workman ML. Medical-Surgical Nursing: Patient-Centered Collaborative Care. 7th ed. St.
Louis: Saunders; 2013:48. A, Redrawn from Agency for Health Care Policy and Research. Acute Pain Management:
Operative or Medical Procedures and Trauma. AHCPR Publ. No. 92-0032. Rockville, MD: US Department of Health and
Human Services; 1992. B, Redrawn from Fishman B etal. The Memorial Pain Assessment Card: A valid instrument for
the evaluation of cancer pain. Cancer. 1987;60(5):1151–1158. C, Redrawn from the Pain Research Group. Brief Pain
Inventory. Madison, WI: Department of Neurology, University of Wisconsin–Madison.)

• Duration: Is the pain continuous or intermittent?
How often does it occur and, once felt, how long
does it persist? Is there a cyclic pattern to the pain?
• Severity: Have the patient rate the pain using the
pain scale methodology that is standard for the
clinical setting. Self-reporting pain assessment tools
are used for most children 3 years and older. After
age 8, children understand numerical values, so one
of the visual analog scales or word-graphic rating
scales can be used.
Nonverbal observations . Note the patient’s general
body position during an episode of pain. Look for
subtle clues such as facial grimaces, immobility of a
particular part, and holding or resisting movement
of an extremity. With pediatric patients, facial expres-
sions, squinting, grimacing, and crying may also be
used as indicators of pain level and pain relief.
Developmental differences inuence the pain ex-
perience and how children in different age groups ex-
press pain. Infants may express pain through continual
inconsolable crying, irritability, poor oral intake, and
alterations in sleep pattern. Preschool children may
verbalize pain; exhibit lack of cooperation; be “clingy”
to parents, nurses, or signicant others; and not want
the site of the pain touched—they may actually push
308 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
you away as you approach the painful area. Older chil-
dren may deny pain in the presence of peers and dis-
play regressive behaviors in the presence of support
personnel.
Pain relief. What specic measures relieve the pain?
What has already been tried for pain relief, and what,
if anything, has been benecial?
Physical data. In the presence of pain, always exam-
ine the affected part for any alterations in appearance,
change in sensation, or limitation in mobility or range
of motion. In older adults, it is particularly important
to evaluate the musculoskeletal and neurologic sys-
tems during the physical examination.
Behavioral responses. What coping mechanisms does
the patient use to manage the pain experience: cry-
ing, anger, withdrawal, depression, anxiety, fear, or
hopelessness? Is the individual introspective and self-
focusing? Does the individual continue to perform
ADLs despite the pain? Does the individual alter life-
style patterns appropriately to enhance pain relief
measures prescribed? Is the individual able to continue
to work? Is the individual socially withdrawn? Is the
person seeing more than one healthcare provider to try
to obtain an answer about the origin of the pain or to
obtain more pain medication from a different health-
care provider?
Life Span Considerations
Pain in the Older Adult Patient
Pain assessment in the older adult patient must include more
than a simple rating of pain using a pain scale. Many older
adults suffer from more than one chronic illness, so obtain
a nursing history and perform a physical and functional as-
sessment to understand the effect of pain on the patient’s
ability to meet self-care needs.
Implementation
Comfort measures
• Provide for the patient’s basic hygiene and comfort.
Use techniques such as back rubs, massage, or hot
and cold applications as ordered.
• Ask the patient what measures have been successful
in the past in providing pain relief.
• Relieve pain by doing any or all of the following,
as appropriate: (1) support an affected part during
movement, provide appropriate assistance during
movement or activities, or apply binders or splint an
incisional area before initiating activities such as deep
breathing and coughing; (2) give analgesics before
starting painful activities and plan for the activity to
take place during the medication’s peak action; and/
or (3) use hot or cold applications, massage, pressure,
and vibration as interventions for pain relief.
Exercise and activity. Unless contraindicated, moder-
ate exercise should be encouraged. Often, pain causes
the individual not to move the affected part or to posi-
tion it in a manner that provides relief. Stress the need
to prevent complications by using passive range of
motion.
Regularly scheduled exercise is important to pre-
vent further deterioration of the musculoskeletal sys-
tem, especially in older patients who may also have
diminished capacity.
Nonpharmacologic approaches . To enhance the ef-
fects of the medication therapy, use nonpharmacologic
strategies such as relaxation techniques, visualization,
meditation, biofeedback, and transcutaneous electri-
cal nerve stimulation (TENS) units. (The patient will
require instruction for using each of these prescribed
techniques.) Assist with referral to a pain clinic for
management of pain, especially chronic pain.
Goals should be established when initiating a treat-
ment regimen. Prevention, reduction, or elimination
of pain is an important therapeutic goal. The patient
and caregiver(s) should be involved in the establish-
ment of these goals so that outcomes important to the
patient are incorporated into the treatment goals and
so that they have realistic expectations. Pain, espe-
cially chronic pain, may not be completely eliminated
but must be managed. Additional important goals
include improving the patient’s quality of life, func-
tional capacity, and ability to retain independence.
Specic therapeutic goals established may include
the following:
• Pain at rest: <3 on pain scale
• Pain with movement: <5 on pain scale
• Able to have at least 6 hours of sleep uninterrupted
by pain
• Able to work at a hobby (e.g., doing crafts, playing
cards, gardening) for 1 hour
Medication. Even though pain medicine administra-
tion may be scheduled, encourage the patient to re-
quest pain medication before the pain escalates and
becomes severe. Encourage open communication be-
tween the patient and the healthcare team regarding
the effectiveness of the medications used. Although the
smallest dose possible to control the pain is the goal of
therapy, it is also important that the dose be sufcient
to provide adequate relief. Therefore the patient must
understand the importance of expressing the degree
of relief being obtained so that appropriate dosage ad-
justments can be made.
The medication prole may list more than one anal-
gesic order for the same patient. This requires the nurse
to use judgment in choosing the correct medication for
the patient based on pain assessment data collected.
The nurse must identify when the last dose of pain
medication was administered by checking the patient’s

medication administration record. It is common prac-
tice for analgesics to be ordered intermittently on an
“as-needed” (PRN) basis. Many clinical institutions
have established policies for pain medications ordered
on a PRN basis, referred to as range orders. Medication
range order policies provide guidelines for the clinical
staff to interpret the PRN ranges using the pain scale
assessment as a guideline. However, in the case of
chronic pain or intractable pain, it has been found that
administering analgesics around the clock, such as ev-
ery 3 to 4 hours, will maintain a more constant plasma
level of the drug (steady state), resulting in more effec-
tive analgesia.
Patient-controlled analgesia (PCA) has gained ac-
ceptance in both the inpatient and ambulatory set-
tings. Pumps are available for inpatient use and in
ambulatory units for home or nursing home settings.
The PCA method of administration allows the patient
to control a small infusion pump containing an opi-
ate agonist, usually morphine or fentanyl, which is
connected to an indwelling IV catheter. When ini-
tiating the PCA pump procedure, a loading dose is
often given to gain rapid blood levels necessary for
analgesia. The patient then receives a slow continu-
ous infusion from the infusion pump; this is referred
to as a basal rate. Depending on the activity level and
level of analgesia needed, the patient may push a but-
ton, self-administering a small bolus of analgesic to
meet their immediate need. A timing device on the
pump limits the amount and frequency of the dose
that can be self-administered per hour. This approach
allows the patient to have some control over the pain
relief and eliminates the need for the patient to wait
for a nurse to answer the call light, check the last dose
of analgesics given, and prepare and administer the
medication. When PCA is used, the nurse should ex-
plain the use of the PCA pump to the patient and ob-
serve the patient using it to validate understanding.
Education includes allowing only the patient to use
the control device, not the family. The degree of pain
relief achieved should always be recorded. When
pain relief is inadequate, assess for other causes and
contact the prescriber to discuss a modication of the
regimen.
PCA pumps are also used for chronic pain; howev-
er, the dose can be delivered intravenously or subcu-
taneously. For chronic pain treatment, the largest dose
of the medication is given continuously with demand.
Continuous subcutaneous opioid analgesia uses either
a buttery-type (25- to 27-gauge) needle or a special
needle device placed subcutaneously into the subcla-
vicular tissue or in the abdomen.
Epidural analgesia has long been used in obstet-
rics but is now recognized as an effective means for
controlling acute pain in a variety of postoperative
procedures. Epidural analgesia most commonly deliv-
ers morphine or fentanyl (sometimes combined with
bupivacaine) into the subarachnoid space. It can be
Drugs Used for Pain Management CHAPTER 19 309
administered continuously with an infusion pump,
intermittently by bolus administration, or via an im-
planted port. Nursing responsibilities during epidural
analgesia involve the following:
• Check institutional policies for qualications need-
ed to administer and monitor the epidural analgesia.
• Use assessment tools to determine the degree of pain
relief and assess the respiratory function, neurologic
function, degree of sedation, and catheter status.
• Observe for narcotic-related adverse effects (i.e., re-
spiratory depression, nausea and vomiting, pruri-
tus, headaches) and catheter-related complications.
Always have drugs and supplies in the immediate
area to reverse a drug overdose.
Transdermal opioid analgesia uses fentanyl
(Duragesic) or buprenorphine (Butrans) for relief of
chronic pain. Fentanyl takes approximately 12 to 24
hours for the initial patch of medication to reach a
steady blood level, so other analgesics must be used
during this time. Once placed, the patch provides relief
for up to 72 hours. Intermittent “rescue” dosing may
still be needed during patch use. When the patch is ter-
minated, the patient still needs to be monitored for an
additional 24 hours because the drug may still be pres-
ent in body tissues.
Buprenorphine takes approximately 3 days for
the initial patch of medication to reach a steady
blood level, so other analgesics must be used dur-
ing this time. Once placed, the patch provides relief
for 7 days. Intermittent “rescue” dosing may still be
needed during patch use. When the patch is to be ter-
minated, it should be gradually tapered over several
weeks preferably under the care of a pain manage-
ment specialist.
Pain control. Some patients will not ask for pain medi-
cation, so it is important to intervene and anticipate
their needs. Ask the patient at what pain level is being
perceived and then treat as appropriate.
Nutritional aspects. The patient should eat a well-
balanced diet high in B-complex vitamins and limit
or eliminate sugar, nicotine, caffeine, and alcohol in-
take. Drinking 8 to 10 eight-ounce glasses of water
daily helps maintain normal elimination patterns.
To minimize or avoid the constipating effects of opi-
ates, the patient should increase intake of fiber and
fluids. If long-term use of opiates is planned, stool
softeners may be necessary.
Patient Education
Teach the patient, family, and signicant others the
benets of adequate pain control. Work with them to
determine their perception of pain management, use
of drug therapy, and nonpharmacologic approaches to
pain management. If the patient is hesitant about these
approaches, determine why. Stress that physical de-
pendence is not a major factor with short-term use of
310 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
analgesics and that during long-term use, such as with
cancer, it is not the primary concern.
The major issues involved with long-term use of
analgesics include obtaining sufcient pain control to
provide comfort, ensuring that the patient has ample
rest, and enhancing the patient’s quality of life.
Inform the patient what medications are available
for pain control and when and how to request them.
Discuss the patient’s expectations of pain manage-
ment and how to rate the severity of pain honestly
so that expectations can be met. Ask what level of
exercise is attainable without severe pain. Is the pain
control adequate for the individual to maintain ADLs
or work?
Assist the patient to learn to cope effectively with
the pain. Discuss changes in lifestyle needed to sup-
port adequate pain control. Include family members
in discussions of pain management. Give praise when
techniques are attempted, regardless of whether suc-
cess is achieved.
Teach the patient how to self-administer the analge-
sics ordered on an outpatient basis. This will include
transdermal, transmucosal, oral, and rectal routes of
administration and care of infusion ports and central
lines. Record the degree of understanding of the pre-
scribed pain regimen.
Include social services information in the patient
education process, especially how to connect with
community resources available for the patient and
family. Make sure that the patient and family under-
stand how to obtain assistance with pain medication
administration and patient care needs (e.g., visiting
nurse, hospice).
Fostering health maintenance . Throughout the course
of treatment, discuss medication information and
how it will benet the patient. Drug therapy for the
management of pain should be coupled with comfort
measures, relaxation techniques, meditation, stress
management, and meeting the total care needs of the
individual to ensure maintenance of ADLs. Provide
the patient and signicant others with important infor-
mation contained in the specic drug monograph for
the medicines prescribed. Additional health teaching
and nursing interventions for adverse effects are de-
scribed in the drug monographs that follow.
Seek cooperation and understanding of the follow-
ing points so that medication adherence is increased:
name of medications; dosage, route, and times of
administration; and common and serious adverse
effects.
Patient self-assessment. Enlist the patient’s aid in de-
veloping and maintaining a written record of moni-
toring parameters (e.g., frequency of pain attacks,
activity performed when pain occurs, techniques
used to control pain, degree of pain relief, exercise
tolerance). See the Patient Self-Assessment Form
for Analgesics on the Evolve website. Complete the
Premedication Data column for use as a baseline to
track response to drug therapy. Ensure that the pa-
tient understands how to use the form and instruct
the patient to bring the completed form to follow-up
visits. During follow-up visits, focus on issues that
will foster adherence with the therapeutic interven-
tions prescribed.
DRUG CLASS: OPIATE AGONISTS
The term opiate was once used to refer to drugs derived
from opium, such as heroin and morphine. It has been
found that many other analgesics not related to mor-
phine act at the same sites within the brain. It is now
understood that opiate agonists and opiate antagonists
act at the same site as morphine to stimulate analgesic
effects (opiate agonists) or block the effects of opiate
agonists (opiate antagonists).
Another outdated term is narcotic. Originally, it re-
ferred to medications that induced a stupor or sleep.
The Harrison Narcotic Act of 1914, which placed
morphine-like products under governmental control,
helped promote this association. The development
of analgesics that are as potent as morphine but do
not have its sedative or addictive properties makes
the word narcotic outdated; the terms opiate agonists
and opiate partial agonists should be used where
appropriate.
Actions
Opiate agonists are a group of naturally occurring and
synthetic substances that have the capability to relieve
severe pain without the loss of consciousness. They act
by stimulating the opiate receptors in the CNS. Most
of these agents also produce physical dependence and
are thus considered controlled substances under the
federal Controlled Substances Act of 1970.
These agents can be subdivided into four groups:
morphine and morphine-like derivatives, meperi-
dine-like derivatives, methadone-like derivatives,
and an “other” category (Table 19.1). Administration
of these agents causes primary effects on the CNS
(e.g., analgesia, suppression of the cough reex, re-
spiratory depression, drowsiness, sedation, mental
clouding, euphoria, nausea and vomiting); there are
also signicant effects on the cardiovascular system,
gastrointestinal (GI) system, endocrine system, and
urinary tracts.
With continued, prolonged use, opiate agonists
may produce tolerance and psychological and physi-
cal dependence. Drug tolerance occurs when a pa-
tient requires increases in dosing to receive the same
analgesic relief. Development of tolerance seems to
depend on the extent and duration of CNS depres-
sion. Patients who have prolonged depression by the
continued use of opiate agonists have a higher in-
cidence of developing tolerance. Patients who have

developed tolerance to one opiate agonist usually
require increased dosages of all opiate agonists to
achieve the desired effect.
Patients who are physically dependent on opiate
agonists remain asymptomatic as long as they are
able to maintain their daily opiate agonist require-
ment. Physical dependence may develop after 3 to 6
weeks of continual use of the opiate agonists if used
for recreational purposes. Physical dependence after
the use of opiates agonists for acute pain management
is infrequent, but addiction has been reported after
short courses of opiate agonist therapy. Early signs of
withdrawal are restlessness, perspiration, gooseesh,
lacrimation, runny nose, and mydriasis. Over the next
24 hours, these symptoms intensify, and the patient
develops muscular spasms; severe aches in the back,
abdomen, and legs; abdominal and muscle cramps;
hot and cold ashes; insomnia; nausea, vomiting, and
diarrhea; severe sneezing; and increases in body tem-
perature, blood pressure, and respiratory and heart
rates. These symptoms reach a peak at 36 to 72 hours
after discontinuation of the medication and disappear
over the next 5 to 14 days.
Uses
Opiate agonists are used to relieve acute or chronic
moderate to severe pain such as that associated with
acute injury, postoperative pain, renal or biliary colic,
myocardial infarction (MI), or cancer. These agents
may be used to provide preoperative sedation and to
supplement anesthesia. In patients with acute pulmo-
nary edema, small doses of opiate agonists are used
to reduce anxiety and produce positive cardiovascular
hemodynamic effects to control edema. All opiate
agonists are classied as Schedule II, Schedule III, or
Schedule IV controlled substances because of the po-
tential for abuse and dependence.
Tramadol is a synthetic opiate agonist that acts as
an analgesic by selectively binding to the μ receptors
and inhibiting the reuptake of norepinephrine and
serotonin. It has some potential for abuse and depen-
dence and is classied as a Schedule IV controlled
substance.
Tapentadol is a synthetic opiate agonist that acts as
an analgesic by selectively binding to the μ receptors
and inhibiting the reuptake of norepinephrine. The
opioid agonist action of tapentadol is stronger than
that of tramadol, and tapentadol has a greater poten-
tial for dependence and abuse; thus it is classied as a
Schedule II controlled substance.
Meperidine (Demerol), once a commonly pre-
scribed opioid agonist in the management of pain, is
much less frequently prescribed because of the adverse
effects associated with its active metabolite, normeper-
idine. Use of meperidine for more than 1 to 2 days is
not recommended. Patients receiving large oral doses
of meperidine long term and those with renal impair-
ment are predisposed to accumulating normeperidine.
Drugs Used for Pain Management CHAPTER 19 311
Evidence of toxic levels of normeperidine includes ex-
citation, tremors, and seizures.
Therapeutic Outcomes
The primary therapeutic outcomes from appropriate
opiate agonist therapy are as follows:
1. Relief of pain intensity and reduced duration of
pain complaint
2. Prevention of the conversion of persistent pain to
chronic pain
3. Prevention of suffering and disability associated
with pain
4. Prevention of psychological and socioeconomic
consequences associated with inadequate pain
management
5. Control of adverse effects associated with pain
management
6. Optimization of the ability to perform ADLs
Nursing Implications for Opiate Agonists
Premedication assessment
1. Perform baseline neurologic assessment (e.g., ori-
entation to date, time, and place; mental alertness;
bilateral hand grip; and motor functioning).
2. Obtain vital signs; hold medication if respirations
are below 12 breaths/min, or according to age-re-
lated respiratory parameters, and consult with the
healthcare provider.
3. Check bowel sounds and note consistency and fre-
quency of passed stools. Review the voiding pattern
and urine output.
4. Check prior use of analgesics.
5. Perform pain assessment before administration of
an opiate agonist and at appropriate intervals dur-
ing therapy. Report poor pain control promptly to the
healthcare provider and obtain modication in orders.
Availability, dosage, and administration. See Table 19.1
Antidotes. Naloxone will reverse the effects of opiate
agonists.
Medication Safety Alert
In children younger than 12 years, codeine and tramadol
should not be used to treat pain and codeine should not
be used for cough. In addition, children between 12 and 18
years of age who are obese or who have conditions such as
obstructive sleep apnea or severe lung disease, which may
increase the risk of serious breathing problems, should not
use codeine or tramadol.
Common adverse effects
Neurologic
Lightheadedness, dizziness, sedation, sweating. These
effects tend to occur most often with the initial dose.
Symptoms can be reduced by keeping the patient
supine. Provide for patient safety, reassurance, and
comfort.
 312
Table 19.1 Opiate Agonists
DOSAGE EQUIVALENT TO

UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
MORPHINE (10 MG)
GENERIC NAME BRAND NAME AVAILABILITY INITIAL ADULT DOSAGE RANGE DURATION (HR) IM (MG) ORAL (MG)
Morphine and Morphine-Like Derivatives
codeine Codeine Sulfate, Tablets: 15, 30, 60 mg Analgesic: PO: 15–60 mg 4–6 120 200
Codeine Phosphate q4–6h
Antitussive: PO: 10–20 mg
q4–6h
hydrocodonea Zohydro ER Capsule, extended release (12 hr): 10, 15, 20, — — — 30
Hysingla ER 30, 40, 50 mg
Tablet, extended-release (24-hr) abuse deterrent:
20, 30, 40, 60, 80, 100, 120 mg
hydromorphone Dilaudid Tablets: 2, 4, 8 mg PO: 2 mg q4–6h 4–5 1.5 7.5
Liquid: 1 mg/mL Subcutaneous (subcut), IM:
Suppositories: 3 mg 2 mg q4–6h
Injection: 1, 2, 4, 10 mg/mL IV: 1–2 mg q4–6h
Tablets, extended-release (24-hr) abuse Rectal: 3 mg q6–8h
deterrent: 8, 12, 16, 32 mg
— Tablets: 2, 3 mg PO: 2 mg q6–8h 4–8 2 1 (chronic); 4
(acute)
morphine Morphine Sulfate Tablets: 15, 30 mg PO: 10–30 mg q4h 4–5; 8–24 for 10 30 (chronic);
MS-Contin Tablets, sustained release (12 hr): 15, 30, 60, Subcut, IM: 10 mg/70 kg sustained- 60 (acute)
100, 200 mg IV: 4–10 mg slowly release
Duramorph Capsules, extended release (24 hr): 10, 20, 30, Rectal: 10–20 mg q4h products
40, 45, 50, 60, 75, 80, 90, 100, 120 mg
Morphine Sulfate Oral solution: 10, 20, 100 mg/5 mL; 20 mg/mL
Suppositories: 5, 10, 20, 30 mg
Injection: 0.5, 1, 2, 4, 5, 8, 10, 25, 50 mg/mL;
150 mg/30 mL
oxycodone Roxicodone Tablets: 5, 10, 15, 20, 30 mg PO: 5–10 mg every 4–6h 4–5 15 20
OxyContin Tablets, controlled release (12-hr abuse PO:10–160 mg q12h
deterrent): 10, 15, 20, 30, 40, 60, 80 mg (controlled release)
Oxycodone Capsules: 5 mg PO: 5–10 mg every 4–6h
Oral solution: 5 mg/5 mL
Oral concentrate: 100 mg/5 mL
Xtampza ER Capsules, extended release (12-hr), abuse PO: 9 mg q12h
deterrent, oral: 9, 13.5, 18, 27, 36 mg
Table 19.1 Opiate Agonists—cont’d
DOSAGE EQUIVALENT TO
MORPHINE (10 MG)
GENERIC NAME BRAND NAME AVAILABILITY INITIAL ADULT DOSAGE RANGE DURATION (HR) IM (MG) ORAL (MG)
Oxaydo Tablets, abuse deterrent, oral: 5, 7.5 mg PO: 5–15 mg q4–6h
oxycodone with various Tablets: 4.8 mg plus aspirin 325 mg PO: 1 tablet every 6h as 4–5 15 30
needed. Maximum dose:
12 tablets daily.
oxymorphone Tablets: 5, 10 mg PO: 10–20 mg q4–6h 3–6 1 10
Tablets, extended release (12 hr): 5, 7.5, 10, 15, PO: 5–10 mg q12h
20, 30, 40 mg (sustained release)
Subcut, IM: 1–1.5 mg
q4–6h
Meperidine-Like Derivatives
Injection: 500 mcg/mL in 2-, 5-mL ampules IV: Variable >45 min — —
fentanyl Injection: 50 mcg/mL IM: 50–100 mcg 1–2 0.1 —
Fentora Buccal lozenges: 100, 200, 400, 600, 800 mcg Buccal: 100 mcg 1–2
Actiq Oral transmucosal lollipop: 200, 400, 600, 800, Use for breakthrough pain: Variable

Drugs Used for Pain Management CHAPTER 19

1200, 1600 mcg 200mcg adjust as needed
Subsys Sublingual spray liquid: 100, 200, 400, 600, 800, Use for breakthrough pain;
1200, 1600 mcg 100–200 mcg, adjust as
needed
Lazanda Nasal solution: 100 and 400 mcg/actuation Intranasal: 100 mcg (1 spray)
Do not confuse with
Latuda
– Transdermal patch: 12, 25, 37.5, 50, 62.5, 75, Upper torso: one patch 72
87.5, 100 mcg q72h
meperidine Tablets: 50, 100 mg PO, subcut, IM: 50–150 mg 2–4 50–100 300
Oral solution: 50 mg/5 mL q3–4h
Injection: 25, 50, 75, 100 mg/1 mL IV: 25–100 mg very slowly
sufentanil Dsuvia Tablet, sublingual: 30 mcg Sublingual: 30 mcg, may 2–3 — —
Injection: 50 mcg/mL in 1-, 2-, 5-mL ampules repeat every 1 hour; do
not exceed 12 doses in
24 hours
IV: variable
Continued

313
 314
Table 19.1 Opiate Agonists—cont’d
DOSAGE EQUIVALENT TO
MORPHINE (10 MG)

UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
GENERIC NAME BRAND NAME AVAILABILITY INITIAL ADULT DOSAGE RANGE DURATION (HR) IM (MG) ORAL (MG)
Tablets: 5, 10 mg Analgesia: 4–8 (may 5 (acute) 10 (acute)
Tablets, orally disintegrating: 40 mg PO, subcut, IM: 2.5–10 mg become
Oral solution: 5, 10 mg/5 mL q8–12h substantially
Injection: 10 mg/mL Maintenance: longer due to
Oral concentrate: 10 mg/mL PO: 20–40 mg; up to 120 variable half-
mg daily life)
Other Opiate Agonists
tramadol Ultram Tablets: 50, 100 mg PO: 50–100 mg 4–6 100
Tablets, extended release (24 hr): 100, 200, PO: 100 mg every 24 hours,
300 mg adjust every 5 days as
needed
ConZip Capsules, extended release (24 hr): 100, 200, —
300 mg
Synapryn FusePaq Oral suspension: 10 mg/mL in 500 mL bottle
tapentadol Nucynta Tablets: 50, 75, 100 mg PO: 50–100 mg 4–6 — 75–100
Nucynta ER Tablets, extended release (12 hr): 50, 100, 150,
200, 250 mg
Do not confuse.
High-alert medication.
aHydrocodone is available in combination with other ingredients for pain (e.g., acetaminophen, ibuprofen) (see Table 19.4).

Confusion, disorientation. Perform a baseline assess-
ment of the patient’s degree of alertness and orienta-
tion to name, place, and time before initiating therapy.
Make regularly scheduled evaluations of mental status
and report alterations from baseline. Provide for pa-
tient safety during these episodes.
Cardiovascular
Orthostatic hypotension. Orthostatic hypotension,
manifested by dizziness and weakness, occurs particu-
larly when therapy is being initiated in a patient not
in a supine position. Monitor blood pressure closely,
especially if the patient complains of dizziness or faint-
ness. Provide patient safety, assurance, and comfort.
Gastrointestinal
Nausea, vomiting. Symptoms can be reduced by keep-
ing the patient supine.
Constipation. Continued use may cause constipation.
Maintain the patient’s state of hydration, and obtain
an order for stool softeners or bulk-forming laxatives if
necessary. Encourage the inclusion of sufcient rough-
age, fresh fruits, vegetables, and whole-grain products
in the diet.
Serious adverse effects
Respiratory
Respiratory depression. Opiate agonists make the res-
piratory centers less sensitive to carbon dioxide, caus-
ing respiratory depression. This may occur before the
reduction in respiratory rate or tidal volume is notice-
able. Check the respiratory rate and depth often. Have
equipment for respiratory assistance available.
Endocrine. Long-term use of opiate agonists may
cause secondary hypogonadism and hypocortisolism.
Genitourinary
Urinary retention. Opiate agonists may produce
spasms of the ureters and bladder, causing urinary re-
tention. The patient may also have difculty in start-
ing the stream for urination. If the patient develops
urinary hesitancy, assess for bladder distention. Report
these adverse effects to the healthcare provider for fur-
ther evaluation. Try to stimulate urination by running
water or placing the patient’s hands in water. If permit-
ted, have male patients stand to void; female patients
should sit on a bedpan or toilet with receptacle.
Psychological
Excessive use or abuse. Evaluate the patient’s re-
sponse to the analgesic. Identify underlying needs
and plan for more appropriate management of those
needs. Discuss the case with the healthcare provider
and make plans to cooperatively approach gradual
withdrawal of the medications being abused. Suggest
a change to a milder analgesic when indicated.
Patients do not have to experience the symptoms
of withdrawal to be treated for physical dependence.
Patients may be treated by gradually reducing the dai-
ly dosage of the opiate agonist. If withdrawal symp-
toms become severe, the patient may receive metha-
done. Temporary administration of tranquilizers and
Drugs Used for Pain Management CHAPTER 19 315
sedatives may aid in reducing patient anxiety and
craving for the opiate agonist.
Drug interactions
Medication Safety Alert
A US Food and Drug Administration (FDA) review has found
that the combined use of opioid medicines with benzodiaz-
epines or other drugs that depress the CNS resulted in seri-
ous adverse reactions, including slowed or difcult breathing
and deaths.
Central nervous system depressants. General anesthet-
ics, phenothiazines, tranquilizers, sedative-hypnotics,
tricyclic antidepressants, antihistamines, gabapentin,
pregabalin, and alcohol enhance the depressant effects
of opiate agonists. Respiratory depression, hypoten-
sion, and profound sedation or coma may result from
this interaction unless the dosage of the opiate agonist
has been reduced appropriately, usually by one-third
to one-half the normal dosage.
Drugs that increase adverse effects. Clarithromycin,
diltiazem, erythromycin, isoniazid, itraconazole, and
verapamil can inhibit the metabolism of oxycodone
and methadone and increase toxicity (respiratory
depression).
Drugs that decrease the therapeutic effect.
Carbamazepine, St. John’s wort, phenytoin, and ri-
fampin are enzyme-inducing agents that may enhance
the metabolism of oxycodone and methadone. This
may result in decreased efcacy or onset of a with-
drawal syndrome in patients who have developed
physical dependence.
Selective serotonin reuptake inhibitors, tricyclic anti-
depressants, monoamine oxidase inhibitors. All these
agents increase serotonin levels, potentially causing
serotonin syndrome when taken by a person receiv-
ing tramadol or tapentadol. These medicines should
be used only under the supervision of the prescriber.
There should be a 14-day washout period after dis-
continuation of monoamine oxidase inhibitors before
starting tramadol or tapentadol therapy.
Warfarin. The oral anticoagulant effect of warfarin
may be increased by tramadol. Carefully monitor the
prothrombin time and international normalized ratio
(INR) and adjust the dosage of warfarin as needed
when tramadol is initiated or discontinued.
DRUG CLASS: OPIATE PARTIAL AGONISTS
Actions
Opiate partial agonists (e.g., buprenorphine, butorph-
anol, nalbuphine, pentazocine) are an interesting class
of drugs because their pharmacologic actions depend
on whether an opiate agonist has been administered
previously and the extent to which physical depen-
dence has developed to that opiate agonist. When used
316 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
without prior administration of opiate agonists, the
opiate partial agonists are effective analgesics. Their
potency during the rst few weeks of therapy is simi-
lar to that of morphine; however, after prolonged use,
tolerance may develop. Increasing the dosage does not
signicantly increase the analgesia but denitely in-
creases the incidence of adverse effects. This is called
a ceiling effect because, contrary to the action of the
opiate agonists, a larger dose does not produce a sig-
nicantly greater analgesic effect.
If an opiate partial agonist is given to a patient
with physical dependence on an opiate agonist such
as morphine or oxycodone, the opiate partial agonist
will induce withdrawal symptoms. If the patient is not
physically dependent on the opiate agonist, there is no
interaction and the patient will be relieved of pain.
Uses
Opiate partial agonists may be used for the short-term
relief (up to 3 weeks) of moderate to severe pain associ-
ated with cancer, burns, and renal colic, as well as for
preoperative analgesia and obstetric and surgical anal-
gesia. Nalbuphine has minimal physical dependence
liability and is not a controlled substance. Because na-
lbuphine has a ceiling effect for analgesia and respi-
ratory depression, it is often used as an analgesic for
obstetric patients. Buprenorphine transdermal can be
used for the management of long-term pain for which
alternative treatment options are inadequate.
Therapeutic Outcomes
The primary therapeutic outcomes from opiate partial
agonist therapy are as follows:
1. Relief of pain intensity and reduced duration of
pain complaint
2. Prevention of the conversion of persistent pain to
chronic pain
3. Prevention of suffering and disability associated
with pain
4. Prevention of psychological and socioeconomic
consequences associated with inadequate pain
management
5. Control of adverse effects associated with pain
management
6. Optimization of the ability to perform ADLs
Nursing Implications for Opiate Partial Agonists
Premedication assessment
1. Perform baseline neurologic assessment (e.g., ori-
entation to date, time, and place; mental alertness;
bilateral hand grip; and motor functioning).
2. Obtain vital signs; hold medication if respirations
are below 12 breaths/min, or according to age-relat-
ed respiratory parameters, and consult with health-
care provider.
3. Check bowel sounds and note consistency of stools.
Review voiding pattern and urine output.
4. Check for prior use of opiate agonists.
5. Perform pain assessment before administration of
the opiate agonist and at appropriate intervals dur-
ing therapy. Report poor pain control promptly to
the healthcare provider and obtain modication in
orders.
Availability, dosage, and administration. See Table 19.2.
Antidotes. Naloxone will reverse the effects of opiate
partial agonists.
Common adverse effects
Neurologic
Clamminess, dizziness, sedation, sweating. These ef-
fects tend to occur most often with the initial dose.
Symptoms can be reduced by keeping the patient su-
pine. Provide patient safety, assurance, and comfort.
Gastrointestinal
Nausea, vomiting, dry mouth. These effects tend to oc-
cur most often with the initial dose. Symptoms can be
reduced by keeping the patient supine. Provide patient
safety, assurance, and comfort.
Constipation. Continued use may cause constipation.
Maintain the patient’s state of hydration and obtain an
order for stool softeners or bulk-forming laxatives if
necessary. Encourage the inclusion of sufcient rough-
age, fresh fruits, vegetables, and whole-grain products
in the diet.
Serious adverse effects
Neurologic
Confusion, disorientation, hallucinations. Butorphanol
and pentazocine, and to a lesser degree nalbuphine,
may produce hallucinations. Patients may complain of
seeing multicolored ashing patterns or animals, with
and without sound, or may have very vivid dreams.
These adverse effects have been reported after only
one or two doses of medication and may occur in as
many as one-third of patients taking butorphanol or
pentazocine.
Perform a baseline assessment of the patient’s de-
gree of alertness and orientation to name, place, and
time before initiating therapy. Make regularly sched-
uled subsequent evaluations of mental status, and re-
port alterations from baseline. Provide for patient safe-
ty during these episodes. If recurring, seek a change in
the medication order.
Respiratory
Respiratory depression. Opiate partial agonists make
the respiratory centers less sensitive to carbon dioxide,
causing respiratory depression. This may occur before
the reduction in respiratory rate or tidal volume is no-
ticeable. Check the respiratory rate and depth often.
Endocrine. Long-term use of buprenorphine may
cause secondary hypogonadism and hypocortisolism.
Psychological
Excessive use or abuse. Repeated use may lead to
tolerance and physical dependence. Evaluate the pa-
tient’s response to the analgesic. Identify underlying
 Drugs Used for Pain Management CHAPTER 19 317

Table 19.2 Opiate Partial Agonists

DOSAGE
DURATION EQUIVALENT TO
GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE (HR) MORPHINE (10 MG)
buprenorphine – Tablets, sublingual: 2, 0.3 mg q 6–8h 6 IM/IV: 0.4 mg
8 mg
Injection: 0.3 mg/mL in
1-mL ampules
Butrans Patch (weekly): 5, 7.5, Initiate treatment with a
10, 15, 20 mcg/hr 5 mcg/hour patch every
7 days
Belbuca Buccal lm: 75, 150, 75 mcg daily, may increase
300, 450, 600, 750, every 4 days
900 mcg
Probuphine Subcutaneous (subcut)
Implant implant: 74.2 mg
buprenorphine/ Suboxone Sublingual lm: 2/0.5, 2/0.5 mg q2h
naloxonea 4/1, 8/2, 12/3 mg
buprenorphine/
naloxone
Bunavail Buccal lm: 2.1/0.3, 2.1/0.3 mg q2h
4.2/0.7, 6.3/1 mg
buprenorphine/
naloxone
Zubsolv Tablets, sublingual: 1.4/0.36 mg q1.5–2h
0.7/0.18, 1.4/0.36,
2/0.5, 2.9/0.71,
5.7/1.4, 8/2,
8.6/2.1, 11.4/2.9 mg
buprenorphine/
naloxone
butorphanol — Injection: 1, 2mg/mL in IM: 2 mg, repeat in 3–4 hr; IM: 3–4 IM: 2 mg
1-, 2-mL vials maximum dosage, 4 mg
Nasal spray: 10 mg/mL IV: 1 mg, repeat in 3–4 hr
Nasal: 1 spray in each
nostril repeated in 3–4 hr
nalbuphine — Injection: 10, 20 mg/mL Subcut, IM, IV: 3–6 IM/IV/subcut:
in 1-, 10-mL vials 10 mg/70 kg, repeat 10 mg
q3–6h; maximum daily
dosage, 160 mg
pentazocine/ — Tablets (with naloxone PO: 50–100 mg q3–4h; do 4–5 30–60 mg
naloxone 0.5 mg):a 50 mg not exceed 600 mg daily;
maximum daily dosage,
360 mg
aTablets contain naloxone to prevent abuse.

needs and plan for more appropriate management
of those needs. Discuss the case with the healthcare
provider and make plans to approach gradual with-
drawal of the medications being abused cooperatively.
Suggest a change to a milder analgesic when indicated.
The patient does not have to experience symptoms
of withdrawal to be treated for physical dependence,
which is usually a gradual reduction of the daily opi-
ate agonist dosage. If withdrawal symptoms become
severe, the patient may receive methadone. Temporary
administration of tranquilizers and sedatives may aid
in reducing patient anxiety and craving for the opiate
agonist.
Drug interactions
Central nervous system depressants. General anesthet-
ics, phenothiazines, tranquilizers, sedative-hypnotics,
tricyclic antidepressants, antihistamines, and alcohol
enhance the depressant effects of the opiate partial
agonists. Respiratory depression, hypotension, and
profound sedation or coma may result from this inter-
action unless the dosage of the opiate partial agonist
318 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
has been reduced appropriately, usually by one-third
to one-half the normal dosage.
Opiate agonists. Opiate partial agonists have weak
antagonist activity. When administered to patients
who have been receiving opiate agonists such as mor-
phine or meperidine on a regular basis, it may precipi-
tate withdrawal symptoms.
DRUG CLASS: OPIATE ANTAGONISTS
naloxone (năl-ŎKS-ōn)
Narcan, Kloxxado, LifEMS Naloxone
Actions
Naloxone is a so-called pure opiate antagonist be-
cause it has no other known effect than reversal of the
CNS depressant effects of opiate agonists and opiate
partial agonists. When administered to patients who
have not recently received opiates, there is no respi-
ratory depression, psychotomimetic effect, circula-
tory change, or other pharmacologic activity. If ad-
ministered to a person addicted to opiate agonists or
opiate partial agonists, withdrawal symptoms may
be precipitated.
Uses
Naloxone is a drug of choice for treatment of respiratory
depression when excessive doses of opiate agonists or
opiate partial agonists have been administered, or when
the causative agent is unknown. Naloxone is not effec-
tive in reversing CNS depression induced by tranquiliz-
ers or sedative-hypnotics. Naloxone has been added to
pentazocine formulations to reduce its abuse by block-
ing the euphoric high associated with pentazocine.
Many emergency services (police, re, ambulance)
across the nation now carry prelled syringes of nal-
oxone (Evzio) to administer to patients emergently for
potential overdoses of opiates (heroin, morphine, oxy-
codone, hydromorphone). This is similar to EpiPen or
Auvi-Q use in acute anaphylaxis resulting from aller-
gens (e.g., bee stings).
Therapeutic Outcomes
The primary therapeutic outcome expected from nal-
oxone is reversal of respiratory depression secondary
to opiate overdose.
Nursing Implications for Naloxone
Premedication assessment
1. Perform baseline neurologic assessment (e.g., ori-
entation to date, time, and place; mental alertness;
bilateral hand grip; and motor functioning).
2. Monitor vital signs; blood pressure, pulse, and res-
pirations should be taken at frequent intervals until
resolution of CNS depression. Then schedule vital
signs to be taken at appropriate intervals because
the duration of action of naloxone is short.
3. Check prior use of or dependence on opiate agonists or
opiate partial agonists. Diagnostic testing for narcotic
dependence may be performed in accordance with pol-
icies of the clinical site. Inform patient of risks involved.
4. Have supportive equipment available in immediate
area to maintain respirations.
5. Check bowel sounds. Review voiding pattern and
urine output.
Availability. Injection: 0.4 mg/mL in 1-mL vials, car-
tridges and prelled syringes; 1 mg/mL in 2-mL pre-
lled syringes; 4 mg/10 mL vial.
Nasal solution: 4-, 8-mg/0.1mL nasal spray.
Dosage and administration. Adult: IV: Postoperative
opiate depression: 0.1 to 0.2 mg every 2 to 3 minutes until
the desired response is achieved.
Adult: IM: Opiate overdose: 0.4 to 2 mg every 2 to 3
minutes. If no response is seen after 10 minutes, the de-
pressive condition may be caused by a drug or disease
process not responsive to naloxone.
Adult: Intranasal: Opiate overdose: 4 mg (contents of 1
nasal spray) as a single dose in one nostril; may repeat
every 2 to 3 minutes in alternating nostrils.
Common adverse effects. Naloxone rarely manifests
any adverse effects. In rare cases when extremely high
doses have been used, mental depression, apathy, in-
ability to concentrate, sleepiness, irritability, anorexia,
nausea, and vomiting have been reported. These ad-
verse effects usually occurred in the rst few days
of treatment and dissipated rapidly with continued
therapy.
Cardiovascular. Use with caution in patients with car-
diovascular disease or in patients taking cardiovascular
medicines (e.g., antihypertensives, antiarrhythmics).
Abrupt reversal of opiate overdose by opioid antago-
nists may cause arrhythmias, pulmonary edema, and
ventricular brillation.
Neurologic
Mental depression, apathy. Be aware of the potential
for suicidal thoughts or suicide. Inform the healthcare
provider immediately if the patient has any new or
worsening symptoms of depression.
Gastrointestinal
Nausea, vomiting. Naloxone should be used with
caution following the use of opiates during surgery be-
cause it may result in excitement, increased blood pres-
sure, and a clinically important reversal of analgesia.
The early reversal of opiate effects may induce nausea,
vomiting, sweating, and tachycardia.
Naloxone should be given with caution to patients
known or suspected to be physically dependent on
opioids, including neonates born to women who are
opiate dependent, because the drug may precipitate
severe withdrawal symptoms. The severity of the
symptoms depends on the dose of naloxone and the
degree of dependence.

Drug interactions. There are no drug interactions other
than that of the antagonist activity toward opiate ago-
nists and opiate partial agonists.
naltrexone (năl-TRĔKS-ōn)
Revia (rē-VĒ-ă) Available in Canada.
Vivitrol (viv ih-trol’)
Actions
Naltrexone is a pure opioid antagonist closely related
to naloxone. It differs, however, in that it is active af-
ter oral administration and has a considerably longer
duration of action. Naltrexone blocks the effects of
opioids by competing for binding sites at opioid recep-
tors. The mechanism of action of naltrexone in patients
with alcoholism is not known.
Uses
Naltrexone is used clinically to block the pharmacologic
effects of exogenously administered opiates in patients
who are enrolled in drug abuse treatment programs.
Naltrexone may diminish or eliminate opiate-seeking be-
havior by blocking the euphoric reinforcement produced
by self-administration of opioids and by preventing the
conditioned abstinence syndrome (i.e., opiate craving)
that occurs after opiate withdrawal.
Naltrexone is also used as an adjunct in the treatment
of alcoholism to support abstinence and reduce relapse
rates and alcohol consumption. It must be used with oth-
er treatment forms such as group and behavior therapy;
the expected effect of the drug treatment is a modest im-
provement in the outcome of conventional treatment.
Therapeutic Outcomes
The primary therapeutic outcomes expected from nal-
trexone are as follows:
1. Improved adherence with a substance abuse treat-
ment program by reducing the craving for opioids
2. Improved adherence with an alcohol abuse treat-
ment program by diminishing the craving for
alcohol
Nursing Implications for Naltrexone
Premedication assessment
1. Perform baseline neurologic assessment (e.g., ori-
entation to date, time, and place; mental alertness;
bilateral hand grip; and motor functioning).
2. Monitor vital signs: temperature, blood pressure,
pulse, and respirations.
3. Check laboratory values for hepatotoxicity; urine
screen for opiate use.
4. Monitor for GI symptoms before and during
therapy.
5. The manufacturer recommends that baseline deter-
minations of liver function should be obtained in
all patients before initiating therapy and repeated
monthly for the next 6 months.
Drugs Used for Pain Management CHAPTER 19 319
6. The manufacturer recommends a minimum of 7 to
10 days of abstinence from all opiates, a urinalysis to
conrm the absence of opiates, and the use of a nal-
oxone challenge test to ensure that the patient will
not develop withdrawal symptoms.
Availability. PO: 50-mg tablets.
IM: 380 mg/vial suspension, extended-release
injection.
Dosage and administration
Behavior modication. Naltrexone therapy in com-
bination with behavior therapy is more effective than
naltrexone or behavior therapy alone in prolonging
opiate or alcohol cessation in patients formerly physi-
cally dependent on opiates or alcohol.
Treatment of opiate agonist dependence. PO: Induction
dose of 25 mg. Observe for development of withdrawal
symptoms. If none occur, administer 50 mg the next day.
The maintenance regimen is 50 mg daily. Alternative
regimens of 100 mg every other day or 150 mg every
third day have been used to improve adherence during
a behavior modication program (see Chapter 48).
Withdrawal symptoms. Naltrexone may precipitate
acute and severe withdrawal symptoms in patients
who are physically dependent on opioids. Addicts
must be completely detoxified and opioid free be-
fore taking naltrexone. The manufacturer recom-
mends a minimum of 7 to 10 days of abstinence from
all opiates, a urinalysis to confirm the absence of
opiates, and the use of a naloxone challenge test to
ensure that the patient will not develop withdrawal
symptoms.
Patients undergoing naltrexone therapy must be
carefully instructed about the expectations of behav-
ior modication associated with therapy. They should
also be advised that self-administration of small doses
of opiates (e.g., heroin) during naltrexone therapy will
not result in any euphoric effect and that large doses
may result in serious adverse effects, including coma
and death. Patients should also be given identication
to notify medical personnel that they are taking a long-
acting opiate antagonist.
Treatment of alcoholism. PO: 50 mg once daily (see
also Chapter 48).
IM: 380 mg IM every 4 weeks as a gluteal injection,
alternating buttocks.
Common adverse effects. Many adverse effects have
been associated with naltrexone therapy, but it is dif-
cult to know exactly which ones are secondary to nal-
trexone alone because some patients may experience
mild opiate withdrawal symptoms as well. The ad-
verse effects of drug and alcohol abuse and poor nutri-
tional states may contribute to the patient’s discomfort.
Gastrointestinal
Nausea, vomiting, anorexia. Adverse effects are usu-
ally mild and tend to resolve with continued therapy.
320 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
Encourage the patient not to discontinue therapy with-
out rst consulting the healthcare provider and treat-
ment program.
Neurologic
Headache. Adverse effects are usually mild and
tend to resolve with continued therapy. Encourage
the patient not to discontinue therapy without rst
consulting the healthcare provider and treatment
program.
Serious adverse effects
Gastrointestinal
Hepatotoxicity. Hepatotoxicity has been reported af-
ter doses of 300 mg daily for 3 to 8 weeks. The symp-
toms of hepatotoxicity are jaundice, nausea, vomiting,
anorexia, hepatomegaly, splenomegaly, and abnormal
liver function test results (e.g., elevated bilirubin, as-
partate aminotransferase [AST], alanine aminotrans-
ferase [ALT], and alkaline phosphatase levels [ALP];
increased prothrombin time [PT]). Because many of
these patients do not develop clinical symptoms but
do develop abnormal liver function, strongly encour-
age patients to report for blood tests as scheduled.
Report abnormal values to the appropriate healthcare
provider.
Drug interactions
Opioid-containing products. Patients taking naltrex-
one will probably not benet from opioid-containing
medicines such as analgesics, cough and cold prepara-
tions, and antidiarrheal preparations. These products
should be avoided during naltrexone therapy when
nonopiate therapy is available.
Clonidine. Clonidine may be administered in pa-
tients to reduce the severity of withdrawal symptoms
precipitated or exacerbated by naltrexone.
DRUG CLASS: PROSTAGLANDIN INHIBITORS
acetaminophen (ă-sēt-ă-MĬN-ō-fĕn)
Tylenol (TĪ-lĕ-nŏl)
Actions
Acetaminophen is a synthetic nonopiate analgesic that
works by prostaglandin inhibition in the CNS and
blocks generation of pain impulses in the peripheral
tissue. Control of elevated body temperature (anti-
pyresis) results from inhibition of the heat-regulating
center in the hypothalamus. Antipyretic effectiveness
and analgesic potency are similar to those of aspirin in
equal doses.
Uses
Acetaminophen is an effective analgesic-antipyretic
for discomfort associated with bacterial and viral
infections, headache, and musculoskeletal pain. It
is a good substitute for patients who cannot take
products containing aspirin or nonsteroidal antiin-
flammatory drugs (ibuprofen) because of allergic
reactions; hypersensitivities; anticoagulant therapy;
or possible bleeding problems from gastric or duo-
denal ulcers, gastritis, and hiatus hernia. This drug
has no antiinflammatory activity and is therefore
ineffective (other than as an analgesic) for the re-
lief of symptoms of rheumatoid arthritis or other
inflammation.
Therapeutic Outcomes
The primary therapeutic outcomes expected from acet-
aminophen are reduced pain and fever.
Nursing Implications for Acetaminophen
Premedication assessment
1. Take vital signs: temperature, blood pressure, pulse,
and respirations.
2. Check laboratory data for hepatotoxicity or
nephrotoxicity.
3. Monitor for GI symptoms before and during
therapy.
4. Check bowel sounds and review voiding pattern
and urine output.
5. When used as an analgesic, perform pain assess-
ment before administering acetaminophen and at
appropriate intervals during therapy. Report poor
pain control promptly to the healthcare provider
and obtain modication in orders.
6. When used as an antipyretic, take baseline tempera-
ture and continue monitoring temperature at appro-
priate intervals (e.g., every 2 to 4 hours, depending
on severity of temperature elevation).
Availability. PO: 325- and 500-mg caplets; 325- and
500-mg capsules and tablets; 80- and 160-mg chewable
tablets; 650-mg extended-release tablets; 80- and 160-
mg dispersible tablets; 160 mg/5 mL, 500 mg/15 mL,
and 650 mg/20.3 mL liquid; 160 mg/5 mL oral gel.
Rectal: 80-, 120-, 325-, or 650-mg suppositories.
IV: 10 mg/mL solution in 50 and 100 mL containers.
To avoid toxicity, it is recommended that the
adult receive no more than 4 g of acetaminophen
daily. Patients who are chronic alcoholics should
take no more than 2 g/day. The American Geriatrics
Society guideline on the management of persistent
pain recommends a prudent approach of less than
3 g/day.
Dosage and administration. Adult: PO: 325 to 650 mg
every 4 to 6 hours. Doses up to 1000 mg may be giv-
en four times daily for short-term therapy. Maximum
dose is 3250 mg daily unless directed by healthcare
provider; under healthcare provider supervision, do
not exceed 4 g daily. IV: Greater than 50 kg: 1 g every 6
hours. Do not exceed 4 g in 24 hours. Less than 50 kg: 15
mg/kg (up to 750 mg) as a single dose and 75 mg/kg
(up to 3750 mg) in 24 hours.

Pediatric: PO: 0 to 3 months, 40 mg; 4 to 11 months,
80 mg; 12 to 24 months, 120 mg; 2 to 3 years, 160 mg; 4
to 5 years, 240 mg; 6 to 8 years, 320 mg; 9 to 10 years,
400 mg; 11 to 12 years, 480 mg; older than 14 years, 650
mg. Rectal: 6 to 11 months: 80 mg every 6 hours, maxi-
mum daily dose: 320 mg; 12 to 36 months: 80 mg every
4 to 6 hours, maximum daily dose: 400 mg; 4 to 6 years:
120 mg every 4 to 6 hours, maximum daily dose: 600
mg; 7 up to 12 years: 325 mg every 4 to 6 hours, maxi-
mum daily dose: 1625 mg. IV: 15 mg/kg as a single
dose and 75 mg/kg in 24 hours. 13 years of age and older,
50 kg or more: 1000 mg every 6 hours or 650 mg every
4 hours. Do not exceed 1000 mg as a single dose and
4000 mg in 24 hours. 13 years and older, less than 50 kg: 15
mg/kg every 6 hours or 12.5 mg/kg every 4 hours. Do
not exceed 15 mg/kg (up to 750 mg) as a single dose
and 75 mg/kg (up to 3750 mg) in 24 hours.
Antidote. The antidote is acetylcysteine.
Common adverse effects. When used as directed,
acetaminophen is extremely well tolerated.
Gastrointestinal
Gastric irritation. If gastric irritation occurs, admin-
ister medication with food, milk, antacids, or large
amounts of water. If symptoms persist or increase in
severity, report for healthcare provider evaluation.
Serious adverse effects
Gastrointestinal
Hepatotoxicity. Overdosage caused by acute and
chronic ingestion has risen dramatically in the past
few years. Severe life-threatening hepatotoxicity has
been reported in patients who ingest 5 to 8 g daily
for several weeks or attempt suicide by consuming
large quantities at one time. Hepatotoxicity is also
more frequent with heavy alcohol use and ingestion of
acetaminophen.
Early indications of toxicity include anorexia, nau-
sea, vomiting, low blood pressure, drowsiness, con-
fusion, and abdominal pain—symptoms often attrib-
uted to other causes. Within 2 to 4 days, symptoms of
hepatotoxicity develop (jaundice and a rise in the AST
and ALT levels and prothrombin time). If acetamino-
phen toxicity is suspected, consult the manufacturer,
a university drug information center, or a poison con-
trol center for the most current recommendations for
therapy.
Drug interactions
Phenobarbital, carbamazepine, phenytoin. If acetami-
nophen is taken in large doses or over the long term,
these agents may enhance hepatotoxicity.
Alcohol. Chronic excessive ingestion of alcohol may
increase the potential for hepatotoxicity with thera-
peutic doses or overdoses of acetaminophen.
salicylates (săl-ĭ-SĬL-āts)
Drugs Used for Pain Management CHAPTER 19 321
Actions
Salicylates are the most common analgesics used for
the relief of slight to moderate pain. Salicylates were
introduced into medicine in the late 19th century be-
cause of their three primary pharmacologic effects as
analgesic, antipyretic, and antiinammatory agents.
Although the mechanisms of action are not fully
known, most of the activity of salicylates comes from
inhibiting prostaglandin synthesis. Salicylates inhibit
the formation of prostaglandins that sensitize pain re-
ceptors to stimulation causing pain (analgesia), they
inhibit the prostaglandins that produce the signs and
symptoms of inammation (e.g., redness, swelling,
warmth), and they inhibit the synthesis and release of
prostaglandins in the brain that cause the elevation of
body temperature (antipyresis). A major benet of sa-
licylates is that they do not dull the consciousness level
and do not cause mental sluggishness, memory distur-
bances, hallucinations, euphoria, or sedation.
A unique property of aspirin, compared with other
salicylates, is inhibition of platelet aggregation and
enhancement of bleeding time. The platelet loses its
ability to aggregate and form clots for the duration of
its lifetime (7 to 10 days). The mechanism of action is
inhibition of the synthesis of thromboxane A2, a potent
vasoconstrictor and inducer of platelet aggregation.
Uses
The combination of pharmacologic effects makes salic-
ylates the drug of choice for symptomatic relief of dis-
comfort, pain, inammation, or fever associated with
bacterial and viral infections, headache, muscle aches,
and rheumatoid arthritis. Salicylates can be taken to re-
lieve pain on a long-term basis without causing drug
dependence. The use of salicylates in children is not
recommended because of the associated risk of Reye
syndrome.
Because of its antiplatelet activity, aspirin is also
indicated for reducing the risk of recurrent transient
ischemic attacks or stroke. Aspirin is also used to re-
duce the risk of MI in patients with previous MI or
unstable angina pectoris. Aspirin is administered on
arrival to the emergency department to those patients
experiencing an acute MI.
Therapeutic Outcomes
The primary therapeutic outcomes expected from sa-
licylates are reduced pain, reduced inammation, and
elimination of fever. The primary therapeutic outcomes
expected from aspirin when used for antiplatelet thera-
py are reduced frequency of transient ischemic attack,
stroke, or MI.
Nursing Implications for Salicylates
Premedication assessment
1. Perform baseline neurologic assessment (e.g., ori-
entation to date, time, and place; mental alertness;
bilateral hand grip; motor functioning).
322 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems
2. Monitor vital signs (i.e., temperature, blood pres-
sure, pulse, respirations).
3. Check laboratory values for hepatotoxicity, renal
impairment, and clotting time.
4. Monitor for GI symptoms before and during thera-
py; conduct stool guaiac test if GI tract bleeding is
suspected.
5. Check for concurrent use of anticoagulant agents.
6. If the patient is taking oral hypoglycemics, review
baseline serum glucose level.
7. When used as an analgesic, perform pain assess-
ment before administering salicylates and at appro-
priate intervals during therapy. Report poor pain
control promptly to the healthcare provider and ob-
tain modication in orders.
Availability. See Tables 19.3 and 19.4
Dosage and administration
Treatment of pain, arthritis, acute rheumatic fever, and
myocardial infarction prophylaxis. See Table 19.3
Stroke prevention. See Table 19.3
Common adverse effects. As benecial as salicylates
are, they are not without adverse effects. In normal
therapeutic dosages, they may produce GI irritation,
occasional nausea, and gastric hemorrhage. Extreme
caution should be used with administration to patients
with a history of peptic ulcer, liver disease, or coagula-
tion disorders.
Gastrointestinal
Gastric irritation. If gastric irritation occurs, give
medication with food, milk, or antacids (1 hour later)
or with large amounts of water. If symptoms persist
or increase in severity, notify the healthcare provider.
Aspirin is available in an enteric-coated form to reduce
gastric irritation.
Serious adverse effects
Gastrointestinal
Gastrointestinal bleeding. Dark, tarry stools and bright
red or coffee-ground emesis may occur. Test any sus-
pect stools or emesis for the presence of occult blood.
Toxicity
Salicylism. Patients receiving higher doses on a contin-
uing basis are susceptible to developing salicylate intoxi-
cation (salicylism). Symptoms include tinnitus (ringing in
the ears), impaired hearing, dimming of vision, sweating,
fever, lethargy, dizziness, mental confusion, nausea, and
vomiting. This condition is reversible on dosage reduc-
tion. Massive overdosage may lead to respiratory depres-
sion and coma. There is no antidote; primary treatment is
discontinuing the drug, gastric lavage, forcing IV uids,
and alkalizing the urine with IV sodium bicarbonate.
Patients who develop signs of salicylate toxicity
should be reevaluated for other underlying diseases
and the possibility that other medications would be
more effective.
Drug interactions
Nonsteroidal antiinammatory drugs. It is possible
that cyclooxygenase-1 (COX-1) inhibitors reduce the
platelet-inhibiting effects of aspirin when adminis-
tered at about the same time. The NSAID may block
the receptor on platelets that aspirin would normally
bind to, preventing the platelet inhibition caused by
aspirin. One approach to avoid this interaction is to
take aspirin several hours before the COX-1 NSAID.
This might not be possible for a patient with severe
rheumatoid arthritis who needs the analgesic effects
around the clock.
Probenecid. Salicylates inhibit the excretion of uric
acid by these agents. Although an occasional aspirin
will not interfere with their effectiveness, regular use
of salicylates or products containing salicylate should
be discouraged. If analgesia is required, suggest
acetaminophen.
Warfarin. Salicylates may enhance the anticoagulant
effects of warfarin. Observe for petechiae; ecchymoses;
nosebleeds; bleeding gums; dark, tarry stools; and
bright red or coffee-ground emesis. Monitor INR and
prothrombin time and reduce the dosage of warfarin
if necessary.
Valproic acid. Monitor the patient with concurrent
therapy for signs of valproic acid toxicity, such as se-
dation or lethargy. Serum levels may be ordered, and
the dosage of valproic acid may need to be reduced.
Oral hypoglycemic agents. Salicylates may enhance
the hypoglycemic effects of these agents. Monitor for
hypoglycemia, headache, weakness, decreased co-
ordination, general apprehension, diaphoresis, hun-
ger, or blurred or double vision. The dosage of the
hypoglycemic agent may need to be reduced. Notify
the healthcare provider if any of the previous symp-
toms appear.
Methotrexate. Monitor for signs of methotrexate
toxicity: bone marrow suppression, decreased white
blood cell (WBC) count, decreased red blood cell (RBC)
count, sore throat, fever, or lethargy.
Corticosteroids. Although often used together, salic-
ylates and corticosteroids may produce GI ulceration.
Monitor for signs of GI bleeding; observe for the devel-
opment of dark, tarry stools and bright red or coffee-
ground emesis.
Ethanol. The patient should avoid aspirin within 8
to 10 hours of heavy alcohol use. Small amounts of GI
bleeding often occur. If aspirin therapy is absolutely
necessary, an enteric-coated product should be used.
DRUG CLASS: NONSTEROIDAL
ANTIINFLAMMATORY DRUGS
Actions
Nonsteroidal antiinammatory drugs are also known
as aspirin-like drugs. They are chemically unrelated to
salicylates but are prostaglandin inhibitors and share
many of the same therapeutic actions and adverse
 Drugs Used for Pain Management CHAPTER 19 323

Table 19.3 Nonsteroidal Antiinammatory Drugs

MAXIMUM DAILY
GENERIC NAME BRAND NAME AVAILABILITY USES AND DOSAGES DOSAGE (MG)
Salicylates
aspirin Ecotrin, St. Tablets: 81, 325, 500 mg Minor aches and pains: 325–600 mg —
Joseph, Bayer Tablets, sustained release: q4h
Aspirin 81, 325 mg Arthritis: 2.6–5.2 g/day in divided
Tablets, chewable: 81, doses
325 mg Acute rheumatic fever: 7.8 g/day
Capsules, sustained Myocardial infarction prophylaxis:
release: 162.5 mg 75–325 mg daily
Suppositories: 60, 120, Ischemic stroke and TIA: 50–325 mg
200, 300 mg daily
diunisal — Tablets: 500 mg Mild to moderate pain: Initially, 1500
1000 mg, then 500 mg q8h
Osteoarthritis and rheumatoid
arthritis: 250–500 mg twice daily

magnesium Doan’s Tablets: 325, 580 mg Mild to Moderate pain: 1160 mg 4640
salicylate every 6 hours as needed

salsalate — Tablets: 500, 750 mg Mild pain: 1,500 mg twice daily or 3000
1,000 mg three times per day
Nonsteroidal Antiinammatory Drugs
Cyclooxygenase-1 (COX-1) Inhibitors
diclofenac Cataam Tablets: 50 mg Rheumatoid and osteoarthritis, 200
Tablets, extended release ankylosing spondylitis: 25–50 mg
(24 hr): 25, 50, 75, 100 two or three times daily
mg Primary dysmenorrhea: 50 mg three
Capsules: 18, 25, 35 mg times daily
Flector Patch, transdermal: 1.3% Apply to pain site twice daily. Do not
Gel, transdermal: 3% apply to broken skin
For actinic keratoses: Apply twice
Voltaren Gel, transdermal: 1%
daily. Avoid direct sun exposure
Osteoarthritis: Apply to affected arm,
hand, foot, and knee joints four
times daily. Do not apply to spine,
hips, or shoulders
etodolac Lodine Capsules: 200, 300 mg Osteoarthritis, pain: 300–400 mg 1200
Taro-Etodolac Tablets: 400, 500 mg three or four times daily
Tablets, extended release:
400, 500, 600 mg
fenoprofen Nalfon Capsules: 200, 400 mg Rheumatoid and osteoarthritis: 300– 3200
Tablets: 600 mg 600 mg three or four times daily
Mild to moderate pain: 200 mg q4–6h
urbiprofen — Tablets: 50, 100 mg Rheumatoid and osteoarthritis: 300
Teva-Flurbiprofen 50–100 mg two or three times daily

ibuprofen Motrin, Advil Tablets: 100, 200, 400, Rheumatoid and osteoarthritis: 300– 3200
Teva-Profen 600, 800 mg 600 mg three or four times daily
Tablets, chewable: 100 Mild to moderate pain: 400 mg q4–6h
mg Primary dysmenorrhea: 400–600 mg
Capsules: 200 mg q4–6h
Suspension: 50 mg/1.25 Fever: Pediatric: 5–10 mg/kg three or
mL; 100 mg/5 mL four times daily
IV: 10 mg/mL; 800 mg/8
mL
Continued
324 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems

Table 19.3 Nonsteroidal Antiinammatory Drugs—cont’d

MAXIMUM DAILY
GENERIC NAME BRAND NAME AVAILABILITY USES AND DOSAGES DOSAGE (MG)
indomethacin Mint-Indomethacin Capsules: 20, 25, 50 mg Rheumatoid and osteoarthritis, 200 for immediate
Capsules, extended ankylosing spondylitis: 25–50 mg release; 150
release: 75 mg three or four times daily for sustained
Oral suspension: 25 mg/5 Acute painful shoulder: 25–50 mg release
mL two or three times daily
Suppository: 50 mg Acute gouty arthritis: 50 mg three
IV: 1 mg/mL/vial times daily
Closure of patent ductus arteriosus:
IV, one to three doses at 12- to 24-
hr intervals
ketoprofen — Capsules: 25, 50, 75 mg Rheumatoid and osteoarthritis: 300
Capsules, extended Initially, 75 mg three times daily
release (24 hr): 200 mg or 50 mg four times daily; reduce
initial dose by to in older patients or
those with impaired renal function
Mild pain, primary dysmenorrhea:
25–50 mg three or four times daily
ketorolac — Tablets: 10 mg Analgesic, antiinammatory, 120–150
Injection 15 mg/mL in antipyretic used for acute, short-
1-mL vial and 30 mg/ term pain management: IM 60 mg
mL in vials and syringe; or IV 30 mg, initially, 15–30 mg
IM 60 mg/2 mL in 2-mL q6h PRN for pain; then PO, up to
vials 40 mg/24 hr; do not exceed 5 days
of therapy
meclofenamate — Capsules: 50, 100 mg Rheumatoid and osteoarthritis: 400
200–400 mg daily in three or four
equal doses
Mild to moderate pain: 50–100 mg
three or four times daily
Primary dysmenorrhea: 100 mg three
times daily
mefenamic acid — Capsules: 250 mg Moderate pain or primary 1000
dysmenorrhea: Initially 500 mg,
Ponstan then 250 mg q6h; do not exceed 7
days of therapy
meloxicam Mobic Tablets: 7.5, 15 mg Osteoarthritis: 7.5–15 mg daily 15
ACT-Meloxicam Capsules: 5, 10 mg
nabumetone Relafen, Relafen Tablets: 500, 750, Rheumatoid and osteoarthritis: 2000
DS 1000 mg 1000–1500 mg daily in one or two
doses
naproxen Naprosyn, Aleve, Tablets: 220, 250, 275, Rheumatoid arthritis, osteoarthritis, 1000
Anaprox DS 375, 500, 550 mg ankylosing spondylitis: 250–500 mg
Pro-Naproxen Tablets, extended release twice daily
EC (24 hr): 375, 500, 750 Acute gout: 750–825 mg initially,
mg followed by 250–275 mg q8h
Capsules: 220 mg Moderate pain, primary
Oral suspension: 125 dysmenorrhea, acute tendonitis,
mg/5 mL bursitis: 500–550 mg followed by
250–275 mg
oxaprozin Daypro Caplets: 600 mg Rheumatoid arthritis, osteoarthritis: 1800
1200 mg once daily
piroxicam Feldene Capsules: 10, 20 mg Rheumatoid arthritis osteoarthritis: 200
20 mg once daily
Apo-Piroxicam

Table 19.3 Nonsteroidal Antiinammatory Drugs—cont’d
GENERIC NAME BRAND NAME AVAILABILITY
sulindac Teva-Sulindac Tablets: 150, 200 mg
Cyclooxygenase-2 (COX-2) Inhibitors
celecoxib Celebrex Capsules: 50, 100, 200,
400 mg
TIA, Transient ischemic attack.
Available in Canada.
High-alert medication.
effects. NSAIDs block COX-1 and cyclooxygenase-2
(COX-2). Cyclooxygenase is an enzyme that is in-
volved in the manufacturing of prostaglandins.
The NSAIDs all have varying degrees of analgesic,
antipyretic, and antiinammatory activity. Celecoxib is
a COX-2 selective inhibitor, whereas all other NSAIDs
are nonselective COX-1 and COX-2 inhibitors.
Uses
In clinical studies, all of these agents (see Table 19.3)
are superior to placebos. Depending on the agent used,
the dosage, and the patient, the adverse effects of ther-
apy tend to be somewhat less than those associated
with salicylate therapy. There is little difference be-
tween them in effectiveness or tolerance, but there is a
difference in response among individuals, and switch-
ing to another NSAID for better therapeutic effect is
appropriate. Longer-acting NSAIDs may be useful for
patients who have difculty remembering to take fre-
quent doses. There is also substantial cost difference
among NSAIDs, so it makes sense to try the lower-cost
agents before moving to the more expensive agents.
Many of these products are also available in generic
form that will further reduce the expense of therapy.
These agents are used to relieve the pain and inam-
mation of rheumatoid arthritis, osteoarthritis, ankylos-
ing spondylitis, and gout. Certain agents (e.g., ibupro-
fen, ketoprofen, naproxen, diclofenac, celecoxib) are
also approved for use to control the discomfort of pri-
mary dysmenorrhea. Ibuprofen, naproxen, and keto-
profen are available over the counter to be used for the
temporary relief of minor aches and pains associated
Drugs Used for Pain Management CHAPTER 19 325
MAXIMUM DAILY
USES AND DOSAGES DOSAGE (MG)
Rheumatoid arthritis, osteoarthritis, 400
ankylosing spondylitis: 150 mg
twice daily
Acute painful shoulder: 200 mg twice
daily
Rheumatoid arthritis, osteoarthritis: —
100–200 mg twice daily
Ankylosing spondylitis: 200–400 mg
daily
Acute pain and primary
dysmenorrhea: 400 mg initially,
followed by 200 mg on the rst day,
then 200 mg twice daily
Familial adenomatous polyposis: 400
mg twice daily taken with food
with the common cold, headache, toothache, muscle
aches, backaches, arthritis, and menstrual cramps, as
well as to reduce fever. COX-2 inhibitors appear to
have the advantage of causing fewer GI adverse ef-
fects, such as upper GI bleeding. This is signicant
because 7% to 8% of patients experience GI bleeding
while using NSAIDs and it is a primary cause of hos-
pitalizations caused by adverse effects of medications.
In April 2005 the FDA issued a warning about an in-
creased risk of potentially fatal cardiovascular adverse
effects (heart attack, stroke) that could be a class effect
of NSAIDs. In 2015 the FDA strengthened the existing
label warning that nonaspirin NSAIDs increase the
potential of an MI or stroke. The prescription NSAID
labels list the following information:
• The risk of MI or stroke can occur in the rst weeks
of using an NSAID, and the risk may increase with
longer use of the NSAID.
• The risk appears greater at higher doses.
• NSAIDs can increase the risk of MI or stroke in pa-
tients with or without heart disease or risk factors
for heart disease.
• Patients treated with NSAIDs following a rst MI
are more likely to die in the rst year after the MI
compared with patients who were not treated with
NSAIDs after their rst MI.
• NSAIDs increase the risk of heart failure.
• NSAIDs should not be used in patients immediately
after coronary artery bypass graft surgery or MI.
In 2020 the FDA recommended that pregnant
women avoid NSAIDS after 20 weeks of gestation
because of potential interference of the fetus’s ability
326 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems

Table 19.4 Ingredients of Selected Analgesic Combination Products

NONCONTROLLED SUBSTANCE CONTROLLED SUBSTANCE
PRODUCT ASPIRIN (MG) ACETAMINOPHENA (MG) OTHER (MG) CODEINE (MG) OTHER (MG)
Anacin caplets and tablets 400 — Caffeine, 32 — —
Anacin Maximum Strength 500 — Caffeine, 32 — —
BC Powder Arthritis 742 — Caffeine, 38 — —
Strength Salicylamide, 222
Endocet — 325 — — Oxycodone 10
Excedrin Extra Strength 250 250 Caffeine, 65 — —
Fioricet 300 Caffeine, 40 — Butalbital, 50
Fioricet with Codeine 300 Caffeine, 40 30 Butalbital, 50
Codeine, 30 mg
Lortab — 300 — — Hydrocodone, 10
Maxidone — 750 — — Hydrocodone, 10
Percocet 7.5 — 325 — — Oxycodone, 7.5
Percogesic — 325 Diphenhydramine, — —
12.5
Prolate — 300 — — Oxycodone, 10
Ultracet — 325 Tramadol, 37.5 —
mg
aAs of January 2014, acetaminophen content in combination products is limited to a maximum of 325 mg per tablet or capsule.

to produce amniotic uid, which may lead to devel-
opmental complications. Fetuses are also susceptible
to closure of the patent ductus arteriosus of the heart
if NSAIDs are administered in the third trimester of
gestation. It is recommended that pregnant women
consult with their obstetrician if analgesia is needed
during pregnancy.
Serious and potentially life-threatening GI bleed-
ing are associated with NSAIDs. Nonsteroidal anti-
inammatory drugs have also been associated with
allergic reactions, including severe skin reactions and
anaphylaxis, some of which occurred in patients with-
out known prior exposure. If an NSAID is prescribed
for chronic use, the lowest effective dose for the short-
est duration should be used.
2. Monitor vital signs (i.e., temperature, blood pres-
sure, pulse, and respirations).
3. Check laboratory data for hepatotoxicity, nephro-
toxicity, bleeding time, and blood dyscrasias.
4. Monitor for GI symptoms before and during thera-
py; conduct a stool guaiac test if GI tract bleeding is
suspected.
5. Check bowel sounds and note stool consistency.
Review voiding pattern and urine output.
6. Check for concurrent use of anticoagulant agents.
7. When used as an analgesic, perform pain assess-
ment before administering NSAIDs and at appro-
priate intervals during therapy. Report poor pain
control promptly to the healthcare provider and ob-
tain modication in orders.

Therapeutic Outcomes Availability, dosage, and administration. See Table 19.3

The primary therapeutic outcomes expected from
NSAIDs are reduced pain, reduced inammation, and Medication Safety Alert
elimination of fever.
Do not administer NSAIDs to patients who are allergic to
aspirin.
Nursing Implications for NSAIDs
Premedication assessment
1. Perform baseline neurologic assessment (e.g., ori- Common adverse effects
entation to date, time, and place; mental alertness; Gastrointestinal
bilateral hand grip; motor functioning; peripheral Gastric irritation, constipation. If gastric irritation oc-
sensations; and vision and hearing). curs, give medication with food, milk, antacids, or large

amounts of water. If symptoms persist or increase in se-
verity, notify the healthcare provider. The use of stool
softeners or bulk-forming laxatives may be necessary.
Maintain the patient’s state of hydration. Encourage the
patient to include sufcient roughage, fresh fruits, veg-
etables, and whole-grain products in the diet.
Serious adverse effects
Gastrointestinal
Gastrointestinal bleeding. Observe for the develop-
ment of dark, tarry stools and bright red or coffee-
ground emesis. Other factors for increased risk of
bleeding include concurrent use of oral corticosteroids,
anticoagulants, smoking, consuming more than three
alcoholic drinks per day, age older than 60 years, and
poor general health status. Special care should be tak-
en in elderly or debilitated patients.
Hepatotoxicity. The symptoms of hepatotoxicity are
anorexia, nausea, vomiting, jaundice, hepatomegaly,
splenomegaly, and abnormal liver function tests (e.g.,
elevated bilirubin, AST, ALT, and ALP; increased PT).
Hypersensitivity
Hives, pruritus, rash, facial swelling. Report symp-
toms for further evaluation by the healthcare provid-
er as soon as possible. This could become a medical
emergency.
Genitourinary
Nephrotoxicity. Monitor urinalysis and kidney func-
tion tests for abnormal results. Report increasing blood
urea nitrogen and creatinine levels, decreasing urine
output or urine specic gravity despite amount of u-
id intake, casts or protein in the urine, frank blood- or
smoky-colored urine, or RBCs in excess of 0 to 3 on the
urinalysis report.
Hematologic
Blood dyscrasias. Routine laboratory studies (e.g.,
RBC, WBC, and differential counts) should be sched-
uled. Monitor for sore throat, fever, purpura, jaundice,
or excessive and progressive weakness.
Drug interactions
Warfarin. Nonsteroidal antiinammatory drugs in-
crease bleeding risk through platelet inhibition. When
used concurrently with warfarin, the patient may be at
greater risk of bleeding even though the PT and INR
are within therapeutic range. Observe for petechiae;
ecchymoses; nosebleeds; bleeding gums; dark, tarry
stools; and bright red or coffee-ground emesis. The
dosage of warfarin may need to be reduced.
Drugs Used for Pain Management CHAPTER 19 327
Phenytoin. Monitor the patient with concurrent ther-
apy for signs of phenytoin toxicity, such as nystagmus,
sedation, or lethargy. Serum levels may be ordered,
and the dosage of phenytoin may need to be reduced.
Valproic acid. Aspirin inhibits valproic acid metabo-
lism, increasing valproic acid blood levels. Monitor for
valproic acid toxicity: sedation, drowsiness, dizziness,
and blurred vision. Serum levels may be ordered, and
the dosage of valproic acid may need to be reduced.
Oral hypoglycemic agents. Monitor for hypoglycemia:
headache, weakness, decreased coordination, general
apprehension, diaphoresis, hunger, and blurred or
double vision. The dosage of the hypoglycemic agent
may need to be reduced. Notify the healthcare provid-
er if any of these symptoms appear.
Furosemide, thiazide diuretics. Nonsteroidal anti-
inammatory drugs inhibit the diuretic activity of these
agents. The dosage of the diuretic agents may need to
be increased or NSAIDs discontinued. Maintain accu-
rate intake and output and blood pressure records, and
monitor for a decrease in diuretic and antihypertensive
activity.
Angiotensin-converting enzyme inhibitors and angioten-
sin II receptor blockers. Nonsteroidal antiinammatory
drugs may diminish the therapeutic effect of angioten-
sin-converting enzyme inhibitors and angiotensin II
receptor blockers. Monitor for inadequate therapeutic
response.
Probenecid. Probenecid inhibits the excretion of
NSAIDs. Monitor for signs of toxicity: headache,
drowsiness, and mental confusion.
Lithium. Nonsteroidal antiinammatory drugs (ex-
cept possibly sulindac and aspirin) may induce lithium
toxicity. Monitor for lithium toxicity: nausea, anorexia,
ne tremors, persistent vomiting, profuse diarrhea, hy-
perreexia, lethargy, and weakness.
Aspirin. COX-1 inhibitors may reduce the platelet-
inhibiting effects of aspirin when administered at
about the same time. An NSAID may block the recep-
tor on platelets that aspirin would normally bind to,
preventing the platelet inhibition caused by aspirin. To
avoid this interaction, take the aspirin several hours
before the COX-1 NSAID. This might not be possible
for the person with severe rheumatoid arthritis who
needs the analgesic effects around the clock.
Cholestyramine. Cholestyramine resins bind to
NSAIDs in the gut, inhibiting absorption. Separate
dosage administration by 2 hours. The NSAID dosage
may need to be increased.
328 UNIT III Drugs Affecting the Autonomic and Central Nervous Systems

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points NCLEX item type: Extended multiple response

• The pain experience is highly subjective and inuenced by
behavioral, physiologic, sensory, emotional (e.g., attention,
anxiety, fatigue, suggestion, prior conditioning), and
cultural factors for a particular person under a certain set
of circumstances.
• Pain is usually described as acute or short term and as
chronic or long term.
• Analgesics are drugs that relieve pain without producing
loss of consciousness or reex activity.
• Analgesic medications have been divided into opiate
agonists, opiate partial agonists, opiate antagonists, and
prostaglandin inhibitors (acetaminophen, salicylates, and
NSAIDs).
• Pain management has made signicant progress, primarily
because of better understanding of the pain experience;
however, there is still a great deal to do in educating
patients, family, and some healthcare providers about
appropriate pain management.
• Nurses can play an important role in providing counseling
and guidance to these groups in understanding pain and
how to maintain an appropriate balance between daily
activities and timing of analgesics to optimize quality of life.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam
ination-Style Questions The following questions are typical of
the NCLEX examination and include both NGN (Next Genera
tion) and traditional questions. See Chapter 1 for further infor-
mation regarding question types.
Cognitive skill: Analysis cues
2. The nurse reviewing an order for pain medication for the patient
in the scenario who was switched from tramadol to oxycodone
explains to the patient what adverse effects may be experienced.
Which statement by the nurse needs to be revised?
1. “You may feel lightheaded and dizzy after initially taking
this, so be careful getting out of bed.”
2. “It is recommended that you do not drive while taking this
medication as it may impair your alertness and reaction
time.”
3. “Some people get nauseated from taking this, and these
types of drugs tend to cause constipation.”
4. “As long as you have pain, you should continue to take
this medication.”
Objective: Discuss the common adverse effects of opiate agonists.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
3. The nurse is assessing the patient from the scenario who was just
started on oxycodone. When assessing the patient for pain and
the effectiveness of the medication, the nurse will do which of the
following? (Select all that apply.)
1. Request that the patient wait until the proper time to take
pain medication.
2. Question the patient about the location of the pain.
3. Offer the patient a pain scale to quantify the pain.
4. Use open-ended questions to nd out about the pain.
5. Ask about what has worked in the past to control the
pain.
Objective: Describe the pain assessment used for patients
receiving opiate agonists.
NCLEX item type: Multiple response
Cognitive skill: Application
4. The nurse reviewed the difference between fentanyl and
buprenorphine and recognized that they have different properties.
Indicate with an X the properties of the opiate agonists, opiate
partial agonists, and opiate antagonists.

Scenario OPIATE
OPIATE PARTIAL OPIATE
A patient came into the urgent care clinic complaining of back AGONISTS AGONISTS ANTAGONISTS
pain. Relieves severe pain
1. The nurse discovered after interviewing the patient in the scenario Has a ceiling effect
that they had been taking tramadol (Ultram) for several months for analgesia
after an injury. What pain assessment data needs to be collected Development of drug
to help the nurse determine the appropriate intervention? (Select tolerance may occur
all that apply.)
Physical dependence
1. Determine the patient’s perception of pain may develop after
2. Obtain height and weight 3–6 weeks of use
3. Gather details regarding the injury Reverses respiratory
4. Ask patient to rate pain on scale of 0 to 10 depression from
5. Determine pupillary response opiates
6. Inquire about medication history
7. Observe nonverbal body positioning May induce
withdrawal
Objective: Describe the pain assessment used for patients symptoms
receiving opiate agonists.
 Drugs Used for Pain Management CHAPTER 19 329

Objective: Differentiate among the properties of opiate agonists, 7. The nurse explains which of the many properties of diunisal to
opiate partial agonists, and opiate antagonists. the patient with osteoarthritis? (Select all that apply.)
NCLEX item type: Matrix 1. “This drug is classied as a prostaglandin inhibitor.”
Cognitive skill: Evaluate outcomes 2. “The adverse effects that need to be monitored include
5. While preparing aspirin for a patient, the nurse reviewed which of GI bleeding and liver function tests.”
the pharmacologic effects of salicylates? (Select all that apply.) 3. “When taking salicylate therapy, you need to be careful
with diuretic agents, because the diunisal may increase
1. Analgesic the effectiveness of the diuretic.”
2. Anesthetic 4. “This drug may require the monitoring of your kidney
3. Antidote function so that adverse effects are identied.”
4. Antiinammatory 5. “If you need to take this long term, we will generally have
5. Antiemetic you take the lowest effective dose to minimize adverse
6. Antipyretic effects.”
7. Antiepileptic
8. Antacid Objective: Describe the three pharmacologic effects of salicylates.
NCLEX item type: Multiple response
Objective: Describe the three pharmacologic effects of salicylates. Cognitive skill: Application
NCLEX item type: Extended multiple response
Cognitive skill: Analyze cues 8. The nurse explained to the patient in the scenario that there are
antidotes in case of an overdose of oxycodone. Which statement by
6. The nurse discussed with the patient in the scenario the difference the nurse is correct?
between adverse effects and drug interactions. Indicate with an
X the common adverse effects, serious adverse effects, and drug 1. “The drug naltrexone is used to block the effects of
interactions associated with salicylates. opiates and can be given sublingually.”
2. “The drug naloxone can be given intranasally and is used
to reverse the respiratory depression secondary to opiate
COMMON SERIOUS overdose.”
ADVERSE ADVERSE DRUG
3. “The drug naloxone is available orally and has no other
EFFECT EFFECT INTERACTION
effect than to reverse the CNS depression caused by
Salicylism opiates.”
Enhanced 4. “The drug naltrexone is used to treat respiratory
hypoglycemic depression with excessive doses of opiates and can be
effect given IV.”
Gastrointestinal Objective: Identify opiate antagonists and expected therapeutic
bleed outcomes to monitor.
Enhanced NCLEX item type: Multiple choice
anticoagulation Cognitive skill: Application
effect
Gastric irritation

Objective: Compare the common and serious adverse effects and

drug interactions associated with salicylates.
NCLEX item type: Matrix
Cognitive skill: Evaluate outcomes
Unit IV Drugs Affecting the Cardiovascular System

20 Introduction to Cardiovascular Disease

and Metabolic Syndrome
https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the major risk factors for the development of
metabolic syndrome.
2. Discuss the importance of lifestyle modication in the
management of metabolic syndrome.
3. Explain the treatment goals for type 2 diabetes management,
lipid management, and hypertension management.
4. Discuss the drug management of the underlying diseases
in patients with metabolic syndrome.

Key Terms
cardiovascular disease (kăr-dē-ō-
VĂS-kyū-lăr) (p. 330)
atherosclerotic cardiovascular
disease (ăth-ĕr-ō-sklĕ-RŎ-tĭk) (p.
330)
coronary artery disease (KŎR-ō-
năr-ē ĂR-tĕr-ē) (p. 330)
angina pectoris (ăn-JĪ-nă PĔK-tŏr-ĭs)
(p. 330)
myocardial infarction (mī-ō-KĂR-dē-
ăl ĭn-FĂRK-shŭn) (p. 330)
stroke (STRŌK) (p. 330)
hypertension (hī-pĕr-TĔN-shŭn) (p.
330)
dysrhythmias (dĭs-RĬTH-mē-ăz) (p.
330)
peripheral vascular disease (pĕ-RĬF-
ĕr-ăl VĂS-kū-lăr) (p. 330)
peripheral arterial disease (pĕ-RĬF-
ĕr-ăl ăr-TĒR-ē-ŭl) (p. 330)
heart failure (HĂRT FĀL-yŭr) (p. 330)
insulin resistance syndrome (ĬN-sŭl-
ĭn rē-ZĬS-tĕns) (p. 331)
metabolic syndrome (mĕt-ĕ-BŎL-ĭk)
(p. 331)
body mass index (BMI) (BŎ-dē MĂS
ĬN-dĕks) (p. 331)

CARDIOVASCULAR DISEASES
Cardiovascular disease is a collective term used to refer
to disorders of the circulatory system (heart, arteries,
veins) of the body. The total and indirect costs of car-
diovascular disease and stroke between 2014 and 2015
were $351.3 billion ($213.8 billion in direct costs and
$137.5 billion in lost productivity/mortality) (Virani
etal., 2020).
These diseases have been subdivided into the areas
or organs of the body in which the pathology is most
obvious, such as atherosclerotic cardiovascular disease,
which refers to narrowing of arteries by atherosclerotic
plaques caused by hypercholesterolemia, and coronary
artery disease (see Chapter 21), which refers to narrow-
ing or obstruction of the arteries of the heart, leading to
angina pectoris and myocardial infarction (Chapter 24).
Stroke (see Chapter 26) refers to either an obstruction
(ischemic stroke) or rupture (hemorrhagic stroke) of
blood vessels in the brain. An increase in the pressure
with which blood circulates through the arteries and
veins is referred to as hypertension (see Chapter 22).
Dysrhythmias (see Chapter 23) are abnormalities in the
electrical conduction pathways of the heart that lead to
inefcient pumping of blood through the circulatory
system. Peripheral vascular disease involves disorders
330
of the blood vessels of the arms and legs. It can be sub-
divided into two types, depending on whether it is
arterial or venous in origin: peripheral arterial disease
(see Chapter 25), such as obstructive arterial disease, or
venous disorders, such as acute deep vein thrombosis
(see Chapter 26). The long-term pathology of any one
or a combination of these diseases affecting the circula-
tory system leads to heart failure (see Chapter 27) and
eventual death.
METABOLIC SYNDROME
Many causative factors lead to cardiovascular disor-
ders. Lifestyle is recognized as the greatest contribu-
tor to a variety of diseases that reduce the quality of
life and end lives prematurely. Research indicates that
persons with hypertension, diabetes mellitus, dys-
lipidemia, and obesity—alone or in combination—are
at greater risk for progressive cardiovascular disease.
In 1988 a unifying pathway of insulin resistance,
called syndrome X, was described In 1998 the World
Health Organization provided a working denition
for this syndrome and renamed it metabolic syndrome.
Insulin resistance leads to type 2 diabetes and in-
duces atherosclerosis, which leads to coronary artery
 Introduction to Cardiovascular Disease and Metabolic Syndrome CHAPTER 20
Table 20.1 Denitions and Characteristics of
Metabolic Syndromea
NATIONAL
CHOLESTEROL
EDUCATION PROGRAM
(UNITED STATES)
RISK FACTOR DEFINING LIMIT MEN WOMEN
Waist circumference (inches)b >40 >35
High-density lipoprotein <40 <50
cholesterol (mg/dL)
Triglycerides (mg/dL)c >150 >150
Blood pressure (mm Hg) >130/85 >130/85
Fasting glucose (mg/dL) >100 >100
aPeople with central obesity and at least two of the remaining four factors are
considered to have metabolic syndrome.
bThere are specic circumferences for different ethnicities in the International
Diabetes Federation document cited below.
cThis also applies to those individuals with previously diagnosed type 2
diabetes.
Data from Alberti KG, Eckel RH, Grundy SM, etal; International Diabetes
Federation Task Force on Epidemiology and Prevention; National Heart, Lung,
and Blood Institute; American Heart Association; World Heart Federation;
International Atherosclerosis Society; International Association for the Study of
Obesity. Harmonizing the metabolic syndrome: a joint interim statement of the
International Diabetes Federation Task Force on Epidemiology and Prevention;
National Heart, Lung, and Blood Institute; American Heart Association; World
Heart Federation; International Atherosclerosis Society; and International
Association for the Study of Obesity. Circulation. 2009;120(16):1640-1645;
and from International Diabetes Federation. The IDF Consensus Worldwide
Denition of the Metabolic Syndrome. Brussels, Belgium: International Diabetes
Federation; 2006. Available at https://www.idf.org/e-library/consensus-
statements.html.
disease. Historically, the hypothesis of insulin resis-
tance has been studied in great depth, and the syn-
drome has been renamed to be more descriptive of
the underlying causes. Other terms include diabe-
sity, insulin resistance syndrome, and, more recently,
cardiometabolic syndrome.
Metabolic syndrome is still the most commonly used
term worldwide. The key characteristics of metabolic
syndrome are the presence of type 2 diabetes mellitus,
abdominal obesity, hypertriglyceridemia, low levels of
high-density lipoproteins (HDLs), and hypertension.
Although metabolic syndrome occurs worldwide,
an estimated 34.7% of adults (i.e., one in three) in the
United States have metabolic syndrome. Hispanics
have the highest rate (35.4%), followed by whites
(33.4%) and blacks (32.7%). It is estimated that about
4.5% of adolescents between the ages of 12 and 17
years also have metabolic syndrome.
Table 20.1 gives the denition of metabolic syn-
drome provided in a consensus statement by several
international organizations that study atherosclerosis,
obesity, cardiovascular disease, and diabetes (Alberti,
2009). People with central obesity and any two of the
four other criteria are dened as having metabolic
syndrome.
RESULTING CONDITIONS
People with metabolic syndrome are three times
more likely to have (and twice as likely to die of)
a heart attack or stroke than people without the
331
syndrome. People with metabolic syndrome have
a vefold greater risk of developing type 2 diabe-
tes. On a global scale, up to 80% of the 200 million
people with diabetes will die as a result of cardio-
vascular disease. This puts the prevalence of meta-
bolic syndrome and diabetes substantially ahead of
HIV/AIDS in terms of morbidity and mortality, yet
the problem is not as well recognized. In addition
to type 2 diabetes and heart disease, other factors
associated with metabolic syndrome include renal
disease, obstructive sleep apnea, polycystic ovary
syndrome, cognitive decline in older adults, and de-
mentia in older adults.
RISK FACTORS
Obesity and Sedentary Lifestyle
Risk factors for the development of metabolic syn-
drome include poor diet, sedentary lifestyle (lack
of exercise), and genetic predisposition. The dietary
habits of most Americans have changed signicantly
over the past 20 years, causing a dramatic increase in
weight gain in the United States. Simply put, weight
gain occurs when energy intake (food calories) exceeds
energy expenditure (burning calories). Categories of
obesity are determined by using the body mass in-
dex (BMI). BMI is described as weight in proportion to
height. BMI is calculated the same way for both adults
and children. The calculation is based on the following
formulas:
Kilograms and Meters (or Centimeters)
Weight in kilograms (kg)
BMI =
(Height in meters [m])2
With the metric system, the formula for BMI is
weight in kilograms divided by height in meters
squared. Because height is commonly measured in
centimeters, divide the height in centimeters by 100
to obtain the height in meters.
Example: Weight = 68 kg, height = 165 cm (1.65 m)
Calculation: 68 ÷ (1.65)2 = 24.98
Pounds and Inches
Weight in pounds (Ib)
BMI = 703
(Height in inches [in])2
Calculate the BMI by dividing the weight in pounds (lb)
by the height in inches (in) squared and multiplying by
a conversion factor of 703.
Example: Weight = 150 lb, height = 5 5″ (65″)
Calculation: (150 ÷ 652) × 703 = 24.96
The National Heart, Blood and Lung Institute guide-
lines also describe overweight and obesity in terms of
the BMI. Table 20.2 shows the relationship between
BMI and weight (healthy weight, overweight, or
obesity).
According to comparison data from the Centers for
Disease Control and Prevention (CDC, 2019), in all
states more than 20% of adults were obese. One state
had a prevalence of 20% to less than 25%; 25 states had
a prevalence of 25% to 30%; 23 states had a prevalence
332 UNIT IV Drugs Affecting the Cardiovascular System
Table 20.2 Relationship Between Body Mass Index
and Categories of Obesity
BODY MASS INDEX (KG/M2) RELATIONSHIP TO WEIGHT
<18.5 Underweight
18.5–24.9 Normal weight
25–29.9 Overweight
30–34.9 Obesity, class I
35–39.9 Obesity, class II
>40 Obesity, class III
(extreme obesity)
of 30% to less than 35%; and 12 states had a prevalence
of 35% or higher. Fig. 20.1 presents a comparison of
obesity rates by race/ethnicity and state.
A sedentary lifestyle contributes to overweight
and obesity. New technologies such as labor-saving
devices and remote-control devices, as well as the
availability of entertainment through television and
computers, have signicantly reduced daily caloric
expenditure. Today, despite common knowledge
that regular exercise promotes health, the CDC re-
ports that all states had more than 15% of adults who
were physically inactive (engaging in no leisure-time
physical activity) and ranged from 17.3% to 47.7%.
Inactivity levels vary among adults by race/ethnicity
and location.
Longer working hours that lead to less time to pre-
pare food at home and larger portions of commercially
prepared food aggravate the problem. The ease and
convenience of food preparation (e.g., fast-food restau-
rants, drive-through windows, the use of a microwave
versus a convection oven) and increases in portion
sizes have placed too many easily consumed calories
on the table. Consequently, reduced physical activity
and increased caloric intake have resulted in a national
epidemic of obesity.
Alcohol, Smoking, and Stress
Other negative lifestyle choices, such as excessive
consumption of alcohol and cigarette smoking, ag-
gravate metabolic syndrome. Excessive alcohol con-
sumption causes fat accumulation in the liver, which
is also associated with metabolic syndrome. Cigarette
smoking is a major contributor to pulmonary disease
(see Chapter 30) and hypertension (see Chapter 22).
One study showed that employees with chronic work
stress were more than twice as likely to have meta-
bolic syndrome as those without work-related stress.
Another study demonstrated that patients with job-
related stress had a twofold increase in the risk of
recurrent unstable angina and myocardial infarction.
Genetic Factors
Genetic factors inuence each component of the syn-
drome, as well as the syndrome itself. A family history
of rst-degree relatives (e.g., parents, siblings) that in-
cludes type 2 diabetes, hypertension, and early heart
disease (e.g., angina, heart attack) greatly increases the
likelihood that an individual will develop metabolic
syndrome (Fig. 20.2).
TREATMENT
The variety of factors associated with the presence of
metabolic syndrome requires an individualized ap-
proach to treatment that is based on a person’s specic
risk factors and diseases present. Lifestyle manage-
ment is critical to prevent and treat the comorbidities
that make up the metabolic syndrome. Research indi-
cates that lifestyle changes alone may delay the onset
of type 2 diabetes mellitus by more than 50%. The
overall treatment goals for metabolic syndrome are
listed in Table 20.3
Weight loss and increased physical activity are usu-
ally the rst steps of treatment. Reducing the number
of calories consumed—while burning more calories—
can have very positive effects in treating metabolic
syndrome. Even a 10- to 15-pound weight loss can im-
prove hypertension and hyperglycemia. Initial thera-
peutic goals are a 7% to 10% weight reduction during
the rst year of treatment, with an ongoing goal of a
BMI less than 25 kg/m2. Several dietary approach-
es can be used to lose weight. Adopting the DASH
(Dietary Approaches to Stop Hypertension) diet may
help patients who also have hypertension (see Chapter
22). The Mediterranean diet—one rich in “good” fats
(e.g., olive oil), containing a reasonable amount of car-
bohydrates, and with protein from sh and chicken—
is frequently recommended. The diet should include
reduced intake of saturated fat (<7% of total calories),
lower cholesterol levels (<200 mg/day), and lower
total fat intake (25% to 35% of total calories). Most
dietary fat should be unsaturated, and the intake of
simple sugars should be reduced. Nonpharmacologic
therapy must include eliminating cigarette smoking,
restricting alcohol intake, reducing stress, and control-
ling sodium (see Chapter 22). Other appropriate diet
plans are the US Department of Agriculture MyPlate
Food Guide or the American College of Cardiology/
American Heart Association diet recommendations
(see Chapter 46).
The American Association of Clinical Endocri-
nologists and the American College of Endocrinology
recommend lifestyle therapy that includes a healthy
meal plan (e.g., DASH diet, Mediterranean diets) and
a physical activity program incorporating both aero-
bic and resistance exercise to maintain a BMI of 18 to
25 kg/m2 (Garvey, 2016). Most patients with the meta-
bolic syndrome are overweight, and weight reduction,
which improves insulin sensitivity, is an important
outcome goal of any diet. If the patient is overweight,
a 10% weight loss is recommended. Physical activity
should include aerobic and resistance training. The
 Introduction to Cardiovascular Disease and Metabolic Syndrome CHAPTER 20 333

Prevalence of Self-Reported Obesity Among Hispanic Adults by State and Territory, BRFSS, 2016-2018

ME
WA

MT ND VT
NH
MN
OR MA
ID NY RI
WI CT
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NV IL IN
WV
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CO
CA KS MO KY
NC
TN
OK SC
AR
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AL GA
MS
20%-<25%
25%-<30%
TX LA
30%-<35%
FL
≥35%
Insufficient data*
AK

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Obesity Among Non-Hispanic Black Adults by State and Territory, BRFSS, 2016-2018

ME
WA

MT ND VT
NH
MN
OR MA
ID NY RI
WI CT
SD MI

WY PA NJ
IA DC
NE OH MD DE
NV IL IN
WV
UT VA
CO
CA KS MO KY
NC
TN
OK SC
AR
AZ NM <20%
AL GA
MS
20%-<25%
25%-<30%
TX LA
30%-<35%
FL
≥35%
Insufficient data*
AK

HI GU PR

Fig. 20.1 Prevalence of self-reported obesity among US adults by race/ethnicity, state, and territory, BRFSS, 2017
to 2019. *Sample size <50 or the relative standard error (dividing the standard error by the prevalence) ≥ 30%. (From
Behavioral Risk Factor Surveillance System [BRFSS], National Center for Chronic Disease Prevention and Health
Promotion, Division of Population Health, Centers for Disease Control and Prevention; retrieved from https://www.cdc.g
ov/obesity/data/prevalence-maps.html.)
334 UNIT IV Drugs Affecting the Cardiovascular System

Prevalence of Self-Reported Obesity Among Non-Hispanic White Adults by State and Territory, BRFSS, 2016-2018

ME
WA

MT ND VT
NH
MN
OR MA
ID NY RI
WI CT
SD MI

WY PA NJ
IA DC
NE OH MD DE
NV IL IN
WV
UT VA
CO
CA KS MO KY
NC
TN
OK SC
AR
AZ NM <20%
AL GA
MS
20%-<25%
25%-<30%
TX LA
30%-<35%
FL
≥35%
Insufficient data*
AK

HI GU PR

Fig. 20.1, cont’d

ultimate goal for aerobic exercise should be ≥150

min/week of moderate exercise (such as brisk walk-
ing) performed during three to ve daily sessions
per week. Resistance training should be done two
to three times per week consisting of single-set exer-
Genetic Environmental cises of the major muscle groups. Resistance training
factors factors helps promote fat loss while preserving fat-free mass.
Abnormal Physical activity should be individualized based on
Inflammation
vascular response the capabilities and preferences of the patient, taking
High
High Metabolic blood glucose into account health-related and physical limitations.
blood pressure Syndrome level A healthy meal plan and physical activity improves
High
triglyceride Insulin
Low
HDL-C level
blood pressure, glucose levels, and triglycerides and
level
resistance increases HDL levels. The exercise sessions do not
Visceral Prothrombotic have to be completed at the same time; rather, they
adiposity state
can be worked into a person’s daily activities. More
recent guidelines to reduce low-density lipoprotein
(LDL) cholesterol and non-HDL cholesterol (see
Cardiovascular Diabetes
Chapter 21) and blood pressure (see Chapter 22) rec-
events ommend exercise.
If, after lifestyle modications and diet and exercise,
the patient is not able to meet the therapeutic goals
for treating metabolic syndrome, drug therapy may
be necessary. Patient education is vitally important
to make patients aware of and to treat metabolic syn-
drome. This education should be emphasized and reit-
erated frequently by the primary healthcare provider,
the pharmacist, and the nurse.
The primary prevention of metabolic syndrome is
becoming a common thread in the curriculum of chil-
Fig. 20.2 Mechanisms of metabolic syndrome. HDL-C, High-density dren in the primary grades. This education focuses on
lipoprotein cholesterol.
 Introduction to Cardiovascular Disease and Metabolic Syndrome CHAPTER 20 335

Table 20.3 General Treatment Goals for Patients With Metabolic Syndrome
LIFESTYLE RISK FACTORS
Abdominal obesity
METABOLIC RISK FACTORS
Elevated blood pressure
Elevated glucose
Dyslipidemia
BP, blood pressure; BMI, body mass index; LDL, low density lipoprotein; HDL, high density lipoprotein.
MANAGEMENT
Diet:
•  Adopting the DASH (Dietary
Approaches to Stop Hypertension)
•  The Mediterranean diet
Physical activity
See lifestyle management
Pharmacotherapy (Table 20.4)
See lifestyle management
Pharmacotherapy (see Table 20.4)
See lifestyle management
Pharmacotherapy (see Table 20.4)
GOALS
Reduce body weight by 7%–10% during year 1 of
therapy. Continue weight loss thereafter to extent
possible with goal to ultimately achieve desirable weight
(BMI 25 kg/m2).
Reduce saturated fat to less than 7% of total calories.
Reduce trans-fat.
Limit total fat to 25%–35% of total calories. Most dietary
fat should be unsaturated.
Dietary cholesterol less than 200 mg/dL; total fat
25%–35% of total calories. Most dietary fat should be
unsaturated.
Simple sugars should be limited.
Regular moderate-intensity physical activity; at least 30
min of continuous or intermittent (and preferably 60 min)
5 days per week but preferably daily.
Reduce BP < 130/80 mm Hg.
Delay progression to type 2 diabetes mellitus.
For diabetes, hemoglobin A1C less than 7.0%.
•  Fasting plasma glucose <120 mg/dL
•  Postprandial plasma glucose <180 mg/dL
LDL less than 100 mg/dL (individualized)
Triglycerides less than 150 mg/dL
HDL > 50 mg/dL for women
HDL > 40 mg/dL for men

the importance of moderate activity, dietary choices,
and the prevention of alcohol consumption and smok-
ing. Resources from the US Department of Agriculture,
such as the MyPlate Food Guide (see Chapter 46), are
often used as guidelines for this education; age- and
gender-related activity and dietary information are
also described.
Drug Therapy to Treat Underlying Conditions for
Metabolic Syndrome and Cardiovascular Disease
Hypertension. A combination of a thiazide diuretic
plus an angiotensin-converting enzyme inhibitor, cal-
cium channel blocker, or angiotensin receptor blocker
will be necessary to treat hypertension in nonblack pa-
tients. In the general black population, including those
with diabetes, initial treatment should include a thia-
zide-type diuretic or calcium channel blocker. Other
combinations of therapy may be used, depending on
the person’s race and the presence of other diseases
(Table 20.4 see Chapter 22 for a discussion of the treat-
ment of hypertension).
Dyslipidemia. The treatment of dyslipidemia is gen-
erally to lower triglyceride and LDL cholesterol
levels and to raise the HDL cholesterol level. After
lifestyle changes, the medicines most commonly used
are 3-hydroxymethylglutaryl coenzyme A reductase
inhibitors (also known as statins). (See Table 20.4
and Chapter 21 for a discussion of the treatment of
dyslipidemias.)
Type 2 diabetes mellitus. Several different classes of
medicines may be used to treat insulin resistance and
type 2 diabetes. The thiazolidinediones reduce in-
sulin resistance in the peripheral tissues. Metformin
decreases the production of glucose by the liver; to a
lesser extent it also reduces insulin resistance in the pe-
ripheral tissues. Alpha-glycosidase inhibitors reduce
the absorption of glucose from the intestine, reducing
postprandial hyperglycemia. Sulfonylureas and meg-
litinides stimulate the beta cells of the pancreas to re-
lease more insulin. The sodium-glucose cotransporter
2 inhibitors (SGLT-2 inhibitors) reduce renal glucose
reabsorption in the kidneys, enhancing urinary glu-
cose excretion. SGLT-2 inhibitors are also effective in
reducing the risk of hospitalization for heart failure
associated with cardiovascular disease. Insulin injec-
tions also benet patients who do not secrete adequate
amounts of insulin. (See Table 20.4 and Chapter 35 for a
discussion of the treatment of type 2 diabetes mellitus.)
336 UNIT IV Drugs Affecting the Cardiovascular System

Table 20.4 Medicines Used to Treat Diseases That Contribute to Cardiovascular Disease a
ANGINA THROMBOSIS, HEART DIABETES
CLASSES OF MEDICINES DYSLIPIDEMIAS HYPERTENSION DYSRHYTHMIAS PECTORIS STROKE FAILURE MELLITUS
See also Chapter(s): 21 22 23 24 25, 26 27 35
Thiazide diuretics X
ACE inhibitors X X X X
ARBs X X
Beta blockers X X X X
Calcium channel blockers X X X
Propafenone X
Amiodarone X
Ranolazine X
Furosemide X
Spironolactone X
Statins X
PSCK-9 inhibitors X
Icosapent X
Nitrates X
Insulins X
Metformin X
SGLT-2 inhibitors X X
Sulfonylureas X
Thiazolidinediones X
Meglitinides X
Factor X inhibitors X
Warfarin X
Key: Thiazide diuretics, peripheral vasodilator, distal tube diuretic; ACE inhibitors, angiotensin-converting enzyme inhibitors; ARBs, angiotensin receptor blocking
agents; beta blockers, beta-adrenergic blocking agents; calcium channel blockers, class IV antidysrhythmic agents; propafenone, class Ic antidysrhythmic agent;
amiodarone, class III antidysrhythmic agent; ranolazine, myocardial cell sodium channel blocker; furosemide, loop diuretic; spironolactone, aldosterone inhibitor that
reduces mortality in heart failure; statins, reduce low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) cholesterol from blood, reducing plaque formation;
PSCK-9 inhibitors, reduce LDL cholesterol by a different pathway than the statins; icosapent, lowers triglyceride blood levels; nitrates, coronary vasodilator; insulins,
prevent reabsorption of glucose in kidneys; metformin, reduces glucose production by liver; SGLT-2 inhibitors, prevent reabsorption of glucose in kidneys; sulfonylureas,
stimulate release of insulin from pancreas to lower blood glucose levels; thiazolidinediones, aid insulin entry into peripheral cells; meglitinides, stimulate release of insulin
from pancreas to lower blood glucose levels; factor X inhibitors, anticoagulants; warfarin, anticoagulant.
aLifestyle changes are required to assist medicine.

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points Additional Learning Resources

• Cardiovascular diseases are a major cause of premature SG Go to your Study Guide for additional Review Questions
death in the United States. for the NCLEX® Examination, Critical Thinking Clinical Situa-
• More than 34% of the US adult population has metabolic tions, and other learning activities to help you master this chap-
syndrome; these individuals are at much greater risk ter content.
for cardiovascular diseases. The key characteristics
of metabolic syndrome are type 2 diabetes mellitus,
abdominal obesity, hypertriglyceridemia, a low HDL Online Resources
cholesterol level, and hypertension.
Centers for Disease Control and Prevention, updated 2017–
• The most cost-effective and successful forms of treatment
2019 Adult Obesity Prevalence Maps and access to other il-
are smoking cessation, weight reduction, exercise, stress
lustrations and information: https://www.cdc.gov/obesity/data
reduction, and dietary modications. If changes in diet and
/prevalence-maps.html
exercise do not produce an acceptable decrease in blood
lipid levels, blood glucose levels, and hypertension, antilipemic
Clinical Judgment and Next-Generation NCLEX® Exam-
agents, antihyperglycemic agents, and antihypertensive
ination-Style Questions The following questions are typical of
agents may be added to the patient’s regimen.
 Introduction to Cardiovascular Disease and Metabolic Syndrome CHAPTER 20 337

the NCLEX examination and include both NGN (Next Genera-
tion) and traditional questions. See Chapter 1 for further infor-
mation regarding question types.
Scenario
4. Patients with metabolic syndrome need to have their diabetes,
hypertension, and hyperlipidemia managed.
Indicate with an arrow which intervention is used to manage
which disease process in metabolic syndrome.

A patient with metabolic syndrome who requires drug therapy Statin medications •  Hypertension
after lifestyle changes were not effective was told by the nurse
Thiazide diuretics
that drugs may be used to manage the underlying diseases (hy-
pertension, hyperlipidemia) causing the metabolic syndrome. Calcium channel blockers •  Diabetes

1. Which risk factors for metabolic syndrome should the nurse SGLT-2 inhibitors
include when assessing the patient in the scenario who came into ACE inhibitor •  Hyperlipidemia
the clinic for a yearly checkup? (Select all that apply.) Metformin
1. Smoking Icosapent
2. Regular exercise
3. Valvular heart disease
4. Genetic predisposition Objective: Explain the treatment goals for type 2 diabetes
5. High blood pressure management, lipid management, and hypertension management.
6. Being underweight NCLEX test item: Extended drop and drag
7. Sedentary lifestyle Cognitive skill: Recognize cues
8. Obesity
5. The patient in the scenario was explaining to the nurse that they
9. Type 2 diabetes
were told that they will have to start taking medications to control
Objective: Identify the major risk factors for the development of their metabolic syndrome. Which medications would the nurse
metabolic syndrome. explain to the patient that are used for this issue? (Select all that
NCLEX test item: Extended multiple response apply.)
Cognitive skill: Analyzed cues
1. Thiazide diuretics
2. The patient in the scenario has a BMI of 29. Which statement by the 2. Testosterone
nurse helps the patient to understand what this number means? 3. Statins
4. Analgesics
1. “This BMI indicates that you are underweight.”
5. Angiotensin-converting enzyme inhibitors
2. “This means that you are within the expected normal
weight.” Objective: Discuss the drug management of the underlying
3. “A BMI over 25 indicates that you are considered diseases in patients with metabolic syndrome.
overweight and close to obese.” NCLEX test item: Multiple response
4. “According to the chart this BMI indicates that you are Cognitive skill: Application
considered obese, class I.”
6. A nurse is explaining to a patient the risk factors that are involved
Objective: Discuss the importance of lifestyle modication in the in developing metabolic syndrome. The nurse realized the patient
management of metabolic syndrome. needs further education after the patient made which statement?
NCLEX test item: Multiple choice
1. “I can control my diet, and get exercise routinely, to try to
Cognitive skill: Explanation
control my weight.”
3. A patient in the clinic asked the nurse for ways to reduce the risk 2. “If I limit eating at restaurants to only three times a week
of developing metabolic syndrome. Which statement by the nurse instead of ve, I should be able to control my weight.”
is appropriate? 3. “I know that diabetes runs in my family, so I will control
my diet and get my blood sugar checked every year.”
1. “You can’t do anything to prevent metabolic syndrome
4. “I routinely check my blood pressure at home and have
because it is in your genes.”
switched to the DASH diet to prevent hypertension.”
2. “The best thing you can do to prevent metabolic syndrome
is to not get diabetes.” Objective: Identify the major risk factors for the development of
3. “Lifestyle modications, including a heart-healthy diet metabolic syndrome.
and exercise, are important to practice to prevent the NCLEX test item: Multiple choice
development of metabolic syndrome.” Cognitive skill: Application
4. “If you routinely get your blood checked for high cholesterol
and eat a low-fat diet, you will not get metabolic syndrome.”
Objective: Discuss the importance of lifestyle modication in the
management of metabolic syndrome.
NCLEX test item: Multiple choice
Cognitive skill: Comprehension
21 Drugs Used to Treat Dyslipidemias

https://evolve.elsevier.com/Willihnganz

Objectives
1. Describe atherosclerosis and identify the ve major types 4. Differentiate between how statins work to control lipid
of lipoproteins. levels and how the bile acid resins work to control lipid
2. Describe the primary approaches to treat lipid disorders. levels.
3. Determine which antilipemic medications are used for
cholesterol control and which can be used for triglyceride
control.

Key Terms
atherosclerotic cardiovascular
disease (ASCVD) (ăth-ĕr-ō-sklĕ-
RŎ-tĭk) (p. 338)
atherosclerosis (ăth-ĕr-ō-sklĕ-RŌ-sĭs)
(p. 338)
hyperlipidemia (hī-pĕr-lĭp-ĭ-DĒ-mē-ă)
(p. 338)
dyslipidemias (dĭs-lĭp-ĭ-DĒ-mē-ăz)
(p.338)
cholesterol (kō-LĔS-tĕ-rŏl) (p. 338)
triglycerides (trī-GLĬ-sĕ-rīdz) (p. 338)
lipoproteins (lī-pō-PRŌ-tēnz) (p. 338)
chylomicrons (kī-lō-MĪ-krŏnz) (p. 338)

ATHEROSCLEROTIC CARDIOVASCULAR TYPES OF LIPOPROTEINS

DISEASE
Fr an inrducin  cardivacular dia, 
Chapr 20. Crnary arry dia (CAD) (al calld
coronary heart disease) i a majr cau f prmaur
dah in h Unid Sa and m hr indurial-
izd nain. Alm n-hird (31.9%) f h US ppu-
lain will di f a har aack r rk aciad wih
atherosclerotic cardiovascular disease (ASCVD), wih
rk aln accuning fr n in vry 6 dah in h
Unid Sa. Majr raabl cau f ASCVD ar ciga-
r mking, dnary lifyl, and pr aing habi
lading  biy, hyprnin, yp 2 diab mlliu,
and ahrclri (Viranni  al., 2020). Atherosclerosis
i characrizd by h accumulain f fay dpi n
h innr wall f h arri and arril hrughu
h bdy ha rduc h bld upply  vial rgan,
ruling in rk, angina pcri, mycardial infarc-
in, and priphral vacular dia. A primary cau f
ahrclri i h abnrmal lvain f chlrl
and riglycrid lvl in h bld. Hyperlipidemia i h
brad rm ud  claify pain wih high lvl f
bld fa (lipid). Dyslipidemias ar furhr dnd un-
dr hyprlipidmia a abnrmalii ha invlv n r
mr f h bld lipid. Dylipidmia can b h rul
f gnic abnrmalii, cndary cau (.g., lifyl,
drug, undrlying dia), r bh. A di ha i high in
aurad fa, chlrl, carbhydra, al calri,
and alchl and a dnary lifyl cnribu igni-
canly  dylipidmia.
338
Cholesterol i a naurally ccurring ubanc ha i
nial fr ynhizing h bdy rid ha ar
ud by h ndcrin ym, fr ynhizing h
bil acid ha ar ndd fr fd abrpin, and fr
cll mmbran ynhi. Th bdy i abl  manu-
facur nugh chlrl  m i mablic nd.
Hwvr, h bdy al cnvr xc diary carb-
hydra in triglycerides (a prcurr f chlrl),
and i cnvr diary fa in chlrl. Afr bing
abrbd frm h garininal (GI) rac, fa (lip-
id), riglycrid, and chlrl ar bund  circu-
laing prin calld lipoproteins fr ranpr hrugh
h bdy.
Lipprin ar ubdividd in v cagri n
h bai f hir cmpiin: chylmicrn, vry-lw-
dniy lipprin (VLDL), inrmdia-dniy
lipprin, lw-dniy lipprin (LDL), and
high-dniy lipprin (HDL). Th v yp diffr
in rlaiv cncnrain f riglycrid, chlrl,
and prin. Clinically, h inrmdia-dniy lip-
prin (IDL) ar includd in h LDL maurmn.
Individually, h IDL cni f 23% riglycrid and
34% chlrl and LDL cni f 6% riglycrid
and 53% chlrl. Chylomicrons cni f abu
90% riglycrid and 5% chlrl; VLDL rprn
abu 15%  20% f al rum chlrl and m
f h al bld riglycrid cncnrain, whra
HDL cnain abu 20%  30% chlrl and 1% 
7% riglycrid.

Vey-low-
Chylomicrons
density
(ultra-low-
lipoproteins
density)
(VLDLs)
90% 55%
triglycerides triglycerides
5% 15% to 20%
cholesterol cholesterol
Fig. 21.1 The ve lipoprotein categories based on their composition: chylomicrons, very-low-density lipoproteins (VLDLs),
intermediate-density lipoproteins (IDLs), low-density lipoproteins (LDLs), and high-density lipoproteins (HDLs). (Redrawn
from McFarlane C, Young IS, Hare L, Mahon G, McEneny J. A rapid methodology for the isolation of intermediate-density
lipoprotein: characterization of lipid composition and apoprotein content. Clinica Chimica Acta 2004;353(2005):117–125.
https://doi.org/10.1016/j.cccn.2004.10.010)
Th purp f HDL appar  b  ranpr
chlrl frm priphral cll  h livr fr mab-
lim. HDL ar mim rfrrd  a h “gd”
lipprin bcau high lvl indica ha chl-
rl i bing rmvd frm vacular iu, whr i
may paricipa in h dvlpmn f CAD. Lw HDL
lvl ar cnidrd a piiv rik facr fr h d-
vlpmn f CAD; high HDL lvl ar a ngaiv rik
facr fr CAD.
LDL accun fr 60%  70% f al rum chl-
rl and ar h majr cnribur  ahrclri.
Th prbabiliy ha ahrclri will dvlp i r-
lad dircly  h cncnrain f LDL chlrl
(LDL-C) in h bld circulain. LDL ar h primary
arg f chlrl-lwring hrapy.
High riglycrid lvl ar al aciad wih an
incrad rik f CAD. Cnqunly, pain a-
mn and chlrl-lwring ramn ar bad n
h al chlrl, LDL-C, HDL chlrl (HDL-C),
and riglycrid lvl fr individual pain. Ohr
markr bing d  a h nd fr hrapy in
pain wih brdrlin rik ar aplipprin B (a
rngr indicar f ahrgniciy); nn–HDL-c (h
um f chlrl in bh LDL-C and riglycrid);
ahrgnic, high-niiviy C-raciv prin (an
indicar f inammain); h ankl-brachial indx
(maurmn f h bld w  h lg and f);
and lipprin (Fig. 21.1).
TREATMENT OF HYPERLIPIDEMIAS
An imad 92.8 (11.7% prvalnc) millin Amrican
adul hav al bld chlrl lvl f 200 mg/dL
r highr. Of h, abu 28.5 (38.2% prvalnc) mil-
lin Amrican adul hav lvl f 240 mg/dL r mr.
Drugs Used to Treat Dyslipidemias CHAPTER 21 339
Intermediate-
Low-density High-density
density
lipoproteins lipoproteins
lipoproteins
(LDLs) (HDLs)
(IDLs)
23% 6% 1% to 7%
triglycerides triglycerides triglycerides
34% 53% 20% to 30%
cholesterol cholesterol cholesterol
Sm f h m cmmn hyprlipidmia f g-
nic rigin ar raabl wih mdicin. Hwvr, i
i nw rcgnizd ha lifyl i h gra cnrib-
ur  h dvlpmn f hyprlipidmia. A clur
f rik facr ha rla dircly  xc in lif-
yl i nw rcgnizd a mablic yndrm (
Chapr 20).
In 2018 h Amrican Cllg f Cardilgy
and h Amrican Har Aciain (ACC/AHA)
publihd nw guidlin  rduc h vrall rik
f ASCVD (Grundy, 2019). Rik rducin i h
crnrn f h guidlin: mainaining a har-
halhy di ( Chapr 46) fr a halhy wigh,
rgular xrci, and avidanc f bacc prduc.
Th 2018 guidlin cagriz pain bad n h
prnc r abnc f clinical ASCVD. I li fur
grup f pain ha wuld bn frm ain
hrapy. Th fur grup wih prvn bn ar a
fllw (Tabl 21.1):
• Clinical ASCVD (cndary prvnin)
• Svr hyprchlrlmia wih balin LDL-C
≥190 mg/dL (primary prvnin)
• Diab, ag 40  75 yar wih LDL-C f 70  189
mg/dL (primary prvnin)
• Ag 40  75 yar, wihu diab, wih LDL-C f
70  189 mg/dL and imad 10-yar ASCVD rik
f ≥7.5% (primary prvnin)
Th guidlin highligh ain and crain nn-
ain ha dmnra prvn rducin in ASCVD.
Sain hrapy i bad n h pncy f h ain d-
nd by h avrag ffc f a crain ain n LDL-C
lvl a a pcic d (Tabl 21.2). Th nnain ar
ranabl  cnidr whn h maximum lrad
ain d i unuccful and addiinal LDL rduc-
in i ncary.
340 UNIT IV Drugs Affecting the Cardiovascular System

Table 21.1 Statin Benet Groups and Recommended Treatment

GROUP RECOMMENDATIONS
SECONDARY PREVENTION
Clinical ASCVD: Patients who have already suffered a For adults who are 75 yr of age or younger with clinical ASCVD,
myocardial infarction, stable or unstable angina, stroke, high-intensity statin therapy should be initiated or continued
transient ischemic attack, or peripheral arterial disease, with the aim of achieving a 50% or greater reduction in
or had a revascularization procedure. Even though these LDL-C levels.
patients have had serious cardiovascular events, there is For adults older than 75 yr of age with clinical ASCVD, it is
strong evidence that statins reduce mortality in patients reasonable to initiate moderate- or high-intensity statin
with a history of ASCVD disease. therapy after evaluation of the potential for ASCVD risk
reduction, adverse effects, and drug–drug interactions, as
well as patient frailty and patient preferences.
In patients with clinical ASCVD at very high risk and who are
receiving maximally tolerated statin therapy with LDL-C
of 70 mg/dL or higher, it is reasonable to add a PCSK9
inhibitor and/or ezetimibe therapy following a clinician–patient
discussion about the net benet, safety, and cost.
PRIMARY PREVENTION FOR PATIENTS WITHOUT CLINICAL ASCVD
Adults, ages 20–75 yr, severe hypercholesterolemia with Evaluate for secondary causes of hyperlipidemia (e.g., high-fat
baseline LDL-C ≥190 mg/dL. diet; hypothyroidism, obstructive liver disease; medicines
such as diuretics, glucocorticoids, cyclosporine, amiodarone).
Initiate maximally tolerated statin therapy.
A reduction in LDL-C of 50% or more is needed to lower
ASCVD risk.
Diabetes, age 40–75 yr with LDL-C of 70–189 mg/dL but no For adults 40–75 yr with type 1 or type 2 diabetes, initiate
clinical ASCVD (ASCVD is the main cause of illness and moderate-intensity statin therapy regardless of 10-yr ASCVD
death in patients with diabetes). risk score.
For adults at higher ASCVD risk (determination based on clinical
judgment), it is reasonable to use high-intensity statin therapy
with a goal LDL-C reduction of 50% or more.
Adults without diabetes with LDL-C of 70–189 mg/dL and For adults without diabetes or ASCVD, start moderate- to high-
estimated 10-yr ASCVD risk of ≥7.5%. intensity statin therapy.
Adults with an ASCVD risk of 5%–7.4% should start with
moderate-intensity statin therapy.
ASCVD, Atherosclerotic cardiovascular disease; LDL-C, low-density lipoprotein cholesterol.
Adapted from Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management
of Blood Cholesterol: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines
[published correction appears in Circulation. 2019 Jun 18;139(25):e1178-e1181]. Circulation. 2019;139(25):e1046-e1081. doi:10.1161/CIR.0000000000000624

Fixed Statin Dosage Recommendations DRUG THERAPY FOR HYPERLIPIDEMIAS

Table 21.2 Based on Intensitya
ACTIONS
HIGH INTENSITY MODERATE LOW INTENSITY
(LOWERS LDL INTENSITY (LOWERS (LOWERS LDL BY S h individual drug mngraph lar in hi chap-
BY >50%) LDL BY 30%–49%) <30%) r fr infrmain abu h mchanim f acin f
atorvastatin atorvastatin simvastatin 10 mg diffrn anilipmic agn.
40–80 mg 10–20 mg pravastatin 10–20
rosuvastatin rosuvastatin mg
20–40 mg 5–10 mg lovastatin 20 mg USES
simvastatin uvastatin 20–40 Anilipmic agn may b ud  ra hyprlipidmia
20–40 mg mg nly if di, xrci, and wigh rducin ar n
pravastatin 40–80 uccful fr adqualy lwring LDL-C lvl. Th
mg
ain ar h r lin f hrapy, bu hr anili-
lovastatin 40 mg
uvastatin 80 mg
pmic agn, r cla (nnain) ha lwr LDL
pitavastatin 2–4 mg lvl ar zimib, h prprin cnvra ub-
iliin kxin yp 9 (PCSK9) inhibir (vlcumab,
LDL, Low-density lipoprotein. alircumab), and h bil acid–binding rin (.g.,
aSee the Drug Class: HMG-CoA Reductase Inhibitors drug monograph later in

this chapter for information on monitoring drug therapy. chlyramin, clipl, clvlam). Anhr
Adapted from Smith SC Jr, Grundy SM. 2013 ACC/AHA Guideline recommends agn, bmpdic acid (Nxl), i ud a an adjunc
xed-dose strategies instead of targeted goals to lower blood cholesterol. J Am
Coll Cardiol. 2014;64:601-612.  di and maximally lrad ain hrapy fr h

ramn f adul wih hrzygu familial hypr-
chlrlmia r ablihd ASCVD wh rquir
addiinal lwring f LDL-C. Niacin and bric acid
(.g., gmbrzil, fnbra) ar ffciv in rducing
riglycrid and ar ud in pain wih vry high
riglycrid lvl (>500 mg/dL). Clinical rial d n
uppr hir u a adjunc hrapy  ain hrapy
whn mr LDL-C lwring i ndd. Omga-3 fay
acid hav bn apprvd by h US Fd and Drug
Adminirain fr ramn f vry high riglyc-
rid lvl (>500 mg/dL) in adul. Icapn hyl
(Vacpa), an mga-3 fay acid, i al ud a an ad-
junc  maximally lrad ain hrapy  rduc
h rik f mycardial infarcin, rk, crnary r-
vacularizain, and unabl angina rquiring hpi-
alizain in adul pain wih lvad riglycrid
lvl (≥150 mg/dL) and ablihd cardivacular
dia r diab mlliu and w r mr addiin-
al rik facr fr cardivacular dia.
Pharmaclgic anilipmic hrapy fr ASCVD i
ard wih a ain bcau f h ain’ afy r-
crd and fcacy in lwring LDL-C and rducing
mrbidiy and mraliy in ASCVD.
Bfr aring hrapy, a lipid panl huld b
drawn and hn rpad in 4  12 wk afr hr-
apy i iniiad. If h rpn  iniial drug hrapy
i inadqua, i migh b an indicain ha h pain
i n cmplian wih hrapy r ha lifyl chang
ar n bing mad. Hav a dicuin wih h pain
 nur ha id ffc ar n limiing hrapy. If
h pain i cmplian, h dag f h ain huld
b incrad r anhr drug huld b addd  h
ramn rgimn. Ohr LDL-C–lwring agn
uch a zimib, PCSK9 inhibir (vlcumab, ali-
rcumab), and a bil acid–binding rin can b ud in
cnjuncin wih a ain. Drug hrapy i likly  cn-
inu fr many yar r h pain’ lifim; plama
lipid lvl rurn  prramn lvl afr 2  3
wk if hrapy i dicninud.
NURSING IMPLICATIONS FOR HYPERLIPIDEMIA
THERAPY
Assessment
History of risk factors. Obain h pain’ ag, n
gndr and rac, and ak a family hiry f h in-
cidnc f lvad chlrl and lipid lvl. Ak
whhr any r-gnrain family mmbr hav a
hiry f r hav did frm ASCVD. Ar hr any
living rlaiv wih lvad chlrl r lvad
riglycrid lvl?
Hypertension. Ak whhr h pain ha vr bn
ld ha hy hav lvad bld prur. If y,
bain dail. Ak abu mdicain ha hav bn
prcribd. Ar h mdicain bing akn rgularly?
If n, why n? Tak h pain’ bld prur in
lying and anding piin.
Drugs Used to Treat Dyslipidemias CHAPTER 21 341
Smoking. Obain a hiry f h numbr f ciga-
r r cigar mkd daily. Hw lng ha h
pain mkd? Ha h pain vr rid  p
mking? Drmin h pain’ knwldg f h
ffc f mking n h vacular ym. Hw d
h individual fl abu mdifying hir mking
habi?
Dietary habits
• Obain a diary hiry. Ak pcic quin 
bain daa rlad  fd an ha ar high in
fa, chlrl, rnd carbhydra, and dium.
Dicu h amun f fa fd and nack fd
cnumd, a wll a h frquncy f rauran
dining. Any f h facr nd  incra fa in-
ak. Uing a calri cunr, ak h prn  i-
ma h numbr f calri an daily. Hw much
ma, h, and pulry i an daily (iz and num-
br f rving)? Eima h prcnag f al
daily calri prvidd by fa.
• Dicu fd prparain (.g., baking, briling, fry-
ing). Hw many rving f frui and vgabl
ar an daily? Wha yp f il r fa ar ud in
fd prparain? S a nuriin x fr addiinal
diary hiry quin.
• Wha ar h frquncy and vlum f alchlic
bvrag ha ar cnumd?
Glucose intolerance. Ak pcic quin rgarding
whhr h individual ha nw r ha vr had an l-
vad rum gluc (bld ugar) lvl. If y, wha
diary mdicain hav bn mad? Hw ucc-
ful ar hy? Wha mdicain ar bing akn fr h
lvad rum gluc lvl (.g., ral hypglycmic
agn, inulin)?
Elevated serum lipid levels. Find u whhr h pa-
in i awar f having lvad lipid, riglycrid,
r chlrl lvl. If , wha maur ha h
pain rid fr rducin, and wha ffc hav h
inrvnin had n h bld lvl a ubqun
xaminain? Rviw availabl labrary daa (.g.,
LDL, VLDL lvl). A faing lipprin prl ha
includ al chlrl, LDL-C, HDL-C, and riglyc-
rid lvl i rcmmndd fr all adul 20 yar ld
r ldr a la nc vry 5 yar.
Obesity. Wigh h pain. Ak abu any rcn
wigh gain r l and whhr i wa innin-
al r uninninal. Uing h prn’ high and
wigh, drmin h prn’ bdy ma indx (
Chapr 20). If biy i prn, wha ragi fr
wigh rducin hav bn rid?
Psychomotor functions
• Typ f lifyl: Ak h pain  dcrib hir
xrci lvl in rm f amun (.g., walking 3
342 UNIT IV Drugs Affecting the Cardiovascular System
mil), inniy (.g., walking 3 mph), and frqun-
cy (.g., walking vry hr day). I h pain’
jb phyically dmanding r f a dnary naur?
• Pychlgical r: Hw much r d h in-
dividual ima having in hir lif? Hw d h
pain cp wih rful iuain a hm and in
h wrk ing?
Patient Education
Nutrition. Pain wh ak bil acid–quring
rin may rquir upplmnal viamin. (Th fa-
lubl viamin—D, E, A, and K—may bcm d-
cin wih lng-rm rin hrapy.)
• Encurag h inak f high-bulk fd (.g.,
whl grain, raw frui and vgabl), a wll a
h inak f 8  10 igh-unc gla f war
daily,  minimiz h cnipaing ffc f h
rin.
• Arrang a diary cnulain wih a nuriini 
addr any diary mdicain ndd (.g., lw
fa, lw chlrl). Nur huld nhanc and
rinfrc hi aching n a cninuum. Sr h
impranc f aaining a nrmal wigh a a majr
ramn gal f hyprlipidmia.
Vitamin K deciency. If h pain i rciving a pr-
cripin fr a bil acid–quring rin, ach h
pain abu h ign and ympm f viamin K
dcincy, including blding gum; bruiing; dark,
arry l; and cff-grund mi. Thi inracin
i rar, bu if ympm ccur, hy huld b rprd
immdialy  h halhcar prvidr.
Follow-up care. Sr h nd fr lng-rm rgular
amn f h rquird rum lvl (.g., lipid
prl valu, livr udi, blding im)  rack
prgr, idnify h nd fr mdicain in hr-
apuic inrvnin, and dc pibl advr
ffc f h mdicain. T bain hi infrmain,
bld udi and rgular vii  h halhcar pr-
vidr ar ncary.
Relating to medication regimen. Examin h individ-
ual drug mngraph fr dail abu mixing drug,
chduling mdicain adminirain, and chniqu
fr imprving cmplianc f pain aking h
mdicain.
Fostering health maintenance
• Thrughu h cur f ramn, dicu mdica-
in infrmain and hw i will bn h pain.
• Drug hrapy i n cmpnn in h managmn
f hyprlipidmia. Thrapuic lifyl chang ar
a impran a drug hrapy; hrfr h nd 
mdify diary habi and  cnrl biy, glu-
c lvl, rum chlrl, lipid, and hyprn-
in mu b rngly mphaizd. Tach h pain
abu which high-chlrl and high-fa fd
 avid (.g., livr, gg ylk, ma, frid fd,
fay dr, nu [cahw, macadamia, Brazil]).
Chlrl i an animal prduc and n fund in
plan. Encurag wiching  kim r 1% fa milk,
ubiuing gg whi, and incraing cnump-
in f frui (pcially grapfrui) and vgabl.
Cain f mking and an incra in daily xr-
ci (30 minu f mdra-inniy xrci m
day f h wk) ar rngly rcmmndd.
• Prvid h pain and ignican hr wih
h impran infrmain cnaind in h p-
cic drug mngraph fr h drug prcribd.
Addiinal halh aching and nuring inrvn-
in fr advr ffc ar dcribd in h drug
mngraph ha fllw.
• Sk h pain’ cprain and undranding f
h fllwing pin  ha mdicain cmplianc
i incrad: h nam f h mdicain; i dag,
ru, and im f adminirain; and i cmmn
and riu advr ffc.
Patient self-assessment. Enli h pain’ hlp
wih dvlping and mainaining a wrin rcrd
f mniring paramr (.g., daily rum gluc
lvl, bld prur, wigh) ( h Pain Slf-
Amn Frm fr Cardivacular Agn n h
Evlv wbi). An individualizd nuriinal di-
ary huld al b kp whil iniuing and larn-
ing abu di mdificain (.g., a rducin in fa
and rfind carbhydra, an incra in lw-ch-
lrl fd). Cmpl h Prmdicain Daa
clumn fr u a a balin  rack h pain’
rpn  drug hrapy. Enur ha h pain
undrand hw  u h frm and inruc h
pain  bring h cmpld frm  fllw-up
vii. During fllw-up vii, fcu n iu ha
will fr adhrnc wih h hrapuic inrvn-
in prcribd.
DRUG CLASS: STATINS (HMG-COA REDUCTASE
INHIBITORS)
Actions
3-Hydrxy-3-mhylgluaryl cnzym A (HMG-
CA) rduca nzym inhibir (Tabl 21.3), al
knwn a h statins, ar pn anilipmic agn.
Th ain cmpiivly inhibi h nzym ha i
rpnibl fr cnvring HMG-CA  mvaln-
a in h biynhic pahway  chlrl in h
livr. Th rducin in livr chlrl incra h
rmval f LDL frm h circulaing bld. Lvl
f LDL-C may b rducd by a much a 50%. Th
ain al cau rducin in VLDL and riglyc-
rid lvl (20%  30%) and mild incra (5% 
15%) in HDL lvl. Th agn ar mr ffciv
if adminird a nigh bcau pak prducin f
 Drugs Used to Treat Dyslipidemias CHAPTER 21 343

Table 21.3 HMG-CoA Reductase Inhibitors (Statins)

MAXIMUM DAILY DOSAGE
GENERIC NAME BRAND NAME AVAILABILITY DAILY DOSAGE RANGE RANGE
atorvastatin Lipitor Tablets: 10, 20, 40, 10–80 mg daily at any Up to 80 mg daily
80 mg time
uvastatin Lescol XL Capsules: 20, 40 mg 20–80 mg at bedtime Up to 80 mg at
Do not confuse Tablets, extended bedtime
uvastatin with release: 80 mg
uoxetine.
lovastatin Altoprev Tablets: 10, 20, 10–80 mg with 80 mg daily (immediate
Do not confuse 40 mg evening meal or release) or 60 mg
lovastatin with Tablets, extended 20–60 mg daily at daily at bedtime
Lotensin or Lovenox. release (Altoprev): bedtime (extended release)
20, 40, 60 mg
pitavastatin Livalo Tablets: 1, 2, 4 mg 2 mg once daily at Typical dosing range is
any time, with or 1–4 mg
without food
pravastatin – Tablets: 10, 20, 40, 10–80 mg daily at any Up to 80 mg daily
80 mg time
rosuvastatin Crestor Tablets: 5, 10, 20, 5–40 mg daily at any Up to 40 mg daily
Ezallor Sprinkles 40 mg time
Capsule sprinkle: 5, 10,
20, 40 mg
simvastatin Zocor Tablets (Zocor): 5, 10, 5–40 mg daily at Up to 40 mg at
Do not confuse 20, 40, 80 mg bedtime bedtime
Zocor with Cozaar, Oral suspension
Zestril, Ziac, or (FloLipid): 20, 40
Zoloft. mg/5 mL in
FloLipid 150-mL bottles
Do not confuse
FloLipid with Flomax.
3-Hydroxy-3-methylglutaryl coenzyme A.
Do not confuse.

chlrl ccur a hi im. Sain al hav h-
r bncial ffc unrlad  hir lipid-lwring
capaciy: hy rduc inammain, plal aggr-
gain, hrmbin frmain, and plama viciy,
hrby rducing h facr ha cnribu  har
aack and rk.
Uses
Sain ar ud in cnjuncin wih diary hrapy
 dcra lvad chlrl cncnrain in pa-
in wih hyprlipidmia and  rduc h rik f
ahrclri lading  ASCVD. Th ain lid in
Tabl 21.3 ar imilar in ffcivn a rcmmndd
aring d and im, bu hy diffr wih rgard 
hir pnial fr drug inracin. Ohr mdicin
al bing akn by h pain may drmin h
m apprpria ain  b prcribd; hi huld
b bad n h avidanc f drug inracin. S
Tabl 21.4 fr cmbinain prduc f arvaain
and amldipin (lipid-lwring agn wih an ani-
hyprniv agn;  Chapr 22 n calcium channl
blckr) and imvaain wih zimib-w lipid-
lwring agn.
Therapeutic Outcomes
Th primary hrapuic ucm xpcd frm
HMG-CA rduca inhibir ar rducin f LDL
and al chlrl lvl.
Nursing Implications for HMG-CoA Reductase
Inhibitors
Premedication assessment
1. Srum riglycrid, lipprin, and chlrl lv-
l huld b drmind bfr iniiaing hrapy,
hn a 4  12 wk, and hn annually afr ha.
2. Livr funcin  (apara aminranfra
[AST], alanin aminranfra [ALT]) huld b
baind bfr iniiaing hrapy and huld b
maurd during hrapy if ympm uggiv
f hpaxiciy dvlp, bu d n nd  b
maurd ruinly. Obain daa rlad  any GI
alrain bfr iniiaing hrapy (.g., prnc
f abdminal pain, naua, r au).
3. Cnrm ha h pain i n prgnan bfr ini-
iaing a ain. Inruc h fmal pain  nify
hr halhcar prvidr bfr prgnancy whil r-
civing ain hrapy.
344 UNIT IV Drugs Affecting the Cardiovascular System

Table 21.4 HMG-CoA Reductase Inhibitor Combination Products

GENERIC NAME
atorvastatin-amlodipine
Rosuvastatin-ezetimibe
simvastatin-ezetimibe
bempedoic acid–
ezetimibe
HMG-CoA, 3-Hydroxy-3-methylglutaryl coenzyme A.
BRAND NAME AVAILABILITY MAXIMUM DAILY DOSAGE RANGE
Caduet Tablets: atorvastatin: 80 mg
10 mg atorvastatin and 2.5 mg amlodipine amlodipine: 10 mg
20 mg atorvastatin and 2.5 mg amlodipine
40 mg atorvastatin and 2.5 mg amlodipine
10 mg atorvastatin and 5 mg amlodipine
20 mg atorvastatin and 5 mg amlodipine
40 mg atorvastatin and 5 mg amlodipine
80 mg atorvastatin and 5 mg amlodipine
10 mg atorvastatin and 10 mg amlodipine
20 mg atorvastatin and 10 mg amlodipine
40 mg atorvastatin and 10 mg amlodipine
80 mg atorvastatin and 10 mg amlodipine
Roszet 5 mg rosuvastatin and 10 mg ezetimibe Rosuvastatin: 40 mg
10 mg rosuvastatin and 10 mg ezetimibe Ezetimibe: 10 mg
20 mg rosuvastatin and 10 mg ezetimibe
40 mg rosuvastatin and 10 mg ezetimibe
Vytorin Tablets: simvastatin: 80 mg
10 mg simvastatin and 10 mg ezetimibe ezetimibe: 10 mg
20 mg simvastatin and 10 mg ezetimibe
40 mg simvastatin and 10 mg ezetimibe
80 mg simvastatin and 10 mg ezetimibe
Nexlizet 180 mg bempedoic acid and 10 mg ezetimibe bempedoic acid: 180 mg
ezetimibe: 10 mg

Availability, dosage, and administration. S Tabl
21.3 and 21.4. Lvaain huld b adminird wih
fd a h vning mal  nhanc abrpin. Th
hr ain may b adminird wihu fd.
Common adverse effects
Neurologic
Headaches. Thi ympm i uually mild and di-
appar wih cninud hrapy.
Gastrointestinal
Nausea, abdominal bloating, gas. Th ympm ar
uually mild and diappar wih cninud hrapy.
Serious adverse effects
Gastrointestinal
Hepatotoxicity. Livr funcin huld b mnird
a dcribd prviuly. If h ranamina (AST,
ALT) ri  hr im h uppr limi f nr-
mal and ar prin, h mdicain huld b
dicninud.
Musculoskeletal
Myopathy, rhabdomyolysis. Sympm f mucl ach,
rn, and wakn may b arly ign f mypa-
hy. Srum crain phphkina lvl mr han 10
im h uppr limi f nrmal cnrm h diagni.
Mypahy i m cmmn wih lvaain (a <1%).
Mypahy i mr cmmn (5%) if ain ar ud in
cmbinain wih niacin, gmbrzil, r cyclprin.
Rhabdmylyi i a vry riu cndiin in which
kidny damag rul frm prgriv mypahy.
An arly indicain f rhabdmylyi i pinkih r
rd-ingd urin cndary  myglbin (mucl
prin) paing hrugh damagd glmruli in h
urin (myglbinuria).
Cultural Considerations
Asian patients should initiate rosuvastatin at 5 mg once a day
because of increased rosuvastatin levels.
Drug interactions
Cyclosporine, itraconazole, ketoconazole, diltiazem,
uconazole, brates, niacin, verapamil, erythromycin,
clarithromycin, ranolazine, amiodarone. Th incidnc f
mypahy i incrad whn lvaain, imvaain,
r arvaain i prcribd in cnjuncin wih h
mdicin. Th mdicin inhibi h mablim f
h ain, inducing xiciy.
Bempedoic acid. Cncmian u wih imvaain
and pravaain rul in incrad lvl f imvaa-
in and pravaain. D n xcd d f imvaa-
in 20 mg r pravaain 40 mg  prvn xiciy.
Fluconazole. Cadminirain f h drug wih u-
vaain rul in ignicanly incrad uvaain lv-
l. Dag rducin f uvaain may b ncary.
Phenytoin, rifampin. Cncurrn adminirain f
rifampin and phnyin, wih arvaain, lvaain,
r imvaain rul in ignicanly lwr lvl f
h ain. Eihr incra h dag f uvaain,
arvaain, r imvaain r wich  anhr ain.
Mnir chlrl lvl 6  8 wk afr chang f
hrapy. D n dicninu h rifampin.

Warfarin. Th ain xcp arvaain may in-
cra h anicagulan ffc f warfarin. Th pr-
hrmbin im (inrnainal nrmalizd rai [INR])
may b prlngd. Obrv h pain fr pibl
xciv anicagulain and blding.
Grapefruit juice. Grapfrui juic inhibi h mab-
lim f arvaain, lvaain, and imvaain, hu
incraing hir plama cncnrain, ruling in a
grar pnial fr mypahy. Ppl wh ar aking
h mdicain huld avid grapfrui juic.
DRUG CLASS: BILE ACID–BINDING RESINS
cholestyramine (co-les-ter-am-MEAN)
Questran (QUEST-tran)
colestipol (co-LES-ti-pol)
Colestid (co-LEST-tid)
colesevelam (cola-SEVA-lam)
Welchol (WEL-coal)
Actions
Chlyramin, clipl, and clvlam ar rin
ha bind bil acid in h inin. Afr ral admini-
rain, h rin frm a nnabrbabl cmplx wih
bil acid, prvning h nrhpaic rcirculain
f h bil acid. Rmval f bil acid cau livr cll
 cmpna by incraing h mablim f chl-
rl  prduc mr bil acid, which rul in a n
rducin in h al chlrl lvl. Bil acid–binding
rin can rduc LDL-C lvl by 15%  30% and
incra HDL lvl by up  5%. Sm pain al
hav a 5%  10% incra in hir riglycrid lvl.
Uses
If pain cann lra ain, chlyramin,
clipl, and clvlam ar ud in cnjuncin
wih diary hrapy  dcra lvad chlrl
cncnrain in pain wih hyprlipidmia and 
rduc h rik f ahrclri lading  ASCVD.
Th agn may al b ud wih ain  lwr
h LDL-C lvl vn furhr. Thy ar gnrally n
ud fr pain wh alrady hav lvad riglycrid
lvl.
Ohr u f h bil acid–binding rin includ
h ramn f pruriu cndary  parial biliary
ai, diarrha cndary  xc fcal bil acid r
pudmmbranu clii, and digiali glycid
xiciy.
Clvlam ha al bn apprvd fr rducing
bld gluc and hmglbin A1c in adul pain
wih yp 2 diab. I may b ud aln r in cm-
binain wih mfrmin, ulfnylura, r inulin. D
n u hi drug in pain wih yp 1 diab.
Therapeutic Outcomes
Th primary hrapuic ucm xpcd frm bil
acid–binding rin hrapy ar h rducin f h
LDL and al chlrl lvl.
Drugs Used to Treat Dyslipidemias CHAPTER 21 345
Nursing Implications for Bile Acid–Binding Resins
Premedication assessment
1. Srum riglycrid, lipprin, and chlrl
lvl huld b drmind bfr h iniiain f
hrapy and pridically hrafr.
2. Obain pain daa rlad  any GI alrain b-
fr h iniiain f hrapy (.g., h prnc f
abdminal pain, naua, au).
Availability
Cholestyramine. PO: 4-g pwdr pack.
Colestipol. PO: 1-g abl; granul in 5-g pack.
Colesevelam. PO: 3.75-mg pack; 625-mg abl.
Dosage and administration
Cholestyramine. PO: 4 g n  ix im daily. Iniial
dag i 4 g daily. Mainnanc dag i 8  16 g/
day. Maximum daily dag i 24 g.
Colestipol. PO: Granules: 5  30 g/day in dividd
d. Iniial dag i 5 g nc r wic daily. Tablets:
2  16 g/day. Iniial dag i 2 g nc r wic daily.
Colesevelam. PO: 6 abl nc daily r in w di-
vidd d wih liquid a mal.
Notes:
 • Th pwdr rin (chlyramin) mu b
mixd wih 2  6 unc f war, juic, up, ap-
plauc, r cruhd pinappl and huld and
fr a fw minu  allw abrpin and dipr-
in. D n amp  wallw h dry pwdr.
Fllw adminirain wih an addiinal gla f
war.
 • Th rcmmndd im f adminirain i wih
mal, bu hi may b mdid  avid inrfr-
nc wih h abrpin f hr mdicain.
 • Tabl huld b wallwd whl; d n cruh,
chw, r cu hm. Tabl huld b akn wih
liquid.
 • Ta may bcm a ran fr nncmplianc.
Plac h pwdr in a favri bvrag r p fr
abl  minimiz h mdicain’ bjcin-
abl a.
Common adverse effects
Gastrointestinal
Constipation, bloating, fullness, nausea, atulence. Th
advr ffc can b minimizd by aring wih a
lw d; mixing h drug wih nncarbnad, pulpy
juic r auc; and wallwing i wihu gulping air.
Mainain adqua br in h di and drink ufcin
war.
Drug interactions
Digoxin, warfarin, thyroid hormones, thiazide diuretics, phe-
nobarbital, nonsteroidal antiinammatory agents, tetracycline,
beta-blocking agents, gembrozil, glipizide, glyburide, oral
contraceptives, phenytoin. Th rin may bind wih h
mdicin, which rduc abrpin. Th inracin can
uually b minimizd by adminiring h mdicin
1 hur bfr r 4 hur afr adminirain f rin.
346 UNIT IV Drugs Affecting the Cardiovascular System
Amiodarone. Th rin ignicanly dcra h ab-
rpin f amidarn. Th rin al blck h n-
rhpaic rcirculain f amidarn. Cnqunly,
amidarn and h rin huld n b ud
cncurrnly.
Fat-soluble vitamins (D, E, A, and K), folic acid. High
d f rin may rduc h abrpin f h
agn, bu hi inracin i n uually ignican in
nrmally nurihd pain.
ezetimibe (ĕ-ZĔT-ĭ-mēb)
Zetia (ZĔ-tē ă)
Actions
Ezimib ac  rduc ahrclri by blck-
ing h abrpin f chlrl frm h mall in-
in. Unlik bil acid–binding rin, zimib
d n bind  chlrl and rduc abrpin.
Inad, i ac n h mall inin  inhibi ab-
rpin f chlrl drivd frm h chlrl
crd in h bil and frm h di. Sudi indi-
ca ha zimib rduc lvl f al chlr-
l by abu 12%, LDL-C by 18%, and riglycrid
by 7%, and ha a minimal ffc n raiing HDL
lvl.
Uses
Ezimib i ud in cnjuncin wih diary hr-
apy  dcra lvad chlrl cncnrain
in pain wih hyprlipidmia and  rduc h
rik f ahrclri lading  ASCVD. Thi agn
may al b ud wih h ain  lwr chlrl
furhr (Vyrin;  Tabl 21.4). Cmbind hrapy
wih bric acid drivaiv i n rcmmndd.
Ezimib may hav an advanag vr h bil
acid–binding rin bcau i d n lva ri-
glycrid lvl.
Therapeutic Outcomes
Th primary hrapuic ucm xpcd frm z-
imib hrapy ar rducin f LDL and al chl-
rl lvl.
Nursing Implications for Ezetimibe
Premedication assessment
1. Srum riglycrid, lipprin, and chlrl lv-
l huld b drmind bfr iniiaing hrapy
and pridically hrafr.
2. Obain pain daa rlad  any GI alrain b-
fr iniiaing hrapy (.g., prnc f abdminal
pain, naua, au).
Availability. PO: 10-mg abl.
Dosage and administration. Adult: PO: 10 mg nc
daily; may b akn wih r wihu mal.
Common adverse effects
Gastrointestinal
Abdominal pain, diarrhea. Th advr ffc ar
mild and gnrally d n rquir dicninuain f
hrapy.
Drug interactions
Bile acid–binding resins. Th rin may bind 
zimib, rducing abrpin. Th inracin can
uually b minimizd by adminiring zimib 1
hur bfr r 4 hur afr adminiring h rin.
DRUG CLASS: ADENOSINE
TRIPHOSPHATE–CITRATE LYASE INHIBITOR
bempedoic acid (BEM-pe-DOE-ik As-id)
Nexletol (NEX-let-ol)
bempedoic acid/ezetimibe
Nexlizet (NEX-lee-zet)
Actions
Bmpdic acid i h r f a nw cla f agn
ud  rduc ahrclri. Bmpdic acid ac by
inhibiing adnin riphpha–cira lya (ACL),
an nzym rquird in h chlrl ynhi pah-
way. Rducin f ACL rduc chlrl prduc-
in. Sudi indica ha an addiin f bmpdic
acid  maximally lrad ain hrapy rducd
LDL-C lvl by an addiinal 15%  17%.
Bmpdic acid al cm in a cmbinain prd-
uc wih zimib calld Nxliz. In pain aking
ain, bmpdic acid plu zimib rducd LDL-C
lvl by abu 36%.
Uses
Bmpdic acid i ud a an adjunc  di and
maximally lrad ain hrapy fr h ramn f
adul wih hrzygu familial hyprchlrlmia
r ablihd ASCVD wh rquir addiinal lwring
f LDL-C.
Therapeutic Outcomes
Th primary hrapuic ucm xpcd frm
bmpdic acid hrapy ar rducin f LDL-C and
al chlrl bld lvl.
Nursing Implications for Bempedoic Acid
Premedication assessment
1. Srum riglycrid, lipprin, and chlrl lvl
huld b drmind bfr iniiaing hrapy and
pridically hrafr  a bn f hrapy.
2. Rqu balin rum uric acid, crain kina,
and livr funcin  (AST, ALT) bfr iniiaing
hrapy. Thy huld b rpad if mucl injury,
gu, r ign f hpaxiciy dvlp, bu d n
nd  b maurd ruinly.
3. D h pain hav a hiry f mucl injury,
uch a mucl ach, rn, r wakn? If ,

cllc mr infrmain n frquncy f rcurrnc
and riggring vn.
4. Cnrm ha h pain i n prgnan bfr ini-
iaing bmpdic acid hrapy. Inruc h fmal
pain  nify hr halhcar prvidr bfr b-
cm prgnancy whil rciving bmpdic acid.
Availability. PO: 180-mg abl.
Dosage and administration. Adult: PO: 180 mg nc
daily.
Common adverse effects
Endocrine and metabolic. Bmpdic acid may in-
cra bld uric acid lvl (hypruricmia), which
may lad  gu. Mnir pain fr ign and ymp-
m f hypruricmia, a rum uric acid lvl,
and iniia ramn wih ura-lwring drug a
apprpria.
Gastrointestinal/hepatic
Abdominal pain, fatigue, anorexia, nausea, malaise, jaun-
dice. Th ar arly ympm ha ar aciad
wih hpaxiciy; rpr h  h halhcar pr-
vidr fr furhr valuain. Mnir fr an incra in
AST and/r ALT livr nzym.
Musculoskeletal
Back pain, limb pain, muscle spasm. Advi pain 
rpr any pain. Mniring crain kina may b
ndd.
Serious adverse effects
Tendon rupture. Bmpdic acid i aciad wih
an incrad rik f ndn rupur r injury. Tndn
rupur ccur wihin wk  mnh f aring
hrapy. Tndn rupur may ccur mr frqunly
in pain vr 60 yar f ag, in h aking a
cricrid r a urquinln anibiic, in pain
wih rnal failur, and in pain wih prviu n-
dn dirdr.
Drug interactions
Simvastatin. D n adminir bmpdic acid
wih d f imvaain grar han 20 mg daily.
Bmpdic acid ubanially incra rum lvl f
imvaain ha may rul in mucl injury.
Pravastatin. D n adminir bmpdic acid
wih d f pravaain grar han 40 mg daily.
Bmpdic acid ubanially incra rum lvl f
pravaain ha may rul in mucl injury.
DRUG CLASS: PCSK9 INHIBITORS
alirocumab (al-i-ROK-ue-mab)
Praluent (PRAHL-u-ent)
evolocumab (e-voe-LOK-ue-mab)
Repatha (ri-PAth-a)
Drugs Used to Treat Dyslipidemias CHAPTER 21 347
Actions
PCSK9 inhibir ar mnclnal anibdi ha bind
 an nzym in h livr, PCSK9, and prvn i frm
binding  LDL rcpr, hrby incraing h num-
br f pn rcpr availabl  bind circulaing
LDL-C, rducing h amun f circulaing LDL-C.
Alircumab r vlcumab rduc LDL-C lvl by
50%  60%.
Uses
Bh PCSK9 inhibir ar ud in cnjuncin wih di
and hr lipid-lwring agn fr pain rquiring
mr LDL-C rducin  cnrl ahrclri.
Thy hav bn hwn  rduc cardivacular vn
uch a angina, mycardial infarcin, and rk.
PCSK9 inhibir may al b prcribd fr pain
wh ar unabl  lra ain hrapy.
Therapeutic Outcomes
Th primary hrapuic ucm xpcd frm
PCSK9 inhibir ar rducin f LDL-C and al
chlrl lvl.
Nursing Implications for PCSK9 Inhibitors
Premedication assessment
1. Lipid prl (faing r nnfaing) bfr iniiaing
ramn. Faing lipid prl huld b rchckd
4  12 wk afr aring hrapy and vry 3  12
mnh hrafr.
2. Rviw h pain’ mdicain hiry  nur
ha h pain d n hav an allrgy  any
immunmdular agn. If h pain d,
infrm h halhcar prvidr immdialy. D
n adminir h mdicain wihu pcic
apprval.
3. Rviw h pain’ mdicain hiry  n
whhr h pain ha a prviu hiry f mu-
cl wakn, myalgia, r mucl pam. Svral
f h mdicin ud  ra dylipidmia may
cau h ympm,  i i impran  n
whhr h pain ha had prviu difculi
wih h ympm. I i n an indicain  wih-
hld PCSK9 inhibir hrapy, bu i i hlpful 
knw if h pain i ucpibl  hm fr lar
valuain f hrapy.
Availability. Alircumab (Pralun): Availabl in
w yp f injcin dvic dpnding n pain
prfrnc.
• Prlld auinjcr: 75 mg/mL and 150 mg/mL
in 1-mL pn; a prlld yring hud in an au-
injcr ha infu h mdicin quickly whn h
auinjcr i acivad by h pain.
• Prlld yring: 150 mg/mL; a prlld yring and
ndl in which h pain puh h plungr 
adminir h mdicin.
Evlcumab (Rpaha): Availabl in hr yp f
injcin dvic dpnding n pain prfrnc.
348 UNIT IV Drugs Affecting the Cardiovascular System
• Prlld auinjcr: 140 mg/mL in 1-mL pn; a
prlld yring hud in an auinjcr ha in-
fu h mdicin quickly whn h auinjcr i
acivad by h pain.
• Prfilld yring: 140 mg/mL in 1 mL yring-
; a prfilld yring and ndl in which h
pain puh h plungr  adminir h
mdicin.
• Sluin carridg: 420 mg/3.5 mL; a prlld car-
ridg ha i inrd in an n-bdy infur ha i
aachd  h bdy. Whn acivad by h pain, i
will lwly infu h mdicin in h ubcuanu
iu vr 9 minu.
Dosage and administration. Adul: Subcutaneous:
• Prparain (alircumab and vlcumab): Sr in
h rfrigrar a 36°F  46°F. Sr in riginal cn-
ainr  prc frm ligh. Bh prduc may b
rd a rm mpraur (up  77°F) fr up 
30 day, bu mu b dicardd afr 30 day if n
ud. Do not shake. Bfr u, allw ihr prduc
 and a rm mpraur fr a la 30 minu
fr h prlld yring r 45 minu fr h bdy
infur wih prlld carridg. D n amp 
ha wih h war.
• Adminir by dp ubcuanu injcin in
ara f h high, uppr arm, r abdmn (xcp
wihin 2 inch f h navl). U ara ha ar n
ndr, bruid, r rd. Ra h injcin i fr
ach adminirain.
• S manufacurr’ dircin n inrucing pa-
in  u h auinjcr pn, prlld yring,
r bdy infur ki.
Dosage ranges
Alirocumab. Adult: Primary hyprlipidmia.
Subcutaneous: 75 mg nc vry 2 wk r 300 mg
nc vry 4 wk; fr bh rgimn. May incra
 a maximum f 150 mg vry 2 wk.
Adult: Scndary prvnin f cardivacular
vn (.g., angina, mycardial infarcin, rk).
Subcutaneous: 75 mg nc vry 2 wk r 300 mg
nc vry 4 wk; fr bh rgimn, if an adqua
LDL-C rpn i n achivd, may incra  a
maximum d f 150 mg vry 2 wk.
Evolocumab. Adult: Primary hyprlipidmia.
Subcutaneous: 140 mg vry 2 wk r 420 mg nc
mnhly.
Adult: Prvnin f cardivacular vn (.g.,
angina, mycardial infarcin, rk) in pain wih
ablihd cardivacular dia. Subcutaneous: 140
mg vry 2 wk r 420 mg nc mnhly.
Adult: Hmzygu familial hyprchlrlmia.
Subcutaneous: 420 mg nc mnhly. Evlcumab may
b adminird vr 9 minu uing h prlld car-
ridg infur ki cnaining 420 mg r adminiring
3 prlld yring cnaining 140 mg ach wihin a
30-minu prid.
Common adverse effects
Local. Mild injcin-i racin hav bn r-
prd, including bruiing, rdn, warmh, burning,
inging, pain, and inammain. M injcin-i
racin ccur wihin 1 hur afr injcin, la l
han 8 day, and gnrally dcra in frquncy wih
ubqun ding. Immdialy rpr a rah r pru-
riu, wih r wihu fvr, and wihhld addiinal
injcin unil apprvd by h halhcar prvidr.
Musculoskeletal. Sympm f mucl ach, r-
n, pam, and wakn hav bn rprd wih
h PCSK9 inhibir and m cla f mdicin
ud  ra dylipidmia. If h pain dvlp nw
ympm, cninu hrapy bu nify h halhcar
prvidr.
Infections. In clinical rial wih alircumab and
vlcumab, hr wa a highr ra f uppr rpirary
infcin (inuii, napharyngii), garnrii,
urinary rac infcin, inunza, and inunza-lik
ympm in h mdicin-rad pain cm-
pard wih h placb-rad grup. Nify h
halhcar prvidr if ympm cnin wih
h infcin (.g., r hra, naal cngin,
cugh, aching jin, fvr, diarrha, burning n
urinain) dvlp during PCSK9 inhibir hra-
py. Dicninuain f PCSK9 inhibir hrapy i
uually n ncary.
Hepatic. Faigu, anrxia, naua, jaundic. Mnir
fr ign and ympm f livr xiciy. Amn f
livr funcin may b ndd, a incra in AST and/
r ALT hav bn rprd. Rpr ympm  h
halhcar prvidr.
Serious adverse effects
Hypersensitivity reactions. Hyprniiviy racin
(angidma, rah, ryhma, uricaria) hav bn r-
prd. Dicninu ramn and iniia uppriv
ramn in pain wh dvlp riu allrgic
ympm. Wihhld furhr injcin unl ap-
prvd by h halhcar prvidr.
Drug interactions. Thr ar n knwn ignican
drug inracin.
DRUG CLASS: NIACIN
Do not confuse niacin with Niaspan or Naprosyn.
Actions
Niacin, al knwn a nicotinic acid, i a war-lubl
B viamin (al knwn a vitamin B3). I mchanim
f acin a an anilipmic agn ar n cmplly
knwn, bu hy ar n rlad  i ffc a a vi-
amin. Niacin inhibi VLDL ynhi by livr cll,
which cau a dcra in LDL and riglycrid pr-
ducin. Triglycrid lvl ar rducd by 20%  50%,
and al chlrl and LDL-C lvl can b rducd
by 5%  25%. Niacin may al rduc h mablim

f HDL, hrby cauing a 15%  35% incra in HDL
lvl. Niacin al cau h rla f hiamin,
cauing priphral vadilain and incrad bld
w (uhing f h kin).
Uses
Nicinic acid i h nly frm f viamin B3 ap-
prvd by h US Fd and Drug Adminirain fr
h ramn f dylipidmia. Accrding  h 2017
Amrican Aciain f Clinical Endcrinlgi and
h Amrican Cllg f Endcrinlgy guidlin
and h 2018 ACC/AHA guidlin fr h manag-
mn f dylipidmia, niacin hrapy i rcmmndd
principally a an adjunc fr rducing riglycrid.
Niacin hrapy huld n b ud in individual
aggrivly rad wih a ain du  h abnc
f imprvd pain ucm and afy cncrn.
In addiin, h u f nicinic acid i fn limid
by pr lrabiliy. Niacin huld b ud wih cau-
in in pain wih diab bcau f hir gluc
inlranc.
Diffrn frm f viamin B3 cann b ud inr-
changably. Ohr frm f viamin B3 ar niacina-
mid and inil hxaniacina, which d n lwr
lvad chlrl lvl. Immdia-rla niacin
prduc cau mr facial and kin uhing, and h
uaind-rla prduc hav a highr pibiliy
f cauing hpaxiciy han h immdia-rla
prduc. Diary upplmn f niacin huld n b
ud  ra dylipidmia. Th rcmmndd Diary
Rfrnc Inak fr nuriinal upplmnain i
l han 20 mg/day. Th dag f niacin rquird 
ra dylipidmia i 1  6 g/day.
Therapeutic Outcomes
Th primary hrapuic ucm xpcd frm nia-
cin ar rducin in LDL (5%  25%) and al ch-
lrl lvl, rducin in riglycrid lvl (20% 
50%), and an incra in HDL lvl (15%  35%).
Nursing Implications for Niacin
Premedication assessment
1. Srum riglycrid and chlrl lvl huld b
drmind bfr iniiain f hrapy and pridi-
cally hrafr.
2. Livr funcin  (AST, ALT, gamma-gluamyl-
ranfra [GGT], and alkalin phphaa lvl
[ALP]; prhrmbin im [PT]) huld b dr-
mind bfr iniiaing hrapy and vry 6  8
wk during h r yar f hrapy.
3. Balin uric acid and bld gluc lvl huld
b drmind bfr iniiaing hrapy. Niacin
hrapy may induc hypruricmia, gu, and
hyprglycmia in ucpibl pain.
4. Balin bld prur and har ra huld b d-
rmind bfr iniiaing hrapy.
5. Obain pain daa rlad  any GI alrain b-
fr iniiaing hrapy (.g., h prnc f abdmi-
nal pain, naua, r au).
Drugs Used to Treat Dyslipidemias CHAPTER 21 349
Availability. PO: 50-, 100-, 250-, r 500-mg abl; 250-
r 500-mg imd-rla capul; 250-, 500-, 750-, r
1000-mg imd-rla abl.
Dosage and administration. PO: Wk 1  4: 500 mg
PO a bdim. Wk 5  8: 1000 mg PO a bdim.
Afr wk 8, ira  pain rpn and lranc.
If rpn  1000 mg/day i inadqua, incra
d  1500 mg/day PO a bdim. If rpn 
1500 mg/day i inadqua, may ubqunly in-
cra d  2000 mg/day.
Common adverse effects
Integumentary. Fluhing, iching, and rah ar cm-
mn. Pain can rduc hir ympm by aking a-
pirin (325 mg) r ibuprfn (200 mg) 30 minu bfr
ach d f niacin.
Neurologic. Tingling and hadach ar frqunly
n wih h drug.
Gastrointestinal
Nausea, gas, abdominal discomfort and pain. GI up
can b minimizd by aring wih lw d f h
drug and adminiring all d wih fd.
Th cmmn advr ffc lid hr uually c-
cur a h bginning f hrapy, pcially wih h im-
mdia-rla prduc. Tlranc dvlp quickly.
Adminir niacin wih fd.
Cardiovascular
Dizziness, faintness, hypotension. Niacin i a va-
dilar, and i may cau hypnin, pcially if
a pain i rciving hr anihyprniv agn.
Anicipa h dvlpmn f hypnin and ak
maur  prvn uch an ccurrnc. Tach h
pain  ri lwly frm a upin r iing piin
and  i r li dwn if hy ar fling fain. Mnir
bld prur wih h pain in bh h upin and
iing piin.
Serious adverse effects
Gastrointestinal
Hepatotoxicity. Thr appar  b a highr inci-
dnc f hpaxiciy aciad wih h imd-
rla prduc. Sm clinician rcmmnd limiing
h imd-rla prduc  1500 mg daily  rduc
h rik.
Fatigue, anorexia, nausea, malaise, jaundice. Th ar
h arly ympm ha ar aciad wih hpa-
xiciy. Rpr h  h halhcar prvidr fr fur-
hr valuain.
Musculoskeletal
Myopathy. Sympm f mucl ach, rn,
and wakn may b arly ign f mypahy.
Srum crain phphkina lvl ha ar mr
han 10 im h uppr limi f nrmal cnrm h
diagni.
Drug interactions
HMG-CoA reductase inhibitors. Th pnial f dvl-
ping mypahy i incrad whn niacin i addd 
350 UNIT IV Drugs Affecting the Cardiovascular System
h ramn rgimn. Th incidnc f hi cndiin
i l han 1%.
DRUG CLASS: FIBRIC ACIDS
Actions
Th mchanim f acin f h bric acid (.g., gm-
brzil, fnbra) i unknwn; hwvr, hy d lw-
r riglycrid lvl by 20%  40%. In pain wih
hyprriglycridmia, h drug rai HDL lvl by
20%  25%. Thy al rduc LDL-C lvl by 10% 
15% in pain wih lvad chlrl. Fnbra
may lwr LDL-C lvl mr ffcivly han gm-
brzil. Hwvr, in pain wih cncurrn hypr-
riglycridmia, gmbrzil may hav n ffc, r i
may lighly incra LDL-C lvl.
Uses
Th bra ar h m ffciv riglycrid-lwring
agn. Gmbrzil and fnbra ar ud in cn-
juncin wih diary hrapy  dcra lvad
riglycrid lvl in pain wh ar a rik fr pan-
craii. Fibric acid mu b ud wih cauin in
cmbinain wih ain bcau f h rik f mypa-
hy and rhabdmylyi.
Therapeutic Outcomes
Th primary hrapuic ucm xpcd frm -
bric acid hrapy ar a 20%  40% rducin in ri-
glycrid lvl and a 20%  25% incra in HDL
lvl.
Nursing Implications for Fibric Acids
Premedication assessment
1. Srum riglycrid, lipprin, and chlrl lv-
l huld b maurd bfr iniiaing hrapy
and pridically hrafr.
2. Livr funcin  huld b run bfr iniiaing
hrapy and hn vry 6 mnh hrafr.
3. Balin bld gluc lvl huld b drmind
bfr gmbrzil hrapy. Gmbrzil may cau
mdra hyprglycmia.
4. Obain pain daa rlad  any GI alrain b-
fr iniiaing hrapy (.g., prnc f abdminal
pain, naua, au).
Availability
Gembrozil (Lopid). PO: 600-mg abl.
Fenobrate. PO: Tabl: 35, 40, 48, 54, 105, 120, 145,
and 160 mg; capul: 30, 43, 50, 67, 90, 130, 134, 150,
and 200 mg; dlayd-rla capul: 45 and 135 mg.
Dosage and administration
Gembrozil. PO: 1200 mg/day in w dividd d,
30 minu bfr h mrning and vning mal.
Fenobrate. PO: Iniially, 45  160 mg/day, givn
wih mal. Incra dag vry 4  8 wk up 
160 mg daily wih a mal. Dag f fnbra nd
 b rducd in ldr adul pain and in pain
wih rnal inufcincy ( h manufacurr’
rcmmndain).
Common adverse effects
Gastrointestinal
Nausea, diarrhea, atulence, bloating, abdominal dis-
tress. Th ar rlaivly cmmn advr ffc.
Saring wih a lwr dag akn bwn mal can
hlp minimiz h ffc. If ympm pri, n-
ify h halhcar prvidr bcau pnially mr
riu cmplicain may b dvlping.
Serious adverse effects
Gastrointestinal
Fatigue, anorexia, nausea, malaise, jaundice. Th ar
h arly ympm aciad wih gallbladdr di-
a and hpaxiciy. Rpr h ympm  h
halhcar prvidr fr furhr valuain.
Musculoskeletal
Myopathy. Sympm f mucl ach, rn,
and wakn may b arly ign f mypahy. Srum
crain phphkina lvl f mr han 10 im
h uppr limi f nrmal cnrm h diagni.
Mypahy i mr cmmn (5%) if ain ar ud in
cmbinain wih gmbrzil; i i m cmmn wih
lvaain and gmbrzil.
Drug interactions
Warfarin. Th bric acid may nhanc h pharma-
clgic ffc f warfarin. Rduc h dag f war-
farin uing h prhrmbin im (INR) a an indicar
 prvn blding.
Sulfonylureas, insulin. Gmbrzil may incra h
pharmaclgic ffc f h agn. Mnir h pa-
in fr ign f hypglycmia and rduc h dag
f h inulin r ulfnylura a ndd.
Bile acid–binding resins. Th rin may bind 
fnbra, rducing abrpin. Th inracin can
uually b minimizd by adminiring fnbra 1
hur bfr r 4 hur afr adminirain f h rin.
HMG-CoA reductase inhibitors. Th pnial fr d-
vlping mypahy i incrad whn bric acid ar
addd  h ain ramn rgimn. Th incidnc
i l han 5%.
omega-3 fatty acids
omega-3-acid ethyl esters
Lovaza (lō-VĂ-ză)
icosapent ethyl -eye-KOE-sa-pent ETH-il
Vascepa vas-EE-puh
Actions
Icapn hyl i an mga-3 fay acid ha cnain
nly icapnanic acid (EPA). Omga-3-acid h-
yl r cnain bh EPA and dcahxanic acid
(DHA). Omga-3 fay acid ar mim rfrrd 
a sh oils bcau highr cncnrain f h fay
acid ar fund in uch il. Th mchanim f acin
i unknwn, bu h nd rul i ha h mga-3

fay acid rduc ynhi f riglycrid in h livr.
Lvaza and Vacpa rduc riglycrid lvl by 20%
 50%. Lvaza can incra LDL-C and HDL-C lvl,
bu Vacpa lwr LDL-C and HDL-C lvl.
Uses
Lvaza and Vacpa ar ud in cnjuncin wih di-
ary hrapy  dcra vry lvad riglycrid
lvl (>500 mg/dL) in adul pain. Vacpa can
al b ud wih maximally lrad ain hrapy
 rduc h rik f mycardial infarcin, rk,
crnary rvacularizain, and unabl angina in
adul pain wih riglycrid lvl ≥150 mg/dL
and in ihr ablihd cardivacular dia r
yp 2 diab mlliu wih w r mr rik fac-
r fr cardivacular dia. Bh agn huld b
ud wih cauin in pain wh ar niiv r al-
lrgic  h.
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm
Lvaza and Vacpa hrapy i h rducin f an l-
vad riglycrid lvl.
Nursing Implications for Omega-3 Fatty Acids
Premedication assessment
1. Srum riglycrid, al chlrl, HDL-C, and
LDL-C lvl huld b drmind bfr iniia-
ing hrapy and pridically hrafr.
2. Livr funcin  (AST, ALT) huld b cmpl-
d bfr iniiaing hrapy and pridically fr h
r yar f hrapy.
3. Obain pain daa rlad  any GI alrain b-
fr iniiaing hrapy (.g., prnc f abdminal
pain, naua, au).
Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• Coronary artery disease is a major cause of premature
death in the United States.
• Major treatable causes of ASCVD are hypertension,
cigarette smoking, and atherosclerosis.
• A primary cause of atherosclerosis is the abnormal
elevation of cholesterol and triglyceride levels in the
blood in a disease known as hyperlipidemia. Diets
high in saturated fats, cholesterol, carbohydrates, total
calories, and alcohol—in combination with a sedentary
lifestyle—are the most common and treatable causes of
hyperlipidemia.
• The most cost-effective and successful forms of treatment
are smoking cessation, weight reduction, exercise, and
dietary modication. If changes in diet and exercise habits
do not produce an acceptable decrease in blood lipid
Drugs Used to Treat Dyslipidemias CHAPTER 21 351
Availability. Omga-3-acid hyl r (Lvaza): PO:
1-g capul.
Icosapent ethyl (Vascepa): PO: 0.5 and 1 g capul.
Dosage and Administration: Lovaza: Adult: PO: 4 g
nc daily r 2 g wic daily fr hyprriglycridmia
Vascepa: Adult: PO: 2 g wic daily wih mal fr
cardivacular rik rducin and hyprriglycridmia.
Common and serious adverse effects. If any f h fl-
lwing advr ffc ccur, rpr hm  h halh-
car prvidr immdialy: arm, back, r jaw pain;
ch pain r dicmfr; ch ighn r havin;
difcul r labrd brahing; fa r irrgular har-
ba; naua; hrn f brah; waing; ighn
in h ch; r whzing.
Ohr minr advr ffc rprd during clinical
udi includ back pain, unuual r unplaan afr-
a, blching, a blad and full fling, a chang in
a, chill, cugh, diarrha, xc air r ga in m-
ach, fvr, a gnral fling f dicmfr r illn,
hadach, harn, jin pain, l f appi, lw-
r back r id pain, mucl ach and pain, painful
r difcul urinain, rah, runny n, hivring, r
hra, waing, rubl lping, unuual irdn
r wakn, r vmiing. Th ympm huld b
rprd  h halhcar prvidr if hy pri.
Drug interactions
Anticoagulants and antiplatelet agents. Omga-3-acid
hyl r and icapn hyl may incra h
rik f blding in pain rciving aniplal
agn (NSAID, apirin, clpidgrl, praugrl) r ani-
cagulan (warfarin). Mnir pain fr bruiing
and/r blding.
levels, an antilipemic agent may be added to the patient’s
regimen.
• Patients should be fully informed of the signicance of
hyperlipidemias, the potential complications involved
with not modifying their lifestyles, and drug therapy. Drug
therapy is likely to continue for many years or a lifetime.
• The primary medicines that are used to lower elevated
cholesterol levels are the statins (rst choice), proprotein
convertase subtilisin kexin type 9 (PCSK9) inhibitors,
ezetimibe, bile acid–binding resins, and bempedoic acid.
Niacin, bric acid derivatives, and omega-3 fatty acids
lower triglyceride levels.
Additional Learning Resources
SG Go to your Study Guide for additional Review Ques-
tions for the NCLEX® Examination, Critical Thinking Clinical
352 UNIT IV Drugs Affecting the Cardiovascular System

Situations, and other learning activities to help you master this
chapter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
4. The nurse discussed the types of medications used for cholesterol
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX examination and include both NGN (Next Genera-
tion) and traditional questions. See Chapter 1 for further infor-
mation regarding question types.
Objective: Determine which antilipemic medications are used for
cholesterol control and which can be used for triglyceride control.
NCLEX item type: Multiple choice
Cognitive skill: Compare
control for the patient in the scenario who was then concerned
about starting on statins. The nurse created a table to help
differentiate between the antilipemic medications available.
Indicate with an X the type of antilipidemic medication that is used
for control of cholesterol and the type of antilipidemic medication
that is used for control of triglycerides.

Scenario
ANTILIPIDEMIC USED TO CONTROL USED TO CONTROL
A patient who is moderately overweight and has hypertension MEDICATIONS LDL CHOLESTEROL TRIGLYCERIDES
was recently informed of a new diagnosis of hyperlipidemia and Omega-3 fatty
needs to be started on a statin. acids
1. The nurse teaching a patient about lipoproteins created a table to Bile acid-binding
explain the composition of each type. Indicate with an X the typical resins
components of each of the ve major types of lipoproteins. HMG-CoA
reductase inhibitors
(statins)
LOW HIGH LOW HIGH
TRIGLYCERIDES TRIGLYCERIDES CHOLESTEROL CHOLESTEROL Fibric acid
<20% >20% <20% >20% derivatives

Chylomicrons PCSK9 inhibitors

VLDLs Bempedoic acid
IDLs Ezetimibe
LDLs
HDLs Objective: Determine which antilipidemic medications are used for
cholesterol control and which can be used for triglyceride control.
NCLEX item type: Matrix
Objective: Describe atherosclerosis and identify the ve major Cognitive skill: Analyze cues
types of lipoproteins.
NCLEX item type: Matrix 5. Choose the most likely option for the information missing from the
Cognitive skill: Recognize cues following sentences by selecting from the list of options provided.

2. The nurse discusses with the patient in the scenario that they need The patient in the scenario was started on
to continue with lifestyle modications in addition to starting on a __________1____________ and then had
statin. The nurse suggests which of these approaches to maintain _______1____________ added. The mechanism of action
lipid control? (Select all that apply.) of the rst drug ______2___________ and the second drug
___________2_______________, respectively.
1. Maintain a heart-healthy diet
2. Daily dental hygiene
3. Avoid tobacco products
OPTION 1 OPTION 2
4. Maintain a healthy weight
5. Regular exercise alirocumab lowers cholesterol by unknown
Objective: Describe the primary approaches to treat lipid disorders. mechanism
NCLEX item type: Multiple response icosapent inhibits the absorption of cholesterol
Cognitive skill: Application gembrozil inhibits the HMG-CoA reductase
3. The patient from the scenario who continues on the statin 3 atorvastatin inhibits the PCSK9
months later has laboratory test results indicating that he still
has high lipids and high triglycerides. Which medication would be Objective: Differentiate between how statins work to control lipid
appropriate to add to the patient’s drug regimen? levels and how the bile acid resins work to control lipid levels.
1. Niacin NCLEX item type: Cloze
2. Gembrozil Cognitive skill: Recognize cues
3. Icosapent
4. Cholestyramine
Drugs Used to Treat Hypertension 22
https://evolve.elsevier.com/Willihnganz

Objectives
1. Differentiate between primary and secondary hypertension.
2. Summarize nursing assessments and interventions used
for the treatment of hypertension.
3. Identify recommended lifestyle modications after a
diagnosis of hypertension.
4. Identify initial options and progression of medicines used
to treat hypertension.
5. Identify and summarize the action of ve drug classes used
to treat hypertension.

Key Terms
arterial blood pressure (ăr-TĒR-ē-ŭl
BLŬD PRĔ-shŭr) (p. 353)
systolic blood pressure (sĭs-TŎL-ĭk)
(p. 353)
diastolic blood pressure (dī-ă-STŎL-
ĭk) (p. 353)
pulse pressure (PŬLS) (p. 353)
mean arterial pressure (MAP) (MĒN
ăr-TĒR-ē-ŭl) (p. 353)
cardiac output (CO) (KĂR-dē-ăk
ŎWT-pŭt) (p. 353)
hypertension (hī-pĕr-TĔN-shŭn) (p. 354)
primary hypertension (PRĪ-mār-ē)
(p. 354)
secondary hypertension (SĔK-ŏn-
dār-ē) (p. 354)
systolic hypertension (p. 354)

Nrmal MAP radings gnrally fall bwn 70

HYPERTENSION
S Chapr 20 fr an inrducin  cardivascular
disass. A primary funcin f h har is  circu-
la bld  h rgans and issus f h bdy. Whn
h har cnracs (sysl), bld is pumpd frm h
righ vnricl u hrugh h pulmnary arry 
h lungs, as wll as frm h lf vnricl u hrugh
h ara  h hr rgans and priphral issus.
Th prssur wih which h bld is pumpd frm
h har is rfrrd  as h arterial blood pressure
r systolic blood pressure. Whn h har muscl r-
laxs bwn cnracins (diasl), h bld prs-
sur drps  a lwr lvl, h diastolic blood pressure.
Whn rcrdd in h pain’s char, h syslic prs-
sur is rcrdd rs, fllwd by h diaslic prs-
sur (.g., 120/80 mm Hg). Th diffrnc bwn h
syslic and diaslic prssurs is calld h pulse pres-
sure, which is an indicar f h n f h arrial
bld vssl walls. Th mean arterial pressure (MAP)
is h avrag prssur hrughu ach cycl f h
harba and is signican bcaus i is h prssur
ha acually pushs h bld hrugh h circulary
sysm  prfus rgans and issus. I is calculad by
adding n-hird f h puls prssur  h diaslic
prssur r by using h fllwing quain, whr DP
is diaslic prssur and SP is syslic prssur:
MAP = DP + 1/3 (SP − DP)
and 110 mm Hg; hwvr, h numbr 60 r highr
has bn argd as nugh prssur  adqualy
prfus rgans and issus. Undr nrmal cndiins,
h arrial bld prssur says wihin narrw limis.
I rachs is pak during high physical r minal
aciviy and is usually a is lws lvl during slp.
Arrial bld prssur (BP) can b dnd as h
prduc f cardiac output (CO) and priphral vascular
rsisanc (PVR):
BP = CO × PVR
Cardiac upu is h primary drminan f syslic
prssur; priphral vascular rsisanc drmins
h diaslic prssur. Cardiac upu is drmind
by h srk vlum (h vlum f bld jcd in
a singl cnracin frm h lf vnricl), har ra
(cnrlld by h aunmic nrvus sysm), and v-
nus capacianc (lasiciy f h bld vssl). Syslic
bld prssur is hus incrasd by facrs ha incras
har ra r srk vlum. Vnus capacianc affcs
h vlum f bld (r prlad) ha is rurnd  h
har hrugh h cnral vnus circulain. Vnus
cnsricin dcrass vnus capacianc, incrasing
prlad and syslic prssur, and vnus dilain in-
crass vnus capacianc and dcrass prlad and
syslic prssur. Priphral vascular rsisanc is rgu-
lad primarily by cnracin and dilain f arrils.
Arrilar cnsricin incrass priphral vascular
353
354 UNIT IV Drugs Affecting the Cardiovascular System
rsisanc and hus diaslic bld prssur. Ohr fac-
rs ha affc vascular rsisanc includ h lasiciy
f h bld vssl walls and h viscsiy f h bld.
Hypertension is a disas characrizd by an lva-
in f h syslic bld prssur, h diaslic bld
prssur, r bh. Th liklihd f having a cardi-
vascular vn (angina, mycardial infarcin, har
failur, srk, rnal failur, rinpahy) incrass as
bld prssur incrass. Sudis hav shwn ha an
incras f 20 mm Hg syslic bld prssur and 10
mm Hg diaslic bld prssur abv 115/75 mm Hg
incrass h risk f dah frm srk, har disas,
and hr vascular disas. Primary hypertension ac-
cuns fr 90% f all clinical cass f high bld prs-
sur. Th caus f primary hyprnsin is unknwn.
A prsn, i is incurabl bu cnrllabl. In h Unid
Sas i is simad ha abu 37% f h ppulain,
r grar han n-hird f h ppulain vr ag
20, has hyprnsin. Th prvalnc incrass sadi-
ly wih bsiy and advancing ag s ha ppl wh
ar nrmnsiv a ag 55 hav a 90% lifim risk f
dvlping hyprnsin. In vry ag grup, h inci-
dnc f hyprnsin is highr fr African Amricans
han whis f bh gndrs. Ohr majr risk facrs
assciad wih high bld prssur ar lisd in Bx
22.1. Secondary hypertension ccurs afr h dvlp-
mn f anhr disrdr wihin h bdy (Bx 22.2).
Box 22.1 Major Risk Factors Associated With
Hypertension and Target Organ Damage
MAJOR RISK FACTORS
• Cigarette smoking
• Obesity (body mass index ≥30 kg/m2)
• Physical inactivity
• Dyslipidemia
• Diabetes mellitus
• Microalbuminuria or estimated glomerular ltration rate
less than 60 mL/min
• Age (older than 55 for men, 65 for women)
• Family history of premature cardiovascular disease
(men younger than age 55; women, age 65)
TARGET ORGAN DAMAGE
• Heart
 • Left ventricular hypertrophy
 • Angina or prior myocardial infarction
 • Prior coronary revascularization
 • Heart failure
• Brain
 • Stroke or transient ischemic attack
• Chronic kidney disease
 • Glomerular ltration rate
• Peripheral arterial disease
• Retinopathy
• Components of metabolic syndrome
Adapted from the Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure. The Seventh Report of the
Joint National Committee on Prevention, Detection, Evaluation, and Treatment
of High Blood Pressure (JNC 7). Bethesda, MD: National Institutes of Health;
2003. NIH publication 03-5233.
Th 2017 Guidlin fr h Prvnin, Dcin,
Evaluain and Managmn f High Bld Prssur
in Aduls jinly publishd by h Amrican Cllg
f Cardilgy and h Amrican Har Assciain in-
cluds a nw dniin f hyprnsin and classica-
in f bld prssur by sags ha rprsn h d-
gr f risk f nnfaal and faal cardivascular disas
vns and rnal disas (Tabl 22.1).
Th guidlins us lvain in bh syslic and
diaslic bld prssur radings abv 115/75 mm
Hg whn making a diagnsis f hyprnsin. In an
ffr  g accura bld prssur radings fr di-
agnsis, h individual shuld b sad quily fr
a las 5 minus in a chair (rahr han n an xami-
nain abl), wih f n h r and arm suppr-
d a har lvl. An apprprialy sizd cuff (cuff
bladdr ncircling a las 80% f h arm) shuld b
usd fr accuracy. A prsn mus hav w r mr
lvad radings n w r mr spara ccasins
afr iniial scrning  b classid as having hypr-
nsin. Whn syslic and diaslic radings fall
in w diffrn sags, h highr f h w sags
is usd  classify h dgr f hyprnsin prs-
n. Tabl 22.2 liss h bld prssur hrshlds
fr classicain f hyprnsin (lvad, sag
1 and sag 2 hyprnsin) and fllw-up rcm-
mndains basd n h iniial s f bld prssur
masurmns.
Th guidlins furhr urg halh praciinrs 
us h syslic bld prssur as h majr cririn
fr h diagnsis and managmn f hyprnsin in
middl-agd and ldr Amricans. Bfr his im,
h diaslic bld prssur had bn h majr d-
rminan fr h cnrl f bld prssur. Evidnc
indicas ha systolic hypertension is h ms cm-
mn frm f hyprnsin and is prsn in abu w-
hirds f hyprnsiv individuals ldr han 60 yars.
Whn a prsn has bn diagnsd wih hypr-
nsin, furhr valuain hrugh mdical hisry,
physical xaminain, and labrary ss shuld b
cmpld  (1) idnify causs f h high bld prs-
sur; (2) assss h prsnc r absnc f arg rgan
Box 22.2 Identiable Causes of Hypertension
• Sleep apnea
• Drug-induced or related causes
• Chronic kidney disease
• Primary aldosteronism
• Renovascular disease
• Chronic steroid therapy and Cushing syndrome
• Pheochromocytoma
• Coarctation of the aorta
• Thyroid or parathyroid disease
Adapted from the Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure. The Seventh Report of the
Joint National Committee on Prevention, Detection, Evaluation, and Treatment
of High Blood Pressure (JNC 7). Bethesda, MD: National Institutes of Health;
2003. NIH publication 03-5233.
 Drugs Used to Treat Hypertension CHAPTER 22 355

damag and cardivascular disas (s Bx 22.1); and
(3) idnify hr cardivascular risk facrs ha may
guid ramn (s Tabl 22.1).
TREATMENT OF HYPERTENSION
Th primary purps fr cnrlling hyprnsin
is  rduc h frquncy f cardivascular dis-
as. T accmplish his gal, h 2017 guidlins
rcmmnd ha bld prssur mus b rducd
and mainaind blw 130/80 mm Hg in adul pa-
ins. Nninsiuinalizd ambulary cmmuniy-
dwlling adul pains 65 yars and ldr shuld
mainain a syslic bld prssur f lss han 130
mm Hg. Fr aduls 65 yars and ldr wih hyprn-
sin and a high burdn f cmrbidiy and limid
lif xpcancy, clinical judgmn, pain prfrnc,
and a am-basd apprach  assss risk/bn ar
rasnabl fr dcisins rgarding innsiy f bld
prssur lwring and chic f anihyprnsiv
drugs. Majr lifsyl mdicains shwn  lwr
bld prssur includ wigh rducin in hs
wh ar vrwigh r bs; adpin f h DASH
(Diary Apprachs  Sp Hyprnsin) di, h
US Dparmn f Agriculur (USDA) Fd Parns,
r h Amrican Cllg f Cardilgy/Amrican
Har Assciain (ACC/AHA) di rcmmnda-
ins; diary sdium rducin; physical aciviy;
and mdrain f alchl cnsumpin (Tabl 22.3).
Tramn schduls shuld inrfr as lil as pssi-
bl wih h pain’s lifsyl; hwvr, nnpharma-
clgic hrapy mus includ liminain f smking,
wigh cnrl, ruin aciviy, rsricin f alchl
inak, srss rducin, a rgular slp parn f a
las 7 hurs ach nigh, and sdium cnrl. If his
hrapy is succssful in cnrlling high bld prs-
sur, drug hrapy is n ncssary. Evn if lifsyl
changs ar n adqua  cnrl hyprnsin,

Table 22.1 Classication and Management of Blood Pressure (BP) for Adults a
BP (MM HG)
BP CLASSIFICATION SYSTOLIC DIASTOLIC LIFESTYLE MODIFICATION INITIAL DRUG
Normal <120 and <80 Encourage No treatment
Elevated 120–129 or <80 Yes Generally no treatment
Stage 1 hypertension 130–139 or 80–89 Yes If risk is less than 10%, start with healthy
lifestyle recommendation; if greater
than 10%, start drug therapy with one
of the following agents: ACEI or ARB,
CCB or diuretic
Stage 2 hypertension ≥140 or ≥90 Yes Two rst-line drug combination from
different classes
aIndividuals with SBP and DBP in two categories should be designated to the higher BP category.
ACEI, Angiotensin-converting enzyme inhibitor; ARB, angiotensin-receptor blocker; CCB, calcium channel blocker.
From Whelton PK, Carey RM, Aronow WS, etal. 2017
ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults:
a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2018;71(19):2199–2269.

Table 22.2 Recommended Follow-up Schedule After Initial Blood Pressure Measurement
INITIAL BLOOD PRESSURE (MM HG)
SYSTOLIC DIASTOLIC FOLLOW-UP RECOMMENDED
<120 <80 Recheck in 1 yr
120–129 <80 Recheck in 3–6 moa
130–139 80–89 Recheck in 3–6 mo, if risk is less than 10% and following healthy lifestyle
recommendations
Recheck in 1 mo, if risk is greater than 10% receiving treatment
≥140 ≥90 Recheck in 1 mo
If goal met in 1 mo, recheck in 3–6 mo
If goal not met in mo, consider different medication or titration
Continue rechecking monthly until control achieved
≥180 ≥110 Evaluate or refer to source of care immediately or within 1 wk, depending on
clinical situation
aProvide advice about lifestyle modications.
From Whelton PK, Carey RM, Aronow WS, etal. 2017
ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults:
a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2018;71(19):2199–2269.
356 UNIT IV Drugs Affecting the Cardiovascular System

Table 22.3 Lifestyle Modications to Manage Hypertension a

APPROXIMATE BLOOD PRESSURE
MODIFICATION RECOMMENDATION REDUCTION (RANGE)
Weight reductionb Maintain normal body weight (body mass index = 18.5– Systolic 5–20 mm Hg/10-kg weight loss
24.9 kg/m2).
Adopt a healthy Consume a diet rich in fruits, whole grains, vegetables; Systolic/diastolic 5–6/3 mm Hg
eating planc includes low-fat dairy products, poultry, sh, legumes,
nontropical vegetable oils, and nuts; limits intake of sweets,
sugar-sweetened beverages, and red meats with a reduced
content of saturated and total fat. Described in DASH diet,
USDA Food Patterns, or AHA/ACC diet.
Dietary sodium Reduce dietary sodium intake to no more than 2.4 g sodium or Systolic/diastolic 2–7/1–3 mm Hg
reductionc 6 g sodium chloride per day.
Physical activityc Engage in regular aerobic physical activity three or four Systolic 4–9 mm Hg
sessions per week, lasting an average of 40 minutes per
session, involving moderate to vigorous intensity.c
Moderation Limit consumption to no more than two drinks (1 oz or 30 mL Systolic 2–4 mm Hg
of alcoholb ethanol [e.g., 24 oz beer, 10 oz wine, or 3 oz 80-proof
consumption whiskey])/day in most men and no more than one drink/day
in women and lighter weight individuals.
aThe effects of implementing these modications are dose and time dependent and could be greater for some individuals. For overall cardiovascular risk reduction, stop
smoking.
bFrom the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The Seventh Report of the Joint National Committee

on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) . Bethesda, MD: National Institutes of Health; 2003. NIH publication 03-5233.
cFrom Eckel RH, Jakcic JM, Ard JD, etal. 2013 AHA/ACC Guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of

Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(25 suppl 2):S76-S99.
ACC, American College of Cardiology; AHA, American Heart Association; DASH, Dietary Approaches to Stop Hypertension; USDA, US Department of Agriculture.

hy may rduc h numbr and dss f anihypr-
nsiv mdicains ndd  manag h cndiin.
Pain ducain is vially impran in raing
hyprnsin. This ducain shuld b mphasizd
and rirad frqunly by h primary halhcar
prvidr, pharmacis, and nurs.
DRUG THERAPY FOR HYPERTENSION
ACTIONS
Drugs usd in h ramn f hyprnsin can b
subdividd in svral cagris f hrapuic
agns basd n si f acin (Fig. 22.1). Pharmaclgic
classs f agns iniially usd  ra hyprnsin
ar anginsin-cnvring nzym (ACE) inhibirs
r anginsin II rcpr blckrs (ARBs), calcium
channl blckrs, and hiazid-yp diurics. Lss fr-
qunly usd agns ar h ba-adrnrgic blckrs,
dirc rnin inhibirs, aldsrn rcpr anag-
niss, alpha-1 adrnrgic blckrs, cnral-acing alpha-
2 agniss, and dirc vasdilars. Agns may b
usd aln r in cmbinain wih hr agns frm
diffrn classs wrking by diffrn mchanisms 
pimiz hrapy whil rducing advrs ffcs f h
mdicins.
USES
A ky  lng-rm succss wih anihyprnsiv hr-
apy is  individualiz hrapy fr a pain basd n
dmgraphic characrisics (.g., ag, gndr, rac),
cxising disass and risk facrs (.g., migrain
hadachs, dysrhyhmias, angina, diabs mllius),
prvius hrapy (wha has r has n wrkd in h
pas), cncurrn drug hrapy fr hr illnsss, and
cs. As ulind in Fig. 22.2, h 2017 guidlins srss
h bn f lifsyl changs  prvn and ra
hyprnsin. Nnpharmaclgic hrapy is spcially
ffciv in managing hyprnsin in pains wih
lvad bld prssur and wih sag 1 hyprnsin
in aduls wih a 10-yar cardivascular risk lss han
10%. Adul pains wih a 10-yar cardivascular risk
f 10% r grar ramn shuld b iniiad wih
n f h fur classs f mdicains rcmmndd:
an ACE inhibir r ARB, a calcium channl blckr,
and/r a diuric and nnpharmaclgic hrapy. In
adul pains wih sag 1 hyprnsin i is rasn-
abl  sar wih n rs-lin agn (.g., a hiazid-
lik diuric), spcially in aduls wih a hisry f
rhsaic hypnsin. I is rcmmndd  inii-
a w rs-lin agns f diffrn classs (.g., an
ACE inhibir and a hiazid-lik diuric r a cal-
cium blckr wih a hiazid-lik diuric) fr aduls
wih sag 2 hyprnsin and a bld prssur mr
han 20/10 mm Hg highr han hir arg (Fig. 22.3).
Us f a cmbinain prduc may simplify h rgi-
mn and nhanc adhrnc. S Tabl 22.4 fr a lis
f ingrdins f anihyprnsiv cmbinain prd-
ucs. Us cauin in ldr aduls bcaus hypnsin
r rhsaic hypnsin may dvlp. In black pa-
ins wih hyprnsin bu wihu har failur and
kidny disas, including hs wih diabs, w r
 Drugs Used to Treat Hypertension CHAPTER 22 357

ALPHA-AND BETA-ADRENERGIC
BLOCKING AGENTS
Labetalol
Cortex
BETA-ADRENERGIC BLOCKING AGENTS 
Propranolol
Hypothalamus Metoprolol

Central-acting ANGIOTENSIN-CONVERTING ENZYME

adrenergic INHIBITORS
antagonists Enalapril
Ramipril
Feedback to Lisinopril
Vasomotor vasomotor center
center ANGIOTENSIN II RECEPTOR BLOCKERS
Candesartan
Sympathetic Irbesartan
ganglion Baroreceptor reflex
Valsartan
Carotid arteries
Aortic arch RENIN INHIBITOR
Peripheral-acting Aliskiren
adrenergic
antagonists ALDOSTERONE RECEPTOR ANTAGONIST
Eplerenone
-Adrenergic receptor blockers CALCIUM CHANNEL (ION) BLOCKERS
Blood vessel
Heart Renin inhibitor Amlodipine
Nifedipine
Calcium
ase

channel
ele

ALPHA-1 ADRENERGIC BLOCKING AGENTS

blockers
in r

Prazosin
Angiotensin-
ren

- and 
Adrenergic converting enzyme CENTRAL-ACTING ALPHA-2 AGONISTS
ibit

Direct arterial Clonidine

blockers
Inh

vasodilators
Angiotensin I Angiotensin II
DIRECT VASODILATORS
Hydralazine

Diuretics Angiotensin II DIURETICS

Decrease sodium Decrease constriction Hydrochlorothiazide
receptor blockers
reabsorption
Representative examples only

Kidney
Fig. 22.1 Sites of action of antihypertensive agents. ACE, Angiotensin-converting enzyme. (Modied from U.S.
Department of Health and Human Services. The Sixth Report of the Joint National Committee on Detection, Evaluation,
and Treatment of High Blood Pressure [JNC-VI]. Washington, DC: National Institutes of Health; 1997.)

mr anihyprnsiv agns ar rcmmndd, such
as a hiazid-lik diuric and/r a calcium channl
blckr. Fr all pains, a lw ds shuld b slcd
 prc agains advrs ffcs, alhugh i may n
immdialy cnrl h bld prssur. I mus b
rcgnizd ha i may ak mnhs  cnrl hypr-
nsin adqualy whil aviding advrs ffcs f
hrapy.
Bcaus f many physilgic cmpnsary mch-
anisms ha may aggrava lwring bld prssur,
abu 75% f hyprnsiv pains rquir a cmbi-
nain f mdicains ha ac by diffrn pahways
 achiv bld prssur gals (<130/80 mm Hg). If,
afr 1 mnh, h rs drug is n ffciv, h dsag
may b incrasd, r a scnd drug frm anhr class
wih a diffrn mchanism f acin may b addd
(s Fig. 22.3). Afr bld prssur is rducd  h
gal lvl and mainnanc dss f mdicins ar
sabilizd, i may b apprpria  chang a pain’s
mdicain  a cmbinain anihyprnsiv prduc
 simplify h rgimn and nhanc cmplianc. S
Tabl 22.4 fr a lis f h ingrdins f anihyprnsiv
cmbinain prducs.
Th guidlins als prvid rcmmndains fr
spcic grups f pains. Fr ms pains wih
cmrbidiis, h bld prssur gal shuld b lss
han 130/80 mm Hg. Fr pains ag 65 yars r ldr,
a arg syslic bld prssur f lss han 130 mm Hg
is rcmmndd. In sm pains wih cmrbidiis,
h gal may b a bld prssur f 140/90 mm Hg.
Fr xampl, ldr pains wih islad syslic
hyprnsin shuld rs b rad wih diurics, wih
r wihu a ba blckr, r a dihydrpyridin cal-
cium channl blckr aln. Pains wih high bld
prssur and har failur, and/r chrnic kidny
disas, shuld b rad wih h ACE inhibirs r
ARBs. Pains wh hav hyprnsin and hav suf-
frd a mycardial infarcin shuld b rad wih a
ba-adrnrgic blcking agn and, in ms cass, an
ACE inhibir. Ohr sudis hav dmnsrad ha
 STATUS OF BLOOD PRESSURE

Stage 1 HTN
Normal BP Elevated BP 130-139/80-89 Stage 2 HTN
<120/80 120-129/<80 ≥140/90

Clinical ASCVD
or estimated
10-year risk ≥10%
Nondrug therapy
No Yes
and BP lowering
Promote medication
Nondrug
healthy therapy Nondrug therapy
lifestyles Nondrug therapy And BP-lowering
medication

Reassess Reassess
in 3-6 months in 1 month
Reassess Reassess
in 1 year in 3-6 months
Yes Reassess in
BP goal met
3-6 months
No

Assess and optimize

adherence to therapy;
consider intensification
of therapy

Fig. 22.2 Treatment algorithm for hypertension. ASCVD, Atherosclerotic cardiovascular disease; BP, blood pressure;
HTN, hypertension. (From Whelton PK, Carey RM, Aronow WS, etal. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/
ASH/ASPC/NMA/PCNA guidelines for the prevention, detection, evaluation, and management of high blood pressure
in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice
Guidelines. J Am Coll Cardiol. 2018;71(19):2199–2269.)

Blood pressure

Cardiac output Peripheral vascular resistance

Heart Stroke Nerve Circulating Local

rate volume transmission regulators regulators

-blockers 1-blockers 1-blockers ACE inhibitors

CCB Central Central ARBs
2-agonists 2-agonists Renin inhibitor
ACE inhibitors Nitroprusside
ARBs
Renin inhibitor

Contractility Preload Direct vasodilators

-blockers CCBs
CCB Nitroprusside
Hydralazine

Venous Vascular
tone volume
1-blockers
ACE inhibitors Sodium/water retention
ARBs
Renin inhibitor Diuretics
Nitroprusside ACE inhibitors
ARBs
Renin inhibitor
Fig. 22.3 Effects of antihypertensive agents. ACE, Angiotensin-converting enzyme; ARB, angiotensin II receptor blocker;
CCB, calcium channel blocker.
 Drugs Used to Treat Hypertension CHAPTER 22 359

Table 22.4 Combination Drugs for Hypertension

COMBINATION TYPE FIXED-DOSE COMBINATION (MG)a BRAND NAME
ACEIs and CCBs amlodipine/benazepril (2.5/10, 5/10, 5/20, 5/40, 10/20, 10/40) Lotrel
trandolapril/verapamil (2/180, 1/240, 2/240, 4/240) Tarka
CCB and statin amlodipine/atorvastatin (2.5/10–10/80) Caduet
CCBs and ARBs amlodipine/valsartan (5/160–10/320) Exforge
amlodipine/olmesartan (5/20–10/40) Azor
amlodipine/telmisartan (5/40, 5/80, 10/40, 10/80) Twynsta
CCBs/diuretic/ARBs amlodipine/hydrochlorothiazide/valsartan (5/12.5/160–10/25/320) Exforge HCT
amlodipine/hydrochlorothiazide/olmesartan (5/12.5/20–10/25/40) Tribenzor
ACEIs and diuretics benazepril/hydrochlorothiazide (5/6.25, 10/12.5, 20/12.5, 20/25) Lotensin HCT
captopril/hydrochlorothiazide (25/15, 25/25, 50/15, 50/25) --
enalapril/hydrochlorothiazide (5/12.5, 10/25) Vaseretic
fosinopril/hydrochlorothiazide (10/12.5, 20/12.5) --
lisinopril/hydrochlorothiazide (10/12.5, 20/12.5, 20/25) Zestoretic
quinapril/hydrochlorothiazide (10/12.5, 20/12.5, 20/25) Accuretic
ARBs and diuretics azilsartan/chlorthalidone (40/12.5–40/25) Edarbyclor
candesartan/hydrochlorothiazide (16/12.5, 32/12.5, 32/25) Atacand HCT
irbesartan/hydrochlorothiazide (150/12.5, 300/12.5) Avalide
losartan potassium/hydrochlorothiazide (50/12.5, 100/12.5, 100/25) Hyzaar
Do not confuse Hyzaar
with Cozaar.
olmesartan/hydrochlorothiazide (20/12.5, 40/12.5, 40/25) Benicar HCT
telmisartan/hydrochlorothiazide (40/12.5, 80/12.5, 80/25) Micardis HCT
valsartan/hydrochlorothiazide (80/12.5, 160/12.5, 320/12.5, 160/25, Diovan HCT
320/25)
BBs and diuretics atenolol/chlorthalidone (50/25, 100/25) Tenoretic
bisoprolol/hydrochlorothiazide (2.5/6.25, 5/6.25, 10/6.25) Ziac
Do not confuse Ziac with
Zocor or Tiazac.
metoprolol/hydrochlorothiazide (25/12.5, 50/12.5, 100/12.5, 50/25, Dutoprol
100/25, 100/50)
nadolol/bendroumethiazide (40/5, 80/5)
Direct renin inhibitor aliskiren/hydrochlorothiazide (150/12.5, 150/25, 300/12.5, 300/25) Tekturna HCT
combination
products
Diuretic and diuretic amiloride HCl/hydrochlorothiazide (5/50) —
combination spironolactone/hydrochlorothiazide (25/25, 50/50) Aldactazide
triamterene/hydrochlorothiazide (37.5/25, 75/50) Maxzide
a

Do not confuse.
ACEI, Angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; BB, beta blocker; CCB, calcium channel blocker.

if a pain has har failur, a diuric, an ACE inhibi-
r, and an aldsrn rcpr anagnis (.g., spi-
rnlacn, plrnn) may b bncial. If a pain
has angina pcris, dihydrpyridin calcium channl
blckrs (.g., amldipin, nifdipin) may b addd
 hr hrapy bcaus hy hav bn prvn 
rliv chs pain and rduc h incidnc f srk.
Ohr cmbinains f hrapy fund  b paricularly
ffciv ar an ACE inhibir plus a diuric r cal-
cium channl blckr, r an ARB plus a diuric. (S
individual drug mngraphs fr mchanisms f ac-
in f ach class f anihyprnsiv agn.) D n
us an ACE inhibir and ARB r dirc rnin inhibir
ghr in h sam pain. Thr is gnrally lil
hrapuic gain cmpard wih pnial advrs f-
fcs ha may dvlp.
360 UNIT IV Drugs Affecting the Cardiovascular System
Pains wh hav mdid hir lifsyls wih
apprpria xrcis, di, wigh rducin, and cn-
rl f hyprnsin fr a las 1 yar may b can-
didas fr sp-dwn hrapy. Th dsag f ani-
hyprnsiv mdicains may b gradually rducd
in a slw, dlibra mannr. Ms pains may sill
rquir sm hrapy, bu ccasinally h mdicin
can b discninud. Pains whs drugs hav bn
discninud shuld hav rgular fllw-up xami-
nains bcaus bld prssur fn riss again 
hyprnsiv lvls, smims mnhs r yars lar,
spcially if lifsyl mdicains ar n cninud.
NURSING IMPLICATIONS FOR HYPERTENSIVE
THERAPY
Assessment
History of risk factors
• Mak n f h pain’s gndr, ag, and rac.
Ppl wh ar ldr, mal, and/r African
Amrican hav a highr incidnc f hyprnsin.
• Has h pain bn ld prviusly abu h l-
vad bld prssur radings? If s, undr wha cir-
cumsancs wr h bld prssur radings akn?
• Is hr a family hisry f hyprnsin, cr-
nary har disas, srk, diabs mllius, r
dyslipidmia?
Smoking. Obain a hisry f h numbr f cigars
r cigars smkd daily. Hw lng has h prsn
smkd? Has h prsn vr rid  sp smking?
Ask whhr h prsn knws wha ffc smking
has n h vascular sysm. Hw ds h individual
fl abu mdifying h smking habi?
Dietary habits. Obain a diary hisry. Ask spcic
qusins  bain daa rlaing  h amun f sal
usd in cking and a h abl, as wll as fds an
ha ar high in fa, chlsrl, rnd carbhydras,
and sdium. Using a calri cunr, ask h prsn 
sima h numbr f calris an daily. Hw much
ma, sh, and pulry ar an daily (siz and num-
br f srvings)? Esima h prcnag f al daily
calris prvidd by fas. Discuss fd prparain
(.g., bakd, brild, frid fds). Hw many srvings
f fruis and vgabls ar an daily? Wha yps
f ils r fas ar usd in fd prparain? Cnsul
a nuriin x fr furhr diary hisry qusins.
Wha is h frquncy and vlum f alchlic bvr-
ags cnsumd?
Elevated serum lipids. Ask whhr h pain is awar
f having lvad lipid, riglycrid, r chlsrl lv-
ls. If lvad, wha masurs has h prsn rid fr
rducin and wha ffc hav h inrvnins had n
h bld lvls a subsqun xaminains? Rviw
labrary daa availabl (.g., chlsrl, riglycrid,
lw-dnsiy lipprin [LDL], vry-lw-dnsiy lip-
prin lvls).
Renal function. Has h pain had any labrary
ss  valua rnal funcin (.g., urinalysis—micr-
albuminuria, prinuria, micrscpic hmauria) r
had a bld analysis shwing an lvad bld ura
nirgn (BUN) r srum crainin lvl? Ds h pa-
in hav ncuria?
Obesity. Ask abu any rcn wigh gains r lsss and
whhr inninal r uninninal. N abnrmal
wais--hip rai. Pains wih mr wigh arund
hir wais hav a highr incidnc f dvlping har
disas, hyprnsin, and diabs (s Chapr 20).
Psychomotor functions
• Drmin h pain’s yp f lifsyl. Hav h
pain dscrib xrcis lvl in rms f amun
(.g., walking 3 mils), innsiy (.g., walking 3
mph), and frquncy (.g., walking vry hr
day). Is h pain’s jb physically dmanding r f
a sdnary naur?
• Drmin h pain’s lvl f psychlgical srss.
Ask h individual  sima h amun f srss
in hir lif. Hw ds h prsn cp wih srss-
ful siuains a hm and in h wrkplac?
• Has h pain xprincd any faigu r rduc-
in in aciviy lvl causd by inlranc r pal-
piains, angina, r dyspna? Whn walking, d
svr lg cramps (claudicain) frc hm  sp
and rs r svrly limi ambulain?
Medication history
• Has h pain vr akn r is currnly aking any
mdicains fr h ramn f high bld prs-
sur? If bld prssur mdicains hav bn pr-
scribd bu ar n bing akn, why was h mdi-
cin discninud? Wr any advrs ffcs nicd
whil aking h mdicains, and hw did h pa-
in manag hm?
• Obain a lis f all mdicains bing akn, includ-
ing prscribd drugs, vr-h-cunr drugs, hrb-
al prparains, and sr drugs. Rsarch hs
mdicains in h drug mngraphs  drmin
pnial drug-drug inracins ha may affc h
individual’s bld prssur r h ffcivnss f
h mdicins prscribd.
• If h pain is fmal, ask whhr sh is nw r
has bn aking ral cnracpivs r is rciving
hrmn rplacmn hrapy.
Physical assessments
Blood pressure. Obain w r mr bld prssur
masurmns.
• Th individual shuld b sad quily fr a las 5
minus in a chair wih a back suppr (rahr han
n an xaminain abl), wih f n h r and
arm supprd a har lvl.
• An apprprialy sizd cuff (cuff bladdr ncircling
a las 80% f h arm) shuld b usd fr accuracy.

• Whn masuring bld prssur, h cuff shuld b
inad  30 mm Hg abv h pin a which h
radial puls disappars. Th sphygmmanmr
prssur shuld hn b rducd a 2  3 mm/sc.
Tw radings shuld b akn a las 1 minu apar.
• Vrify h radings in h ppsi arm. A diffrnc
in bld prssur bwn h w arms can b x-
pcd in abu 20% f pains. Th highr valu
shuld b h n usd in ramn dcisins.
• Ppl mus hav w r mr lvad radings n
w r mr spara ccasins afr iniial scrn-
ing  b classid as having hyprnsin.
• Orhsaic hypnsin is dnd by a dcras
in syslic bld prssur f 20 mm Hg r mr, r
diaslic bld prssur f 10 mm Hg r mr, fl-
lwing rapid chang f psiin frm rcumbn 
sanding r afr 3 minus f qui sanding. Fd
ingsin, im f day, ag, and hydrain can affc
his frm f hypnsin, as can a hisry f parkin-
snism, xcssiv bld lss, diabs, r mulipl
mylma.
• Ensur ha h pain has n ingsd caffin
wihin h pas 2  3 hurs.
Height and weight. Wigh and masur h pain.
Masur h was circumfrnc 2 inchs abv h
navl. Wha has h prsn’s wigh bn? Ask abu
any rcn wigh gains r lsss and whhr inn-
inal r uninninal. Calcula h bdy mass indx
(s Chapr 20 fr mr discussin and classicain
f bdy mass indx).
Bruits. Chck nck, abdmn, and xrmiis fr
h prsnc f bruis.
Peripheral pulses. Palpa and rcrd fmral, pp-
lial, and pdal pulss bilarally.
Eyes. As apprpria  h lvl f ducain, pr-
frm a funduscpic xaminain f h inrir y,
ning arrivnus nicking, hmrrhags, xudas,
r papilldma.
Implementation
• Prfrm nursing assssmns n a schduld basis.
• Mak rfrrals as indicad fr srss managmn,
smking cssain, and diary cunsling and fr
an xrcis prgram apprpria fr h individu-
al’s nds.
• Whn iniiaing anihyprnsiv hrapy in a hs-
pializd pain, prc h pain frm pssibl
falls scndary  hypnsin by assising during
ambulain and carfully assssing fr fainnss.
Tak bld prssur in supin, and sanding psi-
ins  idnify hypnsiv rspnss.
Patient Education
• Examin daa  drmin h individual’s xn
f undrsanding f hyprnsin and is cnrl.
• Using h pain’s hisry, analyz lifsyl l-
mns  drmin halh aching nds f h in-
dividual and signican hrs.
Drugs Used to Treat Hypertension CHAPTER 22 361
Baseline and diagnostic studies Rviw h pain’s
char and all rprs availabl ha ar usd  build
baslin infrmain (.g., lcrcardigram; urinaly-
sis; bld glucs, hmacri, srum passium, BUN,
crainin, and calcium lvls; a lipid prl (al
chlsrl, LDL chlsrl, high-dnsiy lipprin
[HDL] chlsrl, riglycrids) afr a 9-  12-hur
fas).
Smoking
• Suggs ha h pain sp smking. Smking
causs vascnsricin f h bld vssls; ncur-
ag a drasic rducin in—and prfrably al ab-
sinnc frm—smking. Includ infrmain abu
smking cssain and availabl suppr rsurcs.
• Explain h incrasd risk f crnary arry disas
if h habi is cninud. I may b ncssary  s-
l fr a drasic dcras in smking in sm ppl,
alhugh absinnc shuld b h gal.
Nutritional status
• Diary cunsling is ssnial fr h ramn f
hyprnsin. Cnrl f bsiy aln may b suf-
cin  alr h hyprnsiv cndiin. Ms
pains ar placd n a rducd-sdium di (2.4
g sdium r <6 g abl sal pr day). Th gal f di-
ary hrapy is a rducin f chlsrl, lipids,
saurad fa, and alchl cnsumpin. Fds high
in passium and calcium ar ncuragd  d-
cras bld prssur. S h DASH, USDA Fd
Parns, r ACC/AHA di fr furhr infrmain
(s Tabl 22.3).
• Diary planning shuld always invlv h pa-
in in mnu planning s ha prsnal prfr-
ncs, availabiliy f fd prducs, and css ar
discussd. Includ h prsn wh purchass fd
prducs and prpars h mals in h diary
cunsling.
• Shw h pain varius fd labls and xplain
wha ingrdins indica a high sdium cnn
(.g., sal, sdium, sdium chlrid, sdium bicar-
bna, sdium aluminum sulfa). Suggs h us
f a variy f spics as subsius fr sdium whn
cking. Explain fds ha shuld b avidd in
larg quaniis (.g., bacn, smkd mas, crab
ma, una, crackrs, prcssd chss, ham).
• Tach h individual  rcrd wighs in h sam
clhing, a h sam im daily, and using h sam
scal. Gnrally, a wigh gain r lss f mr han
2 punds is rprd  a halhcar prvidr; hw-
vr, spcic paramrs may vary and shuld b
discussd during iniiain f hrapy.
Stress management
• Idnify srss-prducing siuains in h pain’s
lif and sk mans  rduc hs facrs signi-
canly. In sm cass, rfrral fr raining in srss
managmn, rlaxain chniqus, mdiain, r
362 UNIT IV Drugs Affecting the Cardiovascular System
bifdback may b ncssary. If srss is prducd
in h wrk sing, i may b apprpria  invlv
an indusrial nurs.
• Srss wihin h family is fn signican and may
rquir prfssinal cunsling fr h family and
pain.
Exercise and activity. Dvlp a plan fr mdra xr-
cis  imprv h pain’s gnral cndiin. Cnsul
a halhcar prvidr fr any individual mdicains
dmd apprpria. Suggs including aciviis ha
h pain nds hlpful in rducing srss. Nurss can
hlp pains incras physical aciviy hrughu h
day by ncuraging hm  ak par in h fllwing:
• Play aciv gams wih hir childrn.
• Engag in a spr.
• Find a frind wih whm  walk r jg.
• Tak a class in yga r ai chi.
• Walk a dg.
• Gardn n h wknds.
• Walk r bicycl  schl r wrk.
• Tak h sairs, aviding h lvar.
• Park h car a h farhs pin in h parking l a
wrk, schl, r whn shpping.
Blood pressure monitoring. Dmnsra h crrc
prcdur fr aking bld prssur. I is bs  hav
h pain r family bring in h bld prssur quip-
mn ha will b usd a hm  prfrm h bld
prssur masurmn. Valida h pain’s and fam-
ily’s undrsanding by having hm prfrm his ask
n svral ccasins undr suprvisin. Mnir bld
prssur, puls, and rspirains a las vry shif
whil h pain is hspializd and srss h nd
fr h pain  mnir bld prssur in accrdanc
wih a halhcar prvidr’s rdrs afr discharg (usu-
ally daily). Th pain shuld b givn sm numrical
guidlins, as sablishd by a halhcar prvidr, fr
a dsird gal f hrapy and wha  d if his is n
bing achivd. Nrmal hm bld prssur shuld
a las b lwr han 140/90 mm Hg. Nighim hm
bld prssur is usually lwr han dayim prssur.
Medication regimen
• Cauin h pain ha fr h rs 2 wks f
anihyprnsiv hrapy, drwsinss may ccur.
Pains shuld b ld ha his advrs ffc is
slf-limiing. Thy shuld b cauius in praing
pwr quipmn and mr vhicls whil his
sympm ccurs.
• A cmmn advrs ffc f anihyprnsiv mdi-
cains is hypnsin. Insruc h pain  ris
slwly frm a siing r supin psiin. Tll h pa-
in  avid sanding fr lng prids, spcially
wihin 2 hurs f aking anihyprnsiv mdica-
in. Waknss, dizzinss, r fainnss can usually
b rlivd by incrasing muscular aciviy r by
siing r lying dwn.
• Tach h prsn  prfrm xrciss ha prvn
bld pling in h xrmiis whn siing r
sanding fr lng prids. Ths xrciss includ
xing h calf muscls, wiggling h s, rising n
h s, and hn rurning h f  a a psiin.
• Tach h prsn and signican hrs hw  ak
and rcrd bld prssur a prscribd inrvals.
• Th pain shuld always rpr a lack f rspns
 h mdicain prscribd and/r a bld prs-
sur ha cninus  ris afr mdicains hav
bn akn. (Ask a halhcar prvidr fr spcic
paramrs.)
Fostering health maintenance
• Thrughu h curs f ramn, discuss mdica-
in infrmain and hw i will bn h pain.
• Drug hrapy is n cmpnn in h manag-
mn f hyprnsin. Lifsyl changs ar qual in
impranc  drug hrapy; hrfr h nd 
mainain an xrcis prgram and mdify diary
habis  cnrl bsiy and srum chlsrl is
crucial. Cssain f smking and minimal alchlic
inak ar srngly rcmmndd.
• Prvid h pain and signican hrs wih
h impran infrmain cnaind in h sp-
cic drug mngraphs fr h drugs prscribd.
Addiinal halh aching and nursing inrvn-
ins fr cmmn and srius advrs ffcs will
b fund in ach drug mngraph.
• Sk cprain and undrsanding f h fllw-
ing pins s ha mdicain cmplianc is incrasd:
nam f mdicain; dsag, rus, and ims f ad-
minisrain; and cmmn and srius advrs ffcs.
• Th ms ffciv hrapy prscribd by a halh-
car prvidr will cnrl hyprnsin nly if h
pain is mivad. Mivain imprvs whn h
pain has a psiiv xprinc wih and rus in
halhcar prvidrs. Empahy builds rus and is
an xclln mivar.
Patient self-assessment. Enlis h pain’s aid in d-
vlping and mainaining a wrin rcrd f mni-
ring paramrs (.g., bld prssurs, wigh,
xrcis) (s h Pain Slf-Assssmn Frm
fr Cardivascular Agns n h Evlv wbsi).
Cmpl h Prmdicain Daa clumn fr us as
a baslin  rack rspns  drug hrapy. Ensur
ha h pain undrsands hw  us h frm, and
insruc h pain  bring h cmpld frm  fl-
lw-up visis. During fllw-up visis, fcus n issus
ha will fsr adhrnc wih h hrapuic inr-
vnins prscribd.
DRUG CLASS: DIURETICS
Actions
Th diurics ac as anihyprnsiv agns by causing
vlum dplin, sdium xcrin, and vasdilain

f priphral arrils. Th mchanism f priphral
arrilar vasdilain is unknwn.
Uses
Thr ar fur classs f diuric agns: carbnic an-
hydras inhibirs, hiazid and hiazid-yp agns,
lp diurics, and passium-sparing diurics (s
Chapr 28). Th carbnic anhydras inhibirs ar
wak anihyprnsiv agns and hrfr ar n
usd fr his purps. Th passium-sparing diurics
ar rarly usd aln, bu ar cmmnly usd in cm-
binain wih hiazid and lp diurics fr addd
anihyprnsiv ffc and  cunrac h passi-
um-xcring ffcs f hs mr pn diuric-
anihyprnsiv agns.
Th diurics ar h ms cmmnly prscribd
anihyprnsiv agns bcaus hy ar a class f
agns ha hav bn shwn  rduc cardivascu-
lar mrbidiy and mraliy assciad wih hypr-
nsin. Th hiazids ar ms ffciv if h rnal
crainin claranc is highr han 30 mL/min; hw-
vr, as rnal funcin driras, h mr pn
lp diurics ar ndd  cninu xcrin f s-
dium and war.
Diurics ar cmmnly prscribd in cmbinain
hrapy. Thy pnia h hypnsiv aciviy f
h nndiuric anihyprnsiv agns, hav a lw
incidnc f advrs ffcs, and ar fn h las x-
pnsiv f h anihyprnsiv agns.
Diurics ar usd (fn wih hr classs f an-
ihyprnsiv hrapy)  ra all sags f hypr-
nsin. Th agns ar discussd mr xnsivly in
Chapr 28.
Nursing Implications for Diuretic Agents
Premedication assessment
1. Obain baslin bld prssur radings in supin
and sanding psiins.
2. Obain baslin wigh and apical puls.
3. Iniia labrary sudis as rqusd by a halh-
car prvidr (.g., lcrlys).
4. Obain baslin assssmn f pain’s sa f
hydrain.
Availability, dosage, and administration. S Chapr 28.
DRUG CLASS: BETA-ADRENERGIC BLOCKING
AGENTS
Actions
Ba-adrnrgic blcking agns (ba blckrs; s
Tabl 12.3) inhibi cardiac rspns  sympahic
nrv simulain by blcking h ba rcprs. As
a rsul, h har ra, h cardiac upu, and cns-
qunly h bld prssur ar rducd. Ba blckrs
als inhibi rnin rlas frm h kidnys, diminish-
ing h cascad f h rnin-anginsin-aldsrn
sysm (RAAS) ha wuld induc vascnsricin
and sdium rabsrpin, aggravaing hyprnsin.
Drugs Used to Treat Hypertension CHAPTER 22 363
Uses
Ba blckrs rduc h mrbidiy and mraliy as-
sciad wih hyprnsin and ar widly usd as
anihyprnsiv agns. Th clinical advanags f
ba blckrs in raing hyprnsin includ minimal
psural r xrcis hypnsin, minimal ffc n
sxual funcin, bld prssur rducin in h supin
psiin, and lil r n slwing f h cnral nrvus
sysm (CNS).
Th 2017 guidlins rcmmnd ba blckrs
as alrnaiv firs-lin hrapy fr sags 1 and 2
hyprnsin. Hwvr, ba blckrs ar n as f-
fciv in African Amrican pains and shuld b
avidd in pains wih ashma, yp 1 diabs
mllius, har failur causd by syslic dysfunc-
in, and priphral vascular disas. Ohr sud-
is nw rcmmnd hiazid diurics and ACE
inhibirs fr iniial hrapy. Ba blckr hrapy is
sill prfrrd fr hyprnsiv pains wih hr
srng indicains, paricularly hs wih symp-
maic crnary har disas (angina) r prvius
mycardial infarcin.
Nursing Implications for Beta-Adrenergic Blocking
Agents
Premedication assessment
1. Chck h pain’s hisry fr rspirary cndiins
ha culd b aggravad by brnchcnsricin,
yp 1 diabs mllius, har failur, r priphral
vascular disas. If any f hs cndiins ar prs-
n, cnac h halhcar prvidr  discuss h
siuain bfr iniiaing ba blckr hrapy.
2. Obain baslin bld prssur radings in supin
and sanding psiins and apical puls. Hld md-
icain if syslic bld prssur is lss han 100 mm
Hg r h har ra is lss han 50 bas/min, and
cnac h prscribr.
Availability, dosage, and administration. S Tabl 12.3.
Individualization of dosage. Alhugh h ns f ac-
iviy f ba blckrs is rapid, i may fn ak svral
days  wks fr a pain  shw pimal imprv-
mn and bcm sabilizd n an adqua main-
nanc dsag. Pains mus b pridically rvalua-
d  drmin h lws ffciv dsag ncssary
 cnrl h disrdr bing rad.
Sudden discontinuation. Pains mus b cuns-
ld agains pr cmplianc r suddn discninu-
ain f hrapy wihu a halhcar prvidr’s ad-
vic. Suddn discninuain f hrapy has rsuld
in an xacrbain f anginal sympms, fllwd in
sm cass by mycardial infarcin. Whn discn-
inuing lng-rm ramn wih ba blckrs, h
dsag shuld b gradually rducd vr a prid
f 1  2 wks wih carful mniring f h pa-
in. If anginal sympms dvlp r bcm mr
frqun, ba blckr hrapy shuld b rsard,
a las mprarily. Ms f h advrs ffcs
assciad wih ba blckrs ar dsag rlad.
364 UNIT IV Drugs Affecting the Cardiovascular System
Rspns by individual pains is highly variabl.
Many f hs advrs ffcs may ccur bu migh
b ransin. Srngly ncurag pains  s hir
halhcar prvidr bfr discninuing hrapy.
Minr dsag adjusmn may b all ha is rquird
fr ms advrs ffcs.
Serious adverse effects
Cardiovascular
Bradycardia, peripheral vasoconstriction (purple, mottled
skin). Wihhld addiinal dss unil h pain is
valuad by a halhcar prvidr.
Heart failure. Mnir h pain fr an incras in
dma, dyspna, crackls, bradycardia, and rhpna.
Nify a halhcar prvidr if hs sympms dvlp.
Respiratory
Bronchospasm, wheezing. Wihhld addiinal dss
unil h pain has bn valuad by a halhcar
prvidr.
Endocrine
Patients with diabetes. Mnir h pain fr symp-
ms f hypglycmia: hadach, waknss, dcrasd
crdinain, gnral apprhnsin, diaphrsis, hun-
gr, r blurrd r dubl visin. Many f hs symp-
ms may b maskd by h ba blckrs. Nify a
halhcar prvidr if any f hs sympms appar
inrminly.
Drug interactions
Antihypertensive agents. All ba blckrs hav hyp-
nsiv prpris ha ar addiiv wih ani-
hyprnsiv agns (.g., mhyldpa, hydralazin,
clnidin, cappril, diliazm, vrapamil). If i is d-
cidd  discninu hrapy in a pain rciving ba
blckrs and clnidin cncurrnly, h ba blckr
shuld b wihdrawn gradually and discninud sv-
ral days bfr h gradual wihdrawal f h clni-
din. Svr rbund hyprnsin may ccur if h
ba blckr is n gradually discninud rs.
Beta-adrenergic agents. Dpnding n h dsags
usd, h ba simulans (.g., isprrnl, ma-
prrnl, rbualin, alburl; s Tabl 12.2) may
inhibi h acin f h ba blckrs, and vic vrsa.
Amiodarone, verapamil, diltiazem, disopyramide, digoxin,
propafenone. Alhugh hs drugs ar ccasinally
usd cncurrnly, mnir h pain carfully fr ad-
diinal dysrhyhmias, bradycardia, and signs f har
failur.
Enzyme-inducing agents. Enzym-inducing agns
such as phnbarbial, and rifampin nhanc h m-
ablism f prpranll, mprll, pindll, and
imll. This racin prbably ds n ccur wih na-
dll r anll bcaus hy ar n mablizd bu
ar xcrd unchangd. Th dsag f h ba blck-
r may hav  b incrasd  prvid hrapuic ac-
iviy. If h nzym-inducing agn is discninud,
h dsag f h ba-blcking agn will als rquir
rducin.
Nonsteroidal antiinammatory drugs. Indmhacin,
and pssibly hr prsaglandin inhibirs, may in-
hibi h anihyprnsiv aciviy f ba blckrs, r-
suling in lss f hyprnsiv cnrl. Th dsag f
h ba blckr may hav  b incrasd  cmpn-
sa fr h anihyprnsiv inhibiry ffc f nn-
sridal aniinammary drugs (NSAIDs).
DRUG CLASS: ANGIOTENSIN-CONVERTING ENZYME
INHIBITORS
Actions
ACE inhibirs (Tabl 22.5) rprsn a majr brak-
hrugh in h ramn f hyprnsin. Th RAAS
plays a majr rl in h rgulain f bld prssur.
Whn hr is a rducin in bld prssur, sdium
cncnrain, r rnal bld w, rnin is scrd by
h kidnys. Th rnin cnvrs anginsingn, which
is scrd by h livr,  anginsin I. Anginsin I
is hn cnvrd by anginsin I–cnvring nzym
 anginsin II. Anginsin II prducs pn vas-
cnsricin by acing n rcprs wihin bld vssls.
I als prms aldsrn scrin, which causs
sdium rnin by simulain f minralcricid
rcprs in h adrnal crx. Ths acins rsul
in incrasd bld prssur scndary  h vas-
cnsricin and nhancd cardiac upu scndary 
sdium rnin. Th ACE inhibirs inhibi angin-
sin I–cnvring nzym, h nzym rspnsibl fr
h cnvrsin f anginsin I  anginsin II, hus
rducing srum lvls f his pn vascnsricr and
aldsrn simulan. This diminishs h RAAS cas-
cad ha wuld induc vascnsricin and sdium
rabsrpin, aggravaing hyprnsin.
Uses
ACE inhibirs rduc bld prssur, prsrv cardiac
upu, and incras rnal bld w. Thy ar ffc-
iv as singl hrapy fr sag 1 r 2 hyprnsin, s-
vr acclrad hyprnsin, and rnal hyprnsin.
Alhugh hy may b usd aln, hy nd  b mr
ffciv whn cmbind wih diuric hrapy. Thy
ar n as ffciv in lwring bld prssur in African
Amricans unlss usd wih a diuric. Advanags f
ACE inhibirs ar h infrquncy f rhsaic hyp-
nsin; lack f CNS dprssin and sxual dysfuncin
advrs ffcs; lack f aggravain f ashma, bsruc-
iv pulmnary disas, gu, chlsrl lvls, r dia-
bs; and an addiiv ffc wih diurics. Th ACE
inhibirs ar als ffciv in h ramn f har
failur and fllwing mycardial infarcin and ar
ruinly usd  slw h prgrssin f diabic n-
phrpahy. ACE inhibirs shuld n b adminisrd
as chrapy wih ARBs r dirc rnin inhibirs.
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm h
ACE inhibirs is rducin in bld prssur.
 Drugs Used to Treat Hypertension CHAPTER 22 365

Table 22.5 Angiotensin-Converting Enzyme (ACE) Inhibitors

GENERIC NAME BRAND NAME AVAILABILITY APPROVED USES DOSAGE RANGE
benazepril Lotensin Tablets: 5, 10, 20, Hypertension PO: Initial: 10 mg once daily
Do not confuse Do not confuse 40 mg Maintenance: 20–40 mg daily
benazepril with Lotensin with Maximum: 80 mg/day
Benadryl allergy, Lioresal, Loniten ,
Benzonatate, or or Lovastatin.
donepezil.
captopril — Tablets: 12.5, 25, Hypertension, heart PO: Initial: 12.5–25 mg two or
Do not confuse 50, 100 mg failure, diabetic three times daily 1 hr before
captopril with nephropathy meals
carvedilol. Maintenance: 50–450 mg daily 1
hr before meals in two or three
divided doses
enalapril Vasotec Tablets: 2.5, 5, 10, Hypertension, heart PO: Initial: 2.5–5 mg once daily
Do not confuse Do not confuse 20 mg failure Maintenance: 10–40 mg daily
enalapril with Vasotec with Oral solution:
Eldepryl. Norvasc. 1 mg/mL in
150-mL bottle
enalaprilat Vasotec IV Injection: 1.25 mg/ Hypertension IV: 0.625–1.25 mg over 5 min
mL in 1-, 2-mL every 6 hr
vials
fosinopril — Tablets: 10, 20, Hypertension, heart PO: Initial: 10 mg once daily
Do not confuse 40 mg failure Maintenance: 20–40 mg daily
fosinopril with Maximum: 80 mg/day
bisoprolol or
furosemide
lisinopril Prinivil Tablets: 2.5, 5, 10, Hypertension, PO: Initial: 5–10 mg once daily
Do not confuse 20, 30, 40 mg heart failure, Maintenance: 20–40 mg daily
Prinivil with, Oral solution: 1 mg/ post–myocardial Maximum: 80 mg/day
Pravachol, Prevacid, mL in 150-mL infarction
Prilosec, or Zestril. bottle
Zestril
Do not confuse
Zestril with Vistaril,
Zerit, Zocor, or
Zyrtec.
moexipril — Tablets: 7.5, 15 mg Hypertension PO: Initial: with diuretic, 3.75 mg;
without diuretic, 7.5 mg
Maintenance: 7.5–30 mg in one or
two divided doses 1 hr before
meals
perindopril — Tablets: 2, 4, 8 mg Hypertension PO: Initial: 4 mg daily
Maintenance: 4–8 mg daily
Maximum: 16 mg/day
quinapril Accupril Tablets: 5, 10, 20, Hypertension, heart PO: Initial: 10–20 mg daily without
Do not confuse 40 mg failure diuretic; 5 mg daily with diuretic
Accupril with Maintenance: 20–80 mg daily
AcipHex, Accolate,
Altace, or Aricept.
ramipril Altace Capsules: 1.25, 2.5, Hypertension, heart PO: Initial: 1.25–2.5 mg daily
Do not confuse Do not confuse 5, 10 mg failure Maintenance: 2.5–20 mg daily
ramipril with Altace with Accupril,
rifampin. Amaryl, or Norvasc.
trandolapril — Tablets: 1, 2, 4 mg Hypertension, heart PO: Initial: 1 mg daily
Do not confuse failure Maintenance: 2–4 mg daily
trandolapril with
tramadol.
Available in Canada.
Do not confuse.
366 UNIT IV Drugs Affecting the Cardiovascular System
Nursing Implications for Angiotensin-Converting
Enzyme Inhibitors
Premedication assessment
1. Obain baslin bld prssur radings in supin
and sanding psiins and apical puls. Hld md-
icain if syslic bld prssur is lss han 100 mm
Hg r h har ra is lss han 50 bas/min, and
cnac h prscribr.
2. Obain a hisry f bwl liminain parns.
3. Iniia labrary sudis as rqusd by a halh-
car prvidr (.g., rnal funcin ss such as BUN,
srum crainin, and lcrly lvls and cm-
pl bld cun [CBC])  srv as a baslin fr
fuur cmparisn.
4. Ask whhr h pain is prgnan r likly  b-
cm prgnan. If s, discuss wih a halhcar pr-
vidr bfr iniiaing ACE inhibir hrapy.
5. Ask if h pain has a prsisn cugh.
Availability, dosage, and administration. S Tabl 22.5.
Cappril shuld b adminisrd wihu fd and
rquirs w-  hr-ims-daily dsing. All h hr
agns may b adminisrd n r w ims daily.
Note: Th iniial dss f ACE inhibirs may caus
hypnsin wih dizzinss, achycardia, and faining;
hs advrs ffcs ccur mr cmmnly in pains
als rciving diurics. Sympms ccur wihin 3 hurs
afr h rs svral dss. This ffc may b mini-
mizd by discninuing h diuric 1 wk bfr inii-
aing ACE inhibir hrapy. Pains shuld b warnd
ha his advrs ffc may ccur, ha i is ransin,
and ha hy shuld li dwn immdialy if symp-
ms dvlp.
Common adverse effects
Gastrointestinal
Nausea, diarrhea. Ths advrs ffcs ar usu-
ally mild and nd  rslv wih cninud hrapy.
Encurag h pain n  discninu hrapy wih-
u rs cnsuling a halhcar prvidr.
Neurologic
Fatigue, headache. Ths advrs ffcs ar usu-
ally mild and nd  rslv wih cninud hrapy.
Encurag h pain n  discninu hrapy wih-
u rs cnsuling a halhcar prvidr.
Cardiovascular
Orthostatic hypotension (dizziness, weakness, faintness).
Alhugh hs advrs ffcs ar infrqun and
usually mild, crain pains, paricularly hs als
rciving diurics, may suffr sm dgr f rhs-
aic hypnsin, spcially whn hrapy is iniiad.
Obsrv h pain clsly fr a las 2 hurs afr h
iniial ds is givn and fr a las an addiinal hur
unil bld prssur has sabilizd.
Mnir h bld prssur in bh h supin and
sanding psiins. Anicipa h dvlpmn f
psural hypnsin and ak masurs  prvn an
ccurrnc. Tach h pain  ris slwly frm a su-
pin r siing psiin and  si r li dwn if fling
fain.
Inammatory
Chronic cough. As many as n-hird f pains r-
civing ACE inhibirs may dvlp a chrnic, dry,
nnprduciv, prsisn cugh. This is hugh 
b causd by an accumulain f bradykinin. I may
appar frm 1 wk  6 mnhs afr iniiain f
ACE inhibir hrapy. Wmn appar  b mr
suscpibl han mn. Pains shuld b ld  cn-
ac hir halhcar prvidr if h cugh bcms
rublsm. Th cugh rslvs wihin 1  30 days
afr discninuain f hrapy. An ARB may b
subsiud fr h ACE inhibir if h frquncy f
cugh is xcssiv.
Serious adverse effects
Pregnancy. Mdicains ha ac dircly n h RAAS
can caus fal and nnaal harm. Thr is cncrn
abu h pnial fr birh dfcs in nnas whs
mhrs rcivd ACE inhibirs, spcially during h
scnd and hird rimsrs f prgnancy. Wmn wh
wish  bcm prgnan r wh bcm prgnan
whil rciving ACE inhibirs shuld discuss alrna-
iv hrapis wih hir halhcar prvidr as sn
as pssibl.
Hypersensitivity
Swelling of the face, eyes, lips, and tongue; difculty breath-
ing. Angidma has bn rprd  ccur in a small
numbr f pains, spcially afr h rs ds. Th
pain shuld b cauind  discninu furhr
hrapy and sk mdical anin immdialy.
Life Span Considerations
Antihypertensive Therapy
Older adults are more likely to develop orthostatic hypo-
tension with antihypertensive therapy. The patient’s blood
pressure should be monitored in the supine and sitting posi
tions during the initiation of antihypertensive therapy or when
the drug dosage is adjusted. Safety precautions should be
initiated to prevent accidental injury. Teach the patient to rise
slowly from a supine to a sitting and then a standing position.
Medication Safety Alert
Hypotension With ACE Inhibitors
The initial doses of ACE inhibitors may cause hypotension
with dizziness, tachycardia, and fainting; these adverse ef-
fects occur more commonly in patients also receiving diuret
ics. Symptoms occur within 3 hours after the rst several
doses. This effect may be minimized by discontinuing the di-
uretic 1 week before initiating ACE inhibitor therapy. Patients
should be warned that this adverse effect may occur, that
it is transient, and that they should lie down immediately if
symptoms develop.

Hematologic
Neutropenia. Nurpnia (300 nurphils/mm3)
and agranulcysis (drug-inducd bn marrw sup-
prssin) hav rarly bn bsrvd in pains rciv-
ing ACE inhibirs. Th nurpnia appars wihin h
rs 3  12 wks f hrapy and dvlps slwly; h
whi bld cll cun falls  is nadir in 10  30 days.
Th whi bld cll cun rurns  nrmal abu 2
wks afr discninuain f ACE inhibir hrapy.
Th pains ms suscpibl ar hs rciv-
ing cappril wh als hav impaird rnal funcin
r srius auimmun disass, such as lupus ry-
hmasus, r wh ar xpsd  drugs knwn 
affc h whi clls r immun rspns, such as
cricsrids.
Pains a risk shuld hav diffrnial and al
whi bld cll cuns drmind bfr iniiain f
hrapy and hn vry 2 wks hrafr fr h rs
3 mnhs f hrapy. Srss h impranc f rurning
fr his labrary wrk. Pains shuld b ld  n-
ify hir halhcar prvidr prmply if any vidnc
f infcin such as sr hra r fvr, which may b
an indicar f nurpnia, dvlps.
Renal
Hyperkalemia. Bcaus ACE inhibirs inhibi alds-
rn, pains may dvlp sligh incrass in srum
passium lvls. Apprximaly 1% f pains may
dvlp hyprkalmia (passium highr han 5.7
mEq/L). Ms cass rslv wihu discninuain
f hrapy. Pains ms suscpibl  h dvlp-
mn f hyprkalmia ar hs wih rnal impairmn
r diabs mllius and hs alrady rciving a p-
assium supplmn r a passium-sparing diuric.
Many sympms assciad wih alrd uid and
lcrly balanc ar subl and inrsprsd wih
gnral sympms f drug xiciy r h disas pr-
css islf.
Gahr daa rlaiv  changs in h pain’s
mnal saus (.g., alrnss, rinain, and cnfu-
sin), muscl srngh, muscl cramps, rmrs, nau-
sa, and gnral apparanc (.g., drwsy, anxius, r
lhargic).
Always chck h lcrly rprs fr arly indi-
cains f lcrly imbalanc. Kp accura rcrds
f inak and upu, daily wighs, and vial signs.
Nephrotoxicity. A small numbr f hyprnsiv pa-
ins wh ar rciving ACE inhibirs, paricularly
hs wih prxising rnal impairmn and hs als
aking NSAIDs, hav dvlpd incrasd BUN and
srum crainin lvls. Ths lvains hav usually
bn minr and ransin, spcially whn h ACE
inhibir was adminisrd cncmianly wih a diu-
ric. Rnal funcin shuld b mnird during h
rs fw wks f hrapy. Rpr incrasing BUN and
crainin lvls. Dsag rducin f h ACE inhibi-
r r pssibl discninuain f h NSAID r diu-
ric may b rquird.
Drugs Used to Treat Hypertension CHAPTER 22 367
Drug interactions
Drugs that enhance therapeutic and toxic effects. Ths
includ diurics, phnhiazins, alchl, ba-
adrnrgic blcking agns (.g., mprll, carv-
dill), and hr anihyprnsiv agns. Mnir h
bld prssur rspns  h cumulaiv ffcs f
anihyprnsiv agns. Obain bld prssur rad-
ings in supin and sanding psiins. NSAIDs in cm-
binain wih ACE inhibirs may rsul in a signican
dcras in rnal funcin. Mnir srum crainin
lvls and crainin claranc.
Drugs that reduce therapeutic effects. Anacids may
diminish absrpin f ACE inhibirs. Spara h
adminisrain ims by 2 hurs. NSAIDs may rduc
h anihyprnsiv ffcs f h ACE inhibirs.
Rifampin may dcras h anihyprnsiv ffcs
f nalapril. Mnir carfully fr pr bld prssur
cnrl r a gradually incrasing bld prssur.
Digoxin. ACE inhibirs may incras r dcras h
srum lvls f digxin. Mnir fr sympms f an-
rxia, nausa, vmiing, hadachs, blurrd r clrd
visin, bradycardia, har failur, r arrhyhmias. A
digxin srum lvl may b rdrd by a halhcar
prvidr.
Lithium. ACE inhibirs may induc lihium xic-
iy. Mnir fr lihium xiciy manifsd by nausa,
anrxia, n rmrs, prsisn vmiing, prfus di-
arrha, hyprrxia, lhargy, and waknss.
Hyperkalemia. ACE inhibirs may caus small in-
crass in passium lvls by inhibiing aldsrn
scrin. Pains shuld n ak diary suppl-
mns f passium r passium-sparing diurics
(.g., riamrn, spirnlacn, amilrid) wihu
spcic apprval frm h halhcar prvidr. If a pa-
in has rcivd spirnlacn r plrnn up 
svral mnhs bfr ACE inhibir hrapy, h s-
rum passium lvl shuld b mnird clsly b-
caus h passium-sparing ffc f spirnlacn
r plrnn may prsis. Srum passium lvls
shuld b mnird whn h anibiic rimhprim
is usd wih ACE inhibirs.
Capsaicin. Capsaicin may caus r aggrava cugh-
ing assciad wih ACE inhibir hrapy. Mnir fr
incrasd frquncy f dry, prsisn cugh. Rpr 
h halhcar prvidr.
DRUG CLASS: ANGIOTENSIN II RECEPTOR
BLOCKERS
Actions
ARBs (Tabl 22.6) ar a class f anihyprnsiv agns
ha ac by binding  anginsin II rcpr sis, blck-
ing h vry pn vascnsricr frm binding  h
anginsin II yp 1 (AT1) rcpr sis in h vascu-
lar smh muscl, brain, har, kidnys, and adrnal
glands. Th bld prssur–lvaing and sdium-
raining ffcs f anginsin II ar hus blckd.
368 UNIT IV Drugs Affecting the Cardiovascular System

Table 22.6 Angiotensin II Receptor Blockers (ARBs)

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE
azilsartan Edarbi Tablets: 40, 80 mg PO: 80 mg once daily; 40 mg once daily with
high-dose diuretic therapy
candesartan Atacand Tablets: 4, 8, 16, 32 mg PO: Initial: 16 mg once daily; adjust over 4–6 wk
Do not confuse with total daily dosage from 8–32 mg
Atacand with antacid Dose may be administered once or twice daily
or Avandia. for optimal control
eprosartan Teveten Tablets: 400 mg, 600 mg PO: Initial: 600 mg once daily
Maximum: 800 mg/day
Dose may be administered once or twice daily
for optimal control
irbesartan Avapro Tablets: 75, 150, 300 mg PO: Initial: 150 mg once daily; adjust over
Do not confuse 3–4 wk with a total daily dosage of 300 mg
Avapro with Anaprox daily
or Avelox.
losartan Cozaar Tablets: 25, 50, 100 mg PO: 50 mg once daily; adjust over 4–6 wk
Do not confuse Do not confuse with a total daily dosage from 25–100 mg
losartan with Cozaar with Corgard, administered once or twice daily for optimal
loratadine. Hyzaar, or Zocor. control
olmesartan Benicar Tablets: 5, 20, 40 mg PO: Initial: 20 mg once daily; adjust over 2 wk
with total daily dosage of 20–40 mg
Twice-daily dosing offers no benet
telmisartan Micardis Tablets: 20, 40, 80 mg PO: Initial: 40 mg once daily; adjust over 4–6 wk
with total daily dosage from 20–80 mg
valsartan Diovan Tablets: 40, 80, 160, 320 mg PO: Initial: 80 mg once daily; adjust over 4–6 wk
with total daily dosage from 80–320 mg
Available in Canada.
Do not confuse.

This diminishs h RAAS cascad ha wuld induc

vascnsricin and sdium rabsrpin, aggrava-
ing hyprnsin. Th ARBs hav n ffc n rnal
funcin, prsaglandin lvls, riglycrids, chlsr-
l, r bld glucs lvls. Ths agns d n affc
bradykinin and hrfr d n caus a dry cugh.
Uses
ARBs ar as ffciv in lwring bld prssur as ACE
inhibirs and ba blckrs. Mn and wmn usually
hav similar rspnss; hwvr, African Amrican
pains d n rspnd as wll  mnhrapy.
ARBs ar indicad fr h ramn f hyprnsin
and may b usd aln r in cmbinain wih hr
anihyprnsiv agns, paricularly hiazid-yp
diurics. Th bld prssur–lwring ffc is sn
wihin 1 wk, bu i may ak 3  6 wks  achiv
h full hrapuic ffc. If h anihyprnsiv
ffc is n cnrlld by ARBs aln, a lw dsag f
a diuric, usually hydrchlrhiazid, may b addd.
ARBs shuld n b adminisrd as chrapy wih
ACE inhibirs r dirc rnin inhibirs.
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm ARBs
is rducin in bld prssur.
Nursing Implications for Angiotensin II Receptor
Blockers
Premedication assessment
1. Obain baslin bld prssur radings in supin
and sanding psiins and apical puls. Hld md-
icain if syslic bld prssur is lss han 100 mm
Hg r h har ra is lss han 50 bas/min, and
cnac h prscribr.
2. Iniia labrary sudis as rqusd by h
halhcar prvidr (.g., rnal funcin ss such
as BUN, srum crainin, lcrly lvls, and
CBC)  srv as a baslin fr fuur cmparisn.
3. Ask whhr h pain is prgnan r likly  b-
cm prgnan. If s, discuss wih h halhcar
prvidr bfr iniiaing ARB hrapy.
4. Obain a hisry f bwl liminain parns and
any gasrinsinal sympms.
Availability, dosage, and administration. S Tabl 22.6
Common adverse effects
Gastrointestinal
Dyspepsia, cramps, diarrhea. Ths advrs ffcs ar
usually mild and nd  rslv wih cninud hr-
apy. Encurag h pain n  discninu hrapy
wihu rs cnsuling h halhcar prvidr.

Neurologic
Headache. This advrs ffc is usually mild and
nds  rslv wih cninud hrapy. Encurag
h pain n  discninu hrapy wihu rs
cnsuling h halhcar prvidr.
Cardiovascular
Orthostatic hypotension (dizziness, weakness, faint-
ness). Alhugh hs advrs ffcs ar infrqun
and usually mild, crain pains, paricularly hs
als rciving diurics, may suffr sm dgr f r-
hsaic hypnsin, spcially whn hrapy is inii-
ad. Obsrv h pain clsly fr a las 2 hurs
afr h iniial ds and fr a las 1 addiinal hur
unil bld prssur has sabilizd.
Mnir h bld prssur in bh h supin and
sanding psiins. Anicipa h dvlpmn f
psural hypnsin and ak masurs  prvn
an ccurrnc. Tach h pain  ris slwly frm
a supin r siing psiin and  si r li dwn if
fling fain.
Serious adverse effects
Pregnancy. Mdicains ha ac dircly n h
RAAS can caus fal and nnaal harm. Thr is
pnial fr birh dfcs in nnas whs mhrs
hav rcivd ARBs, spcially during h scnd and
hird rimsrs f prgnancy. Wmn wh wish 
bcm prgnan r wh bcm prgnan whil r-
civing ARBs shuld discuss alrnaiv hrapis wih
hir halhcar prvidr as sn as pssibl.
Renal
Hyperkalemia. Bcaus ARBs inhibi aldsrn s-
crin, pains may dvlp sligh incrass in srum
passium lvls. Ms cass rslv wihu discnin-
uain f hrapy. Pains ms suscpibl  h d-
vlpmn f hyprkalmia ar hs wih rnal impair-
mn r diabs mllius and hs alrady rciving
a passium supplmn, plrnn, r a passium-
sparing diuric. Many sympms assciad wih al-
rd uid and lcrly balanc ar subl and inr-
sprsd wih gnral sympms f drug xiciy r h
disas prcss islf.
Gahr daa rlaiv  changs in h pain’s
mnal saus (.g., alrnss, rinain, cnfusin),
muscl srngh, muscl cramps, rmrs, nausa,
and gnral apparanc (.g., bing drwsy, anxius,
lhargic).
Always chck h lcrly rprs fr arly indi-
cains f lcrly imbalanc. Kp accura rcrds
f inak and upu, daily wighs, and vial signs.
Drug interactions
Drugs that enhance therapeutic and toxic effects. Ths in-
clud diurics, phnhiazins, alchl, ba-adrnrgic
blcking agns (.g., mprll, carvdill), and hr
anihyprnsiv agns. Cimidin and ucnazl
inhibi h mablism f lsaran, causing an incrasd
anihyprnsiv ffc. Mnir h bld prssur
Drugs Used to Treat Hypertension CHAPTER 22 369
rspns  h cumulaiv ffcs f anihyprnsiv
agns. Obain bld prssur radings in supin and
sanding psiins. Th cmbinain f a NSAID and an
ARB may signicanly dcras glmrular lrain and
rnal funcin. Mnir srum crainin lvls and cr-
ainin claranc.
Drugs that reduce therapeutic effects. NSAIDs may di-
minish h hrapuic ffc f ARBs. Mnir bld
prssur. Rifampin incrass h mablism f lsar-
an, rducing is anihyprnsiv ffcs. Th dsag
f lsaran may nd  b incrasd, r h pain
may b swichd  anhr ARB.
Hyperkalemia. ARBs may caus small incrass in
passium lvls by rducing aldsrn scrin.
Pains shuld n ak diary supplmns f p-
assium r passium-sparing diurics (.g., riam-
rn, spirnlacn, amilrid) wihu spcic
apprval frm h halhcar prvidr. If a pain has
rcivd spirnlacn r plrnn up  svral
mnhs bfr ARB hrapy, h srum passium lv-
l shuld b mnird clsly bcaus h passium-
sparing ffc f spirnlacn and plrnn may
prsis. Srum passium lvls shuld b mnird
whn h anibiic rimhprim is usd wih ARB
hrapy.
DRUG CLASS: DIRECT RENIN INHIBITOR
aliskiren (ă-lĭs-KĬR-ĕn)
Do not confuse aliskiren with Azilect.
Tekturna (TĔK-tŭrn-ă)
Actions
Rnin is scrd by h kidnys in rspns  dcras-
s in bld vlum and rnal prfusin. I is h rs
sp in h RAAS. By rgulaing lcrly and uid
balanc in h bdy, his sysm plays an impran rl
in h dvlpmn f hyprnsin and ahrsclr-
sis. Rnin is rspnsibl fr h vnual cnvrsin f
anginsingn  h pn vascnsricr angi-
nsin II. Aliskirn, a dirc rnin inhibir, blcks h
rs sp in h RAAS cascad, prvning anginsin
II frm acivaing is rcprs and hus prvning h
rlas f cachlamins, aldsrn scrin, and
sdium rabsrpin ha wuld hrwis rsul in
hyprnsin.
Uses
Aliskirn, a dirc rnin inhibir, lwrs bld prssur
similar  h ACE inhibirs and ARBs. I ds n caus
rx achycardia as dirc vasdilar anihyprnsiv
agns (.g., hydralazin) d. Mn and wmn usually
hav similar rspnss. African Amrican pains and
ldr pains d n rspnd as wll  mnhrapy as
d yungr pains. Aliskirn is indicad fr h ra-
mn f hyprnsin and may b usd aln r in cm-
binain wih hr anihyprnsiv agns. Th bld
370 UNIT IV Drugs Affecting the Cardiovascular System
prssur–lwring ffc is sn wihin 2 wks, bu i
may ak 3  6 wks  achiv h full hrapuic f-
fc. Aliskirn shuld b rsrvd fr hs pains wh
d n rspnd adqualy  ACE inhibirs r ARBs
bcaus hy hav bn prvd  b ffciv ani-
hyprnsiv agns and shuld b rid rs. In gnr-
al, aliskirn shuld n b usd cncurrnly wih ACE
inhibir r ARB hrapy.
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm rnin
inhibirs is rducin in bld prssur.
Nursing Implications for Aliskiren
Premedication assessment
1. Obain baslin bld prssur radings in supin
and sanding psiins and apical puls. Hld md-
icain if syslic bld prssur is lss han 100 mm
Hg r h har ra is lss han 50 bas/min, and
cnac h prscribr.
2. Iniia labrary sudis as rqusd by h
halhcar prvidr (.g., rnal funcin ss
such as BUN, srum crainin, and lcrly
lvls and CBC)  srv as a baslin fr fuur
cmparisn.
3. Ask whhr h pain is prgnan r likly  b-
cm prgnan. If s, discuss wih h halhcar
prvidr bfr iniiaing rnin inhibir hrapy.
4. Obain a hisry f bwl liminain parns and
any gasrinsinal sympms, frquncy f had-
achs, dizzinss, and faigu.
Availability. PO: 150- and 300-mg abls.
Dosage and administration. PO: Iniially, 150 mg nc
daily. Afr a fw wks, if h bld prssur is n
adqualy cnrlld, incras  300 mg nc daily.
Common adverse effects
Gastrointestinal
Dyspepsia, cramps, diarrhea. Ths advrs ffcs ar
usually mild and nd  rslv wih cninud hr-
apy. Encurag h pain n  discninu hrapy
wihu rs cnsuling h halhcar prvidr.
Neurologic
Headache. This advrs ffc is usually mild and
nds  rslv wih cninud hrapy. Encurag
h pain n  discninu hrapy wihu rs
cnsuling h halhcar prvidr.
Cardiovascular
Orthostatic hypotension (dizziness, fatigue, faint-
ness). Alhugh hs advrs ffcs ar infrqun
and usually mild, crain pains, paricularly hs
als rciving diurics, may suffr sm dgr f r-
hsaic hypnsin, spcially whn hrapy is inii-
ad. Obsrv h pain clsly fr a las 2 hurs
afr h iniial ds and fr a las 1 addiinal hur
unil bld prssur has sabilizd.
Mnir h bld prssur in bh h supin and
sanding psiins. Anicipa h dvlpmn f ps-
ural hypnsin and ak masurs  prvn an c-
currnc. Tach h pain  ris slwly frm a supin
r siing psiin and  si r li dwn if fling fain.
Serious adverse effects
Pregnancy. Mdicains ha ac dircly n h
RAAS can caus fal and nnaal harm. Thr is
pnial fr birh dfcs in nnas whs mhrs
hav rcivd rnin inhibirs, spcially during h
scnd and hird rimsrs f prgnancy. Wmn wh
wish  bcm prgnan r wh bcm prgnan
whil rciving rnin inhibirs shuld discuss alr-
naiv hrapis wih hir halhcar prvidr as sn
as pssibl.
Renal
Serum electrolytes. Rnin inhibirs blck aldsr-
n scrin and pains may dvlp sligh incras-
s in srum passium. Ms cass rslv wihu
discninuain f hrapy. Pains ms suscpibl
 h dvlpmn f hyprkalmia ar hs wih r-
nal impairmn r diabs mllius and hs alrady
rciving a passium supplmn, plrnn, r a
passium-sparing diuric. Many sympms asscia-
d wih alrd uid and lcrly balanc ar subl
and inrsprsd wih gnral sympms f drug x-
iciy r h disas prcss islf. Gahr daa rlaiv
 changs in h pain’s mnal saus (.g., alr-
nss, rinain, cnfusin), muscl srngh, muscl
cramps, rmrs, nausa, and gnral apparanc (.g.,
bing drwsy, anxius, lhargic). Chck h lcr-
ly rprs fr arly indicains f lcrly imbal-
anc. Kp accura rcrds f inak and upu, daily
wighs, and vial signs.
Drug interactions
Drugs that enhance therapeutic and toxic effects. Ths
includ diurics, anipsychics, alchl, ba blck-
rs (.g., mprll, carvdill), and hr ani-
hyprnsiv agns. Kcnazl, iracnazl,
and arvasain incras srum cncnrains f
aliskirn, causing an incrasd anihyprnsiv f-
fc. Mnir h pain’s bld prssur rspns
 h cumulaiv ffcs f anihyprnsiv agns.
Obain bld prssur radings in supin and sand-
ing psiins. NSAIDs may nhanc h nphrxic
ffc f aliskirn. Mnir srum crainin lvls
and crainin claranc.
Drugs that reduce therapeutic effects. NSAIDs may di-
minish h anihyprnsiv ffc f aliskirn. Mnir
bld prssur.
In gnral, aliskirn shuld n b usd in cmbina-
in wih ACE inhibirs r ARBs, spcially if h pa-
in als has diabs. Adminisr nly if spcically
apprvd by h halhcar prvidr.
Hyperkalemia. Rnin inhibirs may caus small in-
crass in passium lvls by rducing aldsrn

scrin. Pains shuld n ak diary suppl-
mns f passium r passium-sparing diurics
(.g., riamrn, spirnlacn, amilrid), ARBs,
r ACE inhibirs wihu spcic apprval frm a
halhcar prvidr. If a pain has rcivd spirnl-
acn r plrnn up  svral mnhs bfr rnin
inhibir hrapy, h srum passium lvl shuld b
mnird clsly bcaus h passium-sparing f-
fcs f spirnlacn and plrnn may prsis.
Th anibacrial rimhprim may nhanc h
hyprkalmic ffc f aliskirn, ACE inhibirs, and
ARBs. Mnir srum passium lvls.
DRUG CLASS: ALDOSTERONE RECEPTOR
ANTAGONIST
eplerenone (ĕp-LĔR-ĕ-nōn)
Inspra (ĬN-spră)
Actions
Eplrnn is an anihyprnsiv agn knwn as an
aldosterone receptor blocking agent. Th RAAS plays a ma-
jr rl in h rgulain f bld prssur. Whn hr
is a rducin in bld prssur, sdium cncnrain,
r rnal bld w, rnin is scrd by h kidnys.
Th rnin cnvrs anginsingn, which is scrd
by h livr,  anginsin I. Anginsin I is cnvrd
by anginsin I–cnvring nzym  anginsin II.
Anginsin II prducs pn vascnsricin by
acing n rcprs wihin bld vssls. I als pr-
ms aldsrn scrin, which causs sdium r-
nin by simulain f minralcricid rcprs
in h adrnal crx, bld vssls, and brain. Ths
acins rsul in incrasd bld prssur scndary
 h vascnsricin and nhancd cardiac upu
scndary  sdium rnin. Eplrnn, h ald-
srn rcpr blcking agn, blcks simulain f
h minralcricid rcprs by aldsrn, hus
prvning sdium rabsrpin.
Uses
Eplrnn is usd in raing hyprnsin and har
failur, ihr aln r in cmbinain wih hr ani-
hyprnsiv agns.
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm
plrnn is rducin in bld prssur.
Nursing Implications for Eplerenone
Premedication assessment
1. Obain baslin bld prssur radings in supin
and sanding psiins. Hld mdicain if sys-
lic bld prssur is lss han 100 mm Hg r h
har ra is lss han 50 bas/min, and cnac h
prscribr.
2. Obain a hisry f bwl liminain parns.
Drugs Used to Treat Hypertension CHAPTER 22 371
3. Iniia labrary sudis as rqusd by h
halhcar prvidr—including rnal funcin
ss such as BUN and srum crainin; lcr-
ly, riglycrid, and chlsrl lvls; livr func-
in ss (.g., bilirubin, aspara aminrans-
fras [AST], alanin aminransfras [ALT],
gamma-gluamylransfras [GGT], and alkalin
phsphaas lvls [ALP]; prhrmbin im [PT]);
and uric acid—ha will srv as a baslin fr fu-
ur cmparisn.
4. Ask whhr h pain is prgnan r likly  b-
cm prgnan. If s, discuss wih a halhcar pr-
vidr bfr iniiaing plrnn hrapy.
Availability. PO: 25- and 50-mg abls.
Dosage and administration. PO: Iniially, 50 mg nc
daily, wih r wihu fd. Th full hrapuic ffc
shuld b apparn wihin 4 wks. Fr pains wih
an inadqua bld prssur rspns, h dsag
may b incrasd  50 mg wic daily.
Medication Safety Alert
Eplerenone therapy is contraindicated in patients with the
following:
 • Serum potassium level higher than 5.5 mEq/L.
 • Type 2 diabetes with microalbuminuria.
 • Serum creatinine level higher than 2 mg/dL in men or 1.8
mg/dL in women.
 • Creatinine clearance lower than 50 mL/min.
 • Patients taking potassium-sparing diuretics (e.g.,
amiloride, spironolactone, or triamterene).
 • Patients taking strong metabolic inhibitors (e.g.,
ketoconazole, itraconazole).
For patients older than 65 years, or patients with mild
to moderate hepatic failure, dosages higher than 50 mg
daily are not recommended. For patients taking metabolism
inhibitors such as cimetidine, erythromycin, saquinavir,
verapamil, diltiazem, or uconazole, the starting dosage
should be reduced to 25 mg once daily.
Common adverse effects
Gastrointestinal
Nausea, diarrhea. Ths advrs ffcs ar usu-
ally mild and nd  rslv wih cninud hrapy.
Encurag h pain n  discninu hrapy wih-
u rs cnsuling a halhcar prvidr.
Neurologic
Fatigue, headache. Ths advrs ffcs ar usu-
ally mild and nd  rslv wih cninud hrapy.
Encurag h pain n  discninu hrapy wih-
u rs cnsuling a halhcar prvidr.
Cardiovascular
Orthostatic hypotension (dizziness, weakness, faint-
ness). Alhugh hs advrs ffcs ar infrqun
and usually mild, crain pains, paricularly hs
wh ar als rciving diurics, may suffr sm
372 UNIT IV Drugs Affecting the Cardiovascular System
dgr f rhsaic hypnsin, spcially whn
hrapy is iniiad.
Mnir h bld prssur in bh h supin and
sanding psiins. Anicipa h dvlpmn f ps-
ural hypnsin and ak masurs  prvn an c-
currnc. Tach h pain  ris slwly frm a supin
r siing psiin and  si r li dwn if fling fain.
Serious adverse effects
Gynecomastia, vaginal bleeding. A small numbr f
mn hav dvlpd gyncmasia and a small num-
br f wmn hav dvlpd vaginal blding whil
rciving plrnn hrapy. Rpr hs cndiins
 a halhcar prvidr.
Renal
Nephrotoxicity. A small numbr f hyprnsiv pa-
ins wh ar rciving plrnn, paricularly hs
wih prxising rnal impairmn, hav dvlpd
incrass in BUN and srum crainin lvls. Rnal
funcin shuld b mnird during h rs fw
wks f hrapy. Rpr incrasing BUN and crai-
nin lvls. Dsag rducin r discninuain f
plrnn may b rquird. Eplrnn hrapy is n
rcmmndd in pains wih crainin clarancs
lwr han 50 mL/min.
Hyperkalemia. Bcaus plrnn inhibis aldsrn,
pains may dvlp sligh incrass in srum passi-
um lvls. Pains ms suscpibl  h dvlpmn
f hyprkalmia (passium highr han 5.5 mEq/L) ar
hs wih rnal impairmn r diabs mllius. Many
sympms assciad wih alrd uid and lcrly
balanc ar subl and inrsprsd wih gnral symp-
ms f drug xiciy r h disas prcss islf.
Gahr daa rlaiv  changs in h pain’s mn-
al saus (.g., alrnss, rinain, cnfusin), mus-
cl srngh, muscl cramps, har ra and rhyhm,
rmrs, nausa, and gnral apparanc (.g., drwsy,
anxius, lhargic).
Always chck h lcrly rprs fr arly indi-
cains f lcrly imbalanc. Kp accura rcrds
f inak and upu, daily wighs, and vial signs.
Metabolic
Hypertriglyceridemia, hypercholesterolemia, hyperuricemia.
Incrass in srum riglycrid, chlsrl, and uric
acid lvls hav bn rprd during plrnn hr-
apy. Rpr rising lvls  a halhcar prvidr.
Gastrointestinal
Hepatotoxicity. Th sympms f hpaxiciy ar
anrxia, nausa, vmiing, jaundic, hpamgaly,
splnmgaly, and abnrmal livr funcin s rsuls
(.g., lvad bilirubin, AST, ALT, GGT, ALP, PT).
Drug interactions
Drugs that enhance therapeutic and toxic effects. Ths
includ diurics, anipsychics, kcnazl, alc-
hl, ba blckrs (.g., mprll, carvdill), and h-
r anihyprnsiv agns. Mnir h bld prssur
rspns  h cumulaiv ffcs f anihyprnsiv
agns. Obain bld prssur radings in supin and
sanding psiins. Assss h pain fr hypnsin,
lighhaddnss, dizzinss, and bradycardia. Prvid
fr pain safy; prvn falls.
Drugs that may induce hyperkalemia. Cncurrn us
f plrnn and h fllwing agns may induc
hyprkalmia: ACE inhibirs (.g., lisinpril, cap-
pril, nalapril, ramipril), ARBs (.g., lsaran, cand-
saran, valsaran), passium-sparing diurics (.g.,
riamrn, amilrid, spirnlacn), sal subsi-
us (which fn cnain highr cncnrains f
passium fr avring), and fds markd as “lw
sdium,” which fn hav highr cncnrains f
passium fr avring.
Th anibacrial rimhprim may nhanc h
hyprkalmic ffc f plrnn. Mnir srum p-
assium lvls.
Lithium. Eplrnn may induc lihium xiciy.
Mnir fr lihium xiciy manifsd by nausa, an-
rxia, n rmrs, prsisn vmiing, prfus diar-
rha, hyprrxia, lhargy, and waknss.
Grapefruit juice. Grapfrui juic slws h mab-
lism f plrnn in a minr way. If h pain d-
vlps rhsaic hypnsin, a dsag rducin in
plrnn may b rquird.
Phenobarbital, rifampin, St. John’s wort. Phnbarbial,
rifampin, and S. Jhn’s wr simulas h mab-
lism f plrnn. A dsag incras in plrnn
may b ncssary.
DRUG CLASS: CALCIUM CHANNEL BLOCKERS
Actions
Calcium channl blckrs ar als knwn variusly as
calcium antagonists, calcium ion antagonists, slow channel
blockers, and calcium ion inux inhibitors. Ths agns
inhibi h mvmn f calcium ins acrss a cll
mmbran. This rsuls in fwr dysrhyhmias, a slw-
r ra f cnracin f h har, and rlaxain f
smh muscl f bld vssls, causing vasdilain
and rducd bld prssur. Th calcium channl
blckrs ar classid by srucur: bnzhiazpin
(diliazm), diphnylalkylamin (vrapamil), and di-
hydrpyridins (amldipin, clvidipin, fldipin,
isradipin, nicardipin, nifdipin, nimdipin, and
nisldipin).
Uses
Alhugh ach f hs agns acs by calcium in in-
hibiin, hr ar signican diffrncs in clinical us
bcaus hy ac smwha diffrnly n crnary
bld vssls, sysmic bld vssls, pacmakr clls
f h har, and cnducing issu f h har. Thir
clinical ffcs ar als dpndn n h yp and s-
vriy f h pain’s disas. All h availabl calcium
channl blckrs ar ffciv anihyprnsiv agns,
bu clinicians nd  us hs in h dihydrpyridin
grup mr fn bcaus hy hav br priphral

vasdilaing ffcs, rducing afrlad. Calcium chan-
nl blckrs ar mr ffciv in pains wih highr
prramn bld prssur. Thy incras rnal s-
dium xcrin and ar usually wll lrad. Calcium
channl blckrs ar idal as rs- r scnd-lin mdi-
cins in pains wih hyprnsin and cxising an-
gina and ar an alrnaiv  h us f ba blckrs
in pains wih ashma r diabs mllius. Thy ar
paricularly ffciv in African Amricans and ldr
pains wih hyprnsin, wh ar mr likly 
hav lw-rnin hyprnsin. Th calcium channl
blckrs als d n affc gu r priphral vascu-
lar disas. Vrapamil and diliazm ar als ffciv
anidysrhyhmic agns (s Chapr 23).
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm cal-
cium channl blckr hrapy is rducin in bld
prssur.
Nursing Implications for Calcium Channel
Blockers
Premedication assessment
1. Obain baslin bld prssur radings in h su-
pin and sanding psiins and apical puls. Hld
mdicain if syslic bld prssur is lss han 100
mm Hg r h har ra is lss han 50 bas/min,
and cnac h prscribr.
2. Obain baslin wigh.
3. If h pain is aking digxin cncurrnly, iniia
cls mniring fr pnial digialis xiciy.
Availability, dosage, and administration. S Tabl 22.7
Dosage adjustments. S individual drug mn-
graphs fr dsag paramrs. Adjusmns ar mad
basd n h individual pain’s rspns  hrapy.
Serious adverse effects
Cardiovascular, circulatory
Hypotension and syncope. Cauin h pain ha
hypnsin and syncp may ccur during h rs
wk f hrapy. Ths advrs ffcs dclin nc
h dsag is sabilizd. Tak bld prssur radings
vry shif in h hspializd pain and srss h
nd fr h pain  mnir bld prssur afr
discharg. Prvn hypnsiv pisds by insruc-
ing h pain  ris slwly frm a supin r siing
psiin and prfrm xrciss  prvn bld pl-
ing whn sanding r siing in n psiin fr a pr-
lngd prid. If fainnss ccurs, insruc h pain
 si r li dwn.
Edema. Assss h pain fr dvlpmn f d-
ma. Prfrm daily wighs a h sam im, in simi-
lar clhing, and n h sam scal. Rpr incrass
in wigh  a halhcar prvidr fr furhr valua-
in. Edma is mr cmmn wih diliazm and h
dihydrpyridin calcium channl blckrs.
Drugs Used to Treat Hypertension CHAPTER 22 373
Drug interactions
Drugs that enhance therapeutic and toxic effects. Ths
includ diurics, anipsychics , alchl, ba blck-
rs (.g., mprll, carvdill), hisamin-2 anag-
niss (.g., cimidin, raniidin), and hr ani-
hyprnsiv agns. Mnir h bld prssur
rspns  h cumulaiv ffcs f anihyprnsiv
agns. Obain bld prssur radings in supin and
sanding psiins. Assss h pain fr hypnsin,
lighhaddnss, dizzinss, and bradycardia. Prvid
fr pain safy; prvn falls.
Grapefruit juice. Grapfrui juic (apprximaly 200
mL) may lva srum cncnrains f diliazm,
fldipin, vrapamil, nisldipin, nifdipin, nica-
rdipin, and pssibly amldipin, pnially causing
hypnsin. Grapfrui juic shuld n b cnsumd
wihin 2 hurs bfr r 4 hurs afr adminisrain f
affcd calcium channl blckrs.
Digoxin. Calcium channl blckrs may incras s-
rum lvls f digxin. Mnir h pain fr symp-
ms f anrxia, nausa, vmiing, hadachs, blurrd
r clrd visin, and bradycardia. Th halhcar pr-
vidr may rdr a digxin srum lvl.
Lovastatin and simvastatin. Amldipin, diliazm,
and vrapamil may incras h srum cncnrain
f lvasain and simvasain. Mnir fr signs and
sympms f xiciy (myalgias, rhabdmylysis).
DRUG CLASS: ALPHA-1 ADRENERGIC BLOCKING
AGENTS
Actions
Alpha-1 blckrs—dxazsin, prazsin, and raz-
sin—ac by blcking pssynapic alpha-1 adrnr-
gic rcprs  prduc arrilar and vnus vas-
dilain, rducing priphral vascular rsisanc
wihu rducing cardiac upu r inducing a rx
achycardia. Thy prduc a dcras in sanding
bld prssur slighly grar han in supin bld
prssur. Ths agns als hav a mds psiiv f-
fc n srum lipid lvls, incrasing HDL chlsrl
and rducing LDL chlsrl, al chlsrl, and
riglycrid cncnrains.
Alpha-1 blckrs d n incras cachlamins;
hrfr hr is n incras in har ra r mycar-
dial xygn cnsumpin. Thy als hav n ffc n
uric acid cncnrains.
Bcaus f h prsnc f alpha-1 rcprs n h
prsa gland and crain aras f h bladdr, raz-
sin and dxazsin ar als abl  rduc urinary u-
w rsisanc in mn wih nlargd prsa glands.
Uses
Alpha-1 blckrs may b usd aln r in cmbina-
in wih hr anihyprnsiv agns in h ra-
mn f sag 1 r 2 hyprnsin, paricularly in mn
wih bnign prsaic hyprplasia. Thy hav addi-
iv ffcs wih ba blckrs and diurics. Bld
374 UNIT IV Drugs Affecting the Cardiovascular System

Table 22.7 Calcium Channel Blockers Used to Treat Hypertension

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE
amlodipine Norvasc Tablets: 2.5, 5, 10 mg PO: Initial: 5 mg once daily; adjust over
Do not confuse Do not confuse Suspension: 1 mg/mL in 120-mL 7–14 days to a maximum of 10 mg/
amlodipine with Norvasc with bottles day
amiloride or Altace or Vasotec.
amiodarone.
diltiazem Cardizem Tablets: 30, 60, 90, 120 mg PO: 180–360/day divided every 6-8 h
Do not confuse
Cardizem with
Cardene or
clonidine.
Cardizem LA Tablets, extended release (24 hr): 120, PO: 120-360 mg once a day. Maximum
180, 240, 300, 360, 420 mg of 540 mg/day
Capsule, extended release (12 hr): 60, PO: 120-180 mg twice daily. Maximum
90, 120 mg 0f 360 mg
Cardizem CD Capsules, sustained release (24 hr): PO: 120-360 mg once a day. Maximum
120, 180, 240, 300, 360, 420 mg of 540 mg/day
IV: 5 mg/mL in 5-, 10-, 25-mL vials
Powder for injection: 100 mg
felodipine — Tablets, extended release (24 hr): 2.5, PO: Initial: 5 mg daily; adjust after 14
5, 10 mg days
Maintenance: 2.5–10 mg daily
Maximum:10 mg daily
isradipine — Capsules: 2.5, 5 mg PO: Initial: 2.5 mg twice daily
Maximal response may require 2–4 wk
Maintenance: 10 mg daily
Maximum: 20 mg daily
levamlodipine Conjupri Tablets: 2.5, 5 mg PO: Initial: 1.25–2.5 mg once daily.
Adjust every 1–2 wk based on patient
response
Maximum: 5 mg daily
nicardipine Cardene Capsules: 20, 30 mg PO: Immediate release: Initial: 20 mg
Do not confuse IV: 2.5 mg/mL in 10-mL vial; 0.1 and three times daily
Cardene with 0.2 mg/mL in 200-mL premixed Maximal response may require 2 wk of
Cardizem, containers therapy
Cardura, or Adjust dosage by measuring blood
codeine. pressure about 8 hr after last dose
Peak effect is determined by measuring
blood pressure 1–2 hr after dose
administration
Maintenance: 20–40 mg three times
daily
Maximum: 120 mg daily
Extended release: Initial: 30 mg twice
daily
Maximum: 120 mg daily
IV: 5 mg/hr by continuous infusion
May titrate by 2.5 mg/hr every 15 min
Maximum: 15 mg/hr
nifedipine Procardia XL Capsules: 10, 20 mg PO: Initial: 30–60 mg once daily of
Do not confuse Tablets, sustained release (24 hr): 30, extended-release formulation;
Procardia with 60, 90 mg immediate-release (IR) formulation
Provera or Peri- not indicated for hypertension
Colace. management
Maximum: sustained-release tablets,
120 mg daily
 Drugs Used to Treat Hypertension CHAPTER 22 375

Table 22.7 Calcium Channel Blockers Used to Treat Hypertension—cont’d

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE
nisoldipine Sular Tablets, sustained release (24 hr): 8.5, Sular, PO: Initial: 17 mg once daily;
17, 34 mg Maintenance: 17–34 mg once daily
Generic version, Sular, maximum dose 34 mg/day
extended- Tablets, extended release (24 hr): 10, Nisoldipine ER tablet (original
release original 20, 25.5, 30, 40 mg formulation), PO: Initial 20 mg once
formulation (not a day Maintenance: 20–40 mg once
equivalent to daily; maximum dose 60 mg/day
Sular)
verapamil Calan SR Tablets: 40, 80, 120 mg PO: Initial: 80 mg three or four times daily
Do not confuse Tablets, sustained release (24 hr): 120, Sustained-release tablets and capsules:
Calan with Colace. 180, 240 mg 120–240 mg once daily in the morning
Capsules, sustained release (24 hr): Maintenance: 240–480 mg daily
100, 120, 180, 200, 240, 300, 360 Administer with food
mg
IV: 2.5 mg/mL in 2- and 4-mL ampules
and syringes
Do not confuse.

prssur rspns wih alpha-1 blckrs appars  Medication Safety Alert

b similar in African Amrican and whi pains.
Ths agns can b usd safly in pains wih an-
gina, gu, and hyprlipidmia. Th hr alpha-1
blckrs hav similar anihyprnsiv ffcs and
advrs ffcs. Dxazsin and razsin hav a ln-
gr durain f acin and can b adminisrd nc
daily.
Dxazsin and razsin ar als usd  rduc
mild  mdra urinary bsrucin manifsains
(.g., hsiancy, rminal dribbling f urin, inrrup-
d sram, impaird siz and frc f sram, snsain
f incmpl bladdr mpying) in mn wih bnign
prsaic hyprplasia (s Chapr 40).
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm alpha-1
blckr hrapy ar rducin f bld prssur and r-
ducin f sympms f bnign prsaic hyprplasia
wih imprvmn in urin w.
Nursing Implications for Alpha-1 Adrenergic
Blocking Agents
Premedication assessment
1. Obain baslin bld prssur radings in supin
and sanding psiins and apical puls. Hld md-
icain if syslic bld prssur is lss han 100 mm
Hg r h har ra is lss han 50 bas/min, and
cnac h prscribr.
2. Chck if pain is prgnan r has a hisry f s-
vr crbral r crnary arrisclrsis, gasriis,
r ppic ulcr disas. (Rducin f bld prs-
sur may diminish bld w  hs rgins.)
Availability, dosage, and administration. S Tabl 22.8
The initial doses of doxazosin, prazosin, and terazosin may
cause hypotension with dizziness, tachycardia, and fainting;
these adverse effects occur in less than 1% of patients start-
ing therapy. Symptoms occur 15 to 90 minutes after admin-
istration of the initial dose and occur most often in patients
who are already receiving propranolol and presumably other
beta blockers. These effects may be minimized by giving the
rst doses with food and limiting the initial dose to 1 mg.
Patients should be warned that these adverse effects may
occur, that they are transient, and that the patient should lie
down immediately if symptoms develop.
Common adverse effects
Neurologic. Drowsiness, headache, dizziness,
weakness, lethargy.
Tll h pain ha hs advrs ffcs may ccur
bu ha hy nd  b slf-limiing. Tll h pain n
 sp aking h mdicain and  cnsul a halh-
car prvidr if h prblm bcms unaccpabl.
Cardiovascular
Dizziness, tachycardia, fainting. Ths advrs ffcs
ccur in abu 1% f pains whn hrapy is iniia-
d. Sympms dvlp 15  90 minus afr h rs
fw dss ar akn. T dcras h incidnc, giv
h rs fw dss wih fd and limi h iniial ds
 1 mg. Insruc h pain  li dwn immdialy
if hs sympms sar  ccur, and prvid fr h
pain’s safy.
Drug interactions
Drugs that enhance therapeutic and toxic effects. Ths
includ diurics, anipsychics, alchl, ba
blckrs (.g., mprll, carvdill), and hr
376 UNIT IV Drugs Affecting the Cardiovascular System

Table 22.8 Alpha-1 Adrenergic Blocking Agents

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE
doxazosin Cardura Tablets: 1, 2, 4, 8 mg Hypertension:
Do not confuse Do not confuse Tablets, extended release PO: Initial: 1 mg daily am or pm; hypotensive effects
doxazosin with Cardura with K-Dur, (24 hr): 4, 8 mg are most likely within 2–6 hr; monitor standing
donepezil. Ridaura, Cardene, blood pressure
or Coumadin. Maintenance: increase to 2 mg; then, if needed, to
4, 8, and 16 mg to achieve desired reduction in
blood pressure
Benign prostatic hyperplasia:
PO: Initial: as for hypertension; increase dosage at
weekly intervals to 2 mg, then 4 and 8 mg once
daily
Maintenance: 8 mg daily; monitor blood pressure
Maximum: 8 mg daily
Prazosin Minipress Capsules: 1, 2, 5 mg Hypertension:
PO: Initial: 1 mg two or three times daily, with rst
dose at bedtime to reduce syncopal episodes.
Maintenance: 6–15 mg/day in two or three divided
doses
Maximum dosage: 40 mg/day
terazosin — Capsules: 1, 2, 5, 10 mg Hypertension:
PO: Initial: 1 mg at bedtime; measure blood
pressure 2–3 hr after dosing and evaluate
for symptoms of dizziness or tachycardia; if
response is substantially diminished at 24 hr,
increase dosage
Maintenance: 1–5 mg daily
Maximum dose: 20 mg/day
Benign prostatic hyperplasia:
PO: Initial: as for hypertension; gradually increase
dosage in stepwise fashion to 2, 5, or 10 mg
daily for acceptable urinary output
Maintenance: 10 mg daily for 4–6 wk to assess
urinary response
Maximum dose: 20 mg/day
Do not confuse.

anihyprnsiv agns. Mnir h bld prssur
rspns  h cumulaiv ffcs f anihyprnsiv
agns. Obain bld prssur radings in supin and
sanding psiins. Mnir fr an incras in svriy
f advrs ffcs such as sdain, hypnsin, and
bradycardia r achycardia.
DRUG CLASS: CENTRAL-ACTING ALPHA-2
AGONISTS
Actions
Cnral-acing alpha-2 agniss (.g., clnidin, guanfa-
cin, mhyldpa) ac by simulaing h alpha-adrnrgic
rcprs in h brainsm, rsuling in rducd sympa-
hic uw frm h CNS and dcrasd har ra
and priphral vascular rsisanc, causing a drp in
bh syslic and diaslic bld prssurs.
Uses
Alpha-2 agniss ar cnsidrd adjunciv ani-
hyprnsiv agns and ar rcmmndd fr us
nly in cmbinain wih prfrrd r alrnaiv
anihyprnsiv agns. Clnidin is availabl
as a ransdrmal hrapuic sysm (TTS) ha is
applid nc wkly. Ths drugs caus mr fr-
qun advrs ffcs such as sdain, dizzinss,
dry muh, faigu, and sxual dysfuncin. Whn
usd aln, mhyldpa fn causs fluid rn-
in. Thy can safly b usd in cmbinain wih
hr agns such as diurics, vasdilars, and
ba blckrs.
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm h
alpha-2 agniss is rducin in bld prssur.
Nursing Implications for Central-Acting Alpha-2
Agonists
Premedication assessment
1. Obain baslin bld prssur radings in supin
and sanding psiins and apical puls. Hld md-
icain if syslic bld prssur is lss han 100 mm
 Drugs Used to Treat Hypertension CHAPTER 22 377

Table 22.9 Central-Acting Alpha-2 Agonists

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE
clonidine Tablets: 0.1, 0.2, 0.3 mg PO: Initial: 0.1 mg twice daily
Do not confuse Catapres-TTS Transdermal patch: Maintenance: 0.2–0.8 mg daily in two or three divided
clonidine with TTS-1 = 0.1 mg/day doses
colchicine, TTS-2 = 0.2 mg/day Maximum: 2.4 mg daily
Cardizem, Klonopin, TTS-3 = 0.3 mg/day Transdermal: Apply to hairless area of intact skin
or clonazepam. on upper arm or torso once every 7 days; use a
different site each wk
Initial: Start with 0.1-mg patch; after second wk, add
another 0.1-mg patch or use a larger system
Maximum: Two 0.3-mg patches/wk
Note: Antihypertensive effect starts 2–3 days after
initiation of therapy
Kapvay Tablets extended release Attention-decit/hyperactivity disorder (ADHD):
(12 hr): 0.1 mg PO: Initial: 0.4 mg daily for children over 6 years and
older
guanfacine — Tablets: 1, 2 mg Hypertension (IR only):
PO: Initial: 1 mg daily at bedtime
Maintenance: 1–2 mg
Maximum: 3 mg daily
Intuniv Tablets, extended release: See guanfacine tablets for dosage range for
1, 2, 3, 4 mg (for ADHD) hypertension
Attention-decit/hyperactivity disorder (ADHD):
PO: Initial: 1 mg daily
Maintenance: 1–4 mg daily
When discontinuing, taper the dose no more rapidly
than 1 mg every 3–7 days
methyldopa — Tablets: 250, 500 mg PO: Initial: 250 mg two or three times daily
Do not confuse IV: 50 mg/mL Maintenance: 500 mg to 3 g daily in two to four doses
methyldopa with
levodopa or l-dopa.
TTS, Transdermal therapeutic system.
Do not confuse.

Hg r h har ra is lss han 50 bas/min, and
cnac h prscribr.
2. Assss h pain’s mnal saus; affciv and
cgniiv bhavirs shuld b usd as a baslin fr
subsqun cmparisn. If dprssin is suspcd,
rpr  a halhcar prvidr.
3. Obain baslin daa rlaing  usual slp parn.
Availability, dosage, and administration. S Tabl 22.9
Sudden discontinuation. Nvr suddnly discninu
clnidin bcaus i culd caus a rbund ffc wih
a rapid incras in bld prssur, manifsd by nrv-
usnss, agiain, rslssnss, rmrs, hadach,
nausa, and incrasd salivain. Rbund sympms
ar ms prnuncd afr 1  2 mnhs f hrapy
and may bgin  appar wihin a fw hurs f a
missd ds. Wihin 8  24 hurs, svr sympms
may dvlp.
Whn hrapy is  b discninud, a gradual r-
ducin in dsag is ncssary vr 2  4 days, during
which bld prssur mus b carfully mnird.
If h clnidin TTS pach bcms ls, h adh-
siv vrlay shuld b applid dircly vr h TTS
pach  nsur gd adhsin.
Common adverse effects
Neurologic
Drowsiness, dizziness. Ths sympms may ccur, bu
hy nd  b slf-limiing. Tll h pain n  discn-
inu h mdicain and  cnsul a halhcar prvidr
if h advrs ffcs bcm an unaccpabl prblm.
Gastrointestinal
Dry mouth. Ths sympms may ccur, bu hy
nd  b slf-limiing. Tll h pain n  discn-
inu h mdicain and  cnsul a halhcar pr-
vidr if h advrs ffcs bcm an unaccpabl
prblm.
Genitourinary
Altered urine color. Mhyldpa r is mablis
may disclr h urin, causing i  darkn n xp-
sur  air. I is  b xpcd and is n harmful.
Altered test reactions. Mhyldpa may caus up 
20% f pains  dvlp a psiiv racin  h
378 UNIT IV Drugs Affecting the Cardiovascular System

dirc Cmbs s. Hwvr, lss han 0.2% f hs Actions

pains will dvlp hmlyic anmia. Bld cuns Hydralazin causs dirc arrilar smh muscl
shuld b drmind annually during hrapy  d- rlaxain, rsuling in rducd priphral vascu-
c hmlyic anmia. lar rsisanc. Th rducin in priphral rsisanc
causs a rx incras in har ra, cardiac upu,
Serious adverse effects
and rnin rlas wih sdium and war rnin.
Psychological
Cnsqunly, h hypnsiv ffcivnss is rducd
Depression. Assss h pain’s affc (.g., lnli-
unlss h pain is als aking a sympahic inhibir
nss, sadnss, anxiy, angr), cgniin (.g., cnfu-
(.g., ba blckr) and a diuric.
sin, ambivalnc, lss f inrs), and hr bhaviral
rspnss (.g., agiain, irriabiliy, alrd aciviy
Uses
lvl, wihdrawal) bfr saring hrapy. Afr sar-
Hydralazin is usd  ra sag 2 hyprnsin and
ing hrapy wih clnidin, carfully mnir h pa-
hyprnsin assciad wih rnal disas and x-
in fr changs in usual rspns parns. Assss
mia f prgnancy. I may als b usd  prvid
hrwis nrmal mins fr an incras in durain
sympmaic rlif in pains wih har failur by
r innsiy. N h pain’s dgr f scializain,
rducing rsisanc (afrlad)  lf vnricular u-
rspns  simulain, and changs in inracins
pu. Bcaus f h rx incras in cardiac ra, hy-
wih hrs. All individuals aking his drug shuld b
dralazin is fn usd in cmbinain wih a drug
mnird fr dvlpmn f dprssin, spcially
ha inhibis achycardia (.g., ba blckrs, clnidin,
hs wih a hisry f dprssin.
mhyldpa).
Integumentary
A cmbinain prduc (BiDil) cnaining hydrala-
Rash. Abu 10%  15% f pains using h cl-
zin and issrbid dinira has bn apprvd by
nidin TTS pach dvlp cnac drmaiis. Pains
h US Fd and Drug Adminisrain. This cmbina-
wh dvlp mdra r svr ryhma r vsicl
in has bn shwn  rduc hspializains, im-
frmain a h si f applicain f clnidin TTS
prv qualiy f lif, and rduc mraliy in African
pachs shuld cnsul a halhcar prvidr abu h
Amricans wih hyprnsin and har failur.
pssibl nd  rmv h TTS pach and us alrna-
iv hrapy.
Therapeutic Outcome
Th primary hrapuic ucm f hydralazin is r-
Drug interactions
ducin in bld prssur.
Drugs that enhance therapeutic and toxic effects. Ths
includ digxin, anipsychics, alchl, ba blck-
Nursing Implications for Hydralazine
rs (.g., mprll, carvdill), vrapamil, and hr
Premedication assessment
anihyprnsiv agns. Mnir h bld prssur
1. Obain baslin bld prssur radings in h su-
rspns  h cumulaiv ffcs f anihyprnsiv
pin and sanding psiins and apical puls. Hld
agns. Obain bld prssur radings in supin and
mdicain if syslic bld prssur is lss han 100
sanding psiins. Mnir fr an incras in svriy
mm Hg r h har ra is lss han 50 bas/min,
f advrs ffcs such as sdain, hypnsin, and
and cnac h prscribr.
bradycardia r achycardia.
Drugs that reduce therapeutic effects. Tricyclic ani-
Availability. PO: 10-, 25-, 50-, and 100-mg abls.
dprssans (.g., amiripylin, imipramin, dsipra-
Intramuscular (IM), intravenous (IV): 20 mg/mL in
min), razdn, and mirazapin, may blck h ani-
1-mL vials.
hyprnsiv ffcs f clnidin and mhyldpa. Ba
blckrs (.g., prpranll, anll, pindll) may
Dosage and administration. Adult: PO: Iniially, 10 mg
caus pnially lif-hraning incrass in bld
fur ims daily fr h rs 2  4 days, hn 25 mg
prssur whn akn wih clnidin. Mnir carfully
fur ims daily. Th scnd wk, incras h dsag
fr pr bld prssur cnrl r a gradually incras-
 50 mg fur ims daily as h pain lras h
ing bld prssur.
dsag and h bld prssur is brugh undr cn-
Sedative effects. Alchl, phnbarbial, anipsychics,
rl. Maximum daily dsag is 300 mg.
bnzdiazpins, ricyclic anidprssans, anihisamins,
IM, IV: 10-  20-mg IV blus r 10  50 mg IM,
and any hr drugs ha caus sdain r drwsinss all
rpad as ncssary, usually vry 4  6 hurs.
pnia h sdaiv ffcs f clnidin and mhyld-
Mnir bld prssur fn. Rsuls usually bcm
pa. Pains shuld b warnd ha hir lranc  alc-
vidn wihin 10  20 minus.
hl and hr dprssans may b diminishd.
Common adverse effects
DRUG CLASS: DIRECT VASODILATORS
Neurologic
Dizziness, numbness, tingling in the legs. Alhugh
hydralazine (hī-DRĂL-ă-zēn) hs sympms may b anicipad, hy rquir

mniring. If svr, hy shuld b rprd s ha
h dsag can b adjusd apprprialy.
Nausea. This sympm may b anicipad; mni-
ring is rquird. If svr, rpr  a halhcar pr-
vidr s ha h dsag can b adjusd.
Cardiovascular
Orthostatic hypotension. This may ccur, paricularly
during iniiain f hrapy. Pains can usually avid
his cmplicain by rising slwly frm supin and si-
ing psiins.
Palpitations, tachycardia. Alhugh hs sympms
may b anicipad, hy rquir mniring. If svr,
hy shuld b rprd s ha h dsag can b ad-
jusd apprprialy.
Respiratory
Nasal congestion. Nasal cngsin can b rad
wih an anihisamin such as chlrphniramin.
Serious adverse effects
Immunologic, inammatory
Fever, chills, joint and muscle pain, skin eruptions. Tll pa-
ins  rpr h dvlpmn f hs sympms 
a halhcar prvidr. Mnir labrary rprs fr
lukcy cuns and aninuclar anibdy ir.
Drug interactions
Drugs that enhance therapeutic and toxic effects. Ths
includ diurics, alchl, ba blckrs (.g., prpran-
ll, anll, pindll), and hr anihyprnsiv
Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions
Key Points
• The public has made signicant strides in recognizing the
risk factors associated with cardiovascular disease. This
awareness has led to a reduced incidence of heart attacks
and strokes. Hypertension, however, is still a national
health problem. Nurses can play a signicant role in public
education efforts, monitor for nonadherence, monitor
blood pressure response to therapy, and encourage
patients to make changes in lifestyle to reduce the severity
of hypertension.
• Nonadherence to hypertensive therapy is a major problem,
and nurses need to understand that educating the patient
regarding the consequences of discontinuing therapy is
not enough. Rather, the nurse must investigate the “whys”
for discontinuing the therapy. Many of the reasons the
patient gives may be overcome or reduced by proper
interventions or a change in the type of antihypertensive
agents prescribed.
Drugs Used to Treat Hypertension CHAPTER 22 379
agns. Mnir h bld prssur rspns  h
cumulaiv ffcs f anihyprnsiv agns. Obain
bld prssur radings in supin and sanding psi-
ins. Mnir fr an incras in svriy f advrs f-
fcs, such as sdain, hypnsin, and bradycardia
r achycardia.
nitroprusside sodium (nī-trō-PRŬS-īd)
Nitropress (NĪ-trō-prĕs)
Actions
Nirprussid is a pn vasdilar ha acs dircly
n h smh muscl f bld vssls. I prducs
bh arrial and vnus vasdilain, hus rducing
bh prlad and afrlad n h har.
Uses
Nirprussid is usd in pains wih suddn svr
hyprnsiv crisis and in hs wih rfracry har
failur.
Therapeutic Outcomes
Th primary hrapuic ucms f nirprussid
ar rducin in bld prssur and imprvmn in
sympms assciad wih har failur.
Availability. IV: 25 mg/mL in 2-mL vials
• Current guidelines use the systolic blood pressure as
the major criterion for the diagnosis and management of
hypertension in middle-aged and older Americans.
• The primary purpose for controlling hypertension is to
reduce the frequency of cardiovascular disease (angina,
myocardial infarction, heart failure, stroke), as well as
renal failure and retinopathy. To accomplish this goal, for
most patients the 2017 guidelines recommend that blood
pressure must be reduced and maintained below 130/80
mm Hg.
• The classes of antihypertensive medications include:
diuretics, beta-adrenergic blocking agents, ACE inhibitors,
ARBs, direct renin inhibiters, aldosterone receptor
antagonist, calcium channel blockers, alpha-1 adrenergic
blocking agents, central-acting alpha-2 agonists, direct
vasodilators.
380 UNIT IV Drugs Affecting the Cardiovascular System
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX examination and include both NGN (Next Genera-
tion) and traditional questions. See Chapter 1 for further infor
mation regarding question types.
Scenario
A patient arrived at an outpatient clinic for a follow-up visit to
determine adequate hypertension control. The patient had re-
cently been started on an ACE inhibitor and a thiazide diuretic
after following lifestyle modications for 10 years.
1. The patient in the scenario asks the nurse about the difference
between primary and secondary hypertension. Which statement
by the nurse accurately answers the question?
1. “Primary hypertension accounts for 90% of all clinical
cases of high blood pressure and is readily treatable.”
2. “It does not matter whether you have primary or
secondary hypertension; your treatment plan will be the
same.”
3. “Primary hypertension causes target organ damage and
secondary hypertension causes fast heart rate, as well as
high blood pressure.”
4. “Primary hypertension is curable, and secondary
hypertension is only controllable.”
Objective: Differentiate between primary and secondary
hypertension.
NCLEX item type: Multiple choice
Cognitive skill: Understanding
ALPHA-1
CALCIUM CHAN- ADRENERGIC
NEL BLOCKERS BLOCKERS
Inhibit release of renin from the
kidneys
Cause vasodilation, which reduces
peripheral vascular resistance
Diminish the RAAS cascade
Block stimulation of mineralocorti-
coid receptors by aldosterone
Inhibit the movement of calcium
ions across the cell membrane
Inhibit angiotensin I–converting
enzyme
2. The nurse reviewing the assessments and interventions for
the patient in the scenario who is concerned about starting on
antihypertensive medications. Which statement by the nurse
would be an appropriate response? (Select all that apply.)
1. “It is important that you monitor your blood pressure
regularly and keep a record of it for follow up.”
2. “While you are taking these medications it will be
necessary for your healthcare provider to listen for bowel
sounds.”
3. “Your healthcare provider recommends that we review
your diet history.”
4. “The primary healthcare provider will have you come
back for periodic laboratory checks to determine any
changes in kidney function.”
5. “It is recommended that you continue to engage in
physical activity and maintain this over the course of a
lifetime.”
Objective: Summarize nursing assessments and interventions used
for the treatment of hypertension.
NCLEX item type: Multiple response
Cognitive skill: Application
3. After discussing lifestyle modications with the patient in the
scenario who is hypertensive, the nurse will reinforce teaching
after the patient makes which statement?
1. “I gure that since I have started on these medications
that I don’t have to follow those lifestyle modications
anymore.”
2. “I will walk every day at least 20 minutes.”
3. “I will weigh myself at the same time every day and report
a weight gain of more than 2 pounds.”
4. “I think that I can keep track of my blood pressure using
a journal to record it.”
Objective: Identify recommended lifestyle modications after a
diagnosis of hypertension.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
4. The nurse reviewing the various drug classications used for
hypertension recognizes the drug actions. Indicate with an X the
classication and the action for that drug class.
ALDOSTERONE ANGIOTENSIN-
RECEPTOR CONVERTING EN- BETA-ADRENERGIC
ANTAGONISTS ZYME INHIBITORS BLOCKERS
 Drugs Used to Treat Hypertension CHAPTER 22 381

Objective: Identify and summarize the action of ve drug classes 8. Choose the most likely option for the information missing from the
used to treat hypertension. following sentences by selecting from the list of options provided.
NCLEX item type: Drag and drop
Cognitive skill: Recognize cues The patient in the scenario was started on
__________1____________ and _______1____________,
5. The nurse explains to the patient in the scenario, who needs to which are from the drug classications of
start initial drug therapy for hypertension, that treatment usually ______2___________ and ___________2_______________,
includes one or more agents from which four drug classes? (Select respectively.
all that apply.)
1. Diuretics OPTION 1 OPTION 2
2. Beta blockers amlodipine • beta-adrenergic blocker
3. Aldosterone receptor antagonist metoprolol • ACE inhibitor
4. Angiotensin II receptor blockers lisinopril • calcium channel blocker
5. Calcium channel blockers hydrochlorothiazide • thiazide diuretic
6. ACE inhibitors
7. Direct renin inhibitors
8. Alpha-1 adrenergic blockers Objective: Identify and summarize the action of ve drug classes
used to treat hypertension.
Objective: Identify initial options and progression of medicines NCLEX item type: Cloze
used to treat hypertension. Cognitive skill: Recognize cues
NCLEX item type: Extended multiple response
Cognitive skill: Application 9. While reviewing the drug hydrochlorothiazide for a patient with
hypertension, the nurse also checked which laboratory values
6. The nurse preparing the drug irbesartan (Avapro) from the drug before administration? (Select all that apply.)
class angiotensin II receptor blockers knows that this drug works
by which mechanism? 1. Potassium
2. Bilirubin
1. Inhibiting the conversion of angiotensin I to angiotensin II 3. Serum creatinine
2. Binding to and blocking angiotensin II receptor sites 4. Alkaline phosphatase
3. Preventing the release of catecholamines 5. Sodium
4. Blocking the stimulation of mineralocorticoid receptors 6. Complete blood count
Objective: Identify and summarize the action of ve drug classes 7. Chloride
used to treat hypertension. 8. Prothrombin time
NCLEX item type: Multiple choice Objective: Identify and summarize the action of ve drug classes
Cognitive skill: Compare used to treat hypertension.
7. The nurse is administering amlodipine (Norvasc) to a patient who NCLEX item type: Extended multiple response
asked how the drug works. Which statement is an appropriate Cognitive skill: Compare
response by the nurse? 10. After teaching the patient about the prescription drug lisinopril,
1. “This drug blocks the receptors that stimulate the release an ACE inhibitor, the nurse knew that further education was
of renin from the kidneys.” needed after the patient responded with which statement?
2. “This drug helps relax your blood vessels and slows your 1. “If I start to develop a cough after taking lisinopril, I will
heart rate, which lowers your blood pressure.” notify my primary healthcare provider.”
3. “This drug will help you get rid of excess water, which will 2. “As I understand it, I will have to get out of bed slowly
lower your blood pressure.” to let my blood pressure stabilize.”
4. “This drug is designed to dilate your blood vessels, which 3. “I should take lisinopril with food so it will not upset my
in turn will lower your blood pressure.” stomach.”
Objective: Identify and summarize the action of ve drug classes 4. “This drug will help control my blood pressure and treat
used to treat hypertension. my heart failure.”
NCLEX item type: Multiple choice Objective: Identify and summarize the action of ve drug classes
Cognitive skill: Explain used to treat hypertension.
NCLEX item type: Multiple choice
Cognitive skill: Interpret
23 Drugs Used to Treat Dysrhythmias

https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the classication of drugs used to treat
dysrhythmias.
2. Identify baseline nursing assessments that should be
implemented during the treatment of dysrhythmias.
3. Discuss common adverse effects that may be observed
with the administration of antidysrhythmic drugs.
4. Summarize the six cardinal signs of cardiovascular
disease.

Key Terms
conduction system (kŭn-DŬK-shŭn
SĬS-tĕm) (p. 382)
dysrhythmia (dĭs-RĬTH-mē-ă) (p. 382)
atrial utter (Ā-trē-ŭl FLŬ-tĕr) (p. 383)
atrial brillation (Ā-trē-ŭl fĭb-rĭ-LĀ-
shŭn) (p. 383)
paroxysmal supraventricular torsades de pointes (Tore-sods de
tachycardia (PSVT) (păr-ŏk-SĬZ- pwant) (p. 384)
măl sū-pră-vĕn-TRĬK-yū-lăr tăk-ĕ-
KĂR-dē-ă) (p. 383)
atrioventricular blocks (ā-trē-ō-vĕn-
TRĬK-yū-lăr BLŎKS) (p. 383)

DYSRHYTHMIAS
The funtin f the heart is t sustain life by rhyth-
mially pumping bld t all the vital rgans and the
rest f the bdy’s tissues. The conduction system, r
eletrial system, f the heart is the anatmi struture
that ntrls the sequene f musle ntratins s
that an ptimal vlume f bld is pumped frm the
heart with eah beat (Fig. 23.1). The ndutin system
is mpsed f nerve bers that arry the eletrial im-
pulses t the ardia musle, ausing it t ntrat.
In the nrmal heart, a ntratin f the heart mus-
le begins in the paemaker ells f the sinatrial (SA)
nde. The eletrial wave passes thrugh the ndu-
tin system in the atrial musle and auses it t n-
trat, fring bld frm the atrial hambers int the
ventriles belw. The eletrial urrent then enters the
atriventriular (AV) nde, whih fuses and n-
duts an eletrial urrent thrugh the bundle f His
and Purkinje bers t the ventriular musle tissue.
The musle ntrats frm the apex upward, ausing
bld t be pumped frm the right ventrile int the
pulmnary artery t the lungs and frm the left ven-
trile int the arta t the rest f the bdy.
A dysrhythmia (smetimes alled an arrhythmia) -
urs when there is a disturbane f the nrmal eletri-
al ndutin, resulting in an abnrmal heart musle
ntratin r heart rate. All peple have an a-
sinal irregular ntratin f the heart. The danger
is the frequeny with whih the dysrhythmia urs
beause the heart musle lses its efieny in pump-
ing an adequate vlume f bld. Thus ertain types
f dysrhythmias an prdue additinal dysrhythmias
that an stp the heart frm pumping even thugh it
ntinues t beat fr a shrt time (brillatin). A per-
sn may sense an abnrmal ntratin (dysrhythmia)
beause f a “ip-p” r raing f the heart. A nurse
may als suspet that a patient is having dysrhythmia
beause f an irregular pulse. Dysrhythmias, hwever,
must be identied with the aid f an eletrardigram
(ECG), whih prvides a traing f the eletrial ativ-
ity f the heart.
Dysrhythmias are aused by the ring f abnrmal
paemaker ells, blkage f nrmal eletrial path-
ways, r a mbinatin f bth. Nrmally, the rate and
rhythm f eletrial ativity and musle ntratin are
regulated by the paemaker ells f the SA nde. High
emtinal stress, ishemia (see Chapter 24), r heart
failure (see Chapter 27) may trigger nrmally quiet
paemaker ells in areas f the heart ther than the SA
r AV ndes t re. This sends an eletrial impulse
ut f sequene with thse frm the nrmal paemaker
ells, ausing an irregular musular ntratin, sme-
times sensed as a ip-p f the heart. The send
ause f a dysrhythmia is a partial bstrutin f the
nrmal ndutin pathway, ausing an irregular w
f eletrial impulses that results in an irregular pat-
tern f musle ntratins. This is smetimes alled
a reentrant dysrhythmia. Nrmally, healthy heart tissue
has mehanisms that prtet against reentrant dys-
rhythmias. Varius frms f heart disease ause hang-
es in the ndutin pathways that allw ntinuus
reentrant dysrhythmias.
Dysrhythmias are mst mmnly lassied by
rigin within the heart tissues. Thse that develp

382

Superior
vena cava
Sinoatrial node
Middle
Supra- Intranodal
ventricular Anterior
tracts
Posterior
Inferior
vena cava
Bundle of His
Right bundle
Ventricular branch
Purkinje
fibers
Fig. 23.1 Schematic diagram of the heart, illustrating the conduction system. (Modied from Monahan FD, Sands JK,
Neighbors M, etal. Phipps’ Medical-Surgical Nursing: Health and Illness Perspectives. 8th ed. St. Louis: Mosby; 2007.)
abve the bundle f His (see Fig. 23.1) are alled supra
ventricular. Examples f supraventriular dysrhyth-
mias are atrial utter, atrial brillation, premature atri-
al ntratins, sinus tahyardia, sinus bradyardia,
and paroxysmal supraventricular tachycardia (PSVT).
Juntinal dysrhythmias are thse develping near
r within the AV nde. Dysrhythmias develping be-
lw the bundle f His are referred t as ventricular
dysrhythmias. These inlude premature ventriular
ntratins (PVCs), ventriular tahyardia (VT),
and ventriular brillatin. Dysrhythmias that result
frm bstrutin f ndutin pathways are de-
sribed by latin (e.g., supraventriular r ventri-
ular, left r right bundle branhes). Atrioventricular
blocks an be sublassied by degree f blk: rst
degree = partial blk, delayed AV ndutin; se-
nd degree = partial blk, with asinal blked
beats; and third degree = mplete blk, in whih the
atria and ventriles funtin independently f eah
ther. (It is beynd the spe f this text t desribe
eah type f arrhythmia.) Anther methd f lassi-
atin is based n heartbeat rate: bradyarrhythmia
(less than 60 beats/min) r tahyarrhythmia (mre
than 100 beats/min).
The tissues f the eletrial system an be lassied
by ndutin rate, depending n whether alium r
sdium ins reate the stimulus fr musle ntra-
tin. The SA and AV ndes depend n alium ins
fr eletrial ndutin and are referred t as slow
conduction bers. The atrial musle, His-Purkinje sys-
tem, and ventriular musle depend n sdium fr
ntratin and are smetimes referred t as fast con
duction bers.
Drugs Used to Treat Dysrhythmias CHAPTER 23 383
Pulmonary veins
Bachmann's bundle
(internal tract)
Atrioventricular bundle
Common left
bundle branch
Left posterior fascicle
Left posterior
papillary muscle
Left anterior fascicle
TREATMENT FOR DYSRHYTHMIAS
When a dysrhythmia is suspeted, a patient is ften
admitted t a mnitred r in an aute are setting,
where wire leads are plaed in apprpriate latins t
prvide ntinuus eletrardigraphi mnitring
(telemetry). A mbinatin f the physial examina-
tin, patient histry, and eletrardigraphi pattern
is used t diagnse the underlying ause f the dys-
rhythmia. The gal f treatment is t restre nrmal
sinus rhythm and nrmal ardia funtin and prevent
reurrene f life-threatening dysrhythmias.
DRUG THERAPY FOR DYSRHYTHMIAS
ACTIONS
Antidysrhythmi agents are mplex agents with mul-
tiple mehanisms f atin. They are lassied using
the Vaughan Williams lassiatin system arding
t their effets n the eletrial ndutin system f
the heart (Table 23.1). Class I agents at as myardial
depressants by inhibiting sdium in mvement. The
lass Ia agents prlng the duratin f the eletrial
stimulatin n ells and the refratry time between
eletrial impulses. Class Ib agents shrten the dura-
tin f the eletrial stimulatin and the time between
the eletrial impulses. Class I antidysrhythmis are
the mst ptent myardial depressants and slw the
ndutin rate thrugh the atria and the ventriles.
Class II agents are beta-adrenergi blking agents
(beta blkers). Many dysrhythmias are aused by
stimulatin f the beta ells f the sympatheti ner-
vus system f the heart. Class III agents slw the rate
384 UNIT IV Drugs Affecting the Cardiovascular System

Table 23.1 Classication of Antidysrhythmic Agents

EFFECT
CLASSa DRUGS MECHANISM CV RP AM
Ia quinidine Na channel blockers (intermediate-acting) ↓ — ↓
Ia procainamide Na channel blocker (intermediate-acting) ↓ ↑ ↓
Ib lidocaine (Xylocaine) Na channel blockers (quick-acting) ↓/↔ ↓ ↓
mexiletine
Ic ecainide Na channel blockers (slow-acting) ↓ ↔ ↓
propafenone (Rythmol)
II propranolol (Inderal) Beta blockers ↓ — ↓
esmolol (Brevibloc)
metoprolol (Lopressor)
III amiodarone ( Pacerone) K channel blockers ↓/↔ — ↔
sotalol (Betapace)
ibutilide (Corvert)
dofetilide (Tikosyn)
IV verapamil (Calan) Ca channel blockers ↓ — ↓
diltiazem (Cardizem)
Miscellaneous digoxin (Lanoxin) Vagal stimulation ↓ ↓/↔ ↓
adenosine (Adenocard) Slows conduction
AM, Automaticity; Ca, calcium; CV, conduction velocity; K, potassium; Na, sodium; RP, refractory period.
aVaughan Williams classication system.

f eletrial ndutin and prlng the time interval
between ntratins by blking ptassium hannels.
Class IV agents blk alium in w, prlnging
duratin f the eletrial stimulatin and slwing AV
nde ndutin.
An adverse effet smetimes assiated with lass
Ia, lass I, and lass III antidysrhythmi agents is QT
interval prlngatin. QT interval prlngatin is a
measure f delayed ventriular replarizatin, whih
means the heart takes mre time than nrmal t re-
harge between beats. It is an eletrial disturbane
that an be measured n an ECG. The rreted QT
interval (QT) time adjusts the QT interval rretly
fr heart rate extremes. Exessive QT interval prln-
gatin an trigger torsades de pointes (a ptentially
life-threatening ventriular dysrhythmia). The risk f
QT interval prlngatin inreases when tw r mre
drugs are used nurrently that an ause QT interval
prlngatin (Table 23.2).
USES
See individual drug mngraphs fr uses f anti-
dysrhythmi agents.
NURSING IMPLICATIONS FOR
ANTIDYSRHYTHMIC AGENTS
The infrmatin that nurses assess relative t the ardi-
nal signs f ardivasular disease an prvide a basis
fr subsequent evaluatin f the patient’s respnse t
their drug therapies.
Assessment
Dysrhythmias are initially assessed by eletr-
ardigraphi mnitring. Varius types f telemetry
mnitring equipment are available. It is vitally im-
prtant fr the nurse nt t rely mpletely n m-
puterized systems but rather t perfrm frequent pa-
tient assessments while viewing the telemetry system
as an adjunt t astute nursing bservatins. A 24-hur
ambulatry ECG (Hlter mnitr), eletrphysilgi
studies, exerise eletrardigraphy, and labratry
values are used t analyze and diagnse the patient’s
myardial status.
Patients may be admitted t the rnary are unit,
where speialized mnitring equipment is available
fr ntinuus surveillane f the patient. The nurses
in these are units have advaned eduatin in ardia
physilgy and nursing are needed fr these patients.
(See a general medial-surgial nursing text r ritial
are textbk fr an in-depth explanatin f are f the
patient with a dysrhythmia.)
Medication history. Obtain details f all mediatins
presribed and being taken. Tatfully nd ut if the
presribed mediatins are being taken regularly and,
if nt, why.
History of six cardinal signs of cardiovascular disease
1. Dyspnea (difculty in breathing): Rerd if dyspnea
urs while resting r during exertin. Is the pa-
tient affeted by psitin, suh as lying dwn? D
they awaken frm sleep at night?
2. Chest pain: Rerd data as t the time f nset, fre-
queny, duratin, and quality f the hest pain. Nte
any nditins that the patient has fund that either
aggravate r relieve the hest pain. Are there any
assiated symptms with the pain, suh as sweat-
ing, ashen gray r pale skin, heart skipping a beat,

Table 23.2 Selected Drugs Associated with QT Interval Prolongation
ANTIARRHYTHMIC ANTIDEPRESSANT ANTIMICROBIALS
amiodaronea citaloprama Antibiotics:
dofetilidea escitaloprama azithromycina
ecainidea clarithromycina
ibutilidea erythromycina
procainamidea ciprooxacina
sotalola levooxacina
moxioxacina
Antifungal:
uconazolea
aKnown risk of QT interval prolongation.
bPossible risk of QT interval prolongation.
Sources: Trinkley KE, Page II RL, Lien H, Yamanouye K, etal. QT interval prolongation and the risk of torsades de pointes: essentials for clinicians. Curr Med Res
Opin. 2013;29:12, 1719–1726; Tisdale JE. Drug-induced QT interval prolongation and torsades de pointes: role of the pharmacist in risk assessment, prevention and
management. Can Pharm J (Ott). 2016;149(3):139–152.
shrtness f breath, nausea r vmiting, r raing f
the heart? (Nt all patients with a dysrhythmia have
hest pain.)
3. Fatigue: Determine whether fatigue urs nly at
spei times f the day, suh as evening. Ask the pa-
tient if fatigue dereases in relatin t a derease in
ativity level r if it is present at abut the same time
daily. Can they keep up with family and wrkers?
4. Edema: Rerd the presene r absene f edema. If
present, rerd latin f edema, assessment data
(e.g., degree f pitting present; ankle, midalf, r
thigh irumferene), and any measures that the pa-
tient has used t eliminate edema. Chart the time f
day that the edema is present (e.g., when rising in the
mrning, later in the evening) and the spei parts
where it is present n the bdy. When perfrming
daily weights, use the same sale, at the same time
f day, with the patient in a similar type f lthing.
5. Syncope: Ask the patient abut nditins surrund-
ing any episdes f synpe (faintness r dizziness).
Rerd the degree f symptms suh as general
musle weakness, inability t stand upright, feeling
f faintness, r lss f nsiusness. Rerd what
ativities, if any, bring n these synpal episdes.
6. Palpitations: Rerd the patient’s desriptin f pal-
pitatins, suh as “my heart skips sme beats” r “it
began t feel as if it were raing.” Ask if these n-
ditins are preeded by mild r strenuus exerise
and hw lng the palpitatins last.
Basic mental status. Identify the persn’s level f n-
siusness and larity f thught. Bth f these fatrs
are indiatrs f adequate r inadequate erebral per-
fusin. Subsequent regular bservatins fr these data
shuld be made s that apparent imprvement r de-
teriratin an be assessed. Shedule basi neurlgi
assessments at least ne per shift.
Vital signs. Vital signs shuld be taken as ften as
neessary t mnitr the patient’s status.
Drugs Used to Treat Dysrhythmias CHAPTER 23 385
ANTIPSYCHOTICS OTHERS
chlorpromazinea alfuzosinb
haloperidola cilostazola
asenapineb donepezila
aripiprazoleb droperidola
clozapineb methadonea
iloperidoneb ondansetrona
olanzapineb ranolazineb
paloperidoneb
quetiapineb
risperidoneb
ziprasidoneb
• Blood pressure: Bld pressure readings shuld be
perfrmed at least twie daily in stable ardia pa-
tients and mre ften if indiated by the patient’s
symptms r the healthare prvider’s rders. Be
sure t use the prper-sized bld pressure uff and
have the patient’s arm at heart level.
• Record the blood pressure in both arms: A systli pres-
sure variane f 5 t 10 mm Hg is nrmal; readings
reeting a variane f mre than 10 mm Hg shuld
be reprted fr further evaluatin. Always reprt a
narrwing pulse pressure (differene between sys-
tli and diastli readings).
• Pulse: Assess bilaterally the rhythm, quality, equal-
ity, and strength f the pulses (artid, brahial, ra-
dial, femral, ppliteal, psterir tibial, and drsalis
pedis). If any pulse is diminished r absent, rerd
the level at whih initial hanges are nted. The
usual wrds t desribe the pulse are absent, weak,
normal, increased, r bounding. Reprt irregular rate,
rhythm, and patient-reprted palpitatins. Chek
fr delayed apillary rell.
• Respirations: Observe and hart the rate and depth
f respiratins. Chek breath sunds at least every
shift, making spei ntatins regarding the pres-
ene f abnrmal breath sunds suh as rakles r
wheezes. Observe the degree f dyspnea that urs
and whether it happens with r withut exertin.
• Temperature: Rerd the patient’s temperature at
least every shift.
• Oxygen saturation: Rerd the patient’s O2 satura-
tin using a pulse ximeter with eah vital sign
measurement.
Auscultation. Nurses with advaned skills an per-
frm ausultatin t nte hanges in heart size and
heart and lung sunds. (See a medial-surgial nursing
text fr details abut perfrming assessment skills.)
As apprpriate t nursing skills, nte hanges in ar-
dia rhythm, heart rate, hanges in heart sunds, r
murmurs.
386 UNIT IV Drugs Affecting the Cardiovascular System
Laboratory and diagnostic tests. Review labratry
tests and reprt abnrmal results t the healthare pr-
vider prmptly. Suh tests may inlude levels f serum
eletrlytes, espeially ptassium, alium, magnesi-
um, and sdium; arterial bld gases suh as pH, partial
pressures f xygen (Pao2) and arbn dixide (Paco2),
and biarbnate (HCO3 ) level; agulatin studies t
evaluate the bld ltting; serum enzyme levels, in-
luding aspartate amintransferase (AST), reatine
kinase–MB (CK-MB), trpnin, D-dimer, and latate
dehydrgenase (LDH); serum lipid levels (e.g., hles-
terl, triglyerides); eletrardigraphy; hest radi-
graphy; nulear ardigraphy; ardia atheterizatin;
eletrphysilgi studies; and exerise treadmill.
Examine urinalysis reprts and perfrm hurly
mnitring f intake and utput as rdered. Reprt
utput that is less than intake r belw 30 mL per hur
fr an adult patient. Mnitr ther renal funtin tests
suh as the bld urea nitrgen and serum reatinine.
Abnrmalities f these tests r insufient hurly ut-
put may indiate inadequate renal perfusin.
Implementation
• Mnitr ECG traings n a ntinuum (telemetry).
• Perfrm physial assessments f the patient in a-
rdane with the linial setting’s pliies (e.g., ev-
ery 4 t 8 hurs, depending n the patient’s status).
• Assist the patient, as needed, t perfrm ativities f
daily living (ADLs). Make nte f the degree f im-
pairment r dyspnea seen with and withut exertin.
• Administer xygen as rdered and as neessary.
• Be aware f the pliy fr alling “des,” latin
f the emergeny art, and predures used t hek
the emergeny art supplies. Knw the predure
fr debrillatin and ardiversin.
• Administer presribed mediatins and treatments
per the Advaned Cardia Life Supprt (ACLS) pr-
tl that an best alleviate the patient’s symptms
and prvide the maximum level f mfrt.
• Enurage physial ativity as presribed. D nt
allw the patient t verexert r beme fatigued.
• Institute measures t redue anxiety. Supprt the
patient in a alm manner, even if they respnd in a
hstile r nfrntatinal way.
Patient Education
• Review the patient’s histry t identify mdiable
rnary artery disease fatrs. Design an individu-
alized apprah t help the patient mdify fatrs
that are within their ntrl.
• Cperatively disuss and pratie using ping
mehanisms t handle the individual’s anxiety.
• Teah the patient t take their wn pulse and bld
pressure, and emphasize signs and symptms that
shuld be reprted. The use f tehnlgy t mni-
tr pulse and bld pressure in the frm f ativities
trakers, suh as Fitbits and smart wathes, an as-
sist the patient in keeping trak f these vital signs.
Fostering health maintenance
• Thrughut the urse f treatment, disuss medi-
atin infrmatin and hw it will benet the
patient.
• Drug therapy is ne mpnent f the treatment f
dysrhythmias, and it is ritial that the mediatins
be taken as presribed. Prvide the patient and sig-
niant thers with the imprtant infrmatin n-
tained in the spei drug mngraphs fr the drugs
presribed. Additinal health teahing and nursing
interventins fr adverse drug effets t expet and
reprt will be fund in eah drug mngraph.
• Seek peratin and understanding f the fl-
lwing pints s that mediatin mpliane is
inreased: name f mediatin; dsage, rute, and
times f administratin; and mmn and serius
adverse effets.
Patient self-assessment. Enlist the patient’s aid in de-
velping and maintaining a written rerd f mni-
tring parameters (e.g., pulse rate, bld pressure,
degree f dyspnea and preipitating auses, hest
pain, edema). See the Patient Self-Assessment Frm
fr Cardivasular Agents n the Evlve website.
Cmplete the Premediatin Data lumn fr use as
a baseline t trak respnse t drug therapy. Ensure
that the patient understands hw t use the frm, and
instrut the patient t bring the mpleted frm t fl-
lw-up visits. During fllw-up visits, fus n issues
that will fster adherene t the therapeuti interven-
tins presribed.
DRUG CLASS: CLASS IA ANTIDYSRHYTHMIC
AGENTS
quinidine (KWĬN-ĭ-dēn)
Do not confuse quinidine with quinacrine or quinine.
Actions
Quinidine, riginally btained frm inhna bark, has
been used as an antidysrhythmi agent fr several de-
ades. It is lassied as a lass Ia antidysrhythmi agent,
wrking n the musle f the heart and stabilizing the
rate f ndutin f impulses. It slws the heart and
hanges a rapid, irregular pulse t a slw, regular pulse.
Uses
Quinidine was used mst ften t suppress atrial bril-
latin, atrial utter, PSVT and VT, and life-threatening
PVCs. Beause f infrequeny f use, n additinal in-
frmatin is presented here n quinidine.
Medication Safety Alert
Do not confuse quinidine and quinine. They are both adminis-
tered in dosages of 300 mg but have entirely different clinical
uses.

These effets usually subside within a few days.
Instrut the patient t rise slwly frm a supine psi-
tin. Mnitr the patient’s bld pressure.
procainamide (pro-KANE-a-mide)
Do not confuse procainamide with prochlorperazine.
Actions
Prainamide is a lass Ia antidysrhythmi agent.
Uses
Prainamide is used per ACLS prtl in the treat-
ment f life-threatening widening f the QRS mplex
and ventriular brillatin.
Therapeutic Outcome
The primary therapeuti utme expeted frm pr-
ainamide therapy is nversin f dysrhythmia t
nrmal sinus rhythm.
Nursing Implications for Procainamide
Premedication assessment
1. Obtain data relating t the six ardinal signs f ar-
divasular disease, vital signs, and pulse ximetry
level t be used as a baseline fr subsequent evalua-
tin f respnse t therapy.
2. Assess and rerd any hypersensitivity t prain-
amide, praine, r ther ester-type lal anesthetis.
3. Assess histry fr heart failure and myasthenia gra-
vis. Prainamide shuld be avided in patients
with heart failure r myasthenia gravis, beause it
an wrsen bth nditins.
Availability. Procainamide hydrochloride. IV: Injetin
slutin: 100 mg/mL in 10-mL vials and 500 mg/mL in
2-mL vials.
Dosage and administration
Procainamide. Adult: IV: 10 t 17 mg/kg IV at a rate
f 20 t 50 mg/min or 100 mg IV every 5 minutes;
administer until arrhythmia is ntrlled. Maximum
dse up t 17 mg/kg.
Medication Safety Alert
 • Do not use procainamide in complete AV block, and use
with extreme caution in partial AV block.
 • Blood pressure and ECG should be monitored
because of hypotension and dysrhythmia during IV
administration. Therapeutic blood levels are 4 to 10 mcg/
mL for procainamide and 15 to 25 mcg/mL for N-acetyl
procainamide (NAPA), its active metabolite.
 • The blood sample should be drawn 6 to 12 hours after
the IV infusion has started.
Common Adverse Effects
Cardiovascular
Hypotension. Prainamide may ause hyptensin,
espeially when being administered intravenusly.
Drugs Used to Treat Dysrhythmias CHAPTER 23 387
Mnitr bld pressure lsely. Slw the rate f infu-
sin if bld pressure falls 10 mm Hg r mre.
Serious Adverse Effects
Cardiovascular
Heart failure. Prainamide shuld be avided in pa-
tients with heart failure. It may preipitate r exaer-
bate the nditin.
Dysrhythmias. Prainamide has been assiated
with serius disturbanes suh as ventriular brilla-
tin and QT prlngatin. Mnitr lsely.
Drug interactions
Drugs that enhance therapeutic and toxic effects. These
inlude ther dysrhythmi agents, antipsyhtis,
imetidine, diltiazem, digxin, verapamil, ketna-
zle, urquinlnes (e.g., iprxain), and beta-
adrenergi blking agents (e.g., prpranll, metpr-
ll, atenll). Mnitr fr inreases in severity f drug
effets suh as bradyardia, tahyardia, QT prlnga-
tin, and hyptensin.
Neuromuscular blockade, respiratory depression. Praina-
mide may prlng the effets f the surgial musle
relaxants (e.g., suinylhline). Mnitr the patient’s
respiratry rate and depth. Observe fr signs f yansis
and additinal dysrhythmias. Patients wh are n res-
piratrs may require additinal time t be weaned frm
ventilatry assistane.
DRUG CLASS: CLASS IB ANTIDYSRHYTHMIC
AGENTS
lidocaine (LĪ-dō-kān)
Xylocaine (ZĪ-lō-kān)
Actions
Lidaine is a lass Ib antidysrhythmi agent.
Uses
Lidaine is used in the treatment f life-threatening
PVCs, VT, and ventriular brillatin.
Therapeutic Outcome
The primary therapeuti utme expeted frm lid-
aine therapy is nversin f dysrhythmia t nrmal
sinus rhythm. Beause f infrequeny f use, n addi-
tinal infrmatin is presented here n lidaine.
Life Span Considerations
Lidocaine
Lidocaine for IV use to treat dysrhythmias, often used for
older adults, is different from lidocaine used as a local anes-
thetic. For use with dysrhythmias, check the label carefully to
ensure that it says “lidocaine (or Xylocaine) for cardiac dys-
rhythmia.” Serious dysrhythmias may result if lidocaine with
preservatives or lidocaine with epinephrine is administered
intravenously to the patient.
388 UNIT IV Drugs Affecting the Cardiovascular System
DRUG CLASS: CLASS IC ANTIDYSRHYTHMIC
AGENTS
ecainide acetate (ĕ-KĀ-nīd ĂS-ĭ-tāt)
Actions
Fleainide aetate is a lass I antidysrhythmi agent
that may be taken rally.
Uses
Fleainide may be used in the preventin f parxysmal
atrial brillatin/utter (PAF) assiated with disabling
symptms, PSVTs, and preventin f life-threatening ven-
triular dysrhythmias suh as sustained VT. Fleainide is
usually used fr mre serius ventriular dysrhythmias
that have nt respnded t mre traditinal therapy. In
additin t its therapeuti ativity, a partiular advantage
is its twie-daily dsing shedule. Fleainide has a nega-
tive intrpi effet and may ause r wrsen heart fail-
ure, partiularly in patients with preexisting severe heart
failure. This adverse effet may take hurs t mnths t
develp. New r wrsened heart failure urs in ap-
prximately 5% f patients. Fleainide may als aggra-
vate an existing dysrhythmia and preipitate new nes,
espeially in patients with underlying heart disease.
Therapeutic Outcome
The primary therapeuti utme expeted frm e-
ainide therapy is nversin f dysrhythmia t nr-
mal sinus rhythm.
Nursing Implications for Flecainide
Premedication assessment
1. Obtain data relating t the six ardinal signs f ar-
divasular disease, vital signs, and pulse ximetry
levels t be used as a baseline fr subsequent evalu-
atin f respnse t therapy.
2. If any symptms f heart failure are present, ntify
the healthare prvider befre starting therapy.
Availability. PO: 50-, 100-, and 150-mg tablets.
Dosage and administration
PSVT, PAF. Adult: PO: Initially, 50 mg every 12 hurs,
inreasing 50 mg twie daily every 4 days. Maximum
daily dsage is 300 mg.
Sustained VT. Adult: PO: Initially, 100 mg every 12
hurs; inrease in 50-mg inrements twie daily every
4 days. Mst patients respnd at 150 mg twie daily.
Maximum daily dsage is 400 mg.
Medication Safety Alert
 • Reduce dose of ecainide 50% when administered with
amiodarone.
 • Flecainide should not be used in patients with second-
or third-degree AV block in the absence of an articial
ventricular pacemaker and must be used with caution in
patients with known heart failure. Monitor the ECG before
and during initiation of therapy.
Common adverse effects. The mre frequent adverse
effets that ur with eainide therapy are dizziness,
lightheadedness, faintness, and unsteadiness (19%);
visual disturbanes, suh as blurred visin, difulty
in fusing, and spts befre the eyes (16%); dyspnea
(1%); headahe (10%); nausea (9%); fatigue (8%); n-
stipatin (5%); edema (3%); and abdminal pain (3%).
Neurologic
Dizziness, headache. These adverse effets are usu-
ally mild and tend t reslve with ntinued therapy.
Enurage the patient nt t disntinue therapy with-
ut rst nsulting the healthare prvider.
Gastrointestinal
Constipation, nausea. These adverse effets are usu-
ally mild and tend t reslve with ntinued therapy.
Enurage the patient nt t disntinue therapy with-
ut rst nsulting the healthare prvider.
Sensory
Visual disturbances. Prvide fr patient safety during
temprary visual impairment. Cautin the patient t
avid temprarily any tasks that require visual auity,
suh as driving r perating pwer mahinery. Instrut
the patient nt t rub the eyes with fre when tearing.
These adverse effets are usually mild and tend t
reslve with ntinued therapy. Enurage the patient
nt t disntinue therapy withut rst nsulting the
healthare prvider.
Serious adverse effects
Cardiovascular
Increasing dyspnea, exercise intolerance, ede-
ma. Fleainide may indue r aggravate preexisting
heart failure. If these symptms beme mre pr-
nuned, the patient shuld be instruted t ntat
the healthare prvider fr further evaluatin.
Dysrhythmias. Fleainide may indue r aggravate
preexisting dysrhythmias. The patient shuld be in-
struted t ntat the healthare prvider fr further
evaluatin if sensatins f a jumping r raing heart
develp.
Drug interactions
Drugs that enhance therapeutic and toxic effects. These
inlude amidarne, ziprasidne, urquinlnes
(e.g., iprxain), imetidine, verapamil, and pr-
tease inhibitrs (e.g., ritnavir). Mnitr fr inreases
f drug effets suh as dysrhythmias, heart failure, and
bradyardia.
Digoxin. When multiple dses f eainide are ad-
ministered t patients stabilized n a dse f digxin,
there is a 10% t 20% inrease in serum digxin n-
entratins. This inrease may result in signs f digi-
talis txiity, suh as anrexia, nausea, fatigue, blurred
r lred visin, bradyardia, and dysrhythmias.
Mnitr serum digxin levels, ECG readings, and the
linial urse f the patient lsely.
Urinary acidiers. These agents (e.g., asrbi aid,
ammnium hlride) may lwer the urine pH, aus-
ing an inrease in the urinary exretin f eainide.

Patients shuld be bserved fr redevelpment f dys-
rhythmias, whih may require an inrease in dsage f
eainide.
propafenone (prō-PĂ-fĕ-nōn)
Rythmol SR (RĬTH-mŏl)
Actions
Prpafenne is a lass I antidysrhythmi agent. It als
has weak beta-blking and alium hannel blking
effets.
Uses
Prpafenne is used fr the treatment f PAF and
life-threatening ventriular dysrhythmias suh as VT.
Beause prpafenne an ause additinal dysrhyth-
mias, it is used nly with patients in whm the benets
utweigh the ptential risks.
Therapeutic Outcome
The primary therapeuti utme expeted frm
prpafenne therapy is nversin f dysrhythmia t
nrmal sinus rhythm.
Nursing Implications for Propafenone
Premedication assessment
1. Obtain data relating t the six ardinal signs f ardi-
vasular disease, vital signs, and ntinuus pulse
ximetry and eletrardigraphi mnitring t be
used as a baseline fr subsequent evaluatin f re-
spnse t therapy.
2. Rerd data relating t any gastrintestinal symp-
tms present befre initiatin f therapy.
Availability. PO: 150-, 225-, and 300-mg tablets; 225-,
325-, and 425-mg apsules, extended release (12 hr).
Dosage and administration. PO: Initially, 150 mg eve-
ry 8 hurs. At 3- r 4-day intervals, the dsage may be
inreased t 225 mg every 8 hurs and then 300 mg
every 8 hurs (900 mg/day).
Medication Safety Alert
Because propafenone has mild beta-adrenergic blocking
properties, it should not be used in patients with asthma.
Administer in divided doses around the clock. If a patient
misses a dose of propafenone, the next dose should not be
doubled because of an increased risk of adverse reactions.
Common adverse effects
Neurologic
Dizziness. This may ur, partiularly during
the initiatin f therapy. Dizziness usually subsides
within a few days. Instrut the patient t rise slwly
frm a supine psitin. Mnitr the patient’s bld
pressure.
Drugs Used to Treat Dysrhythmias CHAPTER 23 389
Gastrointestinal
Nausea, vomiting, constipation. Gastrintestinal m-
plaints ur in apprximately 11% f patients, but dis-
ntinuatin f therapy is rarely required. Administer
with fd r milk t alleviate nausea. Enurage the
patient nt t disntinue therapy withut rst n-
sulting the healthare prvider.
Serious adverse effects
Cardiovascular
Dysrhythmias. Prpafenne may indue r aggra-
vate dysrhythmias. Patients with mre serius dys-
rhythmias suh as sustained VT are mre suseptible
t myardial txiity. The patient shuld be instruted
t ntat the healthare prvider fr further evalua-
tin if sensatins f a jumping r raing heart develp.
Drug interactions
Drugs that enhance therapeutic and toxic effects. These
inlude amidarne, imetidine, parxetine, prtease
inhibitrs (e.g., ritnavir), ziprasidne, uxetine,
and urquinlnes (e.g., iprxain). Mnitr
fr an inrease in severity f adverse effets frm
prpafenne, suh as hyptensin, smnlene, brad-
yardia, and dysrhythmias.
Drugs that decrease therapeutic effects
Rifampin. Mnitr patients with nurrent therapy
fr inreased frequeny f dysrhythmias.
Digoxin. Prpafenne prdues dse-related inreases
in serum digxin levels. Measure plasma digxin levels
and redue digxin dsage when prpafenne is started.
Propranolol, metoprolol. Prpafenne appears t in-
hibit the metablism f these beta blkers. A redu-
tin in beta-blker dsage may be neessary during
nurrent therapy with prpafenne.
Warfarin. Prpafenne inreases plasma warfarin
nentratins by inhibiting warfarin metablism,
thus prlnging prthrmbin time. Observe fr the
develpment f petehiae; ehymses; nsebleeds;
bleeding gums; dark, tarry stls; and bright red r
ffee-grund emesis. Mnitr the prthrmbin time
(internatinal nrmalized rati [INR]) and redue the
dsage f warfarin if neessary.
DRUG CLASS: CLASS II ANTIDYSRHYTHMIC
AGENTS: BETA-ADRENERGIC BLOCKING AGENTS
Actions
The beta-adrenergi blking agents (e.g., esm-
ll, metprll) are used widely as antidysrhythmi
agents. These agents inhibit ardia respnse t sym-
patheti nerve stimulatin by blking the beta reep-
trs. As a result, the heart rate, systli bld pressure,
and ardia utput are redued.
Uses
These agents are effetive in the treatment f varius
ventriular dysrhythmias, sinus tahyardia, PSVT,
390 UNIT IV Drugs Affecting the Cardiovascular System
PVCs, and tahyardia assiated with atrial utter r
brillatin beause AV ndutin is diminished.
Therapeutic Outcome
The primary therapeuti utme expeted frm beta-
blker therapy is nversin t, and maintenane f,
nrmal sinus rhythm.
Nursing Implications for Beta-Adrenergic Blocking
Agents
See Chapter 12 fr further disussin f the nursing im-
pliatins assiated with beta-adrenergi inhibitin.
DRUG CLASS: CLASS III ANTIDYSRHYTHMIC
AGENTS
amiodarone hydrochloride (ăm-ē Ō-dă-rōn hī-drō-KLŌR-īd)
Do not confuse amiodarone with trazodone, amanta-
dine, or amlodipine.
Pacerone (pace’ er own)
Actions
Althugh its mehanism f atin is unknwn, amid-
arne is a lass III antidysrhythmi agent that prlngs
the atin ptential f atrial and ventriular tissue
and inreases the refratry perid withut altering
the resting membrane ptential, thus delaying re-
plarizatin. In additin, amidarne has been shwn
t antagnize nnmpetitively bth alpha- and beta-
adrenergi reeptrs, ausing systemi and rnary
vasdilatin.
Uses
Amidarne is being used in the management f life-
threatening supraventriular tahydysrhythmias,
atrial brillatin and utter, bradyardia-tahyardia
syndrmes, ventriular tahyardia and brillatin,
and hypertrphi ardimypathy resistant t ur-
rently available therapy.
Adverse Effects
Adverse reatins are mmn with the use f amida-
rne, partiularly in patients reeiving mre than 400
mg/day. Apprximately 15% t 20% f patients dis-
ntinue therapy beause f adverse effets.
Therapeutic Outcome
The primary therapeuti utme expeted frm ami-
darne therapy is nversin t, and maintenane f,
nrmal sinus rhythm.
Nursing Implications for Amiodarone
Premediatin assessment
1. Obtain data relating t the six ardinal signs f
ardivasular disease, vital signs, pulse ximetry,
and eletrardigraphi traings t be used as a
baseline fr subsequent evaluatin f respnse t
therapy.
2. Initiate requested labratry tests t be used fr
evaluatin f pulmnary, phthalmi, thyrid, and
liver funtin.
3. Rerd data relating t the patient’s usual sleep pat-
tern and any gastrintestinal symptms present be-
fre initiatin f therapy.
Availability. PO: 100-, 200-, and 400-mg tablets.
IV: 50 mg/mL in 3-, 9-, and 18-mL vials; 1.5 mg/mL
in 100-mL and 1.8 mg/mL in 200-mL and 1.8 mg/mL
in 250-mL dextrse IV slutins.
Dosage and administration. The difulty f using
amidarne effetively and safely is that it pses a sig-
niant risk t patients. Patients must be hspitalized
while the lading dse is given, and the respnse f-
ten requires 2 weeks r mre. Beause absrptin and
eliminatin are variable, maintenane dse seletin is
difult, and it is nt unusual fr a redutin in ds-
age r disntinuatin f treatment t be required. The
time at whih a previusly ntrlled life-threatening
dysrhythmia will reur after disntinuatin r dsage
adjustment is unpreditable, ranging frm weeks t
mnths. Attempts t substitute ther antidysrhythmi
agents when amidarne is disntinued are made
difult by the gradually but unpreditably hanging
amidarne bdy stre. A similar prblem exists when
amidarne is nt effetive; it still pses the risk f a
drug interatin with whatever subsequent treatment
is tried.
PO: Loading dose: 800 t 1600 mg daily in divided
dses fr 1 t 3 weeks until an initial therapeuti re-
spnse urs. After the lading dse, a dsage f 600
t 800 mg daily is given fr apprximately 1 mnth.
Maintenance: The lwest effetive dsage shuld be
used, generally 200 t 400 mg daily.
IV: 150 mg intravenus piggybak ver 10 minutes,
fllwed by an infusin f 60 mg/hr fr 6 hurs, then
30 mg/hr fr the next 18 hurs.
Medication Safety Alert
Amiodarone is contraindicated in patients with severe
sinus node dysfunction that causes sinus bradycardia, with
second- and third-degree AV block, and when episodes of
bradycardia have caused syncope (except in the presence
of a pacemaker).
Baseline tests. Befre the start f therapy, baseline
pulmnary, phthalmi, thyrid, and liver funtin
tests shuld be mpleted.
Gastric irritation. If gastri irritatin urs, adminis-
ter with fd r milk. If symptms persist r inrease
in severity, reprt this t the healthare prvider fr
evaluatin.

Serious adverse effects
Neurologic
Fatigue, tremors, involuntary movements, sleep disturbanc-
es, numbness and tingling, dizziness, ataxia, confusion. Many
f these symptms are dse related and reslve with
redutin f dsage r disntinuatin f therapy.
Peripheral neurpathy may be assiated with lng-
term therapy, althugh the nset and presentatin f
symptms are variable. Symptms usually reslve 1
t 4 mnths after the disntinuatin f therapy. Teah
the patient t rise slwly frm a supine r sitting p-
sitin, and enurage the patient t sit r lie dwn if
feeling faint.
Perfrm a baseline assessment f the patient’s de-
gree f alertness and rientatin t name, plae, and
time befre starting therapy. Make regularly shed-
uled subsequent mental status evaluatins and m-
pare ndings. Reprt develpment f mental status
hanges. Prvide fr patient safety during episdes f
dizziness.
Respiratory
Exertional dyspnea, nonproductive cough, pleuritic chest
pain. Pulmnary interstitial pneumnitis r alvelitis
has been reprted in 10% t 15% f patients. Partiular
are shuld be taken nt t assume that suh symp-
tms are related t ardia failure. Tests fr diffu-
sin apaity are mst likely t shw an abnrmality.
Symptms gradually reslve after disntinuatin f
therapy. Peridi hest radigraphs and linial evalu-
atin are remmended every 3 t 6 mnths.
Endocrine
Thyroid disorders. Administratin f amidarne
has been assiated with the develpment f hyp-
thyridism (2% t 10%) and hyperthyridism (1% t 3%).
Patients with a histry f thyrid disrders appear t
be mre suseptible t this mpliatin. Baseline and
peridi thyrid funtin tests shuld be mpleted in
all patients.
Sensory
Yellow-brown pigmentations in the cornea, blurred vision,
halos. Crneal mirdepsits have been bserved by
slit-lamp examinatin as early as 2 weeks after the
initiatin f therapy. Symptms f blurred visin, nar-
rwing peripheral visin, r visual hals develp in
abut 10% f patients. This mpliatin is reversible
after drug withdrawal. Use f methylellulse ph-
thalmi slutin and a minimizatin f the mainte-
nane dses may limit this mpliatin. Prvide fr
patient safety during temprary visual impairment.
Instrut the patient nt t rub the eyes with fre when
tearing.
Gastrointestinal
Nausea, vomiting, constipation, abdominal pain, anorex-
ia. Gastrintestinal mplaints ur in abut 25% f
patients but rarely require disntinuatin f therapy.
These adverse effets mmnly ur during high-
dsage administratin and usually respnd t a ds-
age redutin r divided dsages.
Drugs Used to Treat Dysrhythmias CHAPTER 23 391
Hepatotoxicity. Abnrmal liver funtin test results
(e.g., AST, alanine amintransferase [ALT]) ur
in 4% t 9% f patients. Liver enzyme levels in pa-
tients n relatively high maintenane dses shuld
be mnitred n a regular basis. Persistent signiant
elevatins in the liver enzymes r hepatmegaly are
indiatins fr nsidering a redutin in dsage r
disntinuatin f therapy. Hepatitis and ther liver
abnrmalities may develp in 1% t 3% f patients.
The symptms f hepattxiity are anrexia, nausea,
vmiting, jaundie, hepatmegaly, splenmegaly, and
abnrmal liver funtin tests.
Cardiovascular
Dysrhythmias. Amidarne an ause an exaerba-
tin f the preexisting dysrhythmia and, in 2% t 4% f
patients, indue ther new dysrhythmias as well.
Integumentary
Photosensitivity. Amidarne has prdued pht-
sensitivity resulting in a rash in apprximately 10% f
patients. The severity f the rash may depend n the
degree f sun expsure. Symptms suh as burning,
tingling, erythema, and blistering may ur as early as
2 hurs after expsure t the sun. The use f sunsreens
may minimize this adverse effet. Patients shuld be
enuraged t wear lng-sleeved shirts and t avid
wearing shrts utdrs. Phtsensitivity may persist
fr up t 4 mnths after disntinuatin f therapy.
With lng-term treatment, a blue-gray dislratin f
the expsed skin may ur. The risk is inreased in pa-
tients f fair mplexin and thse with exessive sun
expsure, and may be related t umulative dse and
duratin f therapy. This effet gradually subsides af-
ter disntinuatin f therapy. The patient shuld als
be instruted nt t use artiial tanning lamps.
Drug interactions
Cimetidine, uoroquinolones, azole-type antifungal agents,
protease inhibitors, macrolide antibiotics. Administratin
f these drugs nurrently with amidarne signi-
antly inreases serum levels f amidarne. Redue
the dsage f amidarne and mnitr lsely fr dys-
rhythmias if administered nurrently.
Rifampin. Rifampin signiantly redues the serum
levels f amidarne. The dse f amidarne may
need t be inreased fr therapeuti effet.
Cholestyramine. Chlestyramine signiantly re-
dues the serum levels f amidarne. The dse f
amidarne may need t be inreased fr therapeuti
effet.
Fentanyl. When used nurrently, fentanyl and
amidarne may ause hyptensin, bradyardia, de-
reased ardia utput, and sinus arrest. Mnitr heart
rate, ECG, and pulmnary funtin lsely.
Digoxin. Administratin f amidarne t patients
reeiving digxin therapy regularly results in an in-
rease in the serum digxin nentratin. The dse
f digxin shuld be redued by 50% r disntinued.
Digxin serum levels shuld be lsely mnitred and
392 UNIT IV Drugs Affecting the Cardiovascular System
patients bserved fr linial evidene f txiity (e.g.,
anrexia, nausea, fatigue, blurred r lred visin,
bradyardia, dysrhythmia).
Warfarin. Ptentiatin f warfarin is almst always
seen within 3 t 4 days in patients reeiving nmi-
tant therapy. The dse f the antiagulant shuld be
redued by ne-third t ne-half, and prthrmbin
times (INR) shuld be mnitred lsely. Observe
fr the develpment f petehiae; ehymses; nse-
bleeds; bleeding gums; dark, tarry stls; and bright
red r ffee-grund emesis.
Phenytoin. Elevatin f phenytin serum levels by
200% t 300% is bserved ver several weeks. The ds-
age f phenytin must be gradually redued, based n
patient respnse. Mnitr patients underging n-
urrent therapy fr signs f phenytin txiity: nys-
tagmus, sedatin, and lethargy. Serum levels shuld
be mnitred peridially. Phenytin may als redue
amidarne levels. Mnitr lsely fr lss f thera-
peuti effets.
Beta blockers, calcium channel blockers. Amidarne
shuld be used with autin in patients reeiving beta-
adrenergi blking agents (e.g., prpranll, timll,
nadll, pindll) r alium hannel blkers (e.g.,
diltiazem, verapamil, nifedipine) beause f the ps-
sible ptentiatin f bradyardia, sinus arrest, and AV
blk. If neessary, amidarne an be used after inser-
tin f a paemaker in patients with severe bradyar-
dia r sinus arrest.
Theophylline. Amidarne may inrease thephyl-
line serum levels, resulting in txiity. Effets may nt
be bserved until after at least 1 week f nurrent
therapy. Txiity may persist fr mre than 1 week af-
ter amidarne has been disntinued.
dofetilide (dō-FĔT-ĭ-līd)
Tikosyn (TIK-o-sin)
Actions
Dfetilide is a lass III antidysrhythmi agent. It ats
by blking the ardia ptassium in hannels, delay-
ing replarizatin and thus prlnging the refratry
perid in the atria and ventriles. On an ECG rhythm
strip, the QT interval will be prlnged. In linially
useful dses, dfetilide has n effet n sdium han-
nels r alpha- and beta-adrenergi reeptrs.
Uses
Dfetilide blks reentrant dysrhythmias suh as atrial
brillatin/utter and VT and prevents their refrma-
tin. Thus it is used t nvert atrial brillatin/ut-
ter t nrmal sinus rhythm and maintain sinus rhythm
after nversin.
Adverse Effects
Prlngatin f the QT interval may indue ventri-
ular dysrhythmias, partiularly trsades de pintes
(a ventriular dysrhythmia assiated with prln-
gatin f the QT interval n the ECG), synpe, and
sudden death. Using nly the minimal dse neessary
fr maintenane f nrmal sinus rhythm is imprtant
beause the frequeny f dysrhythmias is diretly r-
related t inrease in dse and further prlngatin f
the QT interval.
Therapeutic Outcome
The primary therapeuti utme expeted frm
dfetilide therapy is nversin t, and maintenane
f, nrmal sinus rhythm.
Nursing Implications for Dofetilide
Premediatin assessment
1. Obtain baseline bld pressure readings in supine
and standing psitins and apial pulse.
2. Initiate labratry studies requested by the health-
are prvider (e.g., renal funtin tests suh as
bld urea nitrgen, serum reatinine, and ele-
trlyte levels) t be used as a baseline fr future
mparisn.
Availability. PO: 125-, 250-, and 500-mg apsules.
Dosage and administration. Befre dfetilide is
initiated:
• Patients must be admitted t a unit with ntin-
uus ECG mnitring available and persnnel
trained in the treatment f serius ventriular dys-
rhythmias and the initiatin f dfetilide. Therapy
must be ntinuusly mnitred fr at least 3
days.
• Patients with atrial brillatin must be anti-
agulated befre eletrial r pharmalgi ardi-
versin t nrmal sinus rhythm.
• Hypkalemia must be rreted befre initiatin f
dfetilide therapy.
• The QT interval must be assessed. If the interval
is mre than 440 t 500 millisends, dfetilide is
ntraindiated.
• The reatinine learane must be alulated.
PO: Initial: Based n alulated reatinine learane
with ntinuus ECG mnitring, give the fllwing
dses:
CALCULATED CREATININE CLEARANCE DOFETILIDE DOSE
>60 mL/min 500 mcg twice daily
40–60 mL/min 250 mcg twice daily
20 to <40 mL/min 125 mcg twice daily
<20 mL/min dofetilide contraindicated
Dosage adjustment: 2 t 3 hurs after administra-
tin f the rst dse, reassess the QT interval. If the
QT interval has inreased 15% r mre mpared with
baseline, r is greater than 500 millisends, adjust the
dse as fllws:

IF THE STARTING DOSE BASED THEN THE NEW DOSE BASED
ONCREATININE CLEARANCE IS: ONQTC INTERVAL IS:
500 mcg twice daily 250 mcg twice daily
250 mcg twice daily 125 mcg twice daily
125 mcg twice daily 125 mcg daily
<20 mL/min dofetilide contraindicated
If, after the send dse, the QT interval is mre
than 500 t 550 millisends, dfetilide shuld be
disntinued.
Renal funtin and QT interval shuld be real-
ulated every 3 mnths. If reatinine learane falls,
adjust the dfetilide dse arding t the initial
dse. If the QT interval is mre than 500 t 550 milli-
sends, dfetilide shuld be disntinued and pa-
tients shuld be mnitred by ECG until the QT re-
turns t baseline.
If a patient misses a dse, the dse shuld nt be
dubled at the next dse. The next dse shuld be tak-
en at the sheduled time.
Common adverse effects
Cardiovascular
Dysrhythmias. Varius dysrhythmias (e.g., ventriu-
lar brillatin, VT, trsades de pintes, AV blk, heart
blk) have been reprted in up t 15% f patients re-
eiving dfetilide. Cntinuus ECG mnitring is ru-
ial until the patient is stable.
Chest pain. Ours in 10% f patients.
Gastrointestinal
Nausea, abdominal pain, diarrhea. Nausea urs in 5%
f patients, abdminal pain in 3% f patients, and diar-
rhea in 3% f patients. These adverse effets are usu-
ally mild and tend t reslve with ntinued therapy.
Enurage the patient nt t disntinue therapy with-
ut rst nsulting the healthare prvider.
Neurologic
Headache. Headahe urs in 11% f patients tak-
ing dfetilide. The headahes are usually mild and
tend t reslve with ntinued therapy. Enurage the
patient nt t disntinue therapy withut rst n-
sulting the healthare prvider.
Other
Dizziness, insomnia, rash. Dizziness urs in 8% f
patients, insmnia in 4%, and rash in 3%.
Drug interactions
Drugs that enhance toxic effects. Cimetidine, tri-
methprim, and ketnazle inhibit urinary exre-
tin f dfetilide, ptentially ausing an inrease in
plasma nentratins and prlngatin f the QT
interval.
Other mediines that prlng the QT interval may
ause serius txiity when used nurrently with
dfetilide. These inlude sme ther antidysrhythmi
agents (amidarne, stall) hlrprmazine, dlas-
etrn, drperidl, mxixain, and ziprasidne.
Drugs Used to Treat Dysrhythmias CHAPTER 23 393
Medication Safety Alert
Dofetilide must be discontinued at least 48 hours before the
initiation of other medicines that may enhance toxic effects
from dofetilide.
sotalol SOE-a-lole
Betapace Beta-pace
Betapace AF
Sotylize SOE-til-eyes
Sorine Sohr-een
Apo-Sotalol
Actions
Stall is a lass III antidysrhythmi agent.
Uses
Stall is used per ACLS prtl in the treatment f
atrial brillatin/utter and life-threatening ventriu-
lar brillatin.
Therapeutic Outcome
The primary therapeuti utme expeted frm s-
tall therapy is nversin f dysrhythmia t nrmal
sinus rhythm.
Nursing Implications for Sotalol
Premedication assessment
1. Obtain data relating t the six ardinal signs f ar-
divasular disease, vital signs, and pulse ximetry
level t be used as a baseline fr subsequent evalua-
tin f respnse t therapy.
2. Obtain histry fr asthma r heart failure. Can
wrsen heart failure and asthma.
Availability. Sotalol hydrochloride. PO: Oral solution:
5 mg/mL, 250- and 480-mL bttles.
Tablets: 80, 120, 160, and 240 mg.
IV injection solution: 150 mg/10-mL vial.
Dosage and administration. Atrial brillatin/atrial
utter (symptmati).
Adult: Oral:
Days 1 t 3: Initial dse f 80 mg tw times daily.
Days 4 t 6: If inmplete respnse, may inrease t
120 mg tw times daily.
Days 7 t 9: If inmplete respnse, may inrease t 160
mg tw times daily. Dse shuld nly be inreased
if exessive QT prlngatin des not ur.
Adult: IV:
Days 1 t 3: 75 mg IV infused ver 5 hurs twie daily.
Days 4 t 6: If inmplete respnse, may inrease t
112.5 mg twie daily.
Days 7 t 9: If inmplete respnse, may inrease t 150
mg twie a day. Dsage shuld nly be inreased if
exessive QT prlngatin des not ur.
394 UNIT IV Drugs Affecting the Cardiovascular System
Medication Safety Alert
Blood pressure, heart rate, and ECG should be monitored
because of hypotension, bradycardia, and QT-interval pro-
longation during intravenous administration.
Common Adverse Effects
Cardiovascular. Stall blks beta reeptrs and
may ause bradyardia. Mnitr heart rate.
Central nervous system. Stall may ause fatigue,
dizziness, and headahe. These effets usually subside
within a few days. Instrut the patient t rise slwly
frm a supine psitin. Mnitr the patient’s bld
pressure. Instrut patient nt t disntinue media-
tin and t nsult a healthare prvider if the adverse
effets beme an unaeptable prblem.
Musculoskeletal. Stall may ause weakness.
Prvide fr safety and prevent falls.
Respiratory. Stall blks beta reeptrs and may
ause dyspnea in patients with asthma r ther res-
piratry disrders. Assess respiratry status and limit
ativity ausing fatigue.
Serious Adverse Effects
Cardiovascular
Heart failure. Stall shuld be avided in patients
with heart failure. May preipitate r exaerbate the
nditin. Mnitr the patient fr an inrease in edema,
dyspnea, rakles, bradyardia, and rthpnea. Ntify
the healthare prvider if these symptms develp.
Dysrhythmias. Stall may be assiated with seri-
us disturbanes suh as ventriular brillatin and
QT prlngatin. Mnitr the patient’s rhythm n the
ECG mnitr and reprt hanges.
Drug interactions
Drugs that enhance therapeutic and toxic effects. These
inlude ther dysrhythmi agents, antipsyhtis,
diltiazem, digxin, verapamil, ketnazle, ur-
quinlnes (e.g., iprxain), and beta-adrenergi
blking agents (e.g., prpranll, atenll). Mnitr
fr inreases in severity f drug effets suh as brady-
ardia, QT prlngatin, and hyptensin.
DRUG CLASS: CLASS IV ANTIDYSRHYTHMIC
AGENTS: CALCIUM CHANNEL BLOCKING AGENTS
Actions
The alium hannel blkers (e.g., verapamil, diltia-
zem) are used widely as antidysrhythmi agents. These
agents inhibit ardia respnse by blking the L-type
alium hannels in the SA and AV ndal tissue. This
slws AV ndutin, prlngs refratriness, and de-
reases autmatiity.
Uses
These agents are effetive in the treatment f autmati
and reentrant tahyardias. They are ntraindiated
in systli heart failure.
Therapeutic Outcome
The primary therapeuti utme expeted frm al-
ium hannel blker therapy is nversin t, and
maintenane f, nrmal sinus rhythm.
Nursing Implications for Calcium Channel
Blocking Agents
See Chapter 22 fr further disussin f nursing implia-
tins assiated with alium hannel blking agents.
DRUG CLASS: MISCELLANEOUS
ANTIDYSRHYTHMIC AGENTS
adenosine (ă-DĔN-ō-sēn)
Actions
Adensine is a naturally urring hemial fund
in every ell within the bdy. It is nt related t ther
antidysrhythmi agents. It has a variety f physilgi
rles, inluding energy transfer, prmtin f prsta-
glandin release, inhibitin f platelet aggregatin, anti-
adrenergi effets, rnary vasdilatin, and suppres-
sin f heart rate.
Uses
Adensine is used per ACLS prtl in the treatment
f PSVT, making it effetive beause f its strng de-
pressant effets n the SA and AV ndes. Adensine
des nt nvert atrial utter, atrial brillatin, r VT
t nrmal sinus rhythm.
Therapeutic Outcome
The primary therapeuti utme expeted frm ade-
nsine therapy is nversin f PVSTs t nrmal sinus
rhythm.
Nursing Implications for Adenosine
Premedication assessment
1. Obtain data relating t the six ardinal signs f ar-
divasular disease, vital signs, pulse ximetry, and
ntinuus eletrardigraphi mnitring t be
used as a baseline fr subsequent evaluatin f re-
spnse t therapy.
Availability. IV: 3 mg/mL in 2-, 4-, 20-, and 30-mL vials.
Dosage and administration. IV: 6 mg administered by
rapid IV blus injetin (ver 1 t 2 sends) fllwed
by a saline ush. A fllw-up dse f 12 mg by rapid
IV blus is remmended if the initial dse is unsu-
essful in restring a nrmal heart rate. The 12-mg
dse may be repeated ne if required. Nrmal saline
(0.9% sdium hlride) is the diluent.
Common adverse effects. The mst mmnly reprt-
ed adverse reatins with adensine inlude ushing f

the fae (18%), shrtness f breath (12%), hest pressure
(7%), nausea (3%), and headahe and lightheadedness
(2%). Beause the half-life f adensine is less than 10
sends, adverse effets are very shrt-lived. Treatment
f any prlnged adverse effet wuld inlude xygen
and pssibly ther antidysrhythmi agents.
Drug interactions
Drugs that enhance therapeutic and toxic effects. Dipyri-
damle and arbamazepine ptentiate the effets f
adensine. Smaller dses f adensine shuld be used
if therapy is required.
Drugs that reduce therapeutic effects. Thephylline,
aminphylline, and affeine mpetitively antagnize
adensine; thus larger dses f adensine are required
with nurrent use.
digoxin (dĭ-JŎKS-ĭn)
Lanoxin (lă-NŎKS-ĭn)
Drugs Used to Treat Dysrhythmias CHAPTER 23 395
Actions
Digxin slws ndutin thrugh the AV nde, re-
duing ndutin velity and autmatiity. It has a
psitive intrpi effet, inreasing ardia utput.
Uses
As an antidysrhythmi agent, digxin may be used t
treat atrial brillatin, atrial utter, and PSVT.
Therapeutic Outcome
The primary therapeuti utme expeted frm di-
gxin therapy is nversin f supraventriular tahy-
ardias t nrmal sinus rhythm and inreased ardia
utput.
Nursing Implications for Digoxin
See Chapter 27 fr further disussin f nursing impli-
atins assiated with digxin therapy.
396 UNIT IV Drugs Affecting the Cardiovascular System

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points 2. The nurse reviewing the laboratory results of a 68-year-old female
patient receiving amiodarone hydrochloride for paroxysmal atrial
• Dysrhythmias are complex in origin, severity, and treatment brillation knows which of the following laboratory tests are monitored
for control. for patients on antidysrhythmic agents? (Select all that apply.)
• Many of the agents used to treat dysrhythmias have
1. Alanine aminotransferase (ALT)
serious adverse effects and must be monitored closely.
2. Creatine kinase–MB (CK-MB)
• Nurses need to check references carefully in advance 3. Aspartate aminotransferase (AST)
of administering these drugs for the correct method of 4. Thyroid-stimulating hormone (TSH)
preparation, preadministration assessments needed, rate 5. Prostate-specic antigen (PSA)
of administration of IV drugs, and monitoring parameters
essential during drug administration. If any monitoring Objective: Identify baseline nursing assessments that should be
parameter (e.g., blood pressure) is not within desired limits, implemented during the treatment of dysrhythmias.
hold the medication and notify the healthcare provider. NCLEX item type: Multiple response
Cognitive skill: Application
• Antidysrhythmic agents include class Ia, Ib, Ic, II, III, and IV,
which work through various mechanisms to slow conduction 3. The patient in the scenario was started on the antidysrhythmic ecainide
of impulses through the heart’s conduction system by and asks the nurse what they need to be aware of while taking this drug.
blocking sodium, potassium, or calcium channels. What common adverse effects should the nurse mention to the patient?
1. Headache
Additional Learning Resources 2. Exertional dyspnea
3. Nausea
SG Go to your Study Guide for additional Review Questions 4. Sinus rhythm
for the NCLEX® Examination, Critical Thinking Clinical Situa- 5. Dizziness
tions, and other learning activities to help you master this chap- 6. Photosensitivity
ter content. 7. Constipation
Go to your Evolve website (https://evolve.elsevier.com/Willihng Objective: Discuss common adverse effects that may be observed
anz) for additional) online resources. with the administration of antidysrhythmic drugs.
NCLEX item type: Extended multiple response
The following questions are typical of the NCLEX examina- Cognitive skill: Evaluate cues
tion and include both NGN (Next Generation) and traditional 4. A nurse assessing a 48-year-old male patient for signs of
questions. See Chapter 1 for further information regarding cardiovascular disease looks for which of these symptoms?
question types. Indicate with an X the assessment signs that indicate one of the six
cardinal signs of cardiovascular disease or whether it is unrelated.
Scenario Objective: Summarize the six cardinal signs of cardiovascular disease.
The nurse is caring for a patient who recently suffered a myo- NCLEX item type: Matrix
cardial infarction (MI) and now is experiencing ectopy and runs Cognitive skill: Evaluate outcomes
of ventricular tachycardia (VT). The patient reports having feel-
ings of palpitations during the ectopy and has been started on CARDINAL SIGN OF
an antidysrhythmic. CARDIOVASCULAR UNRELATED
PATIENT ASSESSMENT DISEASE SIGN
1. The nurse reviewed the classications of drugs that can be used
Patient complaining of not
to treat dysrhythmias and knows they include which mechanisms
sleeping well
of action? (Select all that apply.)
Patient became weak and dizzy
1. Beta-adrenergic blocking
when attempting to stand
2. Calcium channel blocking
3. Chloride channel blocking Patient complaining of
4. Sodium channel blocking blurred vision
5. Potassium channel blocking Patient reports difculty
breathing when lying at
Objective: Identify the classication of drugs used to treat
dysrhythmias. Patient having urinary retention
NCLEX item type: Multiple response Patient experiencing palpitations
Cognitive skill: Application
Patient having pitting edema
around the ankles
Patient reported decrease in
physical activity
Patient complaining of pain
across the chest
Patient reporting ringing in
the ears
Drugs Used to Treat Angina Pectoris
Objectives
1. Discuss angina pectoris and identify assessment data
needed to evaluate an anginal attack.
2. Differentiate between chronic stable angina and unstable
angina.
Key Terms
angina pectoris (ăn-JĪ-nă PĔK-tŏr-ĭs) chronic stable angina (KRŎN-ĭk STĀ-
(p. 397) bŭl) (p. 397)
ischemia (ĭs-KĒ-mē-ă) (p. 397) unstable angina (ŭn-STĀ-bŭl) (p. 397)
ANGINA PECTORIS
Coronary artery disease (CAD) is the leading cause
of disability, socioeconomic loss, and death in the
United States, and angina pectoris is the rst clini-
cal indication of underlying CAD in many patients.
Angina pectoris is the name given to a feeling of chest
discomfort arising from the heart because of lack of
oxygen getting to the heart cells. It is a symptom of
CAD and is also called ischemic heart disease. Ischemia
develops when the supply of oxygen needed by the
heart cells is inadequate. The lack of oxygen occurs
when blood ow through the coronary arteries is
reduced by atherosclerosis or spasm of the arteries.
Atherosclerosis can develop as localized plaques or
as a generalized narrowing of the coronary arteries.
Patients are usually asymptomatic until there is at
least 50% narrowing of the artery. CAD caused by
atherosclerosis is a progressive disease; however, pro-
gression can be slowed with diet control and with the
use of cholesterol-lowering agents (see Chapter 21).
The presentation of angina pectoris is highly variable.
The sensation of discomfort is often described various-
ly as squeezing, tightness, choking, pressure, burning,
or heaviness. This discomfort may radiate to the neck,
lower jaw, shoulder, and arm. The usual anginal attack
begins gradually, reaches its peak intensity over the next
several minutes, and then gradually subsides after the
person stops activity and rests. Attacks can last from
30 seconds to 30 minutes. Anginal episodes are usually
precipitated by factors that require an increased oxygen
supply (e.g., physical activity, such as climbing a ight
of stairs or lifting). Other precipitating factors include
24
https://evolve.elsevier.com/Willihnganz
3. Describe the actions and the adverse effects of the drug
classications used to treat angina.
4. Discuss risk factor management and healthy lifestyle
changes that are taught to prevent disease progression
and myocardial infarction or death.
variant angina (VĂR-ē-ĕnt) (p. 397)
exposure to cold temperatures, emotional stress, sexual
intercourse, and eating a large meal.
Angina pectoris is classied as chronic stable, un-
stable, or variant angina. Chronic stable angina is pre-
cipitated by physical exertion or stress, lasts only a few
minutes, and is relieved by rest or nitroglycerin. It is
usually caused by xed atherosclerotic obstruction in
the coronary arteries. Unstable angina is unpredictable;
it changes in ease of onset, frequency, duration, and in-
tensity. It is probably caused by a combination of athero-
sclerotic narrowing, vasospasm, and thrombus forma-
tion. Variant angina occurs while the patient is at rest; it is
characterized by specic electrocardiographic changes,
and it is caused by vasospasm of a coronary artery re-
ducing blood ow. The type of angina pectoris is diag-
nosed by a combination of history, electrocardiographic
changes during an anginal attack, and exercise tolerance
testing, with or without thallium-201 scintigraphy.
TREATMENT OF ANGINA PECTORIS
The goals for the treatment of angina pectoris are to
prevent myocardial infarction and death (thereby
prolonging life) and to relieve anginal pain symp-
toms (thereby improving the quality of life). In many
cases, percutaneous coronary intervention (PCI; also
known as coronary angioplasty) with stent placement
or coronary artery bypass graft (CABG) surgery will
be considered rst because these treatments have been
proven to save lives over time. The choice of therapy
often depends on the patient’s clinical response to ini-
tial medical therapy.
397
398 UNIT IV Drugs Affecting Cardiovascular System
Life Span Considerations
Anginal Attacks
The goal of the treatment of an anginal attack, which most
often occurs in older adults, is the relief of pain rather than
simply the reduction of pain. If pain is not relieved by nitro-
glycerin, the patient should immediately contact the health-
care provider or be seen in the emergency department.
Analgesics should not be administered in an attempt to elimi-
nate the patient’s pain.
All patients should receive extensive patient educa-
tion to help them reduce their risks related to CAD. The
avoidance of activities that can precipitate attacks (e.g.,
strenuous exercise, exposure to cold weather, drinking
caffeine-containing beverages, cigarette smoking, eat-
ing heavy meals, emotional stress) should be attempt-
ed. Risk factors (e.g., diabetes mellitus, hypertension,
dyslipidemia) must also be treated. A structured exer-
cise program designed for each patient can be success-
ful for weight reduction among overweight patients,
and it can also improve cardiovascular health. Healthy
muscle tissue requires less oxygen. Medications, in
combination with risk reduction and exercise, are ef-
fective in preventing ischemic attacks and myocardial
infarction.
DRUG THERAPY FOR ANGINA PECTORIS
ACTIONS
The underlying pathophysiology of ischemic heart dis-
ease is an imbalance between the oxygen demands of
the heart and the ability of coronary arteries to deliver
the needed oxygen, the spasticity of the coronary arter-
ies, platelet aggregation, and thrombus formation. The
oxygen demand of the heart is determined by the heart
rate, contractility, and ventricular volume. Therefore
the pharmacologic treatment of angina is aimed at
decreasing oxygen demand by decreasing heart rate,
myocardial contractility, and ventricular volume with-
out inducing heart failure. Because platelet aggrega-
tion, blood ow turbulence, and blood viscosity also
play certain roles—especially with unstable angina—
platelet inhibitors are also prescribed to slow the de-
velopment and progression of atherosclerotic disease
and reduce the risk of myocardial infarction (see
Chapter 26). Because atherosclerosis causes narrowing
and closure of the coronary arteries, inducing angina
and myocardial infarction, the use of the 3-hydroxy-
3-methylglutaryl coenzyme A (HMG-CoA) reductase
inhibitors (i.e., the statins) has also become standard
therapy in preventing and treating angina pectoris (see
Chapter 21).
USES
Seven groups of drugs may be used to treat chronic
stable angina: nitrates, beta-adrenergic blockers,
angiotensin-converting enzyme (ACE) inhibitors, cal-
cium channel blockers, statins, platelet-active agents,
and the myocardial cell sodium channel blocker, ra-
nolazine. Combination therapy is benecial for many
patients. Beta blockers, calcium channel blockers,
long-acting nitrates, and ranolazine can reduce the fre-
quency of anginal episodes. Risk factor management,
healthy lifestyle changes, statins, antiplatelet agents,
and ACE inhibitors can prevent disease progression
and myocardial infarction or death.
Drug therapy for patients with angina must be in-
dividualized. Most patients will be given prescrip-
tions for medication (e.g., nitroglycerin in the form
of sublingual tablets or translingual spray) to treat
acute attacks and prescriptions for therapy to prevent
further ischemia and myocardial infarction (and pos-
sible death). Therapy to prevent myocardial infarc-
tion consists of statins to lower the low-density lipo-
protein cholesterol level and to reduce inammation;
platelet inhibitors to prevent platelet aggregation and
thrombus formation; and ACE inhibitors to help dilate
coronary blood vessels and to reduce the potential for
thrombus formation.
The most effective agents for relieving ischemia and
angina are beta blockers, calcium channel blockers,
and nitrates. The drug ranolazine modies metabolism
in the myocardial cells to reduce the oxygen demand
of the contracting heart muscles, thereby reducing
symptoms of angina.
Deciding which medicine to use depends on oth-
er conditions that the patient may have and the
expected adverse effects of therapy. Aspirin or clopi-
dogrel (see Chapter 26), which are platelet-active
agents, may also be considered to slow platelet ag-
gregation. Many patients will have revascularization
procedures (e.g., PCI or CABG) to restore blood ow
and to reduce symptomatology. Even after revascu-
larization, patients will still require antianginal drug
therapy.
NURSING IMPLICATIONS FOR ANGINAL
THERAPY
Assessment
History of anginal attacks . Ask the patient specic ques-
tions to identify the onset, duration, and intensity of
the pain. Ask the patient to describe the chest sensation
and the pattern of occurrence (e.g., under the sternum;
in the jaw, neck, and shoulder; radiation down the left
arm, the right arm, or both; into the wrist, hand, and
ngers). What activities precipitate an attack? Does
the pain occur with or without exertion? Is the pain
relieved by rest? Does the chest pain occur shortly after
eating? Does the individual experience fatigue, short-
ness of breath, indigestion, or nausea in relation to the
anginal attack? Work with the patient to plan interven-
tions that will minimize the factors that trigger attacks.
Mutually establish goals with the patient to alter risk
factors that are modiable.
 Drugs Used to Treat Angina Pectoris CHAPTER 24
Medication history
• What medications—both prescription and non-
prescription—are being taken?
• Does the patient take any herbal or dietary
supplements?
• What medications are being used for the treatment
of the angina?
• What effect does taking nitroglycerin have on the
anginal pain? How many nitroglycerin tablets are
required for the patient to obtain pain relief during
an attack? How many nitroglycerin tablets are being
taken daily? How old is the nitroglycerin that is be-
ing used sublingually? Is it stored properly?
• Have the prescribed medications been taken regu-
larly? If not, determine the reasons for the patient’s
nonadherence. Analyze nonadherence issues, and
plan interventions with the patient. Plan to review
drug administration, as needed.
Central nervous system
• Mental status: Determine the individual’s level of
consciousness and clarity of thought. Check for
orientation to date, time, and place, as well as lev-
el of confusion, restlessness, or irritability. Ask the
patient whether they have noticed any changes in
memory or level of awareness; these factors are in-
dicators of cerebral perfusion.
• Syncope: Ask the patient to describe the conditions
surrounding any episodes of syncope. Record the
degree of presenting symptoms, such as general
mental weakness, inability to stand upright, feeling
faint, or loss of consciousness. Record what activi-
ties, if any, bring on these episodes.
• Anxiety: What degree of apprehension is present?
Did a stressful event precipitate the attack? Plan for
stress reduction education and a discussion of effec-
tive means of coping with stressful events.
Cardiovascular system
• Palpitations: Record the patient’s description of pal-
pitations, such as “my heart skips some beats” or “it
began to feel as if it were racing.” Ask if these con-
ditions are preceded by mild or strenuous exercise
and how long the palpitations last.
• Heart rate: Count and record the rate, rhythm, and
quality of the pulse.
• Blood pressure: Record the blood pressure. It may be
increased or decreased during an attack. Compare
with previous baseline readings.
• Respirations: The patient may be dyspneic. Ask
whether the attack occurred while the patient was
at rest or during exertion.
• Cardiovascular history: What concurrent cardio-
vascular disease does the patient have (e.g., hyper-
tension, dyslipidemia)?
• Peripheral perfusion: Determine the patient’s pe-
ripheral perfusion by checking the pedal pulses
in the lower extremities and the skin color and
399
temperature. Note any loss of hair on the lower legs,
which denotes decreased circulation.
• Smoking: Does the patient smoke? How much? Does
the patient understand the effects of smoking on the
cardiovascular system?
• Ask what, if any, activities of daily living have been
altered to cope with the patient’s symptoms.
Nutritional history
• Diet: Is the patient on a special diet (e.g., low-
sodium diet, low-fat diet)? Is the patient being treat-
ed for high cholesterol? Does eating cause fatigue or
shortness of breath?
• Fluids: Does the patient have any edema, especially
in the ankles? Examine the dietary history to estab-
lish whether a referral to a nutritionist would benet
the individual’s understanding of the diet regimen.
Implementation . Obtain the patient’s vital signs,
and include an assessment of the individual’s pain
rating.
• Adequate tissue perfusion is essential. Instruct the
patient to take measures to avoid fatigue and cold
weather, which can cause vasoconstriction, and pro-
vide for the patient’s personal safety when symp-
toms of hypoxia are present (e.g., lightheadedness,
dyspnea, chest pain).
• When pain is present, comfort measures and pre-
scribed pain medications must be implemented to
allow the individual to decrease the pain. Fatigue
may increase the perception of pain; spacing activi-
ties so that fatigue does not occur is recommended.
Administer oxygen as prescribed and check the pa-
tient’s oxygen saturation.
• For information about medication administration,
see the individual drug monographs.
Patient Education
Medications
• Teach the patient about the signs and symptoms of
hypotension, which may occur when nitrates are
taken. Weakness, dizziness, or faintness can usu-
ally be relieved by increasing muscular activity (i.e.,
alternating exing and relaxing the muscles in the
legs) or by sitting or lying down. Resting for 10 to
15 minutes after taking medication may also assist
the patient with the management of hypotension.
Because lightheadedness or fainting is a possibility
when taking nitroglycerin, safety measures to pre-
vent injury from transient orthostatic hypotension
must be stressed.
• Explain that a headache may occur with the use of
nitroglycerin but that it should subside within 20 to
30 minutes.
• Teach specic administration techniques to the pa-
tient for the type of medication prescribed (e.g., sub-
lingual or transmucosal tablets, translingual spray,
topical ointment, transdermal patches). Refer to
400 UNIT IV Drugs Affecting Cardiovascular System
Chapter 7, Figs. 7.2, 7.3, and 7.4, for further descrip-
tion of percutaneous administration of nitroglycerin.
Lifestyle modications. Lifestyle modications are es-
sential for many individuals with angina. Teach the
patient about appropriate behavioral changes, such as
stress management (e.g., relaxation techniques, medita-
tion, three-part breathing).
• The patient must resume activities of daily living
within the boundaries set by the healthcare provid-
er. Encourage activities such as regular moderate
exercise, meal preparation, the resumption of usual
sexual activity, and social interactions.
• Individuals who are unable to attain the degree of
activity hoped for through drug therapy may be-
come frustrated. Allow for the verbalization of feel-
ings and then implement actions that are appropri-
ate to the circumstances.
• Participation in regular exercise is essential. Follow
the guidelines of the American Heart Association re-
garding an exercise program. Increase the patient’s
exercise demands gradually and monitor the effects
on their cardiovascular system. Changes in the level
of exercise may require participation in a supervised
program (e.g., cardiac rehabilitation). Tell the patient
to avoid overexertion. Anginal pain may occur with
exercise, and taking nitroglycerin before exercise or
before performing certain activities may be recom-
mended. Instruct the patient to always stop exercising
or performing any activity when chest pain is present.
• Discuss the need for smoking cessation and make
referrals to available self-help programs in the area.
Smoking causes vasoconstriction; encourage a dras-
tic reduction in smoking and preferably complete
elimination of smoking. Encourage the patient to set
a date to stop smoking.
• Dietary modications aimed at decreasing the cho-
lesterol level and a reducing program to maintain
the ideal weight are usually prescribed by the pri-
mary healthcare provider. Depending on coexisting
conditions, other dietary modications (e.g., a low-
sodium diet) may be suggested. Discourage the use
of caffeine-containing products, because they may
precipitate an anginal attack when they are taken in
excess.
• If hypertension accompanies the angina, stress the
importance of following prescribed dietary and me-
dicinal regimens to control the disease.
• Instruct the patient not to ingest alcohol while re-
ceiving nitroglycerin therapy. Alcohol causes vaso-
dilation, which potentially results in postural
hypotension.
• Teach the patient about the proper storage of medi-
cation (especially sublingual nitroglycerin) in a dark,
airtight container. Show the patient the medication’s
expiration date and stress the importance of having
the prescription relled before the expiration date.
• Always report poor pain control to the healthcare
provider.
Fostering health maintenance
• Throughout the course of treatment, discuss medi-
cation information and how it will benet the
patient.
• Drug therapy is essential to maintain the adequate
oxygenation of the myocardial cells and body tis-
sues. Although medications can control the anginal
attacks, lifestyle changes to deal with the manage-
ment of precipitating factors must also occur.
• Provide the patient and their signicant others with
the important information contained in the spe-
cic drug monographs for the drugs prescribed.
Additional health teaching and nursing interven-
tions for common and serious adverse effects are
described in the drug monographs later in this
chapter.
• Seek cooperation and understanding with regard to
the following points so that medication adherence
is increased: the name of the medication; its dosage,
route, and times of administration; and its common
and serious adverse effects.
Patient self-assessment. Enlist the patient’s help with
developing and maintaining a written record of moni-
toring parameters (e.g., blood pressure, pulse, de-
gree of pain relief, exercise tolerance, adverse effects
experienced). See the Patient Self-Assessment Form
for Cardiovascular Agents on the Evolve website.
Complete the Premedication Data column for use as a
baseline to track the patient’s response to drug thera-
py. Ensure that the patient understands how to use the
form, and instruct the patient to bring the completed
form to follow-up visits. During follow-up visits, focus
on issues that will foster the patient’s adherence with
the therapeutic interventions prescribed.
DRUG CLASS: NITRATES
Actions
The nitrates are the oldest effective therapy for angina
pectoris. Although they have also been called coronary
vasodilators, these agents do not increase total coro-
nary blood ow. First, nitrates relieve angina pectoris
by inducing the relaxation of the peripheral vascular
smooth muscles, which results in the dilation of the
arteries and veins. This reduces venous blood return
(i.e., reduced preload) to the heart, which in turn leads
to decreased oxygen demands on the heart. Second,
nitrates increase the myocardial oxygen supply by
dilating the large coronary arteries and redistributing
blood ow, thereby enhancing oxygen supply to isch-
emic areas.
Uses
Nitroglycerin is used for the treatment of angina pec-
toris. It is available in different dosages so that it can
be adjusted to patient needs. Sublingual tablets dis-
solve quite rapidly and are used primarily for acute
attacks of angina. The sustained-release tablets and
 Drugs Used to Treat Angina Pectoris CHAPTER 24
capsules, ointments, and transdermal patches are used
prophylactically to prevent anginal attacks. All long-
acting nitrates, including isosorbide dinitrate and mo-
nonitrate, appear to be equally effective when a suf-
cient nitrate-free interval (as discussed under Topical
Ointment Administration and Transdermal Patch
Administration later in this section) is incorporated
into the medicine regimen. The translingual spray may
be used for both the prophylaxis and acute treatment
of anginal attacks.
Continued use of transdermal nitroglycerin patches
and frequent doses of oral nitrates and sustained-release
nitrates causes the development of tolerance and the
loss of the antianginal response. The best way to avoid
tolerance is to have periodic 8- to 12-hour nitrate-free
periods. Depending on the type of angina, patients will
be told when not to use nitrates (e.g., bedtime), unless
they have an acute attack. When used with beta block-
ers or calcium antagonists, nitrates produce greater
antianginal and antiischemic effects than when they
are used alone. These agents also help provide prophy-
laxis against attacks during nitrate-free periods.
Therapeutic Outcomes
The primary therapeutic outcomes from nitrate thera-
py are as follows:
1. Relief of anginal pain during an attack
2. Reduced frequency and severity of anginal attacks
3. Increased tolerance of activities
Nursing Implications for Nitrates
Premedication assessment
1. Assess the level, location, duration, intensity, and
pattern of the patient’s pain.
2. Ask the patient when the last dose of nitrates was
taken and what degree of relief was obtained.
Availability, dosage, and administration. See Table 24.1
Sublingual administration
1. Instruct the patient to sit or lie down at the rst sign
of an oncoming anginal attack.
2. Instruct the patient to place a tablet under the tongue
and allow it to dissolve; encourage the patient not to
swallow the saliva immediately.
3. The American Heart Association (O’Gara etal, 2013)
recommends that if chest pain is not relieved with
one sublingual nitroglycerin tablet within 5 min-
utes, the patient should seek emergency medical at-
tention (i.e., call 911). While waiting for emergency
care, the patient can take one more tablet and then
take a third tablet 5 minutes later if the pain is not
relieved.
4. One or two tablets may be taken prophylactically a
few minutes before engaging in activities that may
trigger an anginal attack.
5. Chart the patient’s ability to place the sublingual
medication under the tongue correctly.
401
Medication deterioration. Every 6 months, the nitro-
glycerin prescription should be relled and the old
tablets safely discarded. (Be sure that the patient
knows how to read the expiration date and have the
prescription relled.)
Medication storage. Store nitroglycerin in its original
dark-colored glass container with a tight lid.
Medication accessibility. Nonhospitalized patients
should carry nitroglycerin at all times, but not in a
pocket directly next to the body, because heat hastens
the deterioration of the medication. When taken, the
drug should produce a slight stinging or burning sen-
sation in the mouth, which usually indicates that it is
still potent.
Allow the hospitalized patient to keep the nitro-
glycerin at the bedside or on their person, if am-
bulatory. Check the hospital policy to see if a fresh
supply of medicine should be issued rather than us-
ing the agents that the patient brought from home.
(Remember that the nurse is still responsible for gath-
ering and charting relevant data regarding all medi-
cation taken by the patient when the medication is
left at the bedside.)
Sustained-release tablet administration. Sustained-
release nitroglycerin is usually taken on an empty
stomach every 8 to 12 hours. If gastritis develops,
the sustained-release tablet may be taken with
food.
Translingual spray administration. Patients should fa-
miliarize themselves with the position of the spray ori-
ce, which can be identied by the nger rest on top
of the valve. This can be particularly helpful for ad-
ministration at night. The spray is highly ammable;
instruct the patient not to use the spray where it may
be ignited.
1. At the time of administration, the patient should
preferably be in a sitting position.
2. The canister should be held vertically, with the valve
head uppermost and the spray orice as close to the
mouth as possible. Do not shake the container, be-
cause any bubbles formed may slow the release of
nitroglycerin.
3. The dose should be sprayed onto or under the
tongue by pressing the button rmly.
4. The patient’s mouth should be closed immediately
after each dose. The spray should not be swallowed
or inhaled.
Medication Safety Alert
The American Heart Association (O’Gara et al, 2013) now
recommends that if chest pain is not relieved by one sublin-
gual nitroglycerin dose within 5 minutes, the patient should
seek emergency medical attention (i.e., call 911).
402 UNIT IV Drugs Affecting Cardiovascular System

Table 24.1 Nitrates

GENERIC NAME BRAND NAME AVAILABILITY ONSET DURATION DOSAGE RANGE
isosorbide dinitrate Isordil Tablets, oral: 5, 10, 30–60 min 4–6 hr PO: 5–40 mg two to three times daily
Do not confuse Titradose 20, 30, 40 mg on empty stomach
isosorbide
dinitrate with
isosorbide
mononitrate.
isosorbide — Tablets, oral: 10, 30–60 min N/A PO: 20 mg twice daily, 7 hr apart
mononitrate 20 mg
Do not confuse — Tablets, sustained 3–4 hr 8–12 hr PO: 30–240 mg once daily; do not
isosorbide release (24 hr): crush or chew tablets
mononitrate 30, 60, 120 mg
with isosorbide
dinitrate.
nitroglycerin Nitrostat Tablets, sublingual: 1–2 min >30 min Sublingual: 0.3–0.6 mg for prophylactic
Do not confuse 0.3, 0.4, 0.6 mg use before activity that may induce
nitroglycerin with angina pectoris or at time of acute
glycerin. attack
Capsules, oral, 30–45 min 3–8 hr PO: 2.5–6.5 mg two to four times daily
sustained for prophylaxis
release: 2.5, 6.5,
9 mg
Nitro-Bid Transdermal 30 min 3 hr Topical: 0.5–2 inches of ointment using
ointment: 2% special applicator every 6 hr for
two doses, then no dose for 12 hr,
followed by two doses for 6 hr each
Nitro-Dur, Patch, transdermal 30–60 min Less than Topical: Initial 0.2–0.4 mg/hr for 12
Minitran : 0.1, 0.2, 0.3, 24 hr hr daily; titrate dose to response;
0.4, 0.6, 0.8 mg/ patient should wait 12 hr after
hr removing old patch before applying
new patch
Nitrolingual Spray, translingual 2 min 30–60 min Spray: One or two sprays onto or
Nitromist metered: 0.4 mg under tongue for acute attack;
repeat if needed in 3–5 min; may
be used prophylactically 5–10 min
before exercise
Nitroglycerin IV: 5 mg/ml in 10 1–2 min 3–5 min IV: Initial: 5 mcg/min through an infusion
IV ml vials; 25, 50, pump; adjust dosage as needed
100 mg in 250 ml
glass containers
Do not confuse.
High-alert medication.

Topical ointment administration. See Chapter 7, Fig. 7.4.
Nitroglycerin ointment is usually applied on arising in
the morning; 6 hours later the rst dose is removed
and a second dose is applied. The second dose of the
ointment is removed after 6 hours, giving a nitrate-free
period of 10 to 12 hours until the next morning.
1. Apply clean gloves before administering the oint-
ment to prevent absorbing the drug through your
skin.
2. Position the dose-measuring applicator paper with
the printed side down.
3. Squeeze the proper amount (usually 1 to 2 inches)
of ointment onto the applicator paper.
4. Place the measuring applicator paper on the skin,
ointment-side down, and spread the ointment in a
thin, uniform layer under the paper. Do not spread
beyond the paper margins. Do not massage the
ointment or rub it in. Any area without hair may be
used; however, many people prefer the chest, the
ank, or the upper arm. The lower extremities are
not used, especially if there is reduced peripheral
perfusion. (Because of the potential for skin irrita-
tion, do not shave an area to apply the medication;
instead use scissors to clip hair if needed.)
5. Help the patient to develop a site rotation sched-
ule to prevent skin irritation. Tell the patient not to
 Drugs Used to Treat Angina Pectoris CHAPTER 24
apply the ointment to an area that still shows signs
of irritation. Use of the applicator allows measur-
ing of the proper dose and prevents absorption
through the ngertips.
6. Cover the area where the patch is placed with a
clear plastic wrap and then tape the plastic wrap
in place. (Alert the patient that the medication may
discolor clothing.)
7. Perform hand hygiene before applying and after
removing gloves.
8. Close the tube tightly and store it in a cool place.
9. When terminating the use of the topical ointment,
gradually reduce the dose and frequency of appli-
cation over the course of 4 to 6 weeks.
10. When removing the ointment paper, apply clean
gloves, wipe the area with tissue to remove the
ointment, and then reapply the ointment to a dif-
ferent area at the appropriate time interval for ro-
tating sites.
Transdermal patch administration. See Chapter 7, Fig.
7.5. The transdermal patch provides a controlled release
of nitroglycerin through a semipermeable membrane
for 24 hours when it is applied to intact skin. The dosage
released depends on the surface area of the patch. The
therapeutic effect can be observed about 30 minutes af-
ter attachment, and it continues for about 30 minutes af-
ter removal. Current recommendations are to apply the
patch and leave it in place for 12 to 14 hours, followed
by a 10- to 12-hour patch-free (nitrate-free) interval. The
patch is then reapplied for another 12 to 14 hours.
1. Apply clean gloves.
2. The patch should be applied to a clean, dry, hair-
less area of skin. Do not apply the patch to shaved
areas, because skin irritation may alter drug absorp-
tion. If hair is likely to interfere with patch adhesion
or removal, then trim the hair but do not shave it.
Optimal locations for patch placement are the up-
per chest or side; the pelvis; and the inner, upper
arm. Avoid scars, skinfolds, and wounds. Rotate the
skin sites daily. (Help the patient develop a rotation
chart.)
3. Perform hand hygiene before applying and after re-
moving gloves.
4. See individual product information to determine
whether the patient’s patch can be worn while
swimming, bathing, or showering.
5. If the patch becomes partially dislodged, discard it
and replace it with a new patch.
6. Sublingual nitroglycerin may be necessary for an-
ginal attacks, especially while the dosage is being
adjusted.
7. Dispose of used patches in a place that is out of reach
of children. Discarded patches still contain enough
of the active ingredient to be dangerous to children.
Intravenous nitroglycerin administration. Intravenous
nitroglycerin is used in an acute inpatient setting (e.g.,
403
intensive care unit, cardiac telemetry unit), and it re-
quires continuous monitoring of vital signs (i.e., blood
pressure, pulse, respirations, oxygen saturation levels,
and central venous pressure).
An infusion pump must be used to monitor the
precise delivery of the infusion. The dose is titrated to
achieve the desired clinical response. Gradual wean-
ing is needed under controlled conditions to prevent a
rebound action.
This medication is never mixed with other medi-
cations and is administered only with intravenous
administration sets known as “nitro tubing,” which
are made specically for use with nitroglycerin. Most
other plastic administration sets absorb the drug. See
the manufacturer’s literature for exact directions for
preparation and administration of the drug.
Common adverse effects
Cardiovascular
Excessive hypotension. Excessive hypotension is an
extension of the nitrate’s pharmacologic activity. Other
possible adverse effects include dizziness, nausea,
ushing, and (rarely) syncope. Report these adverse
effects so that a more appropriate dosage adjustment
may be made.
Neurologic
Prolonged headache. The most common adverse ef-
fect of nitrate therapy is headache. This can range from
a mild sensation of fullness in the head to an intense
and severe generalized headache. Most patients devel-
op a tolerance within a few weeks of starting therapy.
Analgesics (e.g., acetaminophen) may be used, if need-
ed. Report these adverse effects so that a more appro-
priate dosage adjustment may be made.
Tolerance (increasing dosage to attain relief). Tolerance
to the nitrate dosages can develop rapidly, particularly
if large doses are administered frequently. Tolerance
can appear within a few days, and it may be well estab-
lished within a few weeks. The smallest dose needed
to obtain satisfactory results should be used to mini-
mize the development of tolerance. Tolerance is broken
by withdrawing the drug for a short period of time.
Drug interactions
Alcohol. Alcohol accentuates the vasodilation and
postural hypotension caused by the nitrates. Patients
should be warned that drinking alcohol while taking
nitrates may cause hypotension.
Calcium channel blockers and beta-adrenergic block-
ers. Calcium channel blockers and beta-adrenergic
blockers may signicantly lower blood pressure.
Dosage adjustments may be necessary.
Avanal, sildenal, tadalal, and vardenal. The concur-
rent use of nitrates and these agents used for erectile
dysfunction is contraindicated. These agents potentiate
the vasodilatory effects of the nitrates, which results in
a signicant drop in blood pressure that may be fatal.
404 UNIT IV Drugs Affecting Cardiovascular System
DRUG CLASS: BETA-ADRENERGIC BLOCKERS
Actions
The beta-adrenergic blockers (i.e., beta blockers) (see
Table 12.3) reduce myocardial oxygen demand by
blocking the beta-adrenergic receptors in the heart,
thereby preventing stimulation from norepineph-
rine and epinephrine that would normally cause an
increased heart rate. Beta blockers also reduce blood
pressure (see Chapter 22).
Uses
The goals of beta blocker therapy are to reduce the
number of anginal attacks, reduce nitroglycerin use,
and improve exercise tolerance while minimizing ad-
verse effects. It is recommended that a patient who is
admitted to the hospital with an acute myocardial in-
farction receive a beta blocker on arrival and be pre-
scribed a beta blocker on discharge.
All beta blockers are effective for the treatment of an-
gina pectoris, so product selection should be based on
other conditions that the patient may have (e.g., diabe-
tes, chronic obstructive airway disease, peripheral vas-
cular disease) and adherence issues. The cardioselective
agents (see Chapter 12) will have less effect on the beta-
2 receptors of the lungs and the peripheral vasculature,
thereby minimizing the adverse effects involving these
body systems. Atenolol and metoprolol are examples
of beta blockers that can be administered once daily to
minimize anginal attacks if adherence is a problem.
Dosages of beta blockers needed to control angina
are extremely patient specic; therefore therapy should
start at low doses and be increased, depending on the
patient’s needs. Optimally, exercise stress tests should
be used to determine the most appropriate dosage.
Combination therapy with nitrates and beta blockers ap-
pears to be more effective than nitrates or beta blockers
alone. Beta blockers may also be combined with long-
acting dihydropyridines. Combining verapamil or dil-
tiazem with beta blockers should be used with caution
because of potentially adverse effects on AV nodal con-
duction, heart rate, or cardiac contractility; see the dis-
cussion of these drugs in the next section of this chapter.
Therapeutic Outcomes
The primary therapeutic outcomes expected from beta
blocker therapy are as follows:
1. Decreased frequency and severity of anginal attacks
2. Increased tolerance of activities
3. Reduced use of nitroglycerin for acute anginal
attacks
Nursing Implications for Beta-Adrenergic
Blockers
Premedication assessment
1. Obtain baseline blood pressure readings with the
patient in both the supine and standing positions;
assess the pulse rate.
2. Check the patient’s history for respiratory disorders
such as bronchospasm, chronic bronchitis, emphy-
sema, and asthma.
3. Check the patient for a history of diabetes. If diabe-
tes is present, determine the patient’s baseline se-
rum glucose level before starting therapy.
See Chapter 12 for further discussion of patient edu-
cation and the nursing process associated with beta-
adrenergic blockers.
DRUG CLASS: CALCIUM CHANNEL BLOCKERS
Actions
These agents are known variously as calcium antag-
onists, calcium ion antagonists, slow channel blockers,
and calcium ion influx inhibitors. Regardless of what
they are called, they all share the ability to inhibit the
movement of calcium ions across a cell membrane.
Calcium channel blockers (Table 24.2) may be used
to treat angina pectoris by decreasing myocardial oxy-
gen demand (i.e., decreasing workload) and increasing
myocardial blood supply by dilating the coronary arter-
ies. By inhibiting smooth muscle contraction, calcium
channel blockers dilate blood vessels and decrease their
resistance to blood ow. The dilation of the peripheral
vessels reduces the workload of the heart. Coronary ar-
tery dilation improves coronary blood ow.
Uses
Although each of these agents acts by calcium ion
inhibition, there are signicant differences in clinical
use. Their clinical effects also depend on the type and
severity of the patient’s disease. The primary calcium
channel blockers used to treat angina are the long-
acting dihydropyridines (e.g., amlodipine, nicardip-
ine, nifedipine), as well as the nondihydropyridines,
diltiazem (a benzothiazepine) and verapamil (a diphe-
nylalkylamine). The overall effect of calcium channel
blockers will be the combined effects of vasodilator
and myocardial actions with reex-mediated adren-
ergic activity. Amlodipine, a potent peripheral arterial
vasodilator, reduces peripheral vascular resistance;
this may cause a reex tachycardia. Verapamil and
diltiazem also have myocardial depressant effects that
prevent tachycardia. However, they must be avoided
in patients with heart failure.
Therapeutic Outcomes
The primary therapeutic outcomes expected from the
calcium channel blockers are as follows:
1. Decreased frequency and severity of anginal attacks
2. Increased tolerance of activities
Nursing Implications for Calcium Channel
Blockers
Premedication assessment
1. Obtain baseline blood pressure readings with the
patient in both the supine and standing positions.
 Drugs Used to Treat Angina Pectoris CHAPTER 24 405

Table 24.2 Calcium Channel Blockers Used to Treat Angina Pectoris

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE
amlodipine Norvasc Tablets: 2.5, 5, 10 mg PO: Initial: 5 mg once daily; adjust over
Do not confuse Do not confuse Norvasc Oral suspension: 1 mg/ 7–14 days to maximum of 10 mg/day
amlodipine with with Altace or Vasotec. mL in 120 and 150 mL
amiloride or bottles
amiodarone.
diltiazem — Tablets: 30, 60, 90, 120 mg PO: Initial: 30 mg four times daily,
gradually increase to 180–320 mg in
three or four divided doses
— Capsules, extended release PO: Initial: 60 mg two times daily.
(12 hr) 60, 90, 120 mg Increase at 7–14 day intervals to
effective antianginal dose: 240–360
mg/day in 2 divided dosages.
Cardizem LA, Cardizem CD Tablets, sustained release PO: Initial: 120–180 mg sustained-release
(24 hr), and capsules capsule once daily; adjust as needed
(24 hr): 120, 180, 240, after 14 days
300, 360, 420 mg Maximum dose: 480 mg daily
nicardipine — Capsules: 20, 30 mg PO: Initial: 20 mg three times daily
Maximal response may require 2 wk of
therapy
Allow at least 3 days between dosage
adjustments
Maintenance: 20–40 mg three times daily
nifedipine — Capsules: 10, 20 mg PO: Initial: 10 mg three times daily; adjust
over 7–14 days to balance antianginal
and hypotensive activity
Maximum dose: 180 mg/day
Procardia XL Tablets, extended release Extended-release tablets: 30–60 mg
Do not confuse Procardia (24 hr): 30, 60, 90 mg once daily
with Provera or Peri- Maximum; extended-release tablets: 120
Colace. mg daily
verapamil — Tablets: 40, 80, 120 mg PO: Initial, immediate release: 80–120 mg
three times daily
Calan SR Tablets and capsules, PO: Initial: 180 mg once daily at bedtime
Do not confuse Calan with sustained release (24 hr): Maintenance: 120–480 mg daily
Colace. 100, 120, 180, 200, 240, Administer with food
300, 360 mg
Do not confuse.

2. Check the patient for a history of heart failure; with-
hold the drug and consult the healthcare provider if
heart failure is present.
3. Check the patient’s laboratory values for hepatotoxicity.
Availability, dosage, and administration. See Table 24.2.
See Chapter 22 for a further discussion of patient edu-
cation and the nursing process associated with calcium
channel blocker therapy.
DRUG CLASS: ANGIOTENSIN-CONVERTING ENZYME
INHIBITORS
Actions
ACE inhibitors represent a major breakthrough
in the treatment of cardiovascular disease. Their
action is more completely described in Chapter 22.
By inhibiting ACE, these drugs have significant ac-
tions on the endothelial walls of coronary arteries;
they promote vasodilation and minimize platelet
cell aggregation, thereby preventing thrombus
formation.
Uses
ACE inhibitors have been proven to reduce the inci-
dence of myocardial infarction, and they should be
used as routine secondary prevention for patients with
known CAD, particularly for patients with diabetes
mellitus without renal failure. ACE inhibitors are rec-
ommended for the treatment of patients with an acute
myocardial infarction or heart failure with left ventric-
ular systolic dysfunction.
406 UNIT IV Drugs Affecting Cardiovascular System
Therapeutic Outcome
The primary therapeutic outcome expected from the
ACE inhibitors is a reduction in the frequency of recur-
rent myocardial infarction.
Nursing Implications for Angiotensin-Converting
Enzyme Inhibitors
Premedication assessment
1. Obtain baseline blood pressure readings with the
patient in both the supine and standing positions;
assess the apical pulse.
2. Obtain a history of the patient’s bowel elimination
patterns.
3. Initiate laboratory studies as requested by the
healthcare provider (e.g., electrocardiography; re-
nal function tests such as blood urea nitrogen,
serum creatinine, and electrolyte levels; and com-
plete blood count) to serve as a baseline for future
comparison.
4. Ask if the patient has a persistent cough.
Availability, dosage, and administration. See Table 22.5
and Chapter 22 for further discussion of patient edu-
cation and the nursing process associated with ACE
inhibitor therapy.
Medication Safety Alert
The initial doses of ACE inhibitors may cause hypotension
with dizziness, tachycardia, and fainting; these adverse ef-
fects occur more commonly in patients who are also receiv-
ing diuretics. Symptoms occur within 3 hours after the rst
several doses. This effect may be minimized by discontinu-
ing the diuretic 1 week before initiating ACE inhibitor therapy.
Patients should be warned that this adverse effect may oc-
cur, that it is transient, and that they should lie down immedi-
ately if symptoms develop.
DRUG CLASS: MYOCARDIAL CELL SODIUM
CHANNEL BLOCKER
ranolazine (răn-Ō-lă-zēn)
Ranexa (răn-ĚKS-ă)
Actions
Ranolazine is a myocardial cell sodium channel block-
er. It is thought that ranolazine produces myocardial
relaxation, reducing anginal symptoms through this
mechanism, although this is uncertain. As the demand
for oxygen is reduced, the imbalance between the oxy-
gen supply and demand diminishes, thereby reducing
myocardial ischemia and angina symptoms.
Uses
Ranolazine is the rst new agent in more than 20 years
to be used to treat chronic stable angina. It is used in
combination with a dihydropyridine calcium channel
blocker (e.g., amlodipine), beta blockers, and nitrates.
Unlike other antianginal medicines, ranolazine does
not affect the blood pressure or heart rate. Because ra-
nolazine prolongs the QT interval (i.e., a potentially
life-threatening event), it should only be used to treat
angina in patients who have not achieved an anti-
anginal response with other agents or in those who
cannot tolerate the adverse effects of the other medi-
cines. Ranolazine will not reduce the symptoms of an
acute anginal episode.
Therapeutic Outcomes
The primary therapeutic outcomes expected from ra-
nolazine therapy are as follows:
1. Reduced frequency and severity of anginal attacks
2. Increased tolerance of activities
3. Reduced use of nitroglycerin during acute anginal
attacks
Nursing Implications for Ranolazine
Premedication assessment. Initiate laboratory studies
as requested by the healthcare provider (e.g., electro-
cardiography; renal function tests such as blood urea
nitrogen, serum creatinine, and electrolyte levels; and
complete blood count) to serve as a baseline for future
comparison.
Availability. PO: 500- and 1000-mg tablets, extended
release (12 hours).
Medication Safety Alert
It is recommended that ranolazine not be taken concurrently
with other medicines that are known to prolong the QT inter-
val, such as quinidine, dofetilide, sotalol, erythromycin, and
antipsychotics (e.g., thioridazine, ziprasidone). Baseline and
follow-up electrocardiograms should be obtained to evaluate
the effects of these drugs on the patient’s QT interval.
Dosage and administration. PO: 500 mg twice dai-
ly; dosage may be increased to 1000 mg twice daily.
Ranolazine may be taken with or without food. Tablets
should be swallowed whole: do not crush, break, or
chew tablets.
Common adverse effects
Neurologic
Dizziness and headache. These adverse effects are
usually mild, occurring in fewer than 5% of patients.
Patients should not operate an automobile or machin-
ery or engage in activities that require mental alertness
until it is known how they will react to the medicine.
Patients should withhold medicine and contact their
healthcare provider if they experience palpitations or
fainting spells while taking ranolazine.
Gastrointestinal
Constipation, nausea. These adverse effects are usu-
ally mild, occurring in fewer than 6% of patients.
 Drugs Used to Treat Angina Pectoris CHAPTER 24 407

Drug interactions with ranolazine. If they are used concurrently, monitor

Drugs that enhance therapeutic and toxic effects. Azole-
type antifungals (e.g., ketoconazole, uconazole), mac-
rolide antibiotics (e.g., erythromycin, clarithromycin),
grapefruit juice, verapamil, diltiazem, and protease
inhibitors (e.g., ritonavir) signicantly increase the
serum levels and potential toxicity of ranolazine. In
general, these agents should not be used concurrently
patients closely for the development of dizziness, nau-
sea, weakness, loss of muscle strength, constipation,
and headache.
Statins, tacrolimus, sirolimus. Ranolazine inhibits the
metabolism of HMG-CoA inhibitors (statins), tacroli-
mus, and sirolimus. Reduce the dosage of these agents
per manufacturers’ recommendations.

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points
ESSENTIAL UNRELATED
• CAD is the leading cause of disability, socioeconomic loss, ASSESSMENT ASSESSMENT
and death in the United States. DATA DATA
• Angina pectoris is the rst clinical indication of underlying
Pain occurring with
CAD in many patients.
exercise
• The frequency of anginal attacks can be reduced by
Shortness of breath with
controlling risk factors and avoiding precipitating causes
chest pain
(e.g., stress).
• Medicines such as nitrates, beta blockers, calcium channel Periods of insomnia
blockers, and ranolazine can reduce the frequency of Indigestion or nausea
anginal attacks. present
• Nurses can play a signicant role in public education Family history for heart
efforts, monitoring for noncompliance, monitoring patients’ disease
responses to therapy, and encouraging patients to make Feeling faint or
changes in their lifestyles to reduce the severity of angina lightheaded
pectoris.
Unable to remember
recent events
Additional Learning Resources Reporting palpitations
SG Go to your Study Guide for additional Review Questions Smoking history
for the NCLEX® Examination, Critical Thinking Clinical Situa-
Reporting muscle cramps
tions, and other learning activities to help you master this chap-
in lower legs
ter content.

Go to your Evolve website (https://evolve.elsevier.com/Clayton) Objective: Discuss angina pectoris and identify assessment data
for additional online resources. needed to evaluate an anginal attack.
NCLEX item type: Matrix
Clinical Judgment and Next-Generation NCLEX® Exami- Cognitive skill: Evaluate cues
nation-Style Questions
2. Choose the most likely option for the information missing from the
The following questions are typical of the NCLEX examination following sentence by selecting from the list of options provided.
and include both NGN (Next Generation) and traditional ques- The nurse discussed with the patient in the sce-
tions. See Chapter 1 for further information regarding question nario that there are different types of angina
types. and stated that __________1____________ oc-
curs with __________2__________; compared with
Scenario ________1______________, which occurs with
________2____________.

A patient seen in the emergency department came in com-

plaining of pain in the chest radiating down the left arm. It start- OPTION 1 OPTION 2
ed while the patient was mowing the lawn.
palpitations vasodilation
1. The patient in the scenario was diagnosed with angina and the chronic stable angina dysrhythmias
nurse was evaluating the anginal attack. Which assessment data unstable angina a xed obstruction
are needed to evaluate the patient? Indicate with an X which data variant angina new thrombus formation
are essential and which are unrelated to evaluating an anginal
attack.
408 UNIT IV Drugs Affecting Cardiovascular System

Objective: Differentiate between chronic stable angina and NCLEX item type: Cloze
unstable angina. Cognitive skill: Recognize cues
NCLEX item type: Cloze
Cognitive skill: Recognize cues 5. The nurse administering the calcium channel blocker amlodipine
(Norvasc) explained to the patient what effect the drug has on
3. After the administration of sublingual nitroglycerin to the patient in the heart. Which statement is appropriate for the nurse to make?
the scenario with angina, the nurse explained to the patient which (Select all that apply.)
of the following adverse effects may be experienced? (Select all 1. “This drug will prevent angina by dilating the coronary
that apply.) vessels.”
1. Drowsiness 2. “This drug will prevent angina by blocking the receptors
2. Nausea in the heart that increase the heart rate.”
3. Lightheadedness 3. “This drug will prevent angina by blocking the movement
4. Vasoconstriction of calcium ions, which in turn decreases oxygen demand
5. Headache on the heart.”
6. Pain control 4. “This drug will prevent angina by blocking the conversion
7. Syncope of angiotensin I to angiotensin II, which is a potent
8. Shortness of breath vasoconstrictor.”
Objective: Describe the actions of the drug classications used to 5. “This drug will prevent angina by blocking the sodium
treat angina and the adverse effects. channels in the myocardial cells.”
NCLEX item type: Extended multiple response Objective: Describe the actions and the adverse effects of the drug
Cognitive skill: Recognize cues classications used to treat angina.
NCLEX item type: Multiple response
4. Choose the most likely option for the information missing from the Cognitive skill: Application
following sentence by selecting from the list of options provided.
6. The nurse was discussing risk factor management with the patient
The patient in the scenario diagnosed with angina will in the scenario who was admitted with chest pain and realized
have their symptoms controlled with medications such as that the patient needed further education after he made which
___________1____________ and _________2________, statement?
which are classied as _______1_________ and
___________2__________, respectively. 1. “I know that I should quit smoking. I have been meaning
to for a while, but this really hits home that I need to.”
2. “I think maybe I should learn to cook because my wife
OPTION 1 OPTION 2 always insists on meat and potatoes and gravy; we have
such heavy meals.”
isosorbide dinitrate • HMG-CoA reductase 3. “I walk every day with my dog for at least 20 minutes and
inhibitor longer in nice weather.”
lisinopril • angiotensin receptor 4. “I gure I don’t need to do anything different; I can just
blocker take my pills for this.”
metoprolol • ACE inhibitor
Objective: Discuss the risk factor management and healthy
atorvastatin • beta-adrenergic blocker
lifestyle changes that are taught to prevent disease progression and
losartan • nitrates
myocardial infarction or death.
NCLEX item type: Multiple choice
Objective: Describe the actions and the adverse effects of the drug Cognitive skill: Comprehension
classications used to treat angina.
Drugs Used to Treat Peripheral Vascular Disease
Objectives
1. Describe the baseline assessments needed to evaluate a
patient with peripheral vascular disease.
2. Identify specic measures that the patient can use
to improve peripheral circulation and prevent the
complications of peripheral vascular disease.
Key Terms
peripheral arterial disease (p. 409) paresthesias (păr-ĕs-THĒ-zē-ăz)
intermittent claudication (ĭn-tĕr-MĬT- (p. 409)
ĕnt klaw-dĭ-KĀ-shŭn) (p. 409) Raynaud disease (rā-NŌZ) (p. 409)
PERIPHERAL VASCULAR DISEASE
Th rm peripheral vascular disease can b applid  a
variy f illnsss assciad wih bld vssls u-
sid h har, bu i gnrally rfrs  disass f h
bld vssls f h arms and lgs (h xrmiis).
Ths illnsss can b subdividd in w yps basd
n arrial r vnus rigin: (1) peripheral arterial dis-
ease and (2) vnus disrdrs, such as acu dp vin
hrmbsis (s Chapr 26). Th arrial disrdrs ar
subdividd in hs ha rsul frm arrial narrw-
ing and cclusin (bsruciv) and hs causd by
arrial spasm (vasspasic).
Th ms cmmn frm f priphral arrial dis-
as is bsruciv arrial disas rsuling frm ah-
rsclric plaqu frmain, wih narrwing f h
lwr ara and h majr arris ha prvid circula-
in  h lgs. As wih ahrsclrsis f h crnary
arris, h risk facrs ha play an impran rl in
h dvlpmn f his bsruciv disas ar high
lvls f lw-dnsiy lipprin (LDL) chlsrl,
hyprnsin, cigar smking, lw lvls f high-
dnsiy lipprin chlsrl, and diabs mllius.
Pains nd  rmain fr f sympms unil hr
is signican narrwing (75%  90%) in ky lcains
f h majr arris and arrils f h lgs. Th ypi-
cal pain parn dscribd is n f aching, cramping,
ighnss, r waknss ha ccurs during xrcis.
Th primary pahphysilgy is bsrucin f bld
w hrugh h arris, rsuling in ischmia  h
issus supplid by hs arris. A rm cmmnly
applid  his cndiin is intermittent claudication;
i manifss as pain scndary  lack f xygn 
h muscls during xrcis. During h arly sags
25
https://evolve.elsevier.com/Willihnganz
3. Identify treatment goals and what to expect when
peripheral vasodilating agents are administered.
4. Explain why hypotension and tachycardia occur frequently
with the use of cilostazol.
vasospasm (VĂ-zō-spă-zĭm) (p. 409)
f sympms, h pain nds rlif by spping h
xrcis fr a fw minus. Wihu ramn, as h
disas prgrsss vr im, h arris bcm b-
srucd, rsuling in hrmbsis and h pnial fr
gangrn. Addiinal sympms ha dvlp ar pain
a rs, numbnss, and paresthesias (numbnss wih a
ingling snsain). Th disas is fn accmpanid
by incrasd bld viscsiy. Physical ndings n h
lwr xrmiis ar rducd arrial pulsains n
palpain; syslic bruis vr h invlvd arris;
waxy, pal, and dry skin; a lwr mpraur f h
skin f h xrmiy; dma; and numbnss  snsa-
in (Fig. 25.1).
Priphral vascular disas causd by arrial va-
sspasm is als knwn as Raynaud disease, namd
afr h man wh rs dscribd h illnss in 1862.
I is unfruna ha, mr han 150 yars lar, h
pahphysilgy and ramn f his cndiin ar
sill n wll dnd. Raynaud disas is classid as
ihr primary, in which h caus is unknwn, r as
scndary, in which hr cndiins cnribu  h
sympms. Scndary causs ar frqun xpsur 
cld wahr, bsruciv arrial disas, ccupainal
rauma (.g., pnumaic hammr usrs, pianiss), and
crain drugs (.g., ba blckrs, imipramin, nicin,
brmcripin, vinblasin, clnidin). Hrdiy may
als play a rl. Th ns f Raynaud disas is usu-
ally during h nag yars  h 40s, and i ccurs
fur ims mr fn in wmn.
Raynaud disas is hugh  b causd by vaso-
spasm (i.., vascnsricin f bld vssls) and
subsqun ischmia f h arris f h skin f h
hands, ngrs, and smims s. Th physilgic
409
410 UNIT IV Drugs Affecting the Cardiovascular System
Fig. 25.1 Example of an extremity with poor circulation demonstrating
waxy, pale, and dry skin. (From Dinulos JGH. Habif’s Clinical
Dermatology. 7th ed. St. Louis: Elsevier; 2021.)
mchanisms ha riggr h vasspasm ar unknwn.
Suddn cldnss applid  h xrmiy, such as cld
war, can induc an aack. Th signs and sympms
assciad wih Raynaud disas ar numbnss, in-
gling, a sns f skin ighnss in h affcd ara,
and blanching f h skin bcaus f suddn vascn-
sricin fllwd by cyansis. As h aack subsids,
vasdilain causs a rdnss, r rubr,  h pal
skin. Th skin appars nrmal xcp during spasm.
During h arly yars f h illnss, nly h ngrips
f bh hands ar invlvd. Hwvr, as h disas
prgrsss, h skin n h hands is als affcd by h
arrispasm.
TREATMENT OF PERIPHERAL VASCULAR
DISEASE
Th gals f ramn fr priphral arrial disas
ar rvrsal f h prgrssin f h ahrsclrsis,
imprvd bld w, pain rlif, and prvnin f
skin ulcrain and gangrn. An impran cncp
ha mus b srssd  ms pains is ha hr dis-
ass ha hy may hav (.g., diabs, hyprnsin,
crnary har disas, dyslipidmia) ar all inr-
rlad. Cnrl f di, high bld prssur, smking,
wigh, and diabs will signicanly hlp all hs
disass.
Implmnain f h Amrican Har Assciain’s
di—an aing plan fr halhy Amricans—can ar-
rs h prgrssin f ahrsclrsis. Lipid-lwring
agns can b sard if di mdicains d n suc-
cssfully ra h hyprchlsrlmia. A daily x-
rcis prgram (usually walking) can signicanly
imprv cllaral bld circulain arund aras f
bsrucin and rduc h frquncy f inrmin
claudicain. Prpr f car (.g., kping f warm
and dry, waring prprly ing shs), spcially if
h pain has diabs, is als xrmly impran
 prvn ulcraiv cmplicains. Ohr nnphar-
maclgic ramns fr imprving bld w  h
xrmiis includ aviding cld, lvaing h had
f h bd by 12  16 inchs, and arrial angiplasy
and surgry.
Ms vasspasic aacks f Raynaud disas can
b sppd by aviding cld mpraurs, minal
srss, bacc, and drugs ha ar knwn  induc a-
acks. Kping h hands and f warm wih glvs
and scks and using fam wraparunds whn han-
dling icd bvrags can rduc xpsur  cld.
DRUG THERAPY FOR PERIPHERAL
VASCULAR DISEASE
ACTIONS
As h causs f priphral vascular disas hav cm
 b br undrsd, clinical sudis hav dnd
which pharmaclgic hrapis ar ruly succssful. I
has bn shwn ha nnpharmaclgic ramn f
priphral arrial disas is subsanially mr suc-
cssful in raing h undrlying pahlgic cndiin.
Plal aggrgain inhibirs ar h primary pharma-
clgic ramn f priphral arrial disas. Aspirin
and clpidgrl ar apprvd fr ramn f priphr-
al arrial disas (s Chapr 26). Anhr plal ag-
grgain inhibir, cilsazl, is apprvd fr h ra-
mn f inrmin claudicain causd by vasspasm.
USES
Cilsazl is apprvd by h US Fd and Drug
Adminisrain fr h ramn f inrmin clau-
dicain causd by chrnic cclusiv arrial disas
f h limbs. In addiin  cilsazl, classs f drugs
ha hav bn smwha succssful in raing inr-
min claudicain ar calcium-channl blckrs, ad-
rnrgic anagniss, anginsin-cnvring nzym
(ACE) inhibirs, and dirc vasdilars.
Th hr calcium-channl blckrs sudid fr h
ramn f inrmin claudicain ar diliazm,
vrapamil, and nifdipin. Of h hr, nifdipin has
had h gras succss in rducing h frquncy f
vasspasic aack in abu w-hirds f pains.
Adrnrgic anagniss (.g., prazsin, rsrpin,
mhyldpa) hav bn usd fr many yars fr h
ramn f Raynaud disas. Unfrunaly, ra-
mn has bn nly mdraly succssful, and many
advrs ffcs ar assciad wih h us f hs
drugs.
Th ACE inhibirs caus an incras in bradykinin,
a pn vasdilar. Cappril has bn h ms x-
nsivly sd, and i has bn shwn  rduc h
frquncy and svriy f aacks.
Fr mr han 50 yars, nirglycrin, a dirc va-
sdilar, has bn applid as an inmn bas  h
hands f pains wih Raynaud disas. Th ramn
rducs h frquncy and svriy f aacks, bu h
advrs ffcs f dizzinss, hadach, and psural
hypnsin limi is us.
 Drugs Used to Treat Peripheral Vascular Disease CHAPTER 25
NURSING IMPLICATIONS FOR PERIPHERAL
VASCULAR DISEASE THERAPY
Assessment
A baslin assssmn f h pain shuld b cm-
pld ha includs h fllwing lmns fr valu-
aing h hisry and dgr f xygnain xising
in h xrmiis. Subsqun rgular assssmns
shuld b prfrmd fr cmparisn and analysis f
hrapuic ffcivnss r lack f rspns  any
ramns iniiad.
History of risk factors. Drmin h pain’s ag,
gndr, and rac and bain a family hisry f h in-
cidnc f sympms f priphral vascular disas,
hyprnsin, and cardiac disas.
Impotence. If h pain is mal, has h xprincd
impnc?
Hypertension. Tak h pain’s bld prssur in si-
ing and supin psiins daily. Ask abu mdicains
ha hav bn prscribd. Ar h mdicains bing
akn rgularly? If n, why n?
Smoking. Obain a hisry f h numbr f cigars
r cigars ha h pain smks daily; includ hr
surcs f nicin, such as chwing bacc and r-
placmn hrapy. Hw lng has h prsn smkd?
Has h prsn vr rid  sp smking? Ask if h
pain undrsands h ffc f smking n h vas-
cular sysm. Hw ds h individual fl abu md-
ifying hir smking habi?
Dietary habits
• Obain h pain’s diary hisry. Ask spcic
qusins  bain infrmain abu fds an
ha ar high in fa, chlsrl, rnd carbhy-
dras, and sdium. Using a calri cunr, ask
h prsn  sima h numbr f calris
an pr day. Hw much ma, sh, and pul-
ry is an daily (siz and numbr f srvings)?
Esima h prcnag f al daily calris pr-
vidd by fas.
• Discuss fd prparain (.g., bakd, brild,
frid). Hw many srvings f fruis and vgabls
ar an daily? Wha yps f ils and fas ar usd
in fd prparain? S a nuriin x fr furhr
diary hisry qusins.
• Wha is h frquncy and vlum f alchlic bv-
rags cnsumd?
Glucose intolerance. Ask spcic qusins abu
whhr h individual currnly has r has vr had
an lvad srum glucs (bld sugar) lvl. If ys,
wha diary mdicains hav bn mad? Hw
succssful hav hy bn? Wha mdicains ar b-
ing akn fr h lvad srum glucs lvl (.g.,
ral hypglycmic agns, insulin)?
411
Elevated serum lipid levels. Find u whhr h pa-
in is awar f having lvad lipid, riglycrid, r
chlsrl lvls. If any f hs lvls ar lvad,
wha masurs has h pain rid fr rducin and
wha ffc hav h inrvnins had n h bld
lvls during subsqun xaminains? Rviw any
labrary daa availabl (.g., LDL, vry-lw-dnsiy
lipprin, livr funcin ss, cling im).
Leg ulcers. Has h individual dvlpd any slw-
-hal r nnhaling srs? This wuld indica pr
circulain.
Obesity. Wigh h pain. Ask abu any rcn
wigh gains r lsss and whhr i was inninal
r uninninal.
Psychomotor functions
Type of lifestyle. Ask h pain  dscrib hir xr-
cis lvl in rms f amun (.g., walking hr blcks),
innsiy (.g., hw lng ds i ak  walk hr
blcks?), and frquncy (.g., walking vry hr day).
Is h pain’s jb physically dmanding r sdnary?
Psychological stress. Hw much srss ds h in-
dividual sima having in hir lif? Hw ds h
individual cp wih srssful siuains a hm and
a wrk?
Assessment of tissue
Oxygenation. Obsrv h clr f ach hand, ngr,
lg, and f; rpr cyansis r rddish-blu aras.
Ds h pain hav dpndn cyansis (cyansis
whn h lgs ar in h dpndn psiin)? Examin
h skin f h xrmiis fr any signs f ulcrain.
Temperature. Fl h mpraur in ach hand, n-
gr, lg, and f. Rpr any palnss r cldnss.
(Note: Ths sympms f pr circulain will b in-
crasd if h limb is lvad abv h lvl f h
har.)
Edema. Assss, rcrd, and rpr dma and is
xn, and drmin whhr i is rlivd r un-
changd whn h limb is dpndn.
Peripheral pulses. Palpa and rcrd h fmral,
pplial, drsal and ibial pdal pulss (Fig. 25.2) a
las vry 4 hurs in any limb in which circulary
impairmn is fund. Cmpar ndings amng h
xrmiis and rpr diminishd r absn pulss
immdialy. Whn pulss ar difcul  palpa r
absn, a Dpplr ulrasund dvic may hlp dr-
min priphral bld w.
Limb pain. Assss pain in h pain carfully. Pain
during xrcis ha is rlivd by rs may b causd
by claudicain. Cnvrsly, pain whn h pain is
412 UNIT IV Drugs Affecting the Cardiovascular System
Fig. 25.2 Assessing for a peripheral pulse. (From Perry AG, Potter
PA, Ostendorf W. Nursing Interventions and Clinical Skills. 6th ed. St.
Louis: Mosby; 2016.)
a rs may rsul frm suddn bsrucin by a hrm-
bus r an mblus. Chck h apprhnsin lvl f
h pain, palpa priphral pulss, bain dails f
ns and lcain f pain, and vial signs. Unil h
saus f h pain’s limb pain is sablishd, hav h
pain rmain n bd rs and adminisr an analgsic
if rdrd. Nify h pain’s halhcar prvidr f
changs in cndiin.
Implementation
• Prpar h pain fr diagnsic ss (.g., ulra-
sngraphy, puls vlum rcrdings, sgmnal
limb prssur, xrcis sing) and pssibl inva-
siv prcdurs, such as arrigraphy.
• D n plac pillws in h pplial spac r x
h kn rs n h pain’s bd. Us a cradl r
fbard  prvn h bd shs frm cnsric-
ing h pain’s circulain.
• Always chck wih h halhcar prvidr bfr
iniiaing any lvain f h pain’s xrmiis.
This acin is cnraindicad in pains wih ar-
rial insufcincy.
• Prfrm baslin assssmns f issu prfusin
(.g., skin mpraur, priphral pulss) a inr-
vals apprpria  h pain’s saus (a las v-
ry 4 hurs).
• Implmn pain managmn masurs.
Patient Education
Prming issu prfusin
• Tach h pain slf-car masurs ha prm
priphral circulain.
• Smking causs vascnsricin f h bld vs-
sls. Thrfr ncurag a drasic rducin in, and
prfrably al absinnc frm, smking. Includ
infrmain abu smking cssain and availabl
suppr rsurcs.
• Encurag pains  war nhing ha cnsrics
priphral bld w (.g., igh-ing ankls,
scks, garrs). Tll h pain n  lva h x-
rmiis abv h lvl f h har wihu spcif-
ic rdrs frm h halhcar prvidr  d s. Th
halhcar prvidr may rdr h pain’s had f
bd  b lvad a nigh.
• Miculus f and hand car is ssnial. Tach h
pain prpr slf-car f h limbs, including vi-
sual inspcin chniqus, and xplain hw  ak
fmral, pplial, and pdal pulss.
• Srss h nd fr h pain  inspc h xrmi-
is fr pssibl skin brakdwn r signs f infc-
in. Th pain shuld nify h halhcar pr-
vidr immdialy f suddn changs in clr, such
as mling r a mr purplish clr.
• Aras f disclrain in nails, cracking f h
skin, and calluss r blisrs n h xrmiis
rquir cmpl fllw-up. Lisn  h pa-
in’s dscripin f any changs ha hav bn
nd. Tll h pain ha ging barf can b
dangrus bcaus f h pnial fr injuris 
h f.
• Cld mpraurs will incras pain r dcras
snsains in h xrmiis. H ubs r h shw-
rs may caus addiinal vasdilain ha adds 
h ffcs f any vasdilars h pain is aking.
Bcaus f h pssibl dcras in snsain in h
xrmiis, ncurag h pain  s h war
mpraur bfr immrsing h hands r f.
Afr bahing, gnly pa (i.., d n vigrusly
rub) h f and hands  dry hm.
• T avid skin brakdwn, h pain shuld alr-
na pairs f shs  allw fr hrugh drying
bwn warings, chang scks r hs daily, and
avid rubbr-sld shs.
• Th pain shuld avid sanding r siing fr pr-
lngd prids. Pains wh mus si fr xndd
prids mus hav a prprly ing chair. Th sa
shuld b f h crrc dph s ha n prssur
is xrd n h pplial spac. Encurag h pa-
in n  si wih kns r ankls crssd and 
ak frqun shr braks fr walks. Furhrmr,
hs wh mus sand fr lng prids shuld sk
u asks f h jb ha can b prfrmd whil si-
ing in a prprly ing chair r hr alrnaivs.
Psychomotor functions
• Maximum mbiliy shuld b mainaind. Dvis
a daily aciviy plan ha includs walks and usu-
al aciviis f daily living, such as shpping and
huswrk.
• Pain managmn and h psychlgical aspcs
f daling wih a prlngd illnss wih prsisn
sympms ar majr challngs fr bh h pain
and h nurs (s Chapr 19).
• Envirnmn
During prids f xpsur  cld mpraur, h
pain shuld war svral layrs f lighwigh
clhing. Cauin shuld b xrcisd during xpsur
 Drugs Used to Treat Peripheral Vascular Disease CHAPTER 25
 h cld  avid frsbi. Bcaus f dcrasd sn-
sain in h xrmiis, frsbi can ccur wihu
h pain’s awarnss.
Nutritional aspects
• Diary ducain is srngly indicad fr h ra-
mn f priphral vascular disas. I is paricular-
ly impran  cnrl bsiy and chlsrl and
riglycrid lvls.
• Whn ulcrains ar prsn, ncurag a high-
prin di wih adqua inak f viamins 
prm h haling prcss.
• Unlss hr mdical cndiins cnraindica, in-
sruc h pain  drink igh 8-unc glasss f
war daily  prm adqua hydrain f bdy
issus. Mainaining bld vlum will hlp rduc
priphral vascnsricin. Chck wih h halh-
car prvidr rgarding rcmmndains fr uid
r caffin rsricin.
Medication regimen
• Crain mdicains fr h ramn f priphral
vascular disas caus dilain f bld vssls. As a
rsul, rhsaic hypnsin may ccur. Tach h
pain  ris slwly frm siing r lying psiins,
adjus balanc fr sabiliy, x h lg muscls, and
hn prcd wih mvmn.
• Tach h pain  ak and rcrd hir wn bld
prssur.
• Adminisr prscribd mdicains, and cnsul
a halhcar prvidr bfr discninuing any
mdicains.
Fostering health maintenance
• Thrughu h curs f ramn, discuss mdi-
cain infrmain and xplain hw h mdicain
will bn h pain.
• Drug hrapy is n a al sluin fr ahrscl-
rsis. Th pain may n b cmmid  h lif-
syl changs ndd  cnrl h mdiabl as-
pcs f h disas. Ofn, sing shr-rm gals
 cnrl h pain and nding hr inrvnins
ha will allw h pain  viw ffrs psiiv-
ly will hlp ncurag prmann adpin f h
ndd changs.
• Pains wh ar unrspnsiv  lifsyl mdi-
cains and drug hrapy may rquir surgical in-
rvnins  rsablish bld w  h affcd
ara. Prcdurs such as bypass grafing, ndarr-
cmy, r angiplasy may b apprpria. Failur
 rsablish bld w  an xrmiy may rsul
in ampuain.
• Prvid h pain and signican hrs wih im-
pran infrmain cnaind in h spcic drug
mngraphs fr h drugs prscribd. Addiinal
halh aching and nursing inrvnins fr cm-
mn and srius advrs ffcs ar dscribd in
ach drug mngraph.
413
• Sk cprain and undrsanding f h fl-
lwing pins s ha mdicain cmplianc is
incrasd: nam f mdicain; dsag, ru, and
ims f adminisrain; and cmmn and srius
advrs ffcs.
Patient self-assessment. Enlis h pain’s hlp
wih dvlping and mainaining a wrin rcrd
f mniring paramrs (.g., clr f limb, pain
in limb, mpraur and pulss in limb, amun f
dma prsn). S h Pain Slf-Assssmn Frm
fr Cardivascular Agns n h Evlv wbsi.
Cmpl h Prmdicain Daa clumn fr us as a
baslin  rack h pain’s rspns  drug hra-
py. Ensur ha h pain undrsands hw  us h
frm, and insruc h pain  bring h cmpld
frm  fllw-up visis. During fllw-up visis, fcus
n issus ha will fsr adhrnc  h hrapuic
inrvnins prscribd.
DRUG CLASS: PLATELET AGGREGATION INHIBITOR
cilostazol (sī-LŌ-stă-zŏl)
Actions
Cilsazl is a slciv inhibir f cllular cyclic ad-
nsin mnphspha (cAMP) phsphdisras
3. Supprssin f his nzym causs incrasd lvls
f cAMP, rsuling in vasdilain and inhibiin f
plal aggrgain. Ohr mchanisms in addiin 
vasdilain ar hugh  play a rl bu ar n fully
knwn a his im.
Uses
Cilsazl is apprvd fr h ramn f inrmin
claudicain. Cilsazl hrapy shuld b cnsidrd
an adjunc —n a rplacmn fr—smking cssa-
in, wigh lss, xrcis hrapy, surgical bypass, r
rmval f arrial bsrucins in h ramn f p-
riphral vascular disas.
Medication Safety Alert
Cilostazol should not be used to treat patients with heart fail-
ure of any severity.
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm ci-
lsazl is singular imprvd issu prfusin wih a
rducd frquncy f pain, imprvd lranc  x-
rcis, and imprvd priphral pulss.
Nursing Implications for Cilostazol
Premedication assessment
1. Assss h pain fr h prsnc f dizzinss r
hadach.
414 UNIT IV Drugs Affecting the Cardiovascular System
2. Obain a baslin assssmn f h dgr f pain
prsn and any sympms f priphral vascular
disas.
3. Ask h pain spcically abu any cardiac symp-
ms, ppic ulcr disas, r har failur. Rpr
hs  h halhcar prvidr if hy ar prsn.
Availability. PO: 50- and 100-mg abls.
Dosage and administration. PO: 100 mg wic daily
akn 30 minus bfr r 2 hurs afr brakfas
and dinnr. Sympmaic rlif may sar wihin 2 
4 wks, bu ramn shuld b cninud fr a las
12 wks  achiv maximum fcacy.
Medication Safety Alert
Do not administer cilostazol to patients with heart failure.
Phosphodiesterase inhibitors have been reported to signi-
cantly worsen heart failure.
Common adverse effects
Gastrointestinal
Dyspepsia, diarrhea. Dysppsia ccurs in 6% f pa-
ins and diarrha ccurs in 19% f pains. Ths
advrs ffcs ar usually mild, and hy nd  r-
slv wih cninud hrapy. Encurag h pain
n  discninu hrapy wihu rs cnsuling h
halhcar prvidr.
Neurologic
Dizziness, headache. Cnral nrvus sysm disur-
bancs characrizd by dizzinss ccur in abu 10%
f pains. Hadach may ccur in 34% f pains,
and i may b svr nugh  caus h discninu-
ain f hrapy. Ths advrs ffcs ar usually
mild, and hy nd  rslv wih cninud hrapy.
Prvid fr pain safy during pisds f dizzinss.
Encurag h pain  si r li dwn if fling fain.
Encurag h pain n  discninu hrapy wih-
u rs cnsuling h halhcar prvidr.
Serious adverse effects
Cardiovascular
Chest pain, palpitations, dysrhythmias, shortness of
breath. Wihu causing undu alarm, srngly ncur-
ag h pain  sk h halhcar prvidr’s an-
in fr furhr valuain.
Drug interactions
Drugs that enhance toxic effects: diltiazem, erythromy-
cin, omeprazole, uconazole, uvoxamine, verapamil, keto-
conazole, grapefruit juice. Ths subsancs will inhibi
h mablism f cilsazl. If cilsazl hrapy is
ncssary fr pains wh ar alrady rciving any
f h prcding drugs, h saring ds f cilsazl
shuld b half f h nrmal saring ds. Mnir
pains clsly fr an incrasd incidnc f advrs
ffcs.
 Drugs Used to Treat Peripheral Vascular Disease CHAPTER 25 415

Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions

Key Points 2. The nurse explained to the patient in the scenario about the
diagnosis of claudication and peripheral vascular disease and
• Peripheral vascular disease is a cause of signicant what can be done for this condition. Which is an appropriate
morbidity in the United States. Major treatable causes of statement by the nurse?
peripheral vascular disease are hypertension, cigarette
1. “There is very little that we can do to impact this disease;
smoking, and atherosclerosis.
you will just have to learn to live with it.”
• The most cost-effective and successful forms of treatment 2. “We have found that most patients who have this
are smoking cessation, weight reduction, exercise, and condition are taught ways to promote circulation and
dietary modication. what to avoid in order to prevent vasoconstriction.”
• Patients should be fully informed about the signicance of 3. “It is recommended that you have a surgical intervention
peripheral vascular disease, the potential complications to unblock your blood vessels prior to trying any drug
of not participating in lifestyle modication, and the use of therapy.”
drug therapy. 4. “Medications are the only way to improve circulation.”
Objective: Identify specic measures that the patient can use to
Additional Learning Resources improve peripheral circulation and prevent the complications of
SG Go to your Study Guide for additional Review Questions peripheral vascular disease.
NCLEX item type: Multiple choice
for the NCLEX® Examination, Critical Thinking Clinical Situa-
Cognitive skill: Comprehension
tions, and other learning activities to help you master this chap-
ter content. 3. The nurse teaching the patient in the scenario about ways to
prevent vasospasms associated with Raynaud disease includes
Go to your Evolve website (https://evolve.elsevier.com/Willihng which of these instructions? (Select all that apply.)
anz) for additional online resources.
1. Avoid holding cold beverages
2. Avoid handling hot beverages
Clinical Judgment and Next-Generation NCLEX® Exam-
3. Keep hands and feet warm with gloves and socks
ination-Style Questions The following questions are typical of
4. Limiting the amount of uids and calories daily
the NCLEX exam and include both NGN (Next Generation) and
5. Avoid smoking and emotional stress when possible
traditional questions. See Chapter 1 for further information re-
garding question types. Objective: Identify specic measures that the patient can use to
improve peripheral circulation and prevent the complications of
peripheral vascular disease.
Scenario
NCLEX item type: Multiple response
A patient recently diagnosed with Raynaud disease came into Cognitive skill: Application
an ambulatory clinic with symptoms of progressive numbness
4. Choose the most likely option for the information missing from the
and tingling on the lower extremities. The healthcare provider
statements below by selecting from the list of options provided.
ordered an arteriography to be performed and the results in-
dicated that the patient has signicant peripheral vascular dis-
The nurse explaining to the patient in the scenario who was being
ease causing the symptoms of claudication.
started on cilostazol effects to watch for and why by stating that the side
1. The nurse performing a baseline assessment on the patient in the effects of ________1__________ and ________1____________
scenario with peripheral vascular disease will include which of the are frequently experienced when starting on cilostazol because
following? (Select all that apply.) the drug acts by _____________2_______________ and
_____________2______________.
1. Checking for renal disease
2. Obtaining a pain rating
3. Evaluating the peripheral pulses
4. Checking the temperature of extremities OPTION 1 OPTION 2
5. Evaluating the level of psychological stress bradycardia • decreases the
6. Taking vital signs concentration of
7. Inquiring about any smoking brinogen in the blood
8. Monitoring pulmonary function tests tachycardia • prevents the aggregation
9. Checking the skin for possible breakdown
of red blood cells
Objective: Describe the baseline assessments needed to evaluate hypertension • causing vasodilation by
a patient with peripheral vascular disease. selectively inhibiting cAMP
NCLEX item type: Extended multiple response hypotension • inhibits platelet
Cognitive skill: Application aggregation
416 UNIT IV Drugs Affecting the Cardiovascular System

Objective: Explain why hypotension and tachycardia occur 5. The nurse educating a patient with peripheral vascular disease on
frequently with the use of cilostazol. the goals of therapy recognizes the need for further education after
NCLEX item type: Cloze the patient makes which statement?
Cognitive skill: Recognize cues 1. “I understand that I will need to keep walking to help
4. The nurse teaches a patient with any venous circulation disorder maintain my circulation.”
that the best way to prevent venous stasis and increase venous 2. “I realize I will have to eat more fruits and vegetables and
return would be to what? eliminate the fried foods to decrease calories provided by
fats.”
1. Ambulate 3. “I already have poor circulation, so there really is nothing
2. Sit with the legs elevated I can do to stop the process.”
3. Frequently rotate the ankles 4. “If I could keep my weight down and manage my blood
4. Continuously wear compression-gradient stockings sugars better, I hope to reduce the need to be on any
Objective: Identify specic measures that the patient can use to drugs for this.”
improve peripheral circulation and prevent the complications of Objective: Identify the treatment goals and what to expect when
peripheral vascular disease. peripheral vasodilating agents are administered.
NCLEX item type: Multiple choice NCLEX item type: Multiple choice
Cognitive skill: Compare Cognitive skill: Understanding
Drugs Used to Treat Thromboembolic Disorders 26
https://evolve.elsevier.com/Willihnganz

Objectives
1. Describe conditions that place an individual at risk for
developing blood clots and nursing interventions used to
prevent these conditions.
2. Identify the actions of platelet inhibitors, anticoagulants,
thrombin inhibitors, and brinolytic agents.
3. Describe specic monitoring procedures and laboratory
data used to detect hemorrhage in the patient taking
anticoagulants.
4. Describe the nursing assessments needed to monitor
therapeutic response and adverse effects from
anticoagulant therapy.

Key Terms
thromboembolic disorder (thrŏm-
bō-ĕm-BŎL-ĭk) (p. 417)
thrombosis (thrŏm-BŌ-sĭs) (p. 417)
thrombus (THRŎM-bŭs) (p. 417)
embolus (ĔM-bō-lŭs) (p. 417)
intrinsic clotting pathway (ĭn-TRĬN-
zĭk KLŎT-ĭng PĂTH-wā) (p. 417)
extrinsic clotting pathway (ĕks-
TRĬN-zĭk) (p. 417)
brinolytic agents (fī-brĭn-ō-LĬT-ĭk
Ā-gĕntz) (p. 418)
Antithrombotic agents (an-ti-throm-
bot-ik) (p. 418)
anticoagulants (ăn-tī-kō-ĂG-yū-lănts)
(p. 418)
platelet inhibitors (PLĀT-lĕt ĭn-HĬB-ĭ-
tĕrz) (p. 418)
glycoprotein IIb/IIIa inhibitors (glī-
cō-PRŌ-tēn ĭn-HĬ-bĭ-tĕrz) (p. 418)
factor Xa inhibitor (fact-tor TEN a in-
HIB-i-terz) (p. 418)
heparins (HEP-rin) (p. 418)
Vitamin K inhibitor (p. 418)
thrombin inhibitors (THRŎM-bĭn)
(p. 418)

THROMBOEMBOLIC DISORDERS
Disorders associated with abnormal clotting within
blood vessels are known as thromboembolic disor-
ders and are major causes of morbidity and mortality.
Thrombosis is the process of formation of a brin blood
clot (thrombus). An embolus is a small fragment of a
thrombus that breaks off and circulates until it becomes
trapped in a capillary, causing ischemia or infarction to
the area distal to the obstruction (e.g., cerebral embo-
lism, pulmonary embolism [PE]).
Major causes of thrombus formation are immobiliza-
tion with venous stasis; surgery and the postoperative
period; trauma to lower limbs; certain illnesses (e.g.,
heart failure, vasospasm, ulcerative colitis); cancers of
the lung, prostate, stomach, and pancreas; pregnancy
and oral contraceptives; and heredity.
Normally, blood clot formation and dissolution con-
stitute a ne balance within the cardiovascular system.
The clotting proteins normally circulate in an inactive
state and must be activated to form a brin clot. When
there is a trigger, such as increased blood viscosity from
bed rest and stasis or damage to a blood vessel wall, the
clotting cascade is activated. For example, if a blood ves-
sel is injured and collagen in the vessel wall is exposed,
platelets rst adhere to the site of injury and release
adenosine diphosphate (ADP), leading to additional
platelet aggregation that forms a “platelet plug.” At the
same time platelets are forming a plug, the intrinsic clot-
ting pathway is triggered by the presence of collagen ac-
tivating factor XII. Activated factor XIIa activates factor
XI to XIa, which activates factor IX to IXa. Factor IXa, in
the presence of calcium, platelet factor 3, and factor VIII,
activates factor X. Activated factor Xa, in the presence
of calcium, platelet factor 3, and factor V, stimulates the
conversion of prothrombin to thrombin (Fig. 26.1).
Sources outside the blood vessels, such as tissue ex-
tract or thromboplastin (tissue factor), can trigger the
extrinsic clotting pathway by activating factors VII to
VIIa. Factor VIIa can also activate factor X, which re-
sults in the formation of thrombin. After stimulation
from the intrinsic or extrinsic pathway, thrombin, in
the presence of calcium, activates brinogen to soluble
brin. With time and the presence of factor XIII, the
loose brin mesh is converted to a tight, insoluble -
brin mesh clot. Thrombin also stimulates platelet ag-
gregation and stimulates further activity of factors V,
VIIa, VII, and Xa. As the brin clot is being formed, it
also triggers the release of brinolysin, an enzyme that
dissolves brin, preventing the clot from spreading.
Historically, thrombi have been classied into red
and white blood clots. A red thrombus is actually a
venous thrombus and is composed almost entirely of
417
418 UNIT IV Drugs Affecting the Cardiovascular System
brin and erythrocytes (red blood cells), with a few
platelets. Venous thrombi generally form in response
to venous stasis after immobility or surgery. The poor
circulation prevents the dilution of activated coagula-
tion factors that normally occurs by rapidly circulating
blood. The most common location of red thrombus for-
mation is deep vein thrombosis (DVT) of the lower ex-
tremities. These thrombi may extend upward into the
veins of the thigh and have the potential of fragment-
ing, subsequently causing life-threatening pulmonary
emboli. White thrombi develop in arteries and are
composed of platelets and brin. This type of throm-
bus forms in areas of high blood ow in response to
injured vessel walls. Coronary artery occlusion leading
to myocardial infarction (MI) is an example of a white
thrombus.
TREATMENT OF THROMBOEMBOLIC
DISEASES
Diseases caused by intravascular clotting (e.g., DVT,
MI, dysrhythmias with clot formation, coronary vaso-
spasm leading to thrombus formation) are major causes
of death. When thrombosis is suspected, patients are
admitted to the hospital where they can be closely ob-
served for further signs and symptoms of thrombo-
sis formation and progression, and anticoagulant or
brinolytic therapy can be started. A combination of
physical examination, patient history, Doppler ultra-
sound, phlebography, radiolabeled brinogen studies,
and angiography is used to diagnose the presence and
cause of a thrombus and embolism. Routine labora-
tory tests that are run to assess the clotting process and
ensure that occult bleeding is not present are platelet
count, hematocrit, prothrombin time (PT) (reported
as the international normalized ratio [INR]), activated
partial thromboplastin time (aPTT), activated clotting
time (ACT), urinalysis, and stool guaiac test.
Nonpharmacologic prevention and treatment of
thromboembolic disorders include patient education
on how to prevent venous stasis (e.g., leg exercises,
leg elevation) and clinical use of sequential compres-
sion devices (SCDs). If a patient having a heart attack
(MI, acute coronary syndrome) can be transported
to a cardiac intensive care facility soon after symp-
toms develop, revascularization treatment to reopen
the coronary arteries may be performed. Fibrinolytic
agents may be used to dissolve the arterial clot before
it is permanently attached to vessel walls, causing
complete obstruction. Revascularization procedures
used may be a percutaneous coronary intervention
(PCI) or coronary artery bypass graft (CABG). In PCI,
also known as angioplasty, a catheter is inserted into
the femoral artery and advanced up the aorta into the
site of the coronary artery obstruction. The tip of the
catheter can be equipped with different types of de-
vices, such as a balloon to dilate the artery obstruc-
tion, or blades or lasers to reduce or remove the ob-
struction. A vascular stent is then often placed in the
artery to keep the formerly obstructed area open. If
a patient has multiple narrowed or obstructed arter-
ies, a CABG procedure is performed, wherein a seg-
ment of the saphenous vein from the leg is harvested
and attached to the coronary artery above and below
the obstruction, forming a bypass for perfusion to
the myocardial tissues below. The internal mammary
artery can also be used in this procedure. The major
pharmacologic treatments used in the prevention and
treatment of thromboembolic disorders are discussed
in the next section.
DRUG THERAPY FOR THROMBOEMBOLIC
DISORDERS
ACTIONS
The pharmacologic agents used to treat thromboem-
bolic disorders are known broadly as Antithrombotic
agents. They act either to prevent platelet aggregation
that may initiate clot formation or inhibit a variety of
steps in the brin clot formation cascade (see Fig. 26.1)
to prevent thrombosis. See individual drug mono-
graphs later in this chapter for a more detailed discus-
sion of mechanisms of action.
USES
The primary purpose of antithrombotic agents is to
prevent the formation of blood clots. Antithrombotic
agents can be divided into two classes: antiplate-
let drugs and anticoagulants. Antiplatelet agents or
platelet inhibitors (e.g, aspirin, clopidogrel), are used
preventively to reduce arterial clot formation (white
thrombi) by inhibiting platelet aggregation. Another
example of agents that act by platelet inhibition are
the glycoprotein IIb/IIIa inhibitors (e.g. eptibatide,
tiroban). Anticoagulants can be subdivided based
on their mechanism of action: factor Xa inhibitors,
heparins {heparin derivitives [dalteparin, enoxapa-
rin] are also known as low-molecular-weight hepa-
rins (LMWHs)}, vitamin K inhibitors and thrombin
inhibitors. Factor Xa inhibitors (e.g., apixaban, rivar-
oxaban), heparins, vitamin K inhibitor (warfarin) and
thrombin inhibitors (e.g., dabigatran) are also used
prophylactically to prevent the formation of arterial
and venous thrombi in predisposed patients. The gly-
coprotein IIb/IIIa inhibitors (e.g., abciximab, epti-
batide, tiroban) are used to prevent clot formation
during PCI procedures. Fibrinolytic agents (e.g., al-
teplase, reteplase) are used to dissolve arterial (brin-
rich, white) thromboemboli once formed.
LABORATORY TESTS FOR MONITORING
ANTICOAGULANT THERAPY
While receiving anticoagulant therapy, the patient will
undergo regular monitoring of coagulation studies,
including monitoring of the PT (reported as the INR),
ecarin clotting time (ECT), thrombin time (TT), ACT,
aPTT, and platelet counts. These laboratory studies
monitor the time it takes for the blood to clot. Results
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26 419

Intrinsic Clotting Pathway Extrinsic Clotting Pathway orthopedic surgery; and those on prolonged bed rest
or inadequately controlled anticoagulant therapy. Does
Blood trauma Tissue trauma the patient have any disease processes that could po-
or tentially increase the risk of bleeding (e.g., ulcer disease,
collagen contact concurrent chemotherapy, or radiation therapy)?

Tissue factor Current symptoms

• Ask the patient to describe the symptoms. Is the
patient currently taking, or has the patient recently
XII XIIa (H) (W) VII VIIa
taken, anticoagulants? Individualize further ques-
tioning to obtain data that would support or rule out
XI XIa (H) thrombosis formation or progression of thrombosis.
• Collect data about reduced tissue perfusion (e.g.,
symptoms relating to cerebral, cardiopulmonary, or
(W) IX IXa (H) peripheral vascular disease, depending on the un-
derlying pathophysiology). Perform a focused as-
Ca PF3 sessment at appropriate intervals that are consistent
with the patient’s status to detect further signs and
VIII (W)
symptoms of thrombosis formation or progression.
• To prevent thrombus extension or progression,
SCDs are used. These devices inate and deate to
Common Pathway (W) X
promote venous return from the legs. SCDs are re-
Xa (H) (LMWH) (Fu) (Ri)
moved when ambulating and discontinued when
the patient resumes full activity.
Ca PF3
Life Span Consideration
V (W) Important to note: If the presence of a thrombus is suspect-
ed in an extremity, do not apply an SCD to that limb because
(H) (F) this may dislodge the clot, causing an embolism that has the
(W) Prothrombin Thrombin (Da) potential for causing a stroke or pulmonary embolism, both
of which may be fatal.
Ca

(F) Ca Medications

Fibrinogen Fibrin • Obtain a thorough medication history of both pre-
(soluble) scribed and over-the-counter medications being taken.
• Ask specic questions relating to medicines being
(H)
taken that affect clotting.
XIIIa XIII • Ask whether the patient has been complying with
medication regimens and if any dosage adjustment
Fibrin has taken place. If anticoagulants are being taken,
(insoluble) has the patient reported for scheduled laboratory
studies? Has the patient had any reactions to the
Fig. 26.1 The clotting cascade. Da, Site of direct thrombin inhibitors; medication?
F, site of brinolytic action; Fu, fondaparinux; H, site of heparin action;
LMWH, site of low-molecular-weight heparins; PF3, platelet factor 3;
Ri, rivaroxaban; W, site of warfarin action. Basic assessment
• Obtain vital signs and admission weight (used to
calculate dosages) and auscultate breath sounds.
of these studies may be used as guidelines for drug Observe for dyspnea at rest or with exertion.
dosing by the prescriber. • Check mental status (e.g., orientation to date, time,
and place; alertness; confusion). Use as a baseline
NURSING IMPLICATIONS FOR ANTICOAGULANT for future comparison.
THERAPY • Assess for specic signs of reduced tissue perfu-
Assessment sion. Perform a focused assessment depending on
History. Ask specic questions to determine whether the underlying pathologic condition (e.g., cardio-
the patient or family members have a history of any type pulmonary, cerebral, or peripheral vascular dis-
of vascular difculty. Patients at greater risk for clot for- ease). If the presence of a thrombus is suspected in
mation are those with a history of clot formation; those an extremity, complete a comparative assessment of
who have recently undergone abdominal, thoracic, or the unaffected extremity.
420 UNIT IV Drugs Affecting the Cardiovascular System
• Collect data about any pain experienced.
• Ask specic questions about the patient’s state of
hydration. Review intake and output.
Diagnostic studies. Review completed diagnostic
studies and laboratory data (e.g., PT, aPTT, INR), he-
matocrit, platelet count, Doppler studies, exercise test-
ing, serum triglyceride levels, arteriogram, and cardiac
enzyme studies.
Implementation
Techniques for preventing clot formation
• Provide early, regular ambulation after surgery. Use
active or passive leg exercises for patients on bed
rest or restricted activity.
• Develop and follow a specic turning schedule
for patients on complete bed rest to prevent tissue
breakdown and venous stasis. Implement regular
back care and deep breathing and coughing exer-
cises as part of general nursing care.
• Do not ex the patient’s knees or place pressure
against the popliteal space with pillows.
• Do not allow the patient to stand or sit motionless
for prolonged periods.
• Apply SCDs as ordered and indicated. Make sure
that they are applied properly.
Patient assessment. Monitor vital signs and mental
status every 4 to 8 hours or more frequently, depend-
ing on the patient’s status. Observe for signs and
symptoms of bleeding caused by medications (e.g.,
blurred vision, hematuria, ecchymosis, occult blood in
the stools, change in mentation).
Nutritional status
• The dietary regimen will depend on the patient’s di-
agnosis and clinical status.
• Adequate hydration to promote uidity of the blood
is important. Unless coexisting diagnoses prohibit,
give at least six to eight 8-ounce glasses of liquid
daily.
Laboratory and diagnostic data. Monitoring and re-
porting laboratory results to the prescriber are essential
during anticoagulant therapy. Coagulation tests that
might be ordered include the following: whole blood
clotting time, ECT, TT, PT, aPTT, and ACT. The PT, re-
ported as the INR, is routinely used to monitor warfa-
rin therapy, and the aPTT and anti–factor Xa levels are
most commonly used to monitor heparin therapy. The
ECT and TT are used to monitor dabigatran therapy.
Medication administration
• Never administer an anticoagulant without rst
checking the patient’s chart for the most re-
cent laboratory results. Be certain that the anti-
coagulant to be administered is ordered after
the most recent results have been reported to the
healthcare provider. Follow policy statements re-
garding checking anticoagulant doses with other
qualied professionals.
• Reduce localized bleeding at the injection site by us-
ing the smallest needle possible for injections, and
rotate injection sites.
• Administer anticoagulants extremely cautiously to
patients who have been given spinal/epidural an-
esthesia or who have undergone spinal puncture.
These patients are at increased risk of developing
an epidural or spinal hematoma, which may cause
paralysis.
• See individual drug monographs later in this chap-
ter for specic administration techniques related to
a particular medicine.
Patient Education
Nutritional status
• While receiving anticoagulant therapy, patients
should maintain their normal intake of green leafy
vegetables that contain vitamin K. (Vitamin K inhib-
its the action of warfarin.) Patients should not start a
major change in diet without discussing it with their
healthcare provider, pharmacist, and nutritionist.
• Unless contraindicated by the healthcare provider,
instruct the patient to drink six to eight 8-ounce
glasses of liquid daily.
Exercise and activity
• Discuss the level of exercise prescribed by the
healthcare provider. Walking may be prescribed to
promote venous blood ow. Elevation of the legs
when seated may be encouraged to promote venous
blood ow.
• Stress the need to prevent body injury while tak-
ing anticoagulants. Tell the patient to avoid using
power equipment, use care in stepping up onto or
down from curbs, not participate in contact sports,
use only an electric razor, and brush teeth gently
with a soft-bristled toothbrush.
Medication regimen
• Instruct the patient to take the dosage of the medica-
tion exactly as prescribed. Explain the importance of
returning for laboratory blood tests to determine its
effectiveness and the need to adjust medicine dos-
ages. Tell the patient to resume a regular schedule if
one dose of warfarin is missed. If two or more doses
are missed, the patient should consult the health-
care provider.
• Instruct the patient on the importance of wearing a
medical alert bracelet.
• Explain symptoms that the patient should report,
such as nosebleeds, tarry stools, coffee-ground or
blood-tinged vomitus, petechiae (tiny purple or
red spots occurring in various sites on the skin), ec-
chymoses (bruises), hematuria (blood in the urine),
bleeding from the gums or any other body opening,
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26
or cuts or injuries from which the bleeding is dif-
cult to control. Check dressings periodically for
bleeding. Report excessive menstrual ow.
• In some cases, the healthcare provider may want
the patient to perform guaiac testing to detect occult
blood in the stool. If ordered, specic patient educa-
tion should be done to teach the patient or support
person how to perform the test.
• Inform patients that because not all bleeding is
clearly visible, they should report immediately a
rapid weak pulse, deep rapid respirations, moist
clammy skin, and a general feeling of weakness or
faintness.
• Instruct the patient not to take any medication, in-
cluding over-the-counter medications, without rst
consulting the healthcare provider because many
drugs interact with warfarin to increase or decrease
its effectiveness. Instruct the patient to never dis-
continue anticoagulant therapy without healthcare
provider agreement.
• Patients should always inform any healthcare pro-
vider (e.g., prescriber, home healthcare provider,
dentist) that anticoagulant therapy is being taken
whenever seeking care.
Fostering health maintenance
• Throughout the course of treatment, discuss medica-
tion information and how it will benet the patient.
• Provide the patient and signicant others with
important information contained in the specic
drug monographs for the medicines prescribed.
Additional health teaching and nursing interven-
tions for common and serious adverse effects are
described in the drug monographs in this chapter.
Urge the patient to use caution in cutting with a
knife or using any other sharp objects.
• Seek cooperation and understanding of the fol-
lowing points so that medication compliance is
increased: name of medication; dosage, route, and
times of administration; and common and serious
adverse effects.
Patient self-assessment. Enlist the patient’s aid in de-
veloping and maintaining a written record of monitor-
ing parameters. See the Patient Self-Assessment Form
for Anticoagulants on the Evolve website. Complete
the Premedication Data column for use as a baseline
to track response to drug therapy. Ensure that the pa-
tient understands how to use the form, and instruct
the patient to bring the completed form to follow-up
visits. During follow-up visits, focus on issues that will
foster adherence with the therapeutic interventions
prescribed.
DRUG CLASS: PLATELET INHIBITORS
aspirin (ĂS-prĭn)
421
Actions
Aspirin is well known as a salicylate and a non-
steroidal antiinammatory drug (NSAID). A unique
property of aspirin, compared with other salicylates,
is platelet aggregation inhibition with prolongation of
bleeding time. The platelet loses its ability to aggregate
and form clots for the duration of its lifetime (7 to 10
days). The mechanism of action is acetylation of the
cyclooxygenase enzyme, which inhibits the synthesis
of thromboxane A2, a potent vasoconstrictor and in-
ducer of platelet aggregation.
Uses
There is controversy in the literature as to whether as-
pirin is equally effective for men and women. When
used as primary prevention, aspirin therapy was as-
sociated with a signicant reduction in MI among men
older than 45 years but had no effect on the incidence of
stroke. Conversely, women taking aspirin had a lower
rate of stroke, but no effect was found in relation to MI.
Nevertheless, aspirin is administered to both men and
women at the onset of an acute MI.
Therapeutic Outcomes
The primary therapeutic outcomes expected from aspi-
rin therapy when used for antiplatelet therapy are re-
duced frequencies of transient ischemic attacks (TIAs),
stroke, or MI.
Nursing Implications for Aspirin Therapy
Premedication assessment
1. Perform baseline neurologic assessment: orientation
to date, time, and place; mental alertness; bilateral
hand grip; motor functioning (balance and hearing).
2. Monitor for gastrointestinal (GI) symptoms before
and during therapy. Stool guaiac testing may be or-
dered if GI tract bleeding is suspected.
3. Check on concurrent use of anticoagulant agents.
4. If the patient is receiving oral hypoglycemic agents,
review baseline serum glucose levels.
Availability, dosage, and administration. See Chapter
19, specically Tables 19.3 and 19.4
Prevention of transient ischemic attacks and
stroke. Adult: PO: 50 to 325 mg daily.
Treatment of suspected myocardial infarction. Adult:
PO: 160 to 325 mg as soon as possible. Continue 160 to
325 mg daily for at least 30 days.
Prevention of myocardial infarction. Adult: PO: 75 to
162 mg daily. Current literature mostly supports the
use of 81 mg daily for prevention.
clopidogrel (klō-PĬD-ō-grĕl)
Plavix (PLĂ-vĭks)
Do not confuse Plavix with Paxil.
422 UNIT IV Drugs Affecting the Cardiovascular System
Actions
Clopidogrel is a second-generation thienopyridine
chemically related to prasugrel. Clopidogrel is a pro-
drug; its active metabolite acts by inhibiting the ADP
pathway required for platelet aggregation. The full
antiplatelet activity is seen after 3 to 7 days of continu-
ous therapy. The antiaggregatory effect persists for ap-
proximately 5 days after discontinuation of therapy.
Clopidogrel also prolongs bleeding time.
Uses
Clopidogrel is used to reduce the risk of additional
atherosclerotic events (e.g., MI, stroke, vascular death)
in patients who have had a recent stroke, a recent MI,
or coronary bypass grafting or have established pe-
ripheral arterial disease. The medical histories of pa-
tients at greatest risk include TIAs, atrial brillation,
angina pectoris, and carotid artery stenosis. Because
clopidogrel has a different mechanism of action from
aspirin, it is used concurrently with aspirin after an MI
or acute coronary syndromes. The overall safety pro-
le of clopidogrel appears to be at least as good as that
of medium-dose aspirin. Clopidogrel remains the rst-
line thienopyridine in treatment of patients with an MI
who have a history of TIA or stroke, in those patients
being treated with CABG, and in those patients older
than 75 years (with the exception of those older than 75
years with diabetes or prior MI).
Therapeutic Outcomes
The primary therapeutic outcomes expected from clop-
idogrel therapy are reduced frequency of TIAs, stroke,
MI, or complications from peripheral vascular disease.
Nursing Implications for Clopidogrel
Premedication assessment
1. Obtain baseline vital signs.
2. Order baseline laboratory studies as requested by
the healthcare provider (e.g., complete blood count
[CBC] with differential count).
3. Assess and record any GI symptoms.
Availability. PO: 75- and 300-mg tablets.
Dosage and administration. Adult: PO: Initial: 300
or 600 mg for acute MI and PCI; otherwise, 75 mg.
Maintenance: 75 mg once daily with food or on an emp-
ty stomach. (Aspirin may be concurrently prescribed.)
Common adverse effects
Gastrointestinal
Nausea, vomiting, anorexia, diarrhea. These effects tend
to occur most frequently with early dosages and tend
to resolve with continued therapy over the next 2
weeks. They can also be minimized by taking the med-
ication with food. Encourage the patient not to discon-
tinue therapy without rst consulting the healthcare
provider.
Serious adverse effects
Hematologic
Thrombotic thrombocytopenic purpura. Thrombotic
thrombocytopenic purpura is a very rare but potential-
ly life-threatening condition that may occur within 2
weeks of the initiation of therapy. Early indications are
abnormal neurologic ndings and fever, followed by
renal impairment. If suspected, contact the healthcare
provider immediately.
Neutropenia, agranulocytosis. Neutropenia (absolute
neutrophil count less than 1200 neutrophils/mm3) was
discovered in 0.4% of patients in clinical trials. While
neutropenic, patients are very susceptible to infection.
Encourage the patient to report symptoms of infection
(e.g., sore throat, fever, excessive fatigue) to the health-
care provider as soon as possible.
Bleeding. A normal physiologic effect of clopidogrel
is prolongation of bleeding time. Patients should re-
port any incidents of bleeding as soon as possible.
Incidents to be reported include nosebleeds; easy
bruising; bright red or coffee-ground emesis; hematu-
ria; and dark, tarry stools.
Patients should inform other healthcare practitio-
ners (e.g., other physicians, dentist) that they are re-
ceiving platelet inhibitor therapy.
Drug interactions
Drugs that increase therapeutic and toxic ef
fects. Heparin, LMWHs, warfarin, aspirin, NSAIDs,
fondaparinux, and direct thrombin inhibitors (e.g.,
argatroban, bivalirudin, dabigatran) will have an ad-
ditive bleeding effect on the patient. Monitor very
closely for indications of bleeding. Caution should be
used when any of these drugs are coadministered with
clopidogrel.
prasugrel (PRĂ-sū-grĕl)
Do not confuse prasugrel with Pravachol.
Efent (ĔF-ē-ĕnt)
Actions
Prasugrel is a third-generation thienopyridine that is
similar to clopidogrel. Prasugrel is a prodrug that must
be metabolized to the active drug, which then irrevers-
ibly binds to the platelet P2Y12 receptors, inhibiting
the ADP pathway required for platelet aggregation.
The antiplatelet activity is seen after 1 to 2 hours and
continues for 24 hours. The antiaggregatory effect per-
sists for 5 to 9 days after discontinuation of therapy
with new platelet production. Prasugrel also prolongs
bleeding time. The steady-state effect is seen after 3
days of continuous therapy.
Uses
Compared with clopidogrel, prasugrel shows a greater
platelet inhibitory effect and has a more rapid onset
of action, but it also has an increased risk of major
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26
bleeding. Prasugrel is approved for use in the preven-
tion of blood clot formation in patients suffering an MI
who are undergoing a PCI with or without stent place-
ment. Although not recommended in patients older
than 75 years, prasugrel appears to be more effective
and should be considered in patients older than 75
with a history of MI or with diabetes. Aspirin therapy
should be continued with prasugrel therapy.
Therapeutic Outcome
The primary therapeutic outcome expected from pra-
sugrel is reduced blood clot formation in the treatment
of an MI with a PCI procedure.
Nursing Implications for Prasugrel
Premedication assessment
1. Obtain baseline vital signs and admission weight
(used to calculate dose).
2. Order baseline laboratory studies as requested by
the healthcare provider (e.g., CBC).
3. Ask the patient about a history of active bleeding,
TIA, stroke, or hypersensitivity to prasugrel. Notify
the healthcare provider of these ndings.
Availability. PO: 5- and 10-mg tablets.
Dosage and administration. Adult: PO: Initially, 60-
mg loading dose followed by a daily maintenance dose
of 10 mg. If the patient weighs less than 60 kg, 5 mg
daily is recommended. Patients should also continue
to take aspirin, 75 to 325 mg once daily.
Medication Safety Alert
Patients weighing less than 60 kg (132 lb) have a greater risk
for bleeding secondary to prasugrel therapy.
Common adverse effects
Hematologic
Bleeding. The normal physiologic effect of prasug-
rel is prolongation of bleeding time. Patients should
report any incidents of bleeding as soon as possible.
Incidents to be reported include nosebleeds; easy
bruising; bright red or coffee-ground emesis; hematu-
ria; and dark, tarry stools. Patients weighing less than
60 kg (132 lb) have a greater risk for bleeding second-
ary to prasugrel therapy.
Patients should inform other healthcare practitio-
ners (e.g., another physician, dentist) that they are re-
ceiving platelet inhibitor therapy.
Serious adverse effects
Hematologic
Thrombotic thrombocytopenic purpura. Thrombotic
thrombocytopenic purpura is a very rare but poten-
tially life-threatening condition that may occur within
the rst 2 weeks of the initiation of therapy. Early in-
dications are abnormal neurologic ndings and fever,
423
followed by renal impairment. If suspected, contact
the healthcare provider immediately.
Drug interactions
Drugs that increase therapeutic and toxic ef
fects. Heparin, LMWHs, warfarin, aspirin, NSAIDs,
fondaparinux, and direct thrombin inhibitors (e.g., ar-
gatroban, dabigatran, bivalirudin) will have an additive
bleeding effect in the patient. Monitor very closely for
indications of bleeding. Caution should be used when
any of these drugs are coadministered with prasugrel.
ticagrelor (tī-KĂ-grĕ-lŏr)
Brilinta (brĭ-LĬN-tă)
Actions
Ticagrelor is a platelet aggregation inhibitor that binds
to the platelet P2Y12 receptors, inhibiting the ADP
pathway required for platelet aggregation. It is not
chemically related to clopidogrel or prasugrel, is not
a prodrug requiring metabolism for action, and is the
rst platelet inhibitor to have direct, reversible binding
to the receptor site. The maximum antiplatelet activity
is seen at about 2 hours and continues for 8 hours. The
antiaggregatory effect persists for 5 days after discon-
tinuation of therapy.
Uses
Ticagrelor is indicated to reduce the rate of cardio-
vascular death, MI, and stroke in patients with acute
coronary syndrome or a history of MI. It also reduces
the rate of stent thrombosis in those patients who have
received a stent for treatment of acute coronary syn-
drome. Ticagrelor is also approved to reduce the risk of
a rst MI or stroke in patients with high risk coronary
artery disease. Patients should continue low-dose aspi-
rin therapy with ticagrelor.
Therapeutic Outcome
The primary therapeutic outcome expected from ti-
cagrelor is lower frequency of blood clots associated
with MI.
Nursing Implications for Ticagrelor
Premedication assessment
1. Obtain baseline vital signs.
2. Order baseline laboratory studies requested by the
healthcare provider (e.g., CBC).
Availability. PO: 60- and 90-mg tablets.
Dosage and administration
Acute coronary syndrome or history of MI. PO: Loading
dose, 180 mg of ticagrelor with 325 mg of aspirin, fol-
lowed by 90 mg ticagrelor with 75 to 100 mg aspirin
daily for 1 year. After 1 year, ticagrelor 60 mg twice a
day with 75 to 100 mg of aspirin.
424 UNIT IV Drugs Affecting the Cardiovascular System
Patients with coronary arterial disease and no history of
stroke or MI. PO: For patients with coronary artery dis-
ease but no history of stroke or MI, 60 mg twice a day
with 75 to 100 mg of aspirin.
Medication Safety Alert
 • Except for the 325-mg loading dose of aspirin, do not
exceed 100 mg of aspirin daily. Larger doses reduce the
effectiveness of ticagrelor.
 • Ticagrelor is contraindicated in patients who have a
history of intracranial hemorrhage (hemorrhagic stroke).
 • Ticagrelor is contraindicated in moderate to severe liver
failure. Ticagrelor is normally metabolized by enzymes
in the liver, so metabolism may be diminished, causing
higher circulating levels of ticagrelor. Furthermore,
production of clotting factors is reduced in patients
with liver failure, making patients more susceptible to
hemorrhage.
Common adverse effects
Hematologic
Bleeding. A normal physiologic effect of ticagrelor is
prolongation of bleeding time. Patients should report
any incidents of bleeding as soon as possible. Incidents
to be reported include nosebleeds; easy bruising;
bright red or coffee-ground emesis; hematuria; and
dark, tarry stools.
Patients should inform other healthcare practitio-
ners (e.g., another physician, dentist) that they are re-
ceiving platelet inhibitor therapy.
Respiratory
Dyspnea. Fourteen percent of patients receiving
ticagrelor develop mild to moderate dyspnea, which
resolves with continued therapy. If the patient devel-
ops new, prolonged, or worsened dyspnea, notify the
healthcare provider. Seek underlying causes of dysp-
nea. If ticagrelor is determined to be the cause of the
dyspnea, there is no need to discontinue therapy; con-
tinue ticagrelor without interruption.
Drug interactions
Drugs that increase therapeutic and toxic effects
Combined pharmacologic effect. Anticoagulants/
platelet inhibitors that have an additive bleeding ef-
fect in the patient include heparin, LMWHs, warfarin,
aspirin, NSAIDs, fondaparinux, and direct throm-
bin inhibitors (e.g., argatroban, dabigatran, desiru-
din). Monitor very closely for indications of bleeding.
Caution should be used when any of these drugs are
coadministered with ticagrelor.
Reduced metabolism. Drugs that inhibit the metabo-
lism of ticagrelor, increasing the likelihood of bleeding,
include itraconazole, voriconazole, clarithromycin,
and ritonavir. Monitor very closely for indications of
bleeding. Caution should be used when any of these
drugs are coadministered with ticagrelor.
Drugs that decrease therapeutic effects. Drugs that
may decrease the therapeutic activity of ticagrelor by
increasing its rate of metabolism include carbamaz-
epine, dexamethasone, phenobarbital, phenytoin, and
rifampin.
GLYCOPROTEIN IIB/IIIA INHIBITORS
During PCI procedures, it was found that patients were
susceptible to new blood clots forming from the debris
often released from atherosclerotic plaque disruption.
Antiplatelet and antithrombotic agents such as aspirin
and heparin were initially used, but new agents, called
glycoprotein IIb/IIIa inhibitors, have been developed.
Three of these inhibitors are now available: abcix-
imab (ReoPro), eptibatide (Integrilin), and tiroban
(Aggrastat).
Actions
The glycoprotein IIb/IIIa inhibitors act by block-
ing the glycoprotein IIb/IIIa receptor on platelets,
preventing platelet aggregation and clot formation.
Platelet aggregation inhibition persists during con-
tinuous infusion and is reversible on discontinuing
the infusion.
Uses
Glycoprotein IIb/IIIa inhibitors are administered in-
travenously during the PCI procedure and for 12 to
24 hours afterward, signicantly reducing the risk of
acute MI and death. Other antiplatelet and antithrom-
botic agents such as aspirin, clopidogrel, and heparin
are used in conjunction with the glycoprotein IIb/IIIa
inhibitors. Major complications of therapy include
bleeding and thrombocytopenia. The hematocrit,
platelet counts, and ACT must be monitored closely
during and after therapy.
Therapeutic Outcome
The primary therapeutic outcome from glycoprotein
IIb/IIIa inhibitor therapy is prevention of clot forma-
tion during PCI procedures.
DRUG CLASS: ANTICOAGULANTS
FACTOR Xa INHIBITORS
Actions
Apixaban, edoxaban, and rivaroxaban and fond-
aparinux are reversible and selective factor Xa inhibi-
tors that reduce thrombus formation. They do not
affect platelet activity; however, they will prolong PT
(INR) and aPTT.
Uses
Apixaban is used to:
• Reduce the risk of stroke and systemic embolism in
patients with nonvalvular atrial brillation.
• Treat DVT and PE.
• Reduce the risk of recurrence of DVT and PE after
treatment.
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26 425

• Prevent (prophylaxis) DVT, which may lead to PE,
in patients undergoing hip or knee replacement
surgery.
Edoxaban is used to:
• Reduce the risk of stroke and systemic embolism in
patients with nonvalvular atrial brillation.
• Treat DVT and PE.
Rivaroxaban is used to:
• Reduce the risk of stroke and systemic embolism in
patients with nonvalvular atrial brillation.
• Reduce the risk of major cardiovascular events
(stroke, MI, death) in patients with coronary artery
disease or peripheral artery disease.
• Treat DVT and PE.
• Reduce the risk of recurrence of DVT and PE after
treatment.
• Prevent (prophylaxis) DVT, which may lead to PE, in
patients undergoing hip or knee replacement surgery.
The factor Xa inhibitors do not need to be monitored
with anticoagulation tests (PT [INR] and aPTT).
Some of the factor Xa inhibitors may need a dose
reduction because of renal function, age, weight, and
drug interactions.
Therapeutic Outcome
The primary therapeutic outcomes expected from fac-
tor Xa inhibitors are prevention of DVT and PE and
reduction of the risk of thromboembolism in patients
with atrial brillation. They are also used for the treat-
ment of DVT and PE.
Nursing Implications for Factor Xa Inhibitors
Premedication assessment
1. Obtain baseline vital signs.
2. Initiate laboratory studies as requested by the health-
care provider (e.g., renal function tests such as blood
urea nitrogen, serum creatinine, stool occult blood,
and CBC) to serve as a baseline for future comparison.
3. Inspect the skin and mucous membranes for pete-
chiae, ecchymoses, or hematomas. Also, monitor for
hematuria, bleeding gums, and melena before ad-
ministering each dose of medicine.
Availability, dosage, and administration. See Table 26.1
Antidote. Andexanet Alfa (Andexxa) is an antidote that can
reverse anticoagulation in patients treated with apixaban or ri-
varoxaban experiencing life-threatening or uncontrolled bleed-
ing. Although not yet FDA-approved, it may also be used to
reverse edoxaban anticoagulation.

Table 26.1 Factor Xa Inhibitors

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE
apixaban Eliquis Tablets: 2.5, 5 mg DVT and PE:
Treatment: 10 mg twice daily for 7 days followed by 5 mg twice daily
Reduction in the risk of recurrence: 2.5 mg twice daily after at least 6 mo
of treatment for DVT or PE
Nonvalvular atrial brillation (to prevent stroke and systemic embolism):
5 mg twice daily unless patient has any two of the following: Age ≥80
yr, body weight ≤60 kg, or serum creatinine ≥1.5 mg/dL; then reduce
dose to 2.5 mg twice daily
Prophylaxis of DVT and PE:
Hip replacement surgery: 2.5 mg twice daily beginning 12–24 hr
postoperatively; duration: 35 days
Knee replacement surgery: 2.5 mg twice daily beginning 12–24 hr
postoperatively; duration: 12 days
edoxaban Savaysa Tablets: 15, 30, Treatment for DVT and PE: 60 mg once daily after 5–10 days of initial
60 mg therapy with a parenteral anticoagulant. If less than 60 kg (132 lb); 30
mg once daily
Nonvalvular atrial brillation (to prevent stroke and systemic embolism):
60 mg once daily
rivaroxaban Xarelto Tablets: 2.5, 10, DVT and PE:
15, 20 mg Treatment: 15 mg twice daily with food for the rst 21 days
Reduction in the risk of recurrence: 10 mg orally once daily with or
without food, after at least 6 mo of standard anticoagulant therapy
Nonvalvular atrial brillation (to prevent stroke and systemic embolism):
20 mg once daily with the evening meal
Coronary artery disease (stable) or peripheral artery disease (prevention
of major cardiovascular events)
2.5 mg twice daily; administer in combination with daily low-dose aspirin
Prophylaxis of DVT and PE:
Hip replacement surgery: 10 mg once daily beginning at least 6–10 hr
after surgery; total duration of therapy: 35 days
Knee replacement surgery: 10 mg once daily beginning at least 6–10 hr
after surgery; recommended total duration of therapy: 12 days
426 UNIT IV Drugs Affecting the Cardiovascular System
Medication Safety Alert
 • Do not administer to patients who have active major
bleeding or a hypersensitivity to the factor Xa inhibitors.
 • Premature discontinuation of the factor Xa inhibitors
increases the risk of thrombosis. If anticoagulation is
discontinued for a reason other than pathologic bleeding
or completion of a course of therapy, coverage with
another anticoagulant should be considered.
 • Do not administer apixaban or rivaroxaban to patients
with moderate to severe hepatic impairment or a
creatinine clearance less than 30 mL/min.
 • Do not administer edoxaban to patients with creatinine
clearance greater than 95 mL/min.
Common adverse effects
Hematologic
Bleeding. A normal physiologic effect of factor Xa
inhibitors is prolongation of bleeding time. Patients
should report any incidents of bleeding as soon as pos-
sible. Incidents to be reported include nosebleeds; easy
bruising; bright red or coffee-ground emesis; hematu-
ria; and dark, tarry stools.
Patients should inform other healthcare practitio-
ners (e.g., another physician, dentist) that they are re-
ceiving factor Xa inhibitor therapy.
Drug interactions
Drugs that increase therapeutic and toxic effects
Increased pharmacologic effect. Heparin, LMWHs,
warfarin, aspirin, NSAIDs, fondaparinux, vorapaxar,
selective serotonin reuptake inhibitors, omega-3 fatty
acids, and direct thrombin inhibitors (e.g., desirudin,
argatroban, bivalirudin) will have an additive bleed-
ing effect in the patient. Monitor very closely for in-
dications of bleeding. Caution should be used when
any of these drugs is coadministered with factor Xa
inhibitors.
Reduced metabolism or increased blood lev
els. Itraconazole, voriconazole, and clarithromycin,
inhibit the metabolism of apixaban, and rivaroxaban,
increasing the likelihood of bleeding. Amiodarone,
verapamil, and clarithromycin increase the likelihood
of bleeding by increasing the blood levels of edoxaban
by increasing its absorption. Monitor very closely for
indications of bleeding. Caution should be used when
any of these drugs is coadministered with factor Xa
inhibitors.
Drugs that decrease therapeutic effects. When used
concurrently with factor Xa inhibitors, carbamazepine,
dexamethasone, phenobarbital, phenytoin, rifampin,
and St. John’s wort may decrease their therapeutic ac-
tivity by increasing their rate of metabolism. Estrogens
and progestins may diminish their effects because of
their potential prothrombotic effect.
fondaparinux (fŏn-dĕ-PĂR-ĭn-ŭks)
Arixtra (ăr-ĬKS-tră)
Actions
Fondaparinux is a selective factor Xa inhibitor.
Fondaparinux binds to antithrombin III, potentiating
its action against factor Xa, preventing completion of
the coagulation cascade. Fondaparinux has no anti-
platelet activity and has no effect on the PT and aPTT.
Uses
Fondaparinux is used to prevent DVT in patients un-
dergoing hip fracture or hip replacement surgery,
knee replacement surgery, or abdominal surgery and,
in combination with warfarin, to treat patients with
acute DVT. It is also used to treat acute pulmonary
embolism in conjunction with warfarin. When dis-
continued, fondaparinux-mediated anticoagulation
remains for 2 to 4 days in patients with normal renal
function and longer in patients with renal impairment.
Fondaparinux cannot be used interchangeably (unit
for unit) with heparin or LMWHs because they differ
in manufacturing process, anti–factor Xa and anti–
factor IIa activity, units, and dosage. Although they
have similar mechanisms of action, fondaparinux is
not an LMWH product.
Therapeutic Outcomes
The primary therapeutic outcomes from fondaparinux
therapy are prevention of DVT in patients after hip,
knee, or abdominal surgery and treatment of acute
DVT.
Nursing Implications for Fondaparinux
Premedication assessment
1. Perform scheduled laboratory tests, including se-
rum creatinine, CBC, platelet count, and stool occult
blood tests, before starting fondaparinux therapy.
2. Obtain baseline vital signs.
3. Inspect the skin and mucous membranes for pete-
chiae, ecchymoses, or hematomas. Also monitor for
hematuria, bleeding gums, and melena before ad-
ministering each dose of medication.
Availability. Subcutaneous: 2.5 mg in 0.5 mL, 5 mg in 0.4
mL, 7.5 mg in 0.6 mL, and 10 mg in 0.8 mL single-dose
prelled syringes (preservative free) with 27-gauge,
½-inch needles.
Dosage and administration. Adult: Subcutaneous: Do
not expel the air bubble from the prelled syringe be-
fore administration. Administer by deep subcutaneous
injection, rotating the injection sites. The administra-
tion site should vary with each injection. Using the
thumb and forenger, a fold of skin must be lifted for
giving the injection. Insert the entire length of the nee-
dle at a 45- to 90-degree angle. The skinfold should be
held throughout the injection. Inject the drug slowly.
When all contents have been injected from the syringe,
the plunger should be released, allowing it to rise
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26
automatically while the needle withdraws from the
skin and retracts into the security sleeve. Discard into
a sharps container. To minimize bruising, do not rub
the injection site after completion of the injection.
Periodic serum creatinine, CBC (including platelet
count), and stool occult blood tests are recommended
during the course of treatment with fondaparinux. No
special monitoring of clotting times (aPTT) is required.
Medication Safety Alert
 • Do not inject fondaparinux intramuscularly!
 • Use with caution in patients with a creatinine clearance of
30 to 50 mL/min.
 • Do not use in patients with a creatinine clearance less
than 30 mL/min.
Dosage range
DVT prophylaxis. Subcutaneous: 2.5 mg daily at least
6 to 8 hours after hip fracture, hip replacement, or knee
replacement surgery. The usual duration of once dai-
ly administration is 5 to 9 days, and up to 11 days of
administration has been tolerated. In patients under-
going hip fracture surgery, an extended prophylaxis
course of up to 24 additional days is recommended.
After abdominal surgery in patients weighing at least
50 kg, administer 2.5 mg subcutaneously 6 to 8 hours
after surgery. Usual once-daily administration is 5 to
9 days, up to 10 days. Do not administer to patients
weighing less than 50 kg.
Acute DVT and PE treatment. Subcutaneous: 5 mg (body
weight <50 kg), 7.5 mg (body weight = 50 to 100 kg),
or 10 mg (body weight >100 kg) once daily. Continue
treatment for at least 5 days until a therapeutic oral
anticoagulant effect becomes established (INR 2 to 3).
Initiate concomitant treatment with warfarin as soon
as possible, usually within 72 hours. The usual dura-
tion of administration of fondaparinux is 5 to 9 days
(up to 26 days).
Common adverse effects
Hematologic
Hematoma formation and bleeding at injection site.
Inappropriate administration techniques lead to he-
matoma formation at the site of injection. Use proper
technique!
Serious adverse effects
Hematologic
Bleeding. Inspect the skin and mucous membranes
for petechiae, ecchymoses, or hematomas; also moni-
tor for bleeding gums. Assess and record vital signs at
regular intervals. Monitor and report signs and symp-
toms of internal bleeding (e.g., decreasing blood pres-
sure; increasing pulse; cold, clammy skin; feeling faint;
disoriented sensorium).
Check urine and stools for blood. Urine may appear
red, smoke colored, or brownish. Stools may appear
to be dark and tarry. Perform an occult blood test on
427
the stool if necessary. Vomitus may contain bright red
blood or may have a coffee-ground appearance.
Assessment of dressings or drainage tubes for
any signs of bleeding is necessary for postoperative
patients.
Thrombocytopenia. Fondaparinux may cause throm-
bocytopenia. Monitor platelet counts on a daily basis.
It is recommended that fondaparinux therapy be dis-
continued if platelet counts drop to less than 100,000/
mm3
Drug interactions. No clinically signicant drug inter-
actions have been reported, but fondaparinux should
be used cautiously in patients receiving antiplatelet or
warfarin therapy.
HEPARINS
heparin (HĔP-rĭn)
Do not confuse heparin with Hespan.
Actions
Heparin is a natural substance extracted from gut and
lung tissue of pigs and cows. In full therapeutic dos-
es, heparin acts as a catalyst to accelerate the rate of
action of a naturally occurring inhibitor of thrombin,
antithrombin III (sometimes called the heparin cofac-
tor). In the presence of heparin, antithrombin III rap-
idly neutralizes factor IIa; activated factors IX, X, XI,
and XII; and plasmin. Heparin also inhibits activation
of factor VIII, the brin stabilizing factor, preventing
soluble brin clots from becoming insoluble clots (see
Fig. 26.1). Heparin has no brinolytic activity and can-
not lyse established brin clots.
In low doses, heparin causes the neutralization
of only factor Xa, preventing the conversion of pro-
thrombin to thrombin, which allows lower dosages to
be used with fewer complications from therapy. This is
the rationale routinely used in prophylaxis with sub-
cutaneous heparin to prevent postoperative thrombus
formation.
Uses
Heparin is used to treat DVT, PE, peripheral arterial
embolism, and MI and for PCIs. It is used in the treat-
ment of patients with heart valve prostheses. It is also
used prophylactically during cardiovascular surgery;
in postoperative, immobilized patients; and during
hemodialysis to prevent active coagulation and clot
formation and to maintain patency of venous access
devices. When testing for adequate anticoagulation by
heparin, the aPTT is measured. The target range for
full anticoagulation is 1.5 to 2.5 times the control time
(e.g., if the control time is 25 seconds and the patient’s
aPTT is 38 to 64 seconds, the patient is considered to
be adequately anticoagulated). Another laboratory test
that is becoming more frequently used is the measure-
ment of anti–factor Xa levels. Therapeutic ranges of
428 UNIT IV Drugs Affecting the Cardiovascular System
anti–factor Xa for heparin are 0.3 to 0.7 units/mL and
for LMWHs are 0.5 to 1 units/mL.
Therapeutic Outcomes
The primary therapeutic outcomes from heparin ther-
apy are as follows:
1. When used in low doses prophylactically, heparin
prevents DVT.
2. In full doses, heparin is used to treat a thrombo-
embolism and promote neutralization of activated
clotting factors, thus preventing the extension of
thrombi and the formation of emboli. If therapy is
started shortly after the formation of a thrombus,
heparin will minimize tissue damage by prevent-
ing it from developing into an insoluble stable
thrombus.
Nursing Implications for Heparin
Premedication assessment
1. Take baseline vital signs.
2. Always check the most recent laboratory data
(aPTT, anti–factor Xa levels) to ensure that the re-
sults are within the recommended range for hepa-
rin therapy.
3. Inspect the skin and mucous membranes for pete-
chiae, ecchymoses, or hematomas. Also monitor for
hematuria, bleeding gums, and melena before ad-
ministering each dose of medication.
Availability. Subcutaneous, Intravenous (IV): 1000,
2000, 5000, 10,000, and 20,000 units/mL in various
concentrations and sizes of ampules, vials, prelled
syringes, and IV infusion solutions.
Dosage and administration
Accuracy of dose. Always conrm the dosage calcu-
lations with two nurses before IV administration. Be
certain the strength is correct. There is a drastic differ-
ence in clinical response between 1 mL of 1:1000 units
and 1 mL of 1:10,000 units of heparin.
Dosage adjustment. Blood samples for laboratory
studies (aPTT, anti–factor Xa) are usually drawn 4
to 6 hours after the initiation of a continuous IV in-
fusion. Do not draw blood samples from the same
arm being used for heparin infusion. The effects of
heparin only last 4 hours, so a continuous infusion
is needed. When the aPTT or anti–factor Xa level is
too high, the heparin infusion can be stopped for an
hour and then restarted at a lower rate. The use of a
nomogram may be employed to maintain a steady
state of anticoagulation, which adjusts the heparin
infusion according to the aPTT or anti–factor Xa
when appropriate.
Heparin dosage is considered to be in the normal
therapeutic range if the aPTT is 1.5 to 2.5 times the con-
trol aPTT value (e.g., if control is 30 seconds, the pa-
tient receiving full-dose heparin should have an aPTT
of 45 to 75 seconds for optimal therapy). If anti–factor
Xa is used, the normal therapeutic range is 0.3 to 0.7
units/mL.
Subcutaneous: Prophylactic: 5000 units every 8 to
12 hours. Therapeutic: Initially, 10,000 to 15,000 units.
Maintenance: Loading dose: 10,000 to 20,000 units, fol-
lowed by 8000 to 10,000 units every 8 hours, or 15,000
units every 12 hours.
Subcutaneous injection is usually made into the tis-
sue over the abdomen (Fig. 26.2). Do not inject within
2 inches of the umbilicus. The injection site should not
be massaged before or after injection, and sites should
be rotated for each dose to prevent the development of
a massive hematoma.
Needle length and angle need to be adapted to the
patient’s size so that the drug will be deposited into
the subcutaneous tissue. (Usually, a 26- or 27-gauge,
½-inch needle is used.) The injection is usually made at
a 90-degree angle to the skin. Do not aspirate. This will
increase local tissue damage and create the possibility
of hematoma formation. Do not inject into a hematoma
or an area with any infection present. Follow a planned
site rotation schedule.
After injection, apply gentle pressure for 1 or 2 min-
utes to control local bleeding, but do not massage the
area. Ice packs may be used on the site after injection;
check the institutional policy. At this time, there is little
documented evidence that ice packs prevent hemato-
ma formation or affect drug absorption.
Intramuscular (IM): Not recommended because of
the development of hematomas.
IV (intermittent): Initial: 10,000-unit bolus.
Maintenance: 5000 to 10,000 units every 4 to 6 hours.
IV (continuous infusion): Initial: 70- to 100-
unit/kg bolus. Maintenance: 15 to 25 units/kg/hr.
Continuous infusions of heparin provide the advan-
tage of steady heparin levels in the blood. Periodic
dosage adjustment is required based on the response
of the patient.
Medication Safety Alert
When starting a heparin infusion, always have two nurses
conrm calculations and the strength of the heparin to
be used. As a safety measure, heparin drips should be a
single concentration to avoid medication errors (typically
25,000 units in 250 mg [100 units/mL], but conrm with
institutional policy). This protects patients from receiving
massive doses of heparin should the infusion “run away.”
Always use a programmable infusion pump for IV infu
sions. However, the infusion should be monitored at least
every 30 to 60 minutes.
Antidote. Protamine sulfate, 1 mg, will neutralize
approximately 100 units of heparin, dalteparin, and 1
mg of enoxaparin. If protamine sulfate is given more
than 30 minutes after the heparin or LMWHs were ad-
ministered, give only half the dose. Because excessive
doses of protamine may also cause excessive coagula-
tion, it must be used judiciously.
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26
X X
X X
X X X
X
X
X less than the baseline value. This type of thrombocy-
X X
Fig. 26.2 Sites of heparin administration.
Common adverse effects. Patients receiving full-dose
heparin therapy should be monitored for hematocrit,
platelet counts, aPTT, and signs of bleeding.
Adverse effects of heparin therapy are most com-
monly caused by inappropriate administration tech-
nique or overdosage. Factors that can inuence the in-
cidence of complications include age, weight, gender,
and recent trauma. The most common signs of over-
dosage are petechiae, hematomas, hematuria, bleeding
gums, and melena.
Hematologic
Hematoma formation and bleeding at the injection
site. Inappropriate administration techniques lead to
hematoma formation at the site of injection. Use prop-
er technique!
Serious adverse effects
Hematologic
Bleeding. Inspect the skin and mucous membranes
for petechiae, ecchymoses, or hematomas; also moni-
tor for bleeding gums. Assess and record vital signs
at regular intervals. Always monitor menstrual ow
to be certain that it is not excessive or prolonged.
Monitor and report signs and symptoms of internal
bleeding (e.g., decreasing blood pressure; increasing
pulse; cold, clammy skin; feeling faint; disoriented
sensorium).
Check urine and stools for blood. Urine may appear
red, smoke colored, or brownish. Stools may appear
to be dark and tarry. Perform an occult blood test on
the stool if necessary. Vomitus may contain bright red
blood or may have a coffee-ground appearance.
Assessment of dressings or drainage tubes for any
signs of bleeding is necessary for postoperative patients.
Thrombocytopenia. Heparin therapy may cause two
types of HIT. Type I HIT results from a direct effect of
heparin on platelets, causing sequestration and a fall
in the platelet count to as low as 100,000/mm3. This
reversible form of thrombocytopenia occurs within
the rst several days of heparin therapy. The patient
is asymptomatic, and heparin therapy should be
429
continued if therapeutically indicated. The platelet
count should return to normal.
Type II HIT should be suspected when the platelet
count falls to less than 100,000/mm3 or falls to 50%
topenia is an allergic reaction to heparin that causes
aggregation of platelets. The onset of falling platelet
counts is immediate after heparin therapy is started if
the patient has previously received heparin, whereas
it occurs after 5 to 22 days in the previously unex-
posed patient. Type II HIT occurs in about 0.3% to
3% of patients. Patients are at risk for white thrombus
formation caused by sudden aggregation of platelets.
Heparin therapy should be immediately discontinued
if patients develop signs of clot formation, such as pain
in an extremity, symptoms of a stroke, or chest pain
resembling angina. Warfarin therapy may be initiated
or continued when the platelet count is greater than
100,000/mm3, and antiplatelet therapy (aspirin) may
also be started. Direct thrombin inhibitors such as arg-
atroban or bivalirudin may also be used. Fondaparinux
may also be used cautiously. Low-molecular-weight
heparins are contraindicated because of the potential
for cross-allergenicity. Platelet counts should be moni-
tored daily.
Drug interactions
Drugs that increase therapeutic and toxic effects.
Concurrent use of NSAIDs, aspirin, danshen, ginkgo
biloba, dipyridamole, clopidogrel, and direct throm-
bin inhibitors (argatroban, dabigatran, desirudin) may
predispose the patient to hemorrhage.
dalteparin (dăl-TĔ-păr-ĭn)
Do not confuse with dabigatran.
Fragmin (FRĂG-mĭn)
Actions
Dalteparin is the second (after enoxaparin) of the
LMWHs that are essentially the active components of
the heparin protein molecule. The LMWHs have the
advantage of specic action at certain steps of the co-
agulation pathway, resulting in less potential for hemor-
rhage and longer duration of action. Dalteparin enhanc-
es antithrombin activity primarily against factor Xa,
which prevents completion of the coagulation cascade.
Dalteparin has no antiplatelet activity. Because it has no
effect on thrombin, there is no effect on the aPTT.
Uses
Dalteparin is used to prevent and treat DVT after hip
replacement surgery or abdominal surgery, in any
medically ill patients, and in patients with active can-
cer. It may also be used for systemic anticoagulation
and in combination with aspirin to prevent clot forma-
tion in patients with unstable angina pectoris and non–
ST segment elevation MI (NSTEMI). Dalteparin may
430 UNIT IV Drugs Affecting the Cardiovascular System
also be used during hemodialysis in connection with
acute and chronic renal failure. Dalteparin is manufac-
tured from heparin derived from pigs and should not
be used in patients allergic to pork by-products.
Therapeutic Outcomes
The primary therapeutic outcomes from dalteparin
therapy are treatment and prevention of DVT after ab-
dominal or hip replacement surgery and prevention of
clot formation in patients with cancer, angina pectoris,
and NSTEMI.
Nursing Implications for Dalteparin
Premedication assessment
1. Perform scheduled laboratory tests, including CBC,
platelet count, and stool occult blood tests, before
starting dalteparin therapy.
2. Obtain baseline vital signs.
Availability. Subcutaneous: anti–factor Xa: 2500,
5000, 7500, 10,000, 12,500, 15,000, and 18,000 units in
prelled syringes with a 27-gauge, ½-inch needle (pre-
servative free); 25,000 units/mL multidose vial that
also contains benzyl alcohol preservative.
Dosage and administration. Adult: Subcutaneous:
Administer by deep subcutaneous injection into a
U-shaped area around the navel, upper outer side of
the thigh, or upper outer quadrangle of the buttock.
When the area around the navel or the thigh is used, lift
up a fold of skin with the thumb and forenger while
giving the injection. Insert the entire length of the nee-
dle at a 45- to 90-degree angle. The skinfold should be
held throughout the injection. Inject the drug slowly,
leaving the needle in place for 10 seconds after injec-
tion. To minimize bruising, do not rub the injection site
after completion of the injection. Alternate injection
sites every 24 hours.
Periodic CBCs (including platelet count) and stool
occult blood tests are recommended during the course
of treatment with dalteparin. No special monitoring of
clotting times (e.g., aPTT) is required.
Medication Safety Alert
Do not inject dalteparin intramuscularly! To prevent loss
of drug, do not expel air bubble from prelled syringe before
injection.
Dosage Range
Angina, myocardial infarction: clot formation prophylaxis.
Subcutaneous: 120 units/kg (but no more than 10,000
units) every 12 hours with concurrent oral aspirin (75 to
165 mg/day) therapy.
Hip replacement surgery: DVT prophylax
is. Subcutaneous: 2500 to 5000 units before surgery.
At 4 to 8 hours after surgery, 2500 units. Postoperative
days: 5000 units daily. The usual duration of adminis-
tration is 5 to 10 days after surgery.
Abdominal surgery: DVT prophylaxis. Subcutaneous:
2500 units once daily, starting 1 to 2 hours before sur-
gery and repeating for 5 to 10 days postoperatively.
High-risk patients: In abdominal surgery patients at
high risk for thromboembolic complications (e.g.,
malignancy), administer 5000 units the evening be-
fore surgery and repeat once daily for 5 to 10 days
postoperatively. Alternatively, in patients with ma-
lignancy, administer 2500 units 1 to 2 hours before
surgery with an additional 2500 units 12 hours lat-
er, and then 5000 units once daily for 5 to 10 days
postoperatively. In medical patients with severely
restricted mobility during acute illness, 5000 units
administered once daily.
Treatment of symptomatic venous thromboembo
lism. Subcutaneous: In patients with cancer and
symptomatic venous thromboembolism, the recom-
mended dosage of dalteparin for the rst 30 days of
treatment is 200 units/kg total body weight once dai-
ly. Therapy of 150 mg/kg daily may be continued for
2 to 6 months. The total daily dose should not exceed
18,000 units.
Common adverse effects
Hematologic
Hematoma formation and bleeding at injection site.
Inappropriate administration techniques lead to he-
matoma formation at the site of injection. Use proper
technique!
Serious adverse effects
Hematologic
Bleeding. Inspect the skin and mucous membranes
for petechiae, ecchymoses, or hematomas; also moni-
tor for bleeding gums. Assess and record vital signs at
regular intervals. Monitor and report signs and symp-
toms of internal bleeding.
Medication Safety Alert
Signs and symptoms of internal bleeding include decreasing
blood pressure; increasing pulse; cold, clammy skin; feeling
faint; and disoriented sensorium.
Check urine and stools for blood. Urine may ap-
pear red, smoke colored, or brownish. Stools may
appear to be dark and tarry. Perform an occult blood
test on the stool if necessary. Vomitus may con-
tain bright red blood or may have a coffee-ground
appearance.
Assessment of dressings or drainage tubes for
any signs of bleeding is necessary for postoperative
patients.
Thrombocytopenia. Dalteparin may cause type I or II
heparin-induced thrombocytopenia (HIT) (see mono-
graph on heparin later in this chapter). Monitor plate-
let counts daily.
Thrombotic thrombocytopenic purpura. Thrombotic
thrombocytopenic purpura is a very rare but potentially
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26
life-threatening condition that may occur within the
rst 3 months of the initiation of therapy. Early indica-
tions are abnormal neurologic ndings and fever, fol-
lowed by renal impairment. If suspected, contact the
healthcare provider immediately.
Drug interactions. No clinically signicant drug in-
teractions have been reported, but dalteparin should
be used cautiously in patients receiving antiplatelet or
warfarin therapy.
enoxaparin (ĕ-nŏks-ă-PĂR-ĭn)
Do not confuse enoxaparin with enoxacin.
Lovenox (LŌ-vĕn-ŏks)
Do not confuse Lovenox with Avonex, Lanoxin, Lotronex,
Protonix, or Luvox.
Actions
Enoxaparin is the rst of the LMWHs that are essen-
tially the active components of the heparin protein
molecule. The LMWHs have the advantage of spe-
cic action at certain steps of the coagulation path-
way, resulting in less potential for hemorrhage and
longer duration of action. Enoxaparin is specically
active against factor Xa and thrombin; it prevents
completion of the coagulation cascade. Enoxaparin
has no antiplatelet activity and does not affect the PT
or aPTT.
Uses
Enoxaparin is used to prevent DVT after hip replace-
ment surgery, knee replacement surgery, or abdominal
surgery. It is also approved for use with warfarin to
treat acute DVT, with or without PE, and for treat-
ment of ST segment elevation MI. It is also used to
prevent ischemic complications of unstable angina
and NSTEMI when coadministered with aspirin.
Enoxaparin is manufactured from heparin derived
from pigs and should not be used in patients allergic
to pork by-products.
Therapeutic Outcome
The primary therapeutic outcome from enoxaparin
therapy is prevention of DVT after hip or knee replace-
ment surgery and ischemic complications of angina
and MI.
Nursing Implications for Enoxaparin
Premedication assessment
1. Perform scheduled laboratory tests, including CBC,
platelet count, and stool occult blood tests, before
starting enoxaparin therapy.
2. Obtain baseline vital signs.
Availability. Subcutaneous: 30 mg in 0.3 mL, 40 mg in
0.4 mL, 60 mg in 0.6 mL, 80 mg in 0.8 mL, 100 mg in
1 mL, 120 mg in 0.8 mL, and 150 mg in 1 mL. Each
431
concentration is packaged in a prelled syringe (pre-
servative free) with a 27-gauge, ½-inch needle. A
300-mg/3-mL multidose vial is available and contains
benzyl alcohol preservative.
Dosage and administration. Adult: Subcutaneous: Do
not expel the air bubble from the prelled syringe be-
fore administration. Administer by deep subcutaneous
injection into the anterolateral or posterolateral ab-
dominal wall every 12 to 24 hours. The entire length
of the needle should be introduced into a skinfold held
between the thumb and forenger; the skinfold should
be held throughout the injection. Inject the drug slow-
ly, leaving the needle in place for 10 seconds after in-
jection. To minimize bruising, do not rub the injection
site after completion of the injection. Rotate sites every
12 hours.
Periodic CBCs (including platelet count) and stool
occult blood tests are recommended during the course
of treatment with enoxaparin. No special monitoring
of clotting times is required.
Medication Safety Alert
 • Do not inject enoxaparin intramuscularly. To prevent
loss of drug, do not expel air bubble from a prelled
syringe before injection.
 • Dosage adjustment is required in patients with a
creatinine clearance lower than 30 mL/min.
 • Men less than 57 kg (125 lb) and women less than 45 kg
(99 lb) who receive standard doses of enoxaparin of 30
to 40 mg one or two times daily should be more carefully
observed for signs and symptoms of bleeding.
Dosage range. Subcutaneous: Prophylaxis: 30 mg
twice daily or 40 mg once daily, depending on the
medical and surgical condition.
Therapeutic: 1 mg/kg every 12 hours or 1.5 mg/kg
every 24 hours, administered at the same time daily.
Dosage adjustment is recommended for patients older
than 75 years.
Common adverse effects
Hematologic
Hematoma formation and bleeding at injection
site. Inappropriate administration techniques lead to
hematoma formation at the site of injection. Use prop-
er technique!
Serious adverse effects
Hematologic
Bleeding. Inspect the skin and mucous membranes
for petechiae, ecchymoses, or hematomas; also moni-
tor for bleeding gums. Assess and record vital signs
at regular intervals. Watch for and report signs and
symptoms of internal bleeding (e.g., decreasing blood
pressure; increasing pulse; cold, clammy skin; feeling
faint; disoriented sensorium).
432 UNIT IV Drugs Affecting the Cardiovascular System
Check urine and stools for blood. Urine may appear
red, smoke colored, or brownish. Stools may appear
to be dark and tarry. Perform an occult blood test on
the stool if necessary. Vomitus may contain bright red
blood or may have a coffee-ground appearance.
Assessment of dressings or drainage tubes for
any signs of bleeding is necessary for postoperative
patients.
Thrombocytopenia. Enoxaparin may induce type I or
type II HIT (see monograph on heparin later in this
chapter). Monitor platelet counts on a daily basis.
Thrombotic thrombocytopenic purpura. Thrombotic
thrombocytopenic purpura is a very rare but poten-
tially life-threatening condition that may occur within
the rst 3 months after the initiation of therapy. Early
indications are abnormal neurologic ndings and fe-
ver, followed by renal impairment. If suspected, con-
tact the healthcare provider immediately.
Drug interactions. No clinically signicant drug in-
teractions have been reported, but enoxaparin should
be used cautiously in patients receiving antiplatelet or
warfarin therapy.
VITAMIN K INHIBITOR
warfarin (WĂR-făr-ĭn)
Jantoven (jan toh ven)
Actions
Warfarin is a potent anticoagulant that acts by in-
hibiting the activity of vitamin K, which is required
for the activation of clotting factors II, VII, IX, and X
and proteins C and S in the blood. Blockade of the
activation of these factors prevents clot formation
(see Fig. 26.1).
Uses
Warfarin is used for treatment and prophylaxis of ve-
nous thrombosis, embolism associated with atrial -
brillation or heart valve replacement, PE, and coronary
occlusion. The dosage of warfarin is adjusted based on
INR. In general, the target range for the INR with war-
farin therapy is 2 to 3 when treating atrial brillation,
embolic stroke, MI, and DVT. When anticoagulating
the patient with a mechanical prosthetic heart valve,
the target INR range is 2.5 to 3.5.
Therapeutic Outcomes
The primary therapeutic outcomes from warfarin ther-
apy are as follows:
1. Prevention and treatment of venous thrombosis and
embolism
2. Prevention and treatment of thromboemboli associ-
ated with atrial brillation
3. Reduced risk of death, recurrent MI, and thrombo-
embolic events, such as stroke, after MI
4. Prevention and treatment of thromboemboli associ-
ated with cardiac valve replacement
Nursing Implications for Warfarin
Premedication assessment
1. Obtain baseline vital signs.
2. Always check the most recent PT or INR results to
determine whether they are within the recommend-
ed range for warfarin therapy.
3. Inspect the skin and mucous membranes for pete-
chiae, ecchymoses, or hematomas. Also monitor for
hematuria, bleeding gums, and melena before ad-
ministering each dose of medication.
4. Ensure that patients of childbearing age are not
pregnant at the time warfarin therapy is initiated.
Warfarin therapy should be avoided during preg-
nancy, particularly in weeks 6 through 12 and at term.
Warfarin may be administered during pregnancy in
patients with prosthetic heart valves after discussing
the risks and benets of therapy with the patient.
5. Provide dietary education to include information on
those foods high in vitamin K, including green leafy
vegetables.
Availability. PO: Tablets: 1, 2, 2.5, 3, 4, 5, 6, 7.5, and 10 mg.
Dosage and administration. Adult: Dosage adjustment:
Dosage during therapy is based on the PT. The PT
is expressed as the INR, an internationally accepted
standard for adjusting for variability in the PT assay.
The optimal dosage is that which prolongs the INR
at 2 to 3. Certain medical conditions (e.g., mechanical
prosthetic valves, recurrent systemic embolism) re-
quire an INR of 2.5 to 3.5 and concurrent antiplatelet
therapy.
When warfarin therapy is initiated, the patient
should be monitored closely for evidence of hemor-
rhage because of the drug’s cumulative effects.
Stress the need to comply with the prescribed regi-
men and the need for laboratory data to determine the
correct maintenance dose. Instruct the patient to re-
sume a regular schedule if one dose is missed. If two
or more doses are missed, the patient should consult
the healthcare provider.
PO: Initial: 2 to 5 mg/day, adjusting the dosage ev-
ery few days until the INR is in the target range. Use of
a loading dose is not recommended because it does not
anticoagulate the patient any more rapidly than start-
ing with maintenance doses and may result in severe
hemorrhagic complications.
Maintenance: 2 to 10 mg daily as determined by the
INR.
Antidote. Vitamin K is a specic antidote for warf-
arin-induced hemorrhage or reversal of an exces-
sively high INR. Most cases of bleeding induced by
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26 433

warfarin overdose can be controlled by discontinu- Drugs that decrease therapeutic effects. The following
ing warfarin therapy. A prothrombin complex con- drugs, foods, and herbal supplements, when used con-
centrate is available for urgent reversal in patients currently with warfarin, may decrease its therapeutic
with acute major bleeding or a need for an urgent activity:
surgery/invasive procedure. An alternative in se-
vere hemorrhage is a transfusion with fresh frozen
acerola cholestyramine ritonavir
plasma or whole blood. aprepitant coenzyme rose hip
azathioprine Q10 smartweed
Common adverse effects black psyllium dicloxacillin St. John’s
Hematologic blond psyllium etretinate wort
Bleeding. Inspect the skin and mucous membranes bosentan griseofulvin sucralfate
for petechiae, ecchymoses, or hematomas; also moni- cabbage mercaptopurine terbinane
tor for bleeding gums. Assess and record vital signs at carbamazepine mesalamine trazodone
regular intervals. Always monitor menstrual ow to be chlordiazepoxide nafcillin vitamin C
certain that it is not excessive or prolonged. Monitor phenobarbital vitamin K
and report signs and symptoms of internal bleed- rifampin
ing (e.g., decreasing blood pressure; increasing pulse;
cold, clammy skin; feelings of faintness; disoriented All prescription and nonprescription medications. Caution
sensorium). the patient not to take any over-the-counter (includ-
Check urine and stools for blood. Urine may appear ing herbal supplements) or prescription medications
red, smoke colored, or brownish. Stools may appear without rst consulting a healthcare provider or
to be dark and tarry. Perform an occult blood test on pharmacist.
the stool if necessary. Vomitus may contain bright red
blood or may have a coffee-ground appearance. THROMBIN INHIBITORS
Assessment of dressings or drainage tubes for
any signs of bleeding is necessary for postoperative dabigatran (dă-BĬG-ă-trăn)
patients. Do not confuse dabigatran with dalteparin
Pradaxa (pră-DĂK-să
Drug interactions
Drugs that enhance therapeutic and toxic effects. The
following drugs, foods, and herbal supplements, when Actions
used concurrently with warfarin, may enhance its ther- Dabigatran is a direct thrombin inhibitor. Inhibition
apeutic and toxic effects: of thrombin prevents the conversion of fibrinogen
to fibrin, which is required for the formation of a
acetaminophen uorouracil omeprazole thrombus (blood clot). The oral dosage form, dab-
allopurinol uoxetine paclitaxel igatran etexilate, is a prodrug that is rapidly con-
amiodarone utamide papaya verted to dabigatran, which is further metabolized
anabolic steroids uvastatin phenytoin to four active metabolites. Dabigatran and the four
aspirin uvoxamine piroxicam active metabolites also inhibit thrombin-induced
beta blockers gemcitabine propafenone platelet aggregation, another essential step in clot
capecitabine ginkgo biloba propranolol formation.
cimetidine grapefruit quinidine
Three other direct thrombin inhibitors—argatroban,
ciprooxacin ifosfamide ropinirole
cisapride isoniazid salicylates
bivalirudin, and desirudin—are used in specialized
citalopram itraconazole sertraline cases (see Uses section).
clobrate ketoconazole simvastatin
cotrimoxazole levooxacin sulnpyrazone Uses
danshen lovastatin sulfonamides Dabigatran is approved and orally administered to:
devil’s claw lyceum tamoxifen • Reduce the risk of stroke and systemic embolism in
diltiazem methyl salicylate tetracyclines patients with nonvalvular atrial brillation.
disulram (oil of thyroid • Treat DVT and PE in patients who have been
dong quai wintergreen) hormones treated with a parenteral anticoagulant for 5 to 10
entacapone metronidazole tolterodine days.
erythromycin miconazole tramadol
• Reduce the risk of recurrence of DVT and PE in pa-
ethanol moricizine valproate
fenobrate noroxacin voriconazole
tients who have been previously treated.
sh oil NSAIDs ooxacin zarlukast • Provide prophylaxis for DVT and PE in patients
uconazole zileuton who have undergone hip replacement surgery.
434 UNIT IV Drugs Affecting the Cardiovascular System
A major advantage of dabigatran is that it does not
require monitoring of blood tests with resultant dos-
age adjustments, as do warfarin and IV heparin.
The other direct thrombin inhibitors are approved
for the following uses:
• Argatroban is approved as an anticoagulant for use
in patients at risk of HIT undergoing a PCI or in pa-
tients being treated for HIT. It is administered intra-
venously by continuous infusion.
• Bivalirudin is approved as an anticoagulant for
patients undergoing PCI, patients with unstable
angina undergoing PCI, and in patients at risk for
or who are being treated for HIT. It is administered
intravenously by continuous infusion.
• Desirudin is approved for postoperative prophylax-
is for patients undergoing hip replacement surgery.
It is administered subcutaneously.
Therapeutic Outcome
The primary therapeutic outcome expected from the
direct thrombin inhibitors is prevention and treatment
of thrombosis in specialized cases.
Nursing Implications for Dabigatran
Premedication assessment
1. Obtain baseline blood pressure readings in supine
and standing positions and apical pulse.
2. Initiate laboratory studies as requested by the
healthcare provider (e.g., renal function tests such
as serum creatinine, CBC, ECT, TT, and aPTT) to
serve as a baseline for future comparison. If the
ECT is not available, the aPTT may be used. The PT
(INR) is not a good indicator of dabigatran coagula-
tion activity.
3. Ask whether the patient is pregnant or likely to be-
come pregnant. If so, discuss with the healthcare
provider before initiating dabigatran therapy.
4. Obtain a history of bowel elimination patterns and
any GI symptoms, frequency of headaches, dizzi-
ness, and fatigue.
Availability. PO: 75-, 110-, and 150-mg capsules.
Dosage and administration
Nonvalvular atrial brillation. To reduce the risk of stroke
and systemic embolism: PO: 150 mg twice a day. If cre-
atinine clearance is less than 30 mL/min, the dose is 75
mg PO twice a day.
DVT and PE. Treatment and prevention: PO: 150
mg twice daily, after 5 to 10 days of parenteral
anticoagulation.
Reduction of recurrence: PO: 150 mg twice daily.
Prophylaxis after hip replacement surgery: PO: 110 mg
given 1 to 4 hours after completion of surgery and es-
tablishment of hemostasis; if not initiated on the day
of surgery, initiate therapy with 220 mg once daily
after hemostasis has been achieved. Maintenance:
220 mg once daily (total duration of therapy: 28 to 35
days).
Prophylaxis after knee replacement surgery: PO: 150 or
220 mg once daily for 10 to 35 days with a half-dose 1
to 4 hours after surgery.
Medication Safety Alert
 • The capsules must be swallowed whole with a full glass
of water. Do not crush the capsule or pull it apart and
sprinkle the pellets on food. A severe overdose may
potentially result.
 • If a dose is not taken at the scheduled time, it should
be taken as soon as possible on the same day. If the
dose cannot be taken at least 6 hours before the next
scheduled dose, it should not be taken. Do not double up
on doses at the same time.
 • Dabigatran capsules are sensitive to moisture. Reseal the
bottle quickly after taking a capsule out. The container
holds 60 capsules that should be taken within 30 days.
Once the bottle has been opened, use within 30 days.
Antidote. Idarucizumab (Praxbind) is used as an an-
tidote to reverse bleeding caused by dabigatran.
Common adverse effects
Hematologic
Bleeding. A normal physiologic effect of dabigatran
is prolongation of bleeding time. Patients should re-
port any incidents of bleeding as soon as possible.
Incidents to be reported include nosebleeds; easy
bruising; bright red or coffee-ground emesis; hematu-
ria; and dark, tarry stools.
Patients should inform other healthcare practitio-
ners (e.g., another physician, dentist) that they are re-
ceiving thrombin inhibitor therapy.
Gastrointestinal
Dyspepsia, reux, gastritis. These adverse effects may
be early indications of GI bleeding. Observe for dark,
tarry stools and report to the healthcare provider.
Encourage the patient not to discontinue therapy with-
out rst consulting the healthcare provider.
Drug interactions
Drugs that enhance therapeutic and toxic ef
fects. Heparin, LMWHs, warfarin, aspirin, NSAIDs,
fondaparinux, and direct thrombin inhibitors (arga-
troban, bivalirudin, desirudin) will have an additive
bleeding effect in the patient. Monitor very closely
for indications of bleeding. Caution should be used
when any of these drugs are coadministered with
dabigatran.
DRUG CLASS: FIBRINOLYTIC AGENTS
Signicant advances have been made in the treatment
of thromboemboli. Enzymes have been discovered that
work in the clotting system to dissolve recently formed
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26
thrombi. The agents used are called brinolytic agents
because of their ability to cause the dissolution of brin
clots.
All brinolytic agents increase the risk of bleeding,
including intracranial bleeding, and should be used
only in eligible patients. In addition, brinolytic ther-
apy increases the risk of intracranial hemorrhage in
older adult patients.
The goals of brinolytic therapy are to lyse the
thrombi during the early phase of clot formation, limit
the damage to surrounding tissues by restoring circu-
lation to the area distal to the thrombus, and reduce
the morbidity and mortality after the formation of a
thromboembolism.
Actions
Fibrinolytic agents work by stimulating the body’s own
clot-dissolving mechanism, converting plasminogen,
a naturally occurring substance secreted by endothe-
lial cells in response to injury to the artery, to plasmin
(also known as brinolysin), which digests brin. The
clot is then dissolved, restoring blood ow to the area.
There are currently four brinolytic agents available:
alteplase, reteplase, and tenecteplase.
• Alteplase (recombinant tissue plasminogen activa-
tor [rtPA]; Activase) is of proven clinical effective-
ness, more clot specic (a lower potential for hem-
orrhage elsewhere in the body), and nonantigenic.
Disadvantages are a 10- to 20-fold higher cost, a
prolonged administration time, and the need for
concurrent heparin therapy.
• Reteplase (rtPA; Retavase) is administered as two
boluses to dissolve clots. It is of proven clinical
effectiveness, more clot specic (a lower poten-
tial for hemorrhage elsewhere in the body), and
435
nonantigenic. Its disadvantage is the need for con-
current heparin therapy.
• Tenecteplase (rtPA; TNKase) is approved for use to
treat clots associated with MI. It is the rst clot buster
that can be administered over 5 seconds in a single
dose, offering healthcare providers the fastest admin-
istration of a thrombolytic to date in the treatment of
heart attack. Tenecteplase is a bioengineered variant
of alteplase. The ease of administration may allow
this drug to be administered outside the hospital
while the patient is being transported to a cardiovas-
cular center, buying potentially lifesaving time.
Uses
The brinolytic agents are used to dissolve clots second-
ary to coronary artery occlusion (MI, also known as acute
coronary syndrome), PE, and stroke. Alteplase is used
to treat cerebral embolism (stroke). The decisions for
use and selection of the agent depend on the location of
the thrombus, clinical condition and age of the patient,
preference of the patient care team, and availability of al-
ternative therapies, such as angioplasty or bypass graft
surgery. A key factor in the successful treatment of these
conditions is the early treatment with a brinolytic agent.
Fibrinolytic agents tend to be much more successful
against the soluble brin clot in restoring circulation to
the obstructed area, rather than older, insoluble clots.
Alteplase and reteplase may also be used to reopen
IV catheters, including central venous catheters, ob-
structed by blood clots.
Therapeutic Outcome
The primary therapeutic outcome from brinolytic
therapy is reperfusion of the tissues obstructed by the
thrombus.
436 UNIT IV Drugs Affecting the Cardiovascular System

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points
• Disorders caused by intravascular clotting are major PLATELET THROMBIN FIBRINOLYTIC ANTI
causes of death and must be treated rapidly to reduce INHIBITORS INHIBITORS AGENTS COAGULANTS
tissue damage associated with thrombosis.
Breaks
• The major pharmacologic therapeutic agents are platelet up an
inhibitors, factor Xa inhibitors, anticoagulants, thrombin existing
inhibitors, glycoprotein IIb/IIIa inhibitors, and brinolytic thrombus
agents.
Prevents
• Nurses can play a signicant role, especially in the
thrombus
nonpharmacologic prevention and treatment of
formation
thromboembolic disease, which includes patient education
on how to prevent venous stasis and appropriate use of Prevents
prescribed medicines. platelet
aggregation

Additional Learning Resources Decreases

bleeding
SG Go to your Study Guide for additional Review Questions time
for the NCLEX® Examination, Critical Thinking Clinical Situa Prevents
tions, and other learning activities to help you master this chap- the
ter content. extension
of an
Go to your Evolve website (https://evolve.elsevier.com/Willihng existing
anz) for additional online resources. thrombus

Clinical Judgment and Next-Generation NCLEX® Exam

ination-Style Questions The following questions are typical of Objective: Identify the actions of platelet inhibitors, anticoagulants,
the NCLEX exam and include both NGN (Next Generation) and thrombin inhibitors, and brinolytic agents.
traditional questions. See Chapter 1 for further information re- NCLEX item type: Matrix
garding question types. Cognitive skill: Evaluate cues
3. The nurse is reviewing an order for alteplase, a brinolytic agent,
Scenario to be administered for a hospitalized patient and recognizes that
A patient recently developed palpitations and went to see this drug can be used for which reasons? (Select all that apply.)
a healthcare provider who diagnosed atrial brillation. The 1. To prevent the extension of a thrombus
patient was then started on an antiarrhythmic and an anti- 2. To reopen a central venous catheter
coagulant. 3. To maintain patency of a stent after PCI
4. To dissolve a thromboemboli once formed
1. The nurse recognizes which of the following conditions are reasons 5. To prevent a stroke in patients with atrial brillation
for having patients receive anticoagulant therapy? (Select all that
apply.) Objective: Identify the actions of platelet inhibitors, anticoagulants,
thrombin inhibitors, and brinolytic agents.
1. Atrial brillation NCLEX item type: Multiple response
2. History of pulmonary emboli Cognitive skill: Application
3. Recent hip surgery
4. Hematuria 4. The patient in the scenario with atrial brillation is started on
5. Asthma warfarin; which laboratory tests will be monitored to determine
6. At-risk pregnancy the correct dosage? (Select all that apply.)
7. Hypertension 1. INR
Objective: Describe conditions that place an individual at risk for 2. Anti-Xa
developing blood clots and nursing interventions used to prevent 3. Platelets
these conditions. 4. ACT
NCLEX item type: Extended multiple response 5. PT
Cognitive skill: Application Objective: Describe specic monitoring procedures and laboratory
2. The nurse reviewed the mechanism of action for those medications data used to detect hemorrhage in the patient taking anticoagulants.
that are used for patients with blood clots or for those at risk for NCLEX item type: Multiple response
developing blood clots. Indicate with an ‘X’ the effect each drug Cognitive skill: Application
classication will have.
 Drugs Used to Treat Thromboembolic Disorders CHAPTER 26 437

5. The nurse initiates discharge teaching for the patient in the

scenario who is being maintained on warfarin after hospitalization THERAPEUTIC ADVERSE
to prevent clot formation. Which statement by the patient indicates ASSESSMENT FINDING EFFECT EFFECT
that further teaching is needed?
Positive guaiac stool test
1. “I should wear a Medic-Alert bracelet to indicate I am on Stable vital signs after
anticoagulant therapy.” taking these drugs for
2. “I should change my diet to include more green leafy several months
vegetables.”
3. “I will check with my physician or pharmacist before I Hematuria
begin or stop any medication.” Moist clammy skin, weak
4. “I will need to have my blood drawn routinely to monitor rapid pulse
the effects of the warfarin.” INR is 2.2
Objective: Describe the nursing assessments needed to monitor
therapeutic response and adverse effects from anticoagulant
Objective: Describe the nursing assessments needed to monitor
therapy.
therapeutic response and adverse effects from anticoagulant
NCLEX item type: Multiple choice
therapy.
Cognitive skill: Evaluation
NCLEX item type: Matrix
6. The nurse will monitor the therapeutic effect, as well as the Cognitive skill: Evaluate cues
adverse effects of anticoagulation therapy. Indicate with an “X”
which assessment nding is part of the therapeutic effect and
which is an adverse effect from anticoagulation therapy.
27 Drugs Used to Treat Heart Failure

https://evolve.elsevier.com/Willihnganz

Objectives
1. Explain heart failure in terms of the body’s compensatory
mechanisms.
2. Identify the goals of treatment for heart failure.
3. Identify the primary actions on heart failure of digoxin,
angiotensin-converting enzyme inhibitors, angiotensin
receptor blockers (ARBs), the combination of a neprilysin
inhibitor with an ARB (Entresto), and beta blockers.
4. Describe digoxin toxicity and ways to prevent it.
5. Identify essential assessment data and nursing
interventions needed for a patient with heart failure.

Key Terms
heart failure with reduced ejection
fraction (p. 438)
heart failure with preserved
ejection fraction (p. 438)
inotropic agents (ĭn-ō-TRŌ-pĭk
Ā-jĕnts) (p. 440)
digitalis toxicity (dĭ-jĭ-TĂL-ĭs tŏk-SĬS-ĭ- digitalization (dĭ-jĭ-tăl-ī-ZĀ-shŭn)
tē) (p. 445) (p. 448)
positive inotropy (PŎZ-ĭ-tĭv ī-nō-TRŌ-
pē) (p. 448)
negative chronotropy (NĔG-ĕ-tĭv krō-
nō-TRŌ-pē) (p. 448)

HEART FAILURE
Th incidnc f har failur (prviusly knwn as
congestive heart failure)—unlik ha f hr cardi-
vascular disass—cninus  incras as a rsul f
ppulain aging and imprvd survival afr acu
mycardial infarcin (MI). Th lifim risk f dvl-
ping har failur is 20%  45% fr Amricans agd 45
 95 yars. An simad 6.5 millin Amricans hav
his disabling cndiin; mr han 960,000 pains
dvlp har failur annually, and mr han 300,000
ppl di f har failur ach yar. Th 5-yar mr-
aliy ra fr har failur is apprximaly 50%. Th
cnmic burdn is saggring, wih an simad -
al cs f $30 billin fr managing har failur in h
Unid Sas (Bnjamin al, 2019).
Har failur invlvs a clusr f signs and symp-
ms ha aris whn h lf r righ vnricl r bh
vnricls ls h abiliy  pump nugh bld 
m h bdy’s circulary nds. Th ms cmmn
yp f har failur is heart failure with reduced ejec-
tion fraction (HFrEF), Nrmally, h har pumps a a
ra ha supprs h bdy’s nd fr bld w and
xygnain f h vial rgans and muscls. HFrEF
ccurs whn h har lacks sufcin frc (cnrac-
iliy)  pump h bld  m h bdy’s xygn-
ain nds (causing dcrasd issu prfusin). Early
clinical sympms ar dcrasd xrcis lranc and
pr prfusin  h priphral issus. As h cn-
diin prgrsss, h lf vnricl chambr nlargs
438
(lf vnricular hyprrphy) and an incras in bld
vlum is rquird  ll h xpanding vnricl 
mainain cardiac upu. Causs f HFrEF ar hs
ha caus damag  h har muscl islf. Th ms
cmmn caus is crnary arry disas ha lads
 MI. Ohr causs includ dysrhyhmias, cardi-
mypahis, and cngnial har disas. Usually h
lf vnricl fails rs and, as h disas prgrsss,
h righ vnricl als nlargs as a rsul f incrasd
pulmnary rsisanc, and i vnually fails.
Heart failure with preserved ejection fraction (HFpEF)
causs har failur bcaus h lf vnricl dvl-
ps a “siffnss” and fails  rlax nugh bwn
cnracins  allw adqua lling bfr h nx
cnracin. HFpEF includs pulmnary cngsin
and priphral dma. Thr ar many rasns why
HFpEF dvlps, including cnsriciv pricardiis,
vnricular muscl hyprrphy causd by chrnic
hyprnsin, valvular har disas ha rsuls in
w rsisanc, and aric snsis.
Th gnral pahgnsis f har failur is dia-
grammd in Fig. 27.1. Whn h vial rgans and priph-
ral issus ar n adqualy prfusd, cmpnsary
mchanisms bgin  vrcm h inadqua upu
f h har. Th nariuric sysm is acivad primarily
by vlum xpansin. Th nariuric ppids rlasd
ar bncial, causing a dcras in bld prssur
and diursis. Th sympahic nrvus sysm rlas-
s pinphrin and nrpinphrin, which prduc
 Drugs Used to Treat Heart Failure CHAPTER 27 439

Natriuretic peptides Natriuresis/Diuresis

Failing heart
ANP and BNP decrease blood pressure

Neprilysin

Arterial
Inactive fragments
blood pressure

 -adrenergic stimulation

Sympathetic
Renin
activity

 -adrenergic
 blockers ACEI
stimulation

Vasoconstriction Angiotensin II Aldosterone

ARBs ARBs
vasodilators
aldosterone
Afterload antagonists

Na retention

Myocardial O2
demand
diuretics

Worsening Vascular
Preload
heart failure volume

vasodilators

Fig. 27.1 Pathway showing how heart failure develops and how specic classes of medicines block physiologic
mechanisms to reduce the worsening of heart failure. Cardiac glycosides and phosphodiesterase inhibitors are also
used to increase myocardial contractility. ACEI, Angiotensin-converting enzyme inhibitor; ANP, atrial natriuretic peptide;
ARBs, angiotensin II receptor blockers; BNP, B-type natriuretic peptide; β blockers, beta-adrenergic blocking agents.

achycardia and incras cnraciliy. Th incrasd
sympahic simulain als incrass priphral va-
scnsricin, which rsuls in an incrasd afrlad
agains which h har mus pump, causing a furhr
dcras in cardiac upu (s Fig. 27.1). Th rnin-
anginsin-aldsrn sysm simulas rnal disal
ubul sdium and war rnin in an ffr  incras
circulaing bld vlum, which incrass prlad  h
har. Thr is als an incrasd prducin f vasprs-
sin (anidiuric hrmn) frm h piuiary gland ha
incrass war rcvry frm h kidnys and incrass
inravascular vlum and prlad. Wih dcrasd pr-
fusin scndary  lw cardiac upu, h kidnys als
incras sdium rabsrpin in h prximal ubuls 
hlp xpand circulaing bld vlum. Th incrasd in-
ravascular vlum iniially imprvs issu prfusin;
hwvr, vr im, xcssiv amuns f sdium and
war ar raind, causing incrasd prssur wihin
h capillaris, rsuling in dma frmain.
Early sympms f har failur vary dpnding n
h undrlying caus f h disas. Tradiinally, h
signs and sympms f har failur hav bn clas-
sid n h basis f whhr failur is dvlping in
h righ vnricl r h lf vnricl. Hwvr, i has
bn fund ha, bcaus f h cmplxiy f h syn-
drm, h sympms vrlap  such an xn ha
i is difcul  aribu a paricular clinical indicar
 a spcic vnricl. I is als impran  rcgniz
ha h clinical indicars vary cnsidrably vr im
in rspns  h ramns bing applid (Bx 27.1).
TREATMENT OF HEART FAILURE
Th vrall gals fr raing har failur ar  r-
duc h signs and sympms assciad wih uid
vrlad, incras xrcis lranc, imprv qualiy
f lif, and prlng lif. If h har failur is acu, h
pain mus b hspializd fr a diagnsic wrkup
 drmin h undrlying caus. A cmbinain
f h Amrican Cllg f Cardilgy Fundain
and h Amrican Har Assciain (ACCF/AHA) and
h Nw Yrk Har Assciain (NYHA) Funcinal
440 UNIT IV Drugs Affecting the Cardiovascular System

Box 27.1 Clinical and Laboratory Presentation of Heart Failure

GENERAL • Narrow pulse pressure
Patient presentation may range from asymptomatic to • Cardiomegaly
cardiogenic shock. • Peripheral edema
• Jugular venous distention
SYMPTOMS
• Hepatojugular reux
• Dyspnea, particularly on exertion
• Hepatomegaly
• Orthopnea
• Venous stasis changes
• Paroxysmal nocturnal dyspnea
• Lateral displacement of apical impulse
• Exercise intolerance
• Tachypnea LABORATORY TESTS
• Cough • B-type natriuretic peptide (BNP) level >100 pg/mL
• Fatigue • N-terminal proBNP level >300 pg/mL
• Nocturia • Electrocardiography: May be normal or could show
• Hemoptysis numerous abnormalities, including acute ST-T wave
• Abdominal pain changes from myocardial ischemia, atrial brillation,
• Anorexia bradycardia, and left ventricular hypertrophy
• Nausea • Serum creatinine: May be increased as a result of
• Bloating hypoperfusion; preexisting renal dysfunction can
• Poor appetite; early satiety contribute to volume overload
• Ascites • Complete blood count: Useful to determine whether
• Mental status changes heart failure is caused by reduced oxygen-carrying
• Weight gain or loss capacity
• Chest radiography: Useful for detection of cardiac
SIGNS
enlargement, pulmonary edema, and pleural effusions
• Pulmonary crackles
• Echocardiography: Used to assess left ventricular
• Pulmonary edema
size, valve function, pericardial effusion, wall motion
• S3 gallop
abnormalities, and ejection fraction
• Cool extremities
• Hyponatremia: Serum sodium level <130 mEq/L is
• Pleural effusion
associated with reduced survival and may indicate
• Cheyne-Stokes respiration
worsening volume overload or disease progression
• Tachycardia
From Parker RB, Nappi JM, Cavallari LH. Chronic heart failure. In: DiPiro JP, Yee G, Posey M et al, eds. Pharmacotherapy: A Pathophysiologic Approach. 11th ed. New
York: McGraw-Hill; 2020.

Classicain Sysm is cmmnly usd  grup pa-
ins wih har failur accrding  h dgr f im-
pairmn (Tabl 27.1). Th ACCF/AHA sags f har
failur fcus n h dvlpmn and prgrssin f
disas and ar usd  dscrib individuals and pp-
ulains, whras h NYHA classs mphasiz clini-
cal aspcs such as xrcis capaciy and sympms f
har failur. Fig. 27.2 illusras an updad classi-
cain schm ha includs ramn guidlins frm
h ACCF/AHA. Har failur is rad by crrcing
h undrlying disas (.g., crnary arry disas,
hyprnsin, dyslipidmia, hyrid disas), smking
cssain, rgular xrcis whn abl, bd rs whn
ncssary, fllwing a sdium-rsricd di, and
cnrlling sympms wih a cmbinain f pharma-
clgic agns. Halhcar insiuins ar valuad
accrding  h cr masurs ha prm qualiy
ucms fr pains wih har failur. Ths includ
prviding discharg ducain ha is spcic  h
disas managmn f har failur and  smking
cssain, masuring lf vnricular funcin during
hspializain, prscribing an anginsin-cnvring
nzym (ACE) inhibir r an anginsin II rcpr
blckr (ARB) fr pains wih HFrEF, and rpring
h 30-day mraliy ra f pains wih har failur.
DRUG THERAPY FOR HEART FAILURE
ACTIONS
Har failur is rad wih a cmbinain f vas-
dilar, diuric, and inrpic hrapy (s Fig. 27.1).
If h failur is acu, ms hrapy will b adminis-
rd by h inravnus (IV) ru in an innsiv
car uni. Vasdilars ar usd  rduc h srain
n h lf vnricl by rducing h sysmic vascular
rsisanc (afrlad) agains which h lf vnricl
is wrking. Th rducd vascular rsisanc will als
incras issu prfusin  vial rgans and muscls.
Th scnd gal f vasdilar us is  rduc prlad
s ha h high vlum f bld rurning  h har
is dcrasd. Th rducin in prlad dcrass pul-
mnary cngsin and allws h pain  brah
mr asily (Fig. 27.3). As rnal prfusin is imprvd,
pn diurics ar adminisrd  nhanc sdium
and war xcrin. This prvids subsanial symp-
maic rlif  h pain in addiin  rducing h
wrklad n h har.
Inotropic agents simula h har  incras h
frc f cnracins, hrby bsing cardiac upu.
This als hlps rduc pulmnary cngsin and im-
prv issu prfusin.
 Drugs Used to Treat Heart Failure CHAPTER 27 441

Table 27.1 Comparison of ACCF/AHA Stages of Heart Failure and the NYHA Functional Classication System a
ACCF/AHA STAGES OF HEART NYHA FUNCTIONAL CLASSIFICATION SYSTEM
FAILURE FUNCTIONAL CAPACITY OBJECTIVE ASSESSMENT
A At risk for heart failure but no No classication
structural heart disease or
symptoms
B Structural heart disease but Class I: Patients who have cardiac disease but without limitation No objective evidence of
without signs or symptoms of physical activity. Ordinary physical activity does not cause cardiovascular disease.
undue fatigue, palpitation, dyspnea, or anginal pain.
C Structural heart disease with Class I: as above Class II: Patients who have cardiac disease Objective evidence of
prior or current symptoms resulting in slight limitation of physical activity. Comfortable minimal cardiovascular
of heart failure at rest. Ordinary physical activity results in fatigue, disease.
palpitation, dyspnea, or anginal pain.
Class III: Patients who have cardiac disease resulting in Objective evidence of
marked limitation of physical activity. They are comfortable moderately severe
at rest. Less-than-ordinary activity causes fatigue, cardiovascular disease.
palpitation, dyspnea, or anginal pain.
D Refractory heart failure Class IV: Patients who have cardiac disease resulting in Objective evidence of
requiring specialized inability to carry on any physical activity without discomfort. severe cardiovascular
interventions Symptoms of heart failure or the anginal syndrome may be disease.
present even at rest. If any physical activity is undertaken,
discomfort is increased.
ACCF, American College of Cardiology Foundation; AHA, American Heart Association; NYHA, New York Heart Association.
aFunctional Capacity and Objective Assessment are independent categories. Functional Capacity is an estimate of what the patient’s heart will allow the patient to do

and should not be inuenced by the character of the structural lesions or by any opinion regarding the patient’s treatment or prognosis. Objective Assessment is based
on parameters such as electrocardiograms, stress tests, x-ray studies, echocardiograms, and radiologic images.
From Criteria Committee of the New York Heart Association. Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels . 9th ed. Boston:
Little, Brown; 1994; and Yancy CW, Jessup M, Bozkurt B, etal. ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American
Colleges of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2013;128(16):1810-1852.

USES and spirnlacn, Chapr 28) may prvid addi-

IV nirglycrin (s Chapr 24) and nirprussid (s
Chapr 22) ar usd as vasdilars  rduc prlad
and afrlad in criically ill pains. ACE inhibirs,
ARBs (s Chapr 22), and a cmbinain prduc, an-
ginsin rcpr blckr wih a nprilysin inhibir
(ARNI), (valsaran-sacubiril [Enrs]) ar h main-
says f ral vasdilar hrapy fr raing chrnic
har failur. Ms pains wih har failur rquir
a lp diuric such as fursmid r bumanid (s
Chapr 28)  hlp rduc uid and sdium vrlad.
Sudis hav indicad ha crain pains will
als bn frm h us f ba-adrnrgic blcking
agns. A majr cmpnn f h pahphysilgic
causs f har failur is incrasd sympahic aciv-
iy. Carvdill, a nncardislciv ba blckr and
an alpha-1 blckr, blcks adrnrgic aciviy whil
lwring sysmic vascular rsisanc as a vasdilar
(s Chaprs 12 and 22). Ohr vasdilars usd in-
clud issrbid (s Chapr 24) and hydralazin (s
Chapr 22).
A cmbinain prduc cnaining hydralazin and
issrbid dinira (BiDil) has bn apprvd by h US
US Fd and Drug Adminisrain. I has bn shwn
 rduc hspializains, imprv qualiy f lif,
and rduc mraliy amng African Amricans wih
hyprnsin and har failur. Guidlins als rc-
mmnd ha ARBs (s candsaran, Chapr 22) and
aldsrn anagniss (s plrnn, Chapr 22,
inal bn fr pains wh ar sill sympmaic
whil rciving full hrapuic dss f an ACE inhib-
ir and a ba blckr r hs wh hav dvlpd
advrs ffcs frm h sandard hrapis.
Ivabradin is usd wih ba blckrs fr h man-
agmn f har failur. Dapaglizin (Farxiga) (s
Chapr 35) has bn apprvd fr us in pains wih
HRrEF. Th Amrican Cllg f Cardilgy, h AHA,
and h Har Failur Sciy f Amrica publishd a
fcusd upda f h 2013 ACCF/AHA guidlin fr
h managmn f har failur (Yancy al, 2017).
Inrpic agns usd  ra acu har failur in-
clud IV dbuamin (s Chapr 12) and milrinn.
Digxin, a digialis glycsid, has bn usd fr d-
cads  ra har cndiins whn an ral inrpic
agn is ndd.
NURSING IMPLICATIONS FOR HEART FAILURE
THERAPY
Assessment
History of heart disease. Obain h pain’s hisry
f ramn fr har disas, rlad cardivascular
disas (.g., hyprnsin, hyprlipidmia), diabs
mllius, and lung disas.
Medication history. Obain dails f all mdicains
ha hav bn prscribd  h pain. Tacfully d-
rmin whhr h prscribd mdicains ar bing
442 UNIT IV Drugs Affecting the Cardiovascular System

At Risk for Heart Failure Heart Failure

STAGE A STAGE B STAGE C STAGE D

At high risk for HF Structural heart Structural heart disease Refractory HF
but without structural disease but without with prior or current requiring specialized
heart disease or signs or symptoms symptoms of HF. interventions.
symptoms of HF. of HF.

Patients with: Patients with: Patients with: Patients with:

• Hypertension • Previous MI • Known structural Marked symptoms at
• Atherosclerotic disease • LV remodeling heart disease rest despite maximal
• Diabetes including LVH and and medical therapy
• Obesity low EF • Shortness of (e.g., those who are
• Metabolic syndrome Structural • Asymptomatic Development breath and fatigue, Refractory recurrently
or valvular disease of symptoms reduced exercise symptoms of hospitalized or
heart
Patients disease of HF tolerance HF at rest cannot be safely
• Using cardiotoxins discharged from the
• With FHx CM hospital without
specialized
interventions)

HFpEF HFrEF

THERAPY THERAPY THERAPY THERAPY THERAPY

GOALS GOALS GOALS GOALS GOALS
• Treat hypertension • All measures under • Control symptoms • Control symptoms • Appropriate measures
• Encourage smoking Stage A • Improve health-related • Patient education under Stages A, B, C
cessation • Prevent HF quality of life (HRQOL) • Prevent hospitalization • Control symptoms
• Treat lipid disorders symptoms • Prevent hospitalization • Prevent mortality • Improve HRQOL
• Encourage regular • Prevent further • Prevent mortality
DRUGS FOR • Reduce hospital
exercise cardiac remodeling readmissions
STRATEGIES ROUTINE USE
• Discourage alcohol • Establish patient’s
intake, illicit drug use DRUGS
• Identification of • Diuretics for fluid end-of-life goals
• ACEI or ARB in comorbidities retention
• Control metabolic
syndrome appropriate patients • ACEI or ARB or ARNI OPTIONS
• Prevent LV structural • Beta blockers in TREATMENT • Beta blockers
• Advanced care
abnormalities appropriate patients • Diuresis to relieve • Aldosterone antagonists
measures
symptoms of
DRUGS
congestion
DRUGS FOR USE IN • Heart transplant
• ACEI or ARB in IN SELECTED SELECTED PATIENTS • Chronic inotropes
appropriate patients PATIENTS • Follow guideline-driven
• Hydralazine/isosorbide • Temporary or
indications for permanent mechanical
for vascular disease • ICD comorbidities, e.g., dinitrate
• Revascularization or circulatory support
or diabetes atrial fibrillation (AFib), • ACEI and ARB
• Statins as valvular surgery as
coronary artery disease • Digitalis • Experimental surgery
appropriate or drugs
appropriate (CAD), diabetes mellitus • Ivabradine
(DM), hypertension
• Palliative care and
IN SELECTED PATIENTS hospice
(HTN)
• CRT • ICD deactivation
• ICD
• Revascularization or
valvular surgery as
appropriate

Fig. 27.2 Stages in the development of heart failure (HF) and recommended therapy by stage. ACEI, Angiotensin-
converting enzyme inhibitor; ARB, angiotensin II receptor blocker; ARNI, angiotensin receptor-neprilysin inhibitor; CRT,
cardiac resynchronization therapy; EF, ejection fraction; FHx CM, family history of cardiomyopathy; CR/XL, controlled
release/extended release; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection
fraction; ICD, implantable cardioverter-debrillator; LV, left ventricular; LVH, left ventricular hypertrophy; MI, myocardial
infarction. (From Yancy CW, Jessup M, Bozkurt B, etal. 2013 ACCF/AHA guideline for the management of heart failure:
executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force
on practice guidelines. Circulation. 2013;128(16):e240-327; and Yancy CW, Jessup M, Bozkurt B, etal. 2017 ACC/AHA/
HFSA Focused Update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American
College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure
Society of America. J Card Fail. 2017;23(8):628-651.)

akn rgularly. If hy ar n bing akn, ask why
n. Ask h pain fr a lis f all vr-h-cunr
mdicains and any hrbal prducs bing akn.
Prfrm fcusd assssmns  drmin h ffc-
ivnss and h advrs ffcs f any pharmaclgic
inrvnins.
History of six cardinal signs of heart disease
1. Dyspnea (difculty breathing): Rcrd whhr dys-
pna ccurs whil h pain is rsing, if i ccurs
n xrin, r if i ccurs whil h pain is aslp
a nigh (parxysmal ncurnal dyspna). Ar symp-
ms f dyspna accmpanid by a prduciv r
nnprduciv cugh? Ask h pain  dscrib
hir spuum. (Wih har failur, spuum is frhy
and may b ingd wih bld.) Hw has h pain
bn cping wih any rhpnic prblms?
2. Chest pain: Bcaus har failur rsuls in dcrasd
cardiac upu and lwr xygnain f issu, h
har may xprinc inadqua issu prfusin,
 Drugs Used to Treat Heart Failure CHAPTER 27 443

Medicines That Reduce Medicines That Reduce

Preload: Afterload:

• ACE inhibitors • ACE inhibitors

Valsartan-sacubitril Valsartan-sacubitril
Preload and Afterload

• Beta-adrenergic blocking • Beta-adrenergic blocking

agents agents
Pr

d
e lo

rloa
Preload ad Afterload
Volume coming Resistance—left

Afte
• Phosphodiesterase into ventricles ventricle must • Calcium channel blockers
inhibitors (end-diastolic overcome to (dihydropyridine
pressure) circulate blood derivatives)

• Nitrates Increased in: Increased in:

Hypervolemia Hypertension
• nesiritide Regurgitation of Vasoconstriction
cardiac valves • Phosphodiesterase
↑Afterload inhibitors
• nitroprusside ↑Cardiac workload
• Diuretics • hydralazine
• nesiritide
• nitroprusside
Fig. 27.3 Medicines that reduce preload and afterload to reduce heart failure. ACEI, Angiotensin-converting enzyme
inhibitor.

which can rsul in chs pain. Rcrd daa rgard-
ing h im f ns as wll as h frquncy, dura-
in, and qualiy f h chs pain. N any cn-
diins ha h pain has fund  aggrava r
rliv h chs pain.
3. Fatigue: Drmin whhr faigu ccurs nly a
spcic ims f h day, such as ward vning.
Ask h pain if faigu subsids in rlain  a
dcras in aciviy lvl r if i is prsn a abu
h sam im ach day.
4. Edema: Rcrd h prsnc r absnc f dma.
If dma is prsn, rcrd is lcain, any assss-
mn daa (.g., dgr f piing prsn; ankl,
midcalf, r high circumfrnc), h apparanc f
h skin (.g., shiny, wping wih prssur), and
any masurs ha h pain has usd  limina
i. Char h im f day ha h dma is prsn
(.g., whn rising in h mrning, bfr bdim)
and h spcic pars n h bdy whr i is prs-
n. Whn prfrming h pain’s daily wighs,
us h sam scal, wigh h pain a h sam
im f day, and b sur ha h pain is waring
similar clhing ach im.
5. Syncope: Ask h pain abu h cndiins sur-
runding any pisds f syncp. Rcrd h dgr
f sympms, such as gnral muscl waknss, h
inabiliy  sand uprigh, fling fain, r any lss f
cnsciusnss. Rcrd wha aciviis (if any) bring
n hs syncpal pisds.
6. Palpitations: Rcrd h pain’s dscripin f pal-
piains, such as, “My har skips sm bas.” Ask
if hs cndiins ar prcdd by srnuus r
mild xrcis and hw lng h palpiains las.
Indications of altered cardiac function
• Basic mental status: Idnify h individual’s lvl
f cnsciusnss (.g., drwsinss, lhargy, cnfu-
sin; rinain  da, im, and plac). Assss
h clariy f hugh prsn. Bh h lvl f cn-
sciusnss and clariy f hugh ar indicars f
adqua crbral prfusin.
• Vital signs: Obain vial signs and puls ximry
radings as fn as ncssary  mnir h pa-
in’s saus.
• Blood pressure: Obain baslin radings and a his-
ry f prir ramn fr hyprnsin. Mnir
h pain a spcic inrvals and rpr a narrw-
ing puls prssur (i.., h diffrnc bwn h
syslic and diaslic radings). Wih har failur,
hypnsin may b prsn.
• Temperature: Rcrd h pain’s mpraur vry
8 hurs; mnir i mr frqunly if i is lvad.
• Pulse: Rcrd h ra, qualiy, and rhyhm f h
pain’s puls. Wih har failur, achycardia may
rprsn an amp by h bdy  cmpnsa fr
dcrasd cardiac upu. Tachycardia is fn h
rs clinical sympm f har failur.
• Heart and lung sounds: Nurss wih advancd skills
can prfrm ausculain  n changs in har
siz and in h pain’s har and lung sunds.
Lung lds ar assssd wih h pain in a si-
ing psiin  dc abnrmal lung sunds (.g.,
whzs, crackls). (Rfr  a mdical-surgical r
criical car nursing xbk fr dails abu hw
 prfrm hs skills.)
• Skin color: N h clr f h pain’s skin, mu-
cus mmbrans, ngu, arlbs, and nail bds.
444 UNIT IV Drugs Affecting the Cardiovascular System
Char h xac lcain f any pallr r cyansis
ha is prsn.
• Neck veins: Rcrd any jugular vnus disnin.
• Clubbing: Inspc h pain’s ngrnails and -
nails fr clubbing. Assss capillary rll n h n-
grnails and nails.
• Abdomen: Inspc h pain’s abdmn, ning
siz, shap, sfnss, and any disnin. Rad h
pain’s hisry  bain any daa rlad  livr
nlargmn.
• Fluid volume status: Cninu  assss h pain’s
inak and upu a inrvals ha ar apprpria 
h pain’s cndiin (vry hur during an acu
xacrbain f har failur). Rpr inak ha x-
cds upu. Ask h pain abu h frquncy f
ncuria. (Ncuria fn ccurs wih har failur
bcaus rnal prfusin is imprvd whn h pa-
in lis dwn and uid mvs frm h inrsiial
spacs back in h gnral circulain.)
• Diagnostic tests: Rviw labrary and diagns-
ic s rsuls and prmply rpr any abnrmal
rsuls  h halhcar prvidr. Tss includ
srum lcrlys, spcially passium, calcium,
magnsium, and sdium lvls; B-yp nariuric
ppid, arrial bld gass, and srum lipid lv-
ls; lcrcardigraphy; chcardigraphy, which
includs lf vnricular funcin, a diagnsic pa-
ramr idnid as an indicar in h cr ma-
surs; nuclar imaging sudis; chs x-ray lms;
urinalysis; and kidny funcin and hmdynamic
assssmns.
• Nutrition: Tak a hisry f h di ha has bn
prscribd  h pain and assss h pain’s
adhrnc  h di. Obain daa rgarding h
pain’s appi and h prsnc f nausa and
vmiing.
• Activity and exercise: Ask qusins  gahr infr-
main abu h ffc f xrcis n h pain’s
funcining. Is h prsn nrmally sdnary r
mdraly r vry aciv? Has hr bn a rduc-
in in aciviy lvl  handl assciad faigu r
dyspna? Ar h aciviis f daily living (ADLs)
bing prfrmd by h prsn?
• Anxiety level: Pains wih cardiac disrdrs xhibi
varying dgrs f anxiy. N h lvl f anxiy
r dprssin prsn.
Implementation
• Obain baslin arrial bld gass r mnir
h puls ximr, as rdrd. Adminisr xygn
hrapy as prscribd and pridically rviw h
pain’s rsuls.
• Psiin h pain in a Fwlr r smi-Fwlr
psiin  maximiz lung xpansin and xygn-
ain. Rpsiin h pain a las vry 2 hurs,
and prvid skin car  prvn brakdwn.
• Auscula lung sunds a spcid inrvals cn-
sisn wih h pain’s cndiin. Assss h pa-
in fr nck vin disnin.
• Wigh h pain daily a h sam im (usually
bfr brakfas), using h sam scal, and wih h
pain waring similar clhing. Rcrd and rpr
any signican wigh changs. (Wigh gains and
lsss ar h singl bs indicar f uid gain r
lss.) As apprpria  h pain’s cndiin, b-
ain and rcrd abdminal girh masurmns.
• Whn uid rsricins ar prscribd, half f h
uid is usually givn wih mals and h hr
half is dividd vr h rs f h day. Gnrally,
h nurs shuld ncurag h pain  wri
dwn h amun f liquid inak hrughu h
day  br undrsand hw  fllw any uid
rsricin.
• Mainain h dgr f diary sdium rsricin
prscribd.
• Avid using sal subsius whn passium-
sparing diurics ar bing givn  h pain.
• Adminisr prscribd mdicains (.g., brnch-
dilars, ACE inhibirs, niras, digxin, diur-
ics, anianxiy agns) n a schdul r as ndd.
Mnir h dgr f rspns achivd and rpr
any inffcivnss.
• Pac nursing aciviis  avid undu pain fa-
igu; implmn xrcis gradually whil mnir-
ing h pain’s vial signs bfr and afr ambula-
in. Assss fr signs and sympms f faigu r
pr xygnain bfr, during, and afr xrcis.
• D n plan xrcis r ambulain wihin 1 hur
afr aing  avid xcssiv xygn dplin.
• Mnir h pain’s vial signs and ximr rad-
ings, and prfrm a fcusd assssmn f har and
rspirary funcins a spcid inrvals.
• Prfrm nurlgic assssmns  drmin
changs in h pain’s mnal saus.
• Dal calmly wih an anxius pain, ffr xplana-
ins f prcdurs bing prfrmd, and lisn 
hir cncrns and inrvn apprprialy.
• Mnir h ra f IV infusins carfully; cnac
h pain’s halhcar prvidr rgarding h cn-
cnrain f admixurs f drugs  IV infusin s-
luin whn h limiain f uids is indicad.
• Giv h pain sl sfnrs  avid h pain
sraining whil rying  pass a hard sl, which
culd caus syncp by inducing h Valsalva
manuvr.
Patient Education
• Tach h pain and signican hrs abu
h funcinal changs causd by har failur.
Emphasiz h nd fr liflng ramn and ad-
hrnc  drug hrapy, di, and xrcis rgimns
 bain maximum cnrl f h disas prcss.
• Assss h pain’s undrsanding f sympms
ha indica whn  call a halhcar prvidr:
dyspna; a prduciv cugh; wrsning faigu;
dma in h f, ankls, r lgs; wigh gain f 2
punds r mr in a 2-day prid; and dvlpmn
f angina, chs pain, palpiains, r cnfusin.

• Prvid h pain wih insrucins fr aking vi-
al signs such as bld prssur, puls, and rspi-
rains. Giv him r hr infrmain abu h ac-
cpabl paramrs fr ach as prscribd by h
halhcar prvidr.
• Explain any xygn hrapy ha has bn pr-
scribd. If h pain is bing dischargd n xy-
gn, ll him r hr whr  bain xygn quip-
mn and supplis, h ra f adminisrain, and
hw  car fr and mainain h quipmn.
• Dmnsra  h pain hw  g in a Fwlr
psiin. Discuss h adapains ndd a hm
 us hs psiins fr rlif f dyspna. Explain
ha an uprigh psiin prvids maximum
xygnain.
• Tach h pain abu gd skin car and h nd
 chang psiin a las vry 2 hurs, spcially
whn dma is prsn. Hav h pain inspc
hir ankls, f, and abdmn daily fr dma. If
h pain is using a rclinr r bd, h sacral ara
shuld als b chckd rgularly fr dma.
• Discuss h impranc f spacing h ADLs  cn-
srv nrgy and avid faigu. Rviw h pr-
scribd aciviy lvl and srss mniring puls,
dyspna, and faigu lvls as a guid  whn h
pain is vrxring.
• Explr h cping mchanisms ha h prsn
uss in rspns  srss. Discuss hw h pain
is adaping  h ndd changs in hir lifsyl
 manag h disas prcss. Addrss dprssin
issus, if prsn.
• Di hrapy is an ingral par f h ramn f
har failur. Schdul mings wih h nuriin-
is  nabl h pain  larn hw  manag
spcic diary mdicains ha hav bn pr-
scribd (hs usually includ a lw-sdium, high-
passium di wih wigh rducin paramrs
fr pains wh ar bs). If pssibl, hav h pa-
in pracic fd slcin using h daily mnus
whil hy ar sill in h hspial. Tak culural
fd prfrncs in cnsidrain and ffr guid-
anc frm h nuriin saff, as wll as h nurss.
Tach h pain abu fds ha ar lw in sdium
and high in passium. Passium rsricins may
b indicad if h pain is aking a passium-
sparing diuric: sal subsius ar high in pas-
sium, s hir us mus b limid. Alchl inak
shuld b liminad frm h di.
• Tach h pain abu h impranc f main-
aining a rgular, mild xrcis ruin as pr-
scribd by h halhcar prvidr. A n im i
was hugh ha xrcis was harmful wih his
cndiin; hwvr, mild rgular xrcis is nw
prscribd, wih limiains dnd by h halh-
car prvidr.
• Fluid rsricins may b impsd, usually fr pa-
ins wih mdra  advancd har failur; dis-
cuss spcic ways  manag hs limiains.
Drugs Used to Treat Heart Failure CHAPTER 27 445
• Tach h pain abu h signs and sympms f
passium dcincy r xcss, dpnding n h
mdicains prscribd.
Medication regimen
• Har failur rquirs liflng ramn, and adhr-
nc  prscribd hrapy is impraiv  cnrl
h disas.
• Tach h pain h signs and sympms f digitalis
toxicity (.g., anrxia, nausa, vmiing, bradycar-
dia, visual disurbancs, psychiaric disurbancs).
Explain mdicain adminisrain paramrs: if
h puls is lss han 60 r mr han 100 bas/min,
d n adminisr digxin wihu chcking wih
h prscribr. (An anid is availabl fr digxin
xiciy.) Tll h pain ha i is impran  rpr
fr bld draws  chck srum lvls f h drug a
h spcic ims schduld.
• Diurics shuld b akn in h mrning  avid
nighim diursis. Dpnding n h yp f di-
uric prscribd, passium supplmns may b
ncssary. Hwvr, if a passium-sparing diuric
is rdrd, limiing passium inak may b appr-
pria. Sal subsius shuld b avidd bcaus
hy ar high in passium.
• Tll h pain  prfrm daily wighs using h
sam scal, waring similar clhing, a h sam
im ach day (usually bfr brakfas). Rcrd and
rpr signican wigh changs, bcaus wigh
gains and lsss ar h bs indicars f uid gain
r lss. Usually a gain f 2 punds in 2 days shuld
b rprd.
• Whn ACE inhibirs ar rdrd, hypnsin,
hyprkalmia, and a prsisn cugh ar pssibl.
Discuss h managmn f hs advrs ffcs.
Fostering health maintenance
• Thrughu h curs f ramn, discuss mdica-
in infrmain and hw i will bn h pain.
• Drug hrapy is n cmpnn f h ramn f
har failur, and i is criical ha h mdicains
b akn as prscribd. Prvid h pain and hir
signican hrs wih h impran infrmain
cnaind in h spcic drug mngraphs fr h
drugs prscribd. Addiinal halh aching and
nursing inrvnins fr cmmn and srius ad-
vrs ffcs can b fund in ach drug mngraph.
• I is impran  cnrl h undrlying cndiin
causing h har failur (.g., hyprnsin, hypr-
lipidmia). Th pain and hir family mus un-
drsand h impranc f cmplying wih di,
xrcis, and hr prscribd ramns dsignd
 maximiz h pain’s dgr f xygnain.
• Sk cprain and undrsanding f h fllw-
ing pins s ha mdicain adhrnc is incrasd:
h nam f h mdicain; is dsag, ru, and
ims f adminisrain; and cmmn and srius
advrs ffcs.
446 UNIT IV Drugs Affecting the Cardiovascular System
Patient self-assessment. Enlis h pain’s hlp
wih dvlping and mainaining a wrin rcrd f
mniring paramrs (.g., puls ra, bld prs-
sur, dgr f dyspna and wha prcipias i, chs
pain, dma). S h Pain Slf-Assssmn Frm
fr Cardivascular Agns n h Evlv wbsi.
Cmpl h Prmdicain Daa clumn fr us as a
baslin  rack h pain’s rspns  drug hra-
py. Ensur ha h pain undrsands hw  us h
frm and insruc h pain  bring h cmpld
frm  fllw-up visis. During h fllw-up visis,
fcus n issus ha will fsr adhrnc wih h hr-
apuic inrvnins prscribd.
DRUG CLASS: ANGIOTENSIN-CONVERTING ENZYME
INHIBITORS
Actions
ACE inhibirs rprsn a majr brakhrugh in h
ramn f har failur. Larg sudis shw ha
ACE inhibirs rduc h mrbidiy and mraliy
assciad wih har failur. Th ACE inhibirs r-
duc afrlad by blcking anginsin-II–mdiad
priphral vascnsricin, and hy hlp rduc
circulaing bld vlum (prlad) by inhibiing h
scrin f aldsrn. (S Chapr 22 fr a mr
cmpl dscripin f h mchanism f acin f
ACE inhibirs.)
Uses
Th ACE inhibirs rduc bld prssur (afrlad),
prsrv cardiac upu, and incras rnal bld w.
Thy ar nw rcmmndd as h drugs f chic
vr digxin fr h ramn f mild  mdra sys-
lic dysfuncin har failur.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm ACE
inhibirs ar imprvd cardiac upu rsuling in im-
prvd issu prfusin and imprvd lranc  ac-
iviy as dmnsrad by h abiliy  prfrm ADLs
wihu supplmnal xygn hrapy r faigu.
Nursing Implications for Angiotensin-Converting
Enzyme Inhibitors
S Chapr 22 fr a mr cmpl dscripin f h
nursing implicains rlad  ACE inhibirs.
DRUG CLASS: ANGIOTENSIN RECEPTOR BLOCKER–
NEPRILYSIN INHIBITOR
valsartan-sacubitril (văl-SĂR-tăn; săk-Ū-bĭ-trĭl)
Entresto (ĕn-TRĔS-tō)
Actions
Enrs is a cmbinain prduc cnaining an ARB
(valsaran) (s Chapr 22) and a nprilysin inhibir
(sacubiril). Th ARB ras har failur by rducing
afrlad by blcking anginsin-mdiad priphral
vascnsricin, wih rsulan vasdilain, and d-
crass prlad by rducing circulaing bld vlum
by inhibiing h scrin f aldsrn. Aldsrn
inhibiin rsuls in a nariursis (xcrin f sdium
in h urin) and diursis (xcrin f war in h
urin).
Sacubiril inhibis h nzym nprilysin. Nprilysin
nrmally inacivas nariuric ppids and bradyki-
nin. Inhibiin f nprilysin incrass h lvls f na-
riuric ppids scrd by h arial and vnricu-
lar har muscls, rsuling in bld vssl dilain
(rducin in afrlad) and rducin in circulaing
bld vlum (rducd prlad) by nhancd sdium
and war xcrin by h kidnys. Thus h ingrdi-
ns in Enrs wrk by diffrn mchanisms  r-
duc prlad and afrlad, imprving cardiac upu
and rducing har failur.
Uses
Valsaran-sacubiril is usd in h managmn f
har failur, usually in cnjuncin wih hr har
failur mdicains such as diurics and ba blck-
rs. I is usd in plac f an ACE inhibir r anhr
ARB. Th cmbinain rducs h risk f hspializa-
in and cardivascular dah in pains wih chrnic
har failur (NYHA Classs II-IV).
Therapeutic Outcomes
Th primary hrapuic ucms ar rducd risk f
hspializain and f cardivascular dah frm har
failur.
Nursing Implications for Valsartan-Sacubitril
Premedication assessment
1. Tak h pain’s bld prssur in bh h su-
pin and sanding psiins. Rcrd h puls ra,
rhyhm, and rgulariy.
2. Obain h baslin labrary sudis rdrd by
h halhcar prvidr (.g., cmpl bld cun).
3. Obain baslin wigh.
4. Prfrm a baslin assssmn f h pain’s d-
gr f alrnss and rinain  nam, plac, and
im bfr iniiaing hrapy.
Availability. PO: abls: sacubiril/valsaran 24 mg/26
mg, 49 mg/51 mg, and 97 mg/103 mg.
Dosage and administration. Patients not currently tak-
ing an ACE inhibitor or an ARB: PO: Iniial: sacubiril/
valsaran 24 mg/26 mg wic daily. Dubl h ds as
lrad vry 2  4 wks  h arg mainnanc
ds f sacubiril/valsaran 97 mg/103 mg wic daily.
Patients previously taking more than 10 mg/day of enala-
pril or more than 160 mg/day of valsartan or equivalent dose
of another ACE inhibitor or ARB: PO: Initial: sacubiril/
valsaran 49 mg/51 mg wic daily. Dubl h ds as

lrad afr 2  4 wks  h arg mainnanc
ds f sacubiril/valsaran 97 mg/103 mg wic daily.
Patients previously taking low doses of an ACE inhibi-
tor (≤10 mg/day of enalapril or an equivalent dose of an-
other ACE inhibitor) or ARB (≤160 mg/day of valsartan
or an equivalent dose of another ARB): PO: Initial: sa-
cubiril/valsaran 24 mg/26 mg wic daily. Dubl
h ds as lrad vry 2  4 wks  h arg
mainnanc ds f sacubiril/valsaran 97 mg/103
mg wic daily.
Medication Safety Alert
Do not administer Entresto to a patient receiving an ACE in-
hibitor or ARB. If the patient is currently receiving an ACE
inhibitor, wait at least 36 hours before starting Entresto.
Common adverse effects
Cardiovascular
Orthostatic hypotension (dizziness, weakness, faint-
ness). Alhugh hs advrs ffcs ar infrqun
and usually mild, crain pains, paricularly hs
als rciving diurics, may suffr sm dgr f
rhsaic hypnsin, spcially whn hrapy
is iniiad. Obsrv h pain clsly fr a las 2
hurs afr h iniial ds is givn and fr a las an
addiinal hur unil bld prssur has sabilizd.
Mnir h bld prssur in bh h supin and
sanding psiins. Anicipa h dvlpmn f ps-
ural hypnsin and ak masurs  prvn an c-
currnc. Tach h pain  ris slwly frm a supin
r siing psiin and  si r li dwn if fling fain.
Inammatory
Chronic cough. Pains rciving valsaran-sacubiril
may dvlp a chrnic, dry, nnprduciv, prsisn
cugh. This is hugh  b causd by an accumula-
in f bradykinin by h nprilysin inhibir. I may
appar frm 1 wk  6 mnhs afr iniiain f hr-
apy. Pains shuld b ld  cnac h halhcar
prvidr if h cugh bcms rublsm. Th cugh
usually rslvs afr discninuain f hrapy.
Serious adverse effects
Pregnancy. Mdicains ha ac dircly n h rnin-
anginsin-aldsrn sysm can caus fal and
nnaal harm. Thr is cncrn abu h pnial
fr birh dfcs in nnas whs mhrs rciv
valsaran-sacubiril, spcially during h scnd and
hird rimsrs f prgnancy. Wmn wh wish 
bcm prgnan r wh bcm prgnan whil r-
civing valsaran-sacubiril shuld discuss alrnaiv
hrapis wih h halhcar prvidr as sn as
pssibl.
Cardiovascular
Hypotension. Hypnsin may ccur upn ini-
iain, paricularly in pains wih har failur r
ps-MI. I may als ccur in pains rciving high-
ds diurics wh may b vlum dpld. Pains
Drugs Used to Treat Heart Failure CHAPTER 27 447
shuld b warnd ha his may ccur and shuld si r
li dwn immdialy if dizzinss dvlps.
Swelling of the face, eyes, lips, and tongue; difculty breath-
ing. Angidma has bn rprd  ccur in a small
numbr f pains rciving ARBs, spcially afr
h rs ds. Th pain shuld b cauind  dis-
cninu furhr hrapy and sk mdical anin
immdialy.
Renal
Hyperkalemia. Bcaus valsaran-sacubiril bh in-
hibi aldsrn, pains may dvlp sligh incrass
in srum passium lvls. Ms cass rslv wihu
discninuain f hrapy. Pains ms suscpibl
 h dvlpmn f hyprkalmia ar hs wih r-
nal impairmn r diabs mllius and hs alrady
rciving a passium supplmn r a passium-
sparing diuric. Many sympms assciad wih
alrd uid and lcrly balanc ar subl and in-
rsprsd wih gnral sympms f drug xiciy r
h disas prcss islf.
Gahr daa rlaiv  changs in h pain’s mn-
al saus (.g., alrnss, rinain, and cnfusin),
muscl srngh, muscl cramps, rmrs, nausa, and
gnral apparanc (.g., drwsy, anxius, r lhar-
gic). Always chck h lcrly rprs fr arly indi-
cains f lcrly imbalanc. Kp accura rcrds
f inak and upu, daily wighs, and vial signs.
Nephrotoxicity. Pains wh ar rciving valsaran-
sacubiril, paricularly hs wih prxising rnal
impairmn and hs als aking NSAIDs, hav dvl-
pd incrasd bld ura nirgn and srum crai-
nin lvls. Ths lvains hav usually bn minr
and ransin, spcially whn adminisrd cncmi-
anly wih a diuric. Rnal funcin shuld b mni-
rd during h rs fw wks f hrapy. Rpr
incrasing bld ura nirgn and crainin lvls.
Dsag rducin f valsaran-sacubiril r pssibl dis-
cninuain f h NSAID r diuric may b rquird.
Drug interactions
Drugs that enhance therapeutic and toxic effects. Ths
includ diurics, anipsychics, alchl, ba-adrnrgic
blcking agns (.g., mprll, carvdill), and hr
anihyprnsiv agns. ACE inhibirs and ARBs ar
cnraindicad. Mnir h bld prssur rspns 
h cumulaiv ffcs f anihyprnsiv agns. Tak
h bld prssur in supin and sanding psiins.
Drugs that reduce therapeutic effects. Nnsridal
aniinammary drugs may rduc h ffcs f
valsaran-sacubiril and may caus a signican d-
cras in rnal funcin. Mnir srum crainin
clsly.
Lithium. Anginsin II rcpr blckrs may in-
duc lihium xiciy. Mnir fr lihium xiciy
manifsd by nausa, anrxia, n rmrs, prsis-
n vmiing, prfus diarrha, hyprrxia, lh-
argy, and waknss.
448 UNIT IV Drugs Affecting the Cardiovascular System
Hyperkalemia. Valsaran-sacubiril may caus small
incrass in passium lvls by inhibiing aldsr-
n scrin. Pains shuld n ak diary sup-
plmns f passium, passium-cnaining sal
subsius, r passium-sparing diurics (.g., ri-
amrn, spirnlacn, amilrid) wihu spcic
apprval frm h halhcar prvidr. If a pain has
rcivd spirnlacn r plrnn up  svral
mnhs bfr valsaran-sacubiril hrapy, h srum
passium lvl shuld b mnird clsly b-
caus h passium-sparing ffc f spirnlacn
r plrnn may prsis. Srum passium lvls
shuld b mnird whn h anibiic rimh-
prim is usd wih valsaran-sacubiril.
DRUG CLASS: BETA-ADRENERGIC BLOCKING
AGENTS
Actions
Th ba-adrnrgic blcking agns (ba blckrs;
s Tabl 12.3) inhibi cardiac rspns  sympahic
nrv simulain by blcking h ba rcprs. As a
rsul, h har ra, cardiac upu, aggravaing hypr-
nsin—and cnsqunly h bld prssur—ar r-
ducd. Ba blckrs als rduc bld prssur as hy
inhibi rnin rlas, diminishing h cascad f h
rnin-anginsin-aldsrn sysm ha wuld in-
duc vascnsricin and sdium rabsrpin.
Uses
Th ba-adrnrgic blcking agns ar agns f an-
hr class ha hav bn shwn  rduc h mr-
bidiy and mraliy assciad wih har failur. Th
xac mchanism whrby ba blckrs incras sur-
vival in pains wih har failur is unknwn, bu i
is hugh  includ inhibiin f rnin rlas, sup-
prssin f h ffc f lvad circulaing cachl-
amins, and scndary prvnin f angina and MI.
Bcaus ba-adrnrgic blcking agns and ACE in-
hibirs ac hrugh diffrn mchanisms, ba blck-
rs and ACE inhibirs ar cmmnly usd ghr
 ra har failur. Thr is a qusin f whhr all
ba blckrs hav h sam clinical ffc. Th agns
ha ar h ms wll sudid and shwn  b ffc-
iv in raing har failur ar bisprll, lng-acing
mprll (Tprl-XL), and carvdill.
Therapeutic Outcomes
Th primary hrapuic ucms ar rducd risk f
hspializain and f cardivascular dah frm har
failur.
Nursing Implications for Beta-Adrenergic Blocking
Agents
S Chapr 22 fr a mr cmpl dscripin f h
nursing implicains rlad  h ba-adrnrgic
blcking agns.
DRUG CLASS: DIGITALIS GLYCOSIDES
digoxin (dĭ-JŎKS-ĭn)
Do not confuse digoxin with Doxepin.
Lanoxin (lă-NŎKS-ĭn)
Do not confuse Lanoxin with Inapsine, Lomotil, Levoxyl,
Levsin, Lovenox, or Xanax.
Actions
Th digialis glycsids ar amng h lds hra-
puic agns usd  ra har failur. Thir us in
mdicin das  h 18h cnury; in 1785 William
Wihring, an English physician and banis, pub-
lishd xclln bsrvains rgarding h ramn
f varius ailmns wih digxin. Onc drivd nau-
rally frm h drid lavs f Digoxin purpurea (pur-
pl fxglv), h drug is nw prpard synhically.
Digxin is h nly digialis glycsid currnly avail-
abl in h Unid Sas.
Digxin has w primary acins n h har: (1)
incrasing h frc f cnracin (positive inotropy)
and (2) slwing h har ra (negative chronotropy),
hus rducing h cnducin vlciy and prlnging
h rfracry prid a h arivnricular nd. Th
xac mchanisms f hs acins ar unknwn, bu
h n rsul is ha h har is abl  ll and mpy
mr cmplly, hrby imprving cardiac upu
and circulain. Wih imprvd circulain, hr is a
rducin in sysmic and pulmnary cngsin, in
har siz (i.., rurning ward nrmal), and in pri-
phral dma bcaus f h incrasd prfusin f
bld hrugh h kidnys, which xrac war and
lcrlys.
Uses
Digxin is usd  ra mild  svr syslic
har failur ha ds n rspnd  diurics,
ba blckrs, r ACE inhibirs. Digxin may als
b usd  ra arial fibrillain, arial flur, and
parxysmal achycardia. Digxin is n usd 
ra HRpEF bcaus i may acually wrsn his
cndiin.
Th gal f ramn fr har failur is  giv
adqua dss f digxin s ha h ms pimal
cardiac ffcs ar achivd: cardiac upu is in-
crasd, puls ra is slwd, and vascnsricin
dcrass, rsuling in h disapparanc f many
f h signs and sympms f har failur (.g.,
dyspna, rhpna, dma). Th nc-sandard
apprach  giving lading dss (digitalization) f
digxin vr a prid f hurs r days is n lngr
hugh  b ncssary in ms cass  prduc h
dsird cardiac ffc. A mainnanc dsag is nw
givn, usually nc a day. Many pains mus cn-
inu  ak digxin prparains fr h rmaindr
f hir livs.

Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm di-
gxin hrapy ar imprvd cardiac upu rsuling
in imprvd issu prfusin and imprvd lr-
anc  aciviy as dmnsrad by h abiliy  pr-
frm ADLs wihu supplmnal xygn hrapy r
faigu.
Nursing Implications for Digoxin
Premedication assessment
1. Tak h pain’s apical puls fr 1 full minu and
fllw insiuinal guidlins fr wihhlding h
drug (.g., if h puls is <60 r >100 bas/min).
Note: In h lng-rm car sing, a radial puls
may b accpabl.
2. Bfr iniiaing hrapy, bain baslin pain
daa such as vial signs, lung sunds, wigh, and
labrary valus (.g., srum lcrlys, livr and
kidny funcin sudis).
3. As hrapy prgrsss, mnir h pain fr h
dvlpmn f digxin xiciy, hypkalmia, hyp-
magnsmia, r a suddn incras in a prviusly
nrmal r lw puls ra.
Availability. PO: 0.0625-, 0.125-, 0.187.5- and 0.25-mg
abls; pdiaric lixir, 0.05 mg/mL.
IV: 0.1 mg/mL in 1 mL ampuls; 0.25 mg/mL in
2-mL ampuls.
Implementation
Pulse variations. Always ak h apical puls fr 1
full minu bfr adminisring any digxin prpara-
in. D n adminisr h drug whn h puls ra in
an adul is lss han 60 bas/min unil h prscribr
is cnsuld. In a child, rpr a puls ra f lss han
90 bas/min bcaus h prscribr may dcid 
wihhld h mdicain.
Accurate identication. Digxin is fn givn in vry
small incrmns. Always hav h mahmaical cm-
puains chckd by anhr prfssinal nurs.
Us h crrc yp f syring  facilia h ac-
curacy f h dsag masurmn. Always qusin
any rdr ha is unusual bfr adminisrain. Rad
h mdicain labl carfully fr prpr drug and
srngh.
Dosage and administration. Giv digxin afr mals
 minimiz gasric irriain. Note: I is rcmmnd-
d ha a baslin lcrcardigram b baind b-
fr h iniiain f hrapy.
Assuming ha h pain has n ingsd digxin
during h prcding 2 wks, h fllwing dsags
apply:
Adult: PO: Maintenance: 0.125  0.25 mg daily.
Sm pains may rquir 0.375  0.5 mg daily.
IV: Maintenance: Sam as fr PO adminisrain.
Adul hrapuic bld lvls ar 0.5  2.0 ng/mL.
Drugs Used to Treat Heart Failure CHAPTER 27 449
Life Span Considerations
Digoxin Toxicity
Older adults commonly experience digoxin toxicity as a result
of digoxin’s long half-life. Early symptoms of toxicity are an-
orexia and mild nausea, but they are often overlooked or are
not associated with drug toxicity. Any change in pulse rhythm
and rate or central nervous system signs (e.g., mental status,
orientation, hallucinations, behavioral changes) should be in-
vestigated and reported. In children, digoxin toxicity is of-
ten rst detected by the development of atrial dysrhythmias.
Hypokalemia potentiates the effects of digoxin and can lead
to toxicity. Always check the potassium level of the patient
before administration and replace the potassium if low before
giving the dose of digoxin.
Serum levels. Srum lvls f digxin ar masurd
 drmin h amun f digxin in h bldsram.
Bld shuld b drawn bfr h daily ds f mdi-
cain is givn r a las 6 hurs afr adminisrain.
I is impran  b cnsisn wih rgard  h im
f drawing bld and adminisring h ds.
Treatment of digoxin toxicity. Th basic ramn f
digxin-inducd dysrhyhmias cnsiss f spping h
digxin and any passium-dpling diurics, chck-
ing h passium lvl (i.., adminisring passium
as indicad), and adminisring anidysrhyhmic
drugs (.g., phnyin). In sm cass, arpin may b
prscribd fr sinus bradycardia. A pacmakr may b
ncssary  crrc cninuing bradycardia.
Antidote for severe digoxin intoxication. Digxin im-
mun fab (vin) (Digibind).
Serious adverse effects
Digoxin toxicity
Cardiac rhythm. Cnsanly mnir h pain fr
h dvlpmn f a puls dci, bradycardia (har
ra <60 bas/min), and achycardia (har ra >100
bas/min). Ths may b signs f dvlping har
blck. Whnvr h pain is aachd  a mnir,
h parn shuld b clsly wachd fr any yp f
abnrmal cardiac rhyhms. In childrn, digxin xic-
iy is fn rs dcd by h dvlpmn f arial
dysrhyhmias.
Life Span Considerations
Digoxin Dosage
Pediatric dosages for digoxin are extremely small and should
be measured in a tuberculin syringe using the metric scale.
All dosage calculations should be checked with a second
qualied nurse in accordance with the institution’s policy.
Noncardiac effects. Nncardiac sympms f digxin
xiciy ar fn vagu and difcul  spara frm
sympms f har disas. Any pain aking digx-
in prducs wh dvlps h fllwing sympms
shuld b valuad fr digxin xiciy:
• Gastrointestinal: lss f appi, nausa, vmiing
450 UNIT IV Drugs Affecting the Cardiovascular System

• Neurologic: xrm faigu, waknss f h arms

MAY CAUSE HYPERKALEMIA
and lgs amiloride (Midamor) potassium gluconate
• Psychological: psychiaric disurbancs (.g., nigh- angiotensin-converting penicillin G potassium
mars, agiain, lislssnss, hallucinains) enzyme inhibitors potassium supplements
• Sensory: visual disurbancs (.g., hazy r blurrd angiotensin receptor blocking (e.g., K-Lyte, Kaon,
visin, difculy rading, difculy wih rd-grn agents K-Lor)
clr prcpin) beta-adrenergic blockers salt substitutes
Electrolyte balance. Advrs ffcs f digxin may eplerenone spironolactone
als b inducd by lcrly imbalanc (s Drug heparin succinylcholine
Inracins scin lar). Mnir h pain’s lab- mannitol infusions triamterene
potassium chloride trimethoprim
rary rprs, and nify h prscribr f dviains
frm h nrmal rang f 3.6  4.5 mEq/L f pas- MAY CAUSE HYPOMAGNESEMIA
bumetanide furosemide (Lasix)
sium bcaus hypkalmia pnias h ffcs f
chlorthalidone metolazone (Zaroxolyn)
digxin and can lad  xiciy. Always mnir h ethacrynic acid (Edecrin) neomycin
puls carfully if h passium lvl is abnrmal. ethanol thiazide diuretics
Hypkalmia is spcially likly  ccur in a pain
wih nausa, vmiing, diarrha, r havy diursis.
Rplacing passium bfr adminisring digxin is
an accpd pracic. DRUG CLASS: PHOSPHODIESTERASE INHIBITOR
Other diseases. Th pain’s hr clinical cndiins
may als induc digxin xiciy. Pains wh suffr milrinone (MĬL-rĭ-nōn)
frm hyphyridism, acu MI, rnal disas, svr
rspirary disas, r far-advancd har failur may
rquir lwr-han-nrmal dss f digxin; mnir Actions
clsly. Milrinn is an inrpic agn ha incrass h frc
and vlciy f mycardial cnracins by inhibiing
Drug interactions phsphdisras nzyms in h har muscl. I is
Drugs that enhance therapeutic and toxic ef- als a vascular smh muscl rlaxan ha causs
fects. Quinidin, diliazm, vrapamil, ranlazin, vasdilain, hrby rducing prlad and afrlad.
macrlid anibiics (.g., clarihrmycin, ryhr-
mycin), prpafnn, ba blckrs (.g., anll, s- Uses
mll, nadll, prpranll), succinylchlin, hiazid Milrinn is usd fr h shr-rm managmn f s-
and lp diurics, calcium glucna, and calcium vr syslic dysfuncin har failur in pains wh
chlrid nhanc h hrapuic and xic ffcs f hav n rspndd adqualy  digxin, diurics,
digxin. Mnir pains aking hs drugs fr signs r vasdilar hrapy. Th inrpic ffcs f milri-
and sympms f digxin xiciy. nn ar addiiv  hs f digxin, and milrinn
Drugs that reduce therapeutic effects. S. Jhn’s wr, can b usd in fully digializd pains. Milrinn is
aminglycsid anibiics (.g., gnamicin, bramy- usually n usd  ra HFpEF, and i may indd
cin, nmycin), chlsyramin, clsipl, rifampin, wrsn his cndiin.
and anacids rduc h hrapuic ffcs f digxin.
Mnir pain sympms fr rspns  hrapy; Therapeutic Outcomes
rcurrnc r innsicain (xacrbain) f h pa- Th primary hrapuic ucms xpcd frm
in’s disas shuld b rprd  h halhcar milrinn hrapy ar incrasd cardiac upu ha
prvidr. rsuls in imprvd issu prfusin and rducd dys-
Drugs that may alter electrolyte balance, thus altering pna, rhpna, and faigu.
digoxin response. Drugs ha may alr digxin r-
spns, and hus h incidnc f any f h advrs Nursing Implications for Milrinone
ffcs, by alring h lcrly balanc includ h Premedication assessment.
fllwing: 1. Obain h pain’s baslin vial signs, including
pain raing.
MAY CAUSE HYPOKALEMIA 2. Obain h baslin labrary sudis rdrd by
amphotericin B furosemide (Lasix) h halhcar prvidr (.g., cmpl bld cun).
bumetanide metolazone (Zaroxolyn)
chlorthalidone thiazide diuretics Availability. IV: 1 mg/mL in 10-, 20-, and 50-mL vials.
corticosteroids torsemide (Demadex) Premixed infusion: 200 mcg/mL in 100 and 200 mL f
ethacrynic acid (Edecrin) dxrs 5% fr injcin.

Dosage and administration. Diluents: 0.45% r 0.9%
sdium chlrid r dxrs 5% fr injcin may b
usd  prpar diluins f milrinn fr IV infusin.
Adult: IV: A lading ds is n ncssary. Iniia
hrapy wih a mainnanc infusin f 0.5 mcg/kg/
min. In gnral, h al daily ds shuld n xcd
1.13 mg/kg/24 hr.
Serious adverse effects
Cardiovascular
Dysrhythmias, hypotension. Th cardivascular ad-
vrs ffcs f dysrhyhmias (12%) and hypnsin
(1.3%) ar h ms cmmnly rprd advrs f-
fcs. Mnir h pain’s bld prssur and har
ra and rhyhm clsly during hrapy. Ths advrs
ffcs ar fn rlad  h dsag siz, and hy
will rspnd  a rducin in infusin ra. Cnac
h halhcar prvidr immdialy if dysrhyhmias
r signican hypnsin dvlps.
Hematologic
Thrombocytopenia. Thrmbcypnia wih plal
cuns lss han 100,000/mm3 has bn rprd in
0.4% f pains. This cndiin appars  b ds d-
pndn, ccurring wihin 48  72 hurs afr iniiain
f hrapy, and is mr cmmn in pains rciving
highr-han-rcmmndd dsags. Plal cuns
shuld b baind bfr and pridically during
hrapy. If hrmbcypnia ds ccur, discninua-
in f hrapy shuld b cnsidrd, spcially whn
plal cuns dcras  lss han 50,000/mm3. Th
nadir in plal cun appars  b variabl, bu i c-
curs wihin 1  4 wks.
Drug interactions
Furosemide. Milrinn and fursmid ar chmi-
cally incmpaibl. Whn fursmid is mixd wih
milrinn, a prcipia frms immdialy. D n in-
fus hs w drugs in h sam IV lin.
DRUG CLASS: MISCELLANEOUS AGENT
ivabradine (ī-VĀB-ră-dēn)
Corlanor (cor′ la- nor)
Actions
Ivabradin slcivly and spcically inhibis h
cardiac pacmakr lcrical currn in h sinarial
nd, rsuling in a rducin in har ra. Ivabradin
ds n affc h cnraciliy f h har r vascular
sysm. Ivabradin dcrass har ra, which rducs
h risk f hspializain fr wrsning har failur.
Uses
Ivabradin is usd  rduc h risk f hspializa-
in frm wrsning har failur in pains wih
sabl, sympmaic chrnic har failur wh ar
in sinus rhyhm wih a rsing har ra grar r
qual  70 bas/min. Th pain shuld als b n
Drugs Used to Treat Heart Failure CHAPTER 27 451
maximally lrad dss f ba blckrs r hav a
cnraindicain  ba blckrs. Ivabradin ds n
signicanly rduc h risk f cardivascular dah.
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm iv-
abradin is  dcras frquncy f hspializains
as a rsul f har failur.
Nursing Implications for Ivabradine
Premedication assessment.
1. Tak h pain’s apical puls fr 1 full minu and
fllw insiuinal guidlins fr wihhlding h
drug (.g., if h puls is <60 r >100 bas/min).
Note: In h lng-rm car sing, a radial puls
may b accpabl.
2. Bfr iniiaing hrapy, bain baslin pain
daa such as vial signs, lung sunds, and wigh.
3. Obain labrary valus (.g., srum lcrlys,
livr and kidny funcin sudis).
Availability. PO: 5- and 7.5-mg abls; 1 mg/mL in 5
mL ampuls fr ral us
Dosage and administration. Adult: PO: Initial: 5 mg
wic daily r 2.5 mg wic daily in pains wh
may xprinc hmdynamic cmprmis as a r-
sul f bradycardia. Afr 2 wks, adjus ds 
achiv a rsing har ra bwn 50 and 60 bas/
min. Thrafr adjus ds as ndd basd n rs-
ing har ra and lrabiliy. Maximum dose: 7.5 mg
wic daily.
Ivabradin shuld b akn wih mals, and grap-
frui juic shuld b avidd.
Dsag adjusmn basd n rsing har ra:
• Har ra >60 bas/min: Incras ds by 2.5 mg
wic daily (maximum ds: 7.5 mg wic daily).
• Har ra 50  60 bas/min: Mainain ds.
• Har ra <50 bas/min r signs and sympms f
bradycardia: Dcras ds by 2.5 mg wic daily; if
currn ds is 2.5 mg wic daily, discninu hrapy.
Common adverse effects
Cardiovascular
Hypotension and hypertension. Mnir bld prssur
rgularly and rpr changs in rnd  h halhcar
prvidr.
Visual. Ivabradin has bn assciad wih visual
impairmn prsning as ransinly nhancd brigh-
nss, hals, r clrd brigh lighs. This may sar
wihin h rs 2 mnhs f hrapy and may subsid
spnanusly during ramn.
Serious adverse effects
Cardiac
Rhythm disturbances. Rgularly mnir h pain
fr h dvlpmn f a puls dci, bradycardia
(har ra <60 bas/min), and achycardia (har ra
>100 bas/min). Ths may b signs f dvlping
452 UNIT IV Drugs Affecting the Cardiovascular System

har blck. Pains paricularly suscpibl  rhyhm
disurbancs ar hs cncurrnly rciving ami-
darn, ba blckrs, r digxin.
Drug interactions
Drugs that enhance therapeutic and toxic ef-
fects. Diliazm, vrapamil, digxin, ba blckrs,
grapfrui juic, amidarn, macrlid anibiics
(.g., clarihrmycin, ryhrmycin), and iracnazl
nhanc h hrapuic and xic ffcs f ivabradin.
Drugs that reduce therapeutic effects. S. Jhn’s wr,
rifampin, phnbarbial, and carbamazpin rduc
h hrapuic ffcs f ivabradin. Mnir pain
sympms fr rspns  hrapy.
Drugs that may alter electrolyte balance, thus altering ivabra-
dine response. Drugs ha may alr ivabradin rspns,
and hus h incidnc f any f h advrs ffcs, by al-
ring h lcrly balanc includ h fllwing: lp
diurics (bumanid, fursmid, rsmid), hydr-
chlrhiazid, indapamid, and chlrhalidn.

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points process. Which statement by the nurse would be appropriate?

(Select all that apply.)
• Heart failure involves a cluster of signs and symptoms
that arise when the left or right ventricle or both ventricles 1. “You need to remain active and continue to participate
lose the ability to pump enough blood to meet the in the types of exercises you have done in the past, as
body’s circulatory needs. It is an illness that is growing in tolerated.”
frequency as the general population ages. 2. “The type of diet that is recommended is one with limited
calories, low in fat, and low in sodium.”
• The morbidity and mortality associated with heart failure
3. “It is important to conserve energy and avoid becoming
can be reduced through medication, diet, exercise, and
fatigued.”
health monitoring.
4. “If you nd that not being able to use salt is hard, you can
• The major pharmacologic agents used to treat heart failure use salt substitutes on a salt-restricted diet.”
are valsartan-sacubitril, ARBs, ACE inhibitors, beta- 5. “You may have 2 to 3 drinks per day, and drink as much
adrenergic blocking agents, aldosterone antagonists and water as you want.”
diuretics. Other agents that may play an active role are
hydralazine-isosorbide, ivabradine, and digoxin. Objective: Identify the goals of treatment for heart failure.
NCLEX item type: Multiple response
• Nurses can play a signicant role in discussing
Cognitive skill: Application
treatment options, planning for lifestyle changes,
counseling before discharge, and reinforcing key points 2. The nurse recognizes the primary actions of the drugs used to for
during ofce visits. The best results are attained when heart failure. Indicate with an X the effect each drug classication
the patient, the family, and the nurse work together to will have.
develop the care plan.
ARB/
Additional Learning Resources ACE BETA NEPRILYSIN
INHIBITORS ARBS BLOCKERS (ENTRESTO)
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa Decreases
tions, and other learning activities to help you master this chap- peripheral
ter content. vascular
resistance
Go to your Evolve website (https://evolve.elsevier.com/Willihng Reduces
anz) for additional online resources. afterload
Slows heart
Clinical Judgment and Next-Generation NCLEX® Exami rate
nation-Style Questions
Reduces
The following questions are typical of the NCLEX exam and preload
include both NGN (Next Generation) and traditional questions. Inhibits the
See Chapter 1 for further information regarding question types. cardiac
response
to the
Scenario
sympathetic
An elderly patient with known heart failure, who has previously nerve
been stable with lisinopril and metoprolol XL, comes into the stimulation
clinic with an increase in weight and peripheral edema extend- Inactivates
ing halfway up the left calf. natriuretic
peptides
1. The patient in the scenario with chronic heart failure asks the nurse
what else they can do besides drug therapy to control the disease
 Drugs Used to Treat Heart Failure CHAPTER 27 453

Objective: Identify the primary actions on heart failure of digoxin, 5. Hepatomegaly

ACE inhibitors, ARBs, the combination of a neprilysin inhibitor with 6. Widening pulse pressure
an ARB (Entresto), and beta blockers. 7. Splenomegaly
NCLEX item type: Matrix 8. Poor perfusion to the peripheral tissues
Cognitive skill: Recognize cues Objective: Identify essential assessment data and nursing
3. It was decided that the patient in the scenario start on digoxin. interventions needed for a patient with heart failure.
The nurse is providing instructions on what to watch for to detect NCLEX item type: Extended multiple response
developing digitalis toxicity which included which signs and Cognitive skill: Recognizes cues
symptoms? (Select all that apply.) 5. The patient from the scenario asks the nurse to explain the idea of
1. Slow heart rate <60 what is meant by the body’s compensatory mechanisms that occur
2. Anorexia in response to decreases in heart function. The nurse responses
3. Hazy or blurred vision with which correct statement?
4. Hypertension 1. “When patients have heart failure the body compensates
5. Loss of hearing with an increase in energy.”
Objective: Describe digoxin toxicity and ways to prevent it. 2. “Patients with heart failure often have an increase in
NCLEX item type: Multiple response urination as a compensatory response.”
Cognitive skill: Application 3. “The body tries to compensate by increasing heart rate
and blood pressure, but eventually cannot compensate
4. Before treatment is started, the nurse gathers assessment data for leading to shortness of breath and fatigue”
the patient in the scenario with heart failure and recognizes which 4. “Patients in heart failure will have an increase in their
symptoms are related to this condition? (Select all that apply.) peripheral perfusion as a compensatory response.”
1. Decreased exercise tolerance Objective: Explain heart failure in terms of the body’s
2. Bradycardia compensatory mechanisms.
3. Edema present around the ankles NCLEX item type: Multiple choice
4. Anorexia and nausea Cognitive skill: Comprehension
28 Drugs Used for Diuresis

https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the nursing assessments used to evaluate a
patient’s state of hydration and renal function.
2. Describe the actions of diuretics and their effects on blood
pressure and electrolytes.
3. Explain the rationale for administering diuretics cautiously
to older adults and individuals with impaired renal function,
cirrhosis of the liver, or diabetes mellitus.
4. Identify the nursing assessments needed to monitor the
therapeutic response or the development of common or
serious adverse effects of diuretic therapy.

Key Terms
tubule (TŪ-byŭl) (p. 454)
aldosterone (ăl-DŎS-tĕr-ōn) (p. 454)
edema (ĕ-DĒ-mă) (p. 456)
loop of Henle (HĔN-lē) (p. 458)
orthostatic hypotension (ŏr-thō- hyperuricemia (hī-pĕr-yŭr-ĭ-SĒ-mē-ă)
STĂT-ĭk hī-pō-TĔN-shŭn) (p. 459) (p. 459)
electrolyte imbalance (ĕ-LĔK-trō-līt
ĭm-BĂL-ĕns) (p. 459)

DRUG THERAPY WITH DIURETICS

ACTIONS
Diuretics are drugs that act to increase the ow of
urine. The purpose of diuretics is to increase the net
loss of water from the body. To achieve this, they act
on the kidneys in different locations of the nephron
to enhance the excretion of sodium (Fig. 28.1). The os-
motic diuretics (glycerol, mannitol) and the carbonic
anhydrase inhibitors (acetazolamide) act at the proxi-
mal tubule (see Fig. 28.1-1). The loop diuretics (e.g.,
bumetanide, furosemide) act on the ascending limb of
the loop of Henle (see Fig. 28.1-2), and thiazides act
directly on the distal kidney tubules (see Fig. 28.1-3) to
inhibit the reabsorption of sodium and chloride from
the lumen of the tubule Spironolactone, triamterene,
and amiloride inhibit tubular reabsorption of sodium
by inhibiting aldosterone, a hormone that induces re-
absorption of sodium in the distal tubule and collect-
ing duct (see Fig. 28.1-4). Antidiuretic hormone (vaso-
pressin) acts in the collecting duct to reabsorb water,
making the urine more concentrated (see Fig. 28.1-5).
Sodium and chloride that are not reabsorbed are ex-
creted into the collecting ducts and then into the ure-
ters to the bladder, taking large volumes of water to be
excreted from the body through urination.
USES
Diuretics are mainstays of treatment in two major
diseases affecting the cardiovascular system, heart
failure and hypertension. They are routinely used
454
for patients with heart failure to remove excessive
sodium and water, relieving symptoms associated
with pulmonary congestion and edema. The 2017
Guideline for the Prevention, Detection, Evaluation
and Treatment of High Blood Pressure in Adults rec-
ommends that, after lifestyle modications, thiazide
diuretics are one of the primary agents used in the
treatment of hypertension. They have been shown to
reduce cardiovascular morbidity and mortality asso-
ciated with hypertension.
Diuretics have a variety of other medical uses as
well. Mannitol reduces cerebral edema; acetazolamide
is used to reduce intraocular pressure associated with
glaucoma; spironolactone can be effective in reduc-
ing ascites associated with liver disease; thiazide di-
uretics, especially hydrochlorothiazide, are used for
the prevention of recurrent calcium nephrolithiasis
(kidney stones); and furosemide may be used to treat
hypercalcemia.
NURSING IMPLICATIONS FOR DIURETIC
THERAPY
The information the nurse obtains about the patient’s
general clinical symptoms is important to the health-
care provider when analyzing data for the diagnosis
and success of therapy. In addition to assessing overall
clinical symptoms, the nurse should include the fol-
lowing data for subsequent evaluation of the patient’s
response to prescribed therapies that act on the urinary
system.
 Drugs Used for Diuresis CHAPTER 28 455

Proximal convolution Distal convolution

Spironolactone
Triamterene
Acetazolamide Amiloride
HKNa
Isotonic
NaCl and 4
Cortex carbonic
anhydrase– Aldosterone-dependent
dependent and independent Na
Osmotic NaHCO3 reabsorption
diuretics 1 H2O 3 Thiazides
Outer Na
medulla Ethacrynic 2 Na 5
acid, Free-water
furosemide, reabsorption
bumetanide, with ADH
torsemide
Inner
medulla Water impermeable
H2O

Collecting duct
Loop of Henle

Fig. 28.1 Sites of actions of diuretics within the nephron.

Life Span Considerations
Diuretic Therapy
During the use of diuretic therapy, the patient, who is often
an older adult, must be monitored for hydration status and
electrolyte balance, as well as for the response of the pre-
senting symptoms to the therapy. Patients taking digoxin are
particularly susceptible to digitalis toxicity as a result of elec-
trolyte imbalance that may be caused by the use of diuretics.
Assessment
History of related causative disorders and factors. Ask
the patient questions relating to any history of dis-
orders that contribute to uid volume excess: heart
disorders (e.g., myocardial infarction, heart failure,
valvular disease, dysrhythmias); liver disease (e.g.,
ascites, cirrhosis, cancer of the liver); renal disease
(e.g., renal failure); and factors such as immobility,
hypertension, pregnancy, and use of corticosteroid
agents.
History of current symptoms. Ask the patient ques-
tions to ascertain information relating to the onset,
duration, and progression of specic symptoms relat-
ing to edema, weakness, fatigue, dyspnea, productive
cough, and weight gain.
Pattern of urination. Ask the patient to describe their
current urination pattern and to cite any changes.
Details such as frequency, dysuria, incontinence,
changes in the urine stream, hesitancy when starting to
void, hematuria, nocturia, and urgency are all signi-
cant. Provide assistance with voiding for people with
impaired mobility, fatigue, or other impairments.
Medication history. Obtain information from the pa-
tient about all prescribed and over-the-counter medi-
cations being taken. Tactfully ask questions about ad-
herence to the medication regimen.
Hydration status. Obtain the patient’s baseline vital
signs. Note a pulse that is bounding and full or irregu-
lar (i.e., indicating possible dysrhythmias); check the
respiratory rate and quality; listen to the lung sounds
to detect the presence of crackles; ask the patient about
a history of recent weight gain or loss; assess for edema
of the extremities; and assess for neck vein distention.
Blood pressure may also be elevated.
Dehydration. Assess, report, and record signicant
signs of dehydration in the patient. Observe for in-
elastic skin turgor, sticky oral mucous membranes,
a shrunken or deeply furrowed tongue, crusted lips,
weight loss, deteriorating vital signs, soft or sunken
eyeballs, weak pedal pulses, delayed capillary lling,
excessive thirst, a high urine specic gravity (or no
urine output), and possible mental confusion.
Skin turgor. Check the patient’s skin turgor by gen-
tly pinching the skin together over the sternum, on
the forehead, or on the forearm. Elasticity is present
when the skin rapidly returns to a at position in the
well-hydrated patient. In dehydrated patients, the skin
will remain in a peaked or pinched position and return
very slowly to the at, normal position. Skin turgor is
not a reliable indicator in older adults because of the
natural aging changes of the skin.
Oral mucous membranes. With adequate hydration, the
membranes of the mouth feel smooth and glisten. With
dehydration, they appear dull and are sticky. Assess
skin turgor, oral mucosa, and rmness of eyeballs.
456 UNIT IV Drugs Affecting the Cardiovascular System
Laboratory changes. The patient’s hematocrit, hemo-
globin, blood urea nitrogen (BUN), creatinine, osmo-
lality, and electrolytes will appear to uctuate, based
on the state of hydration. When the patient is over-
hydrated, the values appear to drop as a result of
hemodilution. A dehydrated patient will show higher
values because of hemoconcentration.
Overhydration. Increases in abdominal girth,
weight gain, neck vein distention, and circumfer-
ence of the medial malleolus indicate overhydration.
Daily measurements should be obtained of the pa-
tient’s abdominal girth at the umbilical level and
the extremities bilaterally at a level approximately
5 cm above the medial malleolus. The development
of crackles during lung auscultation is also a sign of
overhydration, especially in patients with heart fail-
ure. Weigh the patient daily using the same scale, at
the same time of day, with the patient wearing simi-
lar clothing.
Edema. Edema is a term used to describe excess
uid accumulation in the extracellular spaces, particu-
larly in the lower limbs. Edema is considered “pitting”
when an indentation remains in the tissue after pres-
sure is exerted against a bony part, such as the shin,
ankle, or sacrum. The degree is usually recorded as +1
(slight) to +4 (deep).
Pale, cool, tight, shiny skin is another sign of edema.
Also listen to lung sounds to detect the presence of ex-
cess uid (crackles) in the lungs.
Assess for the presence of edema and record the de-
gree of pitting. Obtain a baseline measurement of ab-
dominal girth when edema is present, and check for
the presence of uid waves in the abdomen.
Electrolyte imbalance. Because the symptoms of most
electrolyte imbalances are similar, the nurse should
obtain information related to changes in the patient’s
mental status (i.e., alertness, orientation, confusion),
muscle strength, muscle cramps, tremors, nausea, and
general appearance.
Susceptible people. Those who are particularly sus-
ceptible to the development of electrolyte disturbances
often have a history of renal or cardiac disease, hor-
monal disorders, or massive trauma or burns, or are
receiving diuretic or steroid therapy. Review the pa-
tient’s available electrolyte studies.
Hypokalemia. Hypokalemia is indicated by a se-
rum potassium (K+) level of less than 3.5 mEq/L.
Hypokalemia is especially likely to occur when a pa-
tient exhibits vomiting, diarrhea, or heavy diuresis. All
diuretics, except the potassium-sparing type, are likely
to cause hypokalemia.
Hyperkalemia. Hyperkaliemia is indicated by a
serum potassium level of more than 5.5 mEq/L.
Hyperkalemia occurs most commonly when a patient
is given excessive amounts of potassium supplementa-
tion, either intravenously or orally. It may also occur
as an adverse effect of potassium-sparing diuretics or
with renal disease.
Hyponatremia. Hyponatremia is indicated by a serum
sodium (Na+) level of less than 135 mEq/L. Remember
the following phrase: “Where sodium goes, water
goes.” Because diuretics act by excreting sodium, as
well as water, monitor the patient for hyponatremia
during and after diuresis.
Hypernatremia. This is indicated by a serum sodium
level of more than 145 mEq/L. Hypernatremia occurs
most commonly when a patient is given intravenous
(IV) uids in excess of the uid excreted.
Implementation
Intake. Measure and record accurately all uids taken
(e.g., oral, parenteral, rectal, via tubes). Ice chips and
foods such as gelatin that turn to a liquid state must
be included. Irrigation solutions should be carefully
measured so that the difference between what is in-
stilled and what is returned can be recorded as intake.
Remember to enlist the help of the patient, family,
and other visitors in this process. Ask them to keep a
record of how many glasses or cups of liquids (e.g.,
water, juice, soda, tea, coffee) are consumed by the pa-
tient. The nurse then converts the household measure-
ments to milliliters.
Nutrition. Patients with edema are routinely placed
on a restricted sodium diet to help control edema as-
sociated with heart failure. Depending on the type
of diuretic prescribed (potassium sparing or non–
potassium sparing), the patient may be placed on po-
tassium restrictions or potassium supplements.
Diet therapy for renal disease is directed at keep-
ing a normal equilibrium of the body while decreasing
the excretory load on the kidneys. See a nutrition text
for modications specic to acute and chronic renal
failure.
Output. Record all output from the mouth, urethra,
rectum, wounds, and tubes (e.g., surgical drains, na-
sogastric tubes, indwelling catheters). Liquid stools
should be recorded according to consistency, color, and
quantity. Urine output should include information on
quantity, color, pH, odor, and specic gravity.
All other secretions should be characterized by col-
or, consistency, volume, and changes from previous
collections, if possible.
Daily output is usually 1200 to 1500 mL, or 30 mL/
hr for the adult patient. Always report urine output be-
low this hourly rate. Low hourly output may indicate
dehydration, renal failure, or cardiac disease. Intake
and output (I&O) should be recorded accurately every
shift and totaled every 24 hours for all patients having
renal evaluations or receiving diuretics.
Keep the urinal or bedpan readily available. Tell pa-
tients and their visitors the importance of not dumping
the bedpan or urinal. Instruct them to use the call light
and allow the hospital personnel to empty and record
all output.

Renal diagnostics. Many laboratory tests are ordered
throughout the treatment of renal dysfunction (e.g.,
BUN, serum creatinine, creatinine clearance, serum os-
molalities, urine osmolalities). Plan schedules for appro-
priate timing of collections of blood and urine samples.
Serum electrolytes. Monitor serum electrolyte reports
especially potassium and sodium levels; notify the
healthcare provider of deviations from normal values.
Nutrition. Order a prescribed special diet, depending
on the underlying pathologic condition. If uid restric-
tions are prescribed, record the amount of uid to be
taken with each meal and the amount that may be tak-
en orally throughout the day.
Patient Education
Purposes of diuresis
• If the disease process is hypertension, stress the
importance of following the prescribed methods to
deal with emotions and the dietary and medication
regimens that can control the disease (see discus-
sion of the nursing process for hypertensive therapy
in Chapter 22).
• Teach the patient and signicant others the func-
tional changes that are caused by hypertension and
heart failure. Emphasize the need for lifelong treat-
ment and adherence to drug therapy, diet, and ex-
ercise regimens to obtain maximum control of the
disease process.
• Diuretics are used in the treatment of several disease
processes—for example, hypertension, glaucoma, as-
cites, hypercalcemia, heart failure, and renal disease.
Be certain that the patient understands the medica-
tion administration schedule and desired therapeutic
outcome for the prescribed therapy.
Medication considerations
• Diuretics should be taken in the morning to avoid
nocturia.
• When the diuretic is prescribed on a scheduled pat-
tern other than daily, assist the patient with develop-
ing ways to remember when to take the medication
(e.g., using a calendar on which to mark dosages or
using a medication holder marked with the days
of the week that is loaded weekly with the medica-
tions to be taken).
• Instruct the patient to perform daily weights using the
same scale, in similar clothing, and at the same time
daily, usually before breakfast. Record and report sig-
nicant weight changes because weight gains and loss-
es are the best indicator of uid loss or gain. Usually a
gain of 2 pounds in 2 days should be reported.
• Potassium supplements may be prescribed concur-
rently with diuretics other than potassium-sparing
diuretics.
Drugs Used for Diuresis CHAPTER 28 457
• Diuretic therapy may produce postural hypo-
tension. Teach the patient to rise slowly from a su-
pine or sitting position, and encourage the patient to
sit or lie down if feeling faint.
Nutrition
• The healthcare provider usually prescribes dietary
modications appropriate to the underlying patho-
logic condition, such as weight reduction or sodium
restriction.
• Patients receiving potassium-sparing diuretics
should be taught which foods are high in potas-
sium content. These foods should be moderately
restricted but not withheld from the diet. Salt sub-
stitutes should be avoided because they are high in
potassium.
• When taking diuretics other than the potassium-
sparing type, the patient is required to eat potassium-
rich foods.
Fostering health maintenance
• Throughout the course of treatment, discuss
medication information and how it will benefit
the patient. Stress the importance of nonpharma-
cologic interventions and the long-term effects
that compliance with the treatment regimen can
provide.
• Provide the patient and significant others with
important information contained in the specific
drug monographs for the medicines prescribed.
Additional health teaching and nursing inter-
ventions for the common and serious adverse ef-
fects are described in the drug monographs that
follow.
• Seek cooperation and understanding of the fol-
lowing points so that medication compliance is in-
creased: name of medication; dosage, route, times
of administration; and common and serious adverse
effects.
Patient self-assessment. Enlist the patient’s aid in de-
veloping and maintaining a written record of moni-
toring parameters. See Patient Self-Assessment Form
for Diuretics on the Evolve website. Complete the
Premedication Data column for use as a baseline to
track response to drug therapy. Ensure that the pa-
tient understands how to use the form, and instruct
the patient to bring the completed form to follow-up
visits. During follow-up visits, focus on issues that will
foster adherence with the therapeutic interventions
prescribed.
DRUG CLASS: CARBONIC ANHYDRASE INHIBITOR
acetazolamide (ă-sē-tă-ZŌL-ă-mīd)
458 UNIT IV Drugs Affecting the Cardiovascular System
Actions
Acetazolamide is a weak diuretic that acts by inhib-
iting the enzyme carbonic anhydrase in the kidneys,
brain, and eyes. As a diuretic, it promotes the excretion
of sodium, potassium, water, and bicarbonate.
Uses
Acetazolamide is not used often as a diuretic because
of the availability of more effective medications; how-
ever, it is used to reduce intraocular pressure in pa-
tients with glaucoma (see Chapter 42).
DRUG CLASS: SULFONAMIDE-TYPE LOOP
DIURETICS
Actions
The loop diuretics are potent diuretics that act pri-
marily by inhibiting sodium and chloride reabsorp-
tion from the ascending limb of the loop of Henle in
the kidneys, enhancing sodium, potassium, chloride,
phosphate, magnesium, and bicarbonate excretion into
the urine.
Furosemide also acts to increase renal blood ow
and glomerular ltration rate and inhibits electrolyte
absorption in the proximal and distal tubules. The
maximum diuretic effect occurs 1 to 2 hours after
oral administration and lasts for 4 to 6 hours. (The
brand name Lasix is derived from “lasts 6 hours.”)
Diuresis occurs 5 to 10 minutes after IV administra-
tion, peaks within 30 minutes, and lasts approxi-
mately 2 hours.
Bumetanide also acts by increasing renal blood ow
into the glomeruli and inhibiting electrolyte absorption
in the proximal tubule but does not act on the distal tu-
bule. Its diuretic activity starts 30 to 60 minutes after oral
administration, peaks within 1 to 2 hours, and lasts 4 to
6 hours. After IV injection, diuresis begins within min-
utes and reaches maximum levels in 15 to 30 minutes.
Torsemide does not appear to affect glomerular
ltration rate or renal blood ow or block reabsorp-
tion of sodium from the proximal or distal tubule.
Maximum diuretic effect occurs 1 to 2 hours after oral
Table 28.1 Sulfonamide-Type Loop Diuretics
GENERIC NAME BRAND NAME
bumetanide — Tablets: 0.5, 1, 2 mg
furosemide Lasix
Do not confuse furosemide with Do not confuse Lasix with
famotidine, uoxetine, fosinopril, Lanoxin or Luvox.
or minoxidil.
torsemide — Tablets: 5, 10, 20, and 100 mg
Do not confuse torsemide with
topiramate.
Do not confuse.
administration and lasts 6 to 8 hours. Diuresis occurs 5
to 10 minutes after IV administration, peaks within 60
minutes, and lasts up to 6 hours.
Uses
Bumetanide, furosemide, and torsemide are used to
treat edema resulting from heart failure, cirrhosis of
the liver, and renal disease, including nephrotic syn-
drome. Although furosemide and torsemide may
be used for the treatment of hypertension, they are
not recommended for the initial treatment of hyper-
tension. Furosemide is also used in combination with
0.9% sodium chloride infusions to enhance the excre-
tion of calcium in patients with hypercalcemia and to
treat edema and heart failure.
Therapeutic Outcome
The primary therapeutic outcome associated with sul-
fonamide loop diuretic therapy is diuresis, with reduc-
tion of edema and improvement in symptoms related
to excessive uid accumulation. Reduction of blood
pressure is an outcome also expected of furosemide
and torsemide.
Nursing Implications for Sulfonamide-Type Loop
Diuretics
Premedication assessment
1. Obtain baseline data such as vital signs, lung
sounds, weight, degree of edema present, and labo-
ratory studies (e.g., serum electrolytes, liver and re-
nal function tests) before initiating therapy.
2. Obtain data relating to the patient’s mental status
(orientation, alertness, confusion), muscle strength,
muscle cramps, tremors, nausea, and general
appearance.
3. Patients with diabetes require baseline measure-
ment of blood glucose levels.
4. Check for symptoms of acute gout. If present, notify
the healthcare provider.
5. Note any reduction in hearing.
Availability See Table 28.1
DOSAGE FORMS AVAILABLE DOSAGE RANGE
0.5–10 mg
Injection: 0.25 mg/mL in 4-, and
10-mL vials
Tablets: 20, 40, 80 mg 20–600 mg
Oral solution: 10 mg/mL in 60 and
120 mL bottles
IV: 10 mg/mL in 2-, 4-, and 10-mL
vials
5–200 mg

Dosage and administration. Adult: PO: Do not ex-
ceed the maximum dosages identied in Table 28.1.
Administer with food or milk to reduce gastric irrita-
tion. Do not administer after midafternoon to prevent
nocturia.
Adult: IM or IV:
• Bumetanide: The IV and oral doses are equivalent.
Administer IV doses over 1 to 2 minutes.
• Furosemide: The IV dose is half the oral dose.
Administer slowly over 2 to 4 minutes.
Common adverse effects
Gastrointestinal
Oral irritation, dry mouth. Start regular oral hygiene
measures when the therapy is initiated. Suggest the
use of 1 teaspoon of hydrogen peroxide in 6 to 8 ounces
of water as a mouthwash. Commercial mouthwashes
contain alcohol, which may cause further drying and
oral irritation. Another method to alleviate dryness is
sucking on ice chips or hard candy.
Cardiovascular
Orthostatic hypotension. Orthostatic hypotension,
a drop in blood pressure that occurs with a change
of position from supine to sitting or standing and
causes dizziness, weakness, and faintness, is infre-
quent and generally mild. All diuretics may cause
orthostatic hypotension to some degree, particularly
when therapy is being initiated. Monitor the blood
pressure daily in both the supine and standing po-
sitions. Anticipate the development of orthostatic
hypotension and take measures to prevent an occur-
rence. Teach the patient to rise slowly from a supine
or sitting position, and encourage the patient to sit or
lie down if feeling faint.
Serious adverse effects
Gastrointestinal
Gastric irritation, abdominal pain. If gastric irritation oc-
curs, administer with food or milk. If symptoms per-
sist or increase in severity, report to the healthcare pro-
vider for evaluation.
Metabolic, renal
Electrolyte imbalance, dehydration. The electrolytes
most commonly altered are potassium, sodium, and
chloride (Cl ). Hypokalemia and hyponatremia are
most likely to occur. Many symptoms associated with
uid and electrolyte imbalance are subtle and inter-
spersed with general symptoms of drug toxicity or
the disease process itself. Gather data about changes
in the patient’s mental status (alertness, orientation,
confusion), muscle strength, muscle cramps, trem-
ors, nausea, and general appearance. Always check
the electrolyte reports for early indications of electro-
lyte imbalance. Keep accurate records of I&O, daily
weights, and vital signs.
Hypomagnesemia. Magnesium depletion caused by
increased excretion of magnesium is a predictable con-
sequence of the chronic use of loop agents. Monitor as
Drugs Used for Diuresis CHAPTER 28 459
clinically warranted. It can be treated by administra-
tion of oral magnesium preparations.
Hyperuricemia. Furosemide may inhibit the excretion
of uric acid, resulting in hyperuricemia. Patients who
have had previous attacks of gouty arthritis are par-
ticularly susceptible to additional attacks as a result
of hyperuricemia. Monitor the laboratory reports for
early indications of hyperuricemia. Report this to the
healthcare provider, who may then add a uricosuric
agent or allopurinol to the patient’s medication regi-
men. (See Chapter 44 for more information on gout.)
Hyperglycemia. Patients with diabetes or prediabe-
tes must be monitored for the development of hyper-
glycemia, particularly during the early weeks of
therapy. Assess regularly for hyperglycemia with a
ngerstick blood sample and home glucometer, and
report to the healthcare provider if it occurs with any
frequency. Patients receiving oral hypoglycemic agents
or insulin may require an adjustment in dosage.
Hypersensitivity
Hives, pruritus, rash. Report symptoms for further
evaluation by the healthcare provider. Pruritus may be
relieved by adding baking soda to the bathwater.
Medication Safety Alert
Patients who are allergic to sulfonamides may also be allergic
to sulfonamide-type loop diuretics. Use cautiously in these
patients.
Drug interactions
Alcohol, sedative-hypnotics, opioids. Orthostatic hypo-
tension associated with sulfonamide-type loop diuret-
ic therapy may be aggravated by these agents.
Digoxin. Sulfonamide-type loop diuretics may cause
excessive potassium excretion, leading to hypokalemia.
If the patient is also receiving digoxin, monitor closely
for digitalis toxicity (anorexia, nausea, fatigue, blurred
or colored vision, bradycardia, dysrhythmias).
Clinical Goldmine
Remember, low potassium levels may cause digitalis toxicity.
Always check potassium levels for patients receiving diuret-
ics before administration of digoxin.
Aminoglycosides. The potential for ototoxicity from the
aminoglycosides (e.g., gentamicin, tobramycin, amikacin)
is increased. Assess the patient for gradual, often subtle,
changes in hearing. Note whether the patient seems to
speak more loudly, asks for statements to be repeated, or
turns the television or radio progressively louder.
Cisplatin. The potential for ototoxicity from the com-
bination of cisplatin and the sulfonamide-type loop
diuretics is increased. Assess the patient for gradual,
often subtle, changes in hearing. Note whether the pa-
tient seems to speak more loudly, asks for statements
to be repeated, or turns the television or radio progres-
sively louder.
460 UNIT IV Drugs Affecting the Cardiovascular System
Nonsteroidal antiinammatory drugs. Nonsteroidal anti-
inammatory drugs (NSAIDs) (e.g., indomethacin,
ibuprofen, naproxen) inhibit the diuretic activity of the
sulfonamide-type loop diuretics. The dose of diuretic
may have to be increased or the NSAID discontinued.
Maintain accurate I&O records and monitor for a de-
crease in diuretic activity.
Corticosteroids. Corticosteroids (e.g., prednisone)
may enhance the loss of potassium. Check potassium
levels and monitor more closely for hypokalemia when
these two agents are used concurrently.
Metolazone. When used concurrently, there is a con-
siderably greater diuresis than when either agent is
used alone. Monitor closely for dehydration and elec-
trolyte imbalance.
ethacrynic acid (ĕth-ă-KRĬN-ĭk)
Edecrin (Ĕ-dĕ-krĭn)
Actions
Ethacrynic acid is another diuretic that acts primarily
on the ascending limb of the loop of Henle but also
the proximal and distal tubules to prevent sodium and
chloride reabsorption. Ethacrynic acid does not appear
to affect renal blood ow or the glomerular ltration
rate. Its diuretic activity begins within 30 minutes,
peaks in approximately 2 hours, and lasts 6 to 8 hours.
Uses
Ethacrynic acid is used to treat edema resulting from
heart failure, cirrhosis of the liver, renal disease, and
malignancy and for hospitalized pediatric patients
with congenital heart disease. It is thought that because
ethacrynic acid inhibits the reabsorption of sodium to
a much greater extent than other diuretics, it may be
more effective for patients with signicant renal fail-
ure. It is also used in conjunction with 0.9% sodium
chloride infusions to enhance excretion of calcium in
patients with hypercalcemia.
Therapeutic Outcome
The primary therapeutic outcome associated with
ethacrynic acid therapy is diuresis with reduction of
edema and improvement in symptoms related to ex-
cessive uid accumulation.
Nursing Implications for Ethacrynic Acid
Premedication assessment
1. Obtain baseline data such as vital signs, lung
sounds, weight, degree of edema present, and labo-
ratory studies (e.g., serum electrolytes, liver and re-
nal function tests) before initiating therapy.
2. Obtain data relating to the patient’s mental status (ori-
entation, alertness, confusion), muscle strength, mus-
cle cramps, tremors, nausea, and general appearance.
3. Patients with diabetes require baseline measure-
ment of blood glucose levels.
Availability. PO: 25-mg tablets.
IV: 50 mg/vial.
Dosage and administration. Adult: PO: 50 to 100 mg
initially, followed by 50 to 200 mg daily. Do not exceed
400 mg/day. Administer with food or milk to reduce
gastric irritation. Do not administer after midafternoon
to prevent nocturia.
Adult: IV: 50 mg or 0.5 to 1 mg/kg. Add 50 mL of
dextrose 5% or saline solution to 50 mg of ethacrynic
acid. This solution is stable for 24 hours. Administer
over several minutes through the tubing of a running
infusion or by direct IV line. Occasionally, the addition
of a diluent may result in a cloudy solution. These so-
lutions should not be used.
Pediatric: PO: 1 mg/kg once daily; may increase
up to 3 mg/kg/day. Adjust dosage at intervals of 2 to
3 days. Always monitor vital signs and I&O at regu-
lar intervals when administering this agent intrave-
nously. Report blood pressure that decreases steadily
or a narrowing pulse pressure, which may indicate
hypovolemia.
Common adverse effects
Cardiovascular
Orthostatic hypotension. Although this effect is infre-
quent and generally mild, all diuretics may cause some
degree of orthostatic hypotension (dizziness, weak-
ness, faintness associated with a drop in blood pres-
sure), particularly when therapy is initiated or dosages
are increased. Monitor the blood pressure daily in both
the supine and standing positions. Anticipate the de-
velopment of orthostatic hypotension and take meas-
ures to prevent its occurrence. Teach the patient to rise
slowly from a supine or sitting position and encourage
the patient to sit or lie down if feeling faint.
Serious adverse effects
Metabolic, renal
Electrolyte imbalance, dehydration. The electrolytes
most commonly altered are potassium, sodium, and
chloride. Hypokalemia and hyponatremia are most
likely to occur. Many symptoms associated with elec-
trolyte imbalance are subtle and interspersed with
general symptoms of drug toxicity or the disease pro-
cess itself. Gather data about changes in the patient’s
mental status (alertness, orientation, confusion), mus-
cle strength, muscle cramps, tremors, nausea, and gen-
eral appearance. Always check the electrolyte reports
for early indications of electrolyte imbalance. Keep ac-
curate records of I&O, daily weights, and vital signs.
Dizziness, deafness, tinnitus. People with impaired re-
nal function may experience these symptoms. Assess
the patient for gradual, often subtle, changes in bal-
ance and hearing. Note whether the patient seems
more unsteady when standing, speaks loudly, asks for
statements to be repeated, or turns the television or ra-
dio progressively louder.
 Drugs Used for Diuresis CHAPTER 28 461

Gastrointestinal and antihypertensive agents since the 1960s. As diuret-

Gastrointestinal bleeding. Observe for coffee-ground
vomitus or dark, tarry stools, particularly in patients
receiving IV therapy.
Diarrhea. Diarrhea may become severe. Report to the
healthcare provider and monitor the patient for dehy-
dration and uid and electrolyte imbalance.
Endocrine
Hyperglycemia. Patients with diabetes or prediabe-
tes must be monitored for the development of hyper-
glycemia, particularly during the early weeks of
therapy. Assess regularly for hyperglycemia with a n-
gerstick blood sample and a glucometer, and report to
the healthcare provider if it occurs with any frequency.
Patients receiving oral hypoglycemic agents or insulin
may require an adjustment in dosage.
Drug interactions
Aminoglycosides. The potential for ototoxicity from
the aminoglycosides (e.g., gentamicin, tobramycin,
amikacin) is increased. Assess the patient for gradual,
often subtle, changes in hearing. Note whether the pa-
tient seems to speak loudly, asks for statements to be
repeated, or turns the television or radio progressively
louder.
Nonsteroidal antiinammatory drugs. NSAIDs (e.g., in-
domethacin, ibuprofen, naproxen) inhibit the diuretic
activity of ethacrynic acid. The dose of ethacrynic acid
may have to be increased or the NSAID discontinued.
Maintain accurate I&O records and monitor for a de-
crease in diuretic activity.
Digoxin. Ethacrynic acid may cause excess potas-
sium excretion, leading to hypokalemia. If the patient
is also receiving digoxin, monitor closely for digitalis
toxicity (anorexia, nausea, fatigue, blurred or colored
vision, bradycardia, dysrhythmias).
Corticosteroids. Corticosteroids (e.g., prednisone)
may enhance the loss of potassium. Check potassium
levels and monitor more closely for hypokalemia when
these two agents are used concurrently.
DRUG CLASS: THIAZIDE DIURETICS
Actions
Benzothiadiazides, more commonly called thiazides,
have been an important and useful class of diuretic
ics, thiazides act primarily on the distal tubule of the
kidney to block the reabsorption of sodium and chlo-
ride ions from the tubule. The sodium and chloride
ions that are not reabsorbed are passed into the collect-
ing ducts, taking molecules of water with them, result-
ing in a diuresis.
Uses
Thiazides are used as diuretics in the treatment of ede-
ma associated with heart failure, renal disease, hepatic
disease, pregnancy, obesity, premenstrual syndrome,
and administration of adrenocortical steroids. The
antihypertensive properties of thiazides result from a
direct vasodilatory action on the peripheral arterioles
(see Chapter 22). Thiazide diuretics tend to lose their
diuretic action after about 6 weeks of therapy, but the
antihypertensive properties continue. Thiazide diuret-
ics also tend to lose their diuretic effect when creati-
nine clearance is less than 30 mL/min.
Therapeutic Outcomes
The primary therapeutic outcomes associated with
thiazide therapy are diuresis with reduction of edema
and improvement in symptoms related to excessive
uid accumulation, and reduction in elevated blood
pressure.
Nursing Implications for Thiazide Diuretics
Premedication assessment
1. Obtain baseline data such as vital signs, lung
sounds, weight, degree of edema present, and labo-
ratory studies (e.g., serum electrolytes, liver and re-
nal function tests) before initiating therapy.
2. Obtain data relating to the patient’s mental status
(orientation, alertness, confusion), muscle strength,
muscle cramps, tremors, nausea, and general
appearance.
3. Patients with diabetes require baseline measure-
ment of blood glucose levels.
4. Note any reduction in hearing.
5. Check for any symptoms of acute gout. If present,
notify the healthcare provider.
Availability. Tables 28.2 and 28.3 list thiazide diuretics
and diuretics chemically related to the thiazides. Most

Table 28.2 Thiazide Diuretics

GENERIC NAME BRAND NAME DOSAGE FORMS AVAILABLE DOSAGE RANGE
chlorothiazide Diuril Tablets: 250, 500 mg 500–1000 mg once or twice
Oral suspension: 250 mg/5 mL daily
Injection: 500 mg
hydrochlorothiazide — Tablets: 12.5, 25, 50 mg 12.5–200 mg
Do not confuse Capsules: 12.5 mg
hydrochlorothiazide with
hydroxychloroquine.
Do not confuse.
462 UNIT IV Drugs Affecting the Cardiovascular System
of the diuretics listed are administered in divided daily
dosages for the treatment of hypertension; however, a
single daily dosage may be most effective for mobiliza-
tion of edema uid.
Dosage and administration. See Tables 28.2 and 28.3.
Administer with food or milk to reduce gastric irrita-
tion. Do not administer after midafternoon to prevent
nocturia.
Common adverse effects
Cardiovascular
Orthostatic hypotension. Although orthostatic hypo-
tension (dizziness, weakness, faintness associated with
a drop in blood pressure) is infrequent and generally
mild, all diuretics may cause some degree of ortho-
static hypotension, particularly when therapy is being
initiated. Monitor the blood pressure daily in both the
supine and standing positions. Anticipate the develop-
ment of orthostatic hypotension and take measures to
prevent it. Teach the patient to rise slowly from a su-
pine or sitting position, and encourage the patient to
sit or lie down if feeling faint.
Serious adverse effects
Gastrointestinal
Gastric irritation, nausea, vomiting, constipation. If gas-
tric irritation occurs, administer with food or milk. If
symptoms persist or increase in severity, report to the
healthcare provider for evaluation.
Dermatologic. Skin photosensitivity is associated
with thiazide diuretics. Advise patients to limit the
amount of time spent in the sun and use sunscreens
when outside.
Metabolic, renal
Electrolyte imbalance, dehydration. Use of thiazides
may cause or aggravate electrolyte imbalance; there-
fore patients should be observed regularly for signs
such as dry mouth, drowsiness, confusion, muscular
weakness, and nausea. The electrolytes most com-
monly altered are potassium, sodium, and chloride.
Hypokalemia is most likely to occur, and supplemen-
tary potassium is often prescribed to prevent or treat
it. Many symptoms associated with altered uid and
electrolyte balance are subtle and interspersed with
Table 28.3 Thiazide-Related Diuretics
GENERIC NAME
chlorthalidone
Do not confuse chlorthalidone with chlorpromazine
or chlorothiazide.
indapamide
metolazone
Do not confuse metolazone with
medroxyprogesterone, metaxalone, methotrexate,
metoclopramide, or metoprolol.
Do not confuse.
general symptoms of drug toxicity or the disease pro-
cess itself. Gather data about changes in the patient’s
mental status (alertness, orientation, confusion), mus-
cle strength, muscle cramps, tremors, nausea, and gen-
eral appearance. Always check the electrolyte reports
for early indications of electrolyte imbalance. Keep ac-
curate records of I&O, daily weights, and vital signs.
Hypomagnesemia. Thiazide diuretics may increase
renal excretion of magnesium. There is the relationship
between magnesium and potassium loss. Monitoring
of magnesium and potassium levels may be needed.
Hypercalcemia. Thiazide diuretics may decrease re-
nal calcium excretion; consider avoiding use in pa-
tients with hypercalcemia.
Hyperuricemia. The plasma uric acid level is often
elevated by the thiazides, which inhibit the excretion
of uric acid. Patients who have had previous episodes
of hyperuricemia or attacks of gouty arthritis are
particularly susceptible to additional attacks when
receiving thiazide therapy. Monitor the laboratory re-
ports for early indications of hyperuricemia. Report
to the healthcare provider, who may then add a uri-
cosuric agent or allopurinol to the patient’s medica-
tion regimen. (See Chapter 44 for more information
on gout.)
Endocrine
Hyperglycemia. The thiazides may induce hyper-
glycemia and aggravate cases of preexisting diabetes
mellitus. Patients with diabetes or prediabetes must
be monitored for the development of hyperglycemia,
particularly during the early weeks of therapy. Assess
regularly for hyperglycemia using a ngerstick blood
sample and glucometer, and report to the healthcare
provider if it occurs with any frequency. Dosages of
oral hypoglycemic agents and insulin may need ad-
justment in patients with diabetes mellitus who also
require diuretic therapy.
Hypersensitivity
Hives, pruritus, rash. Report symptoms for further
evaluation by the healthcare provider. Pruritus may be
relieved by adding baking soda to the bathwater.
Drug interactions
Digoxin. Thiazide diuretics may cause excessive ex-
cretion of potassium, resulting in hypokalemia. If the
BRAND NAME DOSAGE FORMS AVAILABLE DOSAGE RANGE
— Tablets: 15, 25, 50 mg 50–200 mg
— Tablets: 1.25, 2.5 mg 1.25–5 mg
__ Tablets: 2.5, 5, 10 mg 2.5–20 mg

patient is also receiving digoxin, monitor closely for
signs of digitalis toxicity (e.g., anorexia, nausea, fatigue,
blurred or colored vision, bradycardia, dysrhythmias).
Corticosteroids. Corticosteroids (e.g., prednisone)
may enhance the loss of potassium. Check potassium
levels and monitor more closely for hypokalemia when
these two agents are used concurrently.
Lithium. Thiazide diuretics may induce lithium tox-
icity. Monitor patients for lithium toxicity manifested
by nausea, anorexia, ne tremors, persistent vomit-
ing, profuse diarrhea, hyperreexia, lethargy, and
weakness.
Nonsteroidal antiinammatory drugs. NSAIDs (e.g., in-
domethacin, ibuprofen, naproxen) inhibit the diuretic
activity of this agent. The dose of thiazide may have to
be increased or the NSAID discontinued. Maintain ac-
curate I&O records and monitor for a decrease in diu-
retic activity.
Oral hypoglycemic agents, insulin. Because of the hyper-
glycemic effects of the thiazide diuretics, dosage ad-
justments of insulin and oral hypoglycemic agents are
often required.
DRUG CLASS: POTASSIUM-SPARING DIURETICS
amiloride (ă-MĬL-ōr-īd)
Actions
Amiloride is a potassium-sparing diuretic that also has
weak antihypertensive activity. Its mechanism of ac-
tion is unknown, but it acts at the distal renal tubule
to retain potassium and excrete sodium, resulting in a
mild diuresis.
Uses
Amiloride is usually used in combination with other
diuretics in patients with hypertension or heart failure
to help prevent hypokalemia that may result from oth-
er diuretic therapy.
Therapeutic Outcome
The primary therapeutic outcome associated with
amiloride therapy is diuresis with reduction of edema
and improvement in symptoms related to excessive
uid accumulation.
Nursing Implications for Amiloride
Premedication assessment
1. Obtain baseline data such as vital signs, lung
sounds, weight, degree of edema present, and labo-
ratory studies (e.g., serum electrolytes, liver and re-
nal function tests) before initiating therapy.
2. Obtain data relating to the patient’s mental status
(orientation, alertness, confusion), muscle strength,
muscle cramps, tremors, nausea, and general
appearance.
Availability. PO: 5-mg tablets.
Drugs Used for Diuresis CHAPTER 28 463
Dosage and administration. Adult: PO: Initially, 5 mg
daily. Dosage may be increased in 5-mg increments up
to 20 mg daily with close monitoring of electrolytes.
Administer with food or milk to reduce gastric irrita-
tion. Do not administer after midafternoon to prevent
nocturia.
Common adverse effects
Gastrointestinal
Anorexia, nausea, vomiting, atulence. These adverse
effects should be mild, particularly if the dose is ad-
ministered with food. Persistent nausea and vomiting
should be evaluated for other causes, as well as for the
development of electrolyte imbalance.
Neurologic
Headache. Monitor the blood pressure at regularly
scheduled intervals because amiloride is used for
hypertension. Additional readings should be taken
during headaches to determine whether headaches are
caused by the agents or by hypertension. Report per-
sistent headaches to the healthcare provider.
Serious adverse effects
Electrolyte imbalance, dehydration. The electrolytes
most commonly altered are potassium, sodium, and
chloride. Hyperkalemia is most likely to occur. Report
potassium levels greater than 5 mEq/L to the health-
care provider. Many symptoms associated with al-
tered uid and electrolyte balance are subtle and
interspersed with general symptoms of drug toxicity
or the disease process itself. Gather data about chang-
es in the patient’s mental status (alertness, orientation,
confusion), muscle strength, muscle cramps, trem-
ors, nausea, and general appearance. Always check
the electrolyte reports for early indications of electro-
lyte imbalance. Keep accurate records of I&O, daily
weights, and vital signs.
Drug interactions
Lithium. Amiloride may induce lithium toxicity.
Monitor patients who take lithium for lithium toxicity
as manifested by nausea, anorexia, ne tremors, per-
sistent vomiting, profuse diarrhea, hyperreexia, leth-
argy, and weakness.
Potassium supplements, salt substitutes. Amiloride
inhibits potassium excretion. Do not administer with
potassium supplements or use salt substitutes high in
potassium because of the potentially dangerous effects
of hyperkalemia.
Hyperkalemia. Angiotensin-converting enzyme
(ACE) inhibitors (e.g., captopril, lisinopril, ramipril),
angiotensin II receptor blockers (ARBs; e.g., losar-
tan, candesartan), and aldosterone receptor blocking
agents (e.g., eplerenone, spironolactone) inhibit aldos-
terone. Patients may develop hyperkalemia (K+ >5.7
mEq/L). Most cases resolve without discontinuation
of therapy. Patients most susceptible to the develop-
ment of hyperkalemia are those with renal impairment
464 UNIT IV Drugs Affecting the Cardiovascular System
or diabetes mellitus and those already receiving
a potassium supplement. In general, potassium-
sparing diuretics (e.g., amiloride, triamterene) should
not be taken concurrently with these antihypertensive
agents.
Nonsteroidal antiinammatory drugs. NSAIDs (e.g., in-
domethacin, ibuprofen, naproxen) inhibit the diuretic
activity of amiloride. The dose of amiloride may have
to be increased or the NSAID discontinued. Maintain
accurate I&O records and monitor for a decrease in
diuretic activity.
spironolactone (spī-rō-nō-LĂK-tōn)
Aldactone (ăl-DĂK-tōn)
Actions
Spironolactone blocks the sodium-retaining and
potassium-excreting and magnesium-excreting prop-
erties of aldosterone, resulting in a loss of water with
the increased sodium excretion.
Uses
Spironolactone is a diuretic that is particularly use-
ful in relieving edema and ascites that do not re-
spond to the usual diuretics. It may be given with
thiazide diuretics to increase its effect and reduce
the hypokalemia often induced by the thiazides.
Spironolactone has also been shown to further reduce
morbidity and mortality for patients with heart fail-
ure who are also being treated with an ACE inhibitor
and a loop diuretic.
Therapeutic Outcome
The primary therapeutic outcome associated with
spironolactone therapy is diuresis, with reduction of
edema and improvement in symptoms related to ex-
cessive uid accumulation and heart failure.
Nursing Implications for Spironolactone
Premedication assessment
1. Obtain baseline data such as vital signs, lung
sounds, weight, degree of edema present, and labo-
ratory studies (e.g., serum electrolytes, liver and re-
nal function tests) before initiating therapy.
2. Obtain data relating to the patient’s mental status
(orientation, alertness, confusion), muscle strength,
muscle cramps, tremors, nausea, and general
appearance.
3. Tactfully ask about any preexisting problems with
libido.
Availability. PO: 25-, 50-, and 100-mg tablets; oral sus-
pension: 25 mg/5 mL in 118- and 473-mL bottles.
Dosage and administration. Adult: PO: Initially, 100
mg daily. Maintenance dosage is usually 25 to 200
mg daily, but doses up to 400 mg may be prescribed.
Administer with food or milk to reduce gastric
irritation. Do not administer after midafternoon to pre-
vent nocturia.
Common and serious adverse effects
Neurologic
Mental confusion. Perform a baseline assessment of
the patient’s alertness; drowsiness; lethargy; and ori-
entation to time, date, and place before starting drug
therapy. Compare subsequent mental status and assess
on a regular basis.
Headache. Monitor blood pressure at regularly
scheduled intervals because this agent is used for
hypertension. Additional readings should be taken
during headaches to determine whether headaches are
caused by the agent or the hypertension. Report persis-
tent headaches to the healthcare provider.
Gastrointestinal
Diarrhea. The onset of new symptoms occurring af-
ter initiating the drug therapy requires evaluation if
persistent.
Metabolic
Electrolyte imbalance, dehydration. The electrolytes
most commonly altered are potassium, sodium, and
chloride. Hyperkalemia is most likely to occur. Report
potassium levels greater than 5 mEq/L to the health-
care provider. Many symptoms associated with al-
tered uid and electrolyte balance are subtle and
interspersed with general symptoms of drug toxicity
or the disease process itself. Gather data about chang-
es in the patient’s mental status (alertness, orientation,
confusion), muscle strength, muscle cramps, trem-
ors, nausea, and general appearance. Always check
the electrolyte reports for early indications of electro-
lyte imbalance. Keep accurate records of I&O, daily
weights, and vital signs.
Endocrine
Gynecomastia, reduced libido, breast tenderness. Because
the chemical structure of spironolactone is similar to
that of estrogen hormones, an occasional male patient
will report gynecomastia, reduced libido, and dimin-
ished erection. Women may complain of breast sore-
ness and menstrual irregularities. These effects are
reversible after therapy is discontinued.
Drug interactions
Potassium supplements,salt substitutes. Spironolactone
inhibits potassium excretion. Do not administer with
potassium supplements or use salt substitutes high
in potassium because of potentially dangerous effects
from hyperkalemia.
Hyperkalemia. ACE inhibitors (e.g., captopril, lisino-
pril, ramipril), ARBs (e.g., losartan, candesartan), and
aldosterone receptor blocking agents (e.g., eplerenone,
spironolactone) inhibit aldosterone. Patients may de-
velop hyperkalemia (K+ >5.7 mEq/L). Most cases re-
solve without discontinuation of therapy. Patients
most susceptible to the development of hyperkalemia
are those with renal impairment or diabetes mellitus

and those already receiving a potassium supplement.
In general, potassium-sparing diuretics should not be
taken concurrently with these antihypertensive agents.
Nonsteroidal antiinammatory drugs. NSAIDs (e.g., in-
domethacin, ibuprofen, naproxen) inhibit the diuretic
activity of spironolactone. The dosage of spironolac-
tone may have to be increased or the NSAID discon-
tinued. Maintain accurate I&O records and monitor for
a decrease in diuretic activity.
triamterene (trī ĂM-tĕr-ēn)
Dyrenium (dī-RĒ-nē ŭm)
Actions
Triamterene is a very mild diuretic that acts by block-
ing the exchange of potassium for sodium in the distal
tubule of the kidney, resulting in retention of potas-
sium with excretion of sodium and water.
Uses
Triamterene is an effective agent to use in conjunction
with the potassium-excreting diuretics, such as the thi-
azides, and the loop diuretics.
Therapeutic Outcome
The primary therapeutic outcome associated with tri-
amterene therapy is diuresis with reduction of edema
and improvement in symptoms related to excessive
uid accumulation.
Nursing Implications for Triamterene
Premedication assessment
1. Obtain baseline data such as vital signs, lung
sounds, weight, degree of edema present, and labo-
ratory studies (e.g., serum electrolytes, liver and re-
nal function tests) before initiating therapy.
2. Obtain data relating to the patient’s mental status (ori-
entation, alertness, confusion), muscle strength, mus-
cle cramps, tremors, nausea, and general appearance.
Availability. PO: 50- and 100-mg capsules.
Dosage and administration. Adult: PO: 100 to 300 mg/
day given once or twice daily; maximum dose: 300 mg
daily.
Common and serious adverse effects
Metabolic
Electrolyte imbalance, dehydration, leg cramps, weak-
ness. The electrolytes most commonly altered are
potassium, sodium, and chloride. Hyperkalemia is
most likely to occur. Report potassium levels great-
er than 5 mEq/L to the healthcare provider. Many
symptoms associated with altered uid and electro-
lyte balance are subtle and interspersed with general
symptoms of drug toxicity or the disease process
Drugs Used for Diuresis CHAPTER 28 465
itself. Gather data about changes in the patient’s
mental status (alertness, orientation, confusion),
muscle strength, muscle cramps, tremors, nausea,
and general appearance (drowsy, anxious, lethargic).
Always check the electrolyte reports for early indica-
tions of electrolyte imbalance. Keep accurate records
of I&O, daily weights, and vital signs.
Gastrointestinal
Nausea, vomiting. These adverse effects should be
mild, particularly if the dose is administered with
food. Persistent nausea and vomiting should be evalu-
ated for other causes, as well as for the development of
electrolyte imbalance.
Hypersensitivity
Hives, pruritus, rash. Report symptoms for further
evaluation by the healthcare provider. Pruritus may be
relieved by adding baking soda to the bathwater.
Drug interactions
Salt substitutes, potassium supplements. Triamterene
inhibits potassium excretion. Do not administer with
potassium supplements or use salt substitutes high in
potassium because of the potentially dangerous effects
from hyperkalemia.
Hyperkalemia. ACE inhibitors (e.g., captopril, lisino-
pril, ramipril), ARBs (e.g., losartan, candesartan), and
aldosterone receptor blocking agents (e.g., eplerenone,
spironolactone) inhibit aldosterone. Patients may de-
velop hyperkalemia (K+ >5.7 mEq/L). Most cases
resolve without discontinuation of therapy. Patients
most susceptible to the development of hyperkalemia
are those with renal impairment or diabetes mellitus
and those already receiving a potassium supplement.
In general, potassium-sparing diuretics should not
be taken concurrently with these antihypertensive
agents.
Nonsteroidal antiinammatory drugs. NSAIDs (e.g.,
indomethacin, ibuprofen, naproxen) inhibit the diu-
retic activity of triamterene. The dosage of triamterene
may have to be increased or the NSAID discontinued.
Maintain accurate I&O records and monitor for a de-
crease in diuretic activity.
DRUG CLASS: COMBINATION DIURETIC PRODUCTS
A common problem associated with thiazide diuretic
therapy is hypokalemia. In an attempt to minimize this
adverse effect, several products have been manufactured
that contain a potassium-sparing diuretic combined with
a thiazide diuretic (Table 28.4). The goal of these combina-
tion products is to promote diuresis and antihypertensive
effect through different mechanisms of action while
maintaining normal serum potassium levels. Patients
receiving a combination product are at risk for adverse
effects resulting from any of the component drugs. Many
cases of hyperkalemia and hyponatremia have been re-
ported after the use of the combination products.
466 UNIT IV Drugs Affecting the Cardiovascular System

Table 28.4 Combination Diuretics

GENERIC NAME BRAND NAME DOSAGE RANGE
spironolactone 25 mg, hydrochlorothiazide 25 mg Aldactazide-25 1–8 tablets daily
spironolactone 50 mg, hydrochlorothiazide 50 mg Aldactazide-50 1–4 tablets daily
triamterene 37.5 mg, hydrochlorothiazide 25 mg — 1–2 capsules once daily
triamterene 37.5 mg, hydrochlorothiazide 25 mg Maxzide-25 1–2 tablets once daily
triamterene 75 mg, hydrochlorothiazide 50 mg Maxzide 1 tablet daily
amiloride 5 mg, hydrochlorothiazide 50 mg — 1 or 2 tablets daily with meals

Combination products should not be used as initial
therapy for edema or hypertension. Therapy with in-
dividual products should be adjusted for each patient.
If the xed combination represents the appropriate
dosage for each component, the use of a combination
product may be more convenient for patient compli-
ance. Patients must be reevaluated periodically for
appropriateness of therapy and to prevent electrolyte
imbalance.
 Drugs Used for Diuresis CHAPTER 28 467

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points 2. The nurse discusses the importance of careful monitoring of

laboratory values to the patient in the scenario who has been
• Diuretics are drugs that act at various locations in the switched from thiazide to furosemide (Lasix). Which statement by
nephron to increase the ow of urine. the patient indicates the patient needs further education?
• The purpose of diuretics is to increase the net loss of 1. “I have been getting my labs checked monthly, and they
water. tell me that my potassium has been stable.”
• Diuretics are mainstays in the symptomatic treatment of 2. “Because I am going to be switched to this new
heart failure, hypertension, and renal disease. medication, I can stop worrying about any need to have
• Diuretics also have a variety of other medical uses, such my labs checked monthly, as a result of this stabilizing my
as reducing cerebral edema, intraocular pressure, ascites, edema.”
and hypercalcemia. 3. “As I understand it, you are telling me that is it important
• The information that the nurse obtains about the patient’s to keep a close eye on my labs that indicate when I am
general clinical symptoms is important to the healthcare becoming dehydrated from this drug.”
provider when analyzing data for diagnosis and success of 4. “I will get my labs checked more frequently because I
therapy. have just started on this med and I need to see how it will
affect my kidneys.”
Additional Learning Resources Objective: Explain the rationale for administering diuretics
cautiously to older adults and individuals with impaired renal
SG Go to your Study Guide for additional Review Questions function, cirrhosis of the liver, or diabetes mellitus.
for the NCLEX® Examination, Critical Thinking Clinical Situa- NCLEX item type: Multiple choice
tions, and other learning activities to help you master this chap- Cognitive skill: Comprehension
ter content.
3. A nurse is reviewing the common and serious adverse effects of
Go to your Evolve website (https://evolve.elsevier.com/Willihng furosemide (Lasix) therapy with the patient in the scenario. Indicate
anz) for additional online resources. with an X which are the common adverse effects and which are
the serious adverse effects.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX exam and include both NGN (Next Generation) and COMMON ADVERSE SERIOUS ADVERSE
traditional questions. See Chapter 1 for further information re- EFFECT EFFECT
garding question types.
Hypokalemia
Hyperglycemia
Scenario
Muscle cramps
A patient who is diagnosed with heart failure has been taking a Orthostatic
diuretic as part of the treatment and recently developed symp- hypotension
toms of drowsiness, confusion, and muscle weakness.
Hyperuricemia
1. The nurse is assessing the patient in the scenario who has been Confusion
taking diuretics for several months for signs of dehydration. What
Dry mouth
should the nurse assess for in patients taking diuretics? (Select all
that apply.) Tremors
1. Elastic skin turgor
2. Lower lab values of hematocrit and hemoglobin from Objective: Identify the nursing assessment needed to monitor the
baseline therapeutic response or the development of common or serious
3. Dry and sticky oral mucous membranes adverse effect of diuretic therapy.
4. Lab values of hematocrit and hemoglobin elevated from NCLEX item type: Matrix
baseline Cognitive skill: Evaluate cues
5. Sunken eyeballs
6. Weak pedal pulses
7. Crackles in the lung bases
8. Excessive thirst
Objective: Identify the nursing assessments used to evaluate a
patient’s state of hydration and renal function.
NCLEX item type: Extended multiple response
Cognitive skill: Evaluate cues
468 UNIT IV Drugs Affecting the Cardiovascular System
4. The nurse is discussing the possible adverse effects of thiazide
diuretic therapy with a patient. The nurse recognizes that further
education is needed when the patient makes which statement?
1. “I understand that, because I am taking this
hydrochlorothiazide, I can expect my kidneys to shut
down.”
2. “I know that I am taking this for my high blood pressure,
so I should expect that it will control it better once I get
started on this.”
3. “So you are saying that if I develop gout then I need to let
my doctor know.”
4. “I will need to get my blood work done periodically to
determine whether this drug is making my potassium
level drop.”
Objective: Describe the actions of diuretics and their effects on
blood pressure and electrolytes.
NCLEX item type: Multiple choice
Cognitive skill: Evaluate
5. The nurse taking the patient’s blood pressure notes a decrease in
the value from recent readings. What explanation will the nurse
give the patient in the scenario currently taking furosemide (Lasix)
regarding this change?
1. “I believe this blood pressure reading must be in error, I
will need to recheck it.”
2. “You are probably getting worried about how you will
manage at home, so that would explain the change in
your blood pressure.”
3. “Sometimes there is a drop in the blood pressure when
you take these diuretics because they will affect the
volume of circulating blood as a result of diuresis.”
4. “The blood pressure measurement means that you are
not responding to the diuretic like you should be; we will
have to reevaluate the meds you are on.”
Objective: Describe the actions of diuretics and their effects on
blood pressure and electrolytes.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
6. The nurse was caring for a patient who asked for a pain pill
(ibuprofen) for a recent arm fracture and was currently taking
the diuretic furosemide (Lasix). What would be an appropriate
response by the nurse?
1. “Sure, no problem; the two medications do not interact.”
2. “Because these two medications have a known
interaction, I will not be allowed to give you any for pain.”
3. “If I give you the pain pill, it will affect the diuretic and you
will have an increased effect from the diuretic.”
4. “This pain medication may require an increased dosage
of the diuretic.”
Objective: Identify the nursing assessment needed to monitor the
therapeutic response of the development of common or serious
adverse effect of diuretic therapy
NCLEX item type: Multiple choice
Cognitive skill: Recognize cues
7. The nurse knows that individuals with impaired renal function,
cirrhosis of the liver, or diabetes mellitus need to be given diuretics
cautiously because they are known to cause what effect? (Select
all that apply.)
1. Patients with diabetes may experience hyperglycemia.
2. Patients with cirrhosis of the liver may develop orthostatic
hypotension.
3. Patients with renal disease tend to develop electrolyte
imbalances.
4. Patients with diabetes may experience hypoglycemia.
5. Patients with renal disease will develop edema secondary
to diuretics.
Objective: Explain the rationale for administering diuretics
cautiously to older adults and individuals with impaired renal
function, cirrhosis of the liver, or diabetes mellitus.
NCLEX item type: Multiple response
Cognitive skill: Application
8. The nurse monitoring the patient in the scenario using diuretics
to reduce peripheral edema will watch for which therapeutic
response?
1. A reduction in cerebral edema and headaches
2. A reduction in edema and an increased urine output
3. A reduction in ascites associated with liver congestion
4. An improvement in renal function
Objective: Describe the actions of diuretics and their effects on
blood pressure and electrolytes.
NCLEX item type: Multiple choice
Cognitive skill: Understanding
Unit V Drugs Affecting the Respiratory System

Drugs Used to Treat Upper Respiratory Disease 29

https://evolve.elsevier.com/Willihnganz

Objectives
1. Discuss the causes of allergic rhinitis, nasal congestion,
and rhinitis medicamentosa.
2. Explain the major actions (effects) of sympathomimetic,
antihistaminic, and corticosteroid medicines.
3. Explain why all decongestant products should be used
cautiously by people with hypertension, hyperthyroidism,
diabetes mellitus, cardiac disease, increased intraocular
pressure, or prostatic disease.
4. Discuss the nursing assessments needed during therapy
to monitor the therapeutic response to and the common
and serious adverse effects of decongestant drug therapy.

KeyTerms
rhinitis (rī-NĪ-tĭs) (p. 470)
sinusitis (sī-nyū-SĪ-tĭs) (p. 471)
allergic rhinitis (ă-LĔR-jĭk rī-NĪ-tĭs)
(p. 471)
antigen-antibody (ĂN-tĭ-jĕn ĂN-tĭ-bŏ-
dē) (p. 471)
histamine (HĬS-tă-mēn) (p. 471)
rhinorrhea (rī-nō-RĒ-ă) (p. 471)
decongestants (dē-kŏn-JĔS-tănts)
(p. 471)
rhinitis medicamentosa (rī-NĪ-tĭs
mĕd-ĭ-kŏ-mĕn-TŌ-să) (p. 471)
antihistamines (ăn-tĭ-HĬS-tă-mēnz)
(p. 472)
antiinammatory agents (ăn-tī-ĭn-
FLĂ-mă-tō-rē) (p. 473)

UPPER RESPIRATORY TRACT ANATOMY

AND PHYSIOLOGY
The respiratory system is a series of airways that start
with the nose and mouth and end at the alveolar sacs
within the lungs. The upper respiratory tract is com-
posed of the nose and its turbinates, the sinuses, the
nasopharynx, the pharynx, the tonsils, the eustachian
tubes, and the larynx (Fig. 29.1). The nose and its struc-
tures serve two functions: olfactory (i.e., smell) and re-
spiratory. The olfactory region is located in the upper
part of each nostril. It is an area of specialized tissue
cells (i.e., olfactory cells) that contain microscopic hairs
that react to odors in the air and then stimulate the ol-
factory cells. The olfactory cells in turn send signals to
the brain, which processes the sensation that people
perceive as a particular smell.
The respiratory function of the nose is to warm,
humidify, and lter the air inhaled to prepare it for
the lower respiratory airways. Both nasal passages
have folds of skin called turbinates that signicantly
increase the surface area of the passages and contain
massive numbers of blood vessels. The blood circu-
lating through the membranes lining the turbinates
warms and humidies inhaled air. The inhaled air
is also ltered of particulate matter. The hairs at the
entrance to the nostrils remove large particles, and
the turbinates and narrowness of the nasal passag-
es cause turbulence of the airow passing through
with each inhalation. All of the surfaces of the nose
are coated with a thin layer of mucus, which is se-
creted by goblet cells. Because of the turbulence of
the airow, particles are thrown against the walls of
the nasal passages and become trapped in the mu-
cosal secretions. The epithelial cells lining the pos-
terior two-thirds of the nasal passages contain cilia
that sweep the particulate matter back toward the
nasopharynx and pharynx. Once in the pharynx, the
particulate matter is expectorated or swallowed. The
warming, humidication, and ltration processes
continue as the air passes into the trachea, bronchi,
and bronchioles.
The nasal structures are innervated by the autonom-
ic nervous system. Cholinergic stimulation causes va-
sodilation of the blood vessels lining the nasal mucosa
and sympathetic (primarily alpha-adrenergic) stimu-
lation causes vasoconstriction. The cholinergic bers
also innervate the secretory glands. When stimulated,
they produce serous and mucous secretions within the
nostrils.
The paranasal sinuses are hollow, air-lled cavities
in the cranial bones on both sides of and behind the
nose. There are eight sinuses (four on each side). The
469
470 UNIT V Drugs Affecting the Respiratory System
Frontal
sinus
Sphenoid
sinus
Turbinates
Nasal
airway
Mouth
airway
Tongue
Larynx
(vocal cords)
Fig. 29.1 The upper respiratory tract.
purpose of the paranasal sinuses appears to be to act
as resonating chambers for the voice and as a means of
lightening the bones of the head. The sinuses are lined
with the same mucous membranes and ciliated epithe-
lia as those of the upper respiratory tract. The sinuses
are connected to the nasal passages by ducts that drain
secretions into the nasal cavity from activity of the cili-
ated cells.
On either side of the oral pharynx is a pharyngeal
tonsil, a collection of lymphoid tissue that is called the
adenoids when enlarged. The tonsils are located in an
area where mucus laden with particulate matter (e.g.,
virus particles, bacteria) accumulates from the ciliary
action of cells in the nasopharynx above. The lym-
phoid tissue is rich in immunoglobulins and is thought
to play a role in the immunologic defense mechanisms
of the upper airway.
Sneezing is a physiologic reex used by the body to
clear the nasal passages of foreign matter. The sneeze
reex is initiated by irritation of the nasal mucosa by
foreign particulate matter. It is similar to the cough re-
ex, which clears the lower respiratory airways of se-
cretions and foreign matter.
COMMON UPPER RESPIRATORY
DISEASES
Rhinitis is inammation of the nasal mucous mem-
branes. Signs and symptoms include sneezing, na-
sal discharge, and nasal congestion. Rhinitis is often
subclassied as acute or chronic on the basis of the
Respiratory
center
Cough control
center
Nasopharynx
Eustachian tube
(to middle ear)
Soft palate
Tonsil
Pharynx
Esophagus
Trachea
duration of the signs and symptoms. The most com-
mon causes of acute rhinitis are the common cold (vi-
ral infection), bacterial infection, presence of a foreign
body, and drug-induced congestion (rhinitis medica-
mentosa). Common causes of chronic rhinitis are al-
lergy, nonallergic perennial rhinitis, chronic sinusitis,
and a deviated septum.
The common cold is actually a viral infection of
the upper respiratory tissues. When considering the
amount of time lost from school and work and the
number of healthcare provider ofce visits that this
condition causes annually, it is probably the single
most expensive illness in the United States. Seasons
in which viral infections reach near-epidemic propor-
tions are midwinter, spring, and early fall (i.e., a few
weeks after school starts). Six different virus families,
including 120 to 200 subtypes, cause cold-like symp-
toms; the most common are the rhinoviruses and
coronaviruses. Viruses are spread from person to per-
son by direct contact and sneezing. The earliest symp-
toms of a cold are a clear, watery nasal discharge and
sneezing. Nasal congestion from engorgement of the
nasal blood vessels and swelling of nasal turbinates
quickly follows. Over the next 48 hours the discharge
becomes cloudy and much more viscous. Other
symptoms include coughing, a “scratchy” or mildly
sore throat (pharyngitis), and hoarseness (laryngi-
tis). Other symptoms that occur less commonly are
headache, malaise, chills, and fever. A few patients
may develop a fever up to 100°F (37.8°C). Symptoms
should subside within 5 to 7 days.
 Drugs Used to Treat Upper Respiratory Disease CHAPTER 29
Complications occasionally develop as a result of
the challenge to the body’s immune system initiated
by cold viruses. Complications can also arise from
thick, tenacious mucus obstructing the sinus ducts or
the eustachian tubes to the middle ears. Bacteria are
easily trapped behind these obstructions in the sinuses
and ears, resulting in bacterial sinusitis or otitis media
(infection of the middle ear). Viral infections are also
a common cause of exacerbations of obstructive lung
disease and of acute asthmatic attacks in susceptible
individuals. If symptoms of the cold do not begin
to resolve after several days or if symptoms become
worse or additional symptoms appear (e.g., tempera-
ture higher than 100°F [37.8°C], earache), a healthcare
provider should be consulted.
Allergic rhinitis (AR) is inammation of the nasal
mucosa as a result of an allergic reaction. Patients with
AR have had previous exposure to one or more al-
lergens (e.g., pollens, grasses, house dust mites) and
have developed antibodies to those allergens. After
this exposure, when the person inhales the allergen,
an antigen-antibody reaction occurs, causing inam-
mation and swelling of the nasal passages. One of the
major causes of symptoms associated with an allergy
is the release of histamine during the antigen-antibody
reaction.
Histamine is a compound derived from an amino
acid called histidine that is stored in small granules in
most body tissues. Its physiologic functions are not
completely known, but it is released in response to al-
lergic reactions and tissue damage caused by trauma
or infection.
When histamine is released in the area of tissue
damage or at the site of an antigen-antibody reaction
(e.g., a pollen inhaled into the nose of a patient who
is allergic to that specic pollen), it reacts with the
histamine-1 (H1) receptors in the area and the follow-
ing reactions take place:
1. The arterioles and capillaries in the region dilate, al-
lowing increased blood ow to the area that results
in redness.
2. The capillaries become more permeable, resulting in
the outward passage of uid into the extracellular
spaces, causing edema (this is manifested by con-
gestion in the mucous membranes and turbinates of
the patient’s nose).
3. Nasal, lacrimal, and bronchial secretions are re-
leased, resulting in a runny nose (rhinorrhea) and
watery eyes (conjunctivitis) noted in patients with
allergies.
Patients with AR also complain of itching of the pal-
ate, ears, and eyes. Most patients with asthma have an
allergic component to the disease that triggers acute
asthma attacks.
When large amounts of histamine are released
(e.g., during a severe allergic reaction), there is ex-
tensive arterial dilation. Blood pressure drops (hypo-
tension), the skin becomes ushed and edematous,
471
and severe itching (urticaria) develops. Constriction
(narrowing) and spasm of the bronchial tubes make
respiratory effort more difcult (dyspnea), and co-
pious amounts of pulmonary and gastric secretions
are released.
Allergies may be seasonal or perennial. Seasonal
allergies occur when a particular allergen is abun-
dant—tree pollen is prevalent from late March to
early June; ragweed is abundant from early August
until the rst hard freeze in October; and grasses pol-
linate from the middle of May to the middle of July.
Weather conditions (e.g., rainfall, humidity, tempera-
ture) affect the amount of pollen produced during a
particular year but not the actual onset or termination
of the specic allergen’s season. It is common for a
person to be allergic to more than one allergen simul-
taneously, so seasonal allergies may overlap or may
occur more than once per year. People who have al-
lergies to multiple antigens (e.g., smoke, molds, ani-
mal dander, feathers, house dust mites, pollens) have
varying degrees of symptoms all year round and are
said to have perennial allergies. Allergy symptoms
need to be treated, not only for symptomatic relief
but also to prevent irreversible changes within the
nose, such as thickening of the mucosal epithelium,
loss of cilia, loss of smell, recurrent sinusitis and otitis
media, growth of connective tissue, and development
of nasal or sinus polyps that aggravate rhinitis and
secondary infections.
Overuse of topical decongestants may lead to
a rebound of nasal secretions known as rhinitis
medicamentosa.This secondary congestion is thought
to be caused by excessive vasoconstriction of the blood
vessels and by direct irritation of the nasal membranes
by the solution. When the vasoconstrictor effects wear
off, the irritation causes excessive blood ow to the
passages, causing swelling and engorgement to reap-
pear; the nose feels stufer and more congested than it
did before treatment. Over the following few weeks a
vicious cycle develops, involving more frequent use of
the topical decongestant to relieve nasal passage swell-
ing and obstruction. Rhinitis medicamentosa may de-
velop as early as 3 to 5 days after use of long-acting
topical decongestants such as oxymetazoline and xylo-
metazoline, but it usually does not develop until after
2 to 3 weeks of regular use of short-acting topical de-
congestants such as phenylephrine.
TREATMENT OF UPPER RESPIRATORY
DISEASES
COMMON COLD
Treatment of the common cold is limited to relieving
the symptoms associated with rhinitis and, if present,
pharyngitis and laryngitis; reducing the risk of compli-
cations; and preventing the spread of viral infection to
others. Decongestants are the most effective agent for
relieving nasal congestion and rhinorrhea.
472 UNIT V Drugs Affecting the Respiratory System
Life Span Considerations
Decongestants
Sympathomimetic amines, more commonly called decon-
gestants, and antihistamines are commonly used in combi-
nation with analgesics in cold and u remedies. People are
often not fully aware of the ingredients of over-the-counter
(OTC) combination products.
Patients with diabetes mellitus, hypertension, or ischemic
heart disease should use products containing decongestants
only if advised to do so by a healthcare provider or pharmacist.
A paradoxical effect from antihistamines often seen in
young children and older adults is central nervous system
stimulation rather than sedation, which may cause insomnia,
nervousness, and irritability. Antihistamines may also cause
urinary retention and should be used with caution by older
men who have an enlarged prostate gland.
The use of antihistamines (H1-receptor antagonists)
for symptomatic relief of cold symptoms has been con-
troversial. Studies indicate that preschool-age children
do not benet from the use of antihistamines; howev-
er, older children, adolescents, and adults do receive
some benet.
Depending on whether fever, pharyngitis, or cough
is present, patients may also benet from the use of
analgesics (see Chapter 19), antipyretics, expectorants,
and antitussive agents (see Chapter 30). Laryngitis
should be treated by resting the vocal cords as much
as possible. Inhaling cool mist vapor several times dai-
ly to humidify the larynx may be benecial, but put-
ting medication into the inhaled vapor is of no value.
Lozenges and gargles do nothing to relieve hoarseness
because they do not reach the larynx.
ALLERGIC RHINITIS
The rst steps in treating AR are to (1) identify the aller-
gens—through skin testing—and (2) avoid exposure,
if possible. Unfortunately, it often is not possible to
eliminate exposure to many allergens without severe
lifestyle restrictions. Medicines must then be used to
block the allergic reaction or treat the symptoms. The
pharmacologic agents typically used include antihis-
tamines, decongestants, and intranasal corticosteroid
antiinammatory agents. Montelukast (see Chapter
30), a leukotriene receptor antagonist, is approved for
AR but there are concerns that the risk may outweigh
the benet of montelukast. Neuropsychiatric changes
have been reported in association with the use of mon-
telukast, including dream abnormalities, insomnia,
anxiety, depression, suicidal thinking, and in rare cases,
suicide. In 2020 the US Food and Drug Administration
added a boxed warning stating that the use of mon-
telukast in patients with AR should be reserved for
patients who have an inadequate response or intoler-
ance to alternative therapies. Saline nasal sprays can be
effective in reducing nasal irritation between doses of
other pharmacologic agents. If the patient is physically
able, vigorous exercise for 15 to 30 minutes once or
twice daily increases sympathetic output and induces
vascular vasoconstriction.
Mild AR can be treated by an oral antihistamine
(e.g., chlorpheniramine diphenhydramine, loratadine,
cetirizine, fexofenadine). Patients with an inadequate
response to monotherapy may require combination
therapy with the addition of a decongestant if nasal
congestion is present. Patients with moderate to se-
vere symptoms may require an antihistamine, a de-
congestant and a nasal corticosteroid simultaneously.
Immunotherapy may be required if symptoms are
only partially controlled, if high doses of intranasal or
oral corticosteroids are required, or if the AR is com-
plicated by asthma or sinusitis. Therapy should be
started before the anticipated appearance of allergens
and continue during the time of exposure.
RHINITIS MEDICAMENTOSA
The best treatment of rhinitis medicamentosa is pre-
vention. Unfortunately, most patients are not aware of
the condition until it becomes a problem. Following
the directions for a daily dosage and limiting the du-
ration of therapy to that recommended on the topical
decongestant product are the best ways to avoid the
condition.
Several strategies have been successful in treating
rhinitis medicamentosa. Regardless of the approach
used, the patient must understand what caused the
rebound congestion and why it is important to elimi-
nate the problem. One method is to withdraw the
topical decongestant completely at once. The patient
is likely to be congested and uncomfortable for the
next week, but use of a saline nasal spray can help
moisturize irritated nasal tissues. Nasal steroid solu-
tions can also be used, but they still take several days
to reduce inammation and congestion. Probably
the most successful approach, although the longest
to complete, is to have the patient work to clear one
nostril at a time. Start by reducing the strength and
frequency of the decongestant used in the left nostril
while continuing with the normal dosage in the right
nostril. Saline or corticosteroid nasal spray can be
used every other dose in the left nostril. Eventually,
the saline can be used more frequently and the de-
congestant can be discontinued in the left nostril.
Once the patient can breathe normally through the
left nostril, the same approach can be started in the
right nostril. Frequent follow-up with the patient and
reinforcement of progress made are important to the
success of this treatment.
DRUG THERAPY FOR UPPER RESPIRATORY
DISEASES
ACTIONS AND USES
Antihistamines, or H1-receptor antagonists, are used
for treating AR. Antihistamines reduce the symptoms
of nasal itching, sneezing, rhinorrhea, lacrimation, and
 Drugs Used to Treat Upper Respiratory Disease CHAPTER 29
conjunctival itching; however, antihistamines do not
reduce nasal congestion.
Decongestants are alpha-adrenergic stimulants that
cause vasoconstriction of the nasal mucosa, which sig-
nicantly reduces nasal congestion. When treating AR,
decongestants are often administered in conjunction
with antihistamines to reduce nasal congestion.
Antiinammatory agents administered intranasally
are used to treat nasal symptoms resulting from mild
to severe AR depending on the antiinammatory
agent. In general, antiinammatory agents are not
used to treat symptoms associated with a cold because
the symptoms start to resolve before the antiinam-
matory agents can become effective. The antiinam-
matory agents used to treat AR are corticosteroids and
cromolyn sodium.
NURSING IMPLICATIONS FOR UPPER
RESPIRATORY DISEASES
Nasal congestion, AR, and sinusitis are treated with
prescription or OTC medicines. The roles of the nurse
in the healthcare provider’s ofce are to perform the
initial assessment of symptoms and then focus on
teaching the proper techniques for self-administering
and monitoring of the medication therapy. Always re-
view the patient’s history for other diseases currently
being treated (e.g., hypertension, glaucoma, asthma,
prostatic hyperplasia) that may contraindicate the
concurrent use of some upper respiratory medications
used as OTC or prescribed treatments.
Assessment
Description of symptoms
• Which symptoms are present (e.g., frequency of
sneezing or coughing, hoarseness, nasal congestion,
presence of nasal secretions and type [watery, vis-
cous, color])?
• When did the symptoms start?
• Does the patient have a history of allergies? If yes,
what are the known allergens? Are the symptoms
associated with a particular time of year or the re-
lease of pollen from plants? Are the symptoms trig-
gered by exposure to household environmental
factors (e.g., animal dander, dust, molds, certain
foods)?
• Has the individual recently been exposed to some-
one with a common cold or upper respiratory tract
infection?
• Is the individual having pain or discomfort? What
are the specic areas affected and the degree of
pain?
History of treatment
• What prescribed or OTC medicines have been used?
Have any been effective?
• When allergies are suspected, has skin or blood test-
ing been completed to determine what specic al-
lergens are initiating the attacks?
473
• If pain is present, how has pain relief been obtained?
Is the degree of pain relief satisfactory?
History of concurrent medical problems. Ask specic
questions to determine whether the patient has con-
current medical problems (e.g., glaucoma, prostatic
hyperplasia, asthma, hypertension, diabetes mellitus)
as described in the drug monograph preassessments.
Patient Education
• Make sure that the patient understands the impor-
tance of adequate rest, hydration, and personal hy-
giene (i.e., handwashing) to prevent the spread of
infection, when present.
• Discuss the specic medications prescribed, the
therapeutic effects that can be expected, and when
to contact a healthcare provider if therapy does not
yield the expected benet. Explain which symptoms
should be reported to the healthcare provider that
would indicate a poor response to therapy (e.g., es-
calation of symptoms, pain, or fever with sinusitis).
• Make sure that the patient understands when to
take the medicine (e.g., if treating symptoms of al-
lergy, antihistamines should be taken 45 to 60 min-
utes before exposure to the allergen).
• Proper technique is important to therapy success.
Explain the procedures for proper instillation of
nose drops or nasal sprays associated with the pre-
scribed treatment regimen. Document and verify
that the patient can self-administer the medication
as recommended.
• Teach the patient to monitor temperature, pulse,
respirations, and blood pressure as appropriate to
the underlying diagnosis and the medicines used to
treat the diagnosed condition.
Fostering health maintenance
• Throughout the course of treatment, discuss medi-
cation information and how it will benet the pa-
tient. Recognize that nonadherence may occur, es-
pecially when treatment response is not immediate.
• Seek cooperation and understanding regarding the
following points so that medication adherence is
increased: the name of the medication; its dosage,
route, and times of administration; and its common
and serious adverse effects. Numerous OTC prepa-
rations may be contraindicated when other medi-
cations or coexisting diseases are present. For ex-
ample, patients taking antihypertensive medicines
should not take decongestants. (See the individual
drug monographs for details.)
DRUG CLASS: SYMPATHOMIMETIC
DECONGESTANTS
Actions
Sympathomimetic nasal decongestants (Table 29.1)
stimulate the alpha-adrenergic receptors of the nasal
474 UNIT V Drugs Affecting the Respiratory System
Table 29.1 Nasal Decongestants
GENERIC NAME BRAND NAME
oxymetazoline Vicks Sinex Moisturizing
phenylephrine Neo-Synephrine Cold and Allergy
Do not confuse Do not confuse Neo-
phenylephrine with Synephrine with epinephrine.
epinephrine, phenytoin, Sudafed PE Sinus Congestion
or norepinephrine.
pseudoephedrine Sudafed Sinus Congestion
Do not confuse Sudafed Sinus Congestion
pseudoephedrine with 12 hr
prednisone. Sudafed Sinus Congestion
24 hr
Do not confuse.
mucous membranes, causing vasoconstriction. This
constriction reduces blood ow in the engorged nasal
area, resulting in shrinkage of the engorged turbinates
and mucous membranes and promoting sinus drain-
age, improving nasal air passage, and relieving the
feelings of stufness and obstruction.
Uses
Decongestants are used for relieving congestion
associated with rhinitis caused by the common
cold. They are also often used in conjunction with
antihistamines when treating AR to reduce nasal
congestion.
Decongestants can be administered orally or ap-
plied directly to the nose (topically) in the form of na-
sal sprays or drops to treat rhinitis. An advantage of
topical administration is that it has essentially no sys-
temic effects. Disadvantages of nasal sprays and drops
are their lack of effect on conjunctival symptoms, their
inconvenience, and their potential to cause rhinitis
medicamentosa.
Nasal decongestants provide temporary relief of
symptoms, but it is important for the patient to fol-
low the directions on the label carefully. Initially,
the stuffiness or blocked sensation will be relieved;
however, misuse—including excessive use or fre-
quency of administration—may cause a rebound
swelling (i.e., rhinitis medicamentosa) of the nasal
passages.
Alpha-adrenergic agents used as nasal deconges-
tants can stimulate alpha receptors at other sites in
the body as well. Therefore they should be used with
caution when taken orally by patients with hyper-
tension, hyperthyroidism, diabetes mellitus, cardiac
disease, increased intraocular pressure, or prostatic
hyperplasia.
Many states have enacted laws regulating and
tracking the amount of pseudoephedrine-containing
decongestants that can be purchased by an individual.
Pseudoephedrine is one of the ingredients used in the
manufacturing of methamphetamine, an illicit drug
with signicant potential for abuse.
AVAILABILITY ADULT DOSAGE RANGE
Solution: 0.05% Nasal: 2–3 drops or sprays twice
daily; use less than 3 days
Solution: 0.25%, 0.5%, 1% Nasal: 2–3 drops or sprays in
Tablets: 10 mg each nostril q4h; use less than
3 days
Oral: 10–20 mg q4h
Tablets: 30, 60 mg PO: 30–60 mg q4–6h; do not
Liquid: 15, 30 mg/5 mL exceed 240 mg/24 hr
Extended Release 12 hr
tablet: 120 mg
Extended Release 24 hr
tablet: 240 mg
Therapeutic Outcome
The primary therapeutic outcome associated with
sympathomimetic decongestant therapy is reduced
nasal congestion with easier breathing.
Nursing Implications for Sympathomimetic
Decongestants
Premedication assessment
1. Check the patient’s history for evidence of hyper-
tension, hyperthyroidism, diabetes mellitus, cardiac
dysrhythmias, glaucoma, or prostatic hyperplasia.
If any one of these conditions is present, consult the
healthcare provider before initiating therapy.
2. Inquire about urinary pattern, particularly in male
patients older than age 55 who may be developing
prostatic hyperplasia.
3. Obtain the patient’s baseline vital signs.
4. Assess nasal and sinus congestion before therapy.
Availability, dosage, and administration
See Table 29.1; see Chapter 7 for techniques for admin-
istering nose drops and nasal spray.
Common adverse effects
Respiratory
Mild nasal irritation. Burning or stinging may be felt
when sympathomimetic decongestants are adminis-
tered to the nasal membranes. This may be avoided by
using a weaker solution.
Serious adverse effects
Genitourinary
Urinary retention. Some patients, particularly men with
prostatic hyperplasia, may develop urinary partial ob-
struction—difculty with starting a stream of urine—
when taking oral decongestants. The obstruction is dose
related and will resolve with metabolism of the drug.
This adverse effect can be eliminated by using only topi-
cal decongestants rather than oral decongestants.
Cardiovascular
Hypertension. Excessive use of decongestants may
result in signicant hypertension. Patients already
 Drugs Used to Treat Upper Respiratory Disease CHAPTER 29
receiving antihypertensive therapy should avoid using
decongestants. When sympathomimetic decongest-
ants are used, blood pressure monitoring should be
initiated; the healthcare provider should be contacted
if the patient’s blood pressure becomes elevated.
Metabolic
Hyperglycemia. Patients with prediabetes or dia-
betes must be monitored for the development of
hyperglycemia.
Drug interactions
Drugs that enhance toxic effects. Monoamine oxidase
(MAO) inhibitors (e.g., tranylcypromine, phenelzine,
isocarboxazid) may enhance the toxic effects of sym-
pathomimetic decongestants and result in signicant
hypertension. Decongestants should not be used while
taking MAO inhibitor therapy or for 2 weeks after
stopping an MAO inhibitor.
Methyldopa. Frequent decongestant use inhibits the
antihypertensive activity of methyldopa. Concurrent
therapy is not recommended.
DRUG CLASS: ANTIHISTAMINES
Actions
Antihistamines, or H1-receptor antagonists, are chemi-
cal agents that compete with the allergy-liberated hista-
mine for H1-receptor sites in the patient’s arterioles, cap-
illaries, and secretory glands in the mucous membranes.
Antihistamines do not prevent histamine release, but
they reduce the symptoms of an allergic reaction if the
concentration of the antihistamine exceeds the concen-
tration of histamine at the receptor site. Antihistamines
are therefore more effective if they are taken before his-
tamine is released or when symptoms rst appear.
Uses
Oral antihistamines are recommended as rst-line agents
in patients with mild symptoms of AR or those with
sneezing and itching as the primary complaint. These
agents reduce rhinorrhea, lacrimation, nasal and con-
junctival pruritus, and sneezing; however, antihistamines
do not stop nasal congestion. In addition, antihistamine
nasal sprays are available and have similar effectiveness
as oral antihistamine. The antihistamines shown in Table
29.2 have similar histamine-blocking effects when they
are taken in recommended dosages, but they vary in du-
ration of action, sedative effects, and anticholinergic ef-
fects. Occasionally, a patient may develop a tolerance to
the antihistaminic effects; changing to another antihista-
mine is usually effective when this occurs.
Antihistamines work best if taken on a scheduled
basis rather than as needed during the allergy season.
These agents are much more effective if they are taken
before exposure to the allergen (e.g., 45 to 60 minutes
before going outdoors during pollen season).
There is no evidence that one agent is particularly bet-
ter than another at treating symptoms of AR, although
475
there are differences among products regarding their
frequency and type of associated adverse effects. The
most common adverse effect of many antihistaminic
agents is sedation. Most patients acquire a tolerance to
this effect with continued therapy. Reducing the dosage
or changing to another antihistamine may occasion-
ally be necessary. The most sedating antihistamines are
diphenhydramine, cyproheptadine, clemastine, and
doxylamine (doxylamine and diphenhydramine are the
active ingredients in OTC sleep aids). The least sedat-
ing antihistamines (second-generation antihistamines)
are azelastine, fexofenadine, loratadine, cetirizine, levo-
cetirizine, and desloratadine. Although some patients
do not feel a sense of sedation after taking an antihista-
mine, their cognitive functions (e.g., attention, memory,
coordination, psychomotor performance) can be sig-
nicantly impaired. A disturbing observation by these
patients is that they often are not aware that their cogni-
tive abilities are impaired. This is particularly important
when patients who are taking antihistamines perform
potentially dangerous activities (e.g., driving).
All antihistamines display anticholinergic ad-
verse effects, particularly when higher dosages are
used. Symptoms include dry mouth, stuffy nose,
blurred vision, constipation, and urinary reten-
tion. Patients with asthma, prostatic enlargement,
or glaucoma should take antihistamines only with
a healthcare provider’s supervision. The drying ef-
fects may also make respiratory mucus more viscous
and tenacious. Antihistamines should be used with
caution in patients who have a productive cough.
If the cough continues but becomes nonproductive,
consider additional hydration and discontinue the
antihistamine.
Therapeutic Outcome
The primary therapeutic outcome associated with an-
tihistamine therapy is reduced symptoms of AR (e.g.,
rhinorrhea, lacrimation, itching, conjunctivitis).
Nursing Implications for Antihistamines
Premedication assessment
1. Review the patient’s history for evidence of glau-
coma, prostatic hyperplasia, or asthma. If any one
of these is present, consult the healthcare provider
before initiating therapy.
2. Inquire about urinary pattern, particularly in male
patients older than age 55 who may be developing
prostatic hyperplasia.
3. Assess the patient’s work environment and consid-
er whether drowsiness will affect safety and work
performance.
4. Because antihistamines are prescribed for a variety
of symptoms (e.g., hay fever, dermatologic reac-
tions, drug hypersensitivity, rhinitis, transfusion re-
actions), it is necessary to individualize the patient
assessments with regard to the underlying patho-
logic condition.
 Table 29.2 Antihistaminesa
ADULT DOSAGE MAXIMUM DAILY
GENERIC NAME BRAND NAME AVAILABILITY SEDATIONB RANGE DOSAGE
azelastinec – Nasal spray: 0.1%, 0.15%; − 2 sprays per —
137 mcg/spray nostril twice
daily
cetirizinec Zyrtec Allergy Tablets: 5, 10 mg ± 5–10 mg once 10 mg
Do not confuse Do not Capsules: 10 mg daily
cetirizine with cy- confuse Zyrtec Oral solution: 5 mg/5 mL
clobenzaprine. with Zantac, Tablets, chewable: 5, 10 mg
Zestril, or Orally disintegrating tablet: 10 mg
Zyprexa.
chlorpheniramine Chlor-Trimeton Tablets: 4 mg + 4 mg q4–6h 24 mg
maleate Tablets, extended release (12 hr):
12 mg
Syrup: 2 mg/5 mL in 120, 473 mL
bottles
clemastine fumarate – Tablets: 1.34, 2.68 mg +++ 1.34–2.68 mg 8 mg
Syrup: 0.67 mg/ 5mL in 120 mL two or three
bottles times daily
cyproheptadine — Tablets: 4 mg + 4 mg three times 32 mg
hydrochloride Syrup: 2 mg/5 mL in 473 mL daily
Do not confuse cy- bottle
proheptadine with
cyclobenzaprine.
desloratadinec Clarinex Tablets: 5 mg ± 5 mg once daily 5 mg
Orally disintegrating tablets: 2.5,
5 mg
diphenhydramine Benadryl Allergy Injection: 50 mg/mL in 1 mL vials +++ 25–50 mg q4–8h 300 mg
hydrochloride Capsules: 25, 50 mg
Do not confuse Tablets: 25, 50 mg
diphenhydramine Tablets, chewable: 12.5 mg
with dicyclomine or Liquid: 6.25 mg/mL, 12.5 mg/5
dipyridamole. mL
Elixir: 12.5 mg/5 mL
fexofenadinec Allegra Tablets: 60, 180 mg ± 60 mg twice 180 mg
Do not Oral suspension: 30 mg/5 mL in daily; 180 mg
confuse Allegra 120 and 240 mL bottle extended-
with Adalat Orally disintegrating tablets: 30 release
CC, Asacol, or mg formulation
Viagra. daily
levocetirizinec Xyzal Allergy 24 Tablets: 5 mg ± 2.5–5 mg once 5 mg
Oral solution: 2.5 mg/5 mL daily in the
evening
loratadinec Claritin Tablets: 10 mg ± 10 mg daily 10 mg
Do not confuse Tablets, chewable: 5 mg
loratadine with Tablets, disintegrating: 5 mg, 10 mg
losartan. Capsules: 10 mg
Syrup: 5 mg/5 mL
Oral solution: 5 mg/5 mL
olopatadine Patanase Nasal spray: 0.6% − 2 sprays per No established
nostril two dosage
times daily
promethazine hydro- Promethegan Injection: 25, 50 mg/mL +++ 6.25–12.5 mg 100 mg
chlorided Tablets: 12.5, 25, 50 mg three times
Do not confuse Syrup: 6.25 mg/5 mL daily
promethazine with Oral solution: 6.25 mg/5 mL
phenazopyridine or Suppository: 12.5, 25, 50 mg
prochlorperazine.
aMany of these antihistamines are also available in combination with decongestants.
bSedation index: +++, high; ++, moderate; +, low; ±, low to none; −, none.
cNote second-generation antihistamine.
d

Do not confuse.
 Drugs Used to Treat Upper Respiratory Disease CHAPTER 29
Availability, dosage, and administration
See Table 29.2
Common adverse effects
Neurologic
Sedative effects. The types of antihistamines ordered
can produce varying degrees of sedation. Tolerance
may be produced over time, thus diminishing the ef-
fect. Operating machinery or motor vehicles may be
hazardous. Warn the patient to be cautious.
Cognitive impairment. Although newer antihistamines
are less sedating, patients should still be cautioned about
the possibility of impaired memory, coordination, and
psychomotor performance. In many states it is a crime
to operate a motor vehicle while under the inuence
of medicines (in addition to alcohol). Operating ma-
chinery or motor vehicles may be hazardous. Caution
patients to watch closely for signs of impairment (e.g.,
forgetfulness, poor coordination) in these situations.
Respiratory
Drying effects. Monitor the patient’s cough and de-
gree of sputum production when antihistamines are
used. Because of their drying effects, antihistamines
may impair expectoration. Give adequate uids con-
currently with the use of antihistamines. Maintain u-
id intake at 8 to 10 eight-ounce glasses daily.
Anticholinergic
Blurred vision; constipation; urinary retention; dryness of
mouth, throat, and nose mucosa. These symptoms are the
anticholinergic effects produced by antihistamines.
Patients taking these medications should be monitored
for these effects.
Mucosa dryness may be alleviated by sucking hard
candy or ice chips or by chewing gum. Caution the
patient that blurred vision may occur, and make ap-
propriate suggestions for the personal safety of the
individual.
Serious adverse effects
Genitourinary
Urinary retention. Some patients, particularly men
with prostatic hyperplasia, may develop urinary par-
tial obstruction—difculty with starting a stream of
urine—when taking oral antihistamines, particularly
with rst-generation antihistamines (e.g., diphenhy-
dramine). The obstruction is dose related and will re-
solve with metabolism of the drug. This adverse effect
can be eliminated by using only topical antihistamines
(e.g., azelastine) or second-generation antihistamines
(e.g., loratadine, desloratadine, fexofenadine) rather
than rst-generation antihistamines.
Drug interactions
Central nervous system depressants. Central nervous
system depressants—including sleep aids, analgesics,
tranquilizers, and alcohol—will potentiate the seda-
tive effects of antihistamines. People who work around
machinery, operate motor vehicles, or perform other
477
duties that require constant mental alertness should be
particularly cautious until they know how the medi-
cation affects them and should not take these medica-
tions while working.
DRUG CLASS: RESPIRATORY ANTIINFLAMMATORY
AGENTS
intranasal corticosteroids (ĭn-tră-NĀ-zăl cŏr-tĭ-cō-
STĔR-ŏydz)
Actions
Multiple mechanisms are involved with the effects
of nasally administered steroids, which result in
reduced inammation by inhibiting histamine re-
lease; suppression of neutrophil chemotaxis; mild
vasoconstriction, resulting in reduction in intracellu-
lar edema; and inhibition of mast cell–mediated late-
phase reactions.
Uses
Intranasal corticosteroids are the most effective phar-
macologic therapy for AR and are recommended by
guidelines as the best single therapy for patients with
persistent or moderate to severe allergic symptoms.
Systemic corticosteroids should be avoided because
of their adverse effects. In rare cases, a short course
may be a needed if severe symptoms do not respond
to other drugs.
Topically active aerosol steroids (e.g., beclometha-
sone, budesonide, uticasone, unisolide) are highly
effective with few adverse effects. Their therapeutic ef-
fect (i.e., the reduction of sneezing, nasal itching, stuf-
ness, and rhinorrhea) is usually observed by the third
day, although maximal effects may not be evident for
2 weeks. They also appear to have benecial effects on
ocular symptoms reducing itching, redness, tearing,
and pufness.
Concerns with long-term use of systemic cortico-
steroid preparations include adrenal suppression.
With nasal sprays, the risk of adrenal suppression ap-
pears to be small because of the relatively low doses
administered.
Therapeutic Outcomes
The primary therapeutic outcomes associated with
intranasal corticosteroid therapy are reduced rhinor-
rhea, rhinitis, itching, and sneezing.
Nursing Implications for Intranasal Corticosteroid
Therapy
Premedication assessment
1. Blocked nasal passages should be treated with a
topical decongestant just before beginning intra-
nasal corticosteroids.
2. Ask the patient to blow the nose thoroughly before
administering intranasal therapy.
478 UNIT V Drugs Affecting the Respiratory System

Table 29.3 Intranasal Corticosteroids

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE
beclomethasone Beconase AQ, Qnasl Children Nasal spray: 1 or 2 sprays (42–84 mcg) in each
dipropionate, Do not confuse Beconase 40, 42, mcg/actuation nostril twice daily
monohydrate with Beclovent.
Qnasl Nasal spray: 80 mcg/actuation 2 sprays in each nostril once daily
budesonide — Nasal aerosol: 120 doses/ 1–4 sprays in each nostril once daily
canister; 32 mcg/actuation
ciclesonide Omnaris Nasal spray: 50 mcg/actuation 2 sprays in each nostril daily
Zetonna Nasal spray: 37 mcg/actuation 1 spray in each nostril daily
unisolide — Nasal spray: 200 doses/bottle; 2 sprays in each nostril two or three
25 mcg/actuation times daily; maximum daily dosage
is 8 sprays (400 mcg) in 24 hr
uticasone Flonase Sensimist Nasal spray: 27.5 mcg/actuation; Up to 2 sprays (55 mcg) per nostril
60, 120 metered-dose bottles daily
Flonase Allergy Relief Nasal spray: 50 mcg/actuation, Up to 2 sprays (100 mcg each) in
Do not confuse Flonase with 120 actuations/bottle each nostril once daily
Flovent.
Xhance Exhaler 93 mcg/actuation, 120 doses per Nasal polyps: 1–2 sprays in each
16 mL bottle nostril twice daily.
mometasone Nasonex Nasal spray: 120 actuations/ 2 sprays (100 mcg) in each nostril
bottle; 50 mcg/actuation once daily
triamcinolone Nasacort Allergy 24 Hr Nasal spray: 55 mcg/actuation, 2 sprays (110 mcg each) in each
10.8 mL bottle nostril once daily; maximum daily
dosage is 2 sprays in each nostril
in 24 hr
Do not confuse.

Availability, dosage, and administration
See Table 29.3; see Chapter 7 for techniques for admin-
istering intranasal spray.
Counseling. The therapeutic effects—unlike those of
sympathomimetic decongestants—are not immediate.
This should be explained to the patient in advance to
ensure cooperation and the continuation of treatment
with the prescribed dosage regimen. The full thera-
peutic benet requires regular use, and it is usually
evident within a few days, although a few patients
may require up to 3 weeks for maximum benet.
Preparation before administration. Patients with
blocked nasal passages should be encouraged to use
a nasal decongestant 15 to 30 minutes before intra-
nasal corticosteroid administration to ensure adequate
penetration. Patients should also be advised to clear
their nasal passages of secretions before use. Instruct
patients about proper positioning and administration
of intranasal inhaled corticosteroids. Epistaxis can be
minimized by generally pointing the intranasal cortico-
steroid away from the septum within each side of the
nose. Although rare, nasal septal perforation can occur
but may be avoided with proper administration tech-
niques, pointing away from the septum. (See Chapter
7 on technique for administration of nasal drops and
spray.)
Maintenance therapy. After the desired clinical ef-
fect is obtained, the maintenance dosage should be re-
duced to the smallest amount necessary to control the
symptoms.
Common adverse effects
Respiratory
Nasal irritation. Nasal burning is usually mild and
tends to resolve with continued therapy. Encourage
the patient not to discontinue therapy without rst
consulting the healthcare provider.
Drug interactions. No signicant drug interactions
have been reported.
cromolyn sodium (KRŌ-mō-lĭn)
NasalCrom (NĀ-zăl-krŏm)
Actions
Cromolyn sodium is a mast cell stabilizer that inhibits
the release of histamine and other mediators of inam-
mation, making it an indirect antiinammatory agent.
It must be administered before the body receives a
stimulus to release histamine, such as an antigen that
initiates an antigen-antibody allergic reaction.
 Drugs Used to Treat Upper Respiratory Disease CHAPTER 29
Uses
Cromolyn is effective when used shortly (30 minutes)
before exposure to allergen inhalation such as cat dan-
der and seasonal AR. For seasonal AR, it is most effec-
tive when initiated just before the pollen season, rather
than after symptoms have begun.
Therapeutic Outcomes
The primary therapeutic outcomes associated with
cromolyn therapy are reduced rhinorrhea, itching, and
sneezing and fewer incidents of bronchospasm and
asthmatic exacerbations.
Nursing Implications for Cromolyn Sodium
Premedication assessment
1. Cromolyn must be taken before exposure to the
stimulus that initiates an allergic response.
2. Check to see if the concurrent use of antihistamines
or nasal decongestants has been ordered by the
healthcare provider, especially during the initiation
of cromolyn therapy.
3. Have the patient blow their nose before the nasal
instillation of this drug.
Availability. Nasal spray: 5.2 mg/actuation in 13-mL
(100 sprays) and 26-mL (200 sprays) metered-spray
devices.
Inhalation with nebulizer: 20 mg/2 mL in 2-mL plastic
containers.
Oral concentrate: 100 mg/5 mL in 5-mL ampules.
Dosage and administration. See Chapter 7 for tech-
niques to use to administer nasal spray.
479
Counseling. The therapeutic effects of these drugs,
unlike those of sympathomimetic amines, are not im-
mediate. This should be explained to the patient in
advance to ensure cooperation and continuation of
treatment with the prescribed dosage regimen. The
full therapeutic benet requires regular use, and it is
usually evident within 2 to 4 weeks. Therapy must be
continued even when the patient is free of symptoms.
Nasal spray. Adult patients with blocked nasal passag-
es should be encouraged to use a decongestant just before
intranasal cromolyn administration to ensure adequate
penetration. Patients should also be advised to clear their
nasal passages of secretions and then inhale through the
nose during administration. One spray is placed in each
nostril three or four times daily at regular intervals. The
maximum dosage is six sprays in each nostril daily.
Common adverse effects
Respiratory
Nasal irritation. The most common adverse effect is
irritation manifested by sneezing, nasal itching, burn-
ing, and stufness. Patients usually develop a toler-
ance to the irritation, but this is rarely a cause for dis-
continuing intranasal therapy.
Serious adverse effects
Respiratory
Bronchospasm and coughing. Notify the health-
care provider if inhalation causes bronchospasm or
coughing.
Drug interactions. No signicant drug interactions
have been reported.
480 UNIT V Drugs Affecting the Respiratory System

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points 2. The nurse researched the causes of upper respiratory symptoms
and learned their diagnoses. Indicate with an X the causes for
• Rhinitis is dened as the inammation of the nasal mucous allergic rhinitis, nasal congestion, and rhinitis medicamentosa.
membranes that causes sneezing, nasal discharge, and
nasal congestion.
CAUSES OF UPPER ALLERGIC NASAL RHINITIS
• The most common causes of acute rhinitis are the
RESPIRATORY RHINITIS CONGES- MEDICAMEN-
common cold, allergies, bacterial infection, the presence of DISEASES TION TOSA
a foreign body, and drug-induced congestion (i.e., rhinitis
medicamentosa). After regular
• The roles of the nurse when working with patients with use of topical
rhinitis are to perform the initial assessment of symptoms and decongestants
then to focus on teaching the proper techniques for self- Cholinergic
administering and monitoring medication therapy. Frequent stimulation causes
follow-up with the patient and the reinforcement of gains vasodilation of
made are important to the success of these treatments. the blood vessels
lining the nasal
mucosa
Additional Learning Resources
Excessive blood
SG Go to your Study Guide for additional Review Questions ow to nasal
for the NCLEX® Examination, Critical Thinking Clinical Situa- passages causing
tions, and other learning activities to help you master this chap- swelling and more
ter content. congestion
Inammation of
Go to your Evolve website (https://evolve.elsevier.com/Willihng
the nasal mucosa
anz) for additional online resources.
from exposure to
allergen
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of Irreversible
the NCLEX exam and include both NGN (Next Generation) and changes occur
traditional questions. See Chapter 1 for further information re- within the nose if
garding question types. not treated
Serous and
Scenario mucous
secretions within
A patient came into the clinic with complaints of worsening the nostrils
nasal congestion after starting on oxymetazoline (Afrin) for sea-
sonal allergies.
Objective: Discuss the causes of allergic rhinitis, nasal congestion,
1. The patient in the scenario who has been taking Afrin for allergies,
and rhinitis medicamentosa.
asks the nurse about the frequent upper respiratory symptoms
NCLEX item type: Matrix
that have been experienced lately. The nurse responds with which
Cognitive skill: Evaluate cues
appropriate statement?
1. “The medications that you are taking can cause a worsening 3. The nurse is teaching the patient in the scenario who recently
of your symptoms before it will start to improve them.” started an antihistamine. Which statement by the patient indicates
2. “If you use that medication for longer than a few days you that further teaching is needed?
may get a rebound of the symptoms that you are using it 1. “I should drink 8 to 10 glasses of water every day while
for.” taking this medication.”
3. “Apparently, you are not taking your medication the 2. “If my vision starts to blur, I will need to call my doctor.”
proper way or your symptoms would be improving.” 3. “I can suck on candy or chew gum when my mouth gets
4. “I will let your healthcare provider know about this dry from this drug.”
adverse effect that we may have to hospitalize you for.” 4. “I will be able to drive without any problem because I will
Objective: Discuss the causes of allergic rhinitis, nasal congestion, know when I am impaired.”
and rhinitis medicamentosa. Objective: Explain the major actions (effects) of sympathomimetic,
NCLEX item type: Multiple choice antihistaminic, and corticosteroid medications.
Cognitive skill: Comprehension NCLEX item type: Multiple choice
Cognitive skill: Comprehension
 Drugs Used to Treat Upper Respiratory Disease CHAPTER 29 481

4. The nurse knows that intranasal corticosteroids are used to treat

MAJOR EFFECTS OF SYMPATHO- ANTIHIS- CORTICO-
seasonal allergies and explains to the patient that which of the
DECONGESTANTS MIMETIC TAMINIC STEROID
following needs to be done before application? (Select all that apply.)
Stimulate the
1. Rinse mouth before application alpha-adrenergic
2. Blow nose before application receptors in the
3. Suck on hard candy or ice chips before application nasal passages
4. Drink 8 ounces of water before application
5. Use decongestant before use if nasal passages are Compete with
blocked the histamine (H1)
6. Spray both nostrils with 1 to 2 sprays once a day as receptor sites
prescribed in the mucous
membranes
Objective: Discuss the nursing assessments needed during therapy
Causes
to monitor the therapeutic response to and the common and serious
vasoconstriction
adverse effects of decongestant drug therapy.
NCLEX item type: Extended multiple response Reduce
Cognitive skill: Application inammation

5. Before initiating antihistamine medications, the nurse knows that

the patient’s history should be checked for which of the following? Objective: Explain the major actions (effects) of sympathomimetic,
(Select all that apply.) antihistaminic, and corticosteroid medications.
NCLEX item type: Matrix
1. Prostatic hyperplasia
Cognitive skill: Analyze cues
2. Hypothyroidism
3. Glaucoma 7. The patient in the scenario is inquiring about decongestants and
4. Hypertension asks the nurse to explain the common and serious adverse effects.
5. Asthma Which statement by the nurse is correct?
Objective: Explain the major actions (effects) of sympathomimetic, 1. “Topical aerosol products are highly effective in reducing
antihistaminic, and corticosteroid medicines. sneezing and nasal itching, but just remember they are
NCLEX item type: Multiple response for a long period of time only.”
Cognitive skill: Application 2. “This drug prevents histamine from being released so
you will not have allergic rhinitis, make sure to blow your
6. The nurse discussed with the patient in the scenario the effects
nose before spraying the med in your nose and watch for
of the different types of medications used for relief of congestion.
coughing.”
Indicate with an X the major effect each medication has on
3. “This drug will reduce your nasal congestion, but keep
congestion. (More than one effect may apply.)
in mind it may cause urinary retention and sometimes
elevate your blood pressure.”
4. “This drug will not stop the nasal congestion but will
MAJOR EFFECTS OF SYMPATHO- ANTIHIS- CORTICO- reduce the runny nose and runny eyes and itching that
DECONGESTANTS MIMETIC TAMINIC STEROID you have. These types of drugs may cause drowsiness, so
do not drive or operate heavy equipment while taking this.”
Blocks the effects of
histamine Objective: Discuss the nursing assessments needed during therapy
to monitor the therapeutic response to and the common and serious
Reduces sneezing, adverse effects of decongestant drug therapy.
itching and runny NCLEX item type: Multiple choice
eyes Cognitive skill: Analysis
30 Drugs Used to Treat Lower Respiratory Disease

https://evolve.elsevier.com/Willihnganz

Objectives
1. Discuss nursing assessments used to evaluate the
respiratory status of a patient.
2. Distinguish the mechanisms of action of expectorants,
antitussives, and mucolytic agents.
3. Describe the nursing assessments needed to monitor
therapeutic response and the development of adverse
effects from beta-adrenergic bronchodilator therapy.
4. Discuss the nursing assessments needed to monitor
therapeutic response and the development of adverse
effects from anticholinergic bronchodilator therapy.
5. Discuss the nursing assessments needed to monitor
therapeutic response and the development of adverse
effects from corticosteroid inhalant therapy.

Key Terms
ventilation (vĕn-tĭ-LĀ-shŭn) (p. 482)
diffusion (dĭ-FYŪ-zhŭn) (p. 482)
goblet cells (GŎB-lĕt SĔLZ) (p. 483)
obstructive airway diseases (ŏb-
STRŬK-tĭv ĀR-wā dĭ-ZĒ-zĕz) (p. 483)
bronchospasm (BRŎN-kō-spăz-ĕm)
(p. 483)
restrictive airway diseases
(rē-STRĬK-tĭv ĀR-wā) (p. 483)
chronic obstructive pulmonary
disease (COPD) (KRŎN-ĭk ŏb-
STRŬK-tĭv PŬL-mō-nār-ē) (p. 484)
chronic airow limitation disease
(CALD) (KRŎN-ĭk ĀR-ō lĭ-mĭ-TĀ-
shŭn) (p. 484)
arterial blood gases (ABGs) (ăr-TĒR-
ē-ăl BLŬD GĂS-ĕz) (p. 484)
oxygen saturation (ŎKS-ĕ-jĕn să-
chŭr-Ā-shŭn) (p. 484)
spirometry (spĭ-RŎM-ĕ-trē) (p. 484)
cough (KŎF) (p. 485)
asthma (ĂZ-mă) (p. 485)
bronchitis (brŏn-KĪ-tĭs) (p. 485)
emphysema (ĕm-fĭ-SĒ-mă) (p. 486)
expectorants (ĕk-SPĔK-tōr-ănts)
(p. 488)
antitussives (ăn-tĭ-TŬS-ĭvz) (p. 488)
mucolytic agents (myū-kō-LĬ-tĭk)
(p. 488)
bronchodilators (brŏn-kō-DĪ-lā-tŏrz)
(p. 489)
antiinammatory agents (ăn-tī-ĭn-
FLĂ-mă-tō-rē) (p. 489)
immunomodulators (ĭm-yū-nō-MŎD-
yū-lā-tŏrz) (p. 489)

Th primary funin f h lwr rspirary ra

LOWER RESPIRATORY TRACT ANATOMY
AND PHYSIOLOGY
Th rspirary sysm is a sris f airways ha sar
wih h ns and muh and nd a h alvlar sas.
Th ns and muh airways nn a h pharynx.
Passing u f h pharynx, h airways divid in
h sphagus f h gasrinsinal (GI) ra and h
larynx (vi bx) and raha f h rspirary ra.
Th raha divids in h righ and lf mainsm
brnhi, whih nr h lungs. Th brnhi subdivid
in ah lung in many smallr brnhils, whih
furhr subdivid in many smallr airways alld
alvlar dus ha rmina in alvlar sas. Th al-
vlar sas ar surrundd by apillaris f h bld
irulary sysm. Human lungs nain 300  500
millin sas fr gasus xhang and hav a surfa
ara apprximaly qual  ha f a nnis ur. Th
anami pars f h bdy assiad wih h lwr
rspirary sysm ar h larynx, raha, brnhi,
brnhils, and alvlar sas (Fig. 30.1).
is h vnilary yl. Ventilation is h mvmn f
air in and u f h lungs. Inhalain is h prss
f ranspr f air naining xygn  h alvlar
sas, xhang f xygn fr arbn dixid arss
h alvlar mmbrans naining bld apillaris,
and xhalain f “sal air,” inluding arbn dixid.
Vnilain f h lungs is amplishd by nrain
and rlaxain f h diaphragmai and inrsal
musls (musls bwn h ribs). During inspira-
in, h diaphragmai and inrsal musls n-
ra, raing a vauum in h lungs and pulling air
in hrugh h muh and ns. During xhalain, r-
laxain f h musls allws h hs  rurn  is
unxpandd psiin, fring air u f h lungs.
Bld w hrugh h pulmnary arris  h
apillaris surrunding h alvli and hn  h pul-
mnary vins is alld perfusion. Diffusion is h prss
by whih xygn (O2) passs arss h alvlar mm-
bran  h bld in h apillaris and arbn dix-
id (CO2) passs frm h bld  h alvlar sas fr

482
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30
Venule Arterioles
Bronchiole
Alveolus
Air
circulation
Capillaries
Bronchus
Vena cava
Fig. 30.1 The respiratory tract and the alveoli.
xhalain. Oxygn is ransprd by mbining wih
hmglbin in rd bld lls r by disslving in h
bld plasma. Bld irulain prvids disribuin
f xygn  h bdy’s lls fr h susnan f lif.
Vnilain and prfusin mus b qual  mainain
hmsasis.
Th uids f h rspirary ra rigina frm
spializd muus glands (goblet cells) and srus
glands ha lin h rspirary ra. Th gbl lls
prdu glainus muus ha frms a hin layr vr
h inrir surfas f h raha, brnhi, and brn-
hils. Srin f muus is inrasd by xpsur
 irrians, suh as smk, airbrn pariula ma-
r, and baria. Th srus glands ar nrlld by
h hlinrgi nrvus sysm. Whn simulad, h
srus glands sr a wary uid  h inrir sur-
fa f h brnhial r. Thr h muus srins
f h gbl lls and h wary srins f h s-
rus glands mbin  frm rspirary ra uid.
Nrmally, rspirary ra uid frms a pr-
iv layr vr h raha, brnhi, and brnhils.
Frign bdis, suh as smk parils and baria,
ar augh in h rspirary ra uid and ar swp
upward by iliary hairs ha lin h brnhi and ra-
ha  h larynx, whr hy ar rmvd by h
ugh rx. Th xprad (ughd up) marial
nains pulmnary muus srins, frign pariu-
la mar suh as smk and baria, and pihlial
lls slughd frm h lining f h airways. Cmmn
nams givn  h xprad mass ar sputum
and phlegm. If  muh muus is srd as a rsul
f hrni irriain, ilia ar dsryd by hrni
483
Larynx
Trachea
Pulmonary
arteries
(unoxygenated
blood)
Aorta
Pulmonary
blood
circulation
Pulmonary veins
(oxygenated blood)
inhalain f smk, dhydrain dris h muus, r
anihlinrgi agns inhibi wary srins frm
h srus glands, h muus bms visus, frm-
ing hik plugs in h brnhilar airways (Fig. 30.2).
Ths hik plugs ar diful  limina. Th rsul-
an lnizain f pahgni mirrganisms in h
lwr rspirary ra auss inammain and addi-
inal muus srins and h pssibl dvlpmn
f pnumnia frm rappd baria.
Th smh musl f h rahbrnhial r is
innrvad by h parasympahi and sympahi
branhs f h aunmi nrvus sysm. Simulain
f h hlinrgi nrvs auss brnhial nsriin
and inrasd muus srin. Sympahi simula-
in f adrnrgi nrvs auss dilain f brnhial
and brnhilar airways and inhibiin f rspirary
ra uids. Bh ba-1 and ba-2 adrnrgi rp-
rs ar prsn, bu h ba-2 rprs prdmina.
COMMON LOWER RESPIRATORY
DISEASES
Rspirary disass ar fn dividd in w yps:
bsruiv and rsriiv. Obstructive airway diseases
ar hs ha narrw air passags, ra urbuln,
and inras rsisan  airw. Disass aus nar-
rwing f h airways hrugh smh musl n-
sriin (bronchospasm), dma, inammain f h
brnhial walls, r xss muus srin. Exampls
f bsruiv lung disas ar ashma and au brn-
hiis. Restrictive airway diseases ar hs in whih
lung xpansin is limid frm lss f lasiiy (.g.,
484 UNIT V Drugs Affecting the Respiratory System

Table 30.1 Arterial Blood Gases Used to Assess

Trachea Respiratory Function
Lung TEST NORMAL VALUE RESULTS
pH 7.35–7.45 >7.45 = Alkalosis
(arterial) <7.35 = Acidosis
Paco2 35–45 mm Hg Abnormalities indicate
respiratory acid-base
imbalance.
↑ = Hypercapnia = respiratory
Bronchus acidosis
↓ = Hypocapnia = respiratory
Bronchiole
alkalosis
HCO3 24–28 mEq/L Abnormalities indicate
metabolic acid-base
imbalance.
↑ = Metabolic alkalosis
↓ = Metabolic acidosis
Hypersecretion Pao2 80–100 mm Hg Measures the amount of
of mucus oxygen moving through
Edema pulmonary alveoli into blood
for transport to other tissues;
Bronchoconstriction depends on the amount of
inspired oxygen.
Mucous plug
↓ = Hypoxemia, hypoventilation
Alveolus ↑ = Hyperventilation
Sao2 95% Measures the ratio of
actual oxygen content of
Fig. 30.2 Factors restricting the airway. Major factors include hemoglobin compared with
hypersecretion of mucus, mucosal edema, and bronchoconstriction. the hemoglobin’s oxygen-
Mucous plugs may form in the alveoli. (From Clark JB, Queener SF, carrying capacity. When
Karb VB. Pharmacological Basis of Nursing Practice. 3rd ed. St. Louis: decreased, either there is
Mosby–Year Book; 1982.) an impairment of oxygen
binding to hemoglobin
pulmnary brsis) r physial dfrmiy f h hs (e.g., metabolic acidosis)
(.g., kyphslisis). Chrni brnhiis and mphy- or inadequate amounts of
sma ar xampls f bh rsriiv and bsruiv oxygen are being inspired
lung disass. Pains wh hav prsisn airw
limiain assiad wih hrni inammain in h
airways and lung issu ausd by nxius parils h pH and parial prssurs f xygn and arbn
and gass ar rfrrd  as having chronic obstructive dixid in h bld. Anhr masur ha is mr
pulmonary disease (COPD) r chronic airow limitation radily availabl and nninvasiv is h xygn sau-
disease (CALD); h rms ar usd inrhangably. rain f hmglbin. Oxygen saturation (Sao2) is h
Chrni bsruiv pulmnary disas is a lading rai, xprssd as a prnag, f h xygn aually
aus f disabiliy and dah amng individuals ldr bund  hmglbin mpard wih h maximum
han ag 40 in h Unid Sas. amun f xygn ha uld b bund  hmglbin
Pulmnary funin ss hav bn dvlpd  (s Tabl 30.1). Oxygn saurain is ruinly usd
assss h vnilain and diffusin apaiy f h baus a ransuanus mnir r puls ximr is
lungs  assis in diagnsis and  giv an bjiv asily aahd  h skin  masur and rpr xy-
assssmn f imprvmn r drirain f h gn saurain ninuusly. Puls ximr radings
pain’s linial ndiin. Th bs indiars f vrall f xygn saurain shuld gnrally b grar han
pulmnary funin (vnilain and diffusin) ar h 90%; in pains wih nrmal lung funin, ABG val-
parial prssur f arterial blood gases (ABGs) (.g., ar- us f Sao2 shuld b 95%  99%.
rial parial prssur f xygn [Pao2] and arrial par- Spirometry sudis ar ruinly usd  assss
ial prssur f arbn dixid [Paco2]) and pH (Tabl h apabiliy f h pain’s lungs, hrax, and r-
30.1). T drmin ABGs, a sampl f arrial bld spirary musls fr mving vlums f air during
mus b drawn and immdialy analyzd  masur inhalain and xhalain. I is rmmndd ha
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30
Table 30.2 Terminology Used With Spirometry
TERM DEFINITION
Tidal volume (TV) Volume of air inspired or expired
during normal breathing
Vital capacity (VC) Volume of air exhaled after maximal
inspiration to full expiration
Residual volume (RV) Volume of air left in lungs after
maximal exhalation
Functional residual Volume of air left in lungs after
capacity (FRC) normal exhalation
Total lung capacity Vital capacity plus residual volume
(TLC) (VC + RV = TLC)
Forced expiratory Volume of air forced out of the
volume (FEV) lungs by maximal exhalation
Forced expiratory Volume of air forced out in 1 sec to
volume in 1 give the rate of ow
second (FEV1)
Forced vital capacity Maximal volume of air exhaled
(FVC) with maximal forced effort after
maximal inhalation
Peak expiratory ow Maximal rate of airow produced
rate (PEFR) during forced expiration
spirmry b usd  diagns airway bsruin
in sympmai pains, bu i shuld n b usd
as a srning l fr asympmai pains. A spi-
rmr masurs vlums f air. Trms usd wih
spirmry ar lisd in Tabl 30.2. Pains wih b-
sruiv disas usually hav a nrmal al lung
apaiy (TLC), difuly wih xpirain, drasd
vial apaiy (VC), and inrasd rsidual vlum
(RV). Pains wih rsriiv disas hav a dras
in all masurd lung vlums. Th frd xpira-
ry vlum in 1 snd (FEV1) and h frd vial
apaiy (FVC) ar h ms mmnly usd pulm-
nary funin ss. Th FEV1 is usd  drmin h
rvrsibiliy f airway disas and h ffivnss
f brnhdilar hrapy. Th pak xpirary w
ra (PEFR) mr is n as aura bu is muh lss
sly and mr radily availabl han hr pulm-
nary funin s quipmn. This mr is ruinly
usd by pains a hm and by halhar prvidrs
 assss h bns f hrapy fr raing au and
hrni ashmai sympms. A pain is nsidrd
 hav signian rvrsibiliy f airway bsruin
if hr is a 15%  20% imprvmn in h FEV1 r
PEFR afr brnhdilar hrapy.
On f h rs sympms f a rspirary disas is
h prsn f a cough, a rx iniiad by irriain f
h airway. I is a priv bnial mhanism fr
laring xss srins frm h rahbrnhial
r. Th sam irrians rspnsibl fr ashma r al-
lrgy may simula h ugh rprs, r ngsin
f h nasal musa frm a ld may aus a psnasal
485
Box 30.1 Asthma Fact Sheet
In 2016:
• 9.8 million physician ofce visits with asthma as the
primary diagnoses
In 2017:
• There were 1.6 million visits to emergency departments
with asthma as a primary diagnosis.
In 2017:
• There were 3564 deaths due to asthma.
In 2018:
• 19.2 million, or 7.7%, of adults 18 yr and older had
asthma.
• 5.5 million, or 7.5%, of children under 18 yr of age had
asthma.
From Centers for Disease Control and Prevention, National Center for Health
Statistics. FastStats: Asthma; 2018. Retrieved from https://www.cdc.gov/nchs
/fastats/asthma.htm.
drip in h bak f h hra ha simulas h
ugh.
A ugh is prduiv if i hlps rmv aumu-
lad srins and phlgm frm h rahbrnhial
r. A nnprduiv ugh rsuls whn irrians
rpadly simula h ugh rprs bu ar n
rmvd by h ughing rx. Exssiv ughing,
pariularly if i is dry and nnprduiv, is n nly
unmfrabl bu als nds  b slf-prpuaing
baus h rapid air xpulsin furhr irrias h ra-
hbrnhial musa.
Asthma is a mmn hrni airway disas and
majr halh nrn ha affs hildrn and aduls
(Bx 30.1). I is rspnsibl fr an xssiv numbr
f hspializains, mrgny dparmn visis,
halhar prvidr f visis, and dahs. Ashma
is an inammary disas f h brnhi and brnhi-
ls. Thr ar inrmin prids f au, rvrsibl
airw bsruin (brnhnsriin) ausd by
brnhilar inammain and hyprrspnsivnss
 a variy f simuli. Exampls f simuli ha rig-
gr brnhspasm and inammain ar rspirary
viral infins, inhald allrgns, ld air, dry air,
minal srss, and smk. Sympms f ashma in-
lud ugh, whzing, shrnss f brah, ighnss
f h hs, and inrasd muus prduin. Th
xa auss f ashma ar unknwn. Pains wih
ashma ar fn subdividd in agris basd
n svriy f disas: mild, mdra, and svr.
Chrni bronchitis is a ndiin in whih hrni
irriain auss inammain and dma, wih xs-
siv muus srin lading  airw bsruin.
Chronic bronchitis rfrs  a hrni prduiv ugh
ha is prsn fr 3 mnhs in ah f 2 sussiv
yars and has n hr idniabl aus. Cmmn
auss f hrni irriain ar igar smk, grain
and al dus xpsur, and air plluin. A prsisn
prduiv ugh prsn n ms days is n f h
arlis signs f h disas. Th lassi pain wih
hrni brnhiis has a hrni prduiv ugh and
486 UNIT V Drugs Affecting the Respiratory System

mdra dyspna, is fn bs, and suffrs frm
signian hypxia wih yansis. Th ABGs will n-
rm hypxia and rspirary aidsis. Baus f mu-
us vrprduin and frmain f muus plugs,
hs pains ar a risk fr rurrn rspirary in-
fins. As hrni brnhiis prgrsss, pains
fn dvlp plyyhmia (inrasd rd bld ll
prduin)  ranspr xygn and righ-sidd har
failur sndary  h lung disas and pulmnary
hyprnsin.
Emphysema is a disas f alvlar issu dsru-
in wihu brsis. Alvlar sas ls lasiiy and
llaps during xhalain, rapping air wihin h
lung. Th lassi pain wih mphysma is dyspn-
i wih minimal xrin (shr f brah), brahs
hrugh pursd lips, is hin baus f wigh lss, is
barrl hsd frm inrasd us f assry mus-
ls, and has nly sany spuum prduin wih a
minimal ugh. Ths pains mainain nrmal xy-
gnain by inrasing hir brahing ra. Tabl 30.3
lassis h svriy f ah sag f COPD basd n
sympms and spirmry s rsuls.
TREATMENT OF LOWER RESPIRATORY
DISEASES
COUGH
Tramn f h ugh is f sndary impran;
primary ramn is aimd a h undrlying disr-
dr. If h air is dry, a vaprizr r humidir may b
usd  liqufy srins s ha hy d n bm
irriaing. A dhydrad sa hikns rspirary
srins; hrfr drinking larg amuns f u-
ids will hlp rdu srin vissiy (hiknss).
Pains an als suk n hard andis  inras sa-
liva w  a h hra, hrby rduing irriain.
If hs simpl masurs d n rdu h ugh, an
xpran r an aniussiv (ugh supprssan) may
b usd. Th hrapui um is  dras h
innsiy and frquny f h ugh y prmi ad-
qua liminain f rahbrnhial phlgm. In s-
vr ass f pulmnary ngsin, a mulyi agn
may b rquird.
ASTHMA
Th Nainal Ashma Eduain and Prvnin
Prgram (NAEPP) f h Nainal Har, Lung and
Bld Insiu has publishd Expert Panel Report 3:
Guidelines for the Diagnosis and Management of Asthma
(2007; updad 2012, 2020). Ths publiains r-
mmnd h fllwing gals f hrapy fr ashma:
mainain nrmal aiviy lvls; mainain nar-nr-
mal pulmnary funin ras; prvn hrni and
rublsm sympms (.g., ughing r brahlss-
nss in h nigh, in h arly mrning, r afr xr-
in); prvn rurrn xarbains; minimal us
f shr-aing inhald ba-2 agnis (<2 days/wk);
and avid advrs ffs frm ashma mdiains.
Th guidlins dsrib fur mpnns  ashma
hrapy—pain duain, nvirnmnal nrl,
mprhnsiv pharmalgi hrapy, and bjiv
mniring masurs (.g., rgular us f a pak w-
mr). Th guidlins als rmmnd a spwis

Table 30.3 Classication of Airway Limitation Severity, Classication of Group, and Therapy
AIRFLOW LIMITATIONA GROUP CLASSIFICATIONB THERAPYB
GOLD 1: Mild Group A: Mild symptoms and 0–1 Add a bronchodilator (short acting). Continue if symptom
FEV1 ≥ 80% exacerbations not leading to benet is documented.
predicted hospitalization
GOLD 2: Moderate Group B: Moderate to severe Start with a LABA or long-acting anticholinergic agent.
50% ≤ FEV1 < 80% symptoms and 0–1 exacerbations Patients with persistent symptoms should use two
predicted not leading to hospitalization bronchodilators.
GOLD 3: Severe Group C: Mild symptoms and greater Start with a long-acting anticholinergic agent. Patients with
30% ≤ FEV1 < 50% than 2 exacerbations or 1 that led further exacerbations should use two bronchodilators or a
predicted to hospitalization LABA plus an ICS.
GOLD 4: Very severe Group D: Moderate to severe Start with a long-acting anticholinergic agent and a LABA or
FEV1 < 30% symptoms and greater than 2 a LABA plus an ICS. Patients with further exacerbations
predicted exacerbations or 1 that led to should add an ICS to the combination of long-acting
hospitalization bronchodilators or add a long-acting anticholinergic agent
to the LABA and ICS. If further exacerbations occur,
consider adding roumilast if patient has chronic bronchitis.
GOLD, Global Initiative for Chronic Obstructive Lung Disease; ICS, inhaled corticosteroid; LABA, long-acting beta-2 agonist.
GOLD 1–4 provides the severity of airow: The FEV 1 cannot not be used alone to determine all therapeutic options; the letter groups A–D provide information about
symptoms and exacerbations that guides therapy.
aBased on forced expiratory volume in 1 second (FEV ).
1
bBased on symptoms and risk of exacerbations.

Data from https://goldcopd.org/gold-reports/

 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30 487

apprah  ashma hrapy fr hr diffrn ag
grups: 0  5 yars, 6  11 yars, and 12 yars and
ldr. Tabl 30.4 prvids an algrihm fr h rm-
mndd hrapy fr ashma pains agd 12 yars and
ldr. Mdiins usd  ra ashma an b dividd
in w grups: quik-rlif mdiains (Rlivrs)
 ra arly sympms and xarbains and lng-
rm nrl mdiains (Cnrllrs, r mainnan
mdiins)  ahiv and mainain nrl f pr-
sisn ashma. (Tabl 30.5) Th quik-rlif mdia-
ins ar shr-aing inhald ba-2 agniss (SABA)
(Tabl 30.6) and shr-aing inhald anihlinrgi
agns (Tabl 30.7). Lng-rm nrl mdiains
ar h lng-aing ba-2 agniss (LABA) (s Tabl
30.6), lng-aing anihlinrgi (musarini) agns
(LAMA) (s Tabl 30.7), mbinain anihlinrgi
and ba-adrnrgi brnhdilars (Tabl 30.8); in-
hald risrids (Tabl 30.9); mbinain inhald
risrids and ba-adrnrgi brnhdilars
(Tabl 30.10); mbinain inhald anihlinrgi,
ba-adrnrgi, and risrid brnhdilars
(Tabl 30.11); and sysmi risrids, rmlyn
sdium, lukrin mdirs, and immunmdula-
rs agns (Tabl 30.12).
Undr h 2020 NAEPP guidlins, SMART (sin-
gl mainnan and rlivr hrapy) wih lw- r
mdium-ds inhald risrid (budsnid)
and frmrl is rmmndd fr sps 2 hrugh
4 prsisn ashma. This rmmndain allws
h us f a singl inhalr naining bh h
inhald risrid and frmrl (Symbir)
insad f w inhalrs naining ihr a srid r
SABA  b usd as bh a mainnan and rlivr
hrapy.
Evn wih maximal ffrs a fllwing h NAEPP
guidlins, sm pains rmain prly nrlld
dspi us f high-ds inhald risrids, lng-
aing musarini agns, and lng-aing ba agniss.
Subyps f ashma ar bing disvrd and lassi-
d basd n pahgni pahway (.g., sinphili
ashma, airbrn allrgy ashma). Idniain f hs
pahways ras mr argd hrapy, suh as h im-
munmdulars,  ahiv ashma nrl in pains
fr whm ramn sandard prls ar failing.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
I is mmn fr pains wih bsruiv lung dis-
as  hav sympms f bh brnhiis and m-
physma, bu n usually prdminas and vrall
ramn is similar. Arding  h Global Strategy
for the Diagnosis, Management, and Prevention of Chronic
Obstructive Pulmonary Disease, 2020 Report (als knwn
as h GOLD Guidlins—2020) h gals f ffiv
COPD managmn ar h fllwing:
• Rdu sympms
 • Rliv sympms
 • Imprv xris lran
 • Imprv halh saus

Table 30.4 Example of Treatment Algorithm for Patients 12 Years and Older Based on Severity of Asthma
STEP 1 STEP 4
INTERMITTENT STEP 2 MILD STEP 3 MODERATE MODERATE-SEVERE STEPS 5 SEVERE STEP 6 SEVERE
ASTHMA PERSISTENT PERSISTENT PERSISTENT PERSISTENT PERSISTENT
Preferred PRN SABA Daily low-dose Daily and PRN Daily and PRN Daily medium- Daily high-dose
ICS and PRN combination combination high dose ICS-LABA +
SABA or PRN low-dose ICS- medium-dose ICS-LABA + oral systemic
concomitant formoterol ICS- formoterol LAMA and corticosteroids
ICS and SABA PRN SABA + PRN SABA
Alternative Daily LTRA and Daily medium- Daily medium- Daily medium-
PRN SABA; dose ICS and dose ICS- or high-dose
PRN SABA or LABA or daily ICS-LABA or
daily low-dose medium-dose daily high-
ICS-LABA ICS + LAMA dose ICS +
or daily low-dose and PRN SABA LTRA and
ICS + LAMA or daily medium- PRN SABA
or daily low-dose dose ICS +
ICS + LTRA LTRA
and PRN SABA
Consider Adding asthma biologics (e.g.,
omalizumab, benralizumab,
dupilumab)
ICS, Inhaled corticosteroid; LABA, long-acting beta-2 agonist; LAMA, long-acting muscarinic antagonist; LTRA, leukotriene receptor antagonist; PRN, as needed;
SABA, inhaled short-acting beta-2 agonist.aAdjust treatment up and down for individual patient treatment requirements. In stepwise management of chronic asthma
in adults, therapy is stepped up to the next level of therapy every 2 to 6 weeks if control is not achieved at the current step with proper use of medication. Step-down,
or reduction of dosages, should be considered when the desired outcomes have been achieved and sustained for at least 3 months at the current step. Step-down
therapy is desired to identify the minimum dosages of therapy required to maintain the desired outcomes.
Adapted from Expert Panel Working Group of the National Heart, Lung and Blood Institute. Focused updates from the National Asthma Education and Prevention
Program Coordinating Committee, Expert Panel Working Group. J Allergy Clin Immunol. 2020;146:1217-1270.
488 UNIT V Drugs Affecting the Respiratory System
•Rdu risk
 • Prvn disas prgrssin
 • Prvn and ra xarbains
 • Rdu mraliy
Managmn prinipls inlud nsuring ha h
pain undrsands h disas prss, h rai-
nal fr varius prdurs usd  ra h disas,
and h gals f hrapy. Spirmry ss shuld b
mpld pridially  assss ramn suss.
Pains mus als b augh apprpria nuriin;
xris; prpr ughing hniqus; hs prus-
sin and psural drainag  mbiliz muus sr-
ins and plugs; and liminain f risk fars suh
as smking, upainal duss, fums and gass, and
indr r udr plluans. All hs ffrs mus
b baland wih h pain’s prpins f qualiy
f lif.
Nn f h xising mdiains fr COPD hav
bn shwn  mdify h lng-rm dlin in lung
funin assiad wih bsruiv disas. Mdiins
ar usd fr sympmai rlif and  minimiz fr-
quny f mpliains. Brnhdilars ar h r-
nrsn f COPD, bu h xn  whih hy ar f-
fiv dpnds n hw muh rvrsibiliy hr is 
h pain’s airway narrwing. Rgularly shduld
ramn wih lng-aing inhald brnhdilars
is mr ffiv and nvnin han ramn wih
shr-aing brnhdilars. Th anihlinrgi (an-
imusarini) agns and h ba-adrnrgi agniss
ar qually ffiv  sar hrapy. Pharmahrapy
rmmndains ar basd n h pain’s symp-
ms and hisry f xarbains. Arding  h
GOLD guidlins, pains ar lassid in Grup A,
B, C, r D (s Tabl 30.3). Pains in all grups shuld
b augh  avid risk fars ha aus hir COPD 
ar up and shuld riv vainains fr inunza
yarly and pnumal disas whn apprpria.
Pains in Grup A may sar hrapy wih a shr- r
lng-aing brnhdilar. Pains in Grup B iniia
hrapy wih ihr a lng-aing ba r anihlinr-
gi brnhdilar. Pains in Grup C iniia a lng-
aing brnhdilar, prfrably an anihlinrgi
agn (s Tabl 30.6). Pains in Grup D an gnr-
ally als sar wih a lng-aing anihlinrgi agn
(s Tabl 30.6). Pains wih mr svr sympms
an sar bh a lng-aing ba agnis and a lng-
aing anihlinrgi agn, ihr as singl prdus
(s Tabls 30.7 and 30.8) r mbinain prdus (s
Tabl 30.8). Sm pains wih an sinphil un
qual r grar han 300 μL shuld bgin hrapy wih
bh a lng-aing ba agnis (s Tabl 30.6) and
an inhald risrid (s Tabl 30.9). (S Tabl
30.10 fr mbinain prdus naining inhalan
risrids and ba-adrnrgi brnhdilars.)
Sm pains wih svr sympms, mdra  s-
vr airw bsruin, and a hisry f frqun r
svr xarbains may nd ripl hrapy wih a
lng-aing ba agnis, a lng-aing anihlinrgi
agn, and an inhald risrid (s Tabl 30.11).
An ral risrid (.g., prdnisn) may b addd
fr shr urss f hrapy during an au xarba-
in f COPD. Lng-rm ramn (bynd 10  14
days) wih sysmi risrids shuld b avidd.
Th phsphdisras-4 (PDE-4) inhibir rumilas
may b usful in rduing xarbains in pains in
riving ripl hrapy. Azihrmyin (s Chapr
45) may b nsidrd in frmr smkrs xprin-
ing xarbains dspi apprpria ramn. Eah
f hs agns shuld b usd squnially and h
pain rvaluad a ah sp bfr a nw drug is
addd. If spirmry ss r sympms d n shw
imprvmn wih a pariular agn, anhr agn
wih a diffrn mhanism f ain may b addd.
Pulmnary rhabiliain hrapy may als b hlpful
in assising h pain wih COPD by rduing h fr-
quny f xarbains. Th us f anibiis is n
indiad in COPD, hr han fr raing infius
xarbains and hr barial infins.
Oxygn hrapy may als b usd if h pain
is hrnially hypxmi, has nurnal r xris-
indud hypxmia, r has an au xarbain f
bsruiv disas and O2 drps  lss han 55 mm
Hg. Nrmal dss fr xygn hrapy ar 2  3 L/min
via nasal annula.
DRUG THERAPY FOR LOWER
RESPIRATORY DISEASES
ACTIONS AND USES
Expectorants liqufy muus by simulaing h sr-
in f naural lubrian uids frm h srus glands.
Th w f srus uids hlps liqufy hik muus
masss ha may plug h narrw brnhils. A m-
binain f iliary ain and ughing will hn xpl
h phlgm frm h pulmnary sysm. Exprans
ar usd  ra nnprduiv ugh, brnhiis, and
pnumnia, in whih muus plugs inhibi h xpul-
sin f irrians and baria ha aus brnhiis r
pnumnia.
Antitussives a by supprssing h ugh nr in
h brain. Thy ar usd whn h pain has a dry,
haking, nnprduiv ugh. Ths agns will n
sp h ugh mplly bu shuld dras h fr-
quny and supprss h svr spasms ha prvn
adqua rs a nigh. Undr nrmal irumsans,
i is n apprpria  supprss a prduiv ugh,
s aniussivs shuld n b usd in pains wih a
prduiv ugh.
Mucolytic agents rdu h sikinss and viss-
iy f pulmnary srins by aing dirly n h
muus plugs  aus dissluin. This ass h r-
mval f h srins by suin, psural drainag,
and ughing. Mulyi agns ar ms ffiv in
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30
rmving muus plugs bsruing h rahbrn-
hial airway. Thy ar usd in raing pains wih
au and hrni pulmnary disrdrs, bfr and af-
r brnhspy, afr hs surgry, and as par f h
ramn f rahsmy ar.
Bronchodilators rlax h smh musl f h ra-
hbrnhial r. This allws an inras in h pn-
ing f h brnhils and alvlar dus, whih d-
rass h rsisan  airw in h alvlar sas.
Ashma and brnhiis aus rvrsibl bsruin f
h airways. Th airway nsriin assiad wih
mphysma is smwha rvrsibl, dpnding n h
svriy and durain f h disas. Th primary brn-
hdilars usd in h ramn f airway bsruiv
disass inlud ba-adrnrgi agniss and ani-
hlinrgi arsls. Cmbining brnhdilars ha
hav diffrn mhanisms f ain (.g., mbining
a lng-aing anihlinrgi agn wih a lng-aing
ba agnis) and durain f ain may inras h
dgr f brnhdilain and lung funin.
Antiinammatory agents play an impran rl
in h ramn f ashma  rdu inammain.
Crisrids ar h ms ffiv agns and h
mainsay f all ashma hrapy. Ms mmnly usd
ar hs adminisrd by inhalain, fn in mbi-
nain wih ba-adrnrgi agniss (s Tabl 30.10).
Inhalain plas h mdiin a h si f inamma-
in wih minimal sysmi advrs ffs. Dpnding
n h frquny and svriy f au aaks, sm
pains wih ashma will rquir shr “burss” f sys-
mi srids, usually prdnisn, fr 1  2 wks f
hrapy. Oasinally a pain wih ashma may r-
quir alrna-day r daily srid adminisrain 
nrl sympms. All ffrs mus b mad  pi-
miz hr frms f ramn bfr rsring  rgu-
lar sysmi srid adminisrain baus f h p-
nial srius advrs ffs ha ampany his.
Anhr aniinammary agn usd is rumilas.
Rumilas is h rs f a lass f agns, h sl-
iv PDE-4 inhibirs. This agn inhibis h rlas
f inammary mdiars and inhibis immun ll
aivain. I ds n hav brnhdilaing prpris.
Immunomodulators—malizumab, bnralizumab,
dupilumab, rslizumab, r mplizumab—may b
prsribd fr pains wh hav bn diagnsd wih
subyps f ashma. Bnralizumab, dupilumab, rsli-
zumab, and mplizumab ar usd  ra sinphil-
i ashma, and malizumab is usd  ra airbrn
allrgni ashma. Th immunmdulars (s Tabl
30.12) ar usd in addiin  hr mainnan ra-
mn (risrids, brnhdilars)  rdu h
frquny f ashma xarbains.
NURSING IMPLICATIONS FOR LOWER
RESPIRATORY DISEASES
Th nurs mus rs undrsand nrmal rspira-
ry funin bfr prding  h assssmn f
489
pahphysilgi ndiins f h rspirary ra,
suh as ashma, hrni brnhiis, and mphysma.
Bh mphysma and hrni brnhiis ar prgrs-
siv disass wih lil rvrsibiliy, whras ashma
is an inammary prss wih rvrsibl airw
bsruin.
Assessment
History of respiratory symptoms
• Wha pulmnary sympms has h individual x-
prind (.g., hildhd r adul allrgis, pul-
mnary infins, pnumnia, ubrulsis, hs
rauma, surgris)? Has h individual had any
rspirary prblms ha hav rquird rn
halhar prvidr ramn r mrgny dpar-
mn ramn? If ys, g dails. Whn ughing,
whzing, r difuly brahing urs, wha ma-
surs hav hlpd  rliv h sympms?
• Wha is h wrk nvirnmn f h individual? Ask
abu xpsur  allrgns, dus, and hmials.
• Ask spially fr dails f smking r xpsur
 sndhand smk. Hisry f smking is usual-
ly rrdd in pak-yars. (Muliply h numbr f
paks f igars smkd pr day ims h num-
br f yars f smking. Fr xampl, if a prsn
smkd 1½ paks f igars pr day fr 20 yars,
h pain is said  hav a 30 pak-yar [1½ × 20 =
30] hisry f smking.)
• Is hr a family hisry f rspirary disas r
disrdrs? If s, bain dails (.g., diagnsis f dis-
as, ppl affd).
History of respiratory medication
• Wha prsribd mdiains, vr-h-unr
mdiains, r hrbal prdus ar bing usd r
hav bn usd fr h ramn f h sam r
similar rspirary prblms? D any mdiains,
suh as aspirin r nnsridal aniinammary
drugs (NSAIDs, .g., ibuprfn [Advil]), pripia
an ashma aak?
• Hw ffiv hav h mdiains bn in raing
prir r urrn sympms?
Description of current symptoms
• Wha is h pain’s hif mplain?
• Whn did h sympms sar? Ds h pain
hav any ida wha riggrd hm?
• Ask h pain  dsrib h sympms. Wha f-
f d h sympms hav n h pain’s abiliy 
arry u aiviis f daily living (ADLs)?
Respiratory assessment. Note: Th xn f h pul-
mnary xaminain (inspin, palpain, prus-
sin, ausulain) mus b adapd  h nurs’s du-
ain lvl and assssmn skills.
• Obsrv h pain’s gnral apparan and dgr
f rspirary impairmn. Adap h assssmn
490 UNIT V Drugs Affecting the Respiratory System
and pririizain f h xaminain  h dgr
f rspirary impairmn prsn.
• Tak and rrd baslin vial signs and puls xim-
ry lvl.
• Respiratory pattern: Assss h ra, dph, and rgu-
lariy f h pain’s brahing. Th nrmal rspira-
ry ra is apprximaly 12  20 brahs/min in
aduls and up  44 brahs/min in infans.
 • Rapid shallw brahing may b ausd by an
lvad diaphragm, rsriiv lung disas, r
plurii hs pain. Rapid dp brahing may
b ausd by xris, anxiy, r mabli ai-
dsis. Kussmaul rspirain is dp brahing as-
siad wih mabli aidsis. I may b fas,
nrmal, r slw. I is ms fn fund in pains
wih diabi kaidsis.
 • Brahing assiad wih bsruiv lung dis-
as has a prlngd xpirary phas baus
f inrasd airway rsisan. If h rspirary
ra inrass, h pain laks im fr full xpi-
rain. Th hs vrxpands wih rappd air
and brahing bms shallw.
 • Chyn-Sks rspirain is a yli brahing
parn in whih prids f dp brahing alr-
na wih prids f apna. Childrn and ldr
ppl nrmally shw his parn whil aslp.
Ohr auss inlud har failur, drug-indud
rspirary dprssin, urmia, and srk.
• Cough: N whhr a ugh is prduiv r
nnprduiv. Rrd spuum lr, nsisny,
amun, and any apparan f frhinss r bld
(hmpysis). Has h pain xprind any
suddn pisds f svr ughing, whzing, r
shrnss f brah? Ds h pain hav ughing
r whzing during rain sasns f h yar r
whn xpsd  rain plas r ndiins (.g.,
as, dgs, smk, mdiains, fds)? Ds xr-
is indu ughing?
• Mental status: As h xygn lvl in h bdy dimin-
ishs and arbn dixid aumulas ausing aid-
sis, h mnal saus will drira frm alrnss
 prgrssivly lwr lvls f funining (alr →
rslss → drwsy → unnsius → dah).
Inspection
• Skin color: Is h skin lr nrmal, r is h pain
yani? Whr is h yansis visibl? Priphral
yansis is dnd as a bluish lring f an is-
lad ara f h bdy (.g., arlbs, s, f, n-
grs). Cnral yansis indias a gnral lak f
xygn in h hmglbin. Th nir bdy has a
sligh bluish ing. I is ms radily bsrvd n h
lips and muus mmbrans f h muh (irum-
ral yansis).
• Dyspnea: N whhr dyspna urs a rs r
wih xrin. Obsrv h brahing parn (.g.,
pursd lip, xrin rquird  xhal).
• Muscle involvement: Elvaing h shuldrs, r-
raing h spas bwn h ribs, and using h
abdminal musls ar assiad wih advand
rspirary disas.
• Posture: Dyspni pains usually si uprigh r lan
frward frm h wais, rsing h lbws n h
kns. This hlps giv h hs maximal xpansin.
• Chest contour: N hangs in hs nur, suh
as barrl hs (inrasd anrpsrir diamr),
kyphsis, r slisis. Masur and rrd h hs
irumfrn.
• Fingernail clubbing: Assss fr aning r an in-
ras in h angl bwn h ngrnail and h
nail bas f h ngrs. Clubbing has many auss,
inluding hypxia and lung anr.
Palpation. Prfrm palpain f h hs, ning any
ndr r painful aras, masss, and inrasd r d-
rasd ail frmius. N diminishd xpansin f
h hs wall n inspirain.
Auscultation. Prfrm ausulain f h hs; n
h innsiy, pih, and rlaiv durain f inspira-
ry and xpirary phass. Idnify addiinal sunds
(.g., rakls, whzs). Ar h abnrmal sunds in-
spirary, xpirary, r bh? Whr ar hy lad?
D hy lar wih dp brahing r ughing?
Cardiovascular assessment. As apprpria  h
sympms and h diagnsis, prfrm a ardivasu-
lar assssmn (s Chaprs 22 hrugh 27). Whnvr
dyspna is svr, d n vrlk h pssibil-
iy f ardivasular invlvmn—prfrm a ardia
assssmn.
Sleep pattern. Ask whhr h individual has had dif-
uly slping; drmin h numbr f pillws hy
rquir. Obain dails.
Psychosocial assessment. Ask spially abu h
prsn and dgr f dprssin, anxiy, and sial
islain xprind as a rsul f h disas prss,
as wll as adapiv r maladapiv rspnss. Idnify
suppr sysms in pla  assis in prviding fr h
individual’s ar.
Laboratory and diagnostic data. Rviw pulmnary
funin ss, ABGs, hmalgy, spuum ss, and
x-ray rprs as availabl and apprpria  h di-
agnsis. Allrgy sing may b apprpria fr sm
individuals. If alpha-1 anirypsin diny is sus-
pd, an alpha-1 anirypsin s and prinas
inhibir yping may b rdrd  drmin whih
yp f alpha-1 anirypsin diny is prsn.
Implementation
• Prfrm physial assssmns f h pain in a-
rdan wih linial si pliis (.g., vry 4 r 8
hurs, dpnding n h pain’s saus).
• Assis h pain, as ndd,  prfrm slf-ar
aiviis. N h dgr f impairmn r dys-
pna sn wih and wihu xygn.
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30
• During an au ashma aak, ninual rspira-
ry assssmns ar prfrmd. Mnir xygn
saurain. Cmpar pulmnary funin ss wih
nrmal lvls and rpr ndings usid h pa-
ramrs spid by h halhar prvidr.
• Adminisr xygn as rdrd and as ndd.
Rrd spirmr radings whn rdrd.
• Adminisr prsribd mdiains and ramns
ha an bs allvia h pain’s sympms and
prvid h maximum lvl f mfr.
• Enurag physial aiviy as prsribd. D n
allw h pain  vrxr r bm faigud.
• Mainain pain hydrain nsisn wih any -
xising diagnss (.g., har failur). Prvid hu-
midiain as prsribd.
• Insiu masurs  rdu anxiy. Suppr h
pain in a alm mannr.
Patient Education
Peak owmeter. Ppl wih ashma ar ruinly
augh hw  us a pak wmr  masur h
pak xpirary w (PEF)  assss h svriy f
hir sympms. Th fllwing an b drmind us-
ing h PEF as a guid:
• Th grn zn is whr h PEF is a 80%  100%
f h pain’s prsnal bs PEF. Whn in h grn
zn, h pain is brahing wll and having n
ughing, whzing, r hs ighnss and shuld
ninu hrapy as prsribd.
• Th yllw zn is whr h PEF is a 50%  80%
f h prsnal bs PEF. In h yllw zn, h
pain is saring  bm sympmai, having
sympms suh as ughing, whzing, r hs
ighnss. I is im  us quik-rlif mdiin (in-
hald ba-2 agnis).
• Th rd zn is whr h PEF is lss han 50% f h
pain’s prsnal bs PEF. Whn in h rd zn,
h pain shuld na h halhar prvidr
immdialy. Quik-rlif mdiin is ninud,
and risrids ar fn sard a his pin.
Avoiding irritants. Smking, plln, and nvirnmnal
plluans mmnly aggrava rspirary disrdrs.
Chk h hm and wrk nvirnmn fr allrgns ha
may b pripiaing r wrsning an ashmai aak.
Mdiins aln will n allvia h prblm. Th n-
rl f riggrs fr h aaks is f paramun impran.
Activity and exercise
• Faigu and rsuling dyspna may rquir adjus-
mns in physial aiviy and mplymn.
• Suppr h pain’s nrns.
• Plan fr rs prids  alrna wih aiviy.
• Prvid xygnain bfr r during aiviis as
apprpria  h pain’s nds.
• Iniia h us f an inhald ba-2 agnis 30 min-
us bfr undraking xris knwn  indu
an ashma aak.
491
Nutritional status
• A wll-baland di ha prvns xssiv wigh
lss r gain is impran.
• Enurag pains wih dyspna  a svral
small srvings hrughu h day and  ak small
bis. A nuriinal supplmn fr pains wih
rspirary disas (.g., Pulmar) may b pr-
sribd as an adjun  limid daily fd inak.
Avid fds knwn  inras prduin f mu-
us (.g., milk, hla).
Preventing infections
• Enurag pains  avid xpsur  ppl
wih infin, prai gd hygin suh as hand-
washing, g adqua rs, and disps f sr-
ins prprly.
• Pains shuld sk mdial anin a h arlis
sign f suspd infin (.g., inrasd ugh,
inrasd faigu, dyspna, mpraur lvain,
hang in hararisis f srins).
• Annual inunza vainains ar rmmndd
fr pains having prsisn ashma aaks; n-
sidr pnumnia vain.
Increased uid intake. Unlss nraindiad, nur-
ag pains  inras uid inak. This will aid in d-
rasing srin vissiy. Pains shuld drink 8 
10 (r mr) 8-un glasss f war daily as dird
by h halhar prvidr.
Environmental elements. Ppl xprining diful-
y in brahing an bn frm prpr mpraur,
humidiain f h air, r vnilain f h imm-
dia surrundings. Mis air frm a humidir an
radily rliv ns r hra drynss.
Breathing techniques. If rdrd by h halhar pr-
vidr, ah psural drainag and pursd-lip brah-
ing r abdminal brahing and ughing; rfrrals
 pulmnary rhabiliain may b indiad. Rrd
pak w radings and insiu prsribd ramns
as indiad by h halhar prvidr.
Sleep patterns. Disuss adapains ha h individu-
al an mak in daily ruins  nsur adqua rs.
As h disas prgrsss, slping in a rlinr r in
an uprigh psiin may b nssary.
Psychosocial behavior
• Enurag pn disussin f h prsn’s fars and
xpains rgarding hrapy.
• Disuss h xpains f hrapy (.g., lvl f x-
ris, dgr f pain rlif if pain is prsn, lr-
an, frquny f hrapy, rlif f dyspna, abiliy
 mainain ADLs and wrk).
• Idnify suppr ppl wh an assis h indi-
vidual during prids f brahlssnss and mak
hm, as wll as h pain, awar f mmuniy
492 UNIT V Drugs Affecting the Respiratory System
rsurs availabl, suh as h Visiing Nurs
Assiain and hm halhar agnis.
Medications
• Explain h purps and mhd f adminisrain
f ah prsribd mdiain. B rain ha h
individual undrsands h dlivry mhd fr ad-
minisrain f h mdiain (.g., arsl hrapy,
mrd-ds inhalrs, nbulizr, pak xpirary
wmr). Th ar and laning f quipmn
usd fr dlivry f drugs  h rspirary ra
shuld b xplaind  prvn barial grwh.
• Whn adminisring mdiins by arsl hrapy 
a hild r an ldr adul, mak sur ha h pain has
h srngh and dxriy  pra h quipmn b-
fr disharg. Whn musl rdinain is n fully
dvlpd, as in a yungr hild, r whn dxriy has
diminishd, as in an ldr pain, i may b bnial
 us a spar dvi fr mdiins adminisrd by
inhalain (s Fig. 7.13). Hav h pain dmnsra
us f h inhalr a ah f r mrgny dpar-
mn visi. Cnrm ha h pain xhals mpl-
ly bfr iniiaing h rs inhalain f a mdiain
and ha h brah is hld fr apprximaly 10 s-
nds during inhalain f h mdiain. Whnvr
bh a brnhdilar and a srid ar prsribd,
adminisr h brnhdilar as h rs puff f mdi-
ain and hn wai a fw minus bfr adminis-
ring h srid as h snd mdiain. This will
allw brnhdilain s ha whn h srid, r any
snd drug, is givn, h drug is mr likly  rah
h lwr prins f h airway. Advis h pain 
rins h muh (rins and spi) afr inhalain f s-
rid mdiains.
• Oxygn hrapy mus b xplaind in dail. Th
pain wh is in a ninual hypxi sa mus un-
drsand ha i is n bnial and may b harmful
 inras h xygn w  mr han h pr-
sribd ra.
• B rain ha h individual undrsands h prp-
r us f brnhdilars and aniinammary
agns prsribd. Drugs prsribd fr as-ndd
(PRN) us r us during an au aak f ashma
mus b hrughly xplaind. Tah h pain 
hk whhr an inhalr is full r mpy.
Fostering health maintenance
• Thrughu h urs f ramn, disuss mdi-
ain infrmain, h impran f adqua
airway laran, diary and hydrain nds,
brahing xriss, physial xris, pulmnary
hygin, nvirnmnal nrl, h nd  balan
aiviis wih abiliis, and srss rduin and
hw ah f hs masurs an bn h pain.
• Filtration systems: Th us f spializd lrain
sysms n furnas and air ndiinrs an signif-
ianly rdu xpsur  plln and fungal sprs
whn usd wih h windws and usid drs
lsd. Filrs mus b hangd rgularly fr full
ff. War-basd air-ndiining unis mus b
land rgularly  prvn fungal grwh, whih
uld xarba allrgy sympms.
• Dust mites: Th ms mmn aus f allrgy frm in-
dr surs, h dus mi, is fund in arping and
marsss and is n rmvd by air lanrs. T kill
dus mis, wash bdding frqunly in h war and
wash r sam prus surfas; suffd animals and
pillws an b plad insid a plasi bag and pu in h
frzr vrnigh. Enas marsss, pillws, and bx
springs in nnallrgni vrs. Whn laning, us a
damp lh  rmv rahr han sprad h dus.
• Pets: Cas, dgs, and birds ar fn a sur f ash-
ma riggrs. Ps shuld b rmvd frm h hm
r kp usid if a all pssibl.
• Smoking: All smking mus as; prvid smking
ssain duain and unsling.
• Mold: Mlds ar fn ashma riggrs. Rmv
hus plans. D n allw w lhing  li
arund wihu prmp drying.
• Sk prain and undrsanding f h fllw-
ing pins  inras mdiain adhrn: nam
f mdiain; dsag, ru, and ims f adminis-
rain; and mmn and srius advrs ffs.
• I is riial  ah h individual using an inhalr
h prpr hniqu f us. Evalua whhr a
spar is ndd.
• Tah brahing hniqus suh as diaphragmai
r abdminal brahing and h pursd-lip h-
niqu ha will failia brahing.
• Humidid air may b rquird, bu whn usd, i
is ssnial ha h humidir b land hrugh-
ly daily  prvn mld grwh.
• Tah h pain  shdul daily aiviis, inlud-
ing rs,  nsrv nrgy. Eaing smallr mals
mr frqunly spad hrughu h day will
hlp prvid nrgy, and lss nrgy will b n-
sumd mablizing largr mals.
• Tah h pain rlaxain hrapy  avid anxi-
y and srss, knwn riggrs f brnhspasm and
ashma aaks.
• Pulmar, a spially dsignd nuriinal sup-
plmn fr pains wih rspirary disass, may
b rdrd. Avid affin-naining bvrags b-
aus affin is a wak diuri. Diursis prms
hikning f lung srins, making i mr dif-
ul  xpra hm. Milk and hla ar
als knwn  inras h hiknss f srins
and may nd  b liminad frm h di.
• Mak h pain and family awar f h mmu-
niy rsurs availabl.
Patient self-assessment. Enlis h pain’s aid in d-
vlping and mainaining a wrin rrd f mnir-
ing paramrs (.g., rspirains, puls, daily wighs,
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30
dgr f dyspna rlif, xris lran, srins
bing xprad). S Pain Slf-Assssmn Frm
fr Rspirary Agns n h Evlv wbsi. Cmpl
h Prmdiain Daa lumn fr us as a baslin 
rak rspns  drug hrapy. Ensur ha h pain
undrsands hw  us h frm, and insru h pain
 bring h mpld frm  fllw-up visis. During
fllw-up visis, fus n issus ha will fsr adhr-
n wih h hrapui inrvnins prsribd. Tah
h pain  na h halhar prvidr if h PEF is
driraing r if shrnss f brah r whzing pr-
siss dspi aking prsribd mdiains.
DRUG CLASS: EXPECTORANT
guaifenesin (gwĭ-FĔN-ĕ-sĭn)
Actions
Guaifnsin is an xpran ha as by nhaning h
upu f rspirary ra uid. Th inrasd w f
srins drass muus vissiy and prms ili-
ary ain. A mbinain f iliary ain and ughing
hn xpls h phlgm frm h pulmnary sysm.
Uses
Guaifnsin is usd fr h sympmai rlif f n-
diins hararizd by muus in h rspirary ra
wih a dry, nnprduiv ugh. Suh ndiins in-
lud h mmn ld, brnhiis, laryngiis, phar-
yngiis, and sinusiis. Guaifnsin is fn mbind
wih brnhdilars, dngsans, anihisamins,
r aniussiv agns  aid in making a nnprduiv
ugh mr prduiv. Guaifnsin is mr ffiv
if h pain is wll hydrad a h im f hrapy.
Guaifnsin shuld n b givn  a pain if hr
is a dry prsisn ugh ha lass mr han 1 wk; if
hr is a hrni, prsisn ugh, suh as ha whih
ampanis ashma, brnhiis, and mphysma; r
if h ugh is ampanid by xssiv prduin
f phlgm. Ths may b indiains f mr srius
ndiins fr whih h pain shuld sk mdial
anin.
Therapeutic Outcome
Th primary hrapui um xpd frm guai-
fnsin hrapy is hinning f brnhial srins fr
xprain f muus in h rspirary ra and r-
dud frquny f nnprduiv ugh.
Nursing Implications for Guaifenesin
Premedication assessment. Rrd hararisis f
h ugh bfr iniiaing hrapy.
Availability. PO: abls: 200 and 400 mg; xndd-
rlas abls: 600, 1200 mg; ral granuls: 100 mg/
493
pak; liquid: 100 mg/5 mL; 200 mg/10 mL, 300 mg/15
mL, 400 mg/20 mL; syrup: 100 mg/5 mL. I is als
availabl in individual prdus in mbinain wih
psudphdrin, dxrmhrphan, din phs-
pha, and phnylphrin.
Dosage and administration. Adult: PO: 200-400 mg
vry 4 hurs as ndd; d n xd 2400 mg/day.
Pediatric: PO: Fr hildrn 6  11 yars ld, giv
100  200 mg vry 4 hurs; d n xd 1200 mg/
day. Fr hildrn 2  5 yars ld, giv 50  100 mg
vry 4 hurs; d n xd 600 mg/day.
Fluid intake. Mainain uid inak f 8  12 igh-
un glasss f war daily.
Humidication. Suggs h nurrn us f a
humidir.
Common adverse effects
Gastrointestinal
Gastrointestinal upset, nausea, vomiting. Dvlpmn
f hs advrs ffs is rar.
Drug interactions. N signian drug inrains
hav bn rprd.
DRUG CLASS: SALINE SOLUTIONS
Actions
Salin sluins a by hydraing muus, rduing is
vissiy.
Uses
Salin sluins f varying nnrains an b ff-
iv xprans whn adminisrd by nbulizain.
Whn adminisrd by inhalain, hypni sluins
(0.4% r 0.65% sdium hlrid) ar hugh  pr-
vid dpr pnrain in h mr disan airways;
a hyprni sluin (1.8% sdium hlrid) hydras
and simulas a prduiv ugh by irriaing h r-
spirary passags. Isni salin sluins (0.9% s-
dium hlrid) adminisrd by nbulizain ar usd
 hydra rspirary srins.
Salin ns drps/sprays ar smims rdrd
fr pains  rsr misur and rliv nasal n-
gsin sndary  lw humidiy  lar h nasal
passags and aid in brahing.
Therapeutic Outcomes
Th primary hrapui ums xpd frm
nasal and rspirary salin hrapy ar misurizd
muus mmbrans fr lss irriain frm drynss
and a mr prduiv ugh baus f lss visus
muus.
Nursing Implications for Saline Therapy
Premedication assessment. Rrd hararisis f
ugh and muus prduin bfr iniiaing hrapy.
494 UNIT V Drugs Affecting the Respiratory System

DRUG CLASS: ANTITUSSIVE AGENTS Bnznaa is a ugh supprssan. I supprsss

Actions
Aniussiv agns (ugh supprssans) a by supprss-
ing h ugh nr in h brain r by pial anshi
ain (numbing) n h rspirary srh rprs.
Uses
Aniussiv agns ar usd whn h pain has
a bhrsm, dry, haking, nnprduiv ugh.
Ths agns will n sp h ugh mplly bu
shuld dras is frquny and supprss h svr
spasms ha prvn adqua rs a nigh. Undr nr-
mal irumsans, i is n apprpria  supprss a
prduiv ugh.
Cdin is an ffiv ugh supprssan and h
sandard agains whih hr aniussiv agns ar
mpard. In h rlaivly lw dss and shr dura-
in usd  supprss ugh, addiin is n a prblm;
dpndn may dvlp, hwvr, afr lng-rm
ninuus us. Cdin shuld n b usd fr pa-
ins wih hrni pulmnary disas wh may hav
rspirary dprssin r pains wh hav a du-
mnd allrgy  din (rash, prurius).
Medication Safety Alert
The US Food and Drug Administration and Health Canada is-
sued a warning that codeine should not be used in children
younger than 12 years and in some adolescents between 12
and 18 years who are obese, who have undergone tonsillec-
tomy and/or adenoidectomy, who have genetic factors (e.g.,
ultra-rapid metabolism leading to respiratory depression), or
who have conditions that increase the risk of serious breathing
problems (e.g., obstructive sleep apnea, severe lung disease).
a ugh by numbing (anshi ain) h rspira-
ry srh snsrs. Th ain f bnznaa bgins
wihin 15  20 minus and has a durain f apprxi-
maly 3  8 hurs. I shuld n b usd in hildrn
wh ar lss han 10 yars f ag baus uninnin-
al vrds and dah hav bn rprd in his ag
grup.
Dxrmhrphan is a ugh supprssan. I ds
n aus rspirary dprssin r addiin. Th
Amrian Aadmy f Pdiaris warns agains h
us f dxrmhrphan fr rspirary illnsss in
hildrn yungr han 4 yars. Srius advrs ffs
inluding dah hav bn rprd.
Diphnhydramin is an anihlinrgi agn wih
bh anihisamini and aniussiv prpris. As
wih ms hr anihisamins, diphnhydramin
has signian sdaiv prpris. This is fn d-
rimnal during h day, spially if h prsn mus
b mnally alr, bu i is an xlln agn  sup-
prss ugh during slp. Lik hr anihlinrgi
agns, diphnhydramin shuld n b akn by
pains wih lsd-angl glauma r hs wih
prsai hyprplasia. I als may aus muus  dry,
making i hiknd and mr visus, spially if
h pain is n wll hydrad. In addiin, i shuld
b usd auiusly wih hr nral nrvus sysm
dprssans, suh as sdaivs, hypnis, alhl, r
anidprssans.
Therapeutic Outcome
Th primary hrapui um xpd frm ani-
ussiv hrapy is rdud frquny f nnprduiv
ugh.

Table 30.5 Antitussive Agents

ADULT ORAL DOSAGE
GENERIC NAME BRAND NAME AVAILABILITY RANGE
benzonatate Tessalon Perles Capsules: 100, 150, 200 mg 100–200 mg three
Do not confuse times daily
benzonatate with
benazepril or benztropine.
codeinea — Tablets: 15, 30, 60 mg 10–20 mg q4–6h
dextromethorphan Robitussin 12 Hour Strip tablets: 7.5 mg 10–20 mg q4h or
Cough Capsules: 15 mg 30 mg q6–8h;
Do not confuse Syrup: 7.5, 10 mg/5 mL 60 mg q12h
Robitussin with Reglan. Liquid: 7.5 mg/mL; 7.5, 10, 12.5 mg/5 mL (sustained release);
ElixSure Cough Gel: 7.5 mg/5 mL do not exceed
Delsym Suspension, extended release: 30 mg/5 mL 120 mg/24 hr
diphenhydramine Diphen Elixir: 6.25, 12.5 mg/5 mL 25–50 mg every
Do not confuse ZzzQuil Liquid: 6.25, 12.5 mg/5mL; 50 mg/30 mL 4–6 hr; maximum
diphenhydramine Allergy Relief Capsules and tablets: 25, 50 mg dose: 300 mg/day
with dicyclomine or
dipyridamole.
Do not confuse.
aAningredient in combination antitussive products.
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30
Nursing Implications for Antitussive Therapy
Premedication assessment. Rrd hararisis f
ugh and muus bfr iniiaing hrapy.
Availability, dosage, and administration. S Tabl 30.5
Common adverse effects
Neurologic
Drowsiness. All h aniussiv agns aus sm
sdain, bu diphnhydramin has h ms sdaiv
ff. Cauin pains abu bing alr whn driving
and praing mahinry.
Gastrointestinal
Constipation. Cdin is h ms nsipaing f h
aniussiv agns. This ff an b minimizd by
kping h pain wll hydrad and by h us f
bulk sl sfnrs if h pain rquirs mr han 1
r 2 days f din hrapy.
Drug interactions
Central nervous system depressants. Th fllwing
agns may nhan h dprssan ffs f aniussiv
agns: phnhiazins, anidprssans, sdaiv-
hypnis, anihisamins, and alhl.
DRUG CLASS: MUCOLYTIC AGENTS
acetylcysteine (ăs-ĕ-tēl-SĬS-tēn)
Actions
Aylysin as by disslving hmial bnds wih-
in h muus islf, ausing i  spara and liqufy,
rduing vissiy.
Uses
Aylysin is usd  disslv abnrmally visus
muus ha may ur in hrni mphysma, mphy-
sma wih brnhiis, ashmai brnhiis, and pnu-
mnia. Th rdud vissiy allws asir rmval
f srins by ughing, prussin, and psural
drainag. Aylysin is als usd  ra aamin-
phn xiiy.
Therapeutic Outcome
Th primary hrapui um xpd frm a-
ylysin hrapy is imprvd airway w, wih mr
mfrabl brahing.
Nursing Implications for Acetylcysteine Therapy
Premedication assessment
1. Rrd h hararisis f ugh and brnhial
srins bfr saring hrapy.
2. Obain and rrd baslin vial signs, prfrm a
rspirary assssmn and puls ximry, and r-
viw pulmnary funin s rsuls.
3. Obsrv fr and rrd any GI sympms bfr
saring hrapy.
495
4. Prfrm a baslin assssmn f h pain’s
mnal saus (.g., dgr f anxiy, nrvusnss,
alrnss).
Availability. Inhalation: 10% and 20% sluins in 4-,
10-, and 30-mL vials.
Dosage and administration. Adult: Nebulization: Th
rmmndd dsag fr ms pains is 3  5 mL f
h 20% sluin hr r fur ims daily.
Direct application into an intratracheal catheter or
tracheostomy: 1  2 mL f a 20% sluin vry 1 
4 hurs. Afr adminisrain, h vlum f brnhial
srins may inras. Sm pains wih inad-
qua ugh rx may rquir mhanial suining
 mainain an pn airway.
Nebulizer. This sluin nds  nnra as i is
usd. Whn hr-furhs f h riginal amun in h
nbulizr is usd, dilu h rmaining sluin wih
sril war.
Afr hrapy, wash h pain’s fa and hands
baus h drug is siky and irriaing. Thrughly
lans quipmn usd.
Storage. Sr h pnd sluin f h drug in
a rfrigrar fr up  96 hurs. Disard h unusd
prin.
Discoloration. Us mdiain srd nly in plasi
r glass nainrs. Cna wih mals hr han
sainlss sl an aus h sluin  dislr.
Common adverse effects
Gastrointestinal
Nausea, vomiting. Aylysin has a pungn
dr (similar  rn ggs) ha may aus nausa
and vmiing; hav an msis basin availabl. D
n, hwvr, suggs i by having h basin in lar
viw.
Serious adverse effects
Respiratory
Bronchospasm. Aylysin may asinally aus
brnhnsriin and brnhspasm. Cnurrn
us f a brnhdilar may b nssary.
Drug interactions
Antibiotics. Aylysin inaivas ms ani-
biis. D n mix ghr fr arsl adminisra-
in. Shdul adminisrain f inhalain anibiis
1 hur afr adminisrain f aylysin.
DRUG CLASS: BETA-ADRENERGIC
BRONCHODILATING AGENTS
Actions
Ba-adrnrgi agniss simula h ba rprs
in h smh musl f h rahbrnhial r 
rlax, pning h airway passags  grar vl-
ums f air.
496 UNIT V Drugs Affecting the Respiratory System

Uses inhald brnhdilars n a daily basis, i is an india-

Ba-adrnrgi brnhdilars rvrs airway n-
sriin ausd by au and hrni brnhial ash-
ma, brnhiis, and mphysma. Agns wih mr
sliv ba-2 rpr aiviy (.g., alburl, lvalb-
url, frmrl, salmrl, arfrmrl, indaar-
l, ldarl, vilanrl) hav mr dir brnhdi-
laing aiviy and fwr sysmi advrs ffs. (S
Chapr 12 fr a disussin f sliv ba rpr
aiviy.)
Unfrunaly, h rprs simulad by sympa-
hmimi agns, ausing rlaxain f h smh
musl in h rahbrnhial r, ar n fund
nly in h pulmnary sysm. Ths rprs ar
als fund in h musls f h har; in bld vs-
sls; in h urus; and in h GI, urinary, and n-
ral nrvus sysms. Thy als hlp rgula fa and
arbhydra mablism. Thrfr hr ar many
advrs ffs frm hs agns, pariularly if usd
 frqunly r in highr-han-rmmndd ds-
s. Ths adminisrd by inhalain gnrally hav
fwr sysmi ffs baus inhalain plas h
drug a h si f ain s ha smallr dsags may
b usd.
Th shr-aing ba agniss (.g., alburl, lv-
alburl) hav a rapid ns (a fw minus) and ar
usd  ra au brnhspasm. During au xa-
rbains, hs agns an b usd vry 3  4 hurs.
If a pain is using an inrasd amun f hs
in f wrsning ashma. Pains hn mus b ras-
sssd fr adhrn, inhalain hniqu, imprvd
nvirnmnal nrl, and h pssibl addiin f
risrids  h hrapui rgimn.
Salmrl, arfrmrl, frmrl, indaarl,
ldarl, and vilanrl ar lng-aing inhald brn-
hdilars, smims knwn as LABAs. Salmrl
and arfrmrl hav an ns f ain in 10  15
minus wih a durain f ain up  12 hurs.
Thrfr hy ar adminisrd wi daily. Salmrl
is apprvd fr bh ashma and COPD. Arfrmrl
is apprvd fr us in COPD nly.
Frmrl, indaarl, and ldarl hav an
ns f ain in 5  15 minus wih a durain
f ain f 24 hurs and ar hrfr adminisrd
nly n a day. Frmrl is apprvd fr us in
ashma and COPD, whras indaarl and l-
darl ar apprvd nly fr COPD. Vilanrl is
n availabl as a singl agn. I is availabl wih a
risrid (uiasn), an anihlinrgi (um-
lidinium), and wih a risrid (uiasn)
and an anihlinrgi (umlidinium). Usually,
h LABAs ar n usd  ra au pisds f
ashma r COPD, bu ar usd fr lng-rm nrl
f rspirary ffr  prvn au xarbains
f ashma and COPD. Frmrl wih an inhald
risrid an b usd as ndd  ra au
pisds f ashma.

Table 30.6 Beta-Adrenergic Agonist Bronchodilators

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE
SHORT-ACTING BETA-ADRENERGIC BRONCHODILATORS
albuterol Tablets: 2, 4 mg PO: 2–4 mg three or four times daily;
Do not Syrup: 2 mg/5 mL maximum dose 32 mg daily
confuse ProAir Aerosol Powder: Inhale: 2 inhalations q 4–6h; maximum
albuterol with 90 mcg/actuation dose 12 inhalations /24 hr
acebutolol.
Proventil-HFA Aerosol solution: 90 mcg/actuation Inhale: 2 inhalations q4–6h; maximum
Ventolin HFA dose 12 inhalations/24 hr
Solution for Nebulizer inhalation: See manufacturer’s recommendations
0.083%, 0.5%; 0.63, 1.25 mg/3 mL
formoterol Perforomist Solution for nebulization: 20 mcg/2 mL Nebulizer: 20 mcg q12h
levalbuterol Xopenex Solution for inhalation: 0.31, 0.63, 0.31–1.25 mg q8h
1.25 mg/3 mL; Inhale: 1–2 inhalations q4–6h
Xopenex Concentrate 1.25 mcg/0.5 mL
Xopenex HFA Aerosol: 45 mcg/actuation
LONG-ACTING BETA-ADRENERGIC BRONCHODILATORS
arformoterol Brovana Solution for nebulization: 15 mcg/2 mL Inhale: 15 mcg twice daily
olodaterol Striverdi Respimat Aerosol: 2.5 mcg/actuation Two actuations once daily at the same
time of the day
salmeterol Serevent Diskus Powder for inhalation: 50 mcg/ Inhale: 1 inhalation q12h
Do not confuse inhalation
Serevent with Atrovent.
Do not confuse.
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30
Thr is nrn ha alhugh LABAs dras h
frquny f ashmai aaks, hy may aually mak
h aaks ha d ur mr svr. In Fbruary 2010
h US Fd and Drug Adminisrain (FDA) issud
an advisry n LABA us in ashma (bu n COPD),
saing h fllwing:
• Us f LABAs is nraindiad wihu h us f
an ashma nrllr mdiin suh as an inhald
risrid.
• LABAs shuld nly b usd lng rm in pains
whs ashma ann b adqualy nrlld n
ashma nrllr mdiins.
• In 2017 h FDA rprd ha raing ashma wih
lng-aing ba agniss (LABAs) in mbinain
wih inhald risrids (ICS) ds n rsul
in signianly mr srius ashma-rlad sid f-
fs han ramn wih ICS aln.
Pains knwn  hav hyprnsin, hypr-
hyridism, diabs mllius, r ardia disas wih
dysrhyhmias may b pariularly snsiiv  advrs
rains and mus b bsrvd lsly.
Therapeutic Outcome
Th primary hrapui um assiad wih
ba-adrnrgi brnhdilar hrapy is brnh-
dilain rsuling in rdud whzing and asir
brahing.
Nursing Implications for Beta-Adrenergic
Bronchodilators
Premedication assessment
1. Obain and rrd baslin vial signs, prfrm a
rspirary assssmn and puls ximry, and r-
viw pulmnary funin s rsuls.
2. Assss h pain fr h prsn f palpiains
and dysrhyhmias bfr adminisrain f ba-
adrnrgi agns. If suspd, nify h halh-
ar prvidr and ask whhr hrapy shuld b
sard.
3. Prfrm an assssmn f h pain’s baslin
mnal saus (.g., dgr f anxiy, nrvusnss,
alrnss).
Availability, dosage, and administration
S Tabl 30.6. Pains using inhald brnhdilars
shuld wai apprximaly 10 minus bwn
inhalains. This allws h mdiin  dila h
brnhils s ha h snd ds an b inhald
mr dply in h lungs fr a mr hrapui
ff. Assur ha pains undrsand hw  us
h inhalr as dsribd in h manufaurr’s laf-
l ha ampanis h inhalr.
Serious adverse effects
Cardiovascular
Tachycardia, palpitations. Baus ms sympms
ar ds rlad, alrains shuld b rprd
497
 h halhar prvidr. Mnir h pain’s
har ra and rhyhm a rgular inrvals hrugh-
u hrapy wih brnhdilars. An inras f
20 bas/min r mr afr ramn shuld b
rprd  h prsribr. Always rpr palpia-
ins and suspd dysrhyhmias  h halhar
prvidr.
Neurologic
Tremors. Tll h pain  nify h halhar
prvidr if rmrs dvlp afr saring any f hs
mdiains. A dsag adjusmn may b nssary.
Nervousness, anxiety, restlessness, headache. Prfrm a
baslin assssmn f h pain’s mnal saus (.g.,
dgr f anxiy, nrvusnss, alrnss); mpar
subsqun, rgular assssmns wih h baslin.
Dizziness. Prvid fr pain safy during pisds
f dizzinss. Rpr pisds f dizzinss  h halh-
ar prvidr fr furhr valuain.
Gastrointestinal
Nausea, vomiting. Mnir all asps f h dvl-
pmn f hs sympms. Qusin h pain n-
rning hr mdiains bing akn and any hr
sympms ha hav als dvlpd. Adminisr h
mdiain wih fd and a full glass f war r milk.
Rpr if h sympms ar n rlivd.
Drug interactions
Drugs that enhance toxic effects. Triyli anidprs-
sans (.g., imipramin, amiripylin, nrripylin,
dxpin), mnamin xidas inhibirs (.g., ranyl-
yprmin, phnlzin), and hr sympahmimi
agns (.g., isprrnl) nhan h xi ffs f
ba-adrnrgi brnhdilars. Mnir fr inrass
in svriy f drug ffs, suh as nrvusnss, ahy-
ardia, rmrs, and dysrhyhmias.
Drugs that reduce therapeutic effects. Ba-adrnrgi
blking agns (.g., prpranll, nadll, pindll)
rdu h hrapui ffs f ba-adrnrgi brn-
hdilars. Highr dsags r us f anhr lass f
brnhdilar may b rquird.
Antihypertensive agents. Sympahmimi agns
may rdu h hrapui ffs f anihyprnsiv
agns. Mnir bld prssur fr an indiain f
lss f anihyprnsiv nrl.
DRUG CLASS: ANTICHOLINERGIC
BRONCHODILATING AGENTS
Anihlinrgi agns hav bn usd as brnhdi-
lars fr raing bsruiv pulmnary disas fr
mr han 200 yars, bu h pn anihlinrgi
advrs ffs (.g., hra irriain, dry muh, r-
dud muus srins, inrasd srin viss-
iy, mydriasis, ylplgia, urinary rnin, ahyar-
dia) and h availabiliy f sliv sympahmimi
agns hav limid hir us fr pulmnary disrdrs.
Whn adminisrd by inhalain, anihlinrgi
498 UNIT V Drugs Affecting the Respiratory System

agns (alidinium, glypyrrla, iprarpium, rv-
fnain, irpium, umlidinium) hav subsanially
fwr sysmi sid ffs and ar wll lrad.
Actions
Anihlinrgi agns prdu brnhdilain by
mpiiv inhibiin f hlinrgi rprs n brn-
hial smh musl, blking h brnhnsriin
ain f vagal ffrn impulss. Thr is minimal f-
f n iliary aiviy, muus srin, spuum vl-
um, and vissiy wih hs agns.
Uses
Iprarpium is a shr-aing brnhdilaing agn,
whras alidinium, glypyrrla, rvfnain,
irpium, and umlidinium ar lng-aing brn-
hdilars. Iprarpium is adminisrd vry
6 hurs, alidinium and glypyrrla vry 12 hurs,
and rvfnain, irpium, and umlidinium v-
ry 24 hurs. All h anihlinrgi brnhdilaing
agns ar usd in lng-rm ramn f rvrsibl
brnhspasm assiad wih COPD, inluding brn-
hiis and mphysma. Iprarpium, in mbinain
wih a shr-aing ba agnis suh as alburl, is
als usd in h managmn f pains wih ashma
xarbains. Tirpium is als usd in h lng-rm
managmn f ashma. Anihlinrgi brnhdila-
ing agns shuld n b usd as a rsu mdiin in
au pisds f brnhspasm.
Therapeutic Outcome
Th primary hrapui um assiad wih ani-
hlinrgi brnhdilaing agns is brnhdilain
rsuling in rdud whzing and asir brahing.

Table 30.7 Inhaled Anticholinergic Bronchodilators

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE
SHORT-ACTING INHALED ANTICHOLINERGIC BRONCHODILATORS
ipratropium Atrovent HFA Aerosol: 17 mcg/actuation Inhale: 2 inhalations four times daily; maximum dose:
Inhalation Solution: 12 inhalations per 24 hr
0.02%/2.5 mL vial Nebulize: 1 unit-dose vial q6–8h
LONG-ACTING INHALED ANTICHOLINERGIC BRONCHODILATORS
aclidinium Tudorza Pressair Powder for inhalation: Inhale: 1 inhalation twice daily
400 mcg/actuation
glycopyrrolate Seebri Neohaler Powder for inhalation: Inhale: 1 capsule twice daily using Neohaler
15.6 mg/inhalation
Lonhala Magnair Inhalation Solution: Nebulize: 1 vial (25 mcg) inhaled twice daily; using
25 mcg/mL in 1 mL vial only Magnair
revefenacin Yupelri 175 mcg/3 mL Nebulize: 1 unit-dose vial once daily
tiotropium Spiriva HandiHaler 18-mcg capsule Handihaler–Inhaler: 1 capsule once daily (to ensure
Spiriva Respimat 1.25 mcg and 2.5 mcg per drug delivery, the contents of each capsule should
actuation be inhaled twice)
COPD: 2 inhalations (5 mcg) once daily
Asthma: 2 inhalations (2.5 mcg) once daily
umeclidinium Incruse Ellipta Powder for inhalation: Inhale: 1 inhalation once daily
62.5 mcg/actuation

Table 30.8 Combination Anticholinergic and Beta-Adrenergic Bronchodilators

SHORT-ACTING ANTICHOLINERGIC AND BETA AGONIST COMBINATION PRODUCTS
ipratropium/albuterol Combivent Respimat Aerosol: ipratropium 20 mcg and albuterol
100 mcg/inhalation
Inhalation Solution: Ipratropium bromide
0.5 mg and albuterol 2.5 mg/3 mL
LONG-ACTING ANTICHOLINERGIC AND BETA AGONIST COMBINATION PRODUCTS
aclidinium/formoterol Duaklir Pressair Aerosol: aclidinium 400 mcg and
formoterol 12 mcg/actuation
tiotropium/olodaterol Stiolto Respimat Aerosol solution: tiotropium 2.5 mcg and
olodaterol 2.5 mcg/actuation
umeclidinium/vilanterol Anoro Ellipta Aerosol powder: umeclidinium 62.5 mcg
and vilanterol 25 mcg/inhalation
Inhale: 1 inhalation four times
a day
Nebulize: 1 vial (3 mL) via
nebulization q6h
Inhale: 1 inhalations twice a day
Inhale: 2 inhalations at the same
time per 24 hr
Inhale: 1 inhalation per 24 hr
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30
Nursing Implications for Anticholinergic
Bronchodilators
Premedication assessment
1. Obain and rrd baslin vial signs, prfrm r-
spirary assssmn and puls ximry, and rviw
pulmnary funin s rsuls.
2. Chk h mdial rrd  drmin whhr h
pain has a hisry f lsd-angl glauma. If s,
rnrm h adminisrain rdr wih h halh-
ar prvidr bfr adminisrain f anihlinr-
gi brnhdilars.
Availability and dosage
S Tabl 30.7 fr Inhald Anihlinrgi Brnhdilars.
S Tabl 30.8 fr Cmbinain Anihlinrgi and
Ba-Adrnrgi Brnhdilars.
Administration. Ensur ha h pain undrsands
hw  us h inhalr ha ampanis h mdia-
in. Rad h manufaurr’s insruins fr admin-
israin fr h varius yps f inhalrs availabl.
Medication Safety Alert
Use anticholinergic bronchodilators with caution in patients
with the potential for closed-angle glaucoma, prostatic hyper-
plasia, or bladder neck obstruction.
Common adverse effects
Gastrointestinal
Mouth dryness, throat irritation. Ths advrs ffs
ar usually mild and nd  rslv wih ninud
hrapy. Enurag h pain n  disninu hr-
apy wihu rs nsuling h halhar prvidr.
Ohr masurs  allvia drynss inlud suking
n i hips r hard andy.
Serious adverse effects
Anticholinergic
Tachycardia, urinary retention, exacerbation of pulmonary
symptoms. Insru h pain  nsul h prsribr
bfr ninuing wih furhr hrapy.
Drug interactions. N signian inrains hav
bn rprd.
DRUG CLASS: RESPIRATORY ANTIINFLAMMATORY
AGENTS—CORTICOSTEROIDS USED FOR
OBSTRUCTIVE AIRWAY DISEASE
Actions
Crisrids (s Chapr 37), whhr applid
by arsl r adminisrd sysmially, hav bn
shwn  b highly ffiv fr raing bsruiv
airway disas. Th mhanisms f ain ar n
mplly knwn, bu risrids hav a dir
ff n smh musl rlaxain; hy nhan
499
h ff f ba-adrnrgi brnhdilars and
inhibi inammary rspnss ha may rsul in
brnhnsriin.
Uses
Baus inammain is a ky mpnn f ashma,
daily us f inhald risrids has bm h
prfrrd lng-rm nrl mdiin fr mild, mdr-
a, and svr prsisn ashma. Pains wih svr
COPD wh ar unrspnsiv  brnhdilars may
hav an inhald risrids addd  h mdia-
in rgimn  prvid nhand airway w.
Fr pains wih ashma r COPD xprining an
xarbain, a shr urs (5  7 days) f sysmi
risrids (.g., prdnisn) may b ndd. Lng-
rm us f sysmi risrids shuld b avidd.
I is impran  rmmbr ha inhald ri-
srids shuld n b rgardd as ru brnhdila-
rs and shuld n b usd fr rapid rlif f brn-
hspasm. (S Chapr 29 fr h us f inranasal
risrids.)
Therapeutic Outcome
Th primary hrapui um assiad wih r-
isrid hrapy is drasd pulmnary inamma-
in, rsuling in asir brahing wih lss ffr.
Nursing Implications for Corticosteroid Therapy
Premedication assessment. Insp h ral aviy fr
h prsn f any yp f infin.
Availability and dosage
S Tabl 30.9 fr Oral Inhalan Crisrids.
S Tabl 30.10 fr Cmbinain Inhalan Cri-
srid and Ba-Adrnrgi Brnhdilars S
Tabl 30.11 fr Cmbinain Inhalan Crisrid-
Ba-Adrnrgi-Anihlinrgi Brnhdilars
Administration
Counseling, adherence. Th hrapui ffs, un-
lik hs f sympahmimi brnhdilars, ar
n immdia. This shuld b xplaind  h pa-
in bfr hrapy bgins  nsur prain and
ninuain f ramn wih h prsribd dsag
rgimn, vn whn h pain is asympmai. Full
hrapui bn rquirs rgular us and may r-
quir up  4 wks f hrapy fr maximum bn.
Preparation before administration. Pains riving
brnhdilars by inhalain shuld b advisd  us
h brnhdilar bfr h risrid inhalan 
nhan pnrain f h risrid in h brn-
hial r. Afr using h brnhdilar, h pain
shuld wai svral minus bfr h risrid
is inhald  allw im fr h brnhdilar  rlax
h smh musl.
Maintenance therapy. Afr h dsird linial ff has
bn baind, h mainnan ds shuld b rdud
 h smalls amun nssary  nrl sympms.
500 UNIT V Drugs Affecting the Respiratory System

Severe stress or asthma attack. During prids f
srss r a svr ashma aak, pains may rquir
ramn wih sysmi srids. Exarbain f ash-
ma ha urs during h urs f risrid in-
halan hrapy shuld b rad wih a shr urs
f a sysmi srid. Insru pains n  us h
risrid inhalr whn aking sysmi srids
baus h arsl n nly may aus irriain and
xarba sympms, bu als may n pnra dp
nugh in h brnhial r baus f inamma-
in and swlling frm h ashmai aak.
Common adverse effects
Gastrointestinal
Hoarseness, dry mouth. Harsnss and dry muh
ar usually mild and nd  rslv wih ninud
hrapy. Enurag h pain n  disninu hr-
apy wihu rs nsuling h halhar prvidr.

Table 30.9 Oral Inhalant Corticosteroids

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE
beclomethasone Qvar Redihaler Aerosol: 40, 80 mcg/actuation; 120 doses/ Inhale: 1 or 2 inhalations
dipropionate inhaler (80 mcg) twice daily;
maximum 640 mcg daily
budesonide Pulmicort Suspension via inhaler: 0.25, 0.5, Inhale: 2 inhalations twice daily;
phosphate Do not confuse Pulmicort 1 mg/2 mL maximum 4 inhalations twice
with Pulmozyme. daily
Pulmicort Flexhaler Aerosol powder: 90, 180 mcg/actuation
ciclesonide Alvesco Aerosol solution: 80, 160 mcg/actuation 80–160 mcg twice daily
uticasone Flovent HFA Aerosol: 44, 110, 220 mcg/actuation 88–880 mcg twice daily
propionate Do not confuse
Flovent with Flonase.
Flovent Diskus Powder for inhalation: 50, 100, 250 mcg/ 100–500 mcg twice daily
Do not confuse dose
Flovent with Flonase.
ArmonAir Digihaler Powder for inhalation: 55–232 mcg twice daily
55, 113, 232 mcg/actuation
uticasone Arnuity Ellipta Powder for inhalation: 50, 100, 200 mcg/ 50–200 mcg daily
furoate inhalation
mometasone Asmanex HFA Powder for inhalation: 50, 100, 200 mcg/ 200–440 mcg twice daily
furoate Asmanex Metered doses inhalation
Powder, breath activated: 110, 220 mcg/
inhalation
Do not confuse.

Table 30.10 Combination Inhalant Corticosteroid and Beta-Adrenergic Bronchodilators

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE
budesonide/ Symbicort Aerosol: 80 or 160 mcg budesonide Inhale: 2 inhalations twice daily for maintenance
formoterol + 4.5 mcg formoterol/actuation on a regularly scheduled basis; not for acute
bronchospasm
uticasone/ Advair Diskus Powder for inhalation: Inhale: 1–2 inhalations twice daily for
salmeterol Do not 100, 250, or 500 mcg uticasone maintenance therapy on regularly scheduled
confuse + 50 mcg salmeterol/actuation basis; not for acute bronchospasm
Advair with
Advicor.
Advair HFA Aerosol inhalation: Inhale: 2 inhalations twice daily for maintenance
45, 115, or 230 mcg uticasone therapy on regularly scheduled basis; not for
+ 21 mcg salmeterol/actuation acute bronchospasm
uticasone/ Breo Ellipta Aerosol inhalation: Inhale: 1 inhalation once daily
vilanterol 100 or 200 mcg uticasone
+ 25 mcg vilanterol/actuation
mometasone/ Dulera Aerosol inhalation: Inhale: 2 inhalations twice daily for maintenance
formoterol 50, 100, or 200 mcg mometasone on regularly scheduled basis; not for acute
+ 5 mcg formoterol/ actuation bronchospasm
Do not confuse.
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30 501

Table 30.11 Combination Inhalant Corticosteroid–Beta-Adrenergic–Anticholinergic Bronchodilators

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE
uticasone/vilanterol/ Trelegy Ellipta Fluticasone 200 mcg/vilanterol 25 mcg/ Inhale: 1 inhalation once daily
umeclidinium umeclidinium 62.5 mcg per actuation
budesonide/ Breztri Aerosphere Budesonide 160 mcg/glycopyrrolate 9 mcg/ Inhale: 2 inhalations twice daily
glycopyrrolate/ formoterol 4.8 mcg per actuation
formoterol

Serious adverse effects arly and la-phas brnhnsriin, brnhial

Gastrointestinal
Fungal infections (thrush). Inrasd risk fars fr
h dvlpmn f ral hrush inlud nmian
anibii us, diabs, imprpr arsl adminis-
rain, larg ral dss f risrids, and pr
dnal hygin. Pains shuld b insrud n gd
ral hygin hniqu and ld  gargl and rins h
muh wih a muhwash afr ah arsl ramn.
Cmmrial muhwashs nain alhl, whih may
aus furhr drying and ral irriain. If hrush dvl-
ps, i is usually n sufinly rublsm  rquir
disninuing srid arsl hrapy. An anifungal
muhwash suh as nysain will gnrally radia
h ral andidiasis (hrush).
Respiratory
Pneumonia. Alhugh rlaivly unmmn, an in-
rasd risk f pnumnia is assiad wih h us
f inhald risrids in pains wih COPD.
Mnir fr sympms f pnumnia.
Drug interactions. N signian drug inrains
hav bn rprd.
DRUG CLASS: ANTILEUKOTRIENE AGENTS
Whn inammary lls ar riggrd by irrians
suh as smk, allrgns, r viruss, h phsphlip-
id mmbran f h pihlial lining f h airways is
disrupd, ausing a sris f hmial rains frm
arahidni aid ha rlass lukrins, prsaglan-
dins, hrmbxans, and isanids. Th lukrins
prdud aus many f h signs and sympms f
ashma, suh as brnhnsriin, vasular prm-
abiliy lading  dma, and muus hyprsrin.
montelukast (mŏn-tĕ-LŪ-kăst)
Singulair (SĬN-gyū-lār)
Actions
Mnlukas is a sliv and mpiiv rpr
anagnis f h ysinyl lukrin rpr. This
is h rpr ha lukrin D4 simulas  riggr
sympms f ashma.
Uses
Mnlukas is apprvd fr us in njunin wih
hr mdiains fr h prphylai and hrn-
i ramn f ashma. I has bn shwn  rdu
hyprrspnsivnss, dayim ashma sympms, and
nighim awakning; rdu ba-adrnrgi agnis
us; and imprv pulmnary funin ss. Th GINA
guidlins rmmnds anilukrin agns as al-
rnaivs  lw-ds inhald risrids fr mild
prsisn ashma and wih lw  mdium dss f in-
hald risrids fr mdra prsisn ashma.
Mnlukas is n a brnhdilar and shuld n
b usd  ra au pisds f ashma; hwvr,
ramn wih mnlukas an b ninud dur-
ing au xarbains f ashma. Mnlukas us
shuld b ninuus, vn during au ashma xa-
rbains and sympm-fr prids.
Therapeutic Outcome
Th primary hrapui um assiad wih
mnlukas hrapy is fwr pisds f au ash-
mai sympms.
Nursing Implications for Montelukast
Premedication assessment. Obain and rrd baslin
vial signs, prfrm a rspirary assssmn and puls
ximry, and rviw pulmnary funin s rsuls.
Availability. PO: 10-mg abls; 4- and 5-mg hwabl
abls; 4-mg granuls.
Dosage and administration. Adult: PO: 10 mg akn
n daily in h vning. Dss grar han 10 mg
appar  b f n valu. Cninu hr hrapy fr
ashma as prsribd.
Pediatric age 2 to 5 years: PO: 4 mg n daily.
Pediatric age 6 to 14 years: PO: 5 mg n daily.
Medication Safety Alert
Serious neuropsychiatric events such as agitation, aggres-
sion, depression, sleep disturbances, suicidal thoughts and
behavior have been reported with the use of montelukast.
In patients with mild asthma or exercise-induced broncho-
constriction, the benets of montelukast may not outweigh
the risks of adverse events in some patients.
Common adverse effects
Gastrointestinal
Nausea, dyspepsia. Ths sympms ar usually mild
and disappar wih ninud hrapy. Enurag h
pain n  disninu hrapy wihu rs n-
suling h halhar prvidr. Adminisrain wih
fd r milk may hlp minimiz dismfr.
502 UNIT V Drugs Affecting the Respiratory System
Neurologic
Headache. This advrs ff is usually mild and
nds  rslv wih ninud hrapy. Enurag
h pain n  disninu hrapy wihu rs
nsuling h halhar prvidr.
Drug interactions. N linially signian drug inr-
ains hav bn rprd.
DRUG CLASS: PHOSPHODIESTERASE-4 INHIBITOR
roumilast (rō-FLŪ-mĭ-lăst)
Daliresp (dă-lĭ-RĔSP)
Actions
Inrallular yli adnsin mnphspha
(AMP) plays a ky rl in blking inammain in
many issus f h bdy. I is nrmally mablizd
by PDE-4, a ky nzym in lung issu. Rumilas
is a PDE-4 inhibir ha blks PDE-4 frm mab-
lizing AMP, allwing i  aumula and rdu
inammain.
Uses
Rumilas is usd  rdu h frquny f x-
arbains (ar-ups) f inammain (wih n-
squn nsriin f airways) in pains wih
hrni brnhiis and svr COPD. Rumilas is
n a brnhdilar and has n valu in h au
ramn f brnhspasms. I may b usd in n-
junin wih brnhdilars and risrids
in h vrall managmn f COPD. Rumilas is
nraindiad in pains wih svr livr impair-
mn (Child-Pugh lassiain B r C). Ths pa-
ins ar unabl  mabliz rumilas and xi
lvls may rsul.
Therapeutic Outcome
Th primary hrapui um xpd frm ru-
milas is fwr xarbains f COPD.
Nursing Implications for Roflumilast
Premedication assessment
1. Obain and rrd baslin vial signs, prfrm a
rspirary assssmn and puls ximry, and r-
viw pulmnary funin s rsuls.
2. Obain a hisry f bwl liminain parns and
any GI sympms, frquny f hadahs, dizzi-
nss, and faigu ha may b prsn bfr hrapy
is sard.
3. Rrd baslin daa n h lvl f dprssin, in-
smnia, and anxiy prsn.
4. Obain baslin wigh; shdul wkly wigh
masurmn.
Availability. PO: 250-, 500-mg abls.
Dosage and administration. PO: Iniially, 250 mg
n daily fr 4 wks  imprv lrabiliy. Th
aual hrapui mainnan ds is 500 mg n
daily wih r wihu fd.
Common adverse effects
Gastrointestinal
Dyspepsia, cramps, nausea, diarrhea. Ths advrs f-
fs ar usually mild and nd  rslv wih nin-
ud hrapy. Enurag h pain n  disninu
hrapy wihu rs nsuling h halhar prvidr.
Metabolic
Weight loss. Sm pains ls wigh (5%  10% f
bdy wigh) wih rumilas hrapy. Mnir pains
fr unxplaind r linially signian wigh lss.
Neurologic
Headache. This advrs ff is usually mild and
nds  rslv wih ninud hrapy. Enurag
h pain n  disninu hrapy wihu rs
nsuling h halhar prvidr.
Serious adverse effects
Psychiatric/neurologic
Insomnia, anxiety, depression. Pains and argivrs
shuld wah fr h mrgn r wrsning f in-
smnia, anxiy, dprssin, suiidal hughs, r h-
r md hangs. In linial rials, an inras in hs
sympms was rprd mr fn in hs pains
riving h drug mpard wih hs pains r-
iving a plab. Suiidal idain and bhavir hav
bn rprd.
Drug interactions
Drugs that enhance therapeutic and toxic ef-
fects. Ciprxain, knazl, uvxamin, and
imidin inras srum nnrains f rumi-
las. Mnir h pain lsly fr advrs ffs.
Drugs that reduce therapeutic effects. Rifampin, ph-
nbarbial, arbamazpin, and phnyin nhan
h mablism f rumilas. Mnir h frquny
f COPD xarbains as an indiain f hrapui
ff r lss f ff.
DRUG CLASS: IMMUNOMODULATOR AGENTS
benralizumab (ben-rah-LIZ-u-mab)
Fasenra (fa-SEN-rah)
dupilumab (doo PIL ue mab)
Dupixent (doo piks ent)
mepolizumab (me-pol-LIZ-u-mab)
Nucala (new-CAL-ah)
omalizumab (ō-mă-LĪZ-ū-măb)
Xolair (ZŌ- lār)
reslizumab (res-LIZ-u-mab)
Cinqair (sink-air)
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30 503

Actions ashma mdiins. Dupilumab, bnralizumab, and

Fiv immunmdulars ar usd in h managmn
f svr ashma  ahiv nrl in pains wh
hav faild sandard ramn: bnralizumab, dupi-
lumab, mplizumab, rslizumab, and malizumab.
Bnralizumab, mplizumab, and rslizumab ar hu-
manizd mnlnal anibdis ha bind  inrlu-
kin-5. Inrlukin-5 is rspnsibl fr h diffrnia-
in, maurain, rruimn, and aivain f human
sinphils. Whn binding  inrlukin-5, bnrali-
zumab, mplizumab, and rslizumab blk is bilgi
funin, rduing sinphili prduin and ain.
Th xa mhanism by whih hs immun mdula-
rs rdu au pisds f ashma is n knwn.
Dupilumab is a human mnlnal anibdy ha
inhibis inrlukin-4 and inrlukin-13. Whn binding
 inrlukin-4 and inrlukin-13, dupilumab blks
hir bilgi ain, rduing h ykin-indud in-
ammary rspnss. Th mhanism f dupilumab
ain in ashma has n bn dniivly sablishd.
Omalizumab, a DNA-drivd humanizd immun-
glbulin G mnlnal anibdy, binds  h irula-
ing immunglbulin E (IgE) anibdis in h bld,
drasing h numbr f IgE anibdis availabl 
bind  mas lls, hrby inhibiing h mas ll’s r-
las f hs inammary hmials ha an lad 
h sympms f ashma.
Uses
Dupilumab, bnralizumab, mplizumab, and rsli-
zumab ar usd wih hr ashma mdiins fr h
mainnan ramn f svr sinphili ashma.
Whn addd  hr mdiins fr ashma, hs im-
munmdulars hlp prvn svr ashma aaks
(xarbains) and an imprv brahing in pa-
ins whs ashma is n nrlld wih h urrn
mplizumab ar usd in pains agd 12 yars and
ldr and rslizumab in pains 18 yars and ldr.
Omalizumab is usd in pains wh ar a las 12
yars ld, hav mdra  svr prsisn ashma,
hav a psiiv skin rain  a prnnial airbrn
allrgn, and hav sympms ha ar n adqualy
nrlld wih inhald risrids. Omalizumab
drass h inidn f ashma xarbains in
hs pains.
Immunmdulars d n sp au xarba-
ins f ashma and shuld n b usd  ra au
brnhspasm r saus ashmaius. Pains shuld
b unsld ha i may ak a fw wks bfr h
immunmdular has a niabl ff n hir
ashma, s i is impran ha hy ninu aking
all hr ashma mdiins unlss hrwis insru-
d by hir halhar prvidr. Sysmi r inhald
risrids shuld n b abruply disninud
whn an immunmdular is iniiad. Rduins
in risrid dsag shuld b vry gradual and
dn nly undr h suprvisin f a halhar
prvidr.
Dupilumab is als apprvd fr us in raing md-
ra  svr api drmaiis in aduls and hildrn
6 yars and ldr whs illnss is n adqualy n-
rlld wih pial prsripin hrapis. Dupilumab
is als usd  ra hrni rhinsinusiis in h prs-
n f nasal plypsis.
Therapeutic Outcome
Th primary hrapui um assiad wih im-
munmdular agns is rdud frquny f au
ashmai xarbains. Th primary hrapui u-
ms fr dupilumab is als  nrl api drmai-
is and hrni rhinsinusiis.

Table 30.12 Immunomodulator Agents

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE
benralizumab Fasenra Subcutaneous: 30 mg/mL in 1 mL Twelve years old and older:
prelled syringe or auto-injector Subcutaneous: 30 mg every 4 wk for 3 doses,
then q8wk
dupilumab Dupixent Subcutaneous: 200 mg/1.14 mL and Twelve years old and older: Subcutaneous: Initially,
300 mg/2 mL prelled syringe or 400–600 mg
autoinjector Maintenance, 200 mg or 300 mg once every other
week
mepolizumab Nucala Subcutaneous: 100-mg single-use Twelve years old and older: Subcutaneous: 100 mg
vials in powder form; 100 mg/mL q4wk into the upper arm, thigh, or abdomen
in prelled syringe and autoinjector
omalizumab Xolair Subcutaneous: 150-mg single-use Twelve years old and older: Subcutaneous:
vials in powder form; 75 mg/0.5 150–375 mg q2–4wk, based on patient weight
mL and 150 mg/mL prelled and immunoglobulin E serum level
syringe Doses of more than 150 mg (1.2 mL) should be
divided and administered at more than one site
reslizumab Cinqair Intravenous: 100 mg/10 mL solution Twelve years and older: Intravenous infusion:
in single-use vials 3-mg/kg infusion over 20–50 min q4wk
504 UNIT V Drugs Affecting the Respiratory System
Nursing Implications for Immunomodulator
Agents
Premedication assessment
1. Rviw h pain’s mdiain hisry  nsur
ha h pain ds n hav an allrgy  any im-
munmdular agns. If h pain ds, infrm
h harg nurs and h halhar prvidr imm-
dialy. D n adminisr h mdiain wihu
spi apprval.
2. Rviw h pain’s mdial hisry  nsur ha
h pain has psiiv skin rains  a las n
airbrn allrgn r has bn diagnsd wih sin-
phili ashma.
3. Bfr adminisring h rs ds f malizumab,
nsur ha srum IgE lvls hav bn masurd;
his hlps drmin h ds f h malizumab
 b adminisrd. Afr adminisrain f mali-
zumab, srum al IgE lvls bm lvad b-
aus f h frmain f malizumab-IgE mplx-
s. Furhr masurmn f srum IgE lvls is n
nssary.
4. Obain and rrd baslin vial signs, prfrm a
rspirary assssmn and puls ximry and r-
viw pulmnary funin s rsuls.
Availability and dosage. S Tabl 30.12
Preparation and administration. Eah f h immu-
nmdulars has vry spi insruins n hw
h prdu shuld b srd (rfrigrad), warmd
 rm mpraur and mixd bfr injin, h
impran f NOT SHAKING  disslv h pw-
dr, h lr f h nal sluin and siz f ndl
 b usd fr mixing and fr injin. S h manu-
faurr’s insruins fr h spi prdu ha has
bn prsribd.
Medication Safety Alert
Allergic reactions and anaphylaxis have occurred within
hours of administration of dupilumab, benralizumab, mepo-
lizumab, omalizumab, and reslizumab. Symptoms include
urticaria and throat or tongue edema. Patients should be ob-
served after administration of benralizumab, dupilumab, me-
polizumab, omalizumab, or reslizumab, and medications for
the treatment of allergic reactions (e.g., oxygen, epinephrine,
diphenhydramine) should be readily available.
Common and serious adverse effects
Hypersensitivity
Injection site reactions. Th ms mmnly r-
prd advrs ff fr dupilumab, bnralizumab,
mplizumab, and malizumab is injin si ra-
in, inluding bruising, rdnss, warmh, burning,
singing, ihing, hiv frmain, pain, indurains,
mass, and inammain. Ms injin si rains
ur wihin 1 hur afr injin, las lss han 8 days,
and gnrally dras in frquny wih subsqun
dsing. Immdialy rpr a rash r prurius, wih r
wihu fvr, and wihhld addiinal injins unil
apprvd by h halhar prvidr.
Musculoskeletal. Infusin f rslizumab was assi-
ad wih rpharyngal pain, hs pain, nk pain,
musl spasms, xrmiy pain, musl faigu, and
musulsklal pain.
Dupilumab was assiad wih rpharyngal pain.
Drug interactions. N drug inrains hav bn r-
prd wih bnralizumab, mplizumab, malizum-
ab, and rslizumab.
Dupilumab may nhan h advrs r xi ffs
f liv vains. Assur ha h pain’s vain shd-
ul is urrn bfr iniiaing hrapy wih dupilumab.
 Drugs Used to Treat Lower Respiratory Disease CHAPTER 30 505

Clinical Judgment And Next-Generation Nclex ® Examination-Style Questions

Key Points 1. During the respiratory assessment of the patient in the scenario
who was admitted to the hospital, the nurse noted the patient
• Chronic obstructive pulmonary diseases, also known was coughing frequently and appeared to have difculty beathing.
as chronic airow limitation diseases, include chronic Which of the following should be included in the respiratory
bronchitis and emphysema, both of which are progressive, assessment? (Select all that apply.)
irreversible diseases that usually cause death after a long
debilitating illness. 1. Observe the patient’s general appearance
2. Determine the nutrition status of the patient
• Asthma is an inammatory disease that has airow
3. Observe the patient’s degree of respiratory impairment
limitations; however, the episodes are intermittent and the
4. Inquire about the patient’s activity tolerance
limitations are reversible.
5. Take and record baseline vital signs
• Regular use of preventive medicine and removal of triggers 6. Determine whether there is any loss of hearing
such as allergens are key to the long-term treatment of 7. Take and record pulse oximetry level
asthma. 8. Auscultate the patient’s lung elds
• Medications used for lower respiratory diseases include
Objective: Discuss nursing assessments used to evaluate the
inhaled bronchodilators from the drug classes of beta-
respiratory status of a patient.
adrenergic agonists, anticholinergic agents, and inhaled
NCLEX item type: Extended multiple response
corticosteroids and combinations of these drugs. Oral
Cognitive skill: Evaluate cues
medications such as antileukotrienes, phosphodiesterase-4
inhibitors, and immunomodulators are also used. 2. During the evaluation of the patient in the scenario who was
• Emphasize taking medications before exposure to admitted to the hospital complaining of shortness of breath and
a suspected trigger of an attack; treat all respiratory increased sputum production, the nurse asks the patient for
infections early. further information by which of the following statements? (Select
• Regular use of a peak owmeter and appropriate use of an all that apply.)
inhaler are integral to treating asthma successfully. 1. “Tell me about your cough. Does it wake you at night?”
• Nurses can teach patients with irreversible chronic airow 2. “What activities would you say make you short of
disorders techniques to manage their symptoms (e.g., breath?”
adequate uid intake to decrease secretion viscosity, 3. “When you cough up sputum, what color is it?”
breathing techniques, exercise conditioning to strengthen 4. “Is there anyone at home to help you?”
respiratory muscles, controlled coughing, positioning). 5. “Have you had any constipation or diarrhea recently?”
• Nurses can play a signicant role in public education Objective: Discuss nursing assessments used to evaluate the
efforts, monitoring for nonadherence and encouraging respiratory status of a patient.
patients to make changes in lifestyle to reduce the severity NCLEX item type: Multiple response
of chronic obstructive pulmonary diseases. Cognitive skill: Application
• Nurses can help the patient and/or family identify
community resources available in the immediate vicinity. 3. The nurse explained to the patient in the scenario how the various
medications worked to provide symptomatic relief of COPD.
Indicate with an X the mechanism of action for each type of
Additional Learning Resources medication.
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa- MECHANISM MUCOLYTIC
tions, and other learning activities to help you master this chap- OF ACTION EXPECTORANTS ANTITUSSIVES AGENTS
ter content. Stimulates
an increase
Go to your Evolve website (https://evolve.elsevier.com/Willihng in bronchial
anz) for additional online resources. gland
secretions
Clinical Judgment and Next-Generation NCLEX® Examina-
tion-Style Questions The following questions are typical of the Hydrate
NCLEX exam and include both NGN (Next Generation) and tra- respiratory
ditional questions. For Chapters 1 and beyond the use of case secretions
studies will be employed to further develop clinical judgment. Dissolves
thick, sticky
mucus
Scenario
Numbs the
A patient with severe COPD arrived at the u clinic to receive the respiratory
annual inuenza vaccination. The nurse noted that the patient stretch
had difculty talking with frequent pauses between words sensors
to take a breath, was difcult to understand and appeared
dyspneic and uncomfortable.
506 UNIT V Drugs Affecting the Respiratory System
MECHANISM MUCOLYTIC
OF ACTION EXPECTORANTS ANTITUSSIVES AGENTS
Suppress
the cough
center in the
brain
Objective: Distinguish the mechanisms of action of expectorants,
antitussives, and mucolytic agents.
NCLEX item type: Matrix
Cognitive skill: Recognize cues
4. The nurse is preparing to administer the beta-adrenergic
bronchodilator albuterol but rst performs which of the following
preassessments on the patient? (Select all that apply.)
1. Checks liver function test results
2. Checks for a history of glaucoma
3. Performs an assessment of the baseline mental status
(level of anxiety, nervousness, alertness)
4. Asks about concurrent use of antihistamines or nasal
decongestants
5. Checks for history of diabetes mellitus
6. Assesses for the presence of palpitations and
dysrhythmias
7. Checks for history of peptic ulcer disease
8. Obtains baseline vital signs and pulse oximetry
Objective: Describe the nursing assessments needed to monitor
therapeutic response and the development of adverse effects from
beta-adrenergic bronchodilator therapy.
NCLEX item type: Extended multiple response
Cognitive skill: Recognize cues
5. The nurse instructing the patient in the scenario on the drug
tiotropium bromide (Spiriva), which was being started instead
of continuing ipratropium bromide (Atrovent), realized further
teaching was needed after the patient made which statement?
1. “As I understand it, the effects of Spiriva last much longer
than Atrovent so I only have to take it once a day.”
2. “This drug is used to treat an acute attack, like a rescue
drug.”
3. “I can follow the instructions on the package for how to
use this drug.”
4. “When I take this drug, I should notice a reduced amount
of wheezing and easier breathing.”
Objective: Discuss the nursing assessments needed to monitor
therapeutic response and the development of adverse effects from
anticholinergic bronchodilator therapy.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
6. The nurse instructing a patient on the corticosteroid inhalant
budesonide (Pulmicort) realized further teaching was needed after
the patient made which statement?
1. “This drug is used to treat an acute attack, like a rescue
drug.”
2. “You mentioned that this may cause hoarseness and dry
mouth.”
3. “I understand I need to rinse my mouth after taking this
drug so I do not get any oral fungus infection like thrush.”
4. “I know that I need to use my bronchodilator before I use
this med so that I get the full therapeutic benet.”
Objective: Discuss the nursing assessments needed to monitor
therapeutic response and the development of adverse effects from
corticosteroid inhalant therapy.
NCLEX item type: Multiple response
Cognitive skill: Recognize cues
Unit VI Drugs Affecting the Digestive System
Drugs Used to Treat Oral Disorders
Objectives
1. Explain common oral disorders and their treatments.
Key Terms
cold sores (fever blisters) (KŌLD mucositis (myū-kō-SĪ-tĭs) (p. 508)
SŌRZ) (p. 507) plaque (PLĂK) (p. 508)
canker sores (KĂN-kĕr SŌRZ) (p. 507) dental caries (DĔN-tŭl KĂR-ēz) (p. 508)
candidiasis (kăn-dĭ-DĪ-ă-sĭs) (p. 508) tartar (TĂR-tĕr) (p. 508)
ORAL ANATOMY
The mouth, or oral cavity, is the beginning of the diges-
tive tract and contains all the essential structures needed
to consume food and drink to feed the body. The mouth
consists of the upper and lower lips, which are outside
the oral cavity, as well as the jaw bone, tongue, pharynx,
teeth (including the surrounding gums), cheeks (mucous
membranes inside the mouth), hard and soft palate (the
roof of the mouth), uvula, and tonsils. Salivary glands are
also part of the oral cavity; they produce saliva to lubri-
cate the oral cavity and provide enzymes secreted during
eating to help aid digesting of food (Fig. 31.1).
MOUTH DISORDERS
Common disorders affecting the mouth are cold sores
on the lip; canker sores and candidal infections of soft
tissues of the tongue, cheeks, and gums; and plaque
and calculus affecting the gums and teeth. Xerostomia,
or lack of saliva, originates from nonoral causes.
Halitosis can arise from oral or nonoral diseases. A
much less common problem, but one that causes sig-
nicant discomfort, is oral mucositis.
Cold sores (fever blisters) are caused by the herpes
simplex type 1 virus (herpes simplex labialis) and are
most commonly found at the junction of the mucous
membrane and the skin of the lips or nostrils, although
they can occur inside the mouth, especially affecting
the gums and hard and soft palate. It is estimated that
at least half of all Americans ages 20 to 40 years have
had cold sores. Most were infected before age 5 years.
About half of patients will develop recurrent outbreaks
of the lesions, often in the same location, separated by
31
https://evolve.elsevier.com/Willihnganz
2. Identify nursing assessments and interventions associated
with treatment of mucositis.
gingivitis (jĭn-jĭ-VĪ-tĭs) (p. 508)
halitosis (hăl-ĭ-TŌ-sĭs) (p. 508)
xerostomia (zĕr-ŏ-STŌ-mē-ă) (p. 509)
dentifrices (DĔN-tĭ-frĭs-ĕz) (p. 512)
latent periods. The recurrence rate and extent of lesions
are highly variable. Patients often predict when an out-
break may occur because of predisposing factors, such
as systemic illnesses accompanied by fever or cold
such as inuenza (hence the names fever blisters and
cold sores) or by menstruation, extreme physical stress
and fatigue, or sun and wind exposure. Chemotherapy
or radiation therapy that depresses the immune sys-
tem also triggers cold sores.
Patients often report that a are-up of the sores is pre-
ceded by a prodrome of burning, itching, and/or numb-
ness in the area where the lesion develops. The lesions
rst become visible as small, red papules that develop
into uid-lled vesicles (blisters) 1 to 3 mm in diameter.
Smaller lesions often coalesce into larger lesions. Pain
is intense, fever may be present, and increased saliva-
tion and mouth odor occur. Often, the lymph nodes in
the neck are swollen because of the body’s response to
infection. Over the next 10 to 14 days, a crust develops
over the top of many coalesced, burst vesicles; the base
is erythematous. The liquid from the vesicles contains
live virus that is contagious if transferred to other peo-
ple by direct contact (e.g., kissing). If pus develops in the
vesicles or under the crust of a cold sore, a secondary
bacterial infection may be present and should be evalu-
ated for antibiotic therapy.
Canker sores, also known as recurrent aphthous sto-
matitis, affect 20% to 50% of people in the United States.
The exact cause is unknown, but precipitating factors
appear to be stress and local trauma (e.g., chemical ir-
ritation, toothbrush abrasion, irritation from orthodon-
tic braces, biting the inside of the cheeks or lips). The
lesions are not viral infections, as was once thought,
507
508 UNIT VI Drugs Affecting the Digestive System
Upper lip
Gingivae (gums)
Upper central
incisor Canine (cuspid)
Premolar
Hard palate
(bicuspid)
Soft palate Molar
Palatoglossal arch
Fauces
Uvula
Palatine tonsil
Tongue (undersize)
Lingual frenulum
Sublingual fold
Opening
of sublingual Opening of
ducts submandibular
gland
Fig. 31.1 The oral cavity. (From VanMeter KC, Hubert RJ. Gould’s
Pathophysiology for the Health Professions. 5th ed. St. Louis:
Saunders; 2015.)
and they are not contagious. There appears to be a
familial factor as well as nutritional, emotional, and
physiologic factors. They can develop at any age and
affect both sexes in equal numbers. Canker sores affect
the softer parts of the mouth that move, such as the
tongue, soft palate, cheeks, and lips. The lesion is usu-
ally gray to whitish yellow, with an erythematous halo
of inamed tissue surrounding the ulcer crater. There
are three forms. The most common form is minor aph-
thous stomatitis. The sores are usually small (less than
1 cm in diameter) and heal within 7 to 14 days. The
second form is major aphthous stomatitis. This form
is more severe with sores more than 1 cm in diameter
and may last 2 or more weeks. They can be extremely
painful. The third form is herpetiform aphthous sto-
matitis. This form is uncommon, occurring as clusters
of very small ulcers (less than 1 mm in some cases) that
sometimes merge together to form larger ulcers.
Candidiasis is a fungal infection caused by Candida
albicans, the most common organism associated with
oral infections. It is often called “the disease of the
diseased” because it appears in debilitated patients
and patients taking a variety of medicines. The most
common predisposing factors are physiologic (e.g.,
early infancy, pregnancy, old age), diabetes mellitus,
malnutrition, malignancies, and radiation therapy.
Medicines that predispose a patient to candidiasis
are those that depress defense mechanisms (e.g., im-
munosuppressants, corticosteroids, cytotoxics, broad-
spectrum antibiotics) and those that cause xerostomia
(e.g., anticholinergics, antidepressants, antipsychotics,
antihypertensives, antihistamines).
There are several forms of candidiasis, but the
most common is the acute pseudomembranous form
that is often referred to as thrush. It is characterized
by white, milk curd–appearing plaques attached to
the oral mucosa. These plaques usually can be easily
detached, and erythematous, bleeding, sore areas ap-
pear beneath them. Thrush is most common in infants,
pregnant women, and debilitated patients. Treatment
requires local or systemic therapy with antifungal
agents, such as nystatin (Mycostatin) suspension or
clotrimazole lozenges (see discussion of antifungal
agents in Chapter 45).
Mucositis (once called stomatitis) is a general term
used to describe a painful inammation of the mucous
membranes of the mouth. It is commonly associated
with chemotherapy and radiation therapy in the head
and neck area. Both therapies target rapidly divid-
ing cancer cells, but also affect normal healthy cells
that rapidly turnover, such as those lining the mouth.
Mucositis develops 5 to 10 days after antineoplas-
tic therapy and usually develops after the rst 2 to 3
weeks of radiation therapy targeted in the head and
neck region. The sores are erythematous ulcerations
intermixed with white, patchy mucous membranes.
Candidal infections are often present.
Several scales and criteria are commonly used to
standardize the evaluation of mucositis and its ther-
apy. These include the World Health Organization
Oral Mucositis Scale (Table 31.1), the Oral Assessment
Guide, the Oral Mucositis Index, the Oral Mucositis
Assessment Scale, and various visual analog scales. Of
the many oral assessment tools available, there is no
standard scale—all the scales are used to try to deter-
mine the degree of pain and ulceration. Severe mucosi-
tis can affect the patient’s quality of life (QoL) because
it is typically very painful and can be highly debilitat-
ing. It can cause difculty in speaking and swallowing,
as well as pain that prevents eating or drinking, result-
ing in weight loss, anorexia, malnutrition, anemia, and
fatigue.
Plaque is the primary cause of most tooth, gum (gin-
giva), and periodontal disease. Plaque, the whitish yel-
low substance that builds up on teeth and gum lines
around the teeth, is thought to originate from saliva.
Plaque forms a sticky meshwork that traps bacteria
and food particles. If not removed regularly, it thickens
and bacteria proliferate. The bacteria secrete acids that
eat into the enamel of teeth, causing dental caries (cavi-
ties). If the plaque is not removed within 24 hours, it
begins to calcify, forming calculus or tartar The calcu-
lus forms a foundation for additional plaque to form,
eventually eroding under the gum line and causing in-
ammation (gingivitis) and periodontal disease.
Halitosis is the term used to describe a very foul
mouth odor. A temporary foul odor at certain times
is normal in healthy individuals, such as “morning
breath” or after eating certain foods (e.g., garlic, on-
ions). Halitosis can also signify an underlying patho-
logic condition. Halitosis comes from oral and nonoral
sources. Nonoral causes of halitosis include sinus-
itis, tonsillitis, and rhinitis; pulmonary diseases such
as tuberculosis or bronchiectasis; and elimination of
chemicals from the blood, such as acetone exhaled by

World Health Organization Oral Mucositis
Table 31.1 Scale
GRADE CLINICAL FEATURES
0 No mucositis present
1 Oral soreness with erythema
2 Oral erythema, ulcers, solid diet tolerated
3 Oral ulcers, liquid diet tolerated
4 Oral feeding not possible
From Sonis ST, Elting LS, Keefe D, etal. Perspectives on cancer therapy
induced mucosal injury: pathogenesis, measurement, epidemiology, and
consequences for patients. Cancer. 2004;100(9 suppl):19952025.
patients with diabetic ketoacidosis. Paraldehyde and
dimethyl sulfoxide are two medicinal agents excreted
primarily through the lungs that leave a characteristic
foul odor to the breath. “Smoker’s breath” caused by
cigarette smoking is a fairly common cause of halito-
sis. Oral causes of halitosis include decaying food par-
ticles, plaque-coated tongue and teeth, dental caries,
poor oral or denture hygiene, periodontal disease, and
xerostomia.
Xerostomia is a condition in which the ow of saliva
is either partially or completely stopped. About 20%
of those older than 65 years report a change in con-
sistency, decrease in production, or discontinuation
of salivary ow. Xerostomia causes loss of taste, dif-
culty in chewing and swallowing food, and difculty
in talking, and it increases tooth decay. Xerostomia can
also cause a burning sensation of the tongue, cause
mucositis, and reduce how long dentures can be worn
each day. The most common causes of xerostomia are
medicines (e.g., anticholinergic agents, diuretics, anti-
depressants, certain antihypertensive agents), diseases
(e.g., diabetes mellitus, depression), and functional
conditions (e.g., smoking, mouth breathing).
Life Span Considerations
Salivary Flow
About 20% of people older than 65 years report a change
in consistency, decrease in production, or discontinuation of
salivary ow. The most common causes of xerostomia are
medicines such as anticholinergic agents, diuretics, and anti
depressants and certain antihypertensive medicines.
DRUG THERAPY FOR MOUTH
DISORDERS
COLD SORES
The goals of treatment are to control discomfort, allow
healing, prevent spread to others, and prevent compli-
cations. The cold sore should be kept moist to prevent
drying and cracking that may make it more susceptible
to secondary bacterial infection. Docosanol (Abreva) is
the only over-the-counter agent approved by the US
Food and Drug Administration that is clinically proven
Drugs Used to Treat Oral Disorders CHAPTER 31 509
to shorten healing time and the duration of symptoms
such as tingling, pain, burning, and itching. Docosanol
is a saturated aliphatic alcohol with antiviral activity.
It prevents viral entry and replication at the cellular
level. It must be applied ve times daily starting at the
rst sign of outbreak (e.g., tingling, redness, itching).
Besides docosanol, acyclovir (oral or topical), famciclo-
vir (oral), penciclovir (topical), and valacyclovir (oral)
are available by prescription. Local anesthetics (e.g.,
benzocaine, dibucaine, lidocaine) in emollient creams,
petrolatum, gel, liquid or protectants (e.g., Anbesol
[benzocaine 10%]) can temporarily relieve the pain and
itching and prevent drying of the lesion.
Topical analgesics (e.g., Campho-Phenique [cam-
phor, phenol, eucalyptus oil, glycerin, light mineral
oil]) are safe and effective for temporarily reducing
pain. Oral analgesics (e.g., aspirin, acetaminophen,
ibuprofen, naproxen) may also provide signicant
pain relief. Broad-brimmed hats and ultraviolet
blockers (e.g., ChapStick Moisturizer [sun protection
factor (SPF) 15], Natural Ice [SPF 15]) with an SPF of
at least 8 to 15 can be used for patients whose cold
sores occur with sun exposure. Secondary infections
can be treated with a topical antibiotic ointment such
as Neosporin.
CANKER SORES
The goals of treatment are similar to those for cold
sores: to control discomfort and promote healing.
Topical anesthetics to control discomfort, such as
benzocaine (Kank-A Mouth Pain [benzocaine 20% in
oral mucosal protectant]), are particularly effective if
applied just before eating or performing oral hygiene.
Oral analgesics (e.g., aspirin, acetaminophen, ibu-
profen, naproxen) may also provide signicant pain
relief. Aspirin should not be placed on the lesions be-
cause of the high risk of severe chemical burns with
necrosis.
Oxygen-releasing agents (carbamide peroxide [Gly
Oxide], hydrogen peroxide [alcohol-free, Peroxyl
Mouth Sore Rinse]) can be used as debriding and
cleansing agents up to four times daily for 7 days. The
product should not be swallowed. Long-term safety
has not been established, and tissue irritation and
black hairy tongue have been reported. Black hairy
tongue is usually a temporary, harmless condition
and usually resolves by eliminating possible causes
or contributing factors and practicing good oral hy-
giene. Saline rinses (1 to 3 teaspoons of table salt in 4
to 8 ounces of warm tap water) may be soothing and
can be used before topical application of medication.
Sustained use of products containing menthol, phenol,
camphor, and eugenol should be discouraged because
they cause tissue irritation and damage or systemic
toxicity if overused. Silver nitrate should not be used
to cauterize lesions because it may damage healthy tis-
sue surrounding the lesion and predispose the area to
later infection.
510 UNIT VI Drugs Affecting the Digestive System
MUCOSITIS
Treatment of chemotherapy- or radiation-induced mu-
cositis begins with patient education, reinforcing the
importance of good oral care throughout cancer treat-
ment. Before cancer therapy, a baseline pretreatment
oral mucosal assessment should be completed to rule
out preexisting conditions or infections that might ag-
gravate impending mucositis. Although it takes 5 to
10 days for mucositis to develop after a patient begins
chemotherapy or 2 to 3 weeks after a patient begins
radiation therapy, oral hygiene regimens should be
started when chemotherapy or radiation therapy is
initiated. The mainstays of an effective oral care regi-
men include alcohol-free mouth rinses, articial saliva
solutions, tooth brushing, ossing, and denture care.
Mouth rinses are used before and after meals and
at bedtime to remove debris, keeping the oral tissue
moist and healthy. Teeth should be brushed two to
three times daily after eating using a soft bristle brush.
Keeping lips and mouth moisturized by sucking on ice
chips or chewing sugarless gum or an articial saliva
solution can also help.
Pain associated with oral mucositis can be a ma-
jor complication that contributes to poor nutrition
and hydration. To be effective, topical applications
of medications for pain must come into contact with
the tissue. Therefore it is advisable to schedule these
routines before cleaning the oral cavity. In addition to
the previously described protectants, local anesthetics,
and analgesics, the following are routine approaches to
treating pain in the oral area:
• Viscous lidocaine 2% can be used before meals to
relieve pain. Frequent applications are required,
and the sense of taste is diminished. Care must be
taken to make sure the patient is not burned by the
food because the entire mouth and throat are anes-
thetized. The gag reex may also be anesthetized,
allowing for the potential to choke on food. Proper
positioning while eating is important to prevent
choking.
• Milk of magnesia can be used to rinse the mouth
and coat the mucous membranes.
• Nystatin liquid suspension can be swished in the
mouth for 1 minute and then swallowed (“swish
and swallow” routine), or clotrimazole lozenges
may be dissolved slowly in the mouth and then
swallowed to reduce candidal oral infections.
• Mucosal protectants, such as Gelclair or Orabase,
work by coating the mucosa, forming a protective
barrier shielding oral lesions from the effect of food
and liquids.
• Sucralfate suspensions applied topically have been
reported to provide effective pain relief.
• Oral or parenteral analgesics (e.g., morphine)
should be administered for severe pain.
• Palifermin (Kepivance)—recombinant human kera-
tinocyte growth factor—has been approved speci-
cally for stimulating epithelial cell proliferation to
prevent or treat the mucositis that develops in he-
matologic malignancies in patients undergoing che-
motherapy before bone marrow transplantation.
PLAQUE
Plaque is controlled by brushing teeth, ossing be-
tween teeth, and using mouthwashes. If plaque is
removed regularly, calculus will not form. Using a
dentifrice (toothpaste) and ossing between teeth
help remove dental plaque and stain, resulting in less
halitosis and periodontal disease and fewer dental car-
ies. Other devices, such as oral irrigators (Waterpik),
sponge-tipped applicators, or electric toothbrushes,
can be used for patients who wear orthodontic appli-
ances, are physically or mentally handicapped, or lack
manual dexterity and require someone else to clean
their teeth. Therapeutic mouthwashes also help reduce
plaque accumulated above the gum line.
HALITOSIS
Halitosis is treated most easily by eliminating the
causes, such as smoking and certain foods. Regularly
brushing the teeth or dentures and using dental oss
between teeth can remove particles of decaying food.
Mouthwashes and breath mints can mask halitosis but
usually last less than 1 hour. If halitosis is persistent
and has no readily identiable cause such as smoking
or diet, a dentist should be consulted for a thorough
examination to ensure that no other pathologic condi-
tion is the underlying cause.
XEROSTOMIA
Xerostomia is treated by changing the medicines that
cause dry mouth or with articial saliva. Articial sa-
liva products do not stimulate natural saliva produc-
tion, but mimic the viscosity, mineral content, and
taste. Patients with xerostomia should be seen by a
dentist regularly to help avoid additional dental caries
and ensure proper denture t to prevent gum irrita-
tion. Commercially available saliva substitutes include
Mouth Kote, Biotène, Aquoral, and Caphosol. All are
available as sprays for easy administration.
NURSING IMPLICATIONS FOR ORAL HEALTH
THERAPY
Assessment
Drug history. Obtain a history of recent drug therapy.
Some drugs, such as phenytoin (Dilantin), may cause
alterations in the gums, and oral mucositis is common
after chemotherapy and radiation therapy.
Dental history
• Obtain a dental history that includes frequency of
visits to the dentist and a brief summary of dental
procedures that have been performed within the
past 1 to 3 years.
• Ask about usual hygiene practices, such as number
of times per day brushing or ossing is done, type

of toothbrush used, and oral products used (e.g.,
toothpaste, mouthwashes).
• Ask about tobacco and alcohol use, frequency, and
amounts.
• Ask about any difculty chewing, swallowing, or
speaking.
• Ask about any recent changes in the taste of foods
or alterations within the mouth, such as burning or
tingling.
Oral cavity
• Put on gloves and inspect the oral cavity with the
aid of a ashlight and tongue blade. Visually inspect
the mucous membranes covering the lips, hard and
soft palates, gums, tongue, pharynx, and teeth.
• Note the color of the mucous membranes and the
moisture present.
• Inspect the mucous membranes for inamed or re-
ceding gums, ulcerations, crusts, changes in color
(e.g., white patches), and sores from poorly tting
dentures. Inquire how well the dentures t and how
long each day they are worn. Assess for the pres-
ence of teeth, dental caries, and plaque.
• Observe the amount and consistency of the saliva
present.
• Note the presence or absence of halitosis. Its pres-
ence may indicate poor dental hygiene practices or
an oral infection. Some odors occur from a variety
of causes (e.g., garlic, smoking, ingestion of alcohol)
and some from systemic diseases (e.g., acetone from
diabetes, ammonia from liver disease).
• Biopsy of the soft tissues of the oral cavity may be
completed to conrm diagnosis of the oral lesion.
Implementation
• Develop a schedule for oral hygiene measures to
be performed consistent with type and severity of
mouth disorder.
• Make necessary referrals to the dentist, especially
before starting chemotherapy.
• Order prescribed oral hygiene supplies and medica-
tions; list medications used as rinses or “swish and
swallows” in the medication administration record.
• Develop a teaching plan to promote maintaining
a healthy oral cavity and promote daily hygienic
practices.
Cold sores
• Patients who develop cold sores should be taught that
the lesions are common and may occur at any time
from childhood into adulthood. The cold sores are also
contagious when an active lesion is present. Teach the
patient to avoid contaminating other individuals.
• Cold sores should be kept clean by gentle washing
with mild soap solutions. Cold sores should be kept
moist to prevent drying and cracking. Cracking may
render the cold sore more susceptible to second-
ary bacterial infection, delay healing, and increase
Drugs Used to Treat Oral Disorders CHAPTER 31 511
discomfort. Therefore highly astringent products
(e.g., tannic acid, zinc sulfate) should be avoided.
• Apply docosanol (Abreva), local anesthetics, and ul-
traviolet blockers or oral analgesics as prescribed.
• When secondary infections are present, apply topi-
cal antibiotic ointment to the cold sore.
Canker sores
• Apply topical anesthetics before the patient eats or
performs oral hygiene.
• Apply amlexanox (Aphthasol) after meals and oral
hygiene, four times daily.
• Administer oral analgesics; apply oxygen-releasing
agents for (carbamide peroxide, hydrogen peroxide)
debridement and cleansing agents at appropriate
intervals.
• Saline rinses using 1 to 3 teaspoons of table salt
dissolved in 4 to 8 ounces of warm tap water may
be soothing and can be used before topical medica-
tions are applied.
• Changes in diet can also reduce irritation to the sores.
Avoid sharp-edged foods, such as potato chips and
crackers, and spicy foods, pineapple, citrus fruits,
and chocolate. Drinking acidic juices and soft drinks
through a straw can minimize contact and irritation.
Mucositis. Oral hygiene regimens should be started
at the time of chemotherapy or radiation therapy.
Oral hygiene should include a soft-bristled brush, a
Waterpik on low setting, or a sponge-tipped applicator
(in the case of severe lesions). With advanced lesions,
pain and discomfort may be severe and other devices,
such as a gravity ow irrigating system or an oral sy-
ringe, may be helpful.
Commercially prepared mouthwashes containing
alcohol are usually not recommended because they dry
and irritate the mouth rather than relieve symptoms
of mucositis. Alternative preparations for oral hygiene
solutions are 1 tablespoon of salt or ½ teaspoon of bak-
ing soda in 8 ounces of water or 1.5% to 6% solutions
of hydrogen peroxide as a mouthwash. Although each
of these solutions has disadvantages, they remain the
standard for irrigating solutions.
The frequency of oral irrigations is important.
Irrigations should be performed immediately before
and after meals and at bedtime if symptoms are mild.
With moderate lesions, increase the frequency to every
2 hours. In patients with severe symptoms, the mouth
may be rinsed hourly. When fungal infections are pres-
ent, the cleansing regimen should be performed imme-
diately before administering the topical agents (e.g.,
nystatin liquids as a “swish and swallow” or clotrima-
zole lozenges). Performing the cleansing routine im-
mediately before the medication is given will improve
the contact of the medicine with the denuded surface
of the oral mucosa. Caution the patient not to take food
or drink for approximately 15 minutes after the medi-
cation has been given.
512 UNIT VI Drugs Affecting the Digestive System
Mouth dryness can be relieved by chewing gum
and sucking on ice chips or ice pops. Dry lips can be
coated with cocoa butter, K-Y jelly, petroleum jelly, or
lip balm. Articial saliva is available.
Administer pain preparations according to pre-
scribed routines using viscous lidocaine 2% or milk of
magnesia rinses, nystatin liquid as a “swish and swal-
low,” or sucralfate suspension topically. Use oral or
parenteral analgesics for severe pain.
Plaque. Perform toothbrushing and dental ossing
and use mouthwashes on a scheduled basis daily to
prevent plaque.
Halitosis. Brushing dentures and teeth regularly and
using dental oss can remove particles of decaying
food. Mouthwashes and breath mints can mask halito-
sis but usually last less than 1 hour.
Xerostomia. Monitor the medication routine, report
xerostomia to the healthcare provider, and use articial
saliva if prescribed.
Dentures. Dentures should be cleaned each time oral
hygiene is performed. For neutropenic patients, den-
tures should be worn only for eating. Poorly tting
dentures must be repaired to prevent further tissue
breakdown.
Patient Education
• Teach the patient proper cleansing techniques for
oral hygiene consistent with the conditions present
(e.g., normal healthy tissue, mucositis, jaw wiring).
• Instruct patients who are to receive radiation or
chemotherapy to start oral hygiene on a scheduled
regimen immediately rather than waiting until mu-
cositis develops.
• Teach the patient with pain the proper use of pre-
scribed analgesics and comfort measures.
• Discuss dietary practices that may relieve symp-
toms, such as bland foods. For dry mouth, instruct
the person to use gravies or sauces to moisten foods.
When mucous membranes are irritated, suggest
avoiding hot and spicy foods, alcohol, and tobacco.
• Persistent halitosis that is not relieved by brushing
and ossing may have a medical basis. The indi-
vidual should be told to discuss the matter with the
healthcare provider or dentist to ensure appropriate
therapy.
• Fluoride supplements may be recommended in ar-
eas of the United States in which the water supply is
not uoridated or the uoride level is low.
FOSTERING HEALTH MAINTENANCE
• Discuss hygiene practices and medications pre-
scribed for discomfort, infections, or mucosal
breakdown.
• Seek cooperation and understanding of the follow-
ing points to ensure that medication compliance is
increased: name of medication; dosage, route, and
times of administration; and common and serious
adverse effects.
• Discuss a specic schedule for performing oral hy-
giene measures and include details of products to be
used to relieve oral dryness or pain. Discuss basic
dietary modications needed while oral lesions are
present (e.g., avoid citrus juices and spicy foods).
With severe oral lesions, discuss supplemental nu-
trition formulas (e.g., Ensure, Boost). Cold drinks
generally are more soothing to the oral tissue than
hot foods.
• Report to the healthcare provider conditions that
are not relieved by the prescribed therapies.
DRUG CLASS: DENTIFRICES
Actions
Dentifrices contain one or more abrasive agents, a
foaming agent, and avoring materials. They are avail-
able in powder, paste, or gel and are best used with
a soft nylon toothbrush. Although dentifrices vary,
degree of abrasiveness is an essential property for re-
moving plaque. Some toothpastes contain higher con-
centrations of abrasive agents (e.g., silicates, dicalcium
phosphate, calcium pyrophosphate, calcium carbon-
ate) and are advertised as “smokers’ toothpastes” to
remove tobacco stains.
The most common therapeutic agent added to den-
tifrices is uoride for its anticaries activity. Chemicals
such as sanguinarine, zinc citrate, triclosan, thymol,
and eucalyptol have antibacterial properties that may
reduce plaque. Dentifrices advertised as tooth whit-
eners contain oxidizing ingredients, such as hydro-
gen peroxide, carbamide peroxide, and perhydrol
urea. Zinc chloride, zinc citrate, and soluble pyro-
phosphates prevent or retard the formation of new
calculus from plaque but will not remove calculus
already formed. Potassium nitrate is used for reliev-
ing sensitivity to hot and cold liquids and foods in
otherwise normal teeth.
Uses
If possible, everyone should brush at least twice daily
with a uoride toothpaste. If the teeth and gums are
normal, select a uoride-containing dentifrice that
has an acceptable taste. Those of all ages should use
toothpastes that are the least abrasive to the teeth
while controlling tooth decay and gum disease. This
is especially important to patients with receding
gums. People who have a sensitivity to hot or cold
liquids and foods may want to try a sensitivity tooth-
paste containing potassium nitrate. About 2 weeks of
regular use is necessary to eliminate sensitivity to hot
or cold beverages and food.

Therapeutic Outcomes
The primary therapeutic outcomes expected from den-
tifrices are as follows:
1. Reduction in plaque formation and cavities
2. Pleasant, refreshing taste
DRUG CLASS: MOUTHWASHES
Toothbrushing and ossing are optimal for good oral
hygiene; however, they may not be possible for the
patient who has undergone oral surgery or who has
experienced facial trauma. Mouthwashes may be tem-
porarily effective in removing disagreeable tastes and
reducing halitosis. Therapeutic mouthwashes are also
available to reduce plaque.
Actions
Mouthwashes are solutions of avoring, coloring, wa-
ter, surfactants, and sometimes therapeutic ingredi-
ents. Flavoring agents are used to give a pleasant taste
and freshen the breath. Coloring suggests a certain
type of mouthwash: green or blue for minty, red for
spicy, white for whitening, and brown for medicinal.
Surfactants are foaming agents that aid in removing
debris. Alcohol is often present, adding a bite and en-
hancing avor (especially in the medicinal type of prod-
uct) and solubilizing other ingredients. Therapeutic
ingredients include uoride for anticaries protection
and antimicrobial agents (e.g., benzoic acid, thymol,
eucalyptol, menthol, cetylpyridinium chloride, domi-
phen bromide, chlorhexidine) to kill bacteria to reduce
plaque formation and decaying food odor. Phenol is a
local anesthetic, antiseptic, and antibacterial agent that
penetrates and reduces plaque formation. Zinc citrate
and zinc chloride are astringents that neutralize sul-
fur-smelling compounds from decaying debris in the
mouth.
Uses
Mouthwashes can be subdivided into cosmetic and
therapeutic products based on ingredients. Cosmetic
mouthwashes freshen the breath and rinse out some
debris, although the odor-reducing effect lasts only 10
to 30 minutes.
Certain mouthwashes are for specic purposes.
The most common are the uoride-containing mouth-
washes used to prevent dental caries. Medicinal
Drugs Used to Treat Oral Disorders CHAPTER 31 513
mouthwashes (e.g., Listerine) reduce plaque accumu-
lation and gingivitis. Chlorhexidine (Peridex) is an an-
tibacterial agent used to treat oral mucositis. Products
containing zinc chloride are used as astringents for
temporarily decreasing bleeding or irritation. A 0.9%
solution of sodium chloride (normal saline) is an effec-
tive gargle. It can provide temporary, soothing relief of
pharyngeal irritation from nasogastric tubes, endotra-
cheal tubes, sore throat, or oral surgery. Solutions con-
taining hydrogen peroxide cleanse and debride minor
lesions; however, use should be limited to 7 to 10 days
to prevent further tissue irritation. Lidocaine, a local
anesthetic, is available as an oral viscous solution (li-
docaine viscous 2%). The viscous solution is a longer-
lasting local anesthetic and can be used as a gargle for
patients with sore throats or mouth ulcers. This prod-
uct is commonly used for immunosuppressed patients
with painful candidal infections of the mouth and
throat. Caution the patient not to eat or drink anything
for at least 30 minutes after use of viscous lidocaine
because of the absence of the gag reex and potential
risk for aspiration.
Unless a mouthwash is being used to treat a specic
medical condition (e.g., oral mucositis), it should not
become a substitute for normal oral hygiene. Primary
oral hygiene includes proper toothbrushing and
ossing.
All mouthwashes have specic dosage recommen-
dations. It is important not to exceed these recommen-
dations without a healthcare provider’s order because
many of the therapeutic ingredients (e.g., lidocaine,
uoride) can be systemically absorbed, resulting in po-
tentially toxic levels. Most mouthwashes are designed
to be used as a rinse (mouthwash is held in the mouth,
swished around, and expectorated). Again, prolonged
swallowing of mouthwashes may lead to systemic
toxicities. Patients should be advised to refrain from
smoking, eating, or drinking for at least 30 minutes af-
ter use.
Therapeutic Outcomes
The primary therapeutic outcomes expected from
mouthwashes are as follows:
1. Temporary reduction in bleeding or irritation
2. Relief of discomfort
3. A refreshing taste
4. Improvement in halitosis
514 UNIT VI Drugs Affecting the Digestive System
Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• Common disorders affecting the mouth are cold sores on
the lip; canker sores and candidal infections of soft tissues
of the tongue, cheeks, and gums; and plaque and calculus
affecting the gums and teeth. Xerostomia (lack of saliva)
originates from nonoral causes.
• Halitosis can arise from oral or nonoral causes. A much
less common problem but one that causes signicant
discomfort is oral mucositis.
• Health teaching should start with teaching children to carry
out regular brushing, ossing, and dental care. Stress
regular dental checkups, have problems treated promptly
when they occur, and if wearing dentures, be certain that
they t properly.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa
tions, and other learning activities to help you master this chap
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihn
ganz) for additional online resources.
Clinical Judgment and NextGeneration NCLEX® Exam
inationStyle Questions The following questions are typical of
the NCLEX exam and include both NGN (Next Generation) and
traditional questions. See Chapter 1 for further information re
garding question types.
Scenario
A patient with multiple caries and abscessed teeth was admit
ted to the hospital for full dental extraction. The nurse noted
that the patient had poor hygiene and lived alone.
1. The nurse discussed halitosis with the patient in the scenario who
was also a known smoker. After the teaching the nurse knew that
the patient understood the topic when the patient made which
statement?
1. “People can get halitosis from lots of causes and I don’t
believe any apply to me.”
2. “Because I need to get dentures after my teeth are
removed, I will not have any halitosis issues.”
3. “I get it now, my halitosis was from my bad teeth and
smoking.”
4. “If I brush my dentures every day after eating, I will be free
from halitosis.”
Objective: Explain common oral disorders and their treatments.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
2. The nurse is educating a patient with painful oral lesions and
discusses the best approach to oral hygiene. Which statement by
the nurse needs to be reworked?
1. “You may nd that these lesions will heal after 14 days.”
2. “You should start using commercial mouthwashes for
rinsing after meals and at bedtime.”
3. “You could think about using normal saline, baking soda,
or halfstrength hydrogen peroxide rinses for these
lesions.”
4. “You need to get a prescription for pain medication.”
Objective: Explain common oral disorders and their treatments.
NCLEX item type: Multiple choice
Cognitive skill: Understanding
3. A patient was asking the nurse to explain canker sores. What is the
appropriate response by the nurse? (Select all that apply.)
1. “The causes of canker sores are not known.”
2. “Sometimes canker sores are brought on by stress and
trauma to the mouth.”
3. “Canker sores are lesions that are really viral infections.”
4. “Canker sores are not contagious.”
5. “If you take aspirin, it will promote healing of the canker
sores.”
6. “You can get canker sores from biting the inside of your
cheeks.”
7. “There is not cure for canker sores, we only treat the
symptoms.”
Objective: Explain common oral disorders and their treatments.
NCLEX item type: Extended multiple response
Cognitive skill: Application
4. The nurse knows that thrush can occur in which of these patient
populations? (Select all that apply.)
1. Infants
2. Pregnant women
3. Debilitated patients
4. Teens
5. Older adults
Objective: Explain common oral disorders and their treatments.
NCLEX item type: Multiple response
Cognitive skill: Application
5. The nurse can expect that a patient who recently underwent
chemotherapy will develop mucositis during which time frame?
1. Within 2 to 3 days of starting chemotherapy
2. Within 5 to 10 days of starting chemotherapy
3. Within 10 to 12 days of starting chemotherapy
4. Within 2 weeks of starting chemotherapy
Objective: Identify nursing assessments and interventions
associated with treatment of mucositis.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
 Drugs Used to Treat Oral Disorders CHAPTER 31 515

6. The nurse reviewed the medications approved specically for use Objective: Identify nursing assessments and interventions
in preventing and treating the mucositis. Indicate with an ‘X’ which associated with treatment of mucositis.
medications are used to treat which symptom of mucositis. NCLEX item type: Matrix
Cognitive skill: Evaluate cues

FUNGAL
DRY MOUTH INFECTIONS PAIN RELIEF
KY jelly
Nystatin
liquid
Lidocaine
viscous 2%
Lip balm
Articial
saliva
Milk of
magnesia
rinses
Clotrimazole
lozenges
32 Drugs Used to Treat Gastroesophageal Reux
and Peptic Ulcer Disease
https://evolve.elsevier.com/Willihnganz
Objectives
1. Discuss common stomach disorders that require drug
therapy.
2. Identify factors that prevent breakdown of the body’s
normal defense barriers resulting in ulcer formation.
Key Terms
chief cells (CHĒF) (p. 516) gastroesophageal reux disease
parietal cells (pă-RĪ-ĕ-tŭl) (p. 516) (GERD) (găs-trō-ĕs-ŏf-ĕ-JĒ-ŭl RĒ-
hydrochloric acid (hī-drō-KLŎR-ĭk) ŭks) (p. 516)
(p. 516) heartburn (HĂRT-bŭrn) (p. 516)
mucous cells (MŪ-kŭs SĔLZ) (p. 516)
PHYSIOLOGY OF THE STOMACH
As a major part of the gastrointestinal (GI) tract, the
stomach has three primary functions: (1) storing food
until it can be processed in the lower GI tract; (2) mix-
ing food with gastric secretions until it is a partially
digested, semisolid mixture known as chyme; and
(3) slowly emptying the stomach at a rate that allows
proper digestion and absorption of nutrients and med-
icine from the small intestine.
Three types of secretory cells line portions of the
stomach—chief, parietal, and mucous cells. The chief
cells secrete pepsinogen, an inactive enzyme. Parietal
cells secrete hydrochloric acid by way of a hydrogen
ion pump. The hydrochloric acid activates pepsinogen
to pepsin, providing the optimal pH for pepsin to start
protein digestion. Stimulation of histamine-2 (H2) re-
ceptors on the stomach’s parietal cells also causes se-
cretion of hydrochloric acid. Cholinergic nerve bers
that innervate the stomach will also increase parietal
cell secretion of hydrochloric acid when stimulated
by acetylcholine. Normal pH in the stomach ranges
from 1 to 5, depending on the presence of food and
medications. Hydrochloric acid also breaks down
muscle bers and connective tissue ingested as food
and kills bacteria that enter the digestive tract through
the mouth. The parietal cells also secrete intrinsic fac-
tor needed for absorption of vitamin B12. The mucous
cells secrete mucus, which coats the stomach wall. The
1-mm-thick coat is alkaline and protects the stomach
wall from damage by hydrochloric acid and the diges-
tive enzyme pepsin. It also contributes lubrication for
516
3. Discuss the drug classications and actions used to treat
stomach disorders.
4. Identify interventions that incorporate pharmacologic
and nonpharmacologic treatments for an individual with
stomach disorders.
peptic ulcer disease (PUD) (PĔP-tĭk
ŬL-sŭr) (p. 517)
Helicobacter pylori (hĕl-ĭ-kō-BĂK-tŭr
pī-LŎR-ē) (p. 517)
food transport. Small amounts of other enzymes are
also secreted in the stomach: lipases digest fats and
gastric amylase digests carbohydrates. Other digestive
enzymes are also carried into the stomach from swal-
lowed saliva.
Prostaglandins play a major role in protecting the
stomach walls from injury caused by stomach acids
and enzymes. Prostaglandins are produced by cells
lining the stomach and prevent injury by inhibiting
gastric acid secretion, maintaining blood ow, and
stimulating mucus and bicarbonate production.
COMMON STOMACH DISORDERS
Gastroesophageal reux disease (GERD), more com-
monly referred to as heartburn, acid indigestion, or sour
stomach, is a common stomach disorder (Fig. 32.1).
Approximately one-third of the US population experi-
ences heartburn once each month, and 5% to 7% have
heartburn daily. Common symptoms are a burning
sensation, bloating, belching, and regurgitation. Other
symptoms that are reported less frequently are nausea,
a “lump in the throat,” hiccups, and chest pain.
GERD is the reux of gastric secretions, primarily
pepsin and hydrochloric acid, up into the esophagus.
GERD is caused when the lower esophageal sphincter
abnormally weakens or relaxes, allowing acidic gastric
contents to splash up into the esophagus, irritating the
tissues.. Conditions that can increase the risk of GERD
include delayed gastric emptying, hiatal hernia, and
obesity. Factors that aggravate GERD are eating large
 Drugs Used to Treat Gastroesophageal Reux and Peptic Ulcer Disease CHAPTER 32
Lower
esophageal
Delayed sphincter
gastric dysfunction
emptying
Reflux of
gastric
contents
Fig. 32.1 Causes of gastroesophageal reux disease. (From Lewis SL,
Bucher L, Heitkemper MM. Medical-Surgical Nursing: Assessment and
Management of Clinical Problems. 10th ed. St. Louis: Elsevier; 2017.)
meals or eating late at night before bedtime, and acid
secretions increased by smoking, alcohol ingestion,
carbonated beverages, coffee, and spicy foods.
Most cases of GERD pass quickly with only mild
discomfort, but frequent or prolonged bouts of acid
reux cause inammation, tissue erosion, and ulcer-
ations in the lower esophagus. Anyone who has recur-
rent or continuous symptoms of reux, especially if the
symptoms interfere with activities, should be referred
to a healthcare provider. These symptoms may also
accompany more serious conditions, such as ischemic
heart disease, scleroderma, and gastric malignancy.
Clinical Pitfall
Nurses need to be aware that the symptoms of GERD may
also accompany more serious conditions, such as ischemic
heart disease, scleroderma, and gastric malignancy. It is im-
portant to do a thorough physical assessment whenever a
patient presents with heartburn or acid indigestion and not
simply dismiss the symptoms as GI in origin.
Peptic ulcer disease (PUD) refers to several stomach
disorders that result from an imbalance between acidic
stomach contents and the body’s normal defense bar-
riers, causing ulcerations in the GI tract. The most
common illnesses are gastric and duodenal ulcers. It is
estimated that approximately 10% of all Americans
will develop an ulcer at some time in their lives. The in-
cidence in men and women is approximately the same.
Race, economic status, and psychological stress do not
correlate with the frequency of ulcer disease. Often the
only symptom reported is epigastric pain, described as
burning, gnawing, or aching. Patients often report that
varying degrees of pain are present for a few weeks
and are then gone, only to recur a few weeks later. The
pain is most often noted when the stomach is empty,
such as at night or between meals, and is relieved by
517
food or antacids. Other symptoms that cause patients
to seek medical attention are bloating, nausea, vomit-
ing, and anorexia.
Ulcers appear to be caused by a combination of acid
and a breakdown in the body’s defense mechanisms
that protect the stomach wall. Proposed mechanisms are
oversecretion of hydrochloric acid by excessive num-
bers of parietal cells; injury to the mucosal barrier, such as
that resulting from prostaglandin inhibitors (non-
steroidal antiinammatory drugs [NSAIDs], including
aspirin); and infection of the mucosal wall by Helicobacter
pylori. It had been thought that no bacterium could sur-
vive in the highly acidic environment of the stomach;
however, H. pylori was rst isolated from patients with
gastritis in 1983. The bacterium seems able to live below
the mucous barrier, where it is protected from stomach
acid and pepsin. Helicobacter pylori is now thought to be
associated with as many as 90% of duodenal and 70% of
gastric ulcers. The exact mechanism whereby H. pylori
contributes to ulcer formation is not known, but several
hypotheses are being tested.
Several risk factors increase the likelihood of PUD:
1. There seems to be a genetic predisposition to PUD.
Some families have a much greater history of PUD
than others.
2. It is a commonly held belief that stress causes ulcers,
but no well-controlled studies have supported this.
3. Cigarette smoking increases acid secretion, alters
blood ow in the stomach wall, and retards prosta-
glandin synthesis needed for defense mechanisms.
4. NSAIDs have a twofold effect: they inhibit pros-
taglandins that protect the mucosa and directly
irritate the stomach wall. Once ulcerations have
formed, NSAIDs also slow healing.
5. It is commonly thought that certain foods (e.g.,
spicy foods) and alcohol contribute to ulcer forma-
tion. It is true that certain foods increase acid secre-
tion and that alcohol irritates the stomach lining,
but results from studies have not corroborated this
concept.
GOALS OF TREATMENT
The goals of treatment of GERD and PUD are similar:
relieve symptoms, decrease the frequency and dura-
tion of reux, heal tissue injury, and prevent recur-
rence. Both treatment pathways focus on reduction of
acid secretions by using antacids, H2 antagonists, or
proton pump inhibitors (PPIs). An important action for
both conditions is a change in lifestyle, which includes
losing weight (if signicantly over the ideal body
weight), reducing or avoiding foods and beverages
that increase acid production, reducing or stopping
smoking, avoiding alcohol, and consuming smaller
meals. Patients rarely need to be restricted to a bland
diet. If NSAIDs are being taken, consideration should
be given to switching to acetaminophen if feasible.
518 UNIT VI Drugs Affecting the Digestive System
For patients with GERD, additional measures in-
clude remaining upright for 2 hours after meals, not
eating before bedtime, and avoiding tight clothing over
the abdominal area. For patients with nocturnal GERD,
elevation of the head of the bed with 8-inch blocks or
use of a foam wedge pillow to raise the shoulders and
head may be helpful to stop reux. Lozenges may be
used to increase saliva production that may clear acid
secretions that have entered the esophagus and ant-
acid therapy may provide relief for patients who expe-
rience infrequent heartburn. If the patient’s symptoms
do not improve within 2 to 3 weeks, or if the condition
is severe, additional pharmacologic measures such as
H2 antagonists or PPIs should be tried to reduce irrita-
tion. About 5% to 10% of patients with GERD require
surgery.
For decades, PUD treatment focused on reducing
acid secretions (anticholinergic agents, H2 antago-
nists, gastric acid pump inhibitors), neutralizing acid
(antacids), or coating ulcer craters to hasten healing
(sucralfate). Major changes in therapy have come
about by the recognition that PUD is most likely an
infection caused by H. pylori. Various combinations
of antimicrobial agents (e.g., amoxicillin, tetracycline,
metronidazole, clarithromycin, rifabutin), bismuth,
and antisecretory agents (e.g., H2 antagonists, PPIs)
are used to eradicate H. pylori. PPIs are generally pre-
ferred over H2 antagonists. Antibiotics are not recom-
mended for individuals who are asymptomatic with
H. pylori because there is concern that resistant strains
of bacteria may develop.
DRUG THERAPY
ACTIONS
• Antacids neutralize gastric acid, thereby causing the
gastric contents to be less acidic.
• Coating agents (sucralfate) provide a protective
covering over the ulcer crater.
• H2 antagonists decrease the volume of hydrochloric
acid produced, which increases the gastric pH and
thereby results in decreased irritation to the gastric
mucosa.
• PPIs block the formation of hydrochloric acid, re-
ducing irritation of the gastric mucosa.
• Prokinetic agents increase the lower esophageal
sphincter muscle pressure and peristalsis, hastening
emptying of the stomach to reduce reux.
USES
• Antacids decrease hyperacidity associated with
PUD, GERD, gastritis, and hiatal hernia.
• Coating agents provide a protective barrier for the
mucosal lining where hydrochloric acid may come
into contact with inamed eroded areas. They are
used to treat existing ulcer craters on the gastric
mucosa.
• H2 antagonists are used to treat acute PUD and
GERD, as well as for maintenance to prevent ulcer
recurrence.
• PPIs are used to treat hyperacidity conditions (e.g.,
GERD, Zollinger-Ellison syndrome) and PUD.
• Prokinetic agents are used to treat GERD.
NURSING IMPLICATIONS FOR AGENTS USED
FOR STOMACH DISORDERS
Assessment
Nutritional assessment. Obtain patient data about cur-
rent height, weight, and any recent weight gain or loss.
Identify the normal pattern of eating, including snacking
habits. Use a food guide such as the Healthy Eating Plate
(see Fig. 46.3) as a guide when asking questions to identi-
fy the usual foods eaten by the individual. Ask about any
nutritional or cultural restrictions associated with dietary
practices. Are there any food allergies (obtain details) or
foods that particularly cause gastric distress when eaten?
Does the individual take any nutritional supplements?
How often and how much fast food is eaten?
Esophagus, stomach. Ask patients to describe symp-
toms. Question in detail what is meant by the terms in-
digestion, heartburn, upset stomach, nausea, and belching.
Pain, discomfort
• Ask the patient to describe the onset, duration, lo-
cation, and characteristics of pain or discomfort.
Determine whether there is a relationship between
the ingestion of certain types of food or drinks and
the onset of pain. Ask specically about coffee, tea,
cola, chocolate, and alcohol intake.
• What has the patient done to relieve the pain or dis-
comfort? Have there been any changes in taste (e.g.,
bitterness, sourness)? Record pain levels using a rating
scale before and after medications are administered.
Activity, exercise. Ask specically what type of work
or activities the individual performs that may increase
intraabdominal pressure (e.g., lifting heavy objects,
bending over frequently).
History of diseases or disorders
• What other diagnoses have been made for diseases
or disorders (e.g., ulcer, gallbladder, liver, jaundice,
irritable bowel syndrome)?
• Have there been any changes in bowel elimination
or stool color, consistency, or frequency?
Medication history
• What self-medications have been tried?
• What prescribed medications are being taken?
• What is the schedule of medication administration
(e.g., how frequently and when are antacids taken)?
Smoking. What is the frequency of smoking? Has the
patient ever tried to stop smoking?
 Drugs Used to Treat Gastroesophageal Reux and Peptic Ulcer Disease CHAPTER 32
Implementation
• Routine orders: Most healthcare providers order ant-
acids 1 hour before meals, 2 to 3 hours after meals,
and at bedtime. As-needed (PRN) medication dos-
ages must be discussed.
• Each type of medication used to treat GERD or
PUD may require somewhat different scheduling
to avoid drug interactions. When developing the
time frames for administration of medications on
the medication administration record, schedule the
other prescribed drugs 1 hour before or 2 hours after
antacids.
• Changes in diet require careful planning with the
patient and the person responsible for purchasing
and cooking the meals. Schedule teaching sessions
appropriately. Not only may some foods need to be
altered, but also the number of meals per day may
need to be increased with a smaller serving at each
meal.
Patient Education
Nutrition
• Implement prescribed dietary changes: eat small,
more frequent meals to support optimal energy
requirements and healing; avoid overdistention of
the stomach; avoid any seasonings that are intoler-
able or that aggravate the condition; and avoid cof-
fee, teas, colas, alcoholic beverages (including beer),
carbonated beverages, peppermint, spearmint, and
citric juices, which may produce discomfort in those
with GERD.
• Avoid late-night snacks or meals that could result in
increased gastric secretions.
• Observe for foods that aggravate the condition
and eliminate these from the diet. Drink only small
amounts of uid with the meal and drink mostly
between meals. Increase protein foods and decrease
fats to about 45 g/day or less; use nonfat milk.
Pain, discomfort. Keep a written record (see Patient
Self-Assessment later) of the onset, duration, location,
and precipitating factors for any pain. Sit upright at
the table when eating and do not lie down for at least
2 hours after eating. When a hiatal hernia is present,
elevate the head of the bed by 6 to 8 inches using bed
blocks to prevent reux during sleep. Have the patient
keep a log of the pain, including time of day, any fac-
tors that might have precipitated the pain, and degree
of pain relief from medications used.
Medications
• Take prescribed medications at recommended times
to promote optimal healing. See individual drug
monographs for suggested scheduling.
• Avoid NSAIDs and aspirin-containing medicines
that irritate the gastric mucosa. Consult the pre-
scriber or pharmacist regarding scheduling of or
discontinuation of these medications.
519
Fostering health maintenance
• Discuss medication information and how it will
benet the course of treatment to produce an op-
timal response. Medications used in the treatment
of hyperacidity are important measures to alleviate
the irritating effects on the mucosal tissue; stress the
importance of not discontinuing treatment and the
need for continued medical follow-up.
• Seek cooperation and understanding of the follow-
ing points so that medication adherence is increased:
name of medication; dosage, route, and times of
administration; and common and serious adverse
effects. Stress the need to complete a full course of
treatment for H. pylori so that the organisms are in-
deed killed and not only suppressed; H. pylori can
regrow if medications are discontinued too early.
Patient self-assessment. Enlist the patient’s aid in de-
veloping and maintaining a written record of monitor-
ing parameters (e.g., a list of foods causing problems,
degree of pain relief). See Patient Self-Assessment
form for Agents Affecting the Digestive System on
the Evolve website. Complete the Premedication Data
column for use as a baseline to track response to drug
therapy. Ensure that the patient understands how to
use the form and instruct the patient to bring the com-
pleted form to follow-up visits. During follow-up vis-
its, focus on issues that will foster adherence with the
therapeutic interventions prescribed.
DRUG CLASS: ANTACIDS
Actions
Antacids lower the acidity of gastric secretions by buff-
ering the hydrochloric acid (normal pH is 1 to 2) to a
lower hydrogen ion concentration. Buffering hydro-
chloric acid to a pH of 3 to 4 is highly desired because
the proteolytic action of pepsin is reduced and the gas-
tric juice loses its corrosive effect.
Uses
Antacids are commonly used for heartburn, excessive
eating and drinking, and PUD. They are no longer rst-
line agents in the treatment of stomach disorders but
are often the rst agents used by consumers to self-treat
these conditions; however, nurses and patients must be
aware that not all antacids are alike. They should be
used judiciously, particularly by certain types of pa-
tients (e.g., those with heart failure, hypertension, or
renal disease). Long-term self-treatment with antacids
may also mask symptoms of serious underlying dis-
eases, such as a bleeding ulcer.
The most effective antacids available are combina-
tions of aluminum hydroxide, magnesium oxide or
hydroxide, and calcium carbonate. All act by neutral-
izing gastric acid. Combinations of these ingredients
must be used because any compound used alone in
therapeutic quantities may produce severe systemic
520 UNIT VI Drugs Affecting the Digestive System
adverse effects. Other ingredients found in antacid
combination products include simethicone and bis-
muth. Simethicone is a defoaming agent that breaks up
gas bubbles in the stomach, reducing stomach disten-
tion and heartburn. It is effective in patients who have
overeaten or who have heartburn, but it is not effective
in treating PUD. Bismuth compounds have little acid-
neutralizing capacity and are therefore poor antacids.
The following principles should be considered
when antacid therapy is planned:
• For indigestion, antacids should not be adminis-
tered for more than 2 weeks. If after this time the
patient is still experiencing discomfort, the health-
care provider should be contacted.
• Patients with edema, heart failure, hypertension,
renal disease, pregnancy, or salt-restricted diets
should use low-sodium antacids, such as Maalox.
Therapy should continue only on the recommenda-
tion of the healthcare provider.
• Antacid tablets should be used only for the patient
with occasional indigestion or heartburn. Tablets do
not contain enough antacid to be effective in treating
PUD.
• A common complaint of patients consuming large
quantities of calcium carbonate or aluminum hy-
droxide is constipation. Excess magnesium results
in diarrhea. If a patient experiences these symptoms
and still has stomach discomfort, the healthcare pro-
vider should be consulted.
• Effective management of acute PUD requires large
volumes of antacids. The selection of an antacid and
the quantity to be taken depend on its neutralizing
capacity. Any patient with coffee-ground emesis,
bloody stools, or recurrent abdominal pain should
seek medical attention immediately and not attempt
to self-treat the disorder.
• Calcium carbonate and sodium bicarbonate may
cause rebound hyperacidity.
• Patients with renal disease should not use large
quantities of antacids containing magnesium. The
magnesium ions cannot be excreted and may pro-
duce hypermagnesemia and toxicity.
• Most antacids have similar ingredients. Selection of
an antacid for occasional use should be determined
by quantity of each ingredient, cost, taste, and fre-
quency of adverse effects. Patients may need to try
more than one product and weigh the advantages
and disadvantages of each.
Therapeutic Outcomes
The primary therapeutic outcomes expected from ant-
acid therapy are relief of discomfort, reduced frequen-
cy of heartburn, and healing of irritated tissues.
Nursing Implications for Antacids
Premedication assessment
1. Check renal function test results to ensure that renal
function is normal. When renal disease is present,
patients should not take large quantities of ant-
acids containing magnesium. Monitor the patient’s
renal function tests, including blood urea nitrogen,
creatinine, and serum electrolyte levels (including
magnesium and potassium). Magnesium and po-
tassium ions cannot be excreted when patients have
renal disease and may produce hypermagnesemia,
hyperkalemia, and toxicity.
2. Check the pattern of bowel elimination for diarrhea
or constipation.
3. Record the pattern of gastric pain being experi-
enced; report coffee-ground emesis, bloody stools,
or recurrent abdominal pain to the healthcare pro-
vider for prompt attention.
4. If the patient is pregnant or has edema, heart failure,
hypertension, or salt restrictions, ensure that a low-
sodium antacid has been prescribed.
5. Schedule other prescribed medications to be taken
1 hour before or 2 hours after antacids are to be
administered.
Life Span Considerations
Antacids
Those older than 65 years are the most common purchasers
of antacid products. Gastrointestinal disorders such as PUD,
NSAID-induced ulcers, and GERD occur more often in this
age group. Magnesium-containing antacids are often used
as laxatives. Although the primary symptom of ulcer disease
in a younger person is usually burning epigastric pain, the
symptoms in an older person, if present at all, usually include
complaints of vague abdominal discomfort, anorexia, and
weight loss.
Availability. See Table 32.1
• Liquid forms of antacid preparations should be used
for treatment of PUD because tablets do not contain
enough of the active ingredients to be effective.
• Antacid tablets may be used for occasional episodes
of heartburn. They should be well chewed before
swallowing for a more rapid onset of action.
Common adverse effects
Chalky taste. A chalky taste is a common problem
with antacids. Suggest a change in brands or avors.
Suggest using a liquid instead of tablets.
Serious adverse effects
Gastrointestinal
Diarrhea, constipation. Diarrhea or constipation is a com-
mon problem when antacids are used in therapeutic
dosages to treat ulcers. Alternating between calcium- or
aluminum-containing compounds and magnesium-
containing compounds should help alleviate the problem.
Drug interactions
Tetracycline antibiotics, uoroquinolone antibiotics, phe-
nytoin, phenothiazines, ketoconazole, corticosteroids, digox-
in, gabapentin, iron supplements. The absorption of these
 Drugs Used to Treat Gastroesophageal Reux and Peptic Ulcer Disease CHAPTER 32 521

Table 32.1 Ingredients of Commonly Used Antacids

MAGNESIUM
OXIDE,
CALCIUM ALUMINUM HYDROXIDE, OR SODIUM OTHER
PRODUCT FORM CARBONATE HYDROXIDE CARBONATE BICARBONATE SIMETHICONE INGREDIENTS
Baking soda Powder — — — × — —
Gelusil Tablet — × × — × —
Maalox Max Suspension — × × — × —
Phillips’ Milk of Tablet, — — × — — —
Magnesia suspension
Rolaids Tablet × — × — — —
Tums Tablet × — — — — —

medicines is inhibited by antacids. These medications
should be administered 1 hour before or 2 to 3 hours
after antacids.
Levodopa, valproic acid. The absorption of levodo-
pa is increased by magnesium-aluminum antacids.
When antacid therapy is added, toxicity may result in
the patient with Parkinson disease whose condition
is well controlled on a certain dosage of levodopa. If
the patient’s parkinsonism symptoms are well con-
trolled on levodopa and antacid therapy, withdrawal
of antacids may result in a recurrence of parkinsonian
symptoms.
Amphetamines. Frequent use of sodium bicarbonate–
containing antacid therapy may result in increased
urinary pH. Renal excretion of amphetamines may be
inhibited and toxicity may occur.
DRUG CLASS: HISTAMINE-2 RECEPTOR
ANTAGONISTS
Actions
One of the primary mechanisms of hydrochloric acid
secretion has to do with histamine stimulation of H2
receptors on the stomach’s parietal cells. The H2 an-
tagonists act by blocking the H2 receptors, resulting in
a decrease in the volume of acid secreted. The pH of
the stomach contents rises as a consequence of a reduc-
tion in acid.
Cimetidine was the rst approved H2 antagonist
but differs from the other agents by its extensive liver
metabolism and antiandrogenic effect that may result
in gynecomastia. It also has many drug-drug interac-
tions that are not seen with the others. Consequently,
cimetidine is used less commonly than the other H2
antagonists.
Famotidine is similar in action and use to cimetidine
but has the advantages of once-daily dosing, fewer
drug interactions, and no antiandrogenic effect. A par-
enteral dosage form is available.
Nizatidine is similar to famotidine but, in contrast
to the other agents, is not available in a parenteral dos-
age form.
Therapeutic Outcomes
The primary therapeutic outcomes expected from H2
antagonist therapy are relief of discomfort, reduced
frequency of heartburn, and healing of irritated
tissues.
Nursing Implications for H2 Antagonists
Premedication assessment. Perform a baseline as-
sessment of the patient’s mental status for comparison
with subsequent mental status evaluations to detect
central nervous system alterations that may occur, par-
ticularly with cimetidine therapy.

Uses Availability, dosage, and administration. See Table 32.2

The H2 antagonists (cimetidine, nizatidine, famotidine)
are used to treat GERD, duodenal ulcers, and patho-
logic hypersecretory conditions, such as Zollinger-
Ellison syndrome, and for preventing gastric ulcers in
critically ill patients. Unapproved uses are preventing
gastric ulcers in critically ill patients and chronic hives.
Famotidine is also approved in combination with ibu-
profen to reduce the risk of developing a gastric ulcer.
All the H2 antagonists have products that are available
for over-the-counter purchase for symptomatic relief
of overeating and heartburn.
• All H2 antagonists may be administered with or
without food.
• Because antacid therapy is often continued during
early therapy of PUD, administer 1 hour before or 2
hours after the H2 antagonist dose.
Common adverse effects. Approximately 1% to 3% of
patients develop these adverse effects. They are usual-
ly mild and resolve with continued therapy. Encourage
patients not to discontinue therapy without rst con-
sulting the healthcare provider.
522 UNIT VI Drugs Affecting the Digestive System

Table 32.2 Histamine-2 (H2) Receptor Antagonists

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE
cimetidine Tagamet HB Tablets: 200, 300, 400, Duodenal and gastric ulcers:
800 mg PO: 800–1600 mg at bedtime, 400 mg twice daily,
Solution: 300 mg/5 mL or 300 mg four times daily
GERD:
PO: 800 mg twice daily or 400 mg four times daily
famotidine Pepcid Tablets: 10, 20, 40 mg Duodenal and gastric ulcers:
Do not confuse Do not confuse Pepcid Suspension: 40 mg/5 mL PO: 40 mg once daily at bedtime or 20 mg twice
famotidine with with Prevacid. Injection: 10 mg/mL daily
uoxetine. Teva-famotidine GERD:
PO: 20 mg twice daily
nizatidine — Capsules: 150, 300 mg Duodenal and gastric ulcers:
Do not confuse Axid Oral solution: 15 mg/mL PO: 300 mg at bedtime or 150 mg twice daily
nizatidine with GERD:
tizanidine. PO: 150 mg twice daily
Available in Canada.
Do not confuse.
GERD, Gastroesophageal reux disease.

Neurologic
Dizziness, headache, somnolence. Provide for patient
safety during episodes of dizziness. If the patient
develops somnolence and lethargy, encourage using
caution when working around machinery, driving a
car, or performing other duties that require mental
alertness.
Gastrointestinal
Diarrhea, constipation. Maintain the patient’s state of
hydration and obtain an order for stool softeners or
bulk-forming laxatives if necessary. Encourage the in-
clusion of sufcient roughage (fresh fruits, vegetables,
whole-grain products) in the diet.
Serious adverse effects
Neurologic
Confusion, disorientation, hallucinations. If high dos-
ages (particularly of cimetidine) are used in patients
with liver or renal disease or in patients older than
50 years, mental confusion, slurred speech, disorien-
tation, and hallucinations may occur. These adverse
effects dissipate over 3 or 4 days after therapy has
been discontinued. Perform a baseline assessment of
the patient’s degree of alertness and orientation to
name, place, and time before starting therapy. Make
regularly scheduled subsequent mental status evalu-
ations, and compare ndings. Report alterations in
mental status.
Endocrine
Gynecomastia. Mild bilateral gynecomastia and
breast soreness may occur with long-term use (long-
er than 1 month) of cimetidine but will resolve after
discontinuing therapy. Report ndings of gyneco-
mastia for further observation and possible labora-
tory tests.
Gastrointestinal
Hepatotoxicity. Although rare, hepatotoxicity in pa-
tients taking H2 antagonists has been reported. The
symptoms of hepatotoxicity are anorexia, nausea,
vomiting, jaundice, hepatomegaly, splenomegaly, and
abnormal liver function test results (elevated bilirubin,
aspartate aminotransferase [AST], alanine aminotrans-
ferase [ALT], gamma-glutamyl transferase [GGT],
and alkaline phosphatase levels [ALP]; increased pro-
thrombin time [PT]).
Vitamin B12 deciency. Treatment with H2 antago-
nists for more than 2 years may lead to vitamin B12
malabsorption and subsequent vitamin B12 deciency.
The deciency is dose related and the association is
stronger in women. However, patients should not be
routinely screened for vitamin B12 deciency. There is
no evidence for or against testing for B12 deciency
for patients taking H2 antagonists for longer than 2
years.
Drug interactions
Benzodiazepines. Cimetidine inhibits the metabo-
lism or excretion of the following benzodiazepines:
alprazolam, chlordiazepoxide, diazepam, clorazepate,
urazepam, and triazolam. Patients taking cimetidine
and a benzodiazepine concurrently should be ob-
served for increased sedation; a reduction in dosage of
the benzodiazepine may be required. The metabolism
of oxazepam, temazepam, and lorazepam does not ap-
pear to be affected.
Beta-adrenergic blocking agents. Cimetidine may
inhibit the metabolism of beta-adrenergic blocking
agents (e.g., propranolol, labetalol, metoprolol) po-
tentially causing an increased pharmacologic effect.
 Drugs Used to Treat Gastroesophageal Reux and Peptic Ulcer Disease CHAPTER 32
Monitor for signs of toxicity, such as hypotension and
bradycardia.
Phenytoin. Cimetidine inhibits the metabolism of
phenytoin. Monitor patients with concurrent therapy
for signs of phenytoin toxicity: nystagmus, sedation,
and lethargy. Serum levels may be ordered, and a re-
duced dosage of phenytoin may be required.
Antacids. Administer 1 hour before or 2 hours after
administration of cimetidine.
Warfarin. Cimetidine may enhance the anticoagu-
lant effects of warfarin. Observe for the development
of petechiae; ecchymoses; nosebleeds; bleeding gums;
dark, tarry stools; and bright red or coffee-ground
hematemesis. Monitor the prothrombin time (inter-
national normalized ratio [INR]), and reduce the dos-
age of warfarin if necessary.
Calcium antagonists. Cimetidine may inhibit the
metabolism of diltiazem, nifedipine, and verapamil.
Patients should be monitored for increased effects
from the calcium antagonists (e.g., bradycardia, hypo-
tension, dysrhythmias, fatigue).
Tricyclic antidepressants. Cimetidine may inhibit the
excretion of imipramine, desipramine, and nortrip-
tyline, usually within 3 to 5 days after the start of ci-
metidine therapy. If anticholinergic effects or toxicity
becomes apparent, a decreased dosage of the anti-
depressant may be required. If cimetidine is discontin-
ued, the patient should be monitored for a decreased
response to the antidepressant.
Famotidine, nizatidine. In general, there appear to be
only minor interactions with these H2 antagonists.
DRUG CLASS: GASTROINTESTINAL
PROSTAGLANDIN
misoprostol (mĭs-ō-PRŎS-tŏl)
Cytotec (SĪ-tō-tĕk)
Actions
Misoprostol is a synthetic prostaglandin E series drug.
Prostaglandins are normally present in the GI tract
to inhibit gastric acid and pepsin secretion to protect
the stomach and duodenal lining against ulceration.
The prostaglandin E analogs may also induce uterine
contractions.
Uses
Misoprostol is used to prevent gastric ulcers caused
by prostaglandin inhibitors (e.g., NSAIDs, including
aspirin). Whereas prostaglandin inhibition is effec-
tive in reducing pain and inammation, especially in
arthritis, prostaglandin inhibition in the stomach by
NSAIDs makes the patient more predisposed to gas-
tric ulcers.
523
Therapeutic Outcomes
The primary therapeutic outcomes expected from
misoprostol therapy are relief of discomfort and heal-
ing of irritated tissues.
Nursing Implications for Misoprostol Therapy
Premedication assessment
1. Determine whether the patient is pregnant. This
drug is a uterine stimulant and may induce
miscarriage.
2. Check the pattern of bowel elimination; misoprostol
may induce diarrhea.
Availability. PO: 100- and 200-mcg tablets.
Medication Safety Alert
Misoprostol is contraindicated during pregnancy and in
women at risk of becoming pregnant. As a uterine stimulant,
it may induce miscarriage.
Dosage and administration. Adult: PO: 100- to 200-mcg
tablets four times daily with food during NSAID therapy.
Common adverse effects
Gastrointestinal
Diarrhea. Diarrhea associated with misoprostol ther-
apy is dose related and usually develops after approxi-
mately 2 weeks of therapy. It often resolves after about
8 days, but a few patients require discontinuation of
misoprostol therapy. Diarrhea can be minimized by
taking misoprostol with meals and at bedtime and
avoiding magnesium-containing antacids (e.g., Maalox
liquid, Mylanta). Encourage the patient not to discon-
tinue therapy without rst consulting the healthcare
provider. Encourage the patient to include sufcient
roughage or ber (fresh fruits, vegetables, whole-grain
products) in the diet.
Contraindication
Pregnancy. It is crucial that therapy be discontinued if
the patient is pregnant because misoprostol may cause
spontaneous abortion. The patient must receive atten-
tion from the healthcare provider who prescribed the
misoprostol, as well as an obstetrician. The question of
alternative therapies to NSAIDs must also be considered.
Drug interactions. No signicant drug interactions
have been reported.
DRUG CLASS: PROTON PUMP INHIBITORS
Actions
PPIs inhibit gastric secretion of hydrochloric acid by
inhibiting the gastric acid (H+/K+ adenosine triphos-
phate [ATP] pump) of the stomach’s parietal cells.
Uses
PPIs are used to treat severe esophagitis, GERD, gastric
and duodenal ulcers, and hypersecretory disorders,
524 UNIT VI Drugs Affecting the Digestive System

such as Zollinger-Ellison syndrome. They are used in
combination with antibiotics (e.g., amoxicillin, clar-
ithromycin) to eradicate H. pylori, a common cause of
PUD. They are also used for the prevention and treat-
ment of NSAID-induced ulcers. PPIs (e.g., Nexium)
are also available over the counter to treat intermittent
heartburn.
Therapeutic Outcomes
The primary therapeutic outcomes expected from PPIs
are relief of discomfort, reduced frequency of heart-
burn, and healing of irritated tissues.
Nursing Implications for Proton Pump Inhibitor
Therapy
Premedication assessment. Check pattern of bowel
elimination; the PPIs may induce diarrhea.
Common adverse effects. The following symptoms
are relatively mild and rarely result in the discontin-
uation of therapy. Encourage the patient not to dis-
continue therapy without rst consulting the healthcare
provider.
Gastrointestinal
Diarrhea. Maintain the patient’s state of hydration.
Encourage the inclusion of sufcient roughage or ber
(fresh fruits, vegetables, whole-grain products) in the
diet. PPIs may be associated with an increased risk of
Clostridium difcile–associated diarrhea, especially in
hospitalized patients. Consider this diagnosis for diar-
rhea that does not improve. Use the lowest dose and
shortest duration of PPI therapy appropriate to the
condition being treated.
Neurologic. Headache, fatigue.
Musculoskeletal. Muscle pain.

Availability, dosage, and administration. See Table 32.3.
Omeprazole, lansoprazole, and esomeprazole need to
be taken before a meal. Capsules and tablets should
be swallowed whole; instruct the patient not to open,
chew, or crush.
Serious adverse effects
Skeletal
Risk of fractures. Patients older than 50 years who re-
ceived high doses of PPIs or used them for more than
1 year are at greater risk for fractures of the hip, wrist,

Table 32.3 Proton Pump Inhibitors

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE
dexlansoprazole Dexilant Capsules: 30, 60 mg PO: Initial: 60 mg once daily for
4–8 wk
Maintenance: 30 mg once daily
esomeprazole Nexium Capsules, delayed release (24 hr): IV, PO: Initial: 20–40 mg once daily
Do not confuse 20, 40, 49.3 mg for 4–8 wk
esomeprazole Powder for suspension: 2.5-, 5-, Maintenance: 20 mg daily
with 10-, 20-, 40-mg unit dose
omeprazole. IV: 40 mg
lansoprazole Prevacid Capsules, delayed release (24 hr): PO: Initial: 15–30 mg once daily
Do not confuse Prevacid 15, 30 mg 30 min before a meal for 4 wk
with Prinivil, Pepcid, Tablets, disintegrating: 15, 30 mg Maintenance: 15 mg once daily
Pravachol, Premarin, or Suspension: 3 mg/mL in 90, 150, Maximum: 30 mg once daily before
Prilosec. 300 mL bottles a meal
omeprazole Prilosec Capsules, delayed release: 10, 20, PO: Initial: 20 mg once daily for 4 wk
Do not confuse Do not confuse Prilosec 40 mg Maintenance: 20 mg daily
omeprazole with Prinivil, prednisone, Tablets, delayed release: 20 mg Zollinger-Ellison syndrome:
with Prevacid, Prinivil, or Prozac. Granules: 2.5, 10 mg Maximum: 120 mg three times
esomeprazole. Losec Suspension: 2 mg/mL in 90-, 150- daily
and 300-mL bottles
pantoprazole Protonix Tablets, delayed release: 20, 40 mg PO: Initial: 40 mg once daily for 8 wk
Do not confuse Protonix Granules for oral suspension: Maintenance: 40 mg daily
with Lotronex. 40 mg IV: Initial: 40 mg once daily for up
Pantoloc IV: 40 mg/vial to 7–10 days; switch to oral
dosages
rabeprazole Aciphex, Aciphex Sprinkle Tablets, delayed release: 20 mg PO: Initial: 20 mg daily after morning
Do not confuse Aciphex Capsules, sprinkle: 5, 10 mg meal for up to 4 wk
with Accupril, Adipex-P, or Maintenance: 20 mg once daily
Aricept. Maximum: 60 mg twice daily
Pariet
Available in Canada.
Do not confuse.
 Drugs Used to Treat Gastroesophageal Reux and Peptic Ulcer Disease CHAPTER 32
and spine. Patients who continue to receive PPIs and
who are at risk for osteoporosis should receive vitamin
D and calcium supplementation and have their bone
status monitored. Patients should not stop taking their
PPI unless told to do so by their healthcare provider.
Short-term, low-dose use of over-the-counter products
is not likely to cause an increased risk of fractures.
Electrolytes
Hypomagnesemia. Hypomagnesemia has been re-
ported with as little as 3 months of PPI therapy, but it
more commonly occurs in patients receiving PPIs for
more than 1 year. Hypomagnesemia can cause serious
adverse events, including tetany, tremors, seizures,
QT interval prolongation, and cardiac arrhythmias.
Healthcare providers should consider obtaining serum
magnesium levels before beginning long-term PPI
therapy, especially in patients receiving digoxin or pa-
tients receiving diuretics or other medicines known to
cause hypomagnesemia. Magnesium supplementation
may resolve the hypomagnesemia, but discontinuation
of the PPI may be necessary. Magnesium levels return
to normal within about a week of discontinuing PPI
therapy. Patients should not stop PPI therapy without
rst discussing it with their healthcare provider. Use
of over-the-counter PPIs taken according to directions
and for a limited duration has not been associated with
hypomagnesemia.
Vitamin B12 deciency. Treatment with PPIs for more
than 2 years may lead to vitamin B12 malabsorption
and subsequent vitamin B12 deciency; however, pa-
tients should not be routinely screened for vitamin B12
deciency. There is no evidence for or against testing
for B12 deciency for patients taking PPIs for longer
than 2 years.
Integumentary
Rash. Persistent vesicular rash from omeprazole
may be cause for discontinuing therapy. Report rashes
to the healthcare provider for further observation and
possible laboratory tests.
GI infection (e.g., Salmonella, Campylobacter). Use of
PPIs may increase risk of bacterial infections. Report
diarrhea, abdominal pain, or abdominal cramping to
the healthcare provider for further observation and
possible laboratory test assessment.
Drug interactions
Diazepam, triazolam, urazepam. Omeprazole and
esomeprazole signicantly increase the half-life of di-
azepam, triazolam, and urazepam by inhibiting their
metabolism. Observe patients for increased sedative
effects from these medicines. Caution against hazard-
ous tasks, such as driving and operating machinery.
The dosages of diazepam, triazolam, and urazepam
may have to be reduced.
Phenytoin. Omeprazole slows the metabolism of
phenytoin. Observe for nystagmus, sedation, and leth-
argy. The dosage of phenytoin may have to be reduced.
Clopidogrel. There has been a controversy in the
525
literature as to whether PPIs, especially omeprazole and
esomeprazole, prevent conversion of clopidogrel to its
active therapeutic metabolite. A consensus statement
by the American College of Cardiology Foundation, the
American Heart Association, and the American College
of Gastroenterology reports that clopidogrel alone and
aspirin alone and their combination are associated with
an increased risk of GI bleeding; that the risk of GI
bleeding increases as the number of risk factors increases
(e.g., prior GI bleeding, advanced age, concurrent use
of anticoagulants); that PPIs are appropriate in patients
with multiple risk factors for GI bleeding who are also
receiving antiplatelet therapy such as clopidogrel; that
a clinically signicant interaction cannot be excluded in
subgroups who are poor metabolizers of clopidogrel;
and that until solid evidence exists to support staggering
PPIs with clopidogrel, the dosing of PPIs should not be
altered.
Warfarin. Omeprazole and esomeprazole may re-
duce the rate of metabolism of warfarin. Monitor the
patient closely for signs of bleeding tendencies and
monitor the prothrombin time (INR) closely. Reduction
of warfarin dosage may be required.
Sucralfate. Sucralfate inhibits the absorption of PPIs.
Administer PPIs at least 30 minutes before sucralfate.
Altered absorption. The reduction in gastric acid se-
cretion may alter absorption of food and drugs as
follows:
• Ketoconazole, itraconazole capsules, iron: These medi-
cines require an acid medium for absorption. They
should be administered at least 30 to 45 minutes be-
fore PPI therapy.
• Insulin: The absorption of food may be altered and
an adjustment in timing or dosage of insulin in pa-
tients with diabetes may be required.
DRUG CLASS: COATING AGENT
sucralfate (sū-KRĂL-fāt)
Carafate (KĂR-ă-fāt)
Actions
When swallowed, sucralfate forms a complex that ad-
heres to the crater of an ulcer, thereby protecting it from
aggravators such as acid, pepsin, and bile salts; how-
ever, sucralfate does not inhibit gastric secretions (as do
the H2 antagonists) or alter gastric pH (as do antacids).
Uses
Sucralfate is used to treat duodenal ulcers, particularly
in those patients who do not tolerate other forms of
therapy.
Therapeutic Outcomes
The primary therapeutic outcomes expected from su-
cralfate therapy are relief of discomfort and healing of
irritated tissues.
526 UNIT VI Drugs Affecting the Digestive System
Nursing Implications for Sucralfate Therapy
Premedication assessment. Check pattern of bowel
elimination; sucralfate may induce constipation.
Availability. PO: 1-g tablets; 1-g/10-mL suspension.
Dosage and administration. Adult: PO: 1 tablet four
times a day 1 hour before each meal and at bedtime,
all on an empty stomach. Because antacid therapy is
often continued during early therapy of ulcer disease,
administer antacids at least 30 minutes before or after
sucralfate.
Common adverse effects. The following adverse ef-
fects are usually mild and tend to resolve with con-
tinued therapy. Encourage the patient not to discon-
tinue therapy without rst consulting the healthcare
provider.
Gastrointestinal
Constipation, dry mouth. Measures to alleviate dry
mouth include sucking on ice chips or hard candy.
Avoid mouthwashes that contain alcohol because
they cause further drying and irritation. Maintain the
patient’s state of hydration, and obtain an order for
stool softeners or bulk-forming laxatives if necessary.
Encourage the inclusion of sufcient roughage (e.g.,
fresh fruits, vegetables, whole-grain products) in the
diet.
Neurologic
Dizziness. Provide for patient safety during episodes
of dizziness.
Drug interactions
Digoxin. Sucralfate may interfere with the absorp-
tion of digoxin. Administer digoxin at least 2 hours be-
fore sucralfate. Monitor for decreased digoxin levels/
effects with initiation of sucralfate therapy.
Tetracyclines. Sucralfate may interfere with the ab-
sorption of tetracycline. Administer tetracyclines 1
hour before or 2 hours after sucralfate.
DRUG CLASS: PROKINETIC AGENT
metoclopramide (mĕt-ō-KLŌ-pră-mīd)
Reglan (RĔG-lăn)
Actions
Metoclopramide is a gastric stimulant whose mecha-
nisms of action are not fully known. It increases lower
esophageal sphincter pressure, thereby reducing re-
ux; increases stomach contractions; relaxes the py-
loric valve; and increases peristalsis in the GI tract,
resulting in an increased rate of gastric emptying and
intestinal transit. Metoclopramide is an antiemetic that
blocks dopamine in the chemoreceptor trigger zone.
It inhibits serotonin (5-hydroxytryptamine) when ad-
ministered in higher dosages.
Uses
Metoclopramide is used to relieve the symptoms of gas-
tric reux esophagitis and diabetic gastroparesis, as an
aid in small bowel intubation, and to stimulate gastric
emptying and intestinal transit of barium after radiolog-
ic examination of the upper GI tract. It is also given as
an antiemetic to patients undergoing cancer chemother-
apy. Treatment should be limited to less than 12 weeks.
Therapeutic Outcomes
The primary therapeutic outcomes expected from
metoclopramide therapy are relief of discomfort, re-
duced frequency of heartburn, and healing of irritated
tissues.
Nursing Implications for Metoclopramide Therapy
Premedication assessment
1. Determine whether other drugs being taken may in-
duce extrapyramidal symptoms; do not administer
metoclopramide concurrently.
2. Check for a history of epilepsy. If present, check
with the healthcare provider before starting drug
therapy.
3. Do not administer to an individual with symp-
toms of GI perforation, mechanical obstruction, or
hemorrhage.
4. For diabetic patients, food absorption may be al-
tered and more frequent monitoring for hypoglyce-
mia may be required.
Availability. PO: 5- and 10-mg tablets; 5-, 10-mg dis-
integrating tablets; 5-mg/5-mL solution.
Injection: 5 mg/mL in 2 mL vials.
Nasal spray: 15 mg in each 70-μL spray in 9.8 mL
nasal solution
Adults younger than 65 years: Nasal spray: Diabetic
gastroparesis: 1 spray (15 mg) in one nostril, 30 minutes
before each meal and at bedtime (maximum of four
times daily) for 2 to 8 weeks, depending on symptom-
atic response.
Caution. Approximately 1 in 500 patients may develop
extrapyramidal symptoms manifested by restlessness,
involuntary movements, facial grimacing, and possibly
oculogyric crisis, torticollis, or rhythmic tongue protru-
sion. Children and young adults are most susceptible, as
are patients receiving higher doses of metoclopramide
as an antiemetic. Metoclopramide should not be used
in patients with epilepsy or those receiving drugs likely
to cause extrapyramidal reactions (e.g., phenothiazines)
because the frequency and severity of seizures or extra-
pyramidal reactions may be increased. Metoclopramide
must not be used in patients when increased gastric
motility may be dangerous, such as with GI perforation,
mechanical obstruction, or hemorrhage.
Dosage and administration. Adult: PO: Diabetic gastro-
paresis: 10 mg four times a day 30 minutes before each
 Drugs Used to Treat Gastroesophageal Reux and Peptic Ulcer Disease CHAPTER 32
meal and at bedtime. Duration of therapy depends on
response and continued well-being after discontinua-
tion of therapy. It is not recommended to use for more
than 12 weeks.
Adult: PO: Gastroesophageal reux: 10 to 15 mg up to
four times daily 30 minutes before meals and at bed-
time. It is not recommended to use for more than 12
weeks.
Adult: IV: Chemotherapy antiemesis: Initially two
doses, 1 to 2 mg/kg, or 2 mg/kg if highly emeto-
genic chemotherapy is being used. If vomiting is sup-
pressed, follow with 1 mg/kg. Dilute the dose in 50 mL
of parenteral solution (dextrose 5% in water, normal
saline [0.9%], dextrose 5%/0.45% saline, Ringer solu-
tion, or lactated Ringer solution). Infuse over at least 15
minutes, 30 minutes before beginning chemotherapy.
Repeat every 2 hours for two doses, followed by one
dose every 3 hours for three doses.
Medication Safety Alert
Rapid IV infusion of metoclopramide (Reglan) may cause
sudden, intense anxiety and restlessness, followed by
drowsiness. If extrapyramidal symptoms should develop,
treat with diphenhydramine.
Common adverse effects. The following adverse ef-
fects are usually mild and tend to resolve with con-
tinued therapy. Encourage the patient not to discon-
tinue therapy without rst consulting the healthcare
provider.
Neurologic
Drowsiness, fatigue, lethargy, dizziness. People who
work around machinery, drive a car, or perform other
duties that require mental alertness should be particu-
larly cautious. Provide patient safety during episodes
of dizziness.
527
Gastrointestinal. Nausea.
Serious adverse effects
Extrapyramidal symptoms. Provide for patient safe-
ty and then report extrapyramidal symptoms to the
healthcare provider immediately.
Drug interactions
Drugs that increase sedative effects. Antihistamine,
alcohol, analgesics, phenothiazines, and sedative-
hypnotics increase the sedative effects of metoclopra-
mide. Monitor the patient for excessive sedation and
reduce dosage if necessary.
Drugs that decrease therapeutic effects. Anticholinergic
agents (e.g., atropine, benztropine, antihistamines, di-
cyclomine) and opiate agonists (e.g., meperidine, mor-
phine, oxycodone) decrease the therapeutic effects of
metoclopramide. Instruct the patient to avoid taking
these agents while using metoclopramide.
Altered absorption. The GI stimulatory effects of me-
toclopramide may alter absorption of food and drugs
as follows:
• Digoxin: Monitor for decreased activity (e.g., return
of edema, weight gain, heart failure).
• Levodopa: Metoclopramide may decrease the effects
of levodopa. Monitor for increased parkinsonian ac-
tivity (e.g., restlessness, nightmares, hallucinations,
additional involuntary movements such as bobbing
of head and neck, facial grimacing, active tongue
movements).
• Alcohol: Monitor for signs of sedation and intoxica-
tion with smaller amounts of alcohol.
• Insulin: The absorption of food may be altered, and
an adjustment in timing or dosage of insulin in pa-
tients with diabetes mellitus may be required.
528 UNIT VI Drugs Affecting the Digestive System

Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions

Key Points NCLEX item type: Cloze

Cognitive skill: Recognize cues
• GERD and PUD continue to be common illnesses
that are often self-treated initially. Once medication 2. A nurse caring for a patient with diabetes who was diagnosed
therapy has been instituted, it is important to explain with gastroparesis would expect which drug to work as a gastric
thoroughly the medications prescribed and adverse effects stimulant?
that should be expected or reported. Some medications 1. Pantoprazole (Protonix)
taken for GERD and PUD can have signicant 2. Metoclopramide (Reglan)
adverse effects that will need healthcare provider 3. Sucralfate (Carafate)
management. 4. Misoprostol (Cytotec)
• Solicit information about whether symptoms have
Objective: Discuss the drug classications and actions used to
decreased and whether the patient is experiencing adverse
treat stomach disorders.
effects from therapy. Have the patient maintain a record of
NCLEX item type: Multiple choice
the pain using a standard pain rating scale. Also, have the
Cognitive skill: Understanding
patient record the degree of relief obtained at a specied
interval after medications have been taken. 3. Which statement by the patient would indicate to the nurse that
• Assess and make recommendations regarding lifestyle further teaching is needed about how the defense mechanisms of
changes that are necessary to prevent symptom the stomach can be compromised to cause PUD?
recurrence. If symptoms have not begun to diminish over 1. “I should be careful about taking aspirin because it may
2 weeks, the nurse should encourage the person to seek cause damage to my stomach lining.”
medical attention. 2. “My doctor tells me that my stomach has an infection
called H. pylori that caused this ulcer.”
Additional Learning Resources 3. “As I understand it, I have an overproduction of stomach
SG Go to your Study Guide for additional Review Questions acid that caused my ulcer.”
for the NCLEX® Examination, Critical Thinking Clinical Situa- 4. “I need to be careful about drinking too much orange
tions, and other learning activities to help you master this chap- juice because it is acidic and can damage my stomach
ter content. lining.”
Objective: Identify factors that prevent breakdown of the body’s
Go to your Evolve website (https://evolve.elsevier.com/Willihng normal defense barriers resulting in ulcer formation.
anz) for additional online resources. NCLEX item type: Multiple choice
Cognitive skill: Comprehension
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of 4. The nurse was discussing the mechanism of action for pantoprazole
the NCLEX exam and include both NGN (Next Generation) and with the patient in the scenario recently diagnosed with GERD and
traditional questions. See Chapter 1 for further information re- realized further education was needed after the patient made
garding question types. which statement?
1. “I understand that pantoprazole will inhibit my stomach
Scenario from producing acid.”
2. “So this drug will coat the lining of my stomach so I do
A patient came to the clinic with complaints of frequent bouts not get GERD symptoms.”
of acid reux to the point that it was causing waking in the mid- 3. “When I take this, it will not affect how fast my food is
dle of the night. digested.”
4. “I can expect that pantoprazole will relieve my symptoms
1. Choose the most likely options for the information missing from
of heartburn.”
the sentence below by selecting from the lists of options provided.
Objective: Discuss the drug classications and actions used to
Proton pump inhibitors and antibiotics are often used in treat stomach disorders.
combination to eradicate_______1_________, which is NCLEX item type: Multiple choice
caused by ________2___________. Cognitive skill: Comprehension
5. The nurse instructing the patient in the scenario on how to reduce
OPTION 1 OPTION 2 acid production in the stomach to prevent GERD indicated which
measures should be taken? (Select all that apply.)
Gastroparesis Helicobacter pylori
1. Decrease or stop smoking.
GERD Clostridium difcile
2. Decrease the amount of coffee consumed.
Peptic ulcer disease Giardia lamblia 3. Increase the amount of spicy foods consumed.
Heartburn Listeria monocytogenes 4. Decrease the amount of alcohol intake.
5. Increase the amount of carbonated beverages.
GERD, Gastroesophageal reux disease.
6. Increase the amount of caffeinated beverages.
Objective: Discuss common stomach disorders that require drug 7. Decrease the amount of stress experienced every day.
therapy. 8. Increase the amount of uids consumed during meals.
 Drugs Used to Treat Gastroesophageal Reux and Peptic Ulcer Disease CHAPTER 32 529

Objective: Identify interventions that incorporate pharmacologic
and nonpharmacologic treatments for an individual with stomach
disorders.
NCLEX item type: Extended multiple response
Cognitive skill: Application
6. The nurse is reviewing the medications used for common stomach
disorders. Indicate with an X which common stomach disorder is
treated with which class of drug.

PPI H2 BLOCKERS ANTACIDS COATING AGENTS PROKINETIC AGENTS

Hypersecretory disorders
Duodenal ulcers
Gastroparesis
GERD
GERD, Gastroesophageal reux disease; H2 blockers, histamine-2 receptor antagonists; PPI, proton pump inhibitors.

Objective: Discuss the drug classications and actions used to

treat stomach disorders.
NCLEX item type: Matrix
Cognitive skill: Recognize cues
33 Drugs Used to Treat Nausea and Vomiting

https://evolve.elsevier.com/Willihnganz

Objectives
1. Describe the common causes of nausea and vomiting and 3. Compare the therapeutic classes of antiemetics with their
the interventions that apply. uses.
2. Discuss the three types of nausea associated with
chemotherapy and the nursing considerations.

Key Terms
nausea (NŎ-zē-ă) (p. 530)
vomiting (VŎ-mĭt-ĭng) (p. 530)
emesis (ĔM-ĕ-sĭs) (p. 530)
retching (RĔCH-ĭng) (p. 530)
regurgitation (rē-gŭr-jĭ-TĀ-shŭn)
(p. 530)
postoperative nausea and vomiting
(PONV) (pōst-ŎP-ĕr-ă-tĭv)
(p. 531)
hyperemesis gravidarum (hī-pĕr- emetogenicity (ĕ-MĔ-tō-gĕ-NĬ-sĭ-tē)
ĔM-ĕ-sĭs gră-vĭ-DĂR-ŭm) (p. 532) (p. 532)
psychogenic vomiting (sī-kō-JĔN-ĭk) delayed emesis (p. 533)
(p. 532) radiation-induced nausea and
chemotherapy-induced nausea and vomiting (RINV) (p. 533)
vomiting (CINV) (kē-mō-THĔR-ă-
pē) (p. 532)
anticipatory nausea and
vomiting (ăn-TĬ-sĕ-pĕ-tō-rē) (p. 532)

NAUSEA AND VOMITING

Nausea is the sensation of abdominal discomfort that
is intermittently accompanied by a desire to vomit.
Vomiting is the forceful expulsion of gastric contents
(emesis) up the esophagus and out the mouth. Nausea
may occur without vomiting and sudden vomiting
may occur without prior nausea, but the two symp-
toms often occur together. Retching is the involuntary
labored, spasmodic contractions of the abdominal and
respiratory muscles without emesis (also known as
dry heaves). Nausea and vomiting accompany almost
any illness, are experienced by virtually everyone at
one time or another, and have a wide variety of causes
(Box 33.1).
The primary anatomic areas involved in vomiting
are shown in Fig. 33.1. The vomiting center (VC; also
referred to as the central pattern generator), located in
the medulla of the brain, coordinates the vomiting re-
ex. Nerves from sensory receptors in the pharynx,
stomach, intestines, and other tissues connect directly
with the VC through the vagus and splanchnic nerves
and produce vomiting when stimulated. The VC also
responds to stimuli originating in other tissues, such as
the cerebral cortex, the vestibular apparatus of the in-
ner ear, and blood. These stimuli travel rst to the che-
moreceptor trigger zone (CTZ), which then activates
the VC to induce vomiting. The CTZ is also located in
the medulla. An important function of the CTZ is to
530
sample blood and spinal uid for potentially toxic sub-
stances and, when detected, to initiate the vomiting re-
ex. The CTZ cannot initiate vomiting independently,
but only by stimulating the VC. Both the VC and the
CTZ are much smaller than shown in Fig. 33.1
The cerebral cortex of the brain can be a source
of stimulus or suppression of the VC (see Fig. 33.1).
Vomiting can occur as a conditioned response (e.g., see
Anticipatory Nausea and Vomiting later in this chap-
ter) or as a reaction to unpleasant sights and smells.
Suppression of motion sickness by the person’s con-
centration on some mental activity is an example of
cortical control of the vomiting reex. Psychological
factors can play an important role (see Psychogenic
Vomiting later in this chapter).
When the VC is stimulated, nerve impulses are sent
to the salivary, vasomotor, and respiratory centers. The
vomiting reex begins with a sudden deep inspiration
that increases abdominal pressure, which is further
increased by contraction of the abdominal muscles.
The soft palate rises and the epiglottis closes, thus pre-
venting aspiration of vomitus into the lungs. The py-
loric sphincter contracts and the cardiac sphincter and
esophagus relax, allowing stomach contents to be ex-
pelled. The ow of saliva increases to aid the expulsion.
Autonomic symptoms of pallor, sweating, and tachycar-
dia cause additional discomfort associated with vomit-
ing. Regurgitation occurs when the gastric or esophageal
 Drugs Used to Treat Nausea and Vomiting CHAPTER 33 531

Box 33.1 Causes of Nausea and Vomiting Risk Factors for Postoperative Nausea and
Table 33.1
Vomiting
• Infection
• Gastrointestinal disorders (e.g., gastritis; liver, CATEGORY RISK FACTORS
gallbladder, or pancreatic disease) Patient related Women
• Overeating or irritation of the stomach by certain foods History of PONV
or liquids Motion sickness
• Motion sickness Nonsmoking status
• Drug therapy (nausea and vomiting are the most Young age (<50 years old)
common adverse effects of drug therapy) Anesthesia related Prolonged duration of anesthesia
• Surgical procedures (e.g., abdominal surgery, Intraoperative and postoperative
extraocular and middle ear manipulations, testicular administration of:
traction) •  Opioid analgesics
• Emotional disturbances and mental illness •  Volatile agents
• Pregnancy •  Nitrous oxide
• Pain and unpleasant sights and odors Surgery related Prolonged surgery procedures
Type of surgery:
•  Neurosurgery
Unpleasant stimuli •  Intraabdominal surgery
from environment •  Cholecystectomy
(e.g., sight, smell, •  Laparoscopic surgery
emotional shock) •  Gynecologic surgery
PONV, Postoperative nausea and vomiting.
Disturbances of Modied from Apfel CC, Heidrich FM, Jukar-Rao S, etal. Evidence-based analysis of
Cortical input balance (e.g., risk factors for postoperative nausea and vomiting. Br J Anaesth. 2012;109(5):742-
motion sickness) 753; and Matthews C. A review of nausea and vomiting in the anesthetic and post
1 anesthetic environment. J Perioper Pract. 2017;27(10):224-227.

3
2 Vestibular
4 apparatus
contents rise to the pharynx because of greater pressure
(gas bubbles, tight clothing, body position) in the stom-
ach and should not be confused with vomiting.

COMMON CAUSES OF NAUSEA AND

VOMITING
Vestibular input
Direct input from
POSTOPERATIVE NAUSEA AND VOMITING
drugs, toxins, Postoperative nausea and vomiting (PONV) remains a
metabolites, etc.
carried by blood
common complication after anesthesia and surgery.
PONV may result in dehydration, electrolyte imbalance,
pulmonary aspiration, and delayed hospital discharge.
5 Throat, epiglottis,
etc. The risk factors for PONV are categorized as patient
related, anesthesia related, and surgery related (Table
Input from sensory Efferent fibers 33.1). In general, the potential for PONV increases with
receptors in stomach (vagal) mediating the number of risk factors present in a particular patient.
and intestines carried vomiting reflex These risk factors are used for risk score assessments
by afferent fibers
Stomach to estimate a patient’s baseline risk for PONV and to fa-
cilitate the decision-making process about the number
Chemoreceptor and choice of antiemetics used for PONV prevention.
trigger zone (CTZ)
4 Vomiting center MOTION SICKNESS
Nausea and vomiting associated with motion are
3
thought to result from stimulation of the labyrinth sys-
tem of the ear, with subsequent transmission of this
Fig. 33.1 Sites of action of antiemetic medicines. 1, Cerebral
stimulus to the vestibular network located near the VC.
cortex: anxiolytic agents; 2, vestibular apparatus: antihistamine
and anticholinergic agents; 3, chemoreceptor trigger zone and When there is strong or frequent stimulation, such as
gastrointestinal (GI) tract: dopamine antagonists; 4, serotonin receptors from a rocking ship or airplane, the vestibular network
in GI tract and vomiting center (VC): serotonin antagonists; 5, neurokinin is bombarded with an abnormally high number of stim-
receptors in VC: neurokinin-1 receptor antagonists. (Adapted from uli that radiate by cholinergic nerve impulses to the ad-
Clayton BD, Brown BK. Nausea and vomiting. In: Helms RA, Quan
jacent VC. Therefore drugs that inhibit the cholinergic
DJ, Herndel ET, Gourley DR, eds. Textbook of Therapeutics: Drug
and Disease Management. 8th ed. Philadelphia: Lippincott Williams & nerve impulses from the vestibular network to the VC
Wilkins; 2006.) should be effective in treating motion sickness.
532 UNIT VI Drugs Affecting the Digestive System

NAUSEA AND VOMITING IN PREGNANCY

Potential of Emesis With Intravenous
The percentage of women reporting vomiting during Table 33.2
Antineoplastic Agentsa
the rst 16 weeks of gestation is relatively constant at
HIGH (>90%)
about 40%, decreasing to 20% from 17 to 20 weeks; 9%
of women report vomiting after 20 weeks of pregnancy. anthracycline/ cyclophosphamide
cyclophosphamide ≥1500 mg/m2
Vomiting is much more common among primigravidas,
combination dacarbazine
younger women, nonsmokers, African Americans, and
carmustine mechlorethamine
women with obesity. Contrary to commonly held be- cisplatin streptozotocin
liefs, vomiting is not more common in women who have
MODERATE (30%–90%)
experienced prior fetal losses or women with hyper-
tension, proteinuria, or diabetes. There is also no asso- alemtuzumab epirubicin
azacitidine idarubicin
ciation between vomiting and cohabitation; unplanned
bendamustine ifosfamide
pregnancy; or gallbladder, liver, or thyroid disease. carboplatin irinotecan
Although traditionally described as “morning sick- clofarabine oxaliplatin
ness,” most women report that symptoms of nau- cyclophosphamide <1500 mg/ romidepsin
sea and vomiting tend to persist to varying degrees m2 temozolomide
throughout the day. The cause of morning sickness is cytarabine >1 g/m2 thiotepa
unknown, but its occurrence and severity appear to be daunorubicin trabectedin
related to the levels of free and bound estradiol and sex doxorubicin
hormone–globulin-binding capacity. LOW (10%–30%)
A woman with severe persistent vomiting that in- aibercept 5-uorouracil gemcitabine
terferes with nutritional, uid, and electrolyte bal- atezolizumab ipilimumab
ance may be experiencing hyperemesis gravidarum, a belinostat ixabepilone
condition in which starvation, dehydration, and aci- blinatumomab methotrexate
dosis are superimposed on the vomiting syndrome. bortezomib mitomycin
Hospitalization for uid, electrolyte, and nutritional brentuximab vedotin mitoxantrone
therapy may be required. cabazitaxel paclitaxel
carlzomib panitumumab
PSYCHOGENIC VOMITING catumaxomab pemetrexed
cetuximab pertuzumab
Psychogenic vomiting can be self-induced, or it can cytarabine ≤1000 mg/m2 temsirolimus
occur involuntarily in response to situations that the docetaxel topotecan
person considers threatening or distasteful (e.g., eating eribulin trastuzumab-emtansine
food whose origin is considered repulsive). etoposide vinunine
elotuzumab
CHEMOTHERAPY-INDUCED NAUSEA AND MINIMAL
VOMITING
bevacizumab pixantrone
Chemotherapy-induced nausea and vomiting (CINV) is bleomycin pralatrexate
the most unpleasant adverse effect associated with the busulfan ramucirumab
use of cancer chemotherapy. Many patients regard it as cladribine rituximab
the most stressful aspect of their disease, more so even (2-chlorodeoxyadenosine) trastuzumab
than the prospect of dying. Because the object of cancer udarabine vinblastine
therapy is at least to prolong life, the effect of CINV on nivolumab vincristine
the quality of life must be considered. ofatumumab vinorelbine
pembrolizumab
Three types of emesis have been identied in pa-
tients receiving antineoplastic therapy: anticipatory aEstimated incidence without prophylaxis.
Data from Roila F, Moassiotis A, Aapro M, etal. 2016 MASCC and ESMO
nausea and vomiting, acute CINV, and delayed emesis. guideline update for the prevention of chemotherapy- and radiotherapy-
Anticipatory nausea and vomiting is a conditioned induced nausea and vomiting and of nausea and vomiting in advanced cancer
patients. Ann Oncol. 2016;27:19-33; and Hesketh PJ, Kris MG, Basch E, etal.
response triggered by the sight or smell of the clinic Antiemetics: American Society of Clinical Oncology Clinical Practice Guideline
or hospital or by the knowledge that treatment is im- Update. J Clin Oncol. 2017;35:3240-3261.
minent. The onset of anticipatory nausea and vomiting
is usually 2 to 4 hours before treatment and is most type of emesis may begin minutes to hours after che-
severe at the time of chemotherapy administration. motherapy has been administered and usually occurs
Patients who experience anticipatory nausea and vom- within the rst 24 hours. The emetogenicity of antineo-
iting are more likely to be younger (<50 years), female, plastic drugs is highly variable, ranging from an inci-
experienced CINV in previous treatment cycles, and dence of almost 100% with high-dose cisplatin to less
more susceptible to motion sickness. than 10% with chlorambucil. Table 33.2 summarizes
Acute CINV may be stimulated directly by chemo- chemotherapeutic agents in terms of emetogenicity.
therapeutic agents. These agents have emetogenicity, Emetogenicity also is inuenced by dosage, duration,
which refers to having the ability to cause emesis. This and frequency of administration.
 Drugs Used to Treat Nausea and Vomiting CHAPTER 33
Patient factors also affect acute CINV. The incidence
and severity are generally higher in younger people,
women, those in poor general health, and those with
metabolic disorders (e.g., uremia, dehydration, infec-
tion, gastrointestinal [GI] obstruction). Patients with a
history of motion sickness seem to be more sensitive
to the emetic effects of cytotoxic agents. The patient’s
outlook and attitude about cancer and therapy can sig-
nicantly inuence the frequency and severity of nau-
sea and vomiting.
Delayed emesis usually starts more than 24 hours
after treatment ends and can last up to a few days.
The mechanisms are not known, but delayed emesis
in patients receiving chemotherapy may be induced
by metabolic by-products of the chemotherapeutic
agent or by destruction of malignant cells. The eme-
sis experienced is usually less severe than that which
occurs acutely with chemotherapy, but it still can be
signicant in reducing quality of life, nutrition, and
hydration. Patients who have acute emesis also may
experience delayed emesis. Events that often trigger
delayed nausea and vomiting are brushing teeth, us-
ing mouthwash, manipulating dentures, seeing food,
and quickly standing up while getting out of bed after
awakening in the morning.
RADIATION-INDUCED NAUSEA AND VOMITING
Another common cause of emesis associated with the
treatment of cancer is radiation-induced nausea and
vomiting (RINV). The use of high-energy radiation from
x-rays, gamma rays, neutrons, and other sources to
kill cancer cells and shrink tumors also induces nau-
sea and vomiting, especially when concurrent chemo-
therapy is used. Radiation may come from a machine
outside the body (external beam radiation therapy), or
it may come from radioactive material placed in the
body near cancer cells (internal radiation therapy, im-
plant radiation). The frequency of RINV depends on
the treatment site, dose of radiation delivered per frac-
tion, and total dose delivered.
DRUG THERAPY FOR SELECTED
CAUSES OF NAUSEA AND VOMITING
Control of vomiting is important for relieving the ob-
vious distress associated with it and preventing aspi-
ration of gastric contents into the lungs, dehydration,
and electrolyte imbalance. Primary treatment of nau-
sea and vomiting should be directed at the underlying
cause. Because this is not always possible, treatment
with nondrug and drug measures is appropriate. Most
medicines (antiemetics) used to treat nausea and vom-
iting act either by suppressing the action of the VC or
by inhibiting the impulses going to or coming from
the center. These agents are generally more effective if
administered before the onset of nausea, rather than
after it has started. The seven classes of agents used
as antiemetics are dopamine antagonists, serotonin
533
antagonists, anticholinergic agents, corticosteroids,
benzodiazepines, cannabinoids, and neurokinin-1
(NK1) receptor antagonists.
POSTOPERATIVE NAUSEA AND VOMITING
PONV is complex and has no single cause. It involves
a host of patient, anesthesia, surgery- related risk
factors. Therefore successful treatment with a single
pharmacologic agent for all cases is unlikely. Measures
such as limiting patient movement and preventing
gastric distention can reduce PONV. Adequate anal-
gesia can also forestall this complication. Nonsteroidal
antiinammatory analgesics are not emetogenic (opi-
oids are emetogenic) and should be given consider-
ation if appropriate to the type of surgical procedure.
Antiemetics used include dopamine antagonists, an-
ticholinergic agents, and serotonin antagonists. The
histamine-2 antagonists (e.g., cimetidine, famotidine)
are also used to reduce gastric secretions to minimize
nausea and vomiting.
Patients at low risk for PONV usually do not
need prophylactic therapy and may be managed
with an as-needed (PRN) order, but patients who
are considered to be at moderate to high risk should
be considered for prophylactic antiemetic therapy.
In addition to minimizing the risk factors listed, a
multimodal treatment approach is recommended
because of the variety of receptor types associated
with PONV. Therapy may include hydration, sup-
plemental oxygen, a benzodiazepine for anxiolysis,
a combination of antiemetics that work by different
mechanisms (e.g., dexamethasone, serotonin antag-
onist), intravenous (IV) anesthesia induction agents
(e.g., propofol and remifentanil), and analgesia with
a nonsteroidal antiinflammatory drug (NSAID; e.g.,
ketorolac) rather than an opioid. Nonpharmacologic
techniques before surgery using acupuncture, trans-
cutaneous electrical nerve stimulation, and acupres-
sure stimulation have also been shown to reduce
PONV.
The rst step in treating PONV is to identify the
cause. If a nasogastric (NG) tube is in place, check its
patency and placement in preventing abdominal dis-
tention. Do not move an NG tube that was inserted dur-
ing surgery (e.g., gastric resection); in this case, there is
a danger of penetrating the suture line. Irrigation of a
blocked NG tube may alleviate the nausea and vomit-
ing. (A healthcare provider’s order to irrigate the NG
tube is required.) Administration of PRN antiemetics
when the patient rst reports nausea will often prevent
vomiting.
MOTION SICKNESS
Most agents used to reduce nausea and vomiting from
motion sickness are chemically related to antihista-
mines. The effectiveness of antihistamines in motion
sickness probably results from their anticholinergic
properties, not from their ability to block histamine.
534 UNIT VI Drugs Affecting the Digestive System
NAUSEA AND VOMITING IN PREGNANCY
For women experiencing nausea and/or vomiting as-
sociated with pregnancy, an initial treatment approach
is dietary changes, hydration and lifestyle changes,
such as trigger avoidance. The expectant woman
should be advised to eat small, frequent, dry meals
and to avoid fatty foods and other foods found to
cause problems. Sometimes it may be difcult or im-
possible to work in the kitchen around food, and as-
sistance may be required.
In about 10% to 15% of cases, dietary measures
alone will be insufcient and drug therapy should
be considered. Drugs that have been widely used
for treating morning sickness are vitamin B6, anti-
histamines (doxylamine, diphenhydramine, dimen-
hydrinate, meclizine), and phenothiazines such as
promethazine and prochlorperazine. Ginger, an herb
(see Chapter 47), is used in many cultures to treat
pregnancy-induced nausea and vomiting. From a
safety standpoint, vitamin B6 (pyridoxine) alone or
vitamin B6 plus doxylamine are generally recom-
mended rst. If persistent vomiting threatens ma-
ternal nutrition, promethazine may be considered.
If antidopaminergic antiemetic therapy is required,
prochlorperazine is the safest time-tested medicine.
Ondansetron and metoclopramide have been shown
to be effective antiemetics in treating hyperemesis
gravidarum, and no teratogenic effects have been re-
ported to date.
PSYCHOGENIC VOMITING
When a person has chronic or recurrent vomiting,
a diagnosis of psychogenic vomiting is made after
eliminating all other possible causes. The person
with psychogenic vomiting usually does not lose
weight and can control vomiting in certain situa-
tions (e.g., in public). Identication of the causes of
psychogenic vomiting and successful resolution of
the problem may not be possible. After an extensive
workup eliminates other potential causes, a short
course of an antiemetic drug (e.g., metoclopramide)
or an antianxiety drug may be prescribed, along with
counseling.
ANTICIPATORY NAUSEA AND VOMITING
People with a negative attitude toward therapy, such
as the belief that it will be of no benet, are more likely
to develop anticipatory nausea and vomiting. It tends
to become more severe as treatments progress unless
behavior therapy modies the conditioned response.
Such treatments include progressive muscle relax-
ation, guided imagery, hypnosis, self-hypnosis, sys-
tematic desensitization, music therapy, acupressure,
and benzodiazepines (alprazolam, lorazepam). Nurses
can play a signicant role by maintaining a positive
supportive attitude with the patient and making sure
that the patient receives antiemetic therapy before each
course of chemotherapy.
CHEMOTHERAPY-INDUCED NAUSEA AND
VOMITING
Antiemetic therapy to minimize acute CINV is based
on the emetogenic potential of the antineoplastic
agents used (see Table 33.2). Combinations of anti-
emetics are often used, based on the assumption that
antineoplastic agents produce emesis by more than one
mechanism. In general, all patients being treated with
chemotherapeutic agents of moderate to high emeto-
genic potential should receive prophylactic antiemetic
therapy before chemotherapy is started. Combinations
of a serotonin antagonist (ondansetron, granisetron,
or palonosetron) with dexamethasone, NK1 antago-
nists (aprepitant, rolapitant), olanzapine, and possi-
bly lorazepam are used for highly emetogenic agents.
There is also an oral xed-dose combination of an NK1
receptor antagonist (netupitant) and palonosetron
(Akynzeo) available for CINV. Antiemetic therapy
should be continued for 2 to 4 days to prevent delayed
vomiting. Emesis induced by moderately emetogenic
agents may be treated prophylactically with a similar
regimen (without olanzapine), and therapy should
be continued for 24 hours. Dexamethasone is recom-
mended if chemotherapy has low emetic potential; a
phenothiazine (prochlorperazine) or metoclopramide
is recommended if dexamethasone is contraindicated.
Lorazepam may be added to the antiemetic regimen
if necessary. Antiemetic therapy is not recommended
with medications with minimum emetic risk, although
dexamethasone, metoclopramide, or prochlorperazine
may be used to prevent delayed emesis. All antiemet-
ics should be given an adequate amount of time before
chemotherapy is initiated and should be continued for
an appropriate time after the antineoplastic agent has
been discontinued.
DELAYED EMESIS
In general, patients who have acute emesis managed
appropriately have a much lower incidence of delayed-
onset emesis. Studies have indicated that providing
optimal antiemetic therapy with the chemotherapy
will signicantly reduce the frequency of delayed em-
esis. A four-drug combination of an NK1 antagonist
(e.g., aprepitant, fosaprepitant, or rolapitant), a dopa-
mine antagonist (olanzapine), a serotonin antagonist
(e.g., granisetron) and dexamethasone OR the xed
combination of netupitant/palonosetron, olanzapine
and dexamethasone have proven to signicantly re-
duce the incidence of acute and delayed emesis with
highly emetogenic chemotherapy. A combination of
prochlorperazine and lorazepam given orally has suc-
cessfully controlled delayed emesis with chemothera-
peutic agents with lower emetogenicity.
RADIATION-INDUCED NAUSEA AND VOMITING
Clinical guidelines recommend that patients who will
be receiving total body irradiation or upper abdomen
or craniospinal irradiation should receive preventive
 Drugs Used to Treat Nausea and Vomiting CHAPTER 33
antiemetic therapy. The serotonin antagonists (e.g.,
granisetron, ondansetron), with or without dexameth-
asone, are approved and recommended to treat RINV.
Patients at low to intermediate risk for RINV should re-
ceive serotonin antagonists or prochlorperazine before
each dose of radiation. Rescue medicines used to treat
RINV include prochlorperazine and metoclopramide.
Patients who require rescue antiemetic therapy should
be pretreated with a serotonin antagonist before the
next dose of radiation therapy.
NURSING IMPLICATIONS FOR NAUSEA AND
VOMITING
Nausea and vomiting are associated with illnesses of
the GI tract and other body systems and with adverse
effects of medications and food intolerance. Nursing
care must be individualized to the patient’s diagnosis
and needs at all times.
Assessment
History
• Obtain a history of the patient’s symptoms—onset,
duration, frequency, volume, and description of the
vomitus (e.g., color: dark brown or black [coffee-
ground emesis], greenish yellow, red-tinged; consis-
tency; presence of undigested food particles).
• Ask the patient’s perception of precipitating fac-
tors, such as foods, odors, medications, stress, or
treatment (e.g., chemotherapy, radiation therapy,
surgery). Is there actual emesis, or is it primarily
retching?
• Is there a history of obstruction, asthma, and/or
narrow-angle glaucoma?
Medications
• Ask the patient to list all current over-the-counter
medications being taken (including herbal supple-
ments) or those prescribed by a healthcare provider.
Are any used to treat nausea and vomiting?
• Schedule prescribed medications on the medica-
tion prole, and requisition the medicines from the
pharmacy.
• Ensure that antiemetics to be given before chemo-
therapy or irradiation therapy are marked precisely
as ordered on the medication prole, along with
around-the-clock or PRN orders.
Basic assessment. Individualize the assessment pro-
cedure to the underlying cause of the symptoms if
known.
• Vital signs: Obtain baseline vital signs, height, and
weight.
• Abdomen: Assess bowel sounds in all four quadrants
of the abdomen. Observe the size and shape of the
abdomen. Note any signs of distention, ascites, or
masses.
• Hydration: Assess and record signs of dehydration,
such as nonelastic skin turgor, sticky oral mucous
535
membranes, excessive thirst, shrunken and deeply
furrowed tongue, crusted lips, weight loss, deterio-
rating vital signs, soft or sunken eyeballs, delayed
capillary lling, high urine specic gravity or no
urine output, and possible mental confusion.
Laboratory studies. Review laboratory reports for in-
dications that include malabsorption, protein deple-
tion, or dehydration (uid, electrolytes, blood urea
nitrogen, creatinine, and acid-base imbalances), and
for other values (e.g., K+, Cl−, pH, partial pressure of
CO2, bicarbonate, hemoglobin, hematocrit, urinalysis
[urine specic gravity], serum albumin, total protein).
The scope of laboratory data gathered will depend on
the underlying cause of the nausea and vomiting and
severity of the symptoms.
Nursing considerations
• Record intake and output, vital signs every shift or
more frequently depending on patient’s status, and
daily weights.
• Schedule oral hygiene measures.
Implementation
Nutrition
• Obtain specic orders relating to nutrition. Diet or-
ders will depend on the underlying cause and se-
verity of the nausea and vomiting.
• Obtain specic orders for diet, such as nothing by
mouth (NPO) with NG suction, IV uids, or enteral
or parenteral nutrition.
• As the patient’s condition improves, obtain orders
for a gradual progression of diet.
• Maintain hydration via oral or parenteral forms as
prescribed by the prescriber.
 • Adults: The usual treatment includes discontinu-
ation of solid foods and ingestion of oral rehydra-
tion solutions or clear juices. Depending on the
severity of the condition or underlying cause, the
patient may be NPO with an NG tube in place for
decompression of the stomach to reduce the risk
of vomiting. As the patient’s condition improves,
the diet is advanced from clear liquids to small,
frequent, low-fat feedings to bland or normal
diet. Generally, high-fat foods, milk products,
whole grains, and raw fruits and vegetables are
initially avoided.
 • Infants: Formula, milk products, and solid foods
usually are discontinued. Fluids are offered ev-
ery 30 to 60 minutes in small amounts (30 to 60
mL). The volume is gradually increased as toler-
ance improves. Oral rehydration solutions (e.g.,
Pedialyte, diluted gelatin, water, decarbonated
colas, ginger ale) may be offered. Monitor for lac-
tose intolerance when formula is reintroduced.
Formula is generally given in a diluted form
when reinitiated and gradually increased to full
strength.
536 UNIT VI Drugs Affecting the Digestive System
• Monitor hydration status using vital signs, skin tur-
gor, daily weights, and moisture of mucous mem-
branes, as well as intake and output.
• Perform a physical assessment every shift and a fo-
cused assessment at intervals consistent with the pa-
tient’s status and underlying pathologic condition.
• Initiate hygiene measures to provide patient com-
fort during and after emesis. Oral hygiene should
be scheduled at regular intervals, every 2 hours dur-
ing waking hours, whenever an NG tube is in place,
when the patient has stomatitis, or if the condition
warrants it.
• Patients with signicant central nervous system
(CNS) depression may have lost the gag reex; there-
fore institute aspiration precautions as appropriate.
• Initiate measures to eliminate factors that contribute
to nausea and vomiting (e.g., irritating foods, odors,
or medications).
• Give antiemetics as prescribed or recommended.
With postoperative patients, administer when
symptoms of nausea rst occur. Administer before
chemotherapy or radiation therapy; depending on
treatment, schedule on an around-the-clock basis af-
ter chemotherapy or radiation therapy. Administer
30 to 60 minutes before undertaking an activity
known to precipitate motion sickness. If a transder-
mal patch is to be worn during travel, it can be ap-
plied behind the ear 4 hours before departure.
• Nonprescription measures can be used in cases
when the nausea is subacute. Aromatherapy may be
employed with spearmint, peppermint, lavender,
or ginger. A commercially available product called
QueaseEase contains a blend of all four. The patient
should inhale the aroma taking slow breaths to help
with nausea.
• If young children experience motion sickness while
riding in a car, position them so they face forward
and can see the horizon; try covering the side win-
dows with screens so they do not have to turn their
heads suddenly to watch rapidly passing objects.
Provide diversional activities.
• Monitor nutritional needs and status on a
continuum.
Patient Education
Nutritional status
• Ensure the patients’, parents’, or signicant others’
understanding of all aspects of the diet, uid, and
nutritional regimen during hospitalization, as well
as at discharge for home management.
• Stress the importance of maintaining hydration
and following the parameters that must be report-
ed to the healthcare provider (e.g., weight loss of 2
pounds in a specied period, recurrence of nausea
and vomiting).
• For patients receiving cancer treatments, the
American Cancer Society has pamphlets with
suggestions for supplementing dietary needs.
These include, but are not limited to, giving
small, frequent, low-fat meals; food temperature;
and increasing protein content of meals with the
use of powdered milk added to puddings, shakes
made with nutritional supplements, and frozen
yogurt.
• If constipation is present, help patients with cardiac
disease prevent straining and the Valsalva (vasova-
gal) reex by giving stool softeners or bulk-form-
ing laxatives as needed. Ensure that bulk-forming
laxatives are rehydrated with juice, water, or milk
before ingestion. Maintain overall body hydration.
(See Chapter 34 for more information.) For patients
with degenerative neurologic disorders, a bowel
program may be necessary, usually performed ev-
ery other day. Glycerin or bisacodyl suppositories
or digital stimulation may be required as part of the
regimen.
• Discuss ways to decrease environmental stimuli
to vomit, such as removing the emesis basin from
sight.
• Antiemetics cause some degree of sedation, and pa-
tients are often fatigued after receiving chemother-
apy or radiation therapy; therefore caution patients
not to drive or operate power equipment until these
effects have subsided.
Medications. Verify the patient’s and signicant oth-
ers’ understanding of all prescribed medications to be
given on a scheduled or PRN basis.
Fostering health maintenance
• Provide the patient and signicant others with im-
portant information described in the monographs
for drugs prescribed. Additional health teach-
ing and nursing interventions, as well as common
and serious adverse effects, are described in each
monograph.
• Seek cooperation and understanding of the follow-
ing points so that medication adherence is increased:
name of medication; dosage, route, and times of ad-
ministration; and adverse effects.
Patient self-assessment. Enlist the patient’s aid
in developing and maintaining a written record of
monitoring parameters (e.g., weight, details of when
nausea occurs and amount and appearance of vomi-
tus, food diary of what is being eaten, which foods
initiate or aggravate the symptoms) (see Appendix
B: Template for Developing a Written Record for
Patients to Monitor Their Own Therapy). Complete
the Premedication Data column for use as a baseline
to track response to drug therapy. Ensure that the pa-
tient understands how to use the form, and instruct
the patient to bring the completed form to follow-up
visits. During follow-up visits, focus on issues that
will foster adherence with the therapeutic interven-
tions prescribed.
 Drugs Used to Treat Nausea and Vomiting CHAPTER 33
DRUG CLASS: DOPAMINE ANTAGONISTS
Actions
The dopamine antagonists are the phenothiazines,
amisulpride, olanzapine, butyrophenones (e.g., halo-
peridol, trimethobenzamide), and metoclopramide.
These medications inhibit dopamine receptors that
are part of the CTZ and the area postrema in the VC,
reducing emesis impulses. Unfortunately, dopamine
receptors in other parts of the brain are also blocked,
potentially producing extrapyramidal symptoms of
dystonia, parkinsonism, and tardive dyskinesia (see
Chapters 14, 17, and 32) in some patients, especially
when higher dosages are required.
Uses
The phenothiazines are primarily used as antiemetics
for the treatment of mild to moderate nausea and vom-
iting associated with anesthesia and surgery, radiation
therapy, and cancer chemotherapy. Prochlorperazine
and promethazine are the phenothiazines most widely
used as antiemetics.
Amisulpride, a dopamine antagonist, was approved
for the prevention and treatment of PONV either alone
or in combination with an antiemetic of a different
class. Amisulpride has been used in oral form for more
than 30 years in the treatment of acute and chronic psy-
choses in countries other than the United States.
Olanzapine, a dopamine and a serotonin antago-
nist, is effective when used in combination with other
serotonin antagonists, NK1 receptor antagonists, and
dexamethasone to prevent and treat CINV. It is also
classied as an atypical (second generation) antipsy-
chotic agent used to treat schizophrenia and bipolar
disorder (see Chapter 17).
The butyrophenones are seldom used as antiemet-
ics in surgery and cancer chemotherapy. These agents
tend to cause less hypotension than the phenothi-
azines, but they produce more sedation. The butyro-
phenones more likely to be used are haloperidol and
trimethobenzamide.
Metoclopramide is an antagonist of both dopamine
and serotonin receptors. In addition to acting on re-
ceptors in the brain, it acts on similar receptors in the
GI tract, thus making it particularly useful for treat-
ing nausea and vomiting associated with GI cancers,
gastritis, peptic ulcer, radiation sickness, gastroparesis,
and migraine. High-dose metoclopramide was rou-
tinely used to treat nausea and vomiting associated
with certain cancer chemotherapies until the serotonin
antagonists (e.g., ondansetron) became available. In
higher doses, extrapyramidal symptoms are more
common with metoclopramide; therefore many cancer
chemotherapy protocols now include both high-dose
metoclopramide and routine doses of diphenhydr-
amine when highly emetogenic anticancer agents are
used. Metoclopramide appears to be of little value in
treating motion sickness.
537
Therapeutic Outcomes
The primary therapeutic outcome expected from the
dopamine antagonist antiemetics is relief of nausea
and vomiting.
Nursing Implications for Dopamine Antagonists
Premedication assessment
1. Collect data regarding emesis (type, amount, and
frequency, on a continuum).
2. Assess data relative to the underlying cause of
nausea and vomiting (e.g., pregnancy, postsurgical
state, chemotherapy, radiation, bowel obstruction).
3. Obtain baseline data about the patient’s degree of
alertness before starting therapy because these med-
ications tend to produce some degree of sedation.
4. Protect amisulpride from light. It is subject to photo-
degradation. Administer within 12 hours of remov-
al of the vial from the protective carton.
Availability, dosage, administration, and adverse ef-
fects. See Table 33.3. For additional information on
phenothiazines, olanzapine, and haloperidol, see
Chapter 17. For additional information on metoclopra-
mide, see Chapter 32.
The following precautions pertain to amisulpride:
Common adverse effects
Cardiovascular. Amisulpride is associated with
procedural hypotension. Blood pressure should be
monitored.
Endocrine and metabolic. Hypokalemia and increased
serum prolactin have been reported with amisulpride.
Potassium should be monitored. No clinical problems
have reported as a result of elevated prolactin levels.
Gastrointestinal. Amisulpride may cause abdominal
distention.
Local. Infusion-site pain has been reported with
amisulpride.
Serious adverse effects
Cardiovascular. QT prolongation has been asso-
ciated with the IV administration of amisulpride.
Electrocardiogram (ECG) monitoring is recommended
in patients with preexisting arrhythmias or cardiac
conduction disorders and electrolyte abnormalities
(e.g., hypokalemia or hypomagnesemia). Ensure that
electrolyte levels are normal before starting amisul-
pride therapy.
Drug interactions
Dopamine agonists. Dopamine agonists may di-
minish the effect of amisulpride. Avoid using levo-
dopa or other dopamine agonists concurrently with
amisulpride.
Drugs prolonging QT interval. Avoid medications that
are known to prolong QT interval (e.g., ondansetron).
ECG monitoring is recommended in patients taking
other drugs known to prolong the QT interval.
538 UNIT VI Drugs Affecting the Digestive System
DRUG CLASS: SEROTONIN ANTAGONISTS
Actions
The serotonin (5-hydroxytryptamine) type 3 receptor
(5-HT3) antagonists have made major inroads in the
treatment of emesis associated with CINV, RINV, and
PONV over the past few years. Serotonin receptors of
the 5-HT3 type are located centrally in the CTZ of the
medulla and specialized cells of the GI tract and play a
signicant role in inducing nausea and vomiting. The
serotonin antagonists block these receptors and have
been shown to control nausea and vomiting associated
with cisplatin and several other emetogenic chemo-
therapeutic agents.
Uses
Ondansetron, granisetron, and palonosetron are used
to prevent CINV. There are no signicant differences
among the treatment groups with respect to emetic
control, nausea, or adverse reactions. Granisetron and
ondansetron are approved to treat nausea and vomiting
associated with RINV. Palonosetron, and ondansetron
have been approved to prevent and treat PONV. A
particular advantage to this group of compounds is
that there is minimal to no dopaminergic blockade, so
extrapyramidal adverse effects are rare.
Therapeutic Outcomes
The primary therapeutic outcome expected from the
serotonin antagonist antiemetics is relief of nausea and
vomiting.
Nursing Implications for Serotonin Antagonists
Premedication assessment
1. Collect data regarding emesis (type, amount, and
frequency, on a continuum).
2. Assess data relative to the underlying cause
of nausea and vomiting (e.g., pregnancy, post-
surgical state, chemotherapy, radiation, bowel
obstruction).
3. Obtain baseline data about the patient’s degree
of alertness before initiation of therapy because
these medications tend to produce some degree of
sedation.
Availability, dosage, and administration. See Table 33.3
Common adverse effects. Common adverse effects
are fairly mild, especially in relation to the prevention
of nausea and vomiting. Because only a few doses are
administered, the frequency and duration of adverse
effects are minimal.
Neurologic. Headache, sedation.
Gastrointestinal. Diarrhea, constipation.
Serious adverse effects
Cardiovascular. Prolongation of the QTc interval,
inducing potentially fatal dysrhythmias, has been
reported for all drugs in the class. The IV formulations
of 5-HT3 antagonists have been associated more with
QTc interval changes compared with oral formula-
tions, but prolongation is more commonly reported
with ondansetron. Thus the maximum dose for ondan-
setron IV is 16 mg as a single dose.
Drug interactions
Apomorphine. The use of serotonin antagonists
with apomorphine is contraindicated. Profound
hypotension and loss of consciousness have been
reported.
DRUG CLASS: ANTICHOLINERGIC AGENTS
Actions
Motion sickness is thought to be caused by an excess
of acetylcholine at the CTZ and the VC by cholinergic
nerves receiving impulses from the vestibular network
of the inner ear. Anticholinergic agents are used to
counterbalance the excessive amounts of acetylcholine
present.
Uses
Anticholinergic agents, such as scopolamine, and an-
tihistamines (e.g., diphenhydramine, dimenhydrinate,
meclizine) and promethazine are used to treat motion
sickness and, in the case of the antihistamines, nausea
and vomiting associated with pregnancy. The choice
of drug depends on both the period for which antin-
ausea protection is required and the adverse effects.
Scopolamine is the drug of choice for short periods of
motion, and an antihistamine is preferred for longer
periods. Promethazine is the preferred drug in this
class because higher doses act longer, but sedation is
usually a problem. Meclizine has fewer adverse ef-
fects than promethazine but has a shorter duration
of action and is less effective for severe conditions.
Diphenhydramine has a long duration, but excessive
sedation is often a problem, especially after the boat,
plane, or car ride is over. For very severe conditions,
sympathomimetic drugs such as ephedrine are used
in combination with scopolamine or an antihistamine.
Anticholinergic agents are usually not effective in
CINV.
Therapeutic Outcome
The primary therapeutic outcome expected from the
anticholinergic antiemetics is relief of nausea and
vomiting.
Nursing Implications for Anticholinergic Agents
Premedication assessment
1. Collect data regarding emesis (type, amount, and
frequency, on a continuum).
2. Assess data relative to the underlying cause of
nausea and vomiting (e.g., pregnancy, postsurgical
state, chemotherapy, radiation, bowel obstruction).
 Drugs Used to Treat Nausea and Vomiting CHAPTER 33
3. Obtain baseline data about the patient’s degree
of alertness before initiation of therapy because
these medications tend to produce some degree of
sedation.
4. Check the patient’s history to screen for presence
of closed-angle glaucoma; use of an anticholinergic
agent would be contraindicated.
Availability, dosage, and administration. See Table 33.3
Common adverse effects
Neurologic
Sedative effects. Tolerance may develop over time,
thus diminishing the effect. Caution patients to avoid
operating power equipment or motor vehicles.
Anticholinergic effects
Blurred vision; constipation; urinary retention; dry mu-
cosa of the mouth, throat, and nose. These symptoms are
the anticholinergic effects produced by these agents.
Patients should be monitored for these adverse ef-
fects. Maintain uid intake at 8 to 10 eight-ounce
glasses daily. Dryness of the mucosa may be relieved
by sucking hard candy or ice chips, or by chewing
gum. Stool softeners, such as docusate, or the occa-
sional use of a stimulant laxative, such as Bisacodyl,
may be required for constipation. Caution the patient
that blurred vision may occur, and make appropriate
suggestions for personal safety. Patients who devel-
op urinary hesitancy should discontinue the medica-
tion and contact their healthcare provider for further
evaluation.
Drug interactions
Enhanced sedation. Central nervous system depres-
sants, including sleeping aids, analgesics, benzodiaz-
epines, phenothiazines, and alcohol, will enhance the
sedative effects of antihistamines. People who work
around machinery, drive a car, or perform other duties
in which they must remain mentally alert should not
take these medications while working.
DRUG CLASS: CORTICOSTEROIDS
Actions
Several studies have shown that dexamethasone and
methylprednisolone can be effective antiemetics, ei-
ther as single agents or in combination with other an-
tiemetics. The mechanism of action is unknown. Other
actions of the corticosteroids, such as mood elevation,
increased appetite, and a sense of well-being, may also
help in patient acceptance and control of emesis.
Uses
A particular advantage of the steroids, apart from
their efcacy, is their relative lack of adverse effects.
Because only a few doses are administered, the usual
complications associated with long-term therapy do
not arise.
539
Therapeutic Outcome
The primary therapeutic outcome expected from the
corticosteroids as antiemetics is relief of nausea and
vomiting.
Nursing Implications for Corticosteroids
Premedication assessment
1. Collect data regarding emesis (type, amount, and
frequency, on a continuum).
2. Assess data relative to the underlying cause of
nausea and vomiting (e.g., pregnancy, postsurgical
state, chemotherapy, radiation, bowel obstruction).
3. Obtain baseline data about the patient’s degree
of alertness before initiation of therapy because
these medications tend to produce some degree of
sedation.
Availability, dosage, and administration. See Table 33.3.
Common and serious adverse effects. Adverse effects
are infrequent because few doses are administered for
nausea and vomiting. See also Chapter 37.
Drug interactions. See Chapter 37.
DRUG CLASS: BENZODIAZEPINES
Actions
Benzodiazepines act as antiemetics through a com-
bination of effects, including sedation, reduction in
anxiety, possible depression of the VC, and an am-
nesic effect. Of these, the amnesic effect appears to
be most important in treating cancer patients and, in
this respect, lorazepam and midazolam are superior
to diazepam.
Uses
Benzodiazepines (e.g., lorazepam, midazolam, diaz-
epam) are effective in reducing not only the frequency
of nausea and vomiting but also the anxiety often asso-
ciated with chemotherapy. Clinically, benzodiazepines
are most useful in combination with other antiemetics,
such as metoclopramide, dexamethasone, and sero-
tonin antagonists.
Therapeutic Outcome
The primary therapeutic outcome expected from
benzodiazepine antiemetics is relief of nausea and
vomiting.
Nursing Implications for Benzodiazepines
Premedication assessment
1. Collect data regarding emesis (type, amount, and
frequency, on a continuum).
2. Assess data relative to the underlying cause of the
nausea and vomiting (e.g., pregnancy, postopera-
tive state, chemotherapy, radiation therapy, bowel
obstruction).
 540
Table 33.3 Antiemetic Agents
ANTIEMETIC DOSAGE RANGE
GENERIC NAME BRAND NAME AVAILABILITY ADULTS CHILDREN COMMENTS

UNIT VI Drugs Affecting the Digestive System

DOPAMINE ANTAGONISTS
Phenothiazines Comments for All Phenothiazines
prochlorperazine Compro Tablets: 5, 10 mg PO: 5–10 mg q6–8h PO or rectal: 20–29 lb: 2.5 mg once Phenothiazines may suppress the
Prochlorazine Rectal suppositories: Rectal: 25 mg twice or twice daily (maximum of 7.5 mg cough reex.
25 mg daily daily) Ensure that the patient does not
Injection: 5 mg/mL IM: 5–10 mg q3–4h; 30–39 lb: 2.5 mg two or three times aspirate vomitus.
do not exceed 40 daily (maximum of 10 mg daily) Use with caution in patients,
mg/24 hr 40–85 lb: 2.5 mg three times daily or especially children, with
5 mg twice daily (maximum of 15 undiagnosed vomiting.
mg daily) Phenothiazines can mask signs of
IM: 0.132 mg/kg two to three times toxicity of other drugs or mask
per day; same oral maximum symptoms of other diseases, such
limits apply to IM dosing as brain tumor, Reye syndrome, or
promethazinec Phenergan, Tablets: 12.5, 25, PO/PR: 12.5–25 mg PO/PR: Children >2 yr: 0.25–1 mg/ intestinal obstruction.
Promethegan 50 mg q4–6h kg up to 25 mg q4–6h Use with extreme caution in patients
Syrup: 6.25 mg/5 mL IM/IV: Adults: IM/IV: Children ≥2 years and with seizure disorders.
Oral solution: 6.25 12.5–25 mg deep adolescents: 0.25–1 mg/kg IM or Discontinue if rashes develop.
mg/5 mL IM or IV; may IV (maximum: 25 mg/dose) q4–6h May cause orthostatic hypotension.
Suppositories: 12.5, repeat q4–6h as needed; IVPB is preferred
25, 50 mg method of delivery
Injection: 25, 50 mg/
mL in 1-mL ampules
BUTYROPHENONES
haloperidola See earlier comments for phenothiazines.
metoclopramideb
trimethobenzamide Tigan Capsules: 300 mg IM: PO: 300 mg three or Trimethobenzamide Injectable form contains benzocaine. Do not
Do not confuse 100 mg/mL four times daily is generally not use in patients allergic to benzocaine or
Tigan with Tiazac. IM: 200 mg three or recommended for use in local anesthetics.
four times daily children Inject in upper, outer quadrant of gluteal
region. Avoid escape of solution along the
route.
May cause burning, stinging, pain on
injection.
OTHER DOPAMINE ANTAGONISTS
Amisulpride Barhemsys IV: 2.5 mg/mL in single IV: Prophylaxis:5 mg Not recommended Administer at the time of anesthesia
Do not confuse with dose vials. over 1–2 minutes; induction.
amitriptyline. postoperative
treatment of
vomiting: 10 mg
over 1–2 minutes.
Olanzapine Zyprexa Tablets: 2.5, 5, 7.5, 10, Oral: 5 or 10 No dosing recommendations 5 mg with in combination with antiemetics
15, and 20 mg. mg on day of for children is effective and may cause less sedation
Tablets, disintegrating: chemotherapy when used with cisplatin-based high
5, 10, 15, and 20 mg (day 1), followed emetic-risk therapy.
by 5 or 10 mg
once daily on
days 2–4, in
combination with
antiemetics used
for high emetic
risk agents
SEROTONIN ANTAGONISTS
granisetron – Tablets: 1 mg CINV, RINV CINV: CINV: in combination with dexamethasone

Drugs Used to Treat Nausea and Vomiting CHAPTER 33

Injection: 1 mg/mL PO: 2 mg up to PO: 40 mcg/kg/dose every and NK1 antagonist.
1 hr before 12 hr
chemotherapy, IV: Children 2–16 yr: Same as
followed by a PO dose
second dose 12
hr later; or 2 mg
once daily
Sancuso Transdermal patch: Transdermal
(transdermal 3.1 mg/24 hr patch: Apply
patch) one patch to the
upper outer arm
24–48 hr before
chemotherapy.
Patch may be
worn for 7 days;
do not remove for
at least 24 hr after
chemotherapy.

Continued

541
 542
Table 33.3 Antiemetic Agents—cont’d
ANTIEMETIC DOSAGE RANGE
GENERIC NAME BRAND NAME AVAILABILITY ADULTS CHILDREN COMMENTS

UNIT VI Drugs Affecting the Digestive System

ondansetron Zofran Tablets: 4, 8, 24 mg Chemotherapy: Chemotherapy: CINV: with NK1 antagonist and
Do not confuse Tablets, orally PO: Moderately and 6 mo to 18 yr: IV: 0.15 dexamethasone.
Zofran with disintegrating: 4, 8 highly emetogenic mg/kg 30 min before
Reglan, Zantac, or mg chemotherapy: 8 chemotherapy and 0.15
Zosyn. Injection: 2 mg/mL; 40 mg 30 min before mg/kg 4 and 8 hr after the
Zuplenz mg/20 mL chemotherapy), rst dose of ondansetron
Dom-Ondansetron Liquid: 4 mg/5 mL followed by 8 mg PO: 4–11 yr: 4 mg 30 min
Oral lm: 4, 8 mg 8 hr later before chemotherapy and
PONV: repeated 4 and 8 hr after
PO: 16 mg 1 hr initial dose of ondansetron,
before induction of then continue q8h for 1–2
anesthesia days posttreatment
IV: 4 mg just before PO: 12 yr: 8 mg 30 min
induction of before chemotherapy
anesthesia and 4 and 8 hr after initial
dose of ondansetron, then
continue 8 mg every 12 hr
for 1–2 days posttreatment
PONV:
IV: 1 mo to 12 yr: <40 kg:
0.1 mg/kg at end of
anesthesia; >40 kg: 4 mg
at end of anesthesia
palonosetron Aloxi Injection: Chemotherapy: Chemotherapy: CINV: Include NK1 antagonist and
0.25 mg/2ml; 0.25 IV: 0.25 mg over 30 IV: 1 mo dexamethasone.
mg/5 mL in 5-mL seconds 30 min To 17 yr: 20 mcg/kg infused
vials before start of over 15 min beginning
chemotherapy; do 30 min before the start of
not repeat within chemotherapy
2 days Include NK1 antagonist and
PONV: 0.075 mg dexamethasone
over 10 sec IV: 17 yr and older: 0.25 mg
immediately once before chemotherapy
before anesthesia PONV:
induction Not approved in children
ANTICHOLINERGIC AGENTS USED FOR MOTION SICKNESS
dimenhydrinate Dramamine Tablets: 50 mg PO: 50–100 mg q4– PO: 6–12 yr: 25–50 mg May cause sedation.
Gravol Chewable tablet: 50 6h; do not exceed q6–8h; do not exceed Caution patient against operating machinery.
mg 400 mg/24 hr 150 mg/24 hr
Injection: 50 mg/mL IM: 50 mg as 2–5 yr: 12.5–25 mg q6–8h;
needed do not exceed 75 mg/24
hr
diphenhydramine – Tablets: 12.5, 25, PO: 25–50 mg three PO: 12.5–25 mg three or four
Do not confuse 50 mg or four times daily times a day; do not exceed
diphenhydramine Tablets, chewable: IM: 10–50 mg; do 300 mg/24 hr
with dicyclomine or 12.5 mg not exceed 400 IM: 5 mg/kg/24 hr, in four
dipyridamole. Capsules: 25, 50 mg mg/24 hr divided doses; do not
Elixir: 12.5 mg/5 mL exceed 300 mg/24 hr
Suspension: 5 mg/
mL
Injection 50 mg/mL
Liquid: 6.25 mg/mL;
12.5 mg/5 mL; 50
mg/30 mL.

meclizine Antivert Tablets: 12.5, 25, 50 mg PO: 25–50 mg; may Not approved for use in
Bonine Chewable tablet: be repeated every children younger than12 yr
25 mg 24 hr
scopolamine, Transderm-Scop Transdermal patch: Patch: Apply to Not approved for use in Do not cut patches. All medicine will
transdermal 1 mg delivered over skin behind children be released over the next few hours
72 hr ear at least 4 hr potentially causing overdose.
before antiemetic
effect is required;

Drugs Used to Treat Nausea and Vomiting CHAPTER 33

replace in 72 hr if
continued therapy
required
CORTICOSTEROIDS
dexamethasone Decadron Tablets: 0.5, 0.75, 1, PO: 4–16 mg on PO: 8-20 mg on day one Recommended for prevention of nausea and
1.5, 2, 4, 6, 20 mg day 1 vomiting associated with chemotherapy.
Elixir: 0.5 mg/5 mL IV: 8–20 mg before Used in combination with other
Injection: 4, 10 mg/mL administration of antiemetics.
Liquid: 1 mg/mL, 0.5 chemotherapy
mg/5 mL
BENZODIAZEPINES
lorazepam Ativan Tablets: 0.5, 1, 2 mg PO: 0.5–2 mg q6h CINV: Recommended for prevention and treatment
Do not confuse Do not confuse Injection: 2, 4 mg/mL IV: 0.5–2 mg q6h PO: 1 mo or older: 0.04–0.08 of nausea and vomiting associated with
lorazepam with Ativan with Liquid: 2 mg/mL mg/kg/dose at bedtime chemotherapy.
loperamide. Ambien. the evening before
chemotherapy and once
the next day before
chemotherapy; Maximum
dose: 2 mg/dose
Continued

543
 544
Table 33.3 Antiemetic Agents—cont’d
ANTIEMETIC DOSAGE RANGE
GENERIC NAME BRAND NAME AVAILABILITY ADULTS CHILDREN COMMENTS

UNIT VI Drugs Affecting the Digestive System

CANNABINOIDS
dronabinol (THC) Marinol Capsules: 2.5, 5, PO: Initial 5 mg/ Not recommended Schedule III controlled substance. Common
10 mg m2 1–3 hr before adverse effects include drowsiness,
chemotherapy, dizziness, muddled thinking, and possible
then q2–4h for impairment of coordination, sensory, and
a total of 4–6 perceptual functions.
doses/day Use with caution in patients with
Maximum: 15 mg/ hypertension or heart disease.
m2/dose Syndros is a Schedule II controlled
Syndros Oral solution: 5 mg/mL PO: 4.2 mg/m2 substance requiring a new prescription.
(30 mL) 1–3 hr before
chemotherapy
and then
q2–4h after
chemotherapy
for a total of 4–6
doses/day
Maximum: 12.6 mg/
m2/dose and 4–6
doses/day
NEUROKININ-1 RECEPTOR INHIBITOR ANTAGONISTS
aprepitant Emend Capsules: 40, 80, Chemotherapy: Chemotherapy: In combination with other antiemetics
125 mg PO: 125 mg Children at least 12 yr old (dexamethasone, serotonin antagonist),
Oral suspension: 1 hr before and at least 30 kg: As for recommended for prevention of acute and
125 mg chemotherapy on adults delayed nausea and vomiting associated
Cinvanti IV emulsion: day 1; 80 mg daily with initial and repeat courses of highly
130 mg/18 mL in the morning of emetogenic cancer chemotherapy,
days 2 and 3 including high-dose cisplatin.
IV: 100–130 mg 30 Also approved for prevention of PONV in
minutes before adults.
chemotherapy on
day 1
PONV:
PO: 40 mg within 3
hr before induction
of anesthesia
 fosaprepitant Emend Injection: 150 mg Chemotherapy: Chemotherapy: Older than Same as aprepitant but not approved for
IV: 150 mg 12 yr: As for adults PONV.
administered Administer with dexamethasone and a
over 15–20 min serotonin antagonist.
30 min before
chemotherapy on
day 1 only
rolapitant Varubi Tablets: 90 mg Chemotherapy: Not recommended Use in combination with dexamethasone
PO: 180 mg and a serotonin antagonist for the
1–2 hr before prevention of delayed nausea and
chemotherapy on vomiting in adults receiving highly
day 1 only. emetogenic cancer chemotherapy.
Fixed-dose combination: Akynzeo Capsule: netupitant Chemotherapy: Not recommended Prevention of acute and delayed nausea
netupitant and 300 mg and PO: 1 capsule ∼1 hr and vomiting associated with initial and
palonosetron palonosetron 0.5 mg before initiation of repeat courses of cancer chemotherapy,
IV: fosnetupitant chemotherapy on including highly emetogenic
235 mg and day 1 chemotherapy.
palonosetron 0.25 IV: 235/0.25 mg Administered in conjunction with
mg 30 min before dexamethasone.
chemotherapy on
day 1

Drugs Used to Treat Nausea and Vomiting CHAPTER 33

Available in Canada.
CINV, Chemotherapy-induced nausea and vomiting; IM, intramuscular; IVPB, intravenous piggyback; PONV, postoperative nausea and vomiting; THC, tetrahydrocannabinol.
aFor information on haloperidol, see the Drug Class: Antipsychotic Agents section in Chapter 17 and Table 17.1.
bFor a drug monograph for metoclopramide, see the Drug Class: Prokinetic Agents section in Chapter 32.
cPromethazine is a dopamine antagonist and a histamine antagonist and has anticholinergic properties.

545
546 UNIT VI Drugs Affecting the Digestive System
3. Obtain baseline data about the patient’s degree
of alertness before initiation of therapy because
these medications tend to produce some degree of
sedation.
Availability, dosage, and administration. See Table 33.3
Common adverse effects, serious adverse effects, and
drug interactions. See Chapter 15
DRUG CLASS: CANNABINOIDS
Actions
After numerous reports that smoking marijuana re-
duces the frequency of nausea, the antiemetic prop-
erties of the active ingredient tetrahydrocannabinol
(THC) and its synthetic analogs, such as dronabinol
and nabilone, have been studied. The cannabinoids
act through several mechanisms to inhibit pathways
to the VC; however, there is no dopamine antagonist
activity.
Uses
Cannabinoids have been shown to be more effective
than placebo and equally as effective as prochlorper-
azine in patients receiving moderately emetogenic
chemotherapy. They are less effective than metoclo-
pramide. Because of the mind-altering effects and po-
tential for abuse, the cannabinoids serve as antiemetics
only in patients receiving chemotherapy. The cannabi-
noids are of more use in those younger patients who
are refractory to other antiemetic regimens and in
whom combination therapy may be more effective.
Therapeutic Outcome
The primary therapeutic outcome expected from the
cannabinoids is relief of nausea and vomiting.
Nursing Implications for Cannabinoids
Premedication assessment
1. Collect data regarding emesis (type, amount, and
frequency, on a continuum).
2. Assess data relative to the underlying cause of
nausea and vomiting (e.g., pregnancy, postsurgical
state, chemotherapy, radiation, bowel obstruction).
3. Obtain baseline data about the patient’s degree
of alertness before initiation of therapy because
these medications tend to produce some degree of
sedation.
Availability, dosage, and administration. See Table 33.3
Common and serious adverse effects
Psychological
Dysphonic effects. Depressed mood, hallucinations,
dreaming or fantasizing, distortion of perception, par-
anoid reactions, and elation are more common with
moderate to high doses. Younger patients appear to
tolerate these adverse effects better than older patients
or patients who have not previously used marijuana.
Patients should be specically warned not to drive, op-
erate machinery, or engage in any hazardous activity un-
til it is determined that they are able to tolerate the drug
and to perform such tasks safely. Patients should remain
under the supervision of a responsible adult during ini-
tial use of dronabinol and after dosage adjustments.
Drug interactions
Drugs that increase toxic effects. Antihistamines, alco-
hol, analgesics, benzodiazepines, phenobarbital, anti-
depressants, muscle relaxants, and sedative-hypnotics
increase toxic effects. Monitor the patient for excessive
sedation and reduce the dosage of the other sedative
agents, if necessary.
DRUG CLASS: NEUROKININ-1 RECEPTOR
ANTAGONISTS
Actions
Another neurotransmitter thought to play a role in the
vomiting process is substance P. Substance P is a neu-
ropeptide found in high concentrations in the area of
the CNS responsible for vomiting, and it coexists with
serotonin in the enterochromafn cells and vagal af-
ferent nerves of the GI tract. The actions of substance
P are mediated through the NK1 receptor. NK1 an-
tagonists block the effects of substance P in the CNS
and have no afnity for serotonin, dopamine, or corti-
costeroid receptors. The NK1 receptor antagonists are
aprepitant, fosaprepitant, and rolapitant. There is also
a xed-dose combination of netupitant, an NK1 recep-
tor antagonist, and palonosetron, a 5-HT3 antagonist.
Uses
NK1 antagonists are used for the prevention of acute
and delayed CINV caused by moderate and highly
emetogenic antineoplastic agents. They are used in
combination with a corticosteroid and a 5-HT3 receptor
antagonist. Their greatest effect appears to be in reduc-
ing the frequency of delayed emesis; they do not treat
CINV once it has started.
Therapeutic Outcome
The primary therapeutic outcome expected from NK1
antagonists is prevention of nausea and vomiting.
Nursing Implications for NK1 Receptor
Antagonists
Premedication assessment
1. Collect data regarding emesis (type, amount, and
frequency, on a continuum).
2. Assess data relative to the underlying cause of nau-
sea and vomiting (e.g., pregnancy, postsurgical state,
chemotherapy, radiation therapy, bowel obstruction).
 Drugs Used to Treat Nausea and Vomiting CHAPTER 33
3. Assess premedication bowel pattern because diar-
rhea or constipation may occur posttherapy.
Availability. See Table 33.3
Dosage and administration
Postoperative nausea and vomiting. See Table 33.3
Common and serious adverse effects. The most com-
mon adverse effects with NK1 antagonists are tired-
ness, nausea, hiccups, constipation, diarrhea, loss
of appetite, headache, neutropenia, and hair loss.
Because NK1 antagonists are taken only for up to 3
days at a time, adverse effects are short-lived and rare-
ly troublesome.
Drug interactions
Drugs that increase toxic effects of NK1 antago-
nists. Ketoconazole, itraconazole, clarithromycin,
ritonavir, nelnavir, and diltiazem may inhibit the
metabolism of aprepitant, rolapitant, and netupitant.
Monitor the patient for signs of toxicity.
Drugs that reduce therapeutic effects of NK1 antago-
nists. Rifampin, carbamazepine, paroxetine, and
Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• Nausea and vomiting vary from a minor inconvenience to
severe debilitation.
• The six common causes of nausea and vomiting
are PONV, motion sickness, nausea and vomiting in
pregnancy, psychogenic vomiting, CINV, and RINV.
• Nonpharmacologic treatments, such as eliminating
noxious substances, avoiding fatty or spicy foods, and
restricting activity to bed and chair rest to avoid vestibular
irritation, are equally important in reducing the frequency of
nausea and vomiting.
• The causes of nausea and vomiting should be assessed
before treatment is begun, and specic therapy should be
selected for each of the causes.
• Drug therapy for treatment of nausea and vomiting
includes dopamine antagonists, serotonin antagonists,
anticholinergic agents, corticosteroids, benzodiazepines,
cannabinoids, and NK1 receptor antagonists.
Additional Learning Resources
SG Go to your Study Guide for additional Review Ques-
tions for the NCLEX® Examination, Critical Thinking Clinical
Situations, and other learning activities to help you master this
chapter content.
547
phenytoin induce the metabolism of aprepitant, rolapi-
tant, and netupitant, reducing therapeutic effect.
Oral contraceptives. Female patients receiving aprep-
itant who take oral contraceptives should be advised
to use an alternative or additional method of birth
control for the next month because aprepitant may en-
hance the metabolism of estrogens.
Dexamethasone and methylprednisolone. Aprepitant in-
hibits the metabolism of these corticosteroids. Oral dos-
es of dexamethasone and methylprednisolone should
be reduced by approximately 50% when prescribed
concurrently with aprepitant. Intravenous methylpred-
nisolone dosages should be reduced by 25%.
Netupitant also inhibits the metabolism of dexa-
methasone. The oral dose of dexamethasone should be
reduced.
Warfarin. Patients receiving warfarin therapy should
be instructed to have an international normalized ratio
(INR) checked approximately 7 to 10 days after aprepi-
tant therapy because coadministration with aprepitant
may result in increased metabolism of warfarin and a
reduced INR.
Thioridazine. Concurrent use with rolapitant is
contraindicated.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX exam and include both NGN (Next Generation) and
traditional questions. See Chapter 1 for further information re-
garding question types.
Scenario
A patient diagnosed with colon cancer is undergoing chemo-
therapy. The patient remarked to the nurse that they were wor-
ried about the nausea and vomiting that they heard was a side
effect of the therapy.
1. A 21-year-old pregnant woman comes into the clinic complaining
of extreme “morning sickness.” She has not been able to keep
down any food or drink for 2 days. The nurse understands which
treatments are available? (Select all that apply.)
1. Hospitalization with management of uids and
electrolytes by the IV route
2. NPO until the nausea and vomiting passes
3. Antihistamines such as diphenhydramine
4. Ginger (herb) to treat the nausea and vomiting
5. Antihistamine doxylamine plus vitamin B6
548 UNIT VI Drugs Affecting the Digestive System
Objective: Describe the common causes of nausea and vomiting
and the interventions that apply.
NCLEX item type: Multiple response
Cognitive skill: Application
2. After several rounds of chemotherapy the patient in the scenario
started to develop delayed emesis. The nurse is preparing the
drug granisetron prior to the patient receiving chemotherapy and
explains to the patient that relief of nausea will occur when?
1. “Your nausea should not be a problem if you take this
drug by mouth 30 minutes before your chemotherapy.”
2. “When we administer granisetron in the IV form, 60
minutes before your chemotherapy, we anticipate that
you will not have any nausea.”
3. “When we give you granisetron transdermal patch 2
hours prior to the chemotherapy, your nausea should be
alleviated.”
4. “You will need to take this drug as a SQ injection 2 hours
before your chemotherapy it will prevent nausea.”
Objective: Discuss the three types of nausea associated with
chemotherapy and the nursing considerations.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
3. The nurse was comparing the different classes of antiemetics and
knows that the anticholinergic agents are used to prevent which
type of nausea? (Select all that apply.)
1. Anticipatory nausea and vomiting
2. Nausea and vomiting in pregnancy
3. Postoperative nausea and vomiting
4. Motion sickness
5. Chemotherapy induced nausea and vomiting
Objective: Compare the therapeutic classes of antiemetics with
their uses.
NCLEX item type: Multiple response
Cognitive skill: Application
4. The nurse recognized the common and adverse effects of
granisetron for patient with nausea and vomiting as a result of
chemotherapy, and knows these patients should be advised about
which of these symptoms they can expect will be fairly mild?
(Select all that apply.)
1. Constipation
2. Depression
3. Paranoia
4. Blurred vision
5. Hallucinations
6. Headache
7. Prolonged QTc interval
8. Sedation
Objective: Discuss the three types of nausea associated with
chemotherapy and the nursing considerations.
NCLEX item type: Extended multiple response
Cognitive skill: Recognize cues
5. The patient in the scenario with chemotherapy-induced nausea
and vomiting was receiving a benzodiazepine because this class
of drugs work in which way? (Select all that apply.)
1. By depressing the vomiting center (VC)
2. By inhibiting dopamine receptors that are part of the
pathway to the VC
3. By acting through serotonin receptor stimulation in the GI
tract
4. By reducing anxiety associated with chemotherapy-
induced nausea and vomiting
5. By counterbalancing the excessive amounts of
acetylcholine believed to be present
Objective: Discuss the three types of nausea associated with
chemotherapy and the nursing considerations.
NCLEX item type: Multiple response
Cognitive skill: Evaluate cues
6. The nurse discussing with the patient in the scenario different
ways to deal with anticipatory nausea and vomiting included in
the discussion which of the following statements? (Select all that
apply.)
1. “We generally administer antiemetic drugs as soon as
nausea develops, because this will adequately control
your symptoms.”
2. “You can expect anticipatory nausea to become more
severe as your chemotherapy treatments progress.”
3. “We can teach you nonpharmacologic management of
your nausea that includes progressive muscle relaxation
and self-hypnosis.”
4. “It is recommended that we use antiemetic therapy
prior to chemotherapy so that the nausea does not
occur.”
5. “The triggers for this type of nausea are often brushing
teeth, seeing food, or standing up too quickly.”
Objective: Discuss the three types of nausea associated with
chemotherapy and the nursing considerations.
NCLEX item type: Multiple response
Cognitive skill: Application
 Drugs Used to Treat Nausea and Vomiting CHAPTER 33 549

7. The nurse reviewed the therapeutic classes used for antiemetics. Indicate with an X the use for each type of antiemetic.

IN ADDITION TO
TREATMENT OF
REDUCES THE FRE- CINV, RINV, AND USED TO TREAT NAUSEA USED FOR PATIENTS
QUENCY OF NAUSEA PONV, ALSO USED PREVENTION OF AND VOMITING ASSOCI- WHO ARE REFRAC-
AND VOMITING AND FOR GASTROPARE- ACUTE AND DELAYED ATED WITH CINV, RINV, TORY TO OTHER ANTI-
ANXIETY SIS AND MIGRAINES CINV AND PONV EMETIC REGIMENS
Dopamine antagonists
Cannabinoids
Serotonin antagonists
Benzodiazepines
Neurokinin-1 receptor
antagonists

Objective: Compare the therapeutic classes of antiemetics with their uses.

NCLEX item type: Matrix
Cognitive skill: Recognize cues
34 Drugs Used to Treat Constipation and Diarrhea
https://evolve.elsevier.com/Willihnganz
Objectives
1. Identify the mechanism of action for the different classes of
laxatives and describe underlying causes of constipation.
2. Discuss the causes of diarrhea.
3. Differentiate between locally acting and systemically acting
antidiarrheal agents and the conditions that respond
favorably to antidiarrheal agents.
Key Terms
constipation (kŏn-stĭ-PĀ-shŭn) (p. 550) laxatives (LĂKS-ĕ-tĭvz) (p. 550)
CONSTIPATION
There are no xed rules as to what are normal bow
el habits. Usually the stools are formed, brown, and
soft and frequency of bowel movements can range
from three times a day to two to three times per week.
Constipation is dened as:
a symptom-based disorder of unsatisfactory defecation and
is characterized by infrequent stools or feces, difcult stool
passage, or both. Difcult stool passage includes straining,
a sense of difculty passing stool, incomplete evacuation,
hard/lumpy stools, prolonged time to stool defecate, or need
for manual maneuvers to pass stool. Chronic constipation is
dened as the presence of these symptoms for at least 3 months.
American College of Gastroenterology Chronic
Constipation Task Force, 2005
Chronic constipation aficts about 16% of North
Americans and is more predominant in women, affect
ing two females for every male affected. Frequency of
constipation increases with increasing age, particularly
after age 60 years.
Constipation is characterized by decreased motil
ity of the colon or from retention of feces in the lower
colon or rectum. In either case, the longer the feces re
main in the colon, the greater the reabsorption of water
and the drier the stool becomes. The stool is then more
difcult to expel from the anus. Causes of constipation
include the following:
• Improper diet, with too little ber or too little uid
(e.g., lacking fruits and vegetables)
• Lack of exercise and sedentary habits
• Failure to respond to the normal defecation impuls
es; muscular weakness of the colon
550
4. Describe nursing assessments needed to evaluate the
patient’s state of hydration when suffering from either
constipation or dehydration, and identify electrolytes
that should be monitored whenever prolonged or severe
diarrhea is present.
diarrhea (dī-ă-RĒ-ĕ) (p. 550)
• Diseases such as anemia and hypothyroidism
• Medications such as morphine, codeine, oxycodone,
anticholinergic agents
• Tumors of the bowel or pressure on the bowel from
tumors
• Diseases of the rectum.
Occasional constipation is not detrimental to a
person’s health, although it can cause a feeling of
general discomfort or abdominal fullness, anorexia,
and anxiety in some people. Habitual constipation
leads to decreased intestinal muscle tone, increased
straining at the stool as the patient bears down in the
attempt to pass the hardened stool, and an increased
incidence of hemorrhoids. Using laxatives (medica
tions that stimulate the bowels to evacuate stool)
or enemas daily should be avoided because they
decrease the muscular tone and mucus production
of the rectum and may result in water and electro
lyte imbalance. They also become habit forming; the
weakened muscle tone adds to the inability to expel
the fecal contents, which leads to the continued use
of enemas or laxatives.
DIARRHEA
Diarrhea is an increase in the frequency or uid con
tent of bowel movements. Because normal patterns
of defecation and the patient’s perception of bowel
function vary, a careful history must be obtained to
determine the change in a particular patient’s bowel
elimination pattern. An important fact to remember
about diarrhea is that diarrhea is a symptom rather
than a disease.
 Drugs Used to Treat Constipation and Diarrhea CHAPTER 34
CAUSES OF DIARRHEA
Intestinal Infections
Intestinal infections are most frequently associated
with ingestion of food contaminated with bacteria or
protozoa (food poisoning) or eating or drinking water
that contains bacteria foreign to the patient’s gastro
intestinal (GI) tract. People traveling, especially to other
countries, develop what is known as traveler’s diarrhea
from ingestion of microorganisms that are pathogenic
to their GI tracts but not to those of the local residents.
Spicy or Fatty Foods
Spicy or fatty foods may produce diarrhea by irritating
the lining of the GI tract. Diarrhea occurs particularly
when the patient does not routinely eat these types of
foods. This type of diarrhea may occur while an in
dividual is traveling or on vacation (e.g., eating fresh
oysters daily while visiting coastal regions).
Enzyme Deficiencies
Patients with deciencies of digestive enzymes, such
as lactase or amylase, have difculty digesting certain
foods. Diarrhea usually develops because of irritation
from undigested food.
Excessive Use of Laxatives
People who use laxatives on a routine chronic basis but
are not under the care of a healthcare provider for a
specic GI problem are laxative abusers. Some do it for
weight control, and others use laxatives under the mis
conception that a person is not normal if the bowels do
not move daily.
Drug Therapy
Diarrhea is a common adverse effect caused by irritation
of the GI lining by ingested medication. Diarrhea may
also result from the use of antibiotics that may kill certain
bacteria that live in the GI tract and help digest food.
Emotional Stress
Diarrhea is a common symptom of emotional stress
and anxiety.
Hyperthyroidism
Hyperthyroidism induces increased GI motility, result
ing in diarrhea.
Inflammatory Bowel Disease
Inammatory bowel diseases such as diverticulitis,
ulcerative colitis, gastroenteritis, and Crohn disease
cause inammation of the GI lining, resulting in mus
cle spasm and diarrhea.
Surgical Bypass
Surgical bypass procedures of the intestine often result
in chronic diarrhea because of the decreased absorp
tive area remaining after surgery. Incompletely digest
ed food and water rapidly pass through the GI tract.
551
TREATMENT OF ALTERED ELIMINATION
CONSTIPATION
Constipation that does not have a specic cause can
often be treated without the use of laxatives. A high
ber diet (e.g., fruits, grains, nuts, vegetables), ad
equate hydration (e.g., 8 to 10 eightounce glasses of
water daily), and daily exercise (e.g., for physical ac
tivity, stress relief) can eliminate most cases of consti
pation. Overthecounter (OTC) laxatives, other than
when treating acute constipation from a specic cause
(e.g., a change in routine such as traveling), should be
avoided. Patients that should be referred to a health
care provider are those:
• With severe abdominal discomfort or pain
• Who have nausea, vomiting, or fever
• With a preexisting condition (e.g., diabetes mellitus,
abdominal surgery)
• Taking medicines that cause constipation (e.g., iron,
aluminum antacids, anticholinergic agents, opioids)
• Who have used other laxatives without success or
are laxative abusers
DIARRHEA
Diarrhea may be acute or chronic, mild or severe.
Because acute diarrhea may be a defense mechanism
to rid the body of infecting organisms or irritants, it
is usually selflimiting. Chronic diarrhea may be due
to deciency of digestive enzymes, may indicate a dis
ease of the stomach or small or large intestine, or may
be a reaction to antibiotic therapy. If diarrhea is severe
or prolonged, it may cause dehydration, electrolyte de
pletion, and physical exhaustion. Specic antidiarrheal
therapy depends on the cause of the diarrhea.
NURSING IMPLICATIONS FOR CONSTIPATION
AND DIARRHEA
Assessment
History
• Obtain a history of the patient’s usual bowel pat
tern and changes that have occurred in the frequen
cy, consistency, odor, color, and number of stools
per day. Ask whether the patient has a usual time
of defecation (e.g., mornings or afternoon or after
meals). Does the individual respond immediately to
the urge to defecate or delay toileting until a more
convenient time?
• Ask whether the onset of diarrhea or constipation is
recent and if it can be associated with travel or stress.
Has there been a change in water source or foods
lately? Ask what measures (whether prescribed by a
healthcare provider or by selftreatment) the patient
has already initiated to correct the problem, and ask
about the degree of success achieved.
• Obtain a detailed history of the individual’s health.
Are any acute or chronic conditions being treated—
for example, cancer, GI disorders, neurologic condi
tions, or intestinal obstruction?
552 UNIT VI Drugs Affecting the Digestive System
• Plan to perform a focused assessment consistent
with the symptoms and the underlying pathology.
Medications, treatments, and diagnostics
• Ask the patient to provide a list of all current medi
cations prescribed by a healthcare provider, as well
as all OTC medications that are being taken. Are any
used to treat diarrhea or constipation? Are any of
these medications known to slow intestinal transit
time (e.g., opioids, aluminumcontaining antacids,
anticholinergic agents)? Are any known to cause di
arrhea (e.g., magnesiumcontaining antacids)?
• Order baseline laboratory studies requested by the
healthcare provider. Schedule prescribed treatments
(e.g., enema administration) and diagnostic proce
dures (e.g., abdominal radiographs, colonoscopy,
anorectal manometry).
Activity and exercise
• Ask the patient about daily activity level and ex
ercise. Does the patient play vigorous sports, take
walks or jog, or have a sedentary job and hobby?
Elimination pattern. What is the individual’s usual
pattern of stool elimination (i.e., frequency of the urge
to defecate, usual stool consistency, presence of bloat
ing or atus, fecal incontinence)? Does the individual
have a history of, or currently have, anal ssures, hem
orrhoids, or abscesses? Assess intake and output, and
any presence of blood in the stool.
Nutrition
• Ask questions to determine the patient’s usual di
etary practices. How much coffee, tea, soft drinks
(caffeinated or decaffeinated), water, fruit juice, and
alcoholic beverages are consumed each day?
• Ask for a description of what the patient has eaten
over the past 24 hours. Evaluate the data to identify
whether foods from all levels of the food pyramid
(see Fig. 46.4) are being eaten. Are there good sourc
es of dietary ber? Has the patient introduced foods
not usually eaten into the diet?
• Obtain specic orders relating to nutrition. Diet or
ders depend on the cause of constipation or diar
rhea. A dietary consult may be indicated. Schedule
uid intake of at least 3000 mL/day, unless con
traindicated by coexisting conditions (e.g., heart
failure, renal disease). Rehydration solutions may
be required with severe diarrhea. Does the patient
have any food intolerances or foods known to pro
duce diarrhea or constipation?
Basic assessment
• Obtain and record baseline vital signs, height, and
weight.
• Assess bowel sounds in all four quadrants. Observe
the size and shape of the abdomen. Note any signs
of distention, ascites, or masses.
• Assess and record signs of dehydration. Examine
the patient for inelastic skin turgor, sticky oral
mucous membranes, excessive thirst, a shrunken
and deeply furrowed tongue, crusted lips, weight
loss, deteriorating vital signs, soft or sunken eye
balls, delayed capillary lling, high urine specic
gravity or no urine output, and possible mental
confusion.
Laboratory studies
• Review laboratory reports for indications of prob
lems such as malabsorption, dehydration, and uid,
electrolyte, and acidbase imbalances (e.g., K+, Cl−,
pH, partial pressure of carbon dioxide, bicarbonate,
hemoglobin, hematocrit, urinalysis [specic grav
ity], serum albumin, total protein).
• Check reports of stool specimen sent for laboratory
examination.
Implementation
• Maintain hydration with oral or parenteral solu
tions as prescribed by the healthcare provider.
Monitor the hydration status with volume of intake,
urine output, skin turgor, moisturization of mucous
membranes, and daily weights.
• Assess for bowel sounds in all four quadrants.
Report absence of bowel sounds immediately to the
healthcare provider. Assess abdomen for distention;
measure abdominal girth if necessary.
• Give enemas prescribed according to hospital pro
cedures. (These are not used for longterm treat
ment of constipation.) Oil retention enemas may be
required to soften the fecal material.
• Initiate nutritional interventions such as highber
foods and adequate uid intake.
• Give prescribed laxatives or stool softeners. Monitor
for effectiveness and adverse effects.
• Administer prescribed antidiarrheal agents, anti
peristaltic agents (except to patients known to have
infectious diarrhea), and antibiotics for infection
based diarrhea.
• Initiate hygiene measures to prevent perianal skin
breakdown. Cleanse the perianal area thoroughly
after each stool. Apply protective ointment (e.g.,
zinc oxide) as prescribed; with severe diarrhea, a fe
cal collection apparatus may be helpful.
• Monitor vital signs, daily weights, and stool cul
tures and perform a focused assessment appropri
ate to the underlying cause of the constipation or
diarrhea.
Patient Education
Nutritional status
• Be certain that the individual, parent, or signicant
other understands all aspects of the diet and uid
orders prescribed. Ask specically what should and
should not be avoided and how much they should
be drinking.
 Drugs Used to Treat Constipation and Diarrhea CHAPTER 34
• Stress the inclusion of highber foods and ad
equate uids to maintain hydration and alleviate
constipation.
• Depending on the underlying cause of the symp
toms, health teaching is appropriate regarding
proper food preparation, storage, and prevention of
contamination.
• During travel, advise using bottled water when
appropriate.
Activity and exercise
• Encourage regular exercise.
Medications
• Explain the consequences of regular use of laxatives
and the benets of handling constipation with diet,
exercise, and adequate uid intake.
• When opioids are used regularly for pain control
in cancer patients, it is imperative that the patients
know that stool softeners should be initiated and
continued as long as constipating medications are
being taken.
• If laxatives or enemas are prescribed to cleanse the
intestines before diagnostic examination, be cer
tain that the individual has written instructions
for use, the time and amount to be administered,
and where the laxative or enema can be purchased.
Review the correct procedure for selfadminister
ing an enema with the patient, or instruct a family
member.
• Emphasize the need to be in proximity to a bath
room when taking laxatives such as GoLYTELY (a
polyethylene glycol–electrolyte solution [PEGES]).
Fostering health maintenance
• Fecaloral contamination may cause diarrhea. Teach
proper handwashing and cleansing or disinfection
of the toilet, bedpan, or commode.
• For diarrhea associated with chronic GI diseases, it
is imperative to reinforce all aspects of health teach
ing relating to the specic disease underlying the
symptomatology.
• Provide the patient and signicant others with im
portant information contained in the individual drug
monographs to identify drugs that cause constipation
or diarrhea. Additional health teaching and nursing
interventions for common and serious adverse ef
fects are described in each drug monograph.
• Seek cooperation and understanding of the fol
lowing points for judicious use of laxatives or an
tidiarrheals: name of medication; dosage, route,
and times of administration; and common and
serious adverse effects. For infectious diarrhea,
teach the patient precautions to prevent its spread
to others. For all patients with diarrhea, teach the
need for adequate uid intake and any dietary
restrictions.
553
DRUG CLASS: LAXATIVES
Actions
Laxatives are chemicals that act to promote the evacua
tion of the bowel. They are usually subclassied based
on the mechanism of action (Table 34.1).
Stimulant laxatives. Stimulant laxatives (e.g., bisaco
dyl, sennosides A and B) act directly on the intestine,
causing an irritation that promotes peristalsis and
evacuation. If given orally, these agents act within 6 to
10 hours. If administered rectally, they act within 60 to
90 minutes.
Osmotic laxatives. Osmotic laxatives (e.g., lactulose,
PEG, glycerin, lactitol) are hypertonic compounds
that draw water into the intestine from surrounding
tissues. Lactulose and lactitol has an onset of action
within 24 to 48 hours. Glycerin, being administered
as a suppository rectally, usually acts within 15 to 30
minutes.
PEG 3350 and PEGES are similar in osmotic ac
tion, but are quite different in clinical use. PEG 3350
is a granular material that dissolves easily and taste
lessly in a breakfast beverage such as coffee or juice.
It is much milder in action and used for occasional
constipation, usually acting within 24 to 48 hours,
depending on the patient’s normal GI transit time. It
can be used intermittently 2 to 3 mornings per week
in small doses to help regulate the frequency of bowel
movements with formed stools that are easily passed.
PEGES is usually a dry powder that is reconstituted
into 2 to 4 quarts (liters) of a solution of nonabsorb
able ions and electrolytes that act as an osmotic agent.
Each product follows its own protocol, but 8ounce
glasses of solution are consumed every 20 minutes for
several doses. When taken orally, it pulls electrolytes
and water into the solution in the lumen of the bowel
and exchanges sodium ions to replace those removed
from the body. The result is a diarrhea that cleanses
the whole bowel for surgery, colonoscopy, or barium
enema xray examination with no signicant dehydra
tion or loss of electrolytes.
Saline laxatives. Saline laxatives (e.g., magnesium
hydroxide, magnesium citrate, sodium phosphates)
are hypertonic compounds that work in the small
and large intestine, drawing water into the lumen
of the intestine from surrounding tissues. The accu
mulated water affects stool consistency and distends
the bowel, causing peristalsis. The magnesiumcon
taining products also stimulate muscle peristalsis,
helping evacuate the bowel. These agents usually
act within 1 to 3 hours and up to 6 hours for sodium
phosphates. Continued use of these products sig
nicantly alters electrolyte balance and may cause
dehydration.
554 UNIT VI Drugs Affecting the Digestive System

Table 34.1 Laxatives

GENERIC NAME BRAND NAME LAXATIVE TYPE
bisacodyl Dulcolax tablets Stimulant
docusate sodium Colace Stool softener
glycerin Pedia-Lax Osmotic
lactulose Constulose Osmotic
lactitol Pizensy Osmotic
linaclotide Linzess Guanylate cyclase-C agonist
lubiprostone Amitiza Chloride channel activator
magnesium citrate Citrate of Magnesia, Citroma Saline
magnesium hydroxide Phillips’ Milk of Magnesia Saline
methylcellulose Citrucel Bulk forming
methylnaltrexone Relistor Peripheral opioid antagonist
mineral oil Mineral Oil Lubricant
naldemedine Symproic Peripheral opioid antagonist
naloxegol Movantik Peripheral opioid antagonist
plecanatide Trulance Guanylate cyclase-C agonist
polycarbophil FiberLax Bulk forming
polyethylene glycol (PEG) 3350 MiraLAX Osmotic
polyethylene glycol–electrolyte solution (PEG-ES) GoLYTELY Osmotic
MoviPrep Osmotic
psyllium hydrophilic mucilloid Metamucil Bulk forming
sennosides Ex-Lax Stimulant
Senokot Stimulant
sennosides and docusate sodium Peri-Colace Stool softener plus stimulant
sodium phosphates Osmo-Prep Saline

Chloride channel activator. Lubiprostone (Amitiza) in
duces secretion of chloriderich intestinal uid without
altering sodium or potassium concentrations in the se
rum. Increasing intestinal uid secretion increases in
testinal motility with passage of feces.
Guanylate cyclase-C agonists. Linaclotide (Linzess)
and plecanatide (Trulance) are guanylate cyclase
C agonists, drugs approved for chronic idiopathic
constipation. They both activate guanylate cyclaseC,
which stimulates secretion of chloride and bicarbonate
into the intestinal lumen, increasing intestinal uid se
cretion, which can soften stools and increase motility
with passage of feces.
Lubricant laxatives. Lubricant laxatives (e.g., mineral
oil) lubricate the intestinal wall and soften the stool,
allowing a smooth passage of fecal contents. Onset of
action is often 6 to 8 hours but may be up to 48 hours
because the action is highly dependent on the individ
ual patient’s normal GI transit time. Peristaltic activ
ity does not appear to be increased. If used frequently,
these oils may inhibit the absorption of fatsoluble
vitamins.
Bulk-forming laxatives. Psyllium, calcium polycarbo
phil, and methylcellulose are approved bulkforming
laxatives. Psyllium increases stool frequency in pa
tients with chronic constipation, but evidence is lack
ing for the efcacy of the other approved bulkforming
laxatives. Bulkforming laxatives must be administered
with a full glass of water. The laxative causes water to
be retained within the stool. This increases bulk, which
stimulates peristalsis. Onset of action is usually 12 to
24 hours but may be as long as 72 hours, depending
on the patient’s GI transit time. Bulkforming agents
are usually considered the safest laxatives, even when
taken routinely. Fresh fruits, vegetables, and cereals
such as wheat bran are natural bulkforming products.
Stool softeners. Stool softeners, also known as wetting
agents, draw water into the stool, causing it to soften.
Docusate calcium and docusate sodium are US Food
and Drug Administration approved, but there is little
 Drugs Used to Treat Constipation and Diarrhea CHAPTER 34
evidence that they are effective in treating chronic con
stipation. Psyllium is more effective in improving stool
frequency than stool softeners. Stool softeners do not
stimulate peristalsis and may require up to 72 hours
to aid in a soft bowel movement. Action from these
agents depends on the patient’s state of hydration and
the GI transit time.
Peripheral opioid antagonists. Methylnaltrexone
(Relistor), naloxegol (Movantik), and naldemedine
(Symproic) are muopioid receptor antagonists that
bind to opioid receptors in the GI tract, inhibiting
the constipationproducing effects of opioid drugs.
Methylnaltrexone, naloxegol, and naldemedine do not
cross the bloodbrain barrier and do not interfere with
the analgesic effects of the opioids.
Uses
Stimulant, osmotic, chloride channel activa-
tor, guanylate cyclase-C agonist, and saline laxa-
tives. Stimulant, osmotic, and saline laxatives may be
used individually to relieve acute constipation. They
are also effective when used in higher doses and in
combination for cleaning out the intestines prior to
bowel surgery or colonoscopy. PEG 3350, lactulose,
lactitol, and lubiprostone are effective in treating
chronic constipation. Lubiprostone is approved to
treat chronic idiopathic constipation, opioidinduced
constipation in adults with chronic noncancer pain,
and irritable bowel syndrome with constipation.
Smaller doses of lactulose or PEG 3350 can be taken
to regulate stool consistency and frequency. Larger
doses of PEGES are routinely used as bowel prepara
tions to remove gas and feces before radiologic exam
ination of the kidneys, colon, intestine, or gallbladder.
These products should be used only intermittently
because chronic use may cause loss of normal bow
el function and dependency on the agent for bowel
evacuation. The guanylate cyclaseC agonists lina
clotide and plecanatide are used in the treatment of
chronic idiopathic constipation and in the treatment
of irritable bowel syndrome with constipation. The
most common adverse effect is diarrhea.
Lubricant laxatives. Lubricant laxatives are helpful
for producing a soft stool without causing signicant
bowel spasm. Lubricants are also used prophylactical
ly in patients who should not strain during defecation.
Lubricants should not be administered to debilitated
patients who are constantly in a recumbent position.
The oil can be aspirated into the lungs, where it may
cause lipid pneumonia. Lubricant laxatives may be
used in geriatric and pregnant patients because there
is little cramping accompanying their use.
Bulk-forming laxatives. Bulkforming laxatives are
generally considered the drug of choice for someone
555
who is incapacitated and needs a laxative regularly.
These agents may also be used in patients with
irritable bowel syndrome to provide a softer consist
ency to the stools if a highber diet is not adequate.
Bulkforming laxatives are also used to control cer
tain types of diarrhea by absorbance of the irritating
substance, thus allowing its removal from the bowel
during defecation. Bulkforming laxatives may be
used in geriatric and pregnant patients because there
is little cramping accompanying their use. Pediatric
patients should also be treated with a change in diet
to include cereals, fruits, and grains. Constipation in
infants can be treated with malt soup extract, a bulk
forming laxative. It is important that bulkforming
laxatives be dispersed in a glass of water or juice be
fore administration. If adequate volumes of water are
not taken, obstruction within the GI tract may result
from a bulk laxative that forms a sticky mass.
Stool softeners. Stool softeners are routinely used
for prophylactic purposes to prevent constipation or
straining at stool (e.g., in patients recovering from my
ocardial infarction or abdominal surgery).
Peripheral opioid antagonists. Methylnaltrexone, na
loxegol, and naldemedine are used for the treatment of
opioidinduced constipation in patients with advanced
illness who are receiving palliative care when their re
sponse to laxative therapy has not been adequate.
Therapeutic Outcomes
The primary therapeutic outcomes expected from laxa
tive therapy are as follows:
1. Relief from abdominal discomfort.
2. Passage of bowel contents within a few hours of
administration.
Nursing Implications for Laxative Therapy
Premedication assessment
1. Determine the usual pattern of elimination.
2. Ask specically about symptoms that may indi
cate undiagnosed abdominal pain, such as symp
toms associated with intestinal obstruction or
appendicitis.
Medication Safety Alert
Do not administer laxatives to patients with undiagnosed ab-
dominal pain or inammation of the GI tract, such as gastritis,
appendicitis, or colitis.
Availability. For drugs not listed here, see drug mono
graphs for individual products for information on
available formulations.
• Lactitol; oral powder: 10 g in unitdose packets; 280
g and 560 g in multidose bottles
556 UNIT VI Drugs Affecting the Digestive System
• Lubiprostone: 8 and 24mcg capsules
• Methylnaltrexone: 8 mg in a 0.4mL syringe; 12 mg
in a 0.6mL vial and syringe; 150mg tablets
• Naldemedine: 0.2mg tablets
• Naloxegol: 12.5 and 25mg tablets
Dosage and administration. For drugs not listed here,
see drug monographs for individual products for in
formation on dosage and administration.
Bulk-forming laxatives: PO: Be sure to administer
with adequate water to prevent esophageal, gastric,
intestinal, or rectal obstruction.
Lactitol. Chronic idiopathic constipation: PO: 20 g
orally daily, preferably with meals. The dose should be
reduced to 10 g once daily for persistent loose stools.
Other oral medications should be given at least 2 hours
before or 2 hours after lactitol.
Lubiprostone. Chronic idiopathic constipation and
opioid-induced constipation: PO: 24 mcg taken twice
daily with food and water.
Irritable bowel syndrome with constipation: PO: 8
mcg twice daily with food and water.
Methylnaltrexone. Opioid-induced constipation with
chronic noncancer pain: Subcut: 12 mg once daily. PO:
450 mg once daily with water on an empty stomach at
least 30 minutes before the rst meal of the day.
Opioid-induced constipation with advanced illness (re-
ceiving palliative care): Treatment of opioidinduced
constipation in adult patients with advanced illness
who are receiving palliative care and have an inad
equate response to conventional laxative regimens is
based on patient weight:
PATIENT WEIGHT METHYLNALTREXONE DOSAGE
<38 kg 0.15 mg/kg
38–62 kg 8 mg
62–114 kg 12 mg
>114 kg 0.15 mg/kg
• In patients with a creatinine clearance lower than 30
mL/min, reduce the dosage by onehalf.
• Administer by subcutaneous injection every other
day, as needed, but no more than once every 24 hours.
Naldemedine. Opioidinduced constipation with
chronic noncancer pain: PO: 0.2 mg daily.
Naloxegol. Opioid-induced constipation with noncancer
pain: PO: 25 mg once daily in the morning on an empty
stomach. If not tolerated, reduce dose to 12.5 mg once
daily.
Common adverse effects
Gastrointestinal
Abdominal spasms, abdominal discomfort with atulence,
nausea. The most common adverse effect is excessive
bowel stimulation that results in abdominal spasms
and diarrhea. Patients who are severely constipated
may develop abdominal cramps. The patient should
rst experience the urge to defecate, then defecate and
feel a sense of relief.
Cardiovascular. Lactitol may cause an increased
blood pressure. Monitor blood pressure.
Serious adverse effects
Gastrointestinal
Abdominal tenderness, pain, bleeding, vomiting, diarrhea,
increasing abdominal girth. Failure to defecate or defeca
tion of only a small amount may indicate the presence
of an impaction. These also are symptoms of an acute
abdominal condition.
Galactosemia. Patients with galactosemia should not
receive lactitol.
Drug interactions
Bisacodyl. Do not administer with milk, antacids,
cimetidine, famotidine, or nizatidine. These products
may allow the enteric coating to dissolve prematurely,
resulting in nausea, vomiting, and cramping.
Psyllium. Do not administer products containing
psyllium (e.g., Metamucil) at the same time as salicy
lates, nitrofurantoin, or digoxin, because the psyllium
may inhibit absorption. Administer salicylates, nitro
furantoin, or digoxin at least 1 hour before or 2 hours
after psyllium.
Mineral oil. Daily administration of mineral oil for
more than 1 to 2 weeks may cause a deciency of the
fatsoluble vitamins.
Docusate. Docusate enhances the absorption of min
eral oil. Concurrent use is not recommended.
Lactitol. May reduce the absorption of medications
that are administered at the same time. Administer
medications 2 hours before or 2 hours after adminis
tration of lactitol.
Methylnaltrexone, lubiprostone, linaclotide, and plecana-
tide. There are no reported drug interactions for these
medications.
Naldemedine and naloxegol
Drugs that increase toxic effects of naldemedine and na-
loxegol. Fluconazole, aprepitant, diltiazem, verapamil,
erythromycin, itraconazole, ketoconazole, clarithro
mycin, and ritonavir may inhibit the metabolism of
naldemedine and naloxegol. Monitor for signs of
toxicity.
Drugs that reduce therapeutic effects of naldemedine
and naloxegol. Rifampin, carbamazepine, phenytoin,
and St. John’s wort can induce the metabolism of nal
demedine and naloxegol, reducing their therapeutic
effect.
DRUG CLASS: ANTIDIARRHEAL AGENTS
Actions
Antidiarrheal agents include a wide variety of drugs
that can be divided into two broad categories—lo
cally acting agents and systemic agents. Locally acting
 Drugs Used to Treat Constipation and Diarrhea CHAPTER 34
agents such as activated charcoal, pectin, and psyllium
absorb excess water to cause a formed stool and ad
sorb irritants or bacteria that are causing the diarrhea.
Bismuth subsalicylate acts locally to stop secretion of
uids into the GI tract that promote diarrhea; it may
also have local antimicrobial effects, killing bacteria
and viruses that may be inducing diarrhea. Lactobacillus
acidophilus is used to promote normal bacterial growth
in the intestinal tract with chronic (not acute) diarrhea.
The systemic agents act through the autonomic ner
vous system to reduce peristalsis and motility of the
GI tract, allowing the mucosal lining to absorb nutri
ents, water, and electrolytes, leaving a formed stool
in the colon. Representatives of the systemically act
ing agents are loperamide (without atropine) and di
phenoxylate and difenoxin with atropine to prevent
abuse (Table 34.2).
The systemically acting agents are associated with
more adverse effects (see Table 34.2) and should not be
used to treat diarrhea caused by substances toxic to the
GI tract, such as bacterial contaminants or other irritants.
Because these agents act by reducing GI motility, the sys
temically acting antidiarrheals tend to allow the toxin to
remain in the GI tract longer, causing further irritation.
Uses
Although the ingredients of the antidiarrheal products
are, in general, benign and the majority are available
OTC, the decision to recommend treatment or to refer
the patient to a healthcare provider is not to be taken
lightly.
Antidiarrheal products are usually indicated under
the following conditions:
• The diarrhea is of sudden onset, has lasted more
than 2 or 3 days, and is causing signicant uid and
water loss. Young children and elderly patients are
more susceptible to rapid dehydration and electrolyte
imbalance and therefore should start antidiarrheal
therapy earlier.
• Patients with inammatory bowel disease develop
diarrhea. Rapid treatment shortens the course of the
incapacitating diarrhea and allows the patient to
live a more normal lifestyle. Other agents, such as
adrenocorticosteroids or sulfonamides, may also be
used to control the underlying bowel disease.
• Post–GI surgery patients develop diarrhea. These
patients may require chronic antidiarrheal therapy to
allow adequate absorption of uids and electrolytes.
• When the cause of the diarrhea has been diagnosed,
and the healthcare provider determines that an
antidiarrheal product is appropriate for therapy.
Because many cases of diarrhea are selflimiting,
therapy may not be necessary.
557
Therapeutic Outcome
The primary therapeutic outcome expected from
antidiarrheal therapy is relief from the incapacitation
and discomfort of diarrhea.
Nursing Implications for Antidiarrheal Agents
Premedication assessment
1. Confer with patient regarding medications that
may be contributing to diarrhea, including antacids
containing magnesium or laxative products, anti
biotics, or products containing large quantities of
sorbitol.
2. Review history of the onset of diarrhea and pre
cipitating factors. Refer to a healthcare provider
if in doubt about administering antidiarrheal
agents.
Availability, dosage, and administration. See Table 34.2.
PO: Follow directions on the container. Be sure
to give adequate water with bulkforming agents
to prevent esophageal, gastric, intestinal, or rectal
obstruction.
Common adverse effects
Gastrointestinal
Abdominal distention, nausea, constipation. Locally act
ing agents have essentially no adverse effects, but if
used excessively, they may cause abdominal disten
tion, nausea, and constipation.
Stool and tongue discoloration. Bismuth subsalicylate
may cause a grayish black discoloration to stools and
tongue.
Serious adverse effects
Gastrointestinal
Prolonged or worsened diarrhea. This may be an indica
tion that toxins are present in the intestines and that
the systemically acting antidiarrheal is causing reten
tion of these toxins. Refer the patient to a healthcare
provider for medical attention.
Drug interactions
Diphenoxylate, difenoxin. The chemical structure of
these two antidiarrheal agents is similar to meperidine.
These agents should not be used in a patient receiving
monoamine oxidase inhibitors (e.g., phenelzine, iso
carboxazid, tranylcypromine) because of the potential
for a hypertensive crisis.
Sedatives, alcohol, phenothiazines. Sedation caused by
diphenoxylate and difenoxin is potentiated by other
medications with central nervous system depressant
properties.
558 UNIT VI Drugs Affecting the Digestive System

Table 34.2 Antidiarrheal Agents

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE COMMENTS
SYSTEMIC ACTION
difenoxin with Motofen Tablets: 1 mg difenoxin PO: 2 tablets, then 1 tablet Inhibits peristalsis
atropine with 0.025 mg after each loose stool or Atropine added to minimize
atropine every 3–4 hr as needed; potential overdose or
do not exceed 8 tablets in abuse
24 hr May cause drowsiness or
dizziness; use caution in
performing tasks requiring
alertness
Do not use in children
younger than 2 yr
diphenoxylate with Lomotil Tablets: 2.5 mg PO: 5 mg three or four times Inhibits peristalsis
atropine diphenoxylate with daily; do not exceed 20 mg Atropine added to minimize
0.025 mg atropine per 24 hr potential overdose or
Liquid: 2.5 mg abuse
diphenoxylate with May cause drowsiness or
0.025 mg atropine/5 dizziness; use caution in
mL performing tasks requiring
alertness
Do not use in children
younger than 2 yr
loperamide Imodium A-D Tablets: 2 mg PO: 4 mg initially, followed by Inhibits peristalsis
Capsules: 2 mg 2 mg after each unformed Used in acute, nonspecic
Liquid: 1 mg/7.5 mL movement; do not exceed diarrhea and to reduce
16 mg/day volume of discharge from
ileostomy
LOCAL ACTION
Lactobacillus Lactinex Tablets, chewable; PO: 2–4 capsules, two to four Bacteria used to recolonize
acidophilus and Granules times daily, with milk GI tract in an attempt to
L. bulgaricus Granules: 1 packet added to treat chronic diarrhea
cereal, fruit juice, or milk Do not use in acute diarrhea
three or four times daily
bismuth Pepto-Bismol Tablets, chewable: PO: 524 mg every 30–60 min In the GI tract, bismuth
subsalicylate 262 mg or 1050 mg every 60 min subsalicylate dissociates;
Suspension: 262 as needed the salicylate stops
mg/15 mL, 525 Maximum dosage: secretions of uids into
mg/15 mL Approximately 4200 mg (8 the GI tract, and the
doses of 262 mg; 4 doses bismuth has antimicrobial
of 525 mg) per 24 hr action against bacterial
and viral enteropathogens
GI, Gastrointestinal.
 Drugs Used to Treat Constipation and Diarrhea CHAPTER 34 559

Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions

Key Points
• Constipation and diarrhea are common disorders of the GI
tract that most people experience occasionally throughout
their lives. Most cases are self-limiting and do not require
pharmacologic treatment.
• Constipation is most commonly treated by adding bulk
and water to the diet and by exercising regularly. If drug
treatment is required, laxatives that act by a variety of
mechanisms are available: bulk-forming agents, stimulants,
osmotics, lubricants, stool softeners, saline agents,
chloride channel activators, guanylate cyclase-C agonists
and opioid antagonists.
• Acute diarrhea is usually a symptom of an underlying
problem, such as a GI infection. A detailed history of
recent events must be taken to assess whether to
recommend treatment with antidiarrheal agents.
• Antidiarrheal agents are divided into two broad categories,
locally acting agents and systemic agents.
Additional Learning Resources
Objective: Identify the mechanism of action for the different
classes of laxatives and describe underlying causes of constipation.
NCLEX item type: Extended multiple response
Cognitive skill: Application
2. A nurse preparing the drug psyllium (Metamucil) that has been
ordered and explains to the patient in the scenario that oral,
bulk-forming laxatives usually relieve constipation by which time
frame?
1. “You should have relief from constipation in about half an
hour.”
2. “This drug takes about 1 to 3 hours to work.”
3. “Since this drug takes a while to work, do not expect
results for at least 6 to 10 hours.”
4. “This drug works by absorbing water into the stool,
causing a softer stool, and takes about 12 to 24 hours
but may be as long as 72 hours.”
Objective: Identify the mechanism of action for the different
classes of laxatives and describe underlying causes of constipation.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension

SG Go to your Study Guide for additional Review Questions 3. The nurse reviewed the different types of laxatives with their
for the NCLEX® Examination, Critical Thinking Clinical Situa- used. Indicate with an X which class of laxative is used for which
tions, and other learning activities to help you master this chap- purpose.
ter content.
Part A
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
CHLORIDE GUANYLATE PERIPHERAL
Clinical Judgment and Next-Generation NCLEX® Exam- CHANNEL CYCLASE-C OPIOID
ination-Style Questions The following questions are typical of ACTIVATOR STIMULANT AGONISTS ANTAGONISTS
the NCLEX exam and include both NGN (Next Generation) Causes
and traditional questions. See Chapter 1 for further information irritation that
regarding question types. promotes
peristalsis
Scenario and
evacuation
A patient is being seen at the clinic for follow up after being
Used for
treated for anemia and hypothyroidism. After discussing the
chronic
progress of the treatment, the patient mentions that constipa-
idiopathic
tion has been an ongoing issue.
constipation
1. A nurse is providing education to the patient in the scenario who FDA-
has complained about frequent bouts of constipation. Which approved
statements by the patient indicates teaching has been effective? treatment
(Select all that apply.) of opioid
1. “If I exercise for at least 30 minutes every day, my bowels constipation
will move more regularly.” Used in
2. “Drinking adequate amounts of water can help keep irritable
constipation from occurring.” bowel
3. “Taking opioid pain medications regularly will not affect syndrome
my bowel habits.” Used
4. “Eating a diet rich in ber should help alleviate any routinely
irregular bowel movements.” for bowel
5. “As long as I continue to eat my daily yogurt and crackers prep before
and cheese for lunch I should be ne.” GI exami-
6. “I know to use laxatives with caution as they could be nations
habit forming and abused.”
7. “I should have a bowel movement every day to be
normal.”
560 UNIT VI Drugs Affecting the Digestive System

Part B OPTION 1 OPTION 2

Stopping secretions of uids Reducing motility
BULK into the GI tract
SALINE OSMOTIC FORMING LUBRICANT
Reducing peristalsis and Inhibiting peristalsis
Used for motility of GI tract
chronic
Incorporating bacteria to Adsorbing secretions in GI
idiopathic
recolonize GI tract tract
constipation
Absorbs excess water to Incorporating bacteria to
Prophylactic
form stool recolonize GI tract
prevention of
constipation
or straining Objective: Differentiate between locally acting and systemically
Used in acting antidiarrheal agents and the conditions that respond
irritable bowel favorably to antidiarrheal agents.
syndrome NCLEX item type: Cloze
Used Cognitive skill: Evaluate cues
routinely for 1. Choose the most likely options for the information missing from
bowel prep the sentence below by selecting from the lists of options provided.
before GI
examinations The nursing assessments needed to evaluate a pa-
tient’s state of hydration include ________1_________
and _________1__________. The electrolytes that
Objective: Identify the mechanism of action for the different should be monitored with prolonged diarrhea include
classes of laxatives and describe underlying causes of constipation. ________2____________and ________2____________.
NCLEX item type: Matrix
Cognitive skill: Recognize cues OPTION 1 OPTION 2
4. The patient with an ileostomy is receiving loperamide (Imodium Monitoring vital signs and daily weights K+
A-D) for treatment of diarrhea. The nurse knows this is given
Assess for any perianal skin breakdown Na+
because loperamide will have which effects? (Select all that
apply.) Monitor volume of intake, urine output, skin Cl–
turgor, and mucous membranes
1. Softens the stool
2. Inhibit peristalsis Assess bowel sounds in all four quadrants Ca2+
3. Has antimicrobial action
4. Stops the secretion of uids into the GI tract Objective: Describe nursing assessments needed to evaluate the
5. Allows more time for the intestines to absorb excess patient’s state of hydration when suffering from either constipation
water to form stool or dehydration and identify electrolytes that should be monitored
Objective: Differentiate between locally acting and systemically whenever prolonged or severe diarrhea is present.
acting antidiarrheal agents. NCLEX item type: Cloze
NCLEX item type: Multiple response Cognitive skill: Recognize cues
Cognitive skill: Application
5. Choose the most likely options for the information missing from
the sentence below by selecting from the lists of options provided.
The nurse determined that the difference between the lo-
cally acting antidiarrheal agents is that these agents act
by ________1_________and ___________1_____________
versus the systemic agents which act by
________2___________and__________2__________.
Unit VII Drugs That Affect the Endocrine System

Drugs Used to Treat Diabetes Mellitus 35

https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify the major nursing considerations associated
with the management of the patient with diabetes (e.g.,
nutritional evaluation, laboratory values, activity and
exercise, and psychological considerations).
2. Compare the signs, and symptoms of hypoglycemia and
hyperglycemia.
3. Describe the action and use of insulin to control diabetes
mellitus.
4. Discuss the action and use of oral hypoglycemic agents to
control diabetes mellitus.
5. Discuss the educational needs for patients with
complications from diabetes.

Key Terms
diabetes mellitus (dī-ă-BĒ-tēz mĕl-Ī-
tĭs) (p. 561)
hyperglycemia (hī-pĕr-glī-SĒ-mē-ă)
(p. 561)
type 1 diabetes mellitus (p. 562)
type 2 diabetes mellitus (p. 562)
gestational diabetes mellitus
(GDM) (jĕs-TĀ-shŭn-ăl) (p. 563)
impaired glucose tolerance
(IGT) (GLŬ-kōs) (p. 563)
impaired fasting glucose (IFG)
(p. 563)
prediabetes (prē-dī-ă-BĒ-tēz) (p. 563)
microvascular complications
(mīk-rō-VĂS-kyū-lăr) (p. 563)
macrovascular complications
(măk-rō-VĂS-kyū-lăr) (p. 563)
neuropathies (nўr-ŎP-ĕ-thēz) (p. 563)
paresthesia (păr-ĕs-THĒ-zē-ă) (p. 564)
medical nutrition therapy
(MNT) (mĕd-ĭ-KŬL nū-TRĬSH-ĕn
THĔR-ĕ-pē) (p. 564)
hypoglycemia (hī-pō-glī-SĒ-mē-ă)
(p. 564)
intensive therapy (p. 564)

DIABETES MELLITUS
Diabetes mellitus is a group of diseases characterized
by hyperglycemia (fasting plasma glucose level >100
mg/dL) and abnormalities in fat, carbohydrate, and
protein metabolism that lead to microvascular, macro
vascular, and neuropathic complications. Several
pathologic processes are associated with the develop
ment of diabetes, and patients often have impairment
of insulin secretion, as well as defects in insulin action,
resulting in hyperglycemia. It is now recognized that
different pathologic mechanisms are involved that af
fect the development of the different types of diabetes.
“Diabetes is a complex, chronic illness requiring con
tinuous medical care with multifactorial riskreduction
strategies beyond control of blood glucose” (American
Diabetes Association [ADA], 2020, p. S1).
Diabetes mellitus is occurring with increasing fre
quency in the United States as the population increases
in weight and age. In the United States the Centers for
Disease Control and Prevention’s National Diabetes
Statistics Report (CDC, 2020) estimated that the preva
lence of diabetes in the general population is approxi
mately 10.5% (26.9 million people, 7.3 million of whom
are undiagnosed). Direct expenditures of medical care
totaled $327 billion in 2017. An additional $90 billion
was attributed to lost productivity at work, disability,
and premature death. Diabetes is listed as the sixth
leading cause of death in the United States. Most di
abetesrelated deaths are the result of cardiovascular
disease because the risk of heart disease and stroke
is two to four times greater in patients with diabetes
compared with those without the disease.
Adults with undiagnosed diabetes, with few or no
symptoms, present a major challenge to the health
profession. Because early symptoms of diabetes are
minimal, many of these people do not seek medical
advice. Indications of the disease are discovered only
at the time of routine physical examination. Those
with a predisposition to developing diabetes include
people who have relatives with diabetes (they have a
2.5 times greater incidence of developing the disease),
people with obesity (85% of all patients with diabetes
are overweight), and older people (four out of ve
patients with diabetes are older than 45 years). The
incidence of diabetes is higher in African Americans,
Hispanics, American Indians, Alaskan Natives, and
561
562 UNIT VII Drugs That Affect the Endocrine System

women. There also appears to be a signicant increase characterized by a decrease in beta cell activity (insulin
in diabetes among those younger than 20 years. deciency), insulin resistance (reduced uptake of insu
The National Diabetes Data Group of the National lin by peripheral muscle cells), or an increase in glu
Institutes of Health and the World Health Organization cose production by the liver. Over time, the beta cells
Expert Committee on Diabetes have classied diabetes of the pancreas fail, and exogenous insulin injections
by the underlying pathology causing hyperglycemia may be required. Most people with type 2 diabetes
(Box 35.1). mellitus also have metabolic syndrome, also known as
Type 1 diabetes mellitus, formerly known as insulin- insulin resistance syndrome (see Chapter 20). Type 2 dia
dependent diabetes mellitus (IDDM), is present in 5% to betes onset is usually more insidious than that of type
10% of the diabetic population. It is caused by an auto 1 diabetes. The pancreas still maintains some capacity
immune destruction of the beta cells in the pancreas. It to produce and secrete insulin. Consequently, symp
occurs more commonly in juveniles, but patients can toms (polyphagia, polydipsia, polyuria) are minimal
become symptomatic for the rst time at any age. The or absent for a prolonged period. The patient may seek
onset of this form of diabetes usually has a rapid pro medical attention several years later only after symp
gression of symptoms (a few days to a few weeks) char toms of the disease are apparent (see next section on
acterized by polydipsia (increased thirst), polyphagia Complications of Diabetes Mellitus). Fasting hyper
(increased appetite), polyuria (increased urination), glycemia can be controlled by diet in some patients, but
increased frequency of infections, loss of weight and most patients require the use of supplemental insulin
strength, irritability, and often ketoacidosis. Because or oral antidiabetic agents, such as metformin or gly
there is no insulin secretion from the pancreas, patients buride. Although the onset is usually after the fourth
require administration of exogenous insulin. Insulin decade of life, type 2 diabetes can occur in younger pa
dosage adjustment is easily affected by inconsistent tients who do not require insulin for control. See Table
patterns of physical activity and dietary irregularities. 35.1 for a comparison of the characteristics of type 1
It is common for patients with type 1 diabetes mellitus and type 2 diabetes mellitus.
to go into remission in the early stages of the disease, A third subclass of diabetes mellitus (see Box
requiring little or no exogenous insulin. This condition 35.1) includes additional types that have causes
may last for a few months and is referred to as the hon-
eymoon period.
Type 2 diabetes mellitus, formerly known as non–
insulin-dependent diabetes mellitus (NIDDM), is pres Table 35.1 Featuresa of Type 1 and Type 2 Diabetes
Mellitus
ent in 90% to 95% of the diabetic population. In con FEATURE TYPE 1 DIABETES TYPE 2 DIABETES
trast to type 1 diabetes mellitus, type 2 diabetes is
Age (yr) <20b >40b
Onset Over a few days Gradual
to weeks
Box 35.1 Classication of Diabetes Mellitus by
Pathologic Cause Insulin secretion Falling to none Oversecretion
for years
I. Type 1 diabetes (beta cell destruction, usually leading Body image Lean Obese
to absolute insulin deciency)a
Early symptoms Polyuria, Often absent
 • Immune mediated
polydipsia, until
 • Idiopathic
polyphagia complications
II. Type 2 diabetes (caused by a progressive insulin
arise
secretory defect aggravated by insulin resistance)a
III. Other specic types Ketones at Yes No
 • Genetic defects of beta cell function diagnosis
 • Genetic defects in insulin action Insulin required for Yes Noc
 • Disease of the exocrine pancreas (such as cystic treatment
brosis) Acute Diabetic Hyperosmolar
 • Endocrinopathies complications ketoacidosis hyperglycemia
 • Drug or chemical induced (such as after organ
transplantation) Microvascular No Common
 • Infections complications at
 • Uncommon forms of immune-mediated diabetes diagnosis
 • Other genetic syndromes sometimes associated Macrovascular Uncommon Common
with diabetes complications at
IV.Gestational diabetes mellitus diagnosis
aPatients with any form of diabetes may require insulin treatment at some aClinicalpresentation is highly variable.
stage of their disease. Such use of insulin does not, in itself, classify the bAge of onset is most commonly younger than 20 years, but onset may occur
patient. at any age. As the rates of obesity increase, type 2 diabetes is becoming much
Modied from American Diabetes Association. Classication and diagnosis of more prevalent in children, adolescents, and young adults in all ethnic groups.
diabetes. Diabetes Care 2020;43(Suppl. 1):S14–S31. cMay eventually require insulin therapy over time.
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
other than those that cause type 1 and type 2 diabe
tes mellitus. They are part of other diseases having
features not generally associated with the diabetic
state. Diseases that may have a diabetic component
include pheochromocytoma, cystic fibrosis, acro
megaly, and Cushing syndrome. Other disorders
included in this category are malnutrition, infec
tion, drugs and chemicals that induce hyperglyce
mia, defects in insulin receptors, and certain genetic
syndromes.
The fourth category of classication, known as
gestational diabetes mellitus (GDM), is reserved for
women who show abnormal glucose tolerance dur
ing pregnancy. Every year, 2% to 10% of pregnan
cies in the United States are affected by gestational
diabetes. Women with diabetes in the rst trimester
are classied as having type 2 diabetes. GDM is dia
betes diagnosed in the second or third trimester of
pregnancy that is not clearly overt diabetes. Most
women with gestational diabetes have a normal glu
cose tolerance postpartum. Patients with gestational
diabetes must be reclassied 6 weeks after delivery
into one of the following categories: diabetes melli
tus, impaired fasting glucose, impaired glucose tol
erance, or normoglycemia. Patients with gestational
diabetes have been put into a separate category be
cause of the special clinical features of diabetes that
develop during pregnancy and the complications
associated with fetal involvement, such as neona
tal macrosomia, largeforgestationalage births,
and shoulder dystocia. These women are also at a
greater risk of developing diabetes 5 to 10 years after
pregnancy.
There is a group of patients found to have an im-
paired glucose tolerance (IGT) or impaired fasting glu-
cose (IFG). These patients are often normally eugly
cemic but develop hyperglycemia when challenged
with an oral glucose tolerance test. In many of these
patients, the glucose tolerance returns to normal or
persists in the intermediate range for years. This inter
mediate stage between normal glucose homeostasis
and diabetes is now known as prediabetes It is now
thought that patients with IGT or IFG are at a higher
risk for developing type 1 or type 2 diabetes and car
diovascular disease in the future. The CDC has esti
mated that 88 million American adults older than age
18 had prediabetes in 2018. Without lifestyle changes
to improve their health, 15% to 30% of people with pre
diabetes will develop type 2 diabetes within 5 years.
Categories of fasting plasma glucose (FPG) levels are
the following:
• FPG less than 100 mg/dL = normal fasting glucose
• FPG at 100 mg/dL or greater but less than 126 mg/
dL = IFG
• 2hour plasma glucose level at 140 or greater but
less than 199 mg/dL = IGT
See Table 35.2 for criteria for the diagnosis of types 1
and 2 diabetes mellitus.
563
Table 35.2 Criteria for Diagnosis of Diabetes Mellitus a
DIABETES MELLITUS PREDIABETES
Hemoglobin A1c ≥6.5% in certied 5.7%–6.4%
laboratory using DCCT assay
Or
Symptoms of diabetes and a N/A
casualb plasma glucose level
≥200 mg/dL
Or
FPG level ≥126 mg/dLc 100–125 mg/dL (IFG)
Or
2-hr plasma glucose level 140–199 mg/dL (IGT)
≥200 mg/dL during an OGTT
aIn the absence of unequivocal hyperglycemia, these criteria should be
conrmed by repeat testing on a different day. The OGTT is not recommended
for routine clinical use but may be required in the evaluation of patients with
IFG or when diabetes is still suspected despite a normal FPG, as with the
postpartum evaluation of women with gestational diabetes mellitus.
bCasual is dened as any time of day without regard to time since last meal.
The classic symptoms of diabetes include polyuria, polydipsia, and unexplained
weight loss.
cFasting is dened as no caloric intake for at least 8 hours.
DCCT, Diabetes Control and Complications Trial; FPG, fasting plasma glucose;
IFG, impaired fasting glucose; IGT, impaired glucose tolerance; OGTT, oral
glucose tolerance test.
Adapted from American Diabetes Association. Standards of medical care in
diabetes—2020. Diabetes Care. 2020;43(suppl 1):S14-S31.
COMPLICATIONS OF DIABETES
MELLITUS
Longstanding hyperglycemia and abnormalities in
fat, carbohydrate, and protein metabolism lead to
microvascular, macrovascular, and neuropathic com
plications. Microvascular complications are those that
arise from destruction of capillaries in the eyes, kid
neys, and peripheral nerve damage. Diabetes has be
come the leading cause of endstage renal disease and
adult blindness. Macrovascular complications are those
associated with atherosclerosis of middle to large arter
ies, such as those in the heart and brain. Macrovascular
complications, stroke, myocardial infarction, and pe
ripheral vascular disease account for 75% to 80% of
mortality in patients with diabetes. Complications of
diabetes mellitus that often arise include the following
(Fig. 35.1):
• Hypertension
• Cardiovascular disease (atherosclerosis) leading to
myocardial infarction and stroke
• Retinopathy leading to blindness
• Renal disease leading to endstage renal disease and
the need for dialysis
• Peripheral arterial disease leading to nonhealing ul
cers, infections, and lower extremity amputations
• Neuropathies with sexual dysfunction, bladder in
continence, paresthesias, and gastroparesis
• Periodontal disease with loss of teeth
Symptoms associated with complications of diabe
tes may be the rst indication of the disease’s pres
ence. Patients may complain of weight gain or loss.
Blurred vision may indicate hyperglycemia or dia
betic retinopathy. Neuropathies may rst be observed
564 UNIT VII Drugs That Affect the Endocrine System
Retinopathy
and blindness
Cardiovascular disease
Periodontal
• Myocardial infarction
disease
• Stroke
• Hypertension
Kidney
disease
Sexual dysfunction;
bladder incontinence
Peripheral arterial diseases
• Nonhealing ulcers
• Infections
• Paresthesias
• Amputations
Fig. 35.1 Complications of diabetes mellitus.
as numbness or tingling of the extremities (paresthe-
sia), loss of sensation, orthostatic hypotension, impo
tence, vaginal yeast (candidiasis) infections, and dif
culty in controlling urination (neurogenic bladder).
Nonhealing ulcers of the lower extremities may indi
cate chronic vascular disease. Diabetic complications
can be delayed or prevented with continuous normo
glycemia, accomplished by monitoring blood glucose
levels, drug therapy, and treatment of comorbid con
ditions as they arise.
TREATMENT OF DIABETES MELLITUS
Although the classication system of the National
Diabetes Data Group and the World Health
Organization Expert Committee on Diabetes was
developed to facilitate clinical and epidemiologic in
vestigation, the categorization of patients can also be
helpful in determining general principles for therapy.
Because a cure for diabetes mellitus is unknown at
present, the minimal purpose of treatment is to pre
vent ketoacidosis and symptoms resulting from hyper
glycemia. The longterm objective of control of the dis
ease must involve mechanisms to stop the progression
of the complications. Major determinants of success
are a balanced diet, insulin or oral antidiabetic therapy,
routine exercise, and good hygiene.
Patients with diabetes can lead full and satisfy
ing lives. However, unrestricted diets and activities
are not possible. Dietary treatment of diabetes using
medical nutrition therapy (MNT) and exercise constitutes
the basis for management of most patients, especially
those with the type 2 form of the disease. With ade
quate weight reduction, exercise, and dietary control,
patients may not require the use of exogenous insulin
or oral antidiabetic drug therapy. People with type 1
diabetes will always require exogenous insulin injec
tions and dietary control because the pancreas has
lost the capacity to produce and secrete insulin. The
aims of dietary control are the prevention of excessive
postprandial hyperglycemia, the prevention of hypo-
glycemia (blood glucose level less than 70 mg/dL) in
those patients being treated with antidiabetic agents or
insulin, the achievement and maintenance of an ideal
body weight, and a reduction of lipids and cholesterol.
A return to normal weight is often accompanied by a
reduction in hyperglycemia. The diet should also be
adjusted to reduce elevated cholesterol and triglycer
ide levels in an attempt to retard the progression of
atherosclerosis.
To help maintain adherence to dietary restrictions,
the diet should be planned using the MNT recommen
dations of the ADA in relation to the patient’s food
preferences, economic status, occupation, and physical
activity.
Patient education and reinforcement are extreme
ly important to successful therapy. The intelligence
and motivation of the patient with diabetes and their
awareness of potential complications contribute signif
icantly to the ultimate outcome of the disease and the
quality of life that the patient may lead.
All patients with diabetes must receive adequate
instruction on personal hygiene, especially regarding
care of the feet, skin, and teeth. Infection is a common
precipitating cause of ketoacidosis and must be treated
promptly.
Patients with diabetes must also be aggressively
managed for any comorbid diseases (smoking ces
sation [including ecigarettes], treatment of dyslip
idemia, blood pressure control, antiplatelet therapy,
inuenza and pneumococcal vaccinations) to help pre
vent microvascular and macrovascular complications.
The ADA and the American Association of Clinical
Endocrinologists (AACE) have developed programs
of intensive diabetes selfmanagement that applies to
type 1 and type 2 diabetes mellitus. These programs
include the concepts of care, the responsibilities of the
patient and the healthcare provider, and the appro
priate intervals for laboratory testing and followup.
Patient education, understanding, and direct partici
pation by the patient in their treatment are key com
ponents of longterm success in disease management.
Intensive therapy describes a comprehensive program
of diabetes care that includes patientcentered commu
nication, a team approach to care, selfmonitoring of
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35 565

such as walking. The 2020 ADA standards of care sug

Table 35.3 Treatmenta Goals for Diabetes and Comorbid gests that people be encouraged to limit the amount
Diseases
of time they spend being sedentary by breaking up
MONITORING ADA THERAPEUTIC
extended amounts of time spent sitting. Metformin
DISEASE PARAMETER GOALSB
therapy should be considered for treatment of predi
Diabetes Hemoglobin A1c <7%
abetes, especially in those patients whose body mass
Preprandial 80–130 mg/dL index (BMI) is greater than 35 kg/m2, in those who are
plasma glucose younger than 60 years, and in women with prior GDM.
Postprandial <180 mg/dL Patients should be monitored at least annually for the
plasma glucose development of diabetes mellitus.
Hypertension Blood pressure <140/90 mm Hg Other antidiabetic agents are used in the therapy of
Dyslipidemia LDL cholesterol See Chapter 21, type 2 diabetes. They are recommended only for those
Table 21.1 patients whose diabetes cannot be controlled by an
HDL cholesterol >40 mg/dL in males MNT diet and exercise alone and who are not at risk to
>50 mg/dL in females develop ketoacidosis or infections. Patients most likely
to benet from treatment are those who have devel
Triglycerides <150 mg/dL
oped diabetes after age 40 and who require less than
Weight Weight loss BMI <25 kg/m2 (see
40 units of insulin daily.
Chapter 20, Table
A combination of antidiabetic agents working by dif
20.2)
Asian Americans: ferent mechanisms is often required to control hyper
BMI <23 kg/m2 glycemia successfully (Fig. 35.2):
aRecommended
• Biguanide: The only biguanide available in the
by the American Diabetes Association (ADA).
bSee American Diabetes Association. Standards of medical care in United States is metformin. Unless contraindicated,
diabetes—2020. Diabetes Care 2020;43(Suppl. 1):S111–S134. it is the initial drug of choice for treatment of type
BMI, Body mass index; HDL, high-density lipoprotein; LDL, low-density
lipoprotein. 2 diabetes. Metformin decreases hepatic glucose
production by inhibiting glycogenolysis and gluco
neogenesis, reducing absorption of glucose from the
blood glucose four or more times daily, MNT, exercise, small intestine, and increasing insulin sensitivity,
and, for those patients with type 1 diabetes, three or which improves glucose uptake in peripheral mus
more insulin injections daily or use of an insulin pump cle and adipose cells. The net result is a signicant
for continuous insulin infusion. See Table 35.3 for the decrease in fasting and postprandial blood glucose
treatment goals recommended by the ADA. and hemoglobin A1c (A1c) concentrations.
• Secretagogues: The sulfonylureas (e.g., glyburide,
glipizide, glimepiride) and the meglitinides (repa
DRUG THERAPY FOR DIABETES
glinide, nateglinide) stimulate the pancreas to se
MELLITUS
crete more insulin. The sulfonylureas also diminish
“Hyperglycemia denes diabetes, and glycemic con hepatic glucose production and metabolism of insu
trol is fundamental to diabetes management” (ADA, lin by the liver. The net effect is a normalization of
2020, p. S69). The primary treatment goal of type 1 and insulin and glucose levels.
type 2 diabetes is normalization of blood glucose levels. • Thiazolidinediones (TZDs): The TZDs (e.g., piogli
Insulin is required to control type 1 diabetes and other tazone) increase tissue sensitivity to insulin, caus
types of diabetes in patients whose blood glucose can ing greater glucose uptake in muscle, adipose, and
not be controlled by an MNT diet, exercise, weight re liver tissue. They also diminish glucose production
duction, or other antidiabetic agents. Patients normally by the liver.
controlled with other antidiabetic agents require insulin • Alpha-glucosidase inhibitors: Acarbose and miglitol
during situations of increased physiologic and psycho inhibit enzymes in the small intestine that metab
logical stress, such as pregnancy, surgery, and infec olize complex carbohydrates. This slows the ab
tions. The dosage of insulin is usually adjusted accord sorption of carbohydrates, reducing postprandial
ing to the blood glucose levels. The patient should test hyperglycemia.
the blood glucose level before each meal and at bedtime • Sodium-glucose cotransporter 2 (SGLT2) inhibitors:
while the insulin and food intake are being regulated. These agents block the reabsorption of glucose by
The ADA now recommends that patients with pre the kidneys, causing the sugar to be excreted in the
diabetes be treated to prevent or delay the onset of urine, lowering blood glucose. The SGLT2 inhibi
type 2 diabetes. Patients should be referred to an ef tors are canagliozin, dapagliozin, empagliozin,
fective ongoing support program targeting weight loss and ertugliozin.
of 7% of body weight and increasing physical activity • Incretin-related therapy: It is thought that patients
to at least 150 minutes per week of moderate activity with type 2 diabetes have a suppressed incretin
566 UNIT VII Drugs That Affect the Endocrine System
Sulfonylureas
Biguanide
Incretin mimetic agents
• Decreases glucose Liver
glucose output
production
Thiazolidinediones
Peripheral
muscle
Small
Muscle glucose intestine
uptake
Fat cells Biguanide
Thiazolidinediones
• Increase insulin sensitivity,
improving glucose uptake
Fig. 35.2 Sites and mechanisms of action of antidiabetic agents.
hormone system. The incretin hormones act in the
gastrointestinal tract to control blood glucose levels
by enhancing insulin secretion, suppressing gluca
gon secretion from the liver, suppressing glucose
output from the liver, delaying gastric emptying
(thus slowing carbohydrate and lipid absorption),
reducing postprandial hyperglycemia, reducing ap
petite, and maintaining beta cell function. There are
currently two classes of agents that increase incre
tin activity: (1) incretin mimetics (the glucagonlike
peptide1 [GLP1] agonists dulaglutide, exenatide,
exenatide ER, liraglutide, lixisenatide, and sema
glutide) and (2) the dipeptidyl peptidase4 (DPP4)
inhibitors (alogliptin, sitagliptin, saxagliptin, and
linagliptin).
Initial antidiabetic therapy for type 2 diabetes is
highly dependent on the patient’s success with life
style modication and diet control. A consensus state
ment endorsed by the ADA recommends metformin
in combination with MNT and exercise as initial treat
ment of type 2 diabetes mellitus. If the goal A1c level
less than 7% has not been achieved with this mono
therapy within 3 to 6 months and the patient does
not have atherosclerotic cardiovascular disease, add
another agent such as a sulfonylurea, a TZD, an incre
tinrelated DPP4 inhibitor, or GLP1 agonist, or basal
insulin should be added based on the individual pa
tient. If the patient has atherosclerotic cardiovascular
Pancreas Sulfonylureas
Meglitinides
•↑Insulin secretion
Kidneys
SGLT2 Inhibitors
•↑Glucose excretion
Biguanide
Alpha-glucosidase inhibitors
Incretin-related agents
• GLP-1 agonists
• DPP-4 inhibitors
disease, add an agent proven to reduce cardiovascu
lar events and/or cardiovascular mortality, such as
canagliozin, empagliozin, liraglutide, and sema
glutide. Patients with heart failure or chronic kidney
disease add an agent proven to reduce the progres
sion of chronic kidney disease or heart failure, such
as canagliozin, dapagliozin, or empagliozin. If
the A1c level is not at goal, another member of a drug
class not already being used in the initial therapy
should be added. An alphaglucosidase inhibitor may
be added if postprandial hyperglycemia is a problem.
See Table 35.4 for a comparison of antidiabetic agents
and their effects on lowering blood glucose levels and
A1c concentrations.
NURSING IMPLICATIONS FOR PATIENTS WITH
DIABETES MELLITUS
A major challenge in nursing is to teach the recently
diagnosed patient with diabetes all the necessary in
formation to manage selfcare and the disease process
and to prevent complications. The patient must be
taught the entire therapeutic regimen—diet, activity
level, blood or urine testing, medication, selfinjection
techniques, prevention of complications, illness man
agement, and effective management of hypoglyce
mia or hyperglycemia. Patient education may begin
in the hospital and continue for several weeks in the
outpatient setting. Dietitians, nurses, diabetic nurse
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35 567

Table 35.4 Summary of Physiologic Effects of Antidiabetic Agents

DECREASE IN FASTING REDUCTION IN
DRUG INSULIN SECRETION BLOOD GLUCOSE LEVEL HEMOGLOBIN A1C LEVEL WEIGHT GAIN
Insulin Decrease Signicant Signicant Yes
Sulfonylureas Increase 40–60 mg/dL 1%–2% Yes
Meglitinides Increase 30 mg/dL 1.1% Yes
Biguanide (metformin) No change 53 mg/dL 1%–2% No; mild
Thiazolidinediones No change 25–55 mg/dL 0.5%–1.4% Yes
Alpha-glucosidase inhibitors No change 20–30 mg/dL 0.5%–0.8% No
Glucagon-like peptide-1 agonists Increase — 1.0%–1.5% No
Dipeptidyl peptidase-4 inhibitors Increase — 0.5%–0.8% No
Sodium-glucose cotransporter 2 inhibitors Decrease — 0.7%–1% No
Data from Feld S. The American Association of Clinical Endocrinologists medical guidelines for the management of diabetes mellitus: the ACCE system of intensive
diabetes self-management—2002 update. Endocr Pract. 2002;8(suppl 1):S52; Nathan DM, Buse JB, Davidson MB, et al. Medical management of hyperglycemia
in type 2 diabetes mellitus: a consensus algorithm for the initiation and adjustment of therapy. Diabetolgia. 2009;52:17-30; Clinical Resource, Comparison of GLP-1
Agonists. Pharmacist’s Letter/Prescriber’s Letter. January 2017; Clinical Resource, Drugs for Type 2 DM. Pharmacist’s Letter/Prescriber’s Letter. July 2017; U.S.
Department of Health and Human Services and U.S. Department of Agriculture. 2015-2020 Dietary Guidelines for Americans. 8th ed. December 2015 Available at: http
s://health.gov/dietaryguidelines/2015/guidelines/.

educators, and pharmacists are all actively involved
in educating the patient and family. A referral to the
ADA serves as an excellent resource in the community
for the patient and family. Many patients with diabetes
have difculty understanding the critical balance that
must be maintained among the dietary prescription,
prescribed medication, and maintenance of general
health. All are important to the control and effective
management of the disease process.
Assessment and Implementation
Description of current symptoms
• Ask the reasons for seeking the current appoint
ment or admission.
Patient’s understanding of diabetes mellitus
• Assess the individual’s current knowledge of the
treatment of diabetes mellitus. Gather additional
data about the person’s current educational needs
with regard to selfmanagement of the disease pro
cess. Answer questions that the patient has, includ
ing rationale for actions being recommended.
• Will other family members or signicant others be
providing part of the care or participating in the
health education portion of the individual’s care?
• Patients who are readmitted must be assessed for
the understanding of the treatment regimen and for
adherence with the prescribed diet, medications,
and exercise.
• For pregnant women, risk assessment for GDM
should be performed at the rst prenatal visit. High
risk women who have an initial negative testing
for diabetes should be retested between 24 and 28
weeks of gestation.
Psychosocial assessment
• Mental status: Ask specic information to evalu
ate the patient’s current level of consciousness,
alertness, comprehension, and appropriateness of
responses. Evaluate the person’s judgment capabili
ties and ability to solve problems about the manage
ment of the diabetes.
• Adaptation to disease: Ask specically about the per
son’s adjustment to the diagnosis of diabetes mel
litus; in a recently diagnosed individual, identify
prior coping mechanisms used successfully to deal
with life events.
• Feelings: Assess for fears and the person’s perspective
of the impact of the disease on their life. Encourage
expression of the patient’s feelings and concerns;
address the patient’s concerns rst. Involve support
personnel, as appropriate, in the delivery of care or
planning for home management of the diabetes.
• Support system: Obtain information regarding who
can provide support for the patient. Does the indi
vidual live alone? What effect does the disease have
on other members of the family structure (e.g., chil
dren who are diabetic, people with renal or visual
complications)? Does the patient participate in a
support group for patients with diabetes?
Nutrition
• Is the patient on a prescribed MNT diet? The recent
ly diagnosed patient with diabetes requires a thor
ough nutritional assessment. Information collected
by the nurse or dietitian should include identica
tion of the patient’s average daily diet, the ability
and willingness to prepare foods, food budget, and
level of daily activity and exercise.
• Ask about diet prescription—total daily calories
and distribution pattern of carbohydrates, fats, and
proteins.
• Have there been any problems encountered in pur
chasing or preparing foods? Has it been difcult to
comply with the diet? If so, what are the problems
encountered?
568 UNIT VII Drugs That Affect the Endocrine System
• How much alcohol is consumed and how often?
• Has the individual experienced any weight loss or
gain recently?
• If the patient is a child, obtain data relating to the
individual’s growth and development patterns.
Activity and exercise
• Does the individual experience weakness or fatigue
with daily activities? Does the patient get regular
exercise? What type, intensity, and duration is the
exercise? Has there been any signicant variation in
the degree of exercise recently?
• Has the patient made any adjustments in the insu
lin, oral antidiabetic agents, or diet to offset an in
crease or decrease in exercise?
• Has there been a change in occupation that has af
fected the level of exercise?
Medications
• What medications have been prescribed, and
what is the degree of adherence with the regimen?
Monitor for common and serious adverse effects
and document associated monitoring parameters in
the medical records (e.g., blood glucose, ketone test
ing). If the patient is taking insulin, ask specically
about the type and dose being taken and the times
of administration. Assess the ability and accuracy to
selfadminister injections. If a family member gives
the insulin, assess their ability and accuracy in giv
ing injections.
• What overthecounter medications (including
herbal medicines) does the patient take and how
often?
Monitoring. Ask the patient to bring a record of self
monitoring of insulin or antidiabetic agents taken,
as well as any blood glucose testing or A1c testing
that was done. Has the patient done any testing for
ketones? If so, what were the results? Other tests to
be performed periodically include the fasting lipid
profile, which includes measurement of lipid levels
(highdensity lipoprotein [HDL], lowdensity lipo
protein [LDL] cholesterol, triglycerides), as well
as serum creatinine and microalbuminuria. When
hypertension is present, perform a urinalysis and
check for albuminuria. If protein is negative, micro
albumin testing should be performed to deter
mine the presence of protein in the urine. Annual
monitoring of LDL, triglyceride, and A1c levels is
recommended.
Physical Assessment
Generally, data are collected about all body systems
to serve as a baseline for subsequent evaluations
throughout the course of treatment. Periodic focused
assessments are completed to detect signs and symp
toms of complications commonly associated with dia
betes mellitus.
• Hypoglycemia: Have there been any episodes of hy
poglycemia? If so, obtain details of the occurrences
(e.g., has the patient eaten the prescribed diet, taken
the prescribed medications, or altered the exercise
level?). If a hypoglycemic reaction occurs, notify the
team leader or primary nurse, who will then contact
the healthcare provider. The underlying cause of the
hypoglycemia must be identied to prevent further
occurrences. If in doubt about whether a hypoglyce
mic reaction is taking place, treat as though a hypo
glycemic reaction is occurring to prevent neurologic
damage from prolonged reduction in glucose to the
nerve cells (e.g., brain cells). Record all prescription
and overthecounter medications being taken to as
sess whether any drug interactions may be causing
the hypoglycemia.
• Hyperglycemia: With any hyperglycemic reaction,
notify the team leader or primary nurse, who will
then contact the healthcare provider. The goals of
treatment include maintaining normal uid and
electrolyte balance and restoring a normal serum
glucose level.
• Illnesses, stress: Have there been any recent illnesses,
infections, or stressful events? If so, what treatments
have been initiated? Ask specically about any
sores on the skin and feet, periodontal disease, and
occurrence of urinary tract or vaginal (candidiasis)
infections.
• Vascular changes: Obtain baseline vital signs. Does
the person have any symptoms of, or is the patient
being treated for, cerebrovascular, peripheral vas
cular, or cardiovascular disease (including hyper
tension) or diabetic retinopathy or nephropathy?
Obtain a current history of the patient’s blood pres
sure and details of any medications being taken to
treat hypertension.
• Neuropathy: Ask about specic symptoms of pares
thesias (numbness or tingling sensations), foot in
juries and ulcerations, diarrhea, postural hypoten
sion, impotence, or neurogenic bladder.
• Smoking: Obtain a history of smoking and tobacco
use from all patients with diabetes mellitus.
Patient Education
The ADA has developed areas of diabetic education.
Not all aspects of the care outlined in these recommen
dations are presented in the sample teaching plan for
a patient with diabetes mellitus taking one type of in
sulin (see Chapter 5, Box 5.2: “Sample Teaching Plan
for a Patient With Diabetes Mellitus Taking One Type
of Insulin”). The recommendations must be adapted to
the individual’s needs. It may not be possible to teach
the entire program during the hospitalization period.
Teach the individual specics regarding the type of
diabetes that has been diagnosed.
• Type 1 diabetes mellitus results from damage to
the beta cells of the pancreas, where insulin is nor
mally produced. Insulin is needed to transport the
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
glucose required by the body cells from the blood
stream to the individual cells to be used as an en
ergy source. Without beta cells, no insulin is pro
duced and the glucose accumulates in the blood
(hyperglycemia).
• Type 1 diabetes mellitus requires the administration
of insulin injections to replace the insulin that the
body is no longer able to make. The patient must
follow a prescribed diet and exercise program, per
form glucose testing, and, when hyperglycemia is
present, test for ketones in the urine.
• Type 2 diabetes mellitus is an illness characterized
by abnormal beta cell function, resistance to insulin
action, and increased hepatic glucose production.
Type 2 diabetes mellitus requires a prescribed diet
and exercise program, weight loss to a nearideal
body level, glucose testing, and an oral antidiabetic
agent or antihyperglycemic agent if the diabetes
cannot be managed with diet and exercise alone.
During times of illness, or if the oral treatment stops
being effective, insulin may be required. Special
adjustments may be required for patients who are
pregnant or nursing.
Psychological adjustment
• When rst diagnosed, the patient may experience
varying degrees of grief, anger, denial, or accep
tance. Let the patient express these concerns, and
address those items that are considered to be of
greatest importance rst.
• Encourage the idea that the patient can control most
aspects of diabetes by careful management of diet,
medications, and activities. Having a sense of control
is important to everyone. Stress that learning to man
age the disease process is the best longterm approach.
• Discuss the individual’s lifestyle, travel, work or
school schedules, and activities and individualize
the care needs.
• Discuss the need for continued regular monitoring
of the diabetes to minimize the effect that the dis
ease may have on the patient and family.
Smoking. Healthcare providers should emphasize the
need for smoking (including ecigarettes) cessation as
a priority of care for all patients with diabetes.
Nutrition
• Diet is used alone or in combination with insulin or
oral antidiabetic agents to control diabetes mellitus.
The patient with diabetes, whether type 1 or 2, must
follow a prescribed diet to achieve optimal control
of the disease.
• The dietary prescription is based on the nutritional
and energy requirements necessary to maintain an
appropriate weight and lifestyle and normal growth
and development. Patients with diabetes are en
couraged to maintain a reasonable body weight
based on height, gender, and frame size.
569
• MNT is now being recommended for patients with
diabetes. Standardized calorielevel meal patterns
based on exchange lists have traditionally been
used to plan meals for hospitalized patients. Other
meal planning systems include menus based on
the 2020–2025 Dietary Guidelines for Americans (U.S.
Department of Health and Human Services and
U.S. Department of Agriculture, 2020), regular hos
pital menus, individualized meal plans, or menus
using carbohydrate counting. A new system, called
the consistent-carbohydrate diabetes meal plan, is being
developed that uses meal plans without a specic
calorie level; instead, it incorporates a consistent
carbohydrate content for each meal and snack. The
meal plan also includes appropriate fat and protein
modications and emphasizes consistent timing of
meals and snacks. A typical day’s meals and snacks
provide 1500 to 2000 calories with 45% to 65% of the
calories from carbohydrate, 10% to 35% from pro
tein, and 20% to 35% from fat. If a patient’s nutri
tional needs are more or less than provided by these
meal plans, individualized adjustments may be re
quired. Patients who often require adjustments in
clude children, adolescents, metabolically stressed
patients, pregnant women, and older adult patients.
• Weight loss is recommended for all adults who are
overweight (BMI = 25 to 29.9 kg/m2) or obese (BMI
≥30 kg/m2) or who have or are at risk for developing
type 2 diabetes. The primary approach for achieving
weight loss is therapeutic lifestyle change, which in
cludes a reduction in energy (food) intake and/or
an increase in physical activity. A moderate decrease
in caloric balance (500 to 1000 kcal/day) will result
in slow but progressive weight loss (1 to 2 lb/wk).
For most patients, weight loss diets should supply
at least 1000 to 1200 kcal/day for women and 1200
to 1600 kcal/day for men.
• Additional goals for MNT include maintaining a
blood glucose level in the normal range to reduce
the risk of complications of diabetes, a normal lipid
prole to reduce the risk for microvascular disease,
and normal blood pressure levels to reduce the risk
for vascular disease.
• The ADA no longer endorses any single meal plan
or specied percentages of macronutrients as it has
in the past. The Institute of Medicine and the ADA
recommend, in general, that the diet be composed
of 45% to 65% carbohydrates, 15% to 20% protein
(0.8 to 1 g protein/kg of body weight), and no more
than 30% fat. Monounsaturated and polyunsaturat
ed fats should be the primary fat sources; saturated
fats should be limited to no more than 10% of the
diet and cholesterol intake to 300 mg or less daily.
Transfatty acids should be avoided when possible.
Highber foods in the diet (e.g., legumes, oats, bar
ley) are encouraged as they assist in lowering both
blood glucose and blood cholesterol levels. Reduced
sodium, alcohol, and caffeine consumption is also
570 UNIT VII Drugs That Affect the Endocrine System
advisable (see also Chapter 46). The ADA has sever
al cookbooks and pamphlets on nutrition available
for the person with diabetes.
• Patients with diabetes, as well as all individuals,
need to be encouraged to consume an adequate
intake of vitamins and minerals from natural food
sources.
• Inclusion of sucrose is now permitted in limited
amounts in the diabetic diet; however, the amount
eaten must be calculated as part of the carbohydrate
intake for the day. Meal plans such as “no concen
trated sweets,” “no added sugar,” “low sugar,” and
“liberal diabetic diets” are no longer appropriate.
These diets do not reect the diabetes nutrition rec
ommendations and unnecessarily restrict sucrose.
Such meal plans may perpetuate the false notion
that simply restricting sucrosesweetened foods will
improve blood glucose control.
• The US Food and Drug Administration has ap
proved the use of four articial sweeteners as sugar
substitutes: saccharin, aspartame (NutraSweet), su
cralose (Splenda), and acesulfame potassium.
• Patients with diabetes should adhere to the
same guidelines for ingestion of alcohol as for all
Americans—no more than two drinks daily for
men and one drink daily for women. People with
good control of their diabetes may ingest alcohol in
moderation; however, drinking alcohol can result
in hypoglycemia or hyperglycemia in patients with
diabetes. The effects of alcohol are inuenced by the
amount ingested, if ingested on an empty stomach,
or if used chronically or excessively. Many alcoholic
beverages are high in sugar and should be used with
caution; light beer or dry wines are alternatives. One
drink is dened as 12 ounces of beer, 5 ounces of
wine, or 1.5 ounces of distilled spirits, each of which
contains 15 g of alcohol. Because alcohol affects the
blood sugar, it may be prudent to test the blood glu
cose level before and after drinking to identify how
the alcohol reacts in a particular patient. Abstinence
is recommended for pregnant patients, those with
known medical problems aggravated by its use, and
those with a history of alcohol abuse.
• Dietary considerations for children and adolescents
with type 1 or 2 diabetes are similar to the needs for
all other children. They need to maintain a steady
intake of a balanced diet aimed at maintaining nor
mal growth and development. It is important to
obtain height and weight values and to compare
these to the normal growth curve found on charts
to ascertain whether the dietary intake is adequate,
decient, or excessive. The individual’s meal plan
ning must be done in such a way as to accommodate
irregular meal times and schedules and the varying
activity levels of the child or adolescent.
• All women have similar nutritional needs during
pregnancy and lactation whether they have diabetes
or not. A woman with GDM is given education on
food choices that are appropriate for normal weight
gain, normoglycemia, and absence of ketones. Some
patients with GDM may require a modest restriction
in carbohydrates.
• In older adults, a change in body weight of more
than 10 pounds or 10% of the body weight in less
than 6 months is considered sufcient reason to
investigate for nutritionrelated causes. In gen
eral, older people with diabetes in longterm care
settings tend to be underweight rather than over
weight. Administering a daily vitamin supplement
to older adults, especially those with decreased en
ergy intake, may be advisable. Specialized diets do
not appear to be benecial to the older adult in a
longterm care setting, where food choices are de
cidedly limited. It is preferable to make medication
adjustments to control blood glucose rather than
implement food restrictions in the longterm care
setting. Physical activity should be encouraged.
Activity and exercise
• Maintenance of a normal lifestyle is to be encour
aged. This includes exercise and activities enjoyed
by the individual. The normal daily energy level is
used in determining the dietary and medication re
quirements for the patient. The ADA recommends
that initial therapy be modest and based on the pa
tient’s willingness and ability, gradually increasing
the duration and frequency to 30 to 45 minutes of
moderate aerobic activity 3 to 5 days per week (150
minutes per week) when possible. Greater activity
levels of at least 1 hour daily of moderate (walk
ing) or 30 minutes daily of vigorous (jogging) activ
ity may be needed to achieve successful longterm
weight loss.
• As with all individuals who are about to undertake
exercise, a proper period of warmup and cool
down consisting of 5 to 10 minutes of aerobic ac
tivity at a low intensity should be done. It is very
important to maintain proper foot care in a patient
with diabetes who is to start exercising. Use silica
gel or air insoles, as well as polyestercotton blend
socks to prevent blisters, and keep the feet as dry as
possible. Visible inspection of the feet surfaces be
fore and after exercise is an important component
of an exercise regimen and is especially important
for patients with diabetes who already have pe
ripheral neuropathy. Persons with loss of protective
sensation should not use step exercises, jogging,
prolonged walking, or treadmills as an exercise
regimen. Rather, they should substitute swimming,
bicycling, rowing, chair exercises, arm exercises, or
other non–weightbearing exercises.
• Just as it is important for the patient to maintain
a certain diet, it is equally important to maintain
a certain activity level. Patients who suddenly in
crease or decrease their activity level are suscep
tible to developing episodes of hyperglycemia or
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
hypoglycemia. Both dietary and medication pre
scriptions may require adjustment if patients do not
plan to resume the previous exercise level. Patients
should consult with the prescriber before initiating
an exercise program.
• Additional selfmonitoring of the blood glucose
level may be advisable before, during, and approxi
mately 30 minutes after exercise to provide the pre
scriber with data to analyze regarding the effects of
exercise on the individual’s blood glucose level. The
ADA recommends that the patient with diabetes not
exercise if their glucose level is above 250 mg/dL.
Conversely, exercising with hypoglycemia is not ad
visable. A snack high in carbohydrates (10 to 20 g)
should be taken before exercising if the blood glu
cose level is less than 100 mg/dL.
• Exercise helps the cells use glucose; therefore exer
cise lowers the glucose level.
• Drink sufcient uids without caffeine when exer
cising to prevent dehydration.
• Stop exercising if feeling weak, sick, or dizzy or if
experiencing any type of pain.
Medication
• Insulin or oral antidiabetic agent therapy may be
required to control diabetes mellitus. No chang
es in therapy should be made without medical
supervision.
• A variety of combinations of insulin or insulin and
oral antidiabetic agents may be used to provide con
trol of the blood glucose level. The goal of therapy
is to consistently maintain the blood glucose level
within normal range. Administration schedules
have evolved over the years to accomplish this goal.
The schedules commonly used are as follows:
1. Divided doses of intermediateacting insulin
(twothirds in the morning, onethird in the eve
ning before dinner)
2. A combination of rapid or shortacting and
intermediateacting insulin in the morning,
followed by rapid or shortacting insulin at
dinner and intermediateacting insulin before
bedtime
3. Rapid or shortacting insulin before each meal
and intermediateacting or longacting insulin at
bedtime
4. Rapidacting or shortacting and longacting
insulin before breakfast, rapidacting or short
acting insulin before lunch, and rapidacting or
shortacting and longacting insulin again before
dinner
5. Continuous infusion of rapid or shortacting
insulin using a small, portable insulin infusion
pump
• The regimen chosen depends on each person’s re
sponse to medications, schedule of daily activities,
and compliance with blood glucose monitoring, in
sulin injections, and diet.
571
• Medication preparation, dosage, frequency, storage,
and relling should be discussed and taught in de
tail. See Fig. 10.3 for administration of subcutane
ous injections and Fig. 9.26 for mixing of insulins.
Also, discuss proper disposal of used syringes and
needles in the home setting.
• Be certain that the patient understands how to
rell prescriptions for insulin or oral antidiabetic
agents. When purchasing insulin, ask the patient
to doublecheck the type, concentration (usually
U100), and expiration date. Insulin types should
not be changed without the approval of the pre
scribing healthcare provider. The insulin should
be stored in the refrigerator (not the freezer) be
fore use. Once it is opened and being used, it can
be stored at room temperature for up to 1 month.
The patient or nurse should mark the date on the
bottle when rst opened and used. The patient
should always have a spare bottle of each type of
prescribed insulin available for use.
• When a patient is experiencing an acute illness, in
jury, or surgery, hyperglycemia may result. When
ill, the patient should continue with the regular diet
plan and increase noncaloric uids such as broth,
water, and other decaffeinated drinks. The patient
should continue to take the oral agents and/or insu
lin as prescribed and monitor the blood glucose lev
el at least every 4 hours. If the glucose level is higher
than 240 mg/dL, urine should be tested for ketones
(see Urine Testing for Ketones later in this section).
If the patient is unable to eat the normal caloric in
take, they should continue to take the same dose of
oral agents and/or insulin prescribed, but supple
ment food intake with carbohydratecontaining u
ids such as soups, regular juices, and decaffeinated
soft drinks. The healthcare provider should be noti
ed immediately if the patient is unable to “keep
anything down.” Patients should understand that
medication for diabetes, including insulin, should
not be withheld during times of illness because
counterregulatory mechanisms in the body often
increase the blood glucose level dramatically. Food
intake is also necessary because the body requires
extra energy to deal with the stress of illness. Extra
insulin may also be necessary to meet the demand
of illness.
• If pregnancy is suspected, the patient should con
sult an obstetrician as soon as possible about con
tinuing and adjusting medication therapy during
pregnancy.
• Patients with diabetes should receive an annual in
uenza vaccination and at least one pneumococcal
vaccination before age 65. The pneumococcal vac
cination should be repeated at least 5 years later and
after the patient turns 65.
Hypoglycemia. Hypoglycemia, or low blood sugar,
can occur from too much insulin, a sulfonylurea,
572 UNIT VII Drugs That Affect the Endocrine System
insufcient food intake to cover the insulin given,
imbalances caused by vomiting and diarrhea, and
excessive exercise without additional carbohydrate
intake.
Symptoms. Recognize and assess early symptoms of
hypoglycemia; these include:
Adrenergic symptoms
 • Hunger, trembling, pallor, sweating, shaking,
tachycardia, anxiety
Neurologic symptoms
 • Dizziness, poor concentration, drowsiness,
weakness, confusion, lightheadedness, slurred
speech, blurred vision, double vision, unsteadi
ness, poor coordination
Behavioral symptoms
• Tearfulness, confusion, fatigue, irritability,
aggressiveness
If uncorrected, hypoglycemia progresses to blur
ring of vision, lack of coordination, incoherence, coma,
and death. Children younger than 6 to 7 years may not
have the cognitive abilities to recognize and initiate
selftreatment of hypoglycemia.
Treatment. If the patient is conscious and able to
swallow, give 2 to 4 ounces of fruit juice, 1 cup of
skim milk, or 4 ounces of a nondiet soft drink, or give
a piece of candy such as a gumdrop. An alternative is
to carry a glucosecontaining product (e.g., Glutose
gel, Dex4 glucose tablets) and take as recommended
when hypoglycemic. Repeat in 10 to 15 minutes if
relief of symptoms is not evident. Do not use hard
candy if there is a danger of aspiration. If the patient
is unconscious, having a seizure, or unable to swal
low, administer glucagon (administered via subcu
taneous injection or nasal powder) or 20 to 50 mL
of glucose 50% intravenously. (Patients taking insu
lin should have a family member, signicant other,
or coworker who is able to administer glucagon.)
Obtain a blood glucose level at the time of hypo
glycemia, if possible.
Hyperglycemia. Hyperglycemia (elevated blood
sugar) occurs when the glucose available in the
body cannot be transported into the cells for use
because of a lack of insulin necessary for the trans
port mechanism. Hyperglycemia can be caused by
nonadherence, overeating, acute illness, or acute
infection.
Symptoms. Symptoms of hyperglycemia associated
with diabetic ketoacidosis (DKA) are headache, nausea
and vomiting, abdominal pain, dizziness, rapid pulse
(tachycardia), rapid shallow respirations, and a fruity
odor to the breath from acetone. As acidosis becomes
more severe, respirations become slower, deeper and
labored. If untreated, hyperglycemia may also cause
coma and death. Glucose levels higher than 240 mg/
dL and ketones present in the urine are early indica
tions of DKA. Signs of dehydration include a weak
and rapid pulse, dry tongue and tenting skin, as well
as hypotension.
Treatment. Treatment of hyperglycemia often re
quires hospitalization with close monitoring of hydra
tion status; administration of intravenous (IV) uids
and insulin; and blood glucose, urine ketone, and po
tassium levels. Hyperglycemia usually occurs because
of another cause; therefore the problem, often an infec
tion, must also be identied and treated.
Prevention. The risk of hyperglycemia can be mini
mized by taking the prescribed dose of insulin or oral
antidiabetic agent; adhering to the prescribed diet
and exercise; reporting fevers, infection, or prolonged
vomiting or diarrhea to the healthcare provider; and
maintaining an accurate written record for the health
care provider to analyze to determine the individual
patient’s needs. Selfmonitoring of blood glucose re
sults and evaluation of urine ketones can provide the
prescriber with valuable information to manage the
treatment of the individual effectively.
Self-monitoring of blood glucose
• Home blood glucose monitoring (selfmonitoring)
is an accepted practice for managing diabetes melli
tus. It is used to evaluate the degree of control of the
blood glucose. It can also be used to evaluate when
additional insulin must be taken or to determine the
effect of exercise on insulin needs.
• Educate the individual using the equipment for
selfmonitoring that will be used at home. Teach the
person all details of the operation, including cali
bration, care, handling, and cleansing of the glucose
monitor.
• The best time to check blood glucose levels is just
before meals, 1 to 2 hours after meals, and before
bed. The prescriber will give specic instructions re
garding how often and when glucose testing should
be done. When the patient is ill, it is important to
increase the frequency of glucose monitoring.
• A small sample of capillary blood is obtained, gen
erally using an automatic ngersticking lancet. The
blood sample is applied to a reagent strip, which
is then placed into an electronic device that reads
the amount of color change and converts this into
a numerical value representing the blood glucose
level. There also are meters and sensors that do not
use reagent strips for delivering the glucose results.
“Talking” glucometers are on the market for those
who are visually impaired. Written records of the
blood glucose results should be maintained and
taken to all followup visits with the healthcare pro
vider for analysis.
Urine testing for ketones
• Teach the patient to perform urine testing for
ketones at least four times daily during times
of stress, with an infection, or when signs or
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
symptoms of hyperglycemia are suspected or
present. (Ketone testing should be done when the
blood glucose level is consistently higher than
300 mg/dL, during pregnancy, or when symp
toms of ketoacidosis, such as nausea, vomiting, or
abdominal pain, are present.) The healthcare pro
vider may suggest additional times when ketones
should be monitored, depending on the type of
regimen prescribed for controlling blood glucose.
An accurate written record of the results should
be maintained. Guidelines for reporting abnormal
results to the prescriber should be discussed at the
time of discharge. First morning urine tests from
pregnant women and up to 30% of rst morning
specimens in individuals who are fasting may
have positive readings. Several drugs also may
interfere with the results of ketone urine testing,
giving falsepositive values. Blood ketone testing
methods that quantify beta-hydroxybutyric acid
are available for home testing and are preferred
over urine ketone testing for monitoring and di
agnosing ketoacidosis.
• Suggest that ketone testing be initiated when an ill
ness occurs and the serum glucose is elevated above
the individual’s usual range. Explain when to call
the healthcare provider. Suggest increasing uid in
take whenever ketones are positive.
Other laboratory glucose testing
• The A1c test measures the percentage of hemoglobin
that has been irreversibly glycosylated because of
high blood glucose levels. This provides a reection
of the average blood glucose level attained over the
past 2 to 3 months. This test is used in conjunction
with home glucose selfmonitoring to assess overall
glycemic control.
• The fructosamine test measures the amount of glu
cose bonded to the protein fructosamine. This re
ects the average blood level attained over the past
1 to 3 weeks.
Complications associated with diabetes mellitus
Cardiovascular disease. Men and women with dia
betes are at an increased risk of dying from complica
tions of cardiovascular disease. Aspirin therapy may
be considered for primary prevention strategy for both
diabetic men and women with type 1 or type 2 dia
betes who have a 10year cardiovascular risk greater
than 10%. The benet versus the risk of gastrointes
tinal bleeding from aspirin should be discussed with
the patient. This includes most men older than age
50 years or women older than 60 years who have at
least one additional major risk factor (family history
of cardiovascular disease, hypertension, smoking,
dyslipidemia, or albuminuria). Entericcoated aspirin
in doses of 75 to 162 mg daily is taken by individuals
who do not have an aspirin sensitivity. Aspirin therapy
573
is no longer recommended for those who do not meet
the criteria.
Peripheral vascular disease. The patient with diabetes
mellitus is more likely to suffer from peripheral vas
cular disease than the general population. Reduced
blood supply to the extremities may result in inter
mittent claudication, numbness and tingling, and a
greater likelihood of foot infection. The following are
symptoms the patient should look for in caring for the
extremities:
• Color: Observe the color of each hand, nger, leg,
and foot; report cyanosis or reddishblue discolor
ations. Inspect the skin of the extremities for any
signs of ulceration.
• Temperature: Feel the temperature in each hand, n
ger, leg, and foot. Report paleness and coldness.
Note that these symptoms will be increased if the
limbs are elevated above the level of the heart.
• Edema: Report edema, its extent, and whether
relieved or unchanged when in a dependent
position.
• Limb pain: Pain with exercise that is relieved by rest
may be from claudication and should be reported to
the healthcare provider.
• Care of the extremities: Prevent ulcers, injury, and
infection in the lower extremities with meticulous
regular care. Use lotion to prevent dryness. Inspect
the feet daily for any signs of skin breakdown or
loss of sensation; report to the healthcare provider
and do not attempt to selftreat. The presence of
redness, warmth, or calluses may signal an impend
ing breakdown. Always cut toenails straight across
and seek foot care from a podiatrist if problems are
noted.
Visual alterations. Visual changes are common in the
patient with diabetes mellitus. These patients often
suffer from blurred vision associated with an elevated
blood glucose level. Any person with diabetes per
son with intermittently blurred vision should contact
the healthcare provider for a check of the blood glu
cose level. Once the hyperglycemia is controlled, the
blurred vision usually resolves.
Blindness. In advanced stages of diabetes mellitus,
the patient may suffer from changes (microangiopa
thies) in the small blood vessels of the eyes. Retinal
hemorrhages, degeneration of retinal vascular tis
sue, cataracts, and eventual blindness may occur. The
patient with diabetes should have regular eye ex
aminations to allow early treatment of any apparent
alterations.
Renal disease. People with diabetes mellitus are
more susceptible to urinary tract infections; therefore
symptoms such as burning on urination or low back
pain should be evaluated promptly. Patients are also
more susceptible to renal disease. Routine periodic
monitoring of protein in the urine determines the
presence of renal disease. In patients with type 1 or 2
574 UNIT VII Drugs That Affect the Endocrine System
diabetes who have microalbuminuria, even a small re
duction in protein intake has been shown to improve
the glomerular ltration rate and reduce urinary albu
min excretion rates.
Infection. Any type of infection can cause a signi
cant loss of control of diabetes mellitus. Patients should
check themselves carefully for any signs of redness,
tenderness, swelling, or drainage that may occur when
there is any break in the skin. Patients should be taught
to report immediately early signs of infection, such as
fever or sore throat. During an infection the dosage of
insulin may require an adjustment to compensate for
a change in metabolic rate, diet, and exercise. Contact
the healthcare provider for specic directions.
Neuropathies. Explain to appropriate individuals
the complication of degeneration of nerves when it
exists. Ask the patient to describe sensations (e.g.,
numbness, tingling) in the extremities. Inspect the
feet for blisters, ulcerations, ingrown toenails, or
sores. Occasionally, the patient will not be aware of
these lesions because of the degeneration of nerves
in the area. When numbness and lack of sensation are
present, always test the water temperature before im
mersing a limb. Because of impaired sensation, it is
easy to burn the skin, and the patient may be unaware
of the burn until later.
Impotence. Impotence may occur from a number of
causes and should be discussed on an individual basis
with the healthcare provider.
Hypertension. All patients with diabetes should have
a blood pressure measurement, including orthostatic
measurements, completed on every routine ofce visit.
The ADA (2020) recommends that patients with diabe
tes and hypertension who are at lower risk for cardio
vascular disease should be treated to a blood pressure
goal of less than 140/90 mm Hg. A lower blood pres
sure goal of less than 130/80 mm Hg may be appropri
ate in individuals at high risk of cardiovascular disease
if it can be achieved without adverse effects.
Fostering health maintenance
• Throughout the course of treatment, discuss medi
cation, diet, exercise, and the need to achieve and
maintain good glucose control to prevent the com
plications associated with diabetes mellitus. The pa
tient must achieve a high degree of understanding
of diabetes mellitus and its management. The pa
tient and family members must be included in the
entire educational program.
• With shorter hospitalizations, it may be necessary to
incorporate followup care by a health professional
from a visiting nurse association or a home health
agency in the discharge planning.
• Seek cooperation and understanding of the fol
lowing points so that medication compliance is
increased: name of medication; dosage, route, and
time of administration; and common and serious
adverse effects.
At discharge. Develop a list of specic equipment and
supplies that the patient will need when discharged.
Keep in mind the cost of these supplies. Consider the
following:
1. Syringes: Disposable syringes are convenient and
presterilized but are more expensive. Be sure to tell
the patient that disposable syringes are designed
to be used once and then discarded; however, the
literature refers to the repeated use of the same sy
ringe by an individual patient as long as the needle
remains sharp and is kept clean and covered. Check
with the individual prescriber before instituting this
practice. People with diabetes are susceptible to in
fection and healing may be a problem. The newer,
smaller 30 and 31gauge needles can become bent
with even one use, forming a hook at the end of the
needle. If the needle is reused, the hook may result
in a laceration to the tissue and lead to adverse ef
fects. Syringes being reused should be stored at
room temperature. The potential benets of storing
a syringe and needle for reuse in the refrigerator
or of wiping the needle with alcohol are unknown.
Cleansing the needle with alcohol may disrupt the
silicone coating on the needle, resulting in increased
pain at the injection site. Syringes are available in
0.3, 0.5, 1, and 2mL capacities. In some cases, the
insulin pen may also be prescribed for use by ap
propriate individuals. Several medical devices have
been developed to reduce the incidence of needle
sticks and other sharps injuries. When performing
patient education on the selfadministration of in
sulin, it is important to use the type of syringe and
needle device that will be used at home to ensure
that the patient knows how to manipulate the de
vice correctly. Insulin can also be administered us
ing a jet injector for those with a phobia of needles
or unable to use a syringe. They are not a routine
option for use in all patients with diabetes.
2. Insulin pumps: An insulin pump uses regular insulin
or the rapidacting insulin analogs such as lispro,
aspart, or glulisine. The use of mixtures of insulins
in insulin pumps is not recommended because this
approach has not been evaluated.
3. Needles: Disposable needles are more convenient
but also more expensive. Patients usually use a 27,
28, 29, 30, or 31gauge 1/2 ‐or ⅝inch needle, but
needles should be adjusted to the individual. An
obese patient may require a 1 to 1½inchlong nee
dle to inject the insulin properly. Several lengths of
needles are available, and blood glucose should be
monitored when changing from one needle length
to another. Always dispose of insulin syringes, nee
dles, and lancets in sharps containers. (See Chapter
9 for further discussion of syringes, needles, and
safety during use.)
4. Specialized equipment: BD MagniGuides (Becton,
Dickinson and Company, Franklin Lakes, NJ) are
available for the visually impaired patient. This
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
device holds the vial of insulin, acts as a guide in
withdrawing insulin, and has a magnifying glass to
make reading the syringe scale easier. Insulin pens
are available for blind or neurologically impaired
patients. A talking glucosemeasuring device is also
available for the visually impaired individual to per
form selfmonitoring of capillary blood glucose lev
els. Persons with diabetes desiring more information
on insulin delivery aids can contact the ADA.
5. Self-monitoring equipment for blood glucose: Be certain
that the individual has or understands where to
purchase the supplies used with the specic brand
of selfmonitoring glucose machine to be used at
home. Because a number of models of selfmonitor
ing equipment are available, it is important that the
individual be trained on the specic equipment that
will be used at home.
Patient self-assessment. Enlist the patient’s aid in
developing and maintaining a written record of moni
toring parameters (e.g., blood glucose, insulin dosage,
pertinent stress factors, exercise level, illnesses, ma
jor changes in diet or other routine). See the Patient
SelfAssessment Form for Antidiabetic Agents on the
Evolve website. Complete the Premedication Data
column for use as a baseline to track response to drug
therapy. Ensure that the patient understands how to
use the form, and instruct the patient to bring the com
pleted form to followup visits. During followup vis
its, focus on issues that will foster adherence with the
therapeutic interventions prescribed.
Life Span Considerations
Children With Diabetes Mellitus
For children who have diabetes, it is essential that the appro
priate faculty of the school, whether a day care, preschool, or
regular school environment, be familiar with the child’s health
needs. For a sample of a diabetes healthcare plan see the fol
lowing website. https://www.diabetes.org/resources/know-
your-rights/safe-at-school-state-laws/written-care-plans/
diabetes-medical-management-plan
DRUG CLASS: INSULINS
Actions
Insulin, a hormone produced in the beta cells of the
pancreas, is a key regulator of metabolism. Insulin is
required for the entry of glucose into skeletal and heart
muscle and fat. It also plays a signicant role in pro
tein and lipid metabolism. It is not required for glu
cose transport into the brain, kidney, gastrointestinal,
or liver tissue.
The pancreas secretes insulin at a steady rate of 0.5
to 1 unit/hr. It is released in greater quantities when
the blood glucose level rises above 100 mg/dL such as
after a meal. The average rate of insulin secretion in an
adult is 30 to 50 units daily.
Insulin deciency reduces the rate of transport of
glucose into cells, producing hyperglycemia. Other
575
metabolic reactions also are inhibited by the lack of in
sulin and intracellular glucose, resulting in the conver
sion of protein to glucose (gluconeogenesis), hyperlip
idemia, ketosis, and acidosis.
Insulins from the pancreases of different animals
have similar activity and were used in human be
ings for many years. Biosynthetic human insulin is
now used by most patients, especially people newly
diagnosed with diabetes. It has fewer allergic re
actions associated with it than do animalorigin
insulins.
Uses
Three factors—onset, peak, and duration—are impor
tant in the use of insulin therapy. Onset is the time re
quired for the medication to have an initial effect or
action, peak is when the insulin will have the maximum
effect, and duration is how long the agent remains ac
tive in the body. When monitoring insulin therapy, it is
important to understand these terms and to associate
them with the type of insulin being administered to as
certain when a patient is most susceptible to hypergly
cemia or hypoglycemia.
Four types of insulin, based on onset, peak, and du
ration, are in use today: rapidacting, shortacting, in
termediateacting, and longacting insulins (Table 35.5).
The most rapidacting insulins are the insulin analogs,
newer synthetic forms called lispro, aspart, and glulisine.
They are clear solutions that may be injected separately
or mixed in the same syringe with an intermediateacting
insulin. Aspart and lispro are as potent as human regular
insulin but have a more rapid onset and shorter duration
of activity. Aspart appears to have a slightly more rapid
onset than lispro. Glulisine has an onset of action similar
to lispro and aspart but has a slightly shorter duration
of action. Their rapid onset of action is related to a more
rapid absorption rate from subcutaneous tissue than is
the case with regular insulin. Aspart, lispro, and gluli
sine are usually administered within 10 to 15 minutes of
a meal. Aspart is available as a faster acting formulation
called Fiasp and is administered at the beginning of or
within 20 minutes after starting a meal. The rationale for
the development and use of these newer insulins is that
when a meal is ingested, the blood glucose rises for about
2 to 3 hours. After injection, regular insulin takes 30 min
utes to start acting, peaks at 2.5 to 5 hours, and may have
a duration of 5 to 10 hours. Lispro and aspart start to act
within 10 minutes of injection, peak within 1 to 2 hours,
and have a duration of action of 3 to 5 hours. Fiasp starts
to work within 5 to 10 minutes of injection, peaks with
1.5 to 2.2 hours, and has a duration of action 5 to 7 hours.
Glulisine has a similar onset of action but peaks in 30
to 90 minutes with a duration of action up to 4 hours.
Consequently, the newer rapidacting, shorterduration
insulins are used to control hyperglycemia associated
with meals without having longerlasting effects with
the potential for hypoglycemia. These insulins may also
be used without any other insulin in patients with type
2 diabetes who only have hyperglycemia associated with
 576
Table 35.5 Commercially Available Forms of Insulin a
STRENGTH ONSET
TYPE OF INSULIN MANUFACTURER (UNITS/ML) (HR) PEAK (HR) DURATIONB (HR) HYPERGLYCEMIAC HYPOGLYCEMIAC

UNIT VII Drugs That Affect the Endocrine System

RAPID-ACTING INSULIN
Insulin Analog Injection
NovoLog (aspart) Novo Nordisk 100 0.2–0.33 1–3 3–5 After lunch (3) Within 1–3 hr
Fiasp (aspart) Novo Nordisk 100 0.2–0.33 1.5–2.2 5–7 After lunch (3) Within 1–3 hr
Humalog (lispro) Lilly 100 0.2–0.33 0.5–2.5 3–5 After lunch (3) Within 1–3 hr
Lyumjev (lispro aabc) Lilly 100 0.25–0.28 2–2.9 4.6–7.3 After lunch (3) Within 1–3 hr
Apidra (glulisine) Sano-Aventis 100 0.2–0.33 0.5–1.5 3–4 After lunch (3) Within 1–3 hr
SHORT-ACTING INSULIN
Insulin Injection
Humulin R (human) Lilly 100, 500 0.5–1 2.5–5 5–10 Early am (1) Before lunch (3)
Novolin R (human) Novo Nordisk 100 0.5–1 2.5–5 8 Early am Before lunch
INTERMEDIATE-ACTING INSULIN
Isophane Insulin Suspension (NPH)
Humulin N (human) Lilly 100 1–2 4–12 16–28 Before lunch (2) 3 pm to supper (3)
Novolin N (human) Novo Nordisk 100 1–2 4–12 24 Before lunch 3 pm to supper
ISOPHANE INSULIN SUSPENSION (NPH) AND INSULIN INJECTION (REGULAR)
Humulin 70/30 (human) (70% NPH/30% regular) Lilly 100 0.5–1 4–12 24 Before lunch 3 pm to supper
Novolin 70/30 (human) (70% NPH/30% regular) Novo Nordisk 100 0.5–1 2–12 24 Before lunch 3 pm to supper
INSULIN ANALOG PROTAMINE SUSPENSION AND INSULIN ANALOG INJECTION
Humalog Mix 50/50 (50% lispro protamine/50% lispro) Lilly 100 0.8–4.8 0.75–13.5 14–24 — 3 pm to supper
Humalog Mix 75/25 (75% lispro protamine/25% lispro) Lilly 100 0.25–0.5 0.5–4 14–24 — 3 pm to supper
NovoLog Mix 70/30 (70% aspart protamine/30% aspart) Novo Nordisk 100 0.2–0.33 2.4 18–24 — 3 pm to supper
LONG-ACTING INSULIN
Lantus (glargine) Sano-Aventis 100 1.1 —d 24 Mid-am to mid-pm (1) —d
Semglee (glargine) Mylan/Biocon 100 1.1 —d 24 Mid-am to mid-pm —d
Toujeo (glargine) Sano-Aventis 300 1.1 —d 24 Mid-am to mid-pm —d
Basaglar (glargine) Lilly 100 1 —d Up to 24 Mid-pm —d
Levemir (detemir) Novo Nordisk 100 1 —d Up to 24 Mid-am to mid-pm (1) —d
Tresiba (degludec) Novo Nordisk 100, 200 1 —d Up to 42 Mid-am to mid-pm (1) —d
LONG-ACTING INSULIN PLUS RAPID-ACTING INSULIN
Ryzodeg 70/30 (70% degludec/30% aspart) Novo Nordisk 100 0.2–0.33 1.15 Greater than 24 — Mid-am to mid-pm
NPH, Neutral protamine Hagedorn.
aAll forms of insulin listed are from a semisynthetic source.
bThe times listed are averages based on a newly diagnosed patient with diabetes. Factors modifying these times include patient variation, site and route of administration, and dosage.
cMost often occurs when insulin is administered (1) at bedtime the previous night, (2) before breakfast the previous day, or (3) before breakfast the same day.
dNo pronounced peak activity.
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
ingestion of meals (postprandial hyperglycemia). Aspart,
glulisine, and lispro may also be injected intravenously.
Regular insulin has long been used for its short on
set of activity and relatively short duration of action.
But, as noted in Table 35.5, regular insulin is slower in
its onset and longer in duration than the rapidacting
insulins. Regular insulin is approved to be injected by
both IV and subcutaneous routes of administration.
Human regular insulin is usually administered 30 to
60 minutes before meals.
Neutral protamine Hagedorn (NPH) insulin is an in
termediateacting insulin containing specic amounts
of regular insulin and protamine. The protamine binds
to the insulin. When administered subcutaneously,
the insulin is slowly released from the protamine
and becomes active, giving it the intermediateacting
classication.
Lispro and aspart insulin may also be mixed with
protamine to prolong their duration of action. Three
products are available: 50% lispro protamine suspen
sion and 50% lispro solution (50/50 Humalog Mix),
75% lispro protamine suspension and 25% lispro solu
tion (Humalog Mix 75/25) and 70% aspart protamine
suspension and 30% aspart solution (NovoLog Mix
70/30). The combined effect is a rapidacting onset with
an intermediate duration of action of 14 to 24 hours
(Novolog 70/30 is 18 to 24 hours, whereas Humalog
50/50 and Humalog 75/25 are 14 to 24 hours).
Insulin glargine, insulin detemir, and insulin de
gludec are biosynthetic longacting insulins. They are
absorbed from the subcutaneous tissue in a uniform
manner without large uctuations in insulin levels, re
ducing the possibility of hypoglycemic reactions. Most
commonly injected in the evening, these products pro
vide a 24hour basal source of insulin for the body.
Rapidacting insulin is then injected just before meals
to control hyperglycemia secondary to the meal, or in
termediateacting NPH can be injected in the morning
and late afternoon to treat hyperglycemia from meals.
Neither insulin glargine, detemir, nor degludec should
be mixed with other insulins.
Storage of Insulin
Insulin should not be allowed to freeze and should not
be heated to more than 98°F. A general rule of thumb is
that the bottle of insulin should be stored in the refrig
erator (not the freezer) until opened. Because patients
nd it uncomfortable to inject cold insulin, the bottle
(and insulin cartridges for insulin pens) may then be
kept at room temperature (68° to 75°F) until gone. For
all insulins other than regular, lispro, aspart, or gluli
sine, the vial should be gently rolled in the palms of
the hands (not shaken) to warm and resuspend the in
sulin. Once an insulin vial is opened, it should be dis
carded within 30 days. Even though the insulin has not
deteriorated, there is concern that the contents are no
longer sterile and the vial may become a reservoir for
infection, especially with patients who reuse needles.
577
At sustained temperatures warmer than room tem
perature, insulins lose potency rapidly. Do not leave in
a hot car throughout the day.
Excess agitation should be avoided to prevent loss of
potency, clumping, or precipitation. When insulins are
prelled in syringes, the syringes should be stored in a
refrigerator for up to 30 days in a vertical position with
the needle facing upward. The syringe should be taken
out of the refrigerator before use, allowed to warm to
room temperature, and then gently rolled between the
hands to remix the insulin before administration.
Therapeutic Outcomes
The primary therapeutic outcomes expected from in
sulin therapy are as follows:
1. A decrease in both fasting blood glucose levels and
A1c concentrations in the range dened as accept
able for the individual patient
2. Fewer longterm complications associated with
poorly controlled diabetes mellitus
Nursing Implications for Insulin
Premedication assessment
1. Conrm that a blood glucose level was recently
measured and was acceptable for the individual
patient.
2. Conrm that the patient has had a level of activity
reasonable for that patient and that the anticipated
level of activity planned for the next several hours is
balanced with the insulin dose.
3. Conrm that the prescribed diet is being consumed
as planned and that no changes in diet are antici
pated in relation to insulin dosage over the next sev
eral hours (e.g., with patients on nothing by mouth
[NPO] status, consider holding medication).
Availability, dosage, and administration. See Table 35.5,
Fig. 9.26, and Chapter 10 for information regarding
availability and administration. Maintenance therapy
for newly diagnosed patients with diabetes should in
corporate the following information:
• Effective control of diabetes mellitus requires a bal
anced food intake, exercise, blood glucose levels
measured several times daily, and insulin dosage
adjustments based on the blood glucose levels.
• Several methods have been developed to initiate in
sulin therapy. The method chosen depends on such
issues as uctuation of the patient’s blood glucose;
ability of the patient to measure, mix, and adminis
ter the insulin; and adherence to planned exercise
and diet.
• Before starting a standardized regimen, the diet and
physical exercise level must be stabilized. A stan
dard approach is to calculate the initial total daily
dose of insulin based on 0.5 to 0.8 unit/kg of whole
body (not leanbody) weight. NPH (human) insulin
is often used to initiate therapy. This total daily dos
age is then split into two doses so that twothirds
578 UNIT VII Drugs That Affect the Endocrine System
Table 35.6 Compatibility of Insulin Combinations
MIX BEFORE
COMBINATION RATIO ADMINISTRATION
regular + NPH Any combination 2–3 mo
aspart + NPH Any combination Immediately
lispro + NPH Any combination Immediately
glulisine + NPH Any combination Immediately
glargine Do not mix with other insulin
detemir Do not mix with other insulin
degludec Do not mix with other insulin
NPH, Neutral protamine Hagedorn.
are administered in the morning before breakfast
and onethird is administered 30 minutes before the
evening meal. The insulin dosage is then adjusted
over the next several weeks based on blood glucose
measurements taken (usually) four times daily and
on A1c levels. Diet and exercise may also require
adjustment.
• Dosage of insulin may be linked to carbohydrate
consumption. Depending on the healthcare pro
vider orders, nurses must add the total number of
carbohydrates consumed with each meal and us
ing the formula prescribed, calculate the dose of
the insulin. Often the order will state that the pa
tient has “carb counting” and the meal tray comes
with an itemized number of carbohydrate units
for each food item. The amount of insulin ordered
may be 1 unit per 10 carbohydrates or 1 unit per 15
carbohydrates. This is only for rapidacting (e.g.,
lispro, aspart, glulisine) and/or shortacting insu
lins (e.g., regular insulin).
Mixing insulins. Many patients with diabetes mix
rapidacting insulin with intermediateacting or long
acting insulin to manage the hyperglycemia that fol
lows a meal or snack. See Table 35.6 and Chapter 9 for
the technique to follow when mixing insulins. When
regular insulin, insulin lispro, or insulin aspart is com
bined with another insulin in the same syringe, the
rapidacting insulin should be drawn into the syringe
rst to avoid contaminating the rapidacting insulin
vial with the longeracting insulin, which may happen
if the longeracting insulin was drawn into the syringe
rst and then the needle was inserted into the rapid
acting insulin to draw it into the syringe.
Life Span Considerations
Insulin
Almost all patients receiving insulin will experience a hypogly
cemic reaction at some point. Symptoms of a hypoglycemic
reaction vary from patient to patient. Be aware that confusion
and lethargy are signs of hypoglycemia but may sometimes
be overlooked in older adult patients because slowness and
confusion can be interpreted as signs of aging.
Common and serious adverse effects
Metabolic
Hyperglycemia. Patients with diabetes or prediabetes
must be monitored for the development of hypergly
cemia, particularly during the early weeks of therapy.
Assess regularly for abnormal blood glucose levels
and, in certain patients as requested by the healthcare
provider, for glycosuria and ketones. If symptoms oc
cur frequently, the healthcare provider should be noti
ed and the patient’s written records of the results of
selftesting should be supplied to the healthcare pro
vider for analysis. Patients receiving insulin may re
quire an adjustment in dosage.
Hypoglycemia. Insulin overdose or decreased car
bohydrate intake may result in hypoglycemia. If
untreated, irreversible brain damage may occur.
Hypoglycemia occurs most often when the adminis
tered insulin reaches its peak action (see Table 35.5).
Hypoglycemia must be treated immediately.
The following conditions may predispose a patient
with diabetes to a hypoglycemic (insulin) reaction:
improper measurement of insulin dosage, excessive
exercise, insufcient food intake, concurrent ingestion
of hypoglycemic drugs, and discontinuation of drugs
that cause hyperglycemia (see Drug Interactions later
in this section). Monitor the patient for the following
signs of hypoglycemia: headache, nausea, tachycardia,
weakness, hunger, lethargy, decreased coordination,
general apprehension, sweating, or blurred or double
vision.
Hypersensitivity, immune system
Allergic reactions. Allergic reactions, manifested by
itching, redness, and swelling at the site of injection,
are common in patients receiving insulin therapy.
These reactions may be caused by modifying proteins
in NPH insulin, the insulin itself, the alcohol used to
cleanse the injection site, the patient’s injection tech
nique, or the intermittent use of insulin.
Spontaneous desensitization frequently occurs
within a few weeks. Local irritation may be reduced
by changing to insulins derived from biosynthetic
sources (e.g., “human” insulin), by using unscented
alcohol swabs and disposable syringes and needles,
and by checking the patient’s injection technique.
Acute rashes covering the whole body and anaphy
lactic symptoms are rare, but if they occur, they must
be treated with antihistamines, epinephrine, and
steroids.
Lipodystrophies. Rotation of injection sites is impor
tant to avoid atrophy or hypertrophy of subcutaneous
fat tissue. This dermatologic condition may occur at the
site of frequent insulin injections. The hypertrophic ar
eas tend to be used more often by patients with diabetes
because the fat pad becomes anesthetized. In addition to
the adverse cosmetic effects, the absorption rate of insu
lin from these sites becomes signicantly prolonged and
erratic. Loss of diabetic control may result, particularly
in patients with unstable type 1 diabetes.
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
Drug interactions
Hyperglycemia. The following medications may pro
duce hyperglycemia, especially in patients with diabetes
and prediabetes (insulin dosages may require adjust
ment): albuterol, asparaginase, calcitonin, clozapine, olan
zapine, corticosteroids, cyclophosphamide, diltiazem,
diuretics (e.g., thiazides, furosemide, bumetanide), dobu
tamine, epinephrine, glucagon, isoniazid, lithium, mor
phine, niacin, nicotine, oral contraceptives, pentamidine,
phenothiazines, phenytoin, protease inhibitors, terbuta
line, somatropin, and thyroid hormones.
Patients with diabetes or prediabetes must be moni
tored for the development of hyperglycemia, particu
larly during the early weeks of therapy. Assess the
patient regularly for elevated blood glucose level or
glycosuria and notify the healthcare provider if either
occurs with any frequency.
Hypoglycemia. The following drugs may cause hypo
glycemia, thereby decreasing insulin requirements, in
patients with diabetes: anabolic steroids, angiotensin
converting enzyme (ACE) inhibitors, alcohol, nonselec
tive betaadrenergic blocking agents, calcium, clonidine,
uoxetine, ethanol, brates, lithium, monoamine oxidase
inhibitors (MAOIs), pentamidine, pentoxifylline, pyri
doxine, salicylates, sulfonamides, and sulfonylureas.
Monitor for the following signs of hypoglycemia:
headache, nausea, weakness, hunger, lethargy, de
creased coordination, general apprehension, sweating,
or blurred or double vision. Notify the healthcare pro
vider if any of these symptoms appear.
Beta-adrenergic blocking agents. Beta blockers (e.g.,
propranolol, nadolol, metoprolol) may mask many of
the symptoms of hypoglycemia. Notify the healthcare
provider if you suspect that any of these symptoms ap
pear intermittently.
DRUG CLASS: BIGUANIDE ORAL ANTIDIABETIC
AGENT
metformin (mĕt-FŎR-mĭn)
Glucophage (GLŬ-kō-fāj)
Do not confuse metformin with metronidazole.
Actions
Metformin represents a class of oral antihyperglycemic
agents known as the biguanides. It decreases hepatic
glucose production by inhibiting glycogenolysis and
gluconeogenesis, reduces absorption of glucose from
the small intestine, and increases insulin sensitivity,
improving glucose uptake in peripheral muscle and
adipose cells. Metformin may also stimulate glucose
metabolism by anaerobic glycolysis. The net result is a
signicant decrease in fasting and postprandial blood
glucose and A1c concentrations. Insulin must be pres
ent for metformin to be active, and therefore metfor
min is not effective in type 1 diabetes.
579
Uses
Metformin is used as an adjunct to the diet to lower
blood glucose levels in patients with type 2 diabetes
mellitus whose hyperglycemia cannot be controlled
by diet and exercise alone. It has the particular advan
tage that it will not cause hypoglycemia, as can occur
with insulin and the sulfonylureas. It may also be used
in combination with other oral antidiabetic agents to
lower blood glucose because the agents act by different
mechanisms.
Metformin has two other benecial effects: it does not
cause weight gain and actually may cause weight loss,
contrary to the actions of the sulfonylureas, meglitinides,
and insulin; and it also has a favorable effect on triglyc
erides. It produces a modest decrease in concentrations
of serum triglycerides and total and LDL cholesterol,
with modest increases in concentrations of HDL choles
terol. See the Medication Safety Alert in the Dosage and
Administration section later regarding patients with renal
function problems, heart failure, and liver impairment.
Therapeutic Outcomes
The primary therapeutic outcomes expected from bi
guanide oral antidiabetic agent therapy are as follows:
1. A decrease in fasting blood glucose and A1c concen
trations in the range dened as “acceptable” for the
individual patient
2. Fewer longterm complications associated with
poorly controlled type 2 diabetes mellitus
Nursing Implications for Metformin
Premedication assessment
1. Conrm that blood glucose and A1c levels were re
cently measured and were acceptable for the indi
vidual patient.
2. Conrm that the prescribed diet is being consumed
as planned and that no changes in diet are antici
pated in relation to oral hypoglycemic agent dosage
over the next several hours (e.g., in patients on NPO
status, consider holding medication).
Availability. PO: 500, 850, and 1000mg tablets; 500,
750, and 1000mg tablets, extended release (24 hr); 500
mg/5 mL oral solution.
Dosage and administration. Adult: PO: Immediate-
release tablet or solution: Initial: 500 mg twice daily or 850
mg once daily; titrate in increments of 500 mg weekly
or 850 mg every other week; may also titrate from 500
mg twice a day to 850 mg twice a day after 2 weeks. If
a dose greater than 2000 mg/day is required, it may
be better tolerated in three divided doses. Maximum
recommended dose: 2550 mg/day.
PO: Extended-release tablet: Initial: 500 to 1000 mg
once daily; dosage may be increased by 500 mg weekly
up to a maximum of 2500 mg/day. Doses can be ad
ministered twice a day at maximum dose.
580 UNIT VII Drugs That Affect the Endocrine System
If a patient’s blood glucose level is not controlled
with the maximum dosage, a sulfonylurea, a TZD, a
DPP4 inhibitor, a GLP1 agonist, SGLT2 inhibitor, or
basal insulin may be added to the regimen.
Medication Safety Alert
Lactic acidosis is a rare but potentially life-threatening com-
plication that can occur during treatment with metformin. It is
recommended that metformin therapy not be initiated in the
following patients:
 • Those with an estimated glomerular ltration rate of 30 to
45 mL/min/1.73 m2
 • With tissue hypoperfusion, such as in heart failure,
shock, or septicemia, and patients at risk for developing
metabolic acidosis
 • With clinical or laboratory evidence of liver disease
(hyperbilirubinemia; elevated aspartate aminotransferase
[AST] and/or alanine aminotransferase [ALT] levels).
 • Those who are scheduled to receive IV radiopaque
dyes. Radiopaque dyes often induce temporary renal
insufciency, so in patients with an estimated glomerular
ltration rate 30 to 60 mL/min/1.73 m2 or lower,
metformin should be discontinued 24 to 48 hours before
procedures in which radiopaque dye will be administered
(e.g., kidney studies). Metformin should not be reinitiated
for 2 to 3 days until normal renal function has been
proven.
Common adverse effects
Gastrointestinal
Nausea, vomiting, anorexia, abdominal cramps, atu-
lence. These adverse effects are most common and are
the reason for slow dose titration. They are usually mild
and tend to resolve with continued therapy. Taking the
medication with meals will help reduce these adverse
effects. Encourage the patient not to discontinue thera
py without rst consulting the healthcare provider.
Vitamin B12 deciency. Longterm administration of
metformin may cause vitamin B12 deciency; moni
tor vitamin B12 serum concentrations periodically with
longterm therapy, especially in patients with periph
eral neuropathy or anemia.
Serious adverse effects
Metabolic
Malaise, myalgias, respiratory distress, hypotension. A
rare adverse effect of metformin is lactic acidosis. A
gradual onset of these symptoms may be an early in
dication of the development of lactic acidosis. Patients
with reduced renal function, poor circulation, and/or
excessive alcohol intake are most susceptible to devel
oping lactic acidosis.
Drug interactions
Drugs that may enhance toxic effects. Amiloride, cime
tidine, digoxin, furosemide, morphine, quinidine, ra
nitidine, triamterene, trimethoprim, and vancomycin
are excreted by the same route through the kidneys
that metformin depends on for excretion. There is a
possibility that these drugs may block the excretion of
metformin, potentially causing lactic acidosis. Monitor
for signs of lactic acidosis (refer to earlier discussion).
Ethanol. Patients should be cautioned against ex
cessive alcohol intake, acute or chronic, when taking
metformin, because alcohol potentiates the effects of
metformin on lactate metabolism.
Hyperglycemia. The following drugs, when used con
currently with metformin, may decrease its therapeu
tic effects: corticosteroids, phenothiazines, diuretics,
oral contraceptives, thyroid replacement hormones,
phenytoin, and lithium carbonate.
Patients with diabetes and prediabetes must be
monitored for the development of hyperglycemia,
particularly during the early weeks of therapy. Assess
regularly for elevated blood glucose level or glycosuria
and notify the healthcare provider if either occurs with
any frequency.
Nifedipine. Nifedipine appears to increase the ab
sorption of metformin. Reducing the dosage of met
formin may minimize adverse effects.
Fluoroquinolones. Fluoroquinolones (e.g., cipro
oxacin, levooxacin) may cause hyperglycemia or
hypoglycemia. Cases of severe hypoglycemia, includ
ing coma and death, have been reported. Monitor
patients for signs/symptoms of hypoglycemia and
hyperglycemia.
DRUG CLASS: SULFONYLUREA ORAL
HYPOGLYCEMIC AGENTS
Actions
The sulfonylureas lower blood glucose levels by stim
ulating the release of insulin from the beta cells of the
pancreas. The sulfonylureas also diminish glucose pro
duction and metabolism of insulin by the liver.
Uses
The sulfonylureas are effective in patients with type 2
diabetes in whom the pancreas still has the capacity to
secrete insulin, but they are of no value in the patient
with type 1 diabetes who has no beta cell function.
Sulfonylureas are used to treat type 2 diabetes mellitus
in combination with diet and exercise. Sulfonylureas
may induce hypoglycemia as a result of overproduc
tion of insulin.
Therapeutic Outcomes
The primary therapeutic outcomes expected from sul
fonylurea oral hypoglycemic therapy are as follows:
1. A decrease in fasting blood glucose and A1c concen
trations in the range dened as acceptable for the
individual patient
2. Fewer longterm complications associated with
poorly controlled diabetes mellitus
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35 581

Table 35.7 Sulfonylurea Oral Hypoglycemic Agents

DURATIONa
GENERIC NAME BRAND NAME AVAILABILITY INITIAL DOSAGE DOSAGE RANGE (HR)
SECOND GENERATION
glimepiride Amaryl Tablets: 1, 2, 4 mg 1–2 mg daily 1–8 mg daily 24
Do not confuse Amaryl with
Altace, Avandia, Reminyl
glipizide — Tablets: 5, 10 mg 5 mg daily 15–40 mg daily 10–24
Glucotrol XL Tablets, extended release 2.5–10 mg 20 mg daily 24
(24 hr): 2.5, 5, 10 mg
glyburide — Tablets: 1.25, 1.5, 2.5, 3, 2.5–5 mg daily 1.25–20 mg daily 24
5, 6 mg
Glynaseb Tablets, micronized 1.5, 1.5–3 mg daily 0.75–12 mg daily 24
3, 6 mg
aThe times listed are averages based on a newly diagnosed patient with diabetes. Factors modifying these times include patient variation and dosage.
b

Do not confuse.

Nursing Implications for Sulfonylurea Oral
Hypoglycemic Agents
Premedication assessment
1. Conrm that blood glucose and A1c levels were re
cently measured and were hyperglycemic for the
individual patient.
2. Conrm that the patient has had a level of activity
“reasonable” for that patient and that the anticipated
level of activity planned for the next several hours is
balanced with the oral hypoglycemic agent dosage.
3. Conrm that the prescribed diet is being consumed
as planned and that no changes in diet are anticipat
ed in relation to the oral hypoglycemic agent dosage
over the next several hours (e.g., in patients on NPO
status, consider holding medication).
Availability, dosage, and administration. See Table
35.7. Individual dosage adjustment is essential for the
successful use of oral hypoglycemic agents. A patient
should receive a 1month trial on maximum dosage of
the sulfonylurea being used before the medication can
be considered a primary failure. If a patient represents
a secondary failure (a patient initially controlled on oral
agents), changing to an alternative sulfonylurea is oc
casionally successful in controlling blood glucose levels.
Medication Safety Alert
In general, sulfonylureas should not be administered to pa
tients who are allergic to sulfonamides. These patients may
also be allergic to sulfonylureas.
Common adverse effects
Gastrointestinal
Nausea, vomiting, anorexia, abdominal cramps. These ad
verse effects are usually mild and tend to resolve with
continued therapy. Encourage the patient not to dis
continue therapy without rst consulting the health
care provider.
Serious adverse effects
Metabolic
Hypoglycemia. Patients receiving oral hypoglycemic
therapy are as susceptible to hypoglycemia as patients
with diabetes on insulin therapy. Consequently, blood
glucose levels must be monitored closely, especially in
the early stages of therapy. Monitor for the following
signs of hypoglycemia: headache, nausea, weakness,
tachycardia, hunger, lethargy, decreased coordination,
general apprehension, sweating, or blurred or double
vision. Notify the healthcare provider immediately if
any of these symptoms appear.
Hypoglycemia must be treated immediately. Mild
symptoms may be controlled by the oral administra
tion of a glucose source (e.g., a lump of sugar, orange
juice, carbonated cola beverage [not diet], candy [not
chocolate]) or ingestion of a commercially prepared
product such as Glutose. Severe symptoms may be re
lieved by the administration of IV glucose, and paren
teral glucagon may be prescribed in some cases. If in
doubt about whether the patient is hypoglycemic or
hyperglycemic, always treat the individual for hypo
glycemia to prevent the possible neurologic complica
tions that can occur from untreated hypoglycemia. The
dosage of oral hypoglycemic agents may also have to
be reduced.
Gastrointestinal
Hepatotoxicity. The symptoms of hepatotoxicity are
anorexia, nausea, vomiting, jaundice, hepatomegaly,
splenomegaly, and abnormal liver function (e.g., ele
vated bilirubin, AST, ALT, gammaglutamyltransferase
582 UNIT VII Drugs That Affect the Endocrine System
[GGT], and alkaline phosphatase levels [ALP]; in
creased prothrombin time [PT]).
Hematologic
Blood dyscrasias. Routine laboratory studies (e.g.,
red blood cell and white blood cell counts, differential
counts) should be scheduled. Stress the need for the
patient to return for this laboratory work.
Immune system. Monitor for the development of a
sore throat, fever, purpura, jaundice, or excessive and
progressively increasing weakness.
Dermatologic. Report a rash or pruritus immediately.
Withhold additional doses pending approval by the
healthcare provider.
Drug interactions
Hypoglycemia. The following drugs may enhance
the hypoglycemic effects of the sulfonylureas: azole
antifungal agents (e.g., uconazole), uoroquinolo
ne antibiotics, ethanol, androgens (e.g., methandros
tenolone), warfarin, betaadrenergic blocking agents,
salicylates, sulfonamides (e.g., sulfamethoxazoletri
methoprim), and MAOIs.
Monitor the patient for the following signs of hypo
glycemia: headache, nausea, weakness, tachycardia,
hunger, lethargy, decreased coordination, general ap
prehension, sweating, or blurred or double vision.
Notify the healthcare provider if any of these symp
toms appear.
Hyperglycemia. The following drugs, when used
concurrently with the sulfonylureas, may decrease the
therapeutic effects of the sulfonylureas: corticoster
oids, uoroquinolone antibiotics, thiazide diuretics,
phenothiazines, oral contraceptives, thyroid replace
ment hormones, phenytoin, and lithium carbonate.
Patients with diabetes or prediabetes must be
monitored for the development of hyperglycemia,
particularly during the early weeks of therapy. Assess
regularly for elevated blood glucose level or gly
cosuria and notify the healthcare provider if either
occurs with any frequency.
Patients receiving insulin may require an adjust
ment in dosage.
Beta-adrenergic blocking agents. Beta blockers (e.g.,
propranolol, nadolol, metoprolol, carvedilol) may
induce hypoglycemia but may also mask many of
the symptoms of hypoglycemia. Notify the health
care provider if any of these symptoms appear
intermittently.
Alcohol. Ingestion of alcoholic beverages during
sulfonylurea therapy may infrequently result in an
Antabuselike reaction, manifested by facial ushing,
pounding headache, feeling of breathlessness, and
nausea.
In patients who develop an Antabuselike reac
tion to alcohol, the use of alcohol and preparations
containing alcohol (e.g., overthecounter cough medi
cations, mouthwashes) should be avoided during
therapy and for up to 5 days after discontinuation of
sulfonylurea therapy.
DRUG CLASS: MEGLITINIDE ORAL HYPOGLYCEMIC
AGENTS
meglitinides (mĕ-GLĬ-tĭ-nīdz)
Actions
The meglitinides are nonsulfonylurea oral hypoglyce
mic agents. They lower blood glucose levels by stimu
lating the release of insulin from the beta cells of the
pancreas.
Uses
The meglitinides are effective in patients with type 2
diabetes mellitus in whom the pancreas still has the
capacity to secrete insulin, but they are of no value in
patients with type 1 diabetes mellitus who have no
beta cell function. The meglitinides are used to treat
type 2 diabetes mellitus along with diet and exercise.
The meglitinides may be used alone or in combina
tion with metformin to control hyperglycemia. The
meglitinides have the advantage of having a short
duration of action, thus reducing the potential for hy
poglycemic reactions. On the other hand, having to
take doses up to four times daily may reduce compli
ance. The meglitinides may be of particular use for
patients normally well controlled on diet but who
may have periods of transient loss of control, such as
during an infection.
Therapeutic Outcomes
The primary therapeutic outcomes expected from
meglitinide oral hypoglycemic therapy are as
follows:
1. A decrease in fasting blood glucose and the A1c con
centrations in the range dened as “acceptable” for
the individual patient
2. Fewer longterm complications associated with
poorly controlled diabetes mellitus
Nursing Implications for Meglitinide Therapy
Premedication assessment
1. Conrm that blood glucose and A1c levels were re
cently measured and were hyperglycemic for the
individual patient.
2. Conrm that the patient has had a level of activity
“reasonable” for that patient and that the antici
pated level of activity planned for the next several
hours is balanced with the oral hypoglycemic agent
dosage.

Table 35.8 Meglitinide Oral Hypoglycemic Agents
GENERIC NAME BRAND NAME AVAILABILITY
nateglinide — Tablets: 60, 120 mg
repaglinide — Tablets: 0.5, 1, 2 mg
3. Conrm that the prescribed diet is being consumed
as planned and that no changes in diet are anticipat
ed in relation to the oral hypoglycemic agent dosage
over the next several hours (e.g., in patients on NPO
status, consider holding medication).
Availability, dosage, and administration. See Table 35.8.
Doses may be administered within 1 to 30 minutes of
the meal.
• Individual dosage adjustment is essential for
the successful use of the meglitinides. Dosages
may be adjusted weekly, based on fasting blood
glucose.
• Doses may be taken before meals two, three, or four
times daily in response to changes in the patient’s
meal pattern.
Medication Safety Alert
Patients should skip a scheduled dose of repaglinide or na
teglinide if they skip a meal so that the risk of hypoglycemia
is reduced.
Common and serious adverse effects
Metabolic
Hypoglycemia. Patients receiving oral hypoglycemic
therapy are as susceptible to hypoglycemia as patients
with diabetes on insulin therapy. Consequently, blood
glucose levels must be monitored closely, especially in
the early stages of therapy. Monitor for the following
signs of hypoglycemia: headache, nausea, weakness,
hunger, lethargy, decreased coordination, general ap
prehension, sweating, or blurred or double vision.
Notify the healthcare provider immediately if any of
these symptoms appear.
Hypoglycemia must be treated immediately. Mild
symptoms may be controlled by the oral administra
tion of a glucose source (e.g., a lump of sugar, orange
juice, carbonated cola beverage [not diet], candy [not
chocolate]) or ingestion of a commercially prepared
product such as Glutose. Severe symptoms may be
relieved by administering IV glucose, and parenteral
glucagon may be prescribed in some cases. If in doubt
about whether the patient is hypoglycemic or hyper
glycemic, always treat the individual for hypoglyce
mia to prevent the possible neurologic complications
that can occur from untreated hypoglycemia. The dos
age of oral hypoglycemic agents also may have to be
reduced.
Drugs Used to Treat Diabetes Mellitus CHAPTER 35 583
DAILY DOSAGE RANGE MAXIMUM DAILY DOSAGE
Initially, 60–120 mg before each meal 360 mg
Initially, 0.5 mg before each meal 16 mg
Drug interactions
Hypoglycemia. The following drugs may enhance the
hypoglycemic effects of repaglinide and nateglinide:
ethanol, erythromycin, clarithromycin, nonsteroidal
antiinammatory drugs, sulfonylureas, gembrozil,
itraconazole, ketoconazole, androgens (e.g., meth
androstenolone), warfarin, salicylates, sulfonamides
(e.g., sulfamethoxazoletrimethoprim), uoroquinolo
nes (e.g., ciprooxacin, levooxacin, moxioxacin),
probenecid, and MAOIs.
Monitor for the following signs of hypoglycemia:
headache, nausea, weakness, tachycardia, hunger,
lethargy, decreased coordination, general apprehen
sion, sweating, or blurred or double vision. Notify
the healthcare provider if any of these symptoms
appear.
Hyperglycemia. The following drugs, when used
concurrently with the meglitinides, may decrease the
therapeutic effects of the meglitinides: corticosteroids,
uoroquinolones, phenothiazines, diuretics, estrogens,
oral contraceptives, thyroid replacement hormones,
niacin, sympathomimetics, calcium channel blockers,
phenytoin, and lithium carbonate.
Beta-adrenergic blocking agents. Beta blockers (e.g.,
propranolol, nadolol, metoprolol, carvedilol) may in
duce hypoglycemia but may also mask many of the
symptoms of hypoglycemia. Notify the healthcare pro
vider if you suspect that any of these symptoms ap
pear intermittently.
Carbamazepine, barbiturates, rifampin. These agents
may increase repaglinide metabolism. Monitor blood
glucose levels closely when any of these agents are
started or discontinued.
Erythromycin, clarithromycin, ketoconazole. These
agents may inhibit repaglinide metabolism. Monitor
closely for hypoglycemia if any of these agents are
started in a patient receiving repaglinide.
DRUG CLASS: THIAZOLIDINEDIONE ORAL
ANTIDIABETIC AGENTS
thiazolidinediones (thī ă-zŏl-ĭ-dēn-DĪ ōnz)
Actions
The TZDs lower blood glucose levels by increasing the
sensitivity of muscle and fat tissue to insulin, allow
ing more glucose to enter the cells in the presence of
insulin for metabolism. TZDs also may inhibit hepatic
584 UNIT VII Drugs That Affect the Endocrine System
Table 35.9 Thiazolidinedione Oral Hypoglycemic Agents
GENERIC NAME BRAND NAME AVAILABILITY
pioglitazone Actos Tablets: 15, 30, 45 mg PO: Initially, 15–30 mg
Do not confuse Actos with
Actonel.
Do not confuse.
gluconeogenesis and decrease hepatic glucose out
put. Unlike sulfonylureas or meglitinides, TZDs do
not stimulate the release of insulin from the beta cells
of the pancreas, but insulin must be present for these
agents to work.
Uses
TZDs are effective in patients with type 2 diabetes mel
litus in whom the pancreas still has the capacity to se
crete insulin but are of no value in the person with type
1 diabetes who has no beta cell function. TZDs may be
an effective treatment of type 2 diabetes mellitus that
cannot be controlled by diet and exercise. They are not
indicated as initial therapy for patients with type 2 dia
betes mellitus. Pioglitazone may be used as monother
apy (with diet and exercise) or in combination with
insulin, sulfonylureas, or metformin to control blood
glucose levels. Therapy often takes 4 to 6 weeks for
notable effect and several months for full therapeutic
effect. TZDs should not be used in patients with New
York Heart Association class III or IV heart failure (see
Chapter 27).
Therapeutic Outcomes
The primary therapeutic outcomes expected from TZD
oral antidiabetic therapy are as follows:
1. A decrease in fasting blood glucose and A1c concen
trations in the range dened as “acceptable” for the
individual patient
2. Fewer longterm complications associated with
poorly controlled diabetes mellitus
Nursing Implications for Thiazolidinedione
Therapy
Premedication assessment
1. Conrm that blood glucose and A1c levels were re
cently measured and were hyperglycemic for the
individual patient.
2. Perform scheduled baseline laboratory tests. Liver
function, including bilirubin, AST, ALT, GGT, and
ALP tests, should be determined before initiation of
therapy, once a month for the rst year, and quarter
ly after the rst year. A baseline test should also be
completed for body weight; hemoglobin and hema
tocrit; white blood cell count; and total cholesterol,
HDL cholesterol, LDL cholesterol, and triglyceride
levels.
3. Conrm that the prescribed diet is being con
sumed as planned and that no changes in diet are
DAILY DOSAGE RANGE MAXIMUM DAILY DOSAGE
45 mg
once daily
anticipated in relation to the oral hypoglycemic
agent dosage over the next several hours (e.g., in pa
tients on NPO status, consider holding medication).
4. Premenopausal, anovulatory women should be in
formed that TZDs might induce the resumption of
ovulation. These women may be at risk for preg
nancy if adequate contraception is not used (see Oral
Contraceptives in the Drug Interactions section later).
Availability, dosage, and administration. See Table 35.9.
Individual dosage adjustment is essential for the suc
cessful use of hypoglycemic agents. A patient should
be given a multiweek trial (12 weeks for rosiglitazone
and pioglitazone therapy) before adjusting the dosage
or adding other hypoglycemic agents.
Medication Safety Alert
The thiazolidinediones can cause or exacerbate heart fail
ure (HF) in some patients. Observe patients when therapy is
initiated or after a dose increase for signs and symptoms of
HF (including excessive, rapid weight gain, dyspnea, and/or
edema). TZDs are not recommended in patients with symp
tomatic heart failure and are contraindicated in patients with
established New York Heart Association (NYHA) class III or IV
HF (see Chapter 27 for discussion of NYHA classications).
Common adverse effects
Gastrointestinal
Nausea, vomiting, anorexia, abdominal cramps. These ad
verse effects are usually mild and tend to resolve with
continued therapy. Encourage the patient not to dis
continue therapy without rst consulting the health
care provider.
Serious adverse effects
Metabolic
Hypoglycemia. Patients receiving TZDs are not sus
ceptible to hypoglycemia unless they are also receiv
ing other hypoglycemic therapy, such as insulin or
sulfonylureas. If patients are receiving multiple hy
poglycemic therapies, blood glucose levels must be
monitored closely, especially in the early stages of
therapy. Monitor for the following signs of hypoglyce
mia: headache, nausea, weakness, tachycardia, hunger,
lethargy, decreased coordination, general apprehen
sion, sweating, or blurred or double vision. Notify the
healthcare provider immediately if any of the previ
ously mentioned symptoms appear.
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
Hypoglycemia must be treated immediately. Mild
symptoms may be controlled by the oral administra
tion of a glucose source (e.g., a lump of sugar, orange
juice, carbonated cola beverage [not diet], candy [not
chocolate]) or ingestion of a commercially prepared
product such as Glutose. Severe symptoms may be
relieved by IV administration of glucose, and paren
teral glucagon may be prescribed in some cases. If in
doubt about whether the patient is hypoglycemic or
hyperglycemic, always treat the individual for hypo
glycemia to prevent the possible neurologic complica
tions that can occur from untreated hypoglycemia. The
dosage of oral hypoglycemic agents also may have to
be reduced.
Weight gain. Weight gain of a few pounds is a com
mon adverse effect of TZD therapy. It also may be
a sign of uid accumulation and increased plasma
volume. Monitor patients for signs of edema and
heart failure and report to the healthcare provider if
present.
Gastrointestinal
Hepatotoxicity. The symptoms of hepatotoxicity
are anorexia, nausea, vomiting, jaundice, hepato
megaly, splenomegaly, and abnormal liver function
(elevated bilirubin, AST, ALT, GGT, and ALP levels;
increased PT).
Drug interactions
Hypoglycemia. The following drugs may enhance the
hypoglycemic effects of TZDs: sulfonylureas, ethanol,
androgens (e.g., methandrostenolone), warfarin, salic
ylates, sulfonamides (e.g., sulfamethoxazoletrimeth
oprim), uoroquinolones (ciprooxacin, levooxacin,
noroxacin), and MAOIs.
Monitor for the following signs of hypoglycemia:
headache, nausea, weakness, hunger, lethargy, de
creased coordination, general apprehension, sweating,
or blurred or double vision. Notify the healthcare pro
vider if any of these symptoms appear.
Hyperglycemia. The following drugs, when used
concurrently with TZDs, may decrease the therapeu
tic effects of TZDs: corticosteroids, uoroquinolones,
phenothiazines, diuretics, oral contraceptives, thy
roid replacement hormones, phenytoin, and lithium
carbonate.
Patients with diabetes or prediabetes need to be
monitored for the development of hyperglycemia,
particularly during the early weeks of therapy. Assess
regularly for elevated blood glucose level or glycosuria
and notify the healthcare provider if it occurs with any
frequency. Patients receiving insulin may require an
adjustment in dosage.
Beta-adrenergic blocking agents. Beta blockers (e.g.,
propranolol, nadolol, metoprolol, carvedilol) may
induce hypoglycemia but may also mask many of
the symptoms of hypoglycemia. Notify the health
care provider if any of these symptoms appear
intermittently.
585
Oral contraceptives. Pioglitazone may enhance the
metabolism of ethinyl estradiol and norethindrone,
which may cause a resumption of ovulation in patients
taking oral contraceptives. Counseling regarding al
ternative methods of birth control (e.g., contraceptive
foam, condoms) should be planned.
Drugs that inhibit metabolism. Erythromycin, ke
toconazole, itraconazole, calcium channel block
ers, corticosteroids, cyclosporine, triazolam, and
3hydroxy3methylglutaryl coenzyme A (HMG
CoA) reductase inhibitors (statins) may inhibit the
metabolism of pioglitazone.
DRUG CLASS: ALPHA-GLUCOSIDASE INHIBITOR
AGENTS
acarbose (Ă-kăr-bōs)
Precose (PRĒ-kōs)
miglitol (MĬG-lĭ-tŏl)
Actions
Acarbose and miglitol are classied as an antihyper
glycemic agents. They are enzyme inhibitors that in
hibit pancreatic alphaamylase and gastrointestinal
alphaglucoside hydrolase enzymes used in the diges
tion of sugars. In patients with diabetes, this enzyme
inhibition results in delayed glucose absorption and a
lowering of postprandial hyperglycemia.
Uses
Acarbose and miglitol are used as an adjunct to the
diet to lower blood glucose levels in patients with type
2 diabetes mellitus whose hyperglycemia cannot be
controlled by diet and exercise alone. The particular
advantage of the alphaglucosidase inhibitors is that
they will not cause hypoglycemia, as can occur with
insulin and the sulfonylureas. They also may be used
in combination with the sulfonylureas or metformin to
lower the blood glucose level because the agents act by
different mechanisms.
Therapeutic Outcomes
The primary therapeutic outcomes expected from
acarbose and miglitol therapy are as follows:
1. A decrease in postprandial blood glucose and A1c
concentrations in the range dened as “acceptable”
for the individual patient
2. Fewer longterm complications associated with
poorly controlled type 2 diabetes mellitus
Nursing Implications for Acarbose and Miglitol
Premedication assessment
1. If the patient is also receiving an oral hypoglycemic
agent or insulin therapy, ensure that the dosages of
these medications are well adjusted before starting
acarbose or miglitol therapy.
586 UNIT VII Drugs That Affect the Endocrine System
Table 35.10 Alpha-Glucosidase Inhibitor Agents
GENERIC NAME BRAND NAME AVAILABILITY
acarbose Precose Tablets: 25, 50, 100 mg
miglitol — Tablets: 25, 50, 100 mg
2. Review the patient’s history to ensure that there is
no gastrointestinal malabsorption syndrome or ob
struction present.
3. Review the patient’s medical history to ensure that
no liver abnormalities are present before starting
acarbose.
Availability, dosage, and administration
See Table 35.10
Common adverse effects
Gastrointestinal
Abdominal cramps, diarrhea, atulence. These adverse
effects are caused by the metabolism of carbohydrates
in the large intestine that were blocked from metabo
lism in the small intestine by acarbose and miglitol.
These adverse effects are usually mild and tend to re
solve with continued therapy. Encourage the patient
not to discontinue therapy without rst consulting the
healthcare provider.
Serious adverse effects
Metabolic
Hypoglycemia. Although acarbose and miglitol do not
cause hypoglycemia, they can enhance the hypoglyce
mia caused by a sulfonylurea or insulin. Consequently,
blood glucose levels must be monitored closely, espe
cially in the early stages of therapy. Monitor for the
following signs of hypoglycemia: headache, nausea,
weakness, tachycardia, hunger, lethargy, decreased co
ordination, general apprehension, sweating, or blurred
or double vision. Notify the healthcare provider imme
diately if any of these symptoms appear.
Hypoglycemia must be treated immediately.
Treatment should be initiated with oral dextrose
(Glutose) because its metabolism is not blocked by
acarbose or miglitol. Do not use sucrose (table sugar)
because its metabolism is blocked by acarbose and
miglitol. Severe symptoms may be relieved by IV
administration of glucose, and parenteral glucagon
may be prescribed in some cases. If in doubt about
whether the patient is hypoglycemic or hyperglyce
mic, always treat the individual for hypoglycemia to
prevent the possible neurologic complications that
can occur from untreated hypoglycemia. The dos
age of oral hypoglycemic agents may also have to
be reduced.
Gastrointestinal
Hepatotoxicity. Acarbose has been reported to cause
elevations of serum aminotransferase levels (AST and
DAILY DOSAGE RANGE MAXIMUM DAILY DOSE
PO: 25–100 mg three ≤60 kg (132 lb ): 50 mg three times a day
times a day >60 kg (132 lb ): 100 mg three times a
day
PO: 25–100 mg three 100 mg three times a day
times a day
ALT). In rare cases, it causes hyperbilirubinemia. It is
recommended that serum aminotransferase concentra
tions be checked every 3 months during the rst year
of treatment and periodically thereafter.
Drug interactions
Hyperglycemia. The following drugs, when used con
currently with acarbose and miglitol, may decrease the
therapeutic effects of acarbose and miglitol: corticos
teroids, phenothiazines, diuretics, oral contraceptives,
thyroid replacement hormones, phenytoin, diazoxide,
and lithium carbonate.
Digestive enzymes, intestinal adsorbents. Digestive
enzymes (e.g., amylase, pancreatin) and intestinal
adsorbents (e.g., charcoal) may reduce the effect of
acarbose and miglitol. Concurrent therapy is not
recommended.
Digoxin. Acarbose may inhibit the absorption of di
goxin. Monitor serum digoxin levels and therapeutic
effects to assess whether the dosage of digoxin needs
to be adjusted. Monitor closely when the dosage of
acarbose is increased or discontinued.
DRUG CLASS: SODIUM-GLUCOSE COTRANSPORTER
2 INHIBITORS
Actions
In normal physiology, SGLT2 proteins located in the
epithelial cells of the proximal tubules of the nephron
(kidneys) reabsorb about 80% to 90% of the glucose
ltered across the glomerulus, transporting it back
into the circulating blood. In type 2 diabetes, SGLT2
is oversecreted, reabsorbing even more glucose back
into the blood that may aggravate hyperglycemia.
SGLT2 inhibitors block the secretion of the SGLT2
protein, dropping glucose reabsorption from 90% to
less than 10%, causing the glucose to be excreted in
the urine.
Uses
SGLT2 inhibitors are used to treat hyperglycemia in
type 2 diabetes by reducing renal glucose reabsorp
tion in the proximal convoluted tubule, enhancing
increased urinary glucose excretion. They are used as
adjuncts to diet and exercise to improve blood glu
cose control in adults with type 2 diabetes. They may
be used as monotherapy or in combination with met
formin, sulfonylureas, TZDs, DPP4 inhibitors, and
insulin. With continuous use, the A1c is lowered about
0.7%, similar to the reduction with other adjunctive
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
antidiabetic agents. In addition to their indications
for type 2 diabetes, canagliozin and empagliozin
are used to reduce the incidence of cardiovascular
events, heart failure hospitalizations and to slow the
progression of chronic kidney disease. Dapagliozin
is used to reduce the risk of hospitalization for heart
failure in patients with established cardiovascular
disease or multiple cardiovascular risk factors. It is
also approved for patients with heart failure with re
duced ejection fraction with or without type 2 diabe
tes. Patients who have type 1 diabetes or who are sus
ceptible to ketoacidosis are not candidates for SGLT2
inhibitor therapy.
Therapeutic Outcomes
The primary therapeutic outcomes expected from
SGLT2 inhibitor therapy are as follows:
1. A decrease in postprandial blood glucose and A1c
concentrations in the range dened as “acceptable”
for the individual patient
2. Fewer longterm complications associated with
poorly controlled type 2 diabetes mellitus
Nursing Implications for SGLT2 Inhibitors
Premedication assessment
1. Ensure that the dosages of concurrent antidiabetic
therapy are well adjusted before starting SGLT2 in
hibitor therapy.
2. Conrm that blood glucose and A1c levels were re
cently measured and were hyperglycemic for the
individual patient.
3. Review the estimated glomerular ltration rate
(eGFR) as a renal function test to ensure that
the SGLT2 inhibitor being prescribed is accept
able based on the patient’s glomerular ltration
rate. Monitor the eGFR periodically during ther
apy because SGLT2 inhibitors may reduce renal
function.
4. In patients starting canagliozin therapy, ensure
that the patient’s serum potassium level is normal
before starting therapy. Patients predisposed to
hyperkalemia (including those with renal impair
ment or taking potassiumsparing diuretics, ACE
inhibitors, and angiotensin II receptor blockers)
are more likely to develop hyperkalemia; moni
tor serum potassium levels after initiation in those
who are predisposed.
5. Discuss with patients their compliance with cur
rent antidiabetic therapy and ability to do self
monitoring of blood glucose levels.
6. Ensure that the patient and family understand
the signs and symptoms of hypoglycemia and its
causes and treatment.
7. Ensure that patients understand the signs and
symptoms of Fournier gangrene (necrotizing fas
ciitis) of the perineum. Assess patients presenting
with fever or malaise along with genital or peri
anal pain, tenderness, erythema, or swelling for
587
necrotizing fasciitis. Discontinue in patients who
develop necrotizing fasciitis, notify the healthcare
provider and initiate treatment immediately.
8. Ensure that the patient and family understand the
signs and symptoms of ketoacidosis. Risk factors that
may predispose to ketoacidosis include reduction in
insulin therapy, caloric restriction, alcohol abuse, ex
tensive exercise, myocardial infarction, stroke, severe
infection, or other extreme stress event.
9. Discuss with both male and female patients their
histories of urinary tract and genital fungal infec
tions. Ensure that the patients know the signs and
symptoms of these infections and the need to re
port to their healthcare provider.
10. Identify whether the patient is pregnant or
breastfeeding.
11. Monitor the patient’s weight prior to beginning
therapy and on a regular basis thereafter. This class
of medicine is not associated with weight gain
as are some of the other antidiabetic medicines.
Weight losses of 4 to 7 pounds were reported in
clinical trials.
Availability, dosage, and administration
See Table 35.11.
Common and serious adverse effects
Cardiovascular
Hypotension. SGLT2 inhibitors may induce vascular
dehydration caused by excretion of water along with
hypertonic concentrations of glucose in the urine.
Patients may develop hypotension with low systolic
blood pressure, particularly in elderly patients and
those concurrently taking antihypertensive medica
tions and diuretics for other conditions. Maintain ad
equate hydration, especially when initiating therapy.
Increases in low-density lipoprotein cholesterol. It
was noted in clinical trials that LDL cholesterol in
creased 5% to 7% in patients participating in the trials.
The clinical signicance of this mild elevation is un
known. The healthcare provider will decide whether
or not to treat the LDL cholesterol.
Metabolic
Hypoglycemia. Hypoglycemia is quite rare in patients
using the SGLT2 inhibitors as monotherapy but is more
common in concurrent therapy with insulin and those
agents that secrete insulin (secretagogues) (e.g., insulin,
sulfonylureas, meglitinides). When using lower doses of
insulin, the secretagogues or the SGLT2 inhibitors may
be necessary to reduce the incidence of hypoglycemia.
Glycosuria. Based on the mechanism of action of
SGLT2 inhibitors, patients will commonly spill glucose
in the urine. Patients who test urine to monitor their
diabetes should stop doing so because the results will
be meaningless for monitoring.
Genitourinary
Genitourinary tract infections. All patients prescribed
an SGLT2 inhibitor are at slightly greater risk of
588 UNIT VII Drugs That Affect the Endocrine System
Table 35.11 Sodium-Glucose Cotransporter 2 Inhibitors
GENERIC NAME BRAND NAME AVAILABILITY
canagliozin Invokana Tablets: 100, 300 mg
dapagliozin Farxiga Tablets: 5, 10 mg
empagliozin Jardiance Tablets: 10, 25 mg
ertugliozin Steglatro Tablets: 5, 15 mg
eGFR, Estimated glomerular ltration rate; GFR, glomerular ltration rate.
developing bacterial and fungal infections of the genito
urinary tract as a result of glucosuria. Those patients
with chronic or recurrent genitourinary infections are
more likely to develop infections. Report symptoms to
the healthcare provider for appropriate treatment.
Increased urination. Excretion of additional urine glu
cose may result in polyuria and nocturia in 2% to 5%
of patients.
Drug interactions
Antihypertensive agents. Patients taking antihyper
tensive agents (ACE inhibitors, beta blockers, alpha
blockers, calcium channel blockers, diuretics) may be
more susceptible to orthostatic hypotension and hypo
tensive episodes induced by hypovolemic dehydration
caused by SGLT2 inhibitors.
INCRETIN-RELATED ANTIDIABETIC
THERAPY
In normal physiology there are two proteins known as
incretin peptides: GLP1 and glucosedependent insu
linotropic polypeptide (GIP). (The term glucose-depen-
dent means that they are secreted only when glucose
levels start to rise.) These hormones are released from L
cells in the distal ileum and colon in response to inges
tion of carbohydrates and fats. The incretins help con
trol blood glucose levels by the following mechanisms:
• Enhancing insulin secretion
• Suppressing glucagon secretion from the liver,
thereby suppressing glucose output from the liver
• Delaying gastric emptying, thus slowing carbohy
drate and lipid absorption and reducing postpran
dial hyperglycemia
• Reducing appetite
• Maintaining beta cell function
These actions result in reduction in basal glucose
concentration and elevation of postprandial glucose
DAILY DOSAGE RANGE MAXIMUM DAILY DOSAGE
PO: 100 mg once 300 mg; adjust dose in renal impairment;
daily not recommended in patients with eGFR
<45 mL/min/1.73 m2; do not use in patients
with eGFR of <30 mL/min/1.73 m2
PO: 5 mg once daily 10 mg; initiation not recommended with
eGFR <25 mL/min/1.73 m2, however,
patients may continue 10 mg orally once
daily to reduce the risk of eGFR decline,
ESKD, CV death and hospitalization for
heart failure
PO: 10 mg once daily 25 mg; do not use in patients with eGFR
<30 mL/min/1.73 m2
PO: 5 mg once daily 15 mg; do not use in patients with eGFR
<30 mL/min/1.73 m2
concentration. There is also a reduced appetite, with
subsequent weight reduction.
One of the pathophysiologies associated with type 2
diabetes mellitus is low incretin levels. A new approach
to the treatment of this form of diabetes is to enhance
the activity of incretin hormones. There are two classes
of agents that support the incretins: the incretin mimetic
agents (dulaglutide, exenatide, exenatide ER, liraglutide,
lixisenatide, and semaglutide), which are GLP1 ago
nists that improve GLP1 levels, and the DPP4 inhibi
tors (alogliptin, linagliptin, saxagliptin, and sitagliptin).
DRUG CLASS: INCRETIN MIMETIC AGENTS
(GLUCAGON-LIKE PEPTIDE-1 AGONISTS)
Actions
GLP1 agonists mimic the actions of this incretin for
selfregulating glycemic control, resulting in an in
crease in serum insulin and a reduction in glucose
concentrations.
Uses
GLP1 agonists are used as additional therapy to re
duce elevated fasting and postprandial hyperglycemia
in patients with type 2 diabetes mellitus who are taking
metformin, a sulfonylurea, or a combination of metfor
min and a sulfonylurea, but who have not achieved
adequate glycemic control. Particular benets of GLP
1 agonists are that they enhance insulin secretion only
in the presence of hyperglycemia, and insulin secretion
decreases as the blood glucose level approaches nor
mal levels. In addition to their use in type 2 diabetes,
dulaglutide, liraglutide, and semaglutide injection are
used to reduce the risk of major cardiovascular events
(cardiovascular death, nonfatal myocardial infarction,
nonfatal stroke) in adults with type 2 diabetes mellitus
who have established cardiovascular disease or mul
tiple cardiovascular risk factors.
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
Dulaglutide, exenatide ER, liraglutide, and sema
glutide are contraindicated for use in patients with a
personal or family history of medullary thyroid cancer
(MTC) and in patients with multiple endocrine neo
plasia syndrome type 2 (MEN2). All patients should
be monitored for symptoms of thyroid tumors (e.g.,
mass in the neck, dysphagia, dyspnea, persistent
hoarseness).
Therapeutic Outcomes
The primary therapeutic outcomes expected from
GLP1 agonist therapy are as follows:
1. A decrease in fasting and postprandial blood glu
cose levels and A1c concentrations in the range de
ned as “acceptable” for the individual patient
2. Fewer longterm complications associated with
poorly controlled type 2 diabetes mellitus
Nursing Implications for GLP-1 Agonists
Premedication assessment
1. Ensure that the dosages of concurrent oral antidia
betic agents are well adjusted before starting GLP1
therapy.
2. Assess the patient’s or family member’s ability to
selfadminister injections.
Availability, dosage, and administration. See Table
35.12. Administer GLP1 agonists as a subcutaneous in
jection in the thigh, abdomen, or upper arm. Exenatide
is a twicedaily administration, whereas liraglutide is
a oncedaily administration independent of meals. Do
not administer exenatide after a meal. Based on clini
cal response, the dose of the agonist may be increased.
Exenatide ER, semaglutide and dulaglutide are admin
istered once weekly, whereas liraglutide and lixisena
tide are administered once daily and exenatide must
be administered twice daily. All are available in pre
lled syringes for injection. Semaglutide is available in
a prelled syringe for weekly administration and an
oral tablet form for daily use.
The GLP1 agonists are used in conjunction with
metformin and/or a sulfonylurea. Dosage adjustment
of the metformin is not necessary, but a dosage reduc
tion of the sulfonylurea might be necessary to reduce
the risk of hypoglycemia.
GLP1 pens should be stored refrigerated at 36°F to
46°F (2.2°C to 7.8°C). Do not freeze or use the pen if
it has been frozen. Warm to room temperature before
use. After rst use, the pens may be stored at room tem
perature (59°F to 86°F [15°C to 30°C]). The pens should
be discarded 30 days after rst use, even if some of the
drug remains in the pen.
Common adverse effects
Gastrointestinal
Nausea, vomiting, diarrhea, constipation. These adverse
effects are usually mild to moderate and tend to re
solve with continued therapy. Encourage the patient
589
not to discontinue therapy without rst consulting the
healthcare provider.
Neurologic
Headache. This adverse effect is usually mild to
moderate and tends to resolve with continued therapy.
Encourage the patient not to discontinue therapy with
out rst consulting the healthcare provider.
Immune system, respiratory
Upper respiratory infection. In clinical trials with GLP
1 agonists there was a higher rate of upper respiratory
infection in the GLP1 agonist–treated group than in
the placebotreated group. Notify the healthcare pro
vider if symptoms of nasal congestion and sore throat
develop during GLP1 therapy.
Serious adverse effects
Metabolic
Hypoglycemia. Although GLP1 agonists do not cause
hypoglycemia by themselves, they can enhance the hy
poglycemia that may be caused by a sulfonylurea or
other secretagogues. Consequently, blood glucose lev
els must be monitored closely, especially in the early
stages of therapy. Monitor for the following signs of
hypoglycemia: headache, nausea, weakness, tachycar
dia, hunger, lethargy, decreased coordination, general
apprehension, sweating, or blurred or double vision.
Notify the healthcare provider immediately if any of
these symptoms appear.
Hypoglycemia must be treated immediately. Mild
symptoms may be controlled by the oral administration
of a glucose source (e.g., a lump of sugar, orange juice,
carbonated cola beverage [not diet], candy [not choco
late]) or ingestion of a commercially prepared product
such as Glutose. Severe symptoms may be relieved by
IV administration of glucose, and parenteral glucagon
may be prescribed in some cases. If in doubt about
whether the patient is hypoglycemic or hyperglycemic,
always treat the individual for hypoglycemia to prevent
the possible neurologic complications that can occur
from untreated hypoglycemia. The dosage of oral anti
diabetic agents may also have to be reduced.
Pancreatitis. GLP1 agonists may rarely cause pancre
atitis, particularly when treatment is started and after
increases in dosage. Observe for signs and symptoms
of pancreatitis, including persistent, severe abdominal
pain that may radiate around to the back and may be ac
companied by vomiting. If symptoms develop, hold the
dose of medication and contact the healthcare provider.
Drug interactions
Hypoglycemia. The following drugs may enhance
the hypoglycemic effects of the sulfonylureas and
GLP1 agonists: ethanol, androgens (e.g., methandros
tenolone), warfarin, betaadrenergic blocking agents
(e.g., propranolol, metoprolol, carvedilol), salicylates,
sulfonamides (e.g., sulfamethoxazoletrimethoprim),
uoroquinolones (e.g., ciprooxacin, levooxacin,
moxioxacin), and MAOIs.
590 UNIT VII Drugs That Affect the Endocrine System
Table 35.12 Glucagon-like Peptide-1 Agonists
GENERIC NAME BRAND NAME AVAILABILITY DOSAGE RANGE
dulaglutide Trulicity Prelled pen for one-time use: 0.75, Subcutaneous: 0.75 mg to
1.5, 3, 4.5 mg/0.5 mL 4.5 mg one time weekly
exenatide Byetta Prelled pen cartridges: 1.2 mL
of solution to deliver 5 mcg per
injection; 2.4 mL of solution to
deliver 10 mcg per injection (each
prelled pen will deliver 60 doses
to provide a 30-day supply of the
twice-daily medication)
exenatide ER Bydureon Autoinjector pen: 2 mg/0.85 mL
BCise
liraglutide Victoza Prelled pen cartridge: 18 mg/3 mL
lixisenatide Adlyxin Adlyxin Starter Pack: Prelled pen:
10 mcg/0.2 mL in 3 mL prelled
pen and 20 mcg/0.2 mL in
3 mL prelled pen; Prelled Pen
injector 20 mcg/0.2 mL in 3 mL
semaglutide Ozempic Prelled pen 0.25 mg or 0.5 mg per
dose (2 mg/1.5 mL);
1 mg per dose (2 mg/1.5 mL)
Rybelsus Tablets: 3, 7, 14 mg
COMBINATION INSULIN AND GLUCAGON-LIKE PEPTIDE-1 AGONISTS
degludec and Xultophy Prelled pen: degludec 100 units/
liraglutide mL and liraglutide 3.6 mg/mL in
3 mL
glargine and Soliqua Prelled pen: glargine 100 units/
lixisenatide mL and lixisenatide 33 mcg/mL
in 3 mL
MAXIMUM DOSAGE
4.5 mg; 1 injection
weekly
Subcutaneous: 5 mcg twice 10 mcg twice daily
daily within 60 min of morning
and evening meals; 6 or more
hours apart
2 mg once weekly at any time of 2 mg; 1 injection
day, with or without meals weekly
Subcutaneous: 0.6 mg once Use with caution
daily at any time for 1 wk in patients with
May increase dose to 1.2 mg renal or hepatic
once daily impairment
May increase to 1.8 mg for No dosage adjustment
glycemic control is required for these
conditions.
Subcutaneous: 10 mcg once 20 mcg once daily
daily for 14 days; on day 15
increase to 20 mcg once daily.
Maintenance dose: 20 mcg
once daily
Subcutaneously: 0.25 mg once 1 mg once weekly
weekly for 4 wk; after 4 wk
on the initial dose, increase to
0.5 mg subcutaneously once
weekly for at least 4 wk
Initially, 3 mg 30 min before food There is no designated
or beverage once daily for maximum dose for
30 days; then 7 mg 30 min orally administered
before food or beverage once semaglutide.
daily for 30 days; If additional
glycemic control is needed,
start 14 mg daily before
food or beverage once daily,
monitoring glycemic control
Subcutaneous: 16 units of Maximum daily
degludec and 0.58 mg of dosage:
liraglutide once daily 50 units of degludec
and 1.8 mg of
liraglutide
In patients inadequately Maximum dosage:
controlled on <30 units of 60 units
basal insulin or on lixisenatide: glargine/20 mcg
Subcutaneous: 15 units lixisenatide
glargine/5 mcg lixisenatide
given once daily
In patients inadequately
controlled on 30–60 units of
basal insulin: Subcutaneous:
30 units glargine/10 mcg
lixisenatide once daily
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
Table 35.13 Dipeptidyl Peptidase-4 Inhibitors
GENERIC NAME BRAND NAME AVAILABILITY
alogliptin Nesina Tablets: 6.25, 12.5, 25 mg
linagliptin Tradjenta Tablets: 5 mg
saxagliptin Onglyza Tablets: 2.5, 5 mg
sitagliptin Januvia Tablets: 25, 50, 100 mg
Monitor for the following signs of hypoglycemia:
headache, nausea, weakness, tachycardia, hunger,
lethargy, decreased coordination, general apprehen
sion, sweating, and blurred or double vision. Notify
the healthcare provider if any of these symptoms
appear.
Hyperglycemia. The following medications, when
used concurrently with GLP1 agonists, may decrease
the therapeutic effects of GLP1 agonists: corticoster
oids, phenothiazines, diuretics, oral contraceptives,
thyroid replacement hormones, phenytoin, and lithi
um carbonate.
DRUG CLASS: DIPEPTIDYL PEPTIDASE-4
INHIBITORS
Actions
The incretin hormones GIP and GLP1 are quickly me
tabolized by DPP4, which results in hyperglycemia.
DPP4 inhibitors prolong the life of active GLP1 and
GIP, prolonging the benecial effects of the incretin
hormones in reducing hyperglycemia.
Uses
DPP4 inhibitors may be used as monotherapy or as
additional therapy as an adjunct to diet and exercise to
reduce elevated fasting and postprandial hyperglyce
mia in patients with type 2 diabetes mellitus who are
taking metformin, a sulfonylurea, or a combination
of metformin and a sulfonylurea, but who have not
achieved adequate glycemic control. Particular ben
ets of DPP4 inhibitors are that they enhance insulin
secretion only in the presence of hyperglycemia, and
insulin secretion decreases as blood glucose approach
es normal levels. Saxagliptin has been associated with
heart failure that may require hospitalization. Monitor
for signs and symptoms of heart failure during therapy
and consider discontinuation if condition develops
Therapeutic Outcomes
The primary therapeutic outcomes expected from
DPP4 inhibitor therapy are as follows:
1. A decrease in fasting and postprandial blood glu
cose levels and A1c concentrations in the range de
ned as “acceptable” for the individual patient
591
DAILY DOSAGE RANGE MAXIMUM DAILY DOSAGE
PO: 25 mg daily 25 mg; adjust dose in renal
impairment
PO: 5 mg once daily 5 mg
PO: 2.5–5 mg once daily 5 mg; adjust dose in renal
impairment
PO: 100 mg once daily 100 mg; adjust dose in renal
impairment
2. Fewer longterm complications associated with
poorly controlled type 2 diabetes mellitus
Nursing Implications for DPP-4 Inhibitors
Premedication assessment. Ensure that the dosages of
concurrent oral antidiabetic therapy are well adjusted
before starting DPP4 inhibitor therapy.
Availability, dosage, and administration. See Table
35.13. Adult: Administer with or without food.
Adjust DPP4 inhibitor dosage for patients with renal
impairment.
Medication Safety Alert
Dipeptidyl peptidase-4 inhibitors do not cause hypoglycemia
by themselves, but their concurrent use with an agent known
to cause hypoglycemia (e.g., sulfonylureas) should be closely
monitored. Use with caution when given with other agents
that may also cause hypoglycemia. A lower dose of the sul
fonylurea may be required.
Common adverse effects
Gastrointestinal
Nausea, abdominal pain, diarrhea. These adverse effects
are usually mild to moderate and tend to resolve with
continued therapy. Encourage the patient not to dis
continue therapy without rst consulting the health
care provider.
Metabolic
Hyperuricemia. Linagliptin may increase the plasma
uric acid level. Patients who have had previous epi
sodes of hyperuricemia or attacks of gouty arthritis
may be susceptible to additional attacks when receiv
ing linagliptin therapy. Monitor the laboratory reports
for early indications of hyperuricemia.
Neurologic
Headache. This adverse effect is usually mild to
moderate and tends to resolve with continued therapy.
Encourage the patient not to discontinue therapy with
out rst consulting the healthcare provider.
Immunologic, respiratory
Upper respiratory infection, nasopharyngitis. In clinical
trials with DPP4 inhibitors, there was a higher rate
of upper respiratory infection and nasopharyngitis in
592 UNIT VII Drugs That Affect the Endocrine System
the DPP4 inhibitor–treated group than in the placebo
treated group. Notify the prescriber if symptoms of na
sal congestion and sore throat develop during DPP4
inhibitor therapy.
Serious adverse effects
Metabolic
Hypoglycemia. Patients may develop hypoglycemia
when DPP4 inhibitors are used in combination with
other agents that may induce hypoglycemia (e.g., sul
fonylureas). Consequently, blood glucose levels must
be monitored closely, especially in the early stages of
therapy. Monitor for the following signs of hypoglyce
mia: headache, nausea, weakness, tachycardia, hunger,
lethargy, decreased coordination, general apprehen
sion, sweating, or blurred or double vision. Notify the
healthcare provider immediately if any of these symp
toms appear.
Hypoglycemia must be treated immediately. Mild
symptoms may be controlled by the oral administra
tion of a glucose source (e.g., a lump of sugar, orange
juice, carbonated cola beverage [not diet], candy [not
chocolate]) or ingestion of a commercially prepared
product such as Glutose. Severe symptoms may be
relieved by IV administration of glucose, and paren
teral glucagon may be prescribed in some cases. If in
doubt about whether the patient is hypoglycemic or
hyperglycemic, always treat the individual for hypo
glycemia to prevent the possible neurologic complica
tions that can occur from untreated hypoglycemia. The
dosage of oral antidiabetic agents may also have to be
reduced.
Pancreatitis. DPP4 inhibitors infrequently cause
pancreatitis, particularly when treatment is started and
following increases in dosage. Observe for signs and
symptoms of pancreatitis, including persistent, severe
abdominal pain that may radiate around to the back
and may be accompanied with vomiting. If symptoms
develop, hold the dose of medication and contact the
healthcare provider.
Immunologic
Hypersensitivity. With use of DPP4 inhibitors there
have been infrequent reports of hypersensitivity re
actions manifested by skin rashes, angioedema, and
anaphylaxis. If symptoms develop, hold the dose of
medication and contact the healthcare provider.
Arthralgia. Severe and disabling arthralgia has been
reported with DPPIV inhibitor use; onset may occur
within 1 day to years after treatment initiation and
may resolve with discontinuation of therapy. Some
patients may experience a recurrence of symptoms if
DPPIV inhibitor therapy is resumed.
Bullous pemphigoid. DPP4 inhibitors may cause bul
lous pemphigoid characterized by skin eruptions.
Advise patients to report development of skin blisters
or erosions. Discontinue therapy if bullous pemphi
goid is suspected and follow up with the prescribing
healthcare provider.
Drug interactions
Digoxin. Patients taking sitagliptin and digoxin con
currently may experience a 20% increase in digoxin
serum levels. In most patients, this is not a particular
problem, but monitor for bradycardia. Hold the digox
in dose and contact the prescriber if the heart rate is
less than 60 beats/min.
Hypoglycemia. The following drugs may enhance
the hypoglycemic effects of DPP4 inhibitors: etha
nol, androgens (e.g., methandrostenolone), warfarin,
betaadrenergic blocking agents (e.g., propranolol,
metoprolol, carvedilol), salicylates, sulfonamides
(e.g., sulfamethoxazoletrimethoprim), uoroqui
nolones (ciprooxacin, moxioxacin, noroxacin),
and MAOIs.
The following drugs may inhibit the metabolism of
saxagliptin, enhancing hypoglycemic effects: ketocon
azole, itraconazole, clarithromycin, indinavir, nelna
vir, and ritonavir.
Monitor for the following signs of hypoglycemia:
headache, nausea, weakness, tachycardia, hunger,
lethargy, decreased coordination, general apprehen
sion, sweating, or blurred or double vision. Notify the
healthcare provider if any of these symptoms appear.
Hyperglycemia. The following drugs, when used
concurrently with DPP4 inhibitors, may decrease
the therapeutic effects of sitagliptin: corticosteroids,
phenothiazines, diuretics, oral contraceptives, thy
roid replacement hormones, phenytoin, and lithium
carbonate.
The following drugs may enhance the metabo
lism of linagliptin, reducing the therapeutic effects:
rifampin, phenobarbital, phenytoin, and carbamaze
pine. Change therapy to another DPP4 inhibitor.
DRUG CLASS: ANTIHYPOGLYCEMIC AGENTS
glucagon (GLŬ-kă-gŏn)
Actions
Glucagon is a hormone secreted by the alpha cells
of the pancreas that breaks down stored glycogen to
glucose, resulting in elevated blood glucose levels.
Glucagon also aids in converting amino acids to glu
cose (gluconeogenesis). Glucagon is dependent on the
presence of glycogen for its action. It has essentially no
action in cases of starvation, adrenal insufciency, or
chronic hypoglycemia.
Uses
Glucagon is used to treat hypoglycemic reactions in
patients with diabetes mellitus.
Therapeutic Outcome
The primary therapeutic outcome expected from glu
cagon therapy is elimination of symptoms associated
with hypoglycemia.
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35
Nursing Implications for Glucagon
Premedication assessment
1. Conrm patient unresponsiveness before adminis
tration. If patient is conscious, oral antihypoglyce
mic therapy is usually more appropriate.
2. Hypoglycemia is a medical emergency. If suspected,
it should be treated by authorized personnel as soon
as possible.
Availability. Subcutaneous, IM, IV: 1mg vial. Prelled
syringe: 0.5 mg/0.1 mL, 1 mg/0.2 mL.
Intranasal: 3 mg/dose; one or two pack (Baqsimi)
Dosage and administration. Adult: Subcutaneous, IM,
IV: Administer 1 mg. Repeat in 15 minutes as needed.
Administer fastacting and longacting carbohydrates
to patient as soon as possible after response to treat
ment. If the patient is slow to arouse, consider admin
istering glucose by the IV route.
Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions
Key Points
• Diabetes mellitus is a complex group of chronic diseases
that is associated with both short- and long-term
complications. The long-term objective of control of the
disease must involve mechanisms to stop the progression
of the complications of the disease.
• Patient education and reinforcement are extremely
important to successful therapy. Major determinants
to success are the patient’s taking responsibility for a
balanced diet, insulin or oral hypoglycemic therapy, routine
exercise, and good hygiene.
• Medications used to control blood glucose include:
insulin (injection), sulfonylureas, meglitinides, biguanide
(metformin), thiazolidinediones (TZDs), alpha-glucosidase
inhibitors, dipeptidyl peptidase-4 (DPP-4) inhibitors, and
sodium-glucose cotransporter 2 (SGLT2) inhibitors (all oral
agents), and glucagon-like peptide-1 (GLP-1) agonists
(injection) known as antidiabetic agents, used to lower
blood glucose. Another class of medications known
as antihypoglycemic agents are used for patients with
hypoglycemia to elevate blood glucose.
• The nurse plays a critical role as a health educator by
discussing treatment options, planning lifestyle changes,
counseling before discharge, and reinforcing key points
during ofce visits. Best results are attained when the
patient, family, and nurse work together in developing the
care plan.
Additional Learning Resources
SG Go to your Study Guide for additional Review Ques-
tions for the NCLEX® Examination, Critical Thinking Clinical
Situations, and other learning activities to help you master this
chapter content.
593
Adults: Intranasal: 3 mg (one actuation) into a sin
gle nostril; if no response, may repeat in 15 minutes
using an intranasal device.
Common and serious adverse effects
Gastrointestinal
Nausea, vomiting. These adverse effects may also oc
cur with hypoglycemia. Take precautions to prevent
aspiration of vomitus.
Respiratory. For the intranasal glucagon, upper res
piratory system symptoms (e.g., rhinorrhea, nasal con
gestion, cough, and epistaxis, watery eyes, redness of
eyes, and itchy nose, throat and eyes) have occurred in
about 12% of patients.
Drug interactions
Warfarin. Glucagon may potentiate the anticoagu
lant effects of warfarin if used for several days. Monitor
the patient’s international normalized ratio (INR) and
reduce the dosage of warfarin accordingly.
Go to your Evolve website (https://evolve.elsevier.com/Willihn
ganz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX exam and include both NGN (Next Generation) and
traditional questions. See Chapter 1 for further information re-
garding question types.
Scenario
A patient with diabetes and renal disease is hospitalized for left
leg cellulitis requiring close monitoring with the current antibi-
otic therapy ordered.
1. The nurse is educating a patient newly diagnosed with diabetes on
how to manage dietary requirements and prevent hypoglycemia.
The nurse realizes the patient needs further teaching after they
make which statement?
1. “If I increase my carbohydrate intake, I will need to adjust
my daily insulin dose.”
2. “So as I understand it, when I increase my protein intake,
I can decrease my physical activity without affecting my
blood sugar.”
3. “When I take a beta blocker with insulin, it can cause my
blood sugar to drop.”
4. “If I take insulin and do not eat enough carbohydrates, I
could become hypoglycemic.”
Objective: Discuss the educational needs for patients with
complications from diabetes.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
2. After learning the symptoms of hypoglycemia and hyperglycemia
the nurse felt ready to teach the patient. Indicate with an X the
signs for hypoglycemia and hyperglycemia.
594 UNIT VII Drugs That Affect the Endocrine System

5. The nurse needs to discuss diabetic management with the patient

SIGNS OF SIGNS OF
in the scenario who has diabetes and renal disease and was
HYPOGLYCEMIA HYPERGLYCEMIA
hospitalized for left leg cellulitis. Indicate with an X the relevant
Abdominal pain issues needed for diabetic management and those that are not
Rapid, shallow relevant.
respirations
Cold, clammy skin RELEVANT FOR NOT RELEVANT FOR
DM MANAGEMENT DM MANAGEMENT
Sweating
Hunger Review of dietary
intake
Dizziness
Insulin
Weakness and blurred
administration
vision
review
Nausea and vomiting
Discussion of
Fruity odor to breath routine physical
Nervousness activities
Headache Assessment of
Rapid pulse bowel status
(tachycardia) Review of glucose
Apprehension control
Addressing patient
concerns regarding
Objective: Compare the signs, and symptoms of hypoglycemia and DM
hyperglycemia. Monitoring A1c
NCLEX item type: Matrix values
Cognitive skill: Recognize cues
Assessment of lung
3. The nurse is reviewing the types of insulin and identied which sounds
ones as the rapid-acting types? (Select all that apply.) Observing
1. Lispro for diabetic
2. Humulin R complications
3. Glargine Determining brand
4. Glulisine of self-monitoring
5. Aspart equipment
6. Fiasp
7. Detemir
8. Degludec Objective: Identify the major nursing considerations associated
9. Novolog R with the management of the patient with diabetes (e.g.,
nutritional evaluation, laboratory values, activity and exercise, and
Objective: Describe the action and use of insulin to control diabetes psychological considerations).
mellitus. NCLEX item type: Matrix
NCLEX item type: Extended multiple response Cognitive skill: Evaluate cues
Cognitive skill: Application

4. A patient asked the nurse how the antidiabetic drug miglitol works
to lower blood glucose. Which response by the nurse would be
appropriate?
1. “This medication works by stimulating the release of
insulin from beta cells in the pancreas.”
2. “Unfortunately, this medication works by an unknown
mechanism of action.”
3. “This is one of the antidiabetic agents that work by
increasing muscle and fat tissue sensitivity to allow more
glucose to enter the cell in the presence of insulin.”
4. “This medication works by affecting certain enzymes
used in the digestion of sugars, which results in delayed
glucose absorption.”
Objective: Discuss the action and use of oral hypoglycemic agents
to control diabetes mellitus.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
 Drugs Used to Treat Diabetes Mellitus CHAPTER 35 595

6. A patient newly diagnosed with diabetes asks the nurse how long 8. The nurse is educating the patient in the scenario who has diabetes
it takes for insulin to “kick in.” Which response by the nurse would and renal disease and was hospitalized for left leg cellulitis. After
be appropriate? the teaching, the patient was able to recognize which potential
1. “Depending on the type of insulin you receive, it can take complications for which they were susceptible? (Select all that apply.)
as long as 2 hours and as short as 5 minutes.” 1. Arthritis
2. “Insulin lasts as long as there is glucose circulating in 2. Myocardial infarction
your system.” 3. Hypertension
3. “The half-life of insulin is rather short, which is why you 4. Neuropathy
need to take it so frequently.” 5. Retinopathy
4. “Insulin is only effective when it is given before a meal and 6. Gastric ulcers
only lasts as long as it takes to digest the meal.” 7. Infections
Objective: Describe the action and use of insulin to control diabetes 8. Chronic obstructive pulmonary disease (COPD)
mellitus. 9. Seizures
NCLEX item type: Multiple choice 10. Peripheral vascular disease
Cognitive skill: Comprehension Objective: Discuss the educational needs for patients with
complications from diabetes.
7. A patient asked the nurse how the antidiabetic drug pioglitazone NCLEX item type: Extended multiple response
works to lower blood glucose. Which response by the nurse would Cognitive skill: Evaluate cues
be appropriate?
1. “This medication works by stimulating the release of
insulin from beta cells in the pancreas.”
2. “Unfortunately, this medication works by an unknown
mechanism of action.”
3. “This is one of the antidiabetic agents that work by
increasing muscle and fat tissue sensitivity to allow
more glucose to enter the cell in the presence of
insulin.”
4. “This medication works by affecting certain enzymes
used in the digestion of sugars, which results in delayed
glucose absorption.”
Objective: Discuss the action and use of oral hypoglycemic agents
to control diabetes mellitus.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
36 Drugs Used to Treat Thyroid Disease

https://evolve.elsevier.com/Willihnganz

Objectives
1. Describe the signs, symptoms, drugs, and nursing 3. Discuss the drug interactions associated with thyroid
interventions associated with hypothyroidism. hormones and antithyroid medicines.
2. Describe the signs, symptoms, drugs, and nursing
interventions associated with hyperthyroidism.

Key Terms
thyroid-stimulating hormone
(TSH) (THĪ-royd STĬM-yū-lā-tĭng
HŌR-mōn) (p. 596)
triiodothyronine (T3) (trī-ī-ō-dō-THĪ-
rō-nēn) (p. 596)
thyroxine (T4) (thī-RŎKS-ēn) (p. 596)
hypothyroidism (hī-pō-THĪ-royd-ĭzm)
(p. 596)
myxedema (mĭk-sĕ-DĒ-mă) (p. 596)
cretinism (KRĒ-tĭn-ĭzm) (p. 597)
hyperthyroidism (hī-pĕr-THĪ-royd-ĭzm)
(p. 597)
thyrotoxicosis (thī-rō-tŏk-sĭ-KŌ-sĭs)
(p. 597)

THYROID GLAND
The thyroid gland is a large, reddish, ductless gland
in front of and on either side of the trachea. It consists
of two lateral lobes and a connecting isthmus and is
roughly buttery shaped (Fig. 36.1). It is enclosed in
a covering of areolar connective tissue. The thyroid is
made up of numerous closed follicles containing col-
loid matter and is surrounded by a vascular network.
This gland is one of the most richly vascularized tis-
sues in the body. It can be palpated by placing ngers
on either side of the trachea and asking the patient to
swallow (Fig. 36.2).
As with other endocrine glands, thyroid gland func-
tion is regulated by the hypothalamus and the anterior
pituitary gland. The hypothalamus secretes thyrotropin-
releasing hormone (TRH), which stimulates the anterior
pituitary gland to release thyroid-stimulating hormone
(TSH). Thyroid-stimulating hormone stimulates the thy-
roid gland to release its hormones, triiodothyronine (T3)
and thyroxine (T4).
The thyroid hormones regulate general body me-
tabolism. Imbalance in thyroid hormone production
may also interfere with the following body functions:
growth and maturation; carbohydrate, protein, and
lipid metabolism; thermal regulation; cardiovascular
function; lactation; and reproduction.
THYROID DISEASES
Hypothyroidism is the result of inadequate thyroid hor-
mone production. The onset of symptoms is usually
596
mild and vague. Patients develop slowness in motion,
speech, and mental processes. They often develop more
lethargic, sedentary habits, and they have decreased
appetites, gain weight, are constipated, cannot tolerate
cold, become weak, and fatigue easily. Patients often
have decreased blood pressure and heart rate, have el-
evated cholesterol levels, and develop anemia. These
patients have an increased susceptibility to infection
and are sensitive to small doses of sedative-hypnot-
ics, anesthetics, and narcotics. The body temperature
may be subnormal; the skin becomes dry, coarse, and
thickened; and the face appears puffy. The term myx-
edema refers to the thickened, nonpitting edematous
changes to the soft tissues of patients in a hypothyroid
state. Hypothyroidism may be caused by loss of thy-
roid function from excessive use of antithyroid drugs
to treat hyperthyroidism, radiation exposure, thyroid
surgery, acute viral thyroiditis, or chronic thyroiditis.
A rare presentation of hypothyroidism is myxede-
ma coma. Myxedema coma is a severe form of hypo-
thyroidism that can occur as the culmination of severe,
long-standing hypothyroidism or be precipitated by
an acute event in a poorly controlled hypothyroid
patient, such as infection, myocardial infarction, cold
exposure, or the administration of sedative drugs, es-
pecially opioids. It is a medical emergency with a high
mortality rate. Fortunately, it is now a rare presenta-
tion of hypothyroidism.
Congenital hypothyroidism is a condition that af-
fects infants from the time of birth resulting from a par-
tial or complete loss of thyroid function. The historic
 Drugs Used to Treat Thyroid Disease CHAPTER 36
Larynx Thyroid gland
Trachea Isthmus
Thyroid lateral lobes
Clavicle
Sternocleidomastoid
muscle
Fig. 36.1 Location of the thyroid gland. (From Swartz MH. Textbook
of Physical Diagnosis: History and Examination. 7th ed. Philadelphia:
Elsevier; 2014.)
name of the resulting disorder is cretinism. Fortunately,
this disorder is becoming rare (1 case in 2000 to 4000
newborns) because most states require diagnostic test-
ing of the newborn for hypothyroidism.
Although the symptoms of hypothyroidism in both
infants and adults are for the most part classical, the -
nal diagnosis is usually not made until diagnostic tests
have been completed. These tests include determining
serum levels of circulating T3 and T4 hormones. If the
levels are low, the patient is considered to be hypothy-
roid. Further diagnostic testing is required to deter-
mine the cause of thyroid hypofunction.
Hyperthyroidism is caused by excess production of
thyroid hormones. Disorders that may cause hyper-
activity of the thyroid gland are Graves’ disease, nodu-
lar goiter, thyroiditis, thyroid carcinoma, overdoses of
thyroid hormones, and tumors of the pituitary gland.
The clinical manifestations of hyperthyroidism are
a rapid, bounding pulse (even during sleep), as well as
cardiac enlargement, palpitations, and dysrhythmias.
Patients are nervous and easily agitated. They develop
tremors, a low-grade fever, and weight loss, despite an in-
creased appetite. Hyperactive reexes and insomnia are
also usually present. Patients are intolerant of heat; the
skin is warm, ushed, and moist, with increased sweat-
ing; and edema of the tissues around the eyeballs produc-
es characteristic eye changes, including exophthalmos.
Patients develop amenorrhea; dyspnea with minor exer-
tion; hoarse, rapid speech; and an increased susceptibility
to infection. Elevated circulating thyroid hormone levels
easily diagnose hyperthyroidism. Further diagnostic
studies are required to determine the cause.
Excessive formation of thyroid hormones and
their secretion into the circulatory system causes hy-
perthyroidism, potentially leading to thyrotoxicosis.
Symptoms include increased metabolic rate, increased
pulse rate (to perhaps 140 beats/min), increased body
597
Fig. 36.2 Palpation of the thyroid gland. (From Thompson JM, Wilson
SF. Health Assessment for Nursing Practice. St. Louis: Mosby; 1996.)
temperature, restlessness, nervousness, anxiety, sweat-
ing, muscle weakness and tremors, and a sensation of
feeling too warm. This condition is treated with anti-
thyroid drugs or surgical removal of the thyroid gland.
TREATMENT OF THYROID DISEASES
The primary goal of therapy for hyperthyroidism and
hypothyroidism is to return the patient to a normal thy-
roid (euthyroid) state. Hypothyroidism can be treated
successfully by replacement of thyroid hormones (see
drug monographs on individual agents). After therapy
is initiated, the dosage of thyroid hormone is adjusted
until serum levels of the thyroid hormones are within
the normal range.
Three types of treatment can be used to reduce the
hyperthyroid state—subtotal thyroidectomy, radio-
active iodine, and antithyroid medications. Until treat-
ment is underway, the patient requires nutritional and
psychological support.
Life Span Considerations
Treatment of Hypothyroid State
During initial treatment of the hypothyroid state in the older
adult patient, be alert for and report increased frequency of
angina or symptoms of heart failure.
DRUG THERAPY FOR THYROID
DISEASES
Two general classes of drugs are used to treat thyroid
disorders: (1) those used to replace thyroid hormones in
patients whose thyroid glandular function is inadequate
to meet metabolic requirements (hypothyroidism); and
(2) antithyroid agents used to suppress synthesis of thy-
roid hormones (hyperthyroidism). Thyroid hormone
replacements available are levothyroxine (T4), liothy-
ronine (T3), liotrix, and thyroid USP. Antithyroid drugs
interfere with the formation or release of the hormones
produced by the thyroid gland. Antithyroid agents in-
clude iodine-131, propylthiouracil, and methimazole.
598 UNIT VII Drugs Affecting the Endocrine System
NURSING IMPLICATIONS FOR PATIENTS WITH
THYROID DISORDERS
Hypothyroidism and hyperthyroidism are treated pri-
marily on an outpatient basis unless surgery is indicat-
ed or complications occur. Nurses must be able to offer
guidance to the patients requiring treatment on an in-
patient or ambulatory basis. In general, body processes
are slowed with hypothyroidism and accelerated with
hyperthyroidism.
Assessment
Take a history of treatment prescribed for hypo-
thyroidism or hyperthyroidism (e.g., surgery, io-
dine-131, or hormone replacement). Ask for specic
information regarding treatment for any cardiac dis-
ease or adrenal insufciency.
Medications. Request a list of all prescribed and over-
the-counter medications being taken. Ask if any of the
prescribed medications are taken on a regular basis. If
not taken regularly, what factors have caused the pa-
tient to decrease administration?
Description of current symptoms. Ask the patient to
explain symptoms experienced and what changes in
functioning have occurred over the past 2 to 3 months.
Focused assessment. Perform a focused assessment
of the body systems generally affected by hypothyroid
or hyperthyroid states:
• Implement monitoring parameters and regular as-
sessments of vital signs, intake and output, daily
weights, and mental status checks.
• Cardiovascular: Take current vital signs, including
an apical pulse. Note bradycardia or tachycardia
and any alterations in rhythm and pulsations (e.g.,
bounding or thready), subnormal or elevated tem-
perature, and hypertension. Monitor for cardiac
symptoms (e.g., heart failure, dependent edema).
Ask whether the pulse rate is decreased or elevated
on awakening, before any stimulus. Does the pa-
tient experience any palpitations or a feeling that the
pulse is rapid and bounding? Record heart sounds
and any abnormal characteristics heard.
• Respiratory: Does the patient experience dyspnea? Is
it made worse by mild exertion?
• Gastrointestinal: Measure the person’s height and
weight. Check and record bowel sounds. Monitor
bowel patterns and give as-needed (PRN) medica-
tions prescribed for diarrhea or constipation. Ask
for a history of increase or decrease in weight over
the past 3 months. Has there been a change in ap-
petite? Does the individual experience nausea and
vomiting?
• Integumentary: Note the temperature, texture, and
condition of the skin and the characteristics of the
hair and nails. Does the patient complain of intoler-
ance to heat or cold?
• Musculoskeletal: What activity level is maintained?
Does the person feel or act sluggish or hyperactive?
Is the pattern of activity a change from the recent
past? If so, when did this become apparent? Is there
muscle weakness, wasting, or discomfort?
• Neurologic: What is the patient’s mental status—is
the patient oriented to time, date, and place? What
is the degree of alertness and pace of responsiveness
(e.g., sluggish and slow in contrast with being quick
or fast paced)? Is the individual depressed, stupor-
ous, or hyperactive? Has the individual or family
and signicant others noticed any change in per-
sonality in the recent past? Has the individual had
tremors of the hands, eyelids, or tongue? Has the
individual experienced insomnia?
• Sensory: What is the condition of the eyes? Do the
eyelids retract or is exophthalmos present?
• Reproductive: Obtain a history of changes in the pat-
tern of menses and libido.
• Immunologic: Has the individual had any recent in-
fections? What types of infections and at what fre-
quency has the patient had infections over the last
year?
Laboratory and diagnostic studies and surgery. Review
laboratory and diagnostic studies available on the pa-
tient’s record associated with thyroid disorders such as
total thyroxine (TT4) and total triiodothyronine (TT3)
tests, free thyroxine (FT4) and free triiodothyronine
(FT3) tests, TSH levels, TRH stimulation test, thyroid
autoantibodies, thyroglobulin, calcitonin assay, ultra-
sound, ne-needle biopsy, radioactive iodine uptake,
electrocardiography, and thyroid scan. If surgery is
scheduled for hyperthyroidism, schedule routine post-
operative vital signs and order a tracheostomy set for
the bedside. Indicate on care plan to check dressings
for bleeding, perform respiratory assessments, per-
form voice checks for hoarseness, and monitor for
development of tetany for the rst 24 to 48 hours, as
ordered by the healthcare provider.
Implementation
Environment
• For the hyperthyroid individual, plan to provide a
cool, quiet, structured environment because the pa-
tient lacks the ability to respond to change and anxi-
ety-producing situations and has intolerance to heat.
• For the hypothyroid individual, plan to provide a
warm, quiet, structured environment that supports
the patient’s needs. Provide support and give direc-
tions slowly and with patience because the individ-
ual may have difculty processing the information.
Incorporate the family into the provision of care, as
appropriate.
Nutrition
• Hyperthyroid: Order the prescribed diet, usually a
high-calorie diet of 4000 to 5000 calories per day
 Drugs Used to Treat Thyroid Disease CHAPTER 36
with balanced nutrients, and note no caffeine prod-
ucts (e.g., coffee, tea, colas). If diarrhea is present,
note any foods with a laxative or stimulating effect
such as bran products, fruits, and fresh vegetables.
• Hypothyroid: Order the prescribed diet, usually a
low-calorie diet with increased bulk to alleviate con-
stipation. Encourage adequate uid intake, unless
comorbidities prohibit it. Encourage the patient to
comply with dietary orders.
Psychosocial care
• Monitor the mental status at least every shift.
• Plan to incorporate the family into the health teach-
ing plan because the patient may be unable to un-
derstand or implement all facets of the therapeutic
regimen.
Activity and exercise. Note the prescribed level of
activity ordered by the healthcare provider. Institute
safety precautions for individuals with muscle weak-
ness, wasting, or pain that would place them at risk
for injury.
Medications. Give prescribed medications and moni-
tor for response to therapy. Thyroid medications usu-
ally are scheduled early in the day to prevent insomnia.
Patient Education
Medications
• Stress the need for lifelong administration of medi-
cations for the treatment of hypothyroidism and the
need for periodic laboratory studies and evaluation
by the healthcare provider.
• Stress that several medications interact with thyroid
drugs so it is important to inform any prescribing
healthcare provider of the thyroid disease and the
medications being taken.
• Patients scheduled for outpatient diagnostics must
receive detailed written instructions regarding the
prescribed medications to be taken in preparation
for testing.
• The patient and family or signicant others must
understand the anticipated therapeutic response
sought from prescribed medications. Teach specic
indications of a satisfactory response to pharmaco-
logic therapy. Stress the need to contact the health-
care provider if signs of an excess or decit in dos-
age occur. Ensure that the individual can monitor
their resting pulse.
Environment. Explain the need for a cool environment
for a patient with hyperthyroidism or a warm environ-
ment for the person with hypothyroidism.
Nutrition
• In patients with diarrhea secondary to hyperthy-
roidism, explain the need for a high-calorie diet
with reduced ber.
599
• Explain the need for a low-calorie diet with in-
creased ber to the individual with hypothyroid-
ism. Encourage patients with constipation to drink
8 to 10 eight-ounce glasses of water and add ber to
the diet each day.
• As the patient returns to a more normal thyroid
function through medication, the caloric require-
ments of the diet will also change.
Psychosocial. The patient may have had a major per-
sonality change, may be depressed, or (at the other end
of the spectrum) may be hyperactive. Explain these
symptoms to the family and involve them in exam-
ining potential interventions that can be used in the
home environment.
Activity and exercise
• Provide for patient safety during ambulation if
muscle weakness, wasting, or discomfort is pres-
ent. Discuss measures needed to provide for patient
safety with the family and signicant others.
• As the patient returns to a more normal thyroid
function through medication, the activity level
should change. Encourage moderate exercise.
Fostering health maintenance
• Throughout the course of treatment, discuss infor-
mation about the medication and how it will ben-
et the patient. Recognize that nonadherence with
lifelong treatment, when prescribed, may occur, and
stress positive outcomes that result from regular
medication adherence.
• Provide the patient and signicant others with
important information contained in the specic
drug monographs for the medications prescribed.
Additional health teaching and nursing interven-
tions for the common and serious adverse effects are
described in the drug monographs.
• Seek cooperation and understanding of the following
points so that medication adherence is increased: name
of medication; dosage, route, and times of administra-
tion; and common and serious adverse effects.
• When laboratory studies for thyroid function are
scheduled, thyroid preparations may be discontinued
for one or more days in advance of the tests. Always
consult the prescriber for detailed instructions.
Patient self-assessment. Enlist the patient’s aid in de-
veloping and maintaining a written record; see Patient
Self-Assessment Forms for Thyroid Medications
and Antithyroid Medications on the Evolve website.
Complete the Premedication Data column for use as
a baseline to track response to drug therapy. Ensure
that the patient understands how to use the form and
instruct the patient to bring the completed form to fol-
low-up visits. During follow-up visits, focus on issues
that will foster adherence with the therapeutic inter-
ventions prescribed.
600 UNIT VII Drugs Affecting the Endocrine System
DRUG CLASS: THYROID REPLACEMENT HORMONES
Actions
Thyroid hormones either are hormones extracted from
animal thyroid glands or are synthetically manufac-
tured to be equivalent to natural thyroid hormones.
Triiodothyronine and thyroxine are normally se-
creted from the properly functioning thyroid gland.
Thyroxine is partially metabolized to triiodothyronine,
so therapy with thyroxine provides physiologic re-
placement of both hormones.
Uses
The primary goal of thyroid hormone replacement ther-
apy is to return the patient to a normal thyroid (euthy-
roid) state. Several forms of thyroid hormone replace-
ment are available from natural and synthetic sources.
Synthetic levothyroxine (T4) is now considered the
drug of choice for hormone replacement in hypothy-
roidism. All the US Food and Drug Administration
(FDA)–approved brands of T4 are not bioequivalent;
there are subtle differences in their composition. The
bioavailability of a given brand at a given time after
ingestion might be different. This is why endocrinol-
ogists recommend that once a brand is started, the
patient should stick with the same brand. Changing
brands may change the dose slightly, which in turn
may change how the patient feels.
Liothyronine is a synthetic form of the natural thy-
roid hormone T3. Its onset of action is more rapid than
that of levothyroxine, and it is used occasionally as a
thyroid hormone replacement when prompt action
is necessary. It is not recommended for patients with
cardiovascular disease unless a rapid onset of activity
is deemed essential.
Liotrix is a synthetic mixture of levothyroxine and
liothyronine in a ratio of 4:1, respectively. A few en-
docrinologists prefer this combination because the
standardized content of the two hormones produces
consistent laboratory test results that are more in
agreement with the patient’s clinical response.
Thyroid USP (desiccated thyroid) is derived from
pig, cow, and sheep thyroid glands. Thyroid USP is the
oldest thyroid hormone replacement available and the
least expensive. Because of its lack of purity, uniformity,
and stability, however, it is generally not the drug of
choice for the initiation of thyroid replacement therapy.
Therapeutic Outcome
The primary therapeutic outcome expected from thy-
roid hormone replacement therapy is return of the pa-
tient to a euthyroid metabolic state.
Nursing Implications for Thyroid Hormone
Replacement Therapy
Premedication assessment
1. Record baseline vital signs, including apical pulse,
weight, and bowel elimination patterns, before
initiating therapy. Establish a once-daily schedule
in which these assessments are repeated. Assess
for patterns that may indicate early signs of hyper-
thyroidism (e.g., weight loss, nervousness, diapho-
resis, muscle cramps, palpitations, angina pectoris).
2. Ensure that laboratory studies (e.g., thyroid hor-
mone levels) have been completed before adminis-
tration of the medication.
Availability and dosage
See Table 36.1
Administration. Adult: PO: Therapy may be initiated
with low dosages of levothyroxine, such as 50 to 100 mcg
daily. Dosages are gradually increased over the next few
weeks to an average daily maintenance dosage of 100 to
200 mcg daily. The dose should be taken with water on
an empty stomach rst thing in the morning at least 30
minutes, but preferably 60 minutes before ingestion of
food. Another option is taking levothyroxine at bedtime
(3 hours after the evening meal or snack). Levothyroxine
should be the only medication taken at bedtime.
Medication Safety Alert
The age of the patient, severity of hypothyroidism, and other
concurrent medical conditions determine the initial dosage
and the interval of time necessary before increasing the
dosage. Hypothyroid patients are sensitive to replacement
of thyroid hormones. Monitor patients closely for adverse
effects.
Common and serious adverse effects
Endocrine
Signs of hyperthyroidism. Adverse effects of thyroid
replacement preparations are dose related and may oc-
cur 1 to 3 weeks after changes in therapy have been ini-
tiated. Symptoms of adverse effects are anxiety, weight
loss, abdominal cramping and diarrhea, tachycardia,
cardiac palpitations, dysrhythmias, angina pectoris, fe-
ver, and intolerance to heat. Symptoms may require a
reduction or discontinuation of therapy. Patients may
require up to a month without medication for toxic ef-
fects to fully dissipate. Therapy must be restarted at
lower dosages after symptoms have stopped.
Drug interactions
Warfarin. Patients with hypothyroidism require in-
creased dosage of anticoagulants. If thyroid replace-
ment therapy is initiated while the patient is receiving
warfarin therapy, the patient should have frequent
prothrombin time (international normalized ratio
[INR]) determinations and should be counseled to ob-
serve closely for the development of petechiae; ecchy-
moses; nosebleeds; bleeding gums; dark, tarry stools;
and bright red or coffee-ground emesis. The dosage of
warfarin may have to be reduced by one-third to one-
half over the next 1 to 4 weeks.
 Drugs Used to Treat Thyroid Disease CHAPTER 36 601

Table 36.1 Thyroid Hormones

GENERIC NAME BRAND NAME AVAILABILITY COMPOSITION DOSAGE RANGE
levothyroxine Synthroid Tablets/capsules: 13, 25, 50, 75, 88, 100, l-thyroxine (T4) PO: Initial: 12.5–
Do not confuse Tirosint 112, 125, 137, 150, 175, 200, 300 mcg; 50 mcg daily
levothyroxine Levoxyl Solution: 13, 25, 37.5, 44, 50, 62.5, 75, 88, Maintenance:
with Lanoxin or Do not 100, 112, 125, 137, 150, 175, 200 mcg/mL 100–200 mcg
leucovorin. confuse in 1 mL containers. daily
Levoxyl with Injection: 100, 200, 500 mcg/5-mL vials
Lanoxin 100, 200, 500 mcg/vial for reconstitution
liothyronine Cytomel Tablets: 5, 25, 50 mcg liothyronine (T3) PO: Initial: 5–25 mcg
daily
Maintenance: 25–75
mcg daily
– Injection: 10 mcg/mL in 1-mL vials IV: 25–50 mcg
Patients with known
or suspected
cardiovascular
disease: 10–20
mcg
thyroid USP Armour Tablets: 15, 16.25, 30, 32.5, 48.75, 60, 65, Unpredictable PO: Maintenance:
Thyroid 81.25, 90, 97.5, 113.75, 120, 130, 146.25, T4/T3 ratio 30–130 mg daily
162.5, 180, 195, 240, 260, 300, 325 mg
Do not confuse.

Digoxin. Patients with hypothyroidism require a de-
creased dosage of digoxin. If thyroid replacement ther-
apy is started while the patient is receiving digoxin, a
gradual increase in the digoxin will also be necessary
to maintain adequate therapeutic activity.
Estrogens. Patients who have no thyroid function
and who start estrogen therapy may require an in-
crease in dosage of the thyroid hormone. Estrogens
increase thyroid-binding globulin levels, which reduce
the level of circulating free T4. The total level of T4 is
normal or increased. Do not adjust the thyroid hor-
mone dosage until the patient shows clinical signs of
hypothyroidism.
Cholestyramine and calcium- or iron-containing prod-
ucts. To prevent binding of thyroid hormones by
cholestyramine and calcium- or iron-containing prod-
ucts administer doses at least 4 hours apart.
Hyperglycemia. Patients with diabetes should be
monitored for the development of hyperglycemia,
particularly during the early weeks of therapy. Assess
regularly for hyperglycemia or glycosuria and report
if it occurs with any frequency. Patients receiving oral
hypoglycemic agents or insulin may require an adjust-
ment in dosage.
DRUG CLASS: ANTITHYROID MEDICATIONS
Iodine is converted to iodide and stored in the thyroid
gland before reaching the circulation.
Iodine-131 (131I) is a radioactive isotope of iodine.
When administered, it is absorbed into the thyroid
gland in high concentrations. The liberated radioactive
isotope destroys the hyperactive thyroid tissue, with
essentially no damage to other tissues in the body.
Uses
Radioactive iodine is used most commonly for treating
hyperthyroidism in the following individuals: older
patients who are beyond the childbearing years, those
with severe complicating diseases (e.g., heart disease),
those with recurrent hyperthyroidism after previous
thyroid surgery, those who are poor surgical risks, and
those who have unusually small thyroid glands.
It often takes 3 to 6 months after a dose of radio-
active iodine to fully assess the benets gained. A
single dose is usually successful in treating hyperthy-
roidism, but a second or third dose may be necessary.
If more than one dose is required, an interval of at least
3 months between doses is necessary.
Therapeutic Outcome
The primary therapeutic outcome expected from radio-
active iodine is a return to a normal thyroid state.

Nursing Implications for Radioactive Iodine

iodine-131 (131I) (Ī ō-dīn WŬN THŬR-tē WŬN)
Actions
The synthesis of thyroid hormones and their mainte-
nance in the bloodstream in adequate amounts depend
on sufcient iodine intake through food and water.
Premedication assessment
1. Review policy for both institutional personnel and
patients regarding precautions, storage, handling, ad-
ministration, and disposal of radioactive substances.
2. Have all necessary supplies immediately available
in case of a spill.
602 UNIT VII Drugs Affecting the Endocrine System
3. Have all supplies needed according to institution-
al procedure to dispose of patient’s waste, such
as urine and feces, because it will be a radioactive
biohazard.
Availability. Each dose is prepared for an individual
patient by a nuclear pharmacy.
Administration. Administration of a radioactive iodine
preparation seems simple—it is given orally by capsule
or added to water and swallowed. It has no color or
taste. The radiation, however, is extremely dangerous.
• Minimize exposure as much as possible. Maintain
hazardous medication precautions according to the
institution’s policy. Wear latex gloves whenever ad-
ministering radioactive iodine or disposing of the
patient’s urine and feces.
• If the radioactive iodine or the patient’s urine or
feces spills, follow institutional policy. In general,
collect the clothing, bedding, bedpan, urinal, and
any other contaminated materials and place them in
special containers for radioactive waste disposal.
• Avoid spills! Report any accidental contamination
at once to the supervisor and follow directions for
the institution’s contamination cleanup technique,
and then complete an incident report.
Common and serious adverse effects
Gastrointestinal. Radioactive iodine may cause a
metallic taste in the mouth that can last a few days. If
nausea develops it usually subsides 1 or 2 days after
treatment. Radioactive iodine may also cause swollen
salivary glands that can last a few weeks.
Endocrine
Tenderness in the thyroid gland. Adverse effects include
radioactive thyroiditis, which causes tenderness over
the thyroid area and occurs during the rst few days or
few weeks after radioactive iodine therapy.
Hyperthyroidism. A return of symptoms of hyper-
thyroidism occurs in about 40% of patients who have
received one dose of radioactive iodine. Additional
doses may be required.
Hypothyroidism. Some patients who receive radio-
active iodine develop hypothyroidism, which requires
thyroid hormone replacement therapy.
Drug interactions
Lithium carbonate. Lithium and iodine may cause
synergistic hypothyroid activity. Concurrent use may
result in hypothyroidism. Monitor patients for both
hypothyroidism and bipolar disorder.
propylthiouracil (PRŌ-pĭl-thī-ō-YŪ-ră-sĭl)
Do not confuse propylthiouracil with Purinethol.
methimazole (mĕ-THĬM-ă-zōl)
Do not confuse methimazole with methazolamide.
Tapazole (TĂP-ă-zōl)
Actions
Propylthiouracil and methimazole are antithyroid
agents that act by blocking synthesis of T3 and T4 in
the thyroid gland. They do not destroy any T3 or T4
already produced, so there is usually a latent period of
a few days to 3 weeks before symptoms improve once
therapy has been started.
Uses
Propylthiouracil and methimazole may be used for
long-term treatment of hyperthyroidism or for short-
term treatment before subtotal thyroidectomy. Therapy
for long-term use is often continued for 1 to 2 years
to control symptoms. After discontinuation, some pa-
tients gradually return to the hyperthyroid state, and
antithyroid therapy must be reinitiated.
The FDA suggests that because of potential hepa-
totoxicity, it may be appropriate to reserve the use of
propylthiouracil for those who cannot tolerate other
treatments such as methimazole, radioactive iodine,
or surgery. In addition, because of the potential for
birth defects that have been observed with the use
of methimazole in pregnant women during the rst
trimester, propylthiouracil may be the treatment of
choice during and just before the rst trimester of
pregnancy.
Therapeutic Outcome
The primary therapeutic outcome expected from pro-
pylthiouracil or methimazole is a gradual return to
normal thyroid metabolic function.
Nursing Implications for Propylthiouracil and
Methimazole
Premedication assessment
1. Record baseline vital signs, weight, and bowel elim-
ination patterns before initiating therapy. Establish
an alternate-day schedule in which these assess-
ments are repeated. Assess for patterns that may
indicate early signs of hypothyroidism.
2. Ensure that laboratory studies (e.g., complete blood
count with differential; thyroid hormone, TSH,
blood urea nitrogen, serum creatinine, and liver en-
zyme levels) have been completed before adminis-
tering the medication.
Availability
Propylthiouracil. PO: 50-mg tablets.
Methimazole. PO: 5- and 10-mg tablets.
Dosage and administration
Propylthiouracil. Adult: PO: Initially, 100 to 150 mg
every 8 hours. Dosage ranges up to 900 mg daily.
The maintenance dosage is 50 mg two or three times
daily.
Methimazole. Adult: PO: Initially, 5 to 20 mg every 8
hours. Daily maintenance dosage is 5 to 15 mg.
 Drugs Used to Treat Thyroid Disease CHAPTER 36
Common and serious adverse effects
Integumentary
Purpuric maculopapular rash. The most common reac-
tion (in 5% of all patients) that occurs with propylthio-
uracil therapy is a purpuric maculopapular skin erup-
tion. This skin eruption often occurs during the rst 2
weeks of therapy and usually resolves spontaneously
without treatment. If pruritus becomes severe, a change
to methimazole and the use of short-term oral steroids
may be necessary. Cross-sensitivity is uncommon.
This adverse effect is usually mild and tends to re-
solve with continued therapy. Encourage the patient
not to discontinue therapy without rst consulting the
healthcare provider.
Immunologic
Bone marrow suppression, lymph node enlargement. Routine
laboratory studies (e.g., red blood cell, white blood cell,
and differential counts) should be scheduled. Stress the
importance of the patient’s returning for this laboratory
work. Monitor the patient for the development of a sore
throat, fever, purpura, jaundice, or excessive progressive
weakness.
Gastrointestinal
Hepatotoxicity. The symptoms of hepatotoxicity are
anorexia, nausea, vomiting, jaundice, hepatomegaly,
splenomegaly, and abnormal liver function (e.g., ele-
vated bilirubin, aspartate aminotransferase [AST], ala-
nine aminotransferase [ALT], gamma-glutamyl trans-
ferase [GTT], and alkaline phosphatase [ALP] levels;
increased INR).
Renal
Nephrotoxicity. Monitor urinalyses and kidney func-
tion tests for abnormal results. Report increased blood
603
urea nitrogen and creatinine levels, decreased urine
output or decreased specic gravity (despite amount of
uid intake), casts or protein in the urine, frank blood
or smoke-colored urine, or red blood cells in excess of 0
to 3 per high-power eld on the urinalysis report.
Other Adverse Effects
Headaches, salivary gland and lymph node enlargement,
loss of taste. These adverse effects are usually mild and
tend to resolve with continued therapy. Encourage the
patient not to discontinue therapy without rst con-
sulting the health care provider.
Drug interactions
Warfarin. Patients with hyperthyroidism require re-
duced dosage of anticoagulants. If antithyroid thera-
py is initiated while the patient is receiving warfarin
therapy, the patient should have frequent prothrombin
time (INR) determinations and be counseled to ob-
serve closely for the development of petechiae; ecchy-
moses; nosebleeds; bleeding gums; dark, tarry stools;
and bright red or coffee-ground emesis. The dosage of
warfarin may have to be increased over the next 1 to 4
weeks.
Digoxin. Patients with hyperthyroidism require an
increased dosage of digoxin. If antithyroid replace-
ment therapy is started while the patient is receiving
digoxin, a gradual reduction in the digoxin will be
necessary to prevent signs of toxicity. Monitor for the
development of digoxin toxicity.
604 UNIT VII Drugs Affecting the Endocrine System

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points 2. After the patient in the scenario was diagnosed with hypothyroidism
they were started on levothyroxine (Synthroid). The nurse
• Thyroid disease can be manifested as hyperthyroidism or was educating the patient on common adverse effects. Which
hypothyroidism, depending on the amount of circulating statement by the nurse needs to be corrected?
thyroid hormone. These are relatively common disorders
that are easily treated. 1. “Adverse effects from levothyroxine are dose related and
may occur in 1 to 3 weeks after starting therapy.”
• Most therapies for hypothyroidism require lifelong
2. “You may experience the effect of tachycardia, anxiety
treatment to maintain normal thyroid function.
and palpitations.”
• Nurses can play a signicant role in education and 3. “This is a normally occurring hormone, so it is safe to take
reinforcement of the treatment plan. Best results are and rarely has any side effects.”
attained when the patient, family, signicant others, and 4. “The dosage that you get will need to be gradually
nurse work together in reinforcing the care plan. increased so you do not get adverse effects.”
Additional Learning Resources Objective: Describe the signs, symptoms, drugs, and nursing
interventions associated with hypothyroidism.
SG Go to your Study Guide for additional Review Questions for NCLEX item type: Multiple choice
the NCLEX® Examination, Critical Thinking Clinical Situations, and Cognitive skill: Comprehension
other learning activities to help you master this chapter content.
3. The nurse was reviewing the signs and symptoms of
Go to your Evolve website (https://evolve.elsevier.com/Willihng hyperthyroidism. Which of the following symptoms would indicate
anz) for additional online resources. hyperthyroidism ? (Select all that apply.)
1. Tachycardia
Clinical Judgment and Next-Generation NCLEX® Exam- 2. Cold intolerance
ination-Style Questions The following questions are typical of 3. Palpitations
the NCLEX exam and include both NGN (Next Generation) and 4. Anxiousness
traditional questions. See Chapter 1 for further information re- 5. Weight gain
garding question types. 6. Bradycardia
7. Heat intolerance
Scenario 8. Sluggish, slow speech
A patient seen at the express clinic for sore throat mentioned Objective: Describe the signs, symptoms, drugs, and nursing
to the nurse that they were feeling run down and cold over the interventions associated with hyperthyroidism.
past few months and also noticed weight gain. The nurse sug- NCLEX item type: Extended multiple response
gested the patient get tested for hypothyroidism after noticing Cognitive skill: Recognize cues
a slow heart rate and slurred speech.
4. A patient with hyperthyroidism has been prescribed methimazole;
1. The patient in the scenario had which signs and symptoms of the nurse knows this works by which action?
hypothyroidism that alerted the nurse to the possible diagnosis? 1. Destroying T3 and T4
(Select all that apply.) 2. Converting iodine to active iodine
1. Tachycardia 3. Blocking synthesis of T3 and T4 in the thyroid gland
2. Cold intolerance 4. Synthesizing the hormone thyroxine
3. Palpitations Objective: Describe the signs, symptoms, drugs, and nursing
4. Anxiousness interventions associated with hyperthyroidism.
5. Weight gain NCLEX item type: Multiple choice
6. Bradycardia Cognitive skill: Understanding
7. Heat intolerance
8. Sluggish, slow speech
Objective: Describe the signs, symptoms, drugs, and nursing
interventions associated with hypothyroidism.
NCLEX item type: Extended multiple response
Cognitive skill: Recognize cues

5. The nurse is reviewing how a patient treated for hypothyroidism
with levothyroxine who is also being treated with warfarin for a
concurrent clinical condition requires careful management of
warfarin therapy to prevent bleeding. What does this management
include? (Select all that apply.)
1. Frequent INR checks
2. Increasing the dose of warfarin slowly over 1 to 4 weeks
3. Observing for nosebleeds and petechiae
4. Frequent assessment of TSH levels
5. Reducing the dose of warfarin slowly over 1 to 4 weeks
Objective: Discuss the drug interactions associated with thyroid
hormones and antithyroid medicines.
NCLEX item type: Multiple response
Cognitive skill: Application
Drugs Used to Treat Thyroid Disease CHAPTER 36 605
6. The nurse assesses a patient for thyroid enlargement associated
with hyperthyroidism by which method?
1. Palpate the throat and ask the patient to swallow.
2. Auscultate the throat and ask the patient to cough.
3. Palpate the throat and ask the patient to cough.
4. Auscultate the throat and ask the patient to swallow.
Objective: Describe the signs, symptoms, drugs, and nursing
interventions associated with hyperthyroidism.
NCLEX item type: Multiple choice
Cognitive skill: Understanding
37 Corticosteroids
https://evolve.elsevier.com/Willihnganz
Objectives
1. Discuss the normal actions of mineralocorticoids and
glucocorticoids in the body.
2. Identify the baseline assessments needed for a patient
receiving corticosteroids.
Key Terms
corticosteroids (kōrtĭkōSTĔR glucocorticoids (glūkōkŌRtĭ
ōydz) (p. 606) kōydz) (p. 606)
mineralocorticoids (mĭnĕrălōKŌR
tĭkōydz) (p. 606)
CORTICOSTEROIDS
Corticosteroids re horones secreted by the drenl
cortex of the drenl glnd s regulted by the pituitry
glnd. Corticosteroids re divided into two ctego-
ries, inerlocorticoids nd glucocorticoids, bsed on
structure nd biologic ctivity. The priry mineralo
corticoid is ldosterone, secreted by the drenl cortex
to ct on the kidneys to intin uid nd electrolyte
blnce. Fludrocortisone is the only coercilly
vilble inerlocorticoid nd is used to tret drenl
insufciency cused by hypopituitris (Addison dis-
ese). It stiultes the drenl glnds to regulte uid
nd electrolyte blnce through ction on the kidneys.
The glucocorticoids (e.g., cortisone, hydrocortisone,
prednisone) regulte crbohydrte, protein, nd ft
etbolis. Glucocorticoid therpy is used in the tret-
ent of  vriety of disorders becuse of its potent nti-
intory, ntillergenic, nd iunosuppressnt
ctivity. Exples of diseses treted with systeic
corticosteroids include systeic lupus erythetosus,
utoiune throbocytopeni purpur, gint cell r-
teritis, ultiple sclerosis, ulcertive colitis, nd Crohn
disese.
NURSING IMPLICATIONS FOR CORTICOSTEROID
THERAPY
Assessment
The iniu ssessent dt for  ptient receiv-
ing corticosteroids include bseline weight, blood
pressure, nd results of electrolyte nd glucose
studies. Monitoring ll spects of intke, output,
606
3. Discuss the clinical uses and potential adverse effects
associated with corticosteroids.
cortisol (KŌRtĭsōl) (p. 610)
diet, electrolyte blnce, nd stte of hydrtion is
iportnt to the long-ter success of corticosteroid
therpy. Although ny of the preters used for
ssessent initilly y be norl, it is iportnt
tht bseline vlues for these preters be estb-
lished so tht they y be used to onitor steroid
therpy.
• Ask the ptient to describe the current probles
tht initited this visit or dission.
• How long hve the syptos been present?
• Is this  recurrent proble? If so, how hs it been
treted?
• If n infectious process is suspected, deterine
when the ptient ws lst tested for tuberculosis.
History of pain experience. See equivlent subsection
under Assessent in the Nursing Iplictions for Pin
Mngeent section of Chpter 19 (Drugs Used for
Pin Mngeent).
Medication use. Obtin  detiled history of ll pre-
scribed nd over-the-counter edictions (including
herbl edicines). Ask if the ptient understnds why
ech is being tken. Ask speciclly whether cortico-
steroids hve been tken within the pst yer nd for
wht purpose. Tctfully deterine whether the pre-
scribed edictions re being tken regulrly nd if
not, why not.
Physical assessment
• Blood pressure: Tke  bseline blood pressure red-
ing in the sitting, lying, nd stnding positions.

Becuse ptients receiving corticosteroids ccu-
ulte uid nd gin weight, hypertension y
develop.
• Temperature: Record teperture dily nd oni-
tor ore frequently if elevted. Ptients receiving
corticosteroids re ore susceptible to infection,
nd fever is often n erly indictor of infection.
Glucocorticoids, however, soeties suppress  fe-
brile response to infection.
• Weight and fat distribution: Obtin the ptient’s
weight on dission nd use s  bseline in s-
sessing therpy. Becuse ptients receiving cortico-
steroids hve  tendency to ccuulte uid nd
gin weight, the dily weight is n iportnt tool in
ssessing ongoing therpy. Observe ny chnges in
the distribution of ft nd ny uscle wekness or
uscle wsting.
• Pulse: Record rte, qulity, nd rhyth of pulse.
• Heart and lung sounds: Nurses with dvnced skills
cn perfor usculttion to note chnges in hert
nd lung sounds. (Consult  edicl-surgicl nurs-
ing textbook for detils in perforing these ssess-
ents.) Lung elds re ssessed in  sitting posi-
tion to detect bnorl lung sounds (e.g., wheezes,
crckles, nd ccuultion of uid).
• Skin color: Note the color of the skin, ucous e-
brnes, tongue, erlobes, nd nil beds. Note in
prticulr the developent of  rsh or the develop-
ent of ecchyoses (bruises).
• Neck veins: Record ny jugulr vein distention. This
y be n indiction of uid overlod.
Neurologic
• Mental status: A ptient receiving  higher dosge
of corticosteroids is susceptible to psychotic be-
hviorl chnges. The ost susceptible ptient is
one with  previous history of entl dysfunction.
Perfor  bseline ssessent of the ptient’s bil-
ity to respond rtionlly to the environent nd
the dignosis of the underlying disese. Check for
orienttion to dte, tie, nd plce nd ssess for
level of confusion, restlessness, or irritbility. Mke
regulrly scheduled entl sttus evlutions nd
copre the ndings.
• Anxiety: Wht degree of pprehension is present?
Did stressful events precipitte the nxiety?
Status of hydration
• Dehydration: Assess nd record signicnt signs of
dehydrtion in the ptient. Observe for the following
signs: poor skin turgor, sticky orl ucous ebrnes,
 shrunken or deeply furrowed tongue, crusted lips,
weight loss, deteriorting vitl signs, soft or sunken
eyeblls, wek pedl pulses, delyed cpillry lling,
excessive thirst, high urine specic grvity (or no urine
output), nd possible entl confusion.
• Skin turgor: Check skin turgor by gently pinching the
skin together over the sternu, over the forehed,
Corticosteroids CHAPTER 37 607
or on the forer. In the well-hydrted ptient,
elsticity is present nd the skin rpidly returns to
 t position. With dehydrted ptients, the skin
reins pinched or peked nd returns very slowly
to the t, norl position.
• Oral mucous membranes: When dequtely hydrted,
the ebrnes of the outh feel sooth nd glis-
ten. When dehydrted, they re sticky nd pper
dull.
• Laboratory changes: The vlues of the hetocrit, he-
oglobin, blood ure nitrogen (BUN), nd electro-
lytes will pper to uctute bsed on the stte of
hydrtion. A dehydrted ptient will show higher
vlues s  result of heoconcentrtion. When 
ptient is overhydrted, the vlues pper to drop
becuse of heodilution.
• Overhydration: Incresed bdoinl girth nd in-
cresed circuference of the edil lleolus,
weight gin, nd neck vein engorgeent indicte
overhydrtion. Mesure the ptient’s bdoinl
girth dily t the ubilicl level. Mesure the ex-
treities bilterlly every dy, pproxitely 5 c
bove the edil lleolus.
• Edema: Is ede present? Where is it locted? Is it
pitting or nonpitting? It y be n indictor of uid
nd electrolyte iblnce.
Presence of ulcer disease. Ptients receiving cortico-
steroid therpy hve higher incidences of peptic ulcer
disese (PUD). Ask the ptient bout ny previous
tretent for n ulcer, hertburn, or stoch pin.
Periodic testing of stools for occult blood y be
ordered.
Laboratory tests
• Ptients tking corticosteroids re prticulrly sus-
ceptible to the developent of electrolyte ibl-
nce. Physiologiclly, corticosteroids cuse sodiu
retention (hyperntrei) nd potssiu excretion
(hypoklei); hyperglycei y be observed
with high-dose glucocorticoids.
• Ptients ost likely to develop electrolyte dis-
turbnces re those who, in ddition to receiving
corticosteroids, hve histories of renl or crdic
disese, horonl disorders, or ssive tru or
burns or re on diuretic therpy.
• Review lbortory tests nd report bnorl results
to the helthcre provider proptly. Tests y in-
clude seru electrolytes, especilly sodiu, po-
tssiu, clciu, nd gnesiu; rteril blood
gses; glucose; electrocrdiogrphy; chest x-ry ex-
intion; urinlysis nd kidney function; nd he-
odynic ssessent.
• Becuse the syptos of ost electrolyte ibl-
nces re siilr, the nurse should ssess chnges
in the ptient’s entl sttus (lertness, orienttion,
nd confusion), uscle strength, uscle crps,
treors, nuse, nd generl ppernce.
608 UNIT VII Drugs Affecting the Endocrine System
Nutrition. Obtin  history of the ptient’s diet. Ask
questions regrding ppetite nd the presence of nu-
se nd voiting. Anorexi, nuse, nd voiting re
erly indictions of corticosteroid insufciency.
Hyperglycemia. Corticosteroid therpy y induce
hyperglycei, prticulrly in ptients with predi-
betes or dibetes. All ptients ust be onitored for
the developent of hyperglycei, especilly during
the erly weeks of therpy. Assess regulrly for hyper-
glycei nd report bnorlities.
Activity and exercise. Ask questions to obtin infor-
tion bout the effect of exercise on the ptient’s
functioning:
• Is the person norlly sedentry, odertely c-
tive, or very ctive?
• Hs there been  reduction in ctivity level to cope
with ssocited ftigue or dyspne?
• Is the person perforing the ctivities of dily
living?
Implementation
Presence of illness. If n infectious disese process is
suspected nd tuberculosis testing is plnned, it should
be perfored before inititing corticosteroid therpy.
Medication use. Review prescription edictions nd
over-the-counter edictions (including herbl edi-
cines) being tken nd estblish whether they re be-
ing tken correctly. Anlyze nondherence issues nd
pln interventions with the ptient. Pln to review
drug dinistrtion s needed.
Medication administration
• Glucocorticoids y cuse hyperglycei, necessi-
tting the onitoring of blood glucose levels t p-
proprite intervls. If elevted, insulin therpy y
be required.
• During steroid replceent therpy, the din-
istrtion schedule for the replceent drugs
should iic the body’s norl circdin rhyth.
Therefore glucocorticoids ordered twice dily re
usully scheduled with two-thirds of the dose d-
inistered before 9 am (usully with brekfst) nd
one-third of the dose in the lte fternoon (usully
with dinner). Alternte-dy therpy is lso used in
soe cses to intin  ore norl body rhyth.
Minerlocorticoids re usully given once dily in
the evening.
• Steroid replceent therpy is grdully discon-
tinued in sll increents (tpered) to ensure tht
the ptient’s drenl glnds re ble to strt secret-
ing steroids ppropritely s the drug dosge is
reduced.
• Order edictions prescribed nd schedule these
on the ediction prole. Corticosteroids should be
scheduled to be tken with food. Perfor focused
ssessents to deterine effectiveness nd dverse
effects of phrcologic interventions. Monitor for
hyperglycei.
Neurologic. Pln for stress reduction eduction nd
discussion of effective ens of coping with stressful
events. Note the ptient’s entl sttus every shift.
• Perfor neurologic ssessent to deterine chng-
es in entl sttus.
• Del clly with n nxious ptient, offer expln-
tions of procedures being perfored, nd listen to
concerns nd intervene ppropritely.
Fluid volume status. Pln to onitor intke nd out-
put t intervls pproprite to the ptient’s condition.
Report intke tht exceeds output.
Nutrition. Exine the dietry history to deterine
whether referrl to  nutritionist would help the p-
tient understnd the diet regien. Pln interventions
needed to del with dietry nondherence.
Schedule eetings with the nutritionist to lern
how to nge specic dietry odictions pre-
scribed (e.g.,  low-sodiu, high-potssiu diet with
weight reduction preters for obese ptients). If
possible, instruct the ptient to prctice food selections
fro the dily enus while still in the hospitl. Tech
the ptient which foods re low in sodiu nd high in
potssiu. Potssiu restrictions y be indicted if
the ptient is tking  potssiu-spring diuretic. Slt
substitutes re high in potssiu; therefore use ust
be liited.
Pain management. When pin is present, cofort
esures ust be ipleented to llow the ptient to
decrese the pin. Ftigue y increse pin percep-
tion; spcing ctivities so tht ftigue does not occur is
recoended.
Vital signs and status of hydration
• Monitor vitl signs nd perfor focused ssessent
of hert, respirtory, nd hydrtion sttus t speci-
ed intervls.
• Perfor dily weights using the se scle, in
clothing of pproxitely the se weight, nd
t the se tie, usully before brekfst. Record
nd report signicnt weight chnges. (Weight
gins nd losses re the best indictors of u-
id gin or loss.) As pproprite to the ptient’s
condition, obtin nd record bdoinl girth
esureents.
• When uid restrictions re prescribed, hlf of the
uids re generlly given with els. The other hlf
is given on  per-shift bsis.
• Monitor the rte of intrvenous (IV) infusions cre-
fully; contct the helthcre provider regrding the
concentrtion of dixtures of drugs to the IV infu-
sion solution when liited uids re indicted.

Laboratory tests. Check for nd report bnorl
lbortory vlues (e.g., hypoklei, hyperklei,
hypoglycei, hyperglycei, hypontrei, hyper-
ntrei), depending on the underlying disese
pthology.
Patient Education
Contact with healthcare provider
• Assess the ptient’s understnding of syptos
tht should be reported to the helthcre provider:
dyspne; productive cough; worsening ftigue;
ede in the feet, nkles, or legs; weight gin; or
developent of ngin (chest pin), plpittions, or
confusion.
• Instruct the ptient to perfor dily weights using
the se scle, in clothing pproxitely the se
weight, nd t the se tie of dy, usully before
brekfst. Record nd report signicnt weight
chnges; weight gins nd losses re the best indic-
tors of uid gin or loss. Usully,  gin of 2 pounds
in 2 dys should be reported.
Skin care. Tech pproprite skin cre nd the need to
chnge position t lest every 2 hours, especilly when
ede is present. Hve the ptient inspect the nkles,
feet, nd bdoen for ede dily. If the ptient is
using  recliner or bed, the scrl re should lso be
checked regulrly for ede.
Coping with stress
• Ptients receiving high doses of corticosteroids do
not tolerte stress well. Ptients should be instruct-
ed to notify the helthcre provider before exposure
to dditionl stress, such s dentl procedures. If
 ptient sustins n ccidentl injury or sudden
eotionl stress, the ttending helthcre provider
should be told tht the ptient is receiving steroid
therpy. An dditionl steroid dose y be needed
to support the ptient through  stressful sitution.
• Explore the echniss tht the person uses to cope
with stress. Discuss how the ptient is dpting to
the needed lifestyle chnges to nge the disese
process. Address depression issues, if present.
Avoidance of infections. Advise the ptient to void
crowds or people known to hve infections. Report
even inor signs of n infection (e.g., generl -
lise, sore throt, low-grde fever) to the helthcre
provider.
Nutritional status
• Assist the ptient in developing  specic sched-
ule for spcing dily uid intke nd plnning so-
diu restrictions, s prescribed by the helthcre
provider.
• If weight gin is  specic proble (not relted to
uid ccuultion), pln for clorie restrictions nd
spcing of dily intke.
Corticosteroids CHAPTER 37 609
• If  high-potssiu diet is prescribed, help the p-
tient becoe filir with foods tht should be con-
sued. Tech the signs nd syptos of potssiu
deciency or excess, depending on edictions
prescribed.
• Further dietry needs y include increses in vit-
in D nd clciu.
• Fluid restrictions y be iposed; discuss specic
wys to nge these liittions.
Activity and exercise
• Prticiption in regulr exercise is essentil. The
ptient y resue ctivities of dily living with-
in the boundries set by the helthcre provider.
Encourge ctivities such s regulr nd oderte
exercise, el preprtion, resuption of usul sex-
ul ctivity, nd socil interctions. Help the ptient
pln for pproprite ltertions, depending on the
disese process nd degree of ipirent.
• Encourge weight-bering esures to prevent
clciu loss. Active nd pssive rnge-of-otion
exercises intin obility nd joint nd uscle
integrity.
• Individuls unble to ttin the degree of ctiv-
ity nticipted s  result of drug therpy y
becoe frustrted. Allow for verbliztion of feel-
ings nd then ipleent ctions pproprite to the
circustnces.
Fostering health maintenance
• Throughout the course of tretent, discuss edi-
ction infortion nd how the ediction will
benet the ptient.
• Drug therpy is one coponent of the tretent
of illnesses for which steroids re prescribed; it is
criticl tht the edictions be tken s prescribed.
Ensure tht the ptient understnds the entire ed-
iction regien, including the iportnce of not
djusting the dosge without helthcre provider
pprovl. If corticosteroid therpy is to be discon-
tinued,  tpering schedule is used. Stress the i-
portnce of not withdrwing the prescribed edic-
tion suddenly.
• Ptients on steroid therpy should crry identic-
tion crds or  brcelet with the ne of the helth-
cre provider to contct in n eergency, s well
s the drug ne, dosge, nd frequency of use.
Ephsize situtions requiring helthcre provid-
er consulttion for drug dosge djustents (e.g.,
stress, dentl procedures, infection).
• Provide the ptient nd signicnt others with
the iportnt infortion contined in the spe-
cic drug onogrphs for the drugs prescribed.
Additionl helth teching nd nursing interven-
tions for coon nd serious dverse effects re in
ech drug onogrph.
• Seek the ptient’s coopertion nd understnd-
ing of the following points to increse ediction
610 UNIT VII Drugs Affecting the Endocrine System
dherence: ne of ediction; dosge, route, nd
ties of dinistrtion; nd coon nd serious
dverse effects.
Patient self-assessment. Enlist the ptient’s help in de-
veloping nd intining  written record of onitoring
preters (e.g., pulse rte, blood pressure, body weight,
ede, exercise tolernce, pin relief). See the Ptient Self-
Assessent For for Corticosteroids on the Evolve web-
site. Coplete the Preediction Dt colun for use s
 bseline to trck response to drug therpy. Ensure tht
the ptient understnds how to use the for nd instruct
the ptient to tke this written record to follow-up visits.
During follow-up visits, focus on issues tht will foster
dherence with the therpeutic interventions prescribed.
DRUG CLASS: MINERALOCORTICOID
udrocortisone (ū-drō-KŌR-tĭ-sōn)
Actions
Fludrocortisone is n drenl corticosteroid with po-
tent inerlocorticoid nd glucocorticoid effects. It
ffects uid nd electrolyte blnce by cting on the
distl renl tubules, cusing sodiu nd wter reten-
tion nd potssiu nd hydrogen excretion.
Uses
Fludrocortisone is used in cobintion with gluco-
corticoids to replce inerlocorticoid ctivity in p-
tients who suffer fro drenocorticl insufciency
(Addison disese) nd to tret slt-losing drenogeni-
tl syndroe.
Therapeutic Outcomes
The priry therpeutic outcoes expected fro
udrocortisone therpy re s follows.
1. Control of blood pressure
2. Restortion of uid nd electrolyte blnce
Nursing Implications for Fludrocortisone
Premedication assessment
1. Check the electrolyte reports for erly indictions of
electrolyte iblnce.
2. Keep ccurte records of intke nd output, dily
weights, nd vitl signs.
3. Ask the ptient bout ny signs of infection (e.g.,
sore throt, fever, lise, nuse, voiting).
Corticosteroid therpy cn sk syptos of
infection.
4. Perfor  bseline ssessent of the ptient’s de-
gree of lertness; orienttion to ne, plce, nd
tie; nd rtionlity of responses.
5. Ask the ptient bout previous tretent for n ul-
cer, hertburn, or stoch pin. Testing stools for
occult blood should be done periodiclly.
Availability. PO: 0.1-g tblets.
Dosage and administration. Adult: PO: 0.1 g dily.
Dosge y be djusted s needed. Cortisone or hy-
drocortisone re lso usully dinistered to provide
dditionl glucocorticoid effect. Fludrocortisone pro-
duces rked sodiu retention nd potssiu deple-
tion, which could led to high blood pressure.
Common and serious adverse effects and drug inter-
actions. See equivlent sections under Drug Clss:
Glucocorticoids.
DRUG CLASS: GLUCOCORTICOIDS
Actions
The jor glucocorticoid of the drenl cortex is cor
tisol. The hypothlic-pituitry xis regultes the
secretion of cortisol by incresing or decresing the
output of corticotropin-relesing fctor (CRF) fro
the hypothlus. Corticotropin-relesing fctor
stiultes the relese of drenocorticotropic horone
(ACTH) fro the pituitry glnd; ACTH then stiu-
ltes the drenl cortex to secrete cortisol. As seru
levels of cortisol increse, the ount of CRF secreted
by the hypothlus is decresed, resulting in diin-
ished secretion of cortisol fro the drenl cortex.
Uses
Glucocorticoids re usully given becuse of their nti-
intory nd ntillergenic properties. They do
not cure disese, but they relieve the syptos of tis-
sue intion. When glucocorticoids re used to
control rheutoid rthritis, sypto relief is noted
within  few dys. Joint nd uscle stiffness, uscle
tenderness nd wekness, joint swelling, nd sore-
ness re signicntly reduced; however, it is iportnt
to ssess the ptient’s predrug ctivity level becuse
pin relief y led to overuse of the disesed joints.
Appetite, weight, nd energy levels re incresed; fe-
ver is reduced; nd sedienttion rtes re reduced or
return to norl. Antoic chnges nd joint defor-
ities lredy present rein unchnged. Syptos
usully return shortly fter glucocorticoid withdrwl.
Glucocorticoids re lso effective for iunosup-
pression in the tretent of certin cncers, orgn
trnsplnttion, nd utoiune diseses (e.g., lupus
erythetosus, dertoyositis, rheutoid rthritis);
relief of llergic nifesttions (e.g., seru sickness,
severe hy fever, sttus sthticus); nd tretent of
shock. They lso y be used to tret nuse nd voit-
ing secondry to cheotherpy (see Chpter 33).
Therapeutic Outcomes
The priry therpeutic outcoes expected fro gluco-
corticoid therpy re s follows:
1. Reduced pin nd intion
2. Miniized shock syndroe nd fster recovery
 Corticosteroids CHAPTER 37 611

Table 37.1 Topical and Systemic Corticosteroid Preparations a

GENERIC NAME BRAND NAME DOSAGE FORMS
alclometasone – Cream, ointment
amcinonide – Cream, ointment, lotion
betamethasone Celestone Soluspan, Diprolene, Injection, cream, ointment, lotion, emulsion,
Diprolene AF, Luxiq, Sernivo gel, foam
budesonide Entocort EC, Ortikos, Uceris Oral extended-release capsule and tablet,
rectal foam
clobetasol Temovate, Clobex, Olux Cream, ointment, solution, scalp shampoo,
lotion, gel, foam
clocortolone Cloderm Cream
cortisone – Tablets
desonide DesOwen, Verdeso, Desonate Cream, ointment, lotion, foam, gel
desoximetasone Topicort Cream, ointment, gel, liquid spray
dexamethasone Decadron, TopiDex Injection, tablets, elixir, solution, concentrated
solution
diorasone ApexiCon E, Psorcon Cream, ointment
udrocortisone – Tablets
uocinolone Capex, Derma-Smoothe/FS, Synalar Cream, ointment, solution, shampoo, oil
uocinonide Vanos Cream, ointment, gel, solution
Do not confuse uocinonide
with uorouracil.
urandrenolide Cordran, Nolix Cream, ointment, tape, lotion
uticasone Cutivate Cream, ointment, lotion
halcinonide Halog Cream, ointment, solution
halobetasol Ultravate, Lexette Cream, ointment, lotion, foam
hydrocortisone Alkindi Sprinkle, Cortef Cream, ointment, tablets, enema, lotion,
Do not confuse hydrocortisone Do not confuse Cortef with Lortab. solution, suppositories, foam, injection,
with hydralazine or hydrocodone. Solu-Cortef, Hydrocortone capsule sprinkle
methylprednisolone Solu-Medrol, Depo-Medrol, Medrol Tablets, injection
Do not confuse methylprednisolone
with medroxyprogesterone.
mometasone – Cream, ointment, solution
prednicarbate – Ointment
prednisolone Veripred 20, Pediapred Tablets, solution, disintegrating tablets
prednisone Tablets, solution, liquid concentrate
Do not confuse prednisone with Rayos Delayed-release tablets
potassium, Prilosec, primidone,
or pseudoephedrine.
triamcinolone Kenalog, Triderm, Trianex Cream, ointment, lotion, injection, aerosol, paste
aForinformation on ophthalmic corticosteroid products, see Chapter 42; for information on nasal inhalation corticosteroid products, see Chapter 29; for information on
Chapter 30
Do not confuse.

3. Reduced nuse nd voiting ssocited with
cheotherpy
Nursing Implications for Glucocorticoids
Premedication assessment
1. Check the electrolyte nd glucose reports for erly in-
dictions of electrolyte iblnce or hyperglycei.
2. Keep ccurte records of intke nd output, dily
weights, nd vitl signs.
3. Ask the ptient bout ny signs of infection (e.g., sore
throt, fever, lise, nuse, voiting). Corticosteroid
therpy cn sk syptos of infection.
4. Perfor  bseline ssessent of the ptient’s de-
gree of lertness; orienttion to ne, plce, nd
tie; nd rtionlity of responses.
5. Ask the ptient bout previous tretent for n ul-
cer, hertburn, or stoch pin. Testing stools for
occult blood should be done periodiclly.
Availability, dosage, and administration
See Tble 37.1
When  therpeutic dosge is dinistered for 3
weeks or longer, it ust be ssued tht the internl
production of corticosteroids is suppressed. Generl
612 UNIT VII Drugs Affecting the Endocrine System
guidelines re tht if  ptient hs received prednisone
2 g/kg/dy or less, or 20 g/dy for 21 dys or less,
the ptient does not need to be tpered off the cortico-
steroid. Abrupt discontinution of glucocorticoids y
result in drenl insufciency if higher dosges re
being received. Therpy should be withdrwn grdu-
lly (often clled  steroid taper). The tie required to
decrese glucocorticoids depends on the durtion of
tretent, dosge ount, ode of dinistrtion,
nd glucocorticoid being used.
• Abrupt discontinuation: Ptients who hve received
corticosteroids for t lest 3 weeks ust not brupt-
ly discontinue therpy. Syptos of brupt discon-
tinution include fever, lise, ftigue, wekness,
norexi, nuse, orthosttic dizziness, hypoten-
sion, finting, dyspne, hypoglycei, uscle nd
joint pin, nd possible excerbtion of the disese
process.
• Application: Topicl corticosteroids re pplied s
directed by the nufcturer. Specic instructions
regrding use of n occlusive dressing should be
clried before ppliction.
• Alternate-day therapy: Alternte-dy therpy y be
used to tret chronic conditions. Corticosteroids re
usully given between 6 nd 9 am on lternte dys
to iniize suppression of norl drenl func-
tion. Adinister with els to iniize gstric
irrittion.
• Pediatric patients: The correct dosge for  child is
usully bsed on the disese being treted rther
thn the ptient’s weight. Monitoring of skeletl
growth y be required in children if prolonged
therpy is required.
Medication Safety Alert
Glucocorticoids are potent agents that produce many unde-
sirable adverse effects as well as therapeutic benets. Unless
immediate life-threatening conditions exist, other therapeutic
methods should be exhausted before corticosteroid therapy
is initiated. Many of the adverse effects of the steroids are
related to dosage and duration of therapy. These drugs must
be used with caution in patients with diabetes mellitus, heart
failure, hypertension, peptic ulcer disease, mental distur-
bance, immunocompromise, and suspected infections.
Common and serious adverse effects
Fluid and electrolyte disturbances
Electrolyte imbalance, uid accumulation. The electro-
lytes ost coonly ltered re potssiu (K+), so-
diu (N+), nd chloride (Cl−). Hypoklei is ost
likely to occur. Mny syptos ssocited with l-
tered uid nd electrolyte blnce re subtle nd in-
terspersed with generl syptos of drug toxicity or
the disese process itself. Obtin dt bout chnges
in the ptient’s entl sttus (lertness, orienttion,
nd confusion), uscle strength, uscle crps, tre-
ors, nuse, nd generl ppernce (drowsy, nxious,
or lethrgic). Alwys check the electrolyte reports for
erly indictions of electrolyte iblnce. Keep ccu-
rte records of intke nd output, dily weights, blood
glucose, nd vitl signs.
Immune system
Susceptibility to infection. Alwys question the ptient
before initition of therpy bout ny signs nd syp-
tos of possible infection. Corticosteroid therpy often
sks syptos of infection. Monitor the ptient for
signs of infection, such s sore throt, fever, lise,
nuse, nd voiting. Encourge the ptient to void
exposure to infections.
Psychological
Behavioral changes. Psychotic behviors re ore
likely to occur in ptients with previous histories of
entl instbility. Perfor  bseline ssessent of
the ptient’s degree of lertness; orienttion to ne,
plce, nd tie; nd rtionlity of responses before ini-
titing therpy. Mke regulrly scheduled entl st-
tus evlutions, nd copre the ndings. Report the
developent of ltertions.
Metabolic
Hyperglycemia. Ptients with predibetes or dibetes
ust be onitored for the developent of hyperglyce-
i, prticulrly during erly weeks of therpy. Assess
regulrly for hyperglycei nd report ny bnorl
ndings. Ptients receiving orl hypoglyceic gents
or insulin y require n djustent in dosge.
Gastrointestinal
Peptic ulcer formation. Before inititing therpy, sk
the ptient bout ny previous tretent for n ulcer,
hertburn, or stoch pin. Periodic testing of stools
for occult blood y be ordered. Antcids y lso be
recoended by the prescribing helthcre provider
to iniize gstric syptos.
Integumentary
Delayed wound healing. Ptients who hve recently hd
surgery ust hve their surgicl sites onitored closely
for signs of dehiscence (the edges of  surgicl incision
tht strt to open, pull prt, or seprte). Tech surgi-
cl ptients to splint the wounds while coughing nd
brething deeply. Inspect surgicl sites nd report stte-
ents such s, “When I coughed, I felt soething pop.”
Sensory
Visual disturbances. Visul disturbnces noted by
ptients on long-ter therpy ust be reported.
Glucocorticoid therpy y produce ctrcts.
Musculoskeletal
Osteoporosis. Long-ter glucocorticoid therpy y
produce osteoporosis.
Drug interactions
Diuretics (e.g., furosemide, bumetanide, thiazides).
Corticosteroids y enhnce the loss of potssiu.
Check potssiu levels nd onitor the ptient ore
closely for hypoklei when these gents re used
concurrently. Mny syptos of ltered uid nd
electrolyte blnce re subtle nd interspersed with
generl syptos of drug toxicity or the disese pro-
cess itself.

Gther dt bout chnges in the ptient’s entl
sttus (lertness, orienttion, nd confusion), uscle
strength, uscle crps, treors, nuse, nd generl
ppernce (drowsy, nxious, nd lethrgic). Alwys
check the electrolyte reports for erly indictions of
electrolyte iblnce. Keep ccurte records of intke
nd output, dily weights, nd vitl signs.
Warfarin. Steroids y enhnce or decrese the
nticogulnt effects of wrfrin. Observe for the de-
velopent of petechie; ecchyoses; nosebleeds;
bleeding gus; drk, trry stools; nd bright red or
coffee-ground eesis. Monitor the prothrobin tie
(interntionl norlized rtio) nd djust the dos-
ge of wrfrin if necessry. Becuse of the ulcerogenic
Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions
Key Points
• Corticosteroids are potent agents that produce many
therapeutic benets, as well as undesirable adverse effects.
• Many of the adverse effects of the steroids are related
to dosage and duration of therapy. These drugs must
be used with caution in patients with diabetes mellitus,
heart failure, hypertension, peptic ulcer disease, mental
disturbance, and suspected infections.
• Nurses can play a signicant role in helping patients
monitor therapy and can assist them in seeking medical
attention at the earliest signs of impending trouble.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX exam and include both NGN (Next Generation) and
traditional questions. See Chapter 1 for further information re-
garding question types.
Scenario
A patient with known Addison disease called the nurse line to
report recent stomach pain along with nausea. The nurse was
concerned that the patient may be developing an ulcer.
1. The patient in the scenario has been taking udrocortisone a
mineralocorticoid to treat Addison disease. The nurse reviewed
the effects of mineralocorticoids which include which of the
following? (Select all that apply.)
1. Regulation of serum glucose levels
2. Maintenance of electrolyte balance
Corticosteroids CHAPTER 37 613
potentil of steroids, close observtion of ptients tk-
ing nticogulnts is necessry to reduce the possibil-
ity of heorrhge.
Hyperglycemia. Ptients with predibetes or dibetes
ust be onitored for the developent of hypergly-
cei, prticulrly during the erly weeks of therpy.
Assess regulrly for hyperglycei nd report ny
frequent occurrences. Ptients receiving orl hypogly-
ceic gents or insulin y require n djustent in
dosge.
Rifampin. Rifpin y enhnce the etbolis
of corticosteroids, thus reducing therpeutic effect.
Monitor for diinished therpeutic effect nd increse
the corticosteroid dose if necessry.
3. Action on the distal tubules of the kidneys to retain
water
4. Regulation of body temperature
5. Treatment of salt-wasting adrenogenital syndrome
Objective: Discuss the normal actions of mineralocorticoids and
glucocorticoids in the body.
NCLEX item type: Multiple response
Cognitive skill: Application
2. The nurse is discussing with the patient in the scenario the
difference between mineralocorticoids and glucocorticoids. The
nurse pointed out that glucocorticoids regulate carbohydrate,
protein, and fat metabolism and are used in medicine because
they have which of the following properties? (Select all that
apply.)
1. Antiinammatory
2. Anticoagulant
3. Antiallergenic
4. Antihypertensive
5. Antiseizures
6. Antipsychotic
7. Antiemetic
Objective: Discuss the normal actions of mineralocorticoids and
glucocorticoids in the body.
NCLEX item type: Extended multiple choice
Cognitive skill: Recognize cues
3. The nurse is explaining to the patient the reason for corticosteroids
to be prescribed for rheumatoid arthritis. During the teach-back
session, which response by the patient indicates that further
teaching is needed?
1. “I know that I can’t overdo activity, even though I may be
feeling less pain with the prednisone.”
2. “When I take this drug, I can gain water weight, so I need
to weigh myself every day.”
3. “I should let my doctor know if I get a sore throat, fever,
and start to feel crummy.”
4. “I know that this drug will cure my arthritis.”
614 UNIT VII Drugs Affecting the Endocrine System

Objective: Discuss the clinical uses and potential adverse effects 5. Choose the most likely options for the information missing from
associated with corticosteroids. the sentence by selecting from the lists of options provided.
NCLEX item type: Multiple choice
Cognitive skill: Understanding The nurse recognizes that corticosteroids can be used
for ________1__________ and ________1__________
4. The nurse is assessing a patient who is being started on a and __________1_________, but needs to be alert for
corticosteroid. The nurse should ask the patient if there is any adverse effects such as _________2___________ and
history of which disorder? ________2_________ and ________2_________.
1. Gastric ulcers
2. Blood dyscrasias
3. Heart disease OPTION 1 OPTION 2
4. Respiratory disease Lupus erythematosus Bradycardia
Objective: Identify the baseline assessments needed for a patient Anxiety and depression Hyperglycemia
receiving corticosteroids. Rheumatoid arthritis Hypoglycemia
NCLEX item type: Multiple choice
Organ transplantation Osteoporosis
Cognitive skill: Comprehension
Status epilepticus Hypokalemia

Objective: Discuss the clinical uses and potential adverse effects

associated with corticosteroids.
NCLEX item type: Cloze
Cognitive skill: Analyze cues
Gonadal Hormones
Objectives
1. Identify the uses of estrogens and progestins.
Key Terms
gonads (GŌ-nădz) (p. 615) androgens (ĂN-drō-jĕnz) (p. 615)
testosterone (tĕs-TŎS-tĕr-ōn) (p. 615) ovaries (Ō-văr-ēz) (p. 615)
THE GONADS AND GONADAL
HORMONES
The gonads are the reproductive glands: the ovaries of
the female and testicles of the male.
The ovaries produce eggs needed for reproduc-
tion, and the hormones estrogen and progesterone.
These hormones stimulate maturation of the female
sex organs. They inuence breast development, voice
intonation, and the broader pelvis of the female body
form. Menstruation is established because of hormone
production of the ovaries and action on the uterus.
Estrogen is responsible for most of these changes.
Progesterone is thought to be associated mainly with
body changes that favor the implantation of the fer-
tilized ovum, continuation of pregnancy, and prepara-
tion of the breasts for lactation.
The testicles produce androgens, primarily testos-
terone, the male sex hormone, as well as sperm neces-
sary for egg fertilization for reproduction. Testosterone
controls the development of the male sex organs and
inuences characteristics such as voice intonation, hair
distribution, and masculinization of male body form.
NURSING IMPLICATIONS FOR GONADAL
HORMONES
Assessment
History. Ask the patient to describe the current prob-
lem that initiated this visit. How long have the symp-
toms been present? Is this a recurrent problem? If so,
how was it treated?
Reproductive. Ask female patients to describe the
following, as appropriate: age of menarche; usual pat-
tern of menses (i.e., duration, number of pads used,
last menstrual period); number of pregnancies, live
births, miscarriages, and abortions; vaginal discharg-
es, itching, infections, and how treated; and breast
38
https://evolve.elsevier.com/Willihnganz
2. Compare the adverse effects seen with the use of estrogen
hormones with those seen with androgens.
estrogen (ĔS-trō-jĕn) (p. 615)
progesterone (prō-JĔS-tĕr-ōn) (p. 615)
self-examination routine (if not being performed regu-
larly, explain the correct procedure).
Male patients should be asked whether testicular
self-examinations are performed (if not being per-
formed regularly, explain the correct procedure). As
appropriate, obtain information regarding impotence,
sterility, or alterations in libido.
Prior illnesses. Any indication of hypertension, heart
or liver disease, thromboembolic disorders, or cancer
of the reproductive organs is of particular concern.
Medication. Obtain a detailed history of all pre-
scribed medications, including oral contraceptives;
over-the-counter medications, including herbal medi-
cines (e.g., dong quai, black cohosh); and any street
drugs (e.g., “muscle-building” steroids). Ask if the pa-
tient understands why each is being taken. Tactfully
determine whether the prescribed medications are be-
ing taken regularly, and if not, why not?
Smoking. Does the person smoke?
Physical examination
• A complete physical examination is usually done as
part of the preliminary workup before treatment of
any disorders using gonadal hormones. With chil-
dren and adolescent patients, include questions to
collect data regarding growth and development
(note in particular the development of long bones),
changes in hair growth and distribution, and size of
the genitalia.
• Record basic patient data: height, weight, and vital
signs. Baseline blood pressure readings are of par-
ticular concern so that recordings on future visits
can be evaluated for any change.
• Collect urine for urinalysis and blood samples for
hemoglobin, hematocrit, measurement of gonado-
tropic hormones, and other laboratory studies
deemed appropriate by the healthcare provider.
615
616 UNIT VII Drugs Affecting the Endocrine System
Usually, patients with family histories of diabetes
mellitus should be tested for hyperglycemia before
starting gonadal hormone therapy.
• The physical examination for a female patient
should include a breast examination and a pelvic
examination, including a Papanicolaou (Pap) test.
Observe the distribution of body hair and the pres-
ence of scars. Stress the need for periodic physical
examinations while receiving gonadal hormones.
Psychosocial. Patients requiring androgen therapy
may need to be encouraged to discuss feelings relating
to sexuality, sterility, or altered libido.
Life Span Considerations
Diabetes Mellitus
Patients with diabetes mellitus who receive gonadal hor-
mones may experience alterations in the blood glucose lev-
els. Parameters should be established and a written record
for glucose monitoring maintained for reporting to the health-
care provider.
Most gonadal hormones are prescribed to patients
for prolonged self-administration. Therefore planning
should stress patient education specic to the type of
gonadal hormone prescribed and its intended actions,
including monitoring of common and serious adverse
effects. Ensure that the patient understands the dosage
and specic time schedule for administration of the
prescribed medication.
Implementation
Obtain baseline data for subsequent evaluation of ther-
apeutic response to therapy (e.g., weight, vital signs,
and blood pressure in sitting, lying, and standing posi-
tions). Assist with the physical examination.
Patient Education
Expectations of therapy. Discuss the expectations of
therapy with the patient (e.g., degree of pain relief, fre-
quency of use of therapy, relief of menopausal symp-
toms, sexual maturation, regulation of menstrual cy-
cle, sexual activity, maintenance of mobility, activities
of daily living, and work).
Smoking. Explain the risks of continuing to smoke,
especially when the patient is receiving estrogen or
progestin therapy. The incidence of fatal heart attacks,
thromboembolic disorders, and stroke is increased for
women older than 35 years who smoke. Provide smok-
ing cessation education.
Physical examination. Stress the need for regular peri-
odic medical examinations and laboratory studies.
Fostering health maintenance. Discuss medication in-
formation and how it will benet the course of treatment
to produce an optimal response. Seek cooperation and
understanding of the following points so that medica-
tion adherence is increased: name of medication; dos-
age, route, and times of administration; and common
and serious adverse effects. If estrogen has been pre-
scribed for the purpose of delaying the advancement of
osteoporosis, stress the importance of adhering to the
regimen to achieve the maximum effect.
Patient self-assessment. Plan to teach the individual
to monitor vital signs and weight daily. Enlist the pa-
tient’s help in developing and maintaining a written
record of monitoring parameters (e.g., blood pressure,
pulse, daily weight, degree of pain relief, menstrual
cycle information, breakthrough bleeding, nausea,
vomiting, cramps, breast tenderness, hirsutism, gy-
necomastia, masculinization, hoarseness, headaches,
sexual stimulation). See Appendix B: Template for
Developing a Written Record for Patients to Monitor
Their Own Therapy. Complete the Premedication Data
column for use as a baseline to track response to drug
therapy. Ensure that the patient understands how to
use the form, and instruct the patient to take the com-
pleted form to follow-up visits. During follow-up vis-
its, focus on issues that will foster adherence to the
therapeutic interventions prescribed.
DRUG THERAPY WITH GONADAL
HORMONES
DRUG CLASS: ESTROGENS
Actions
The natural estrogenic hormone released from the ova-
ries is composed of several closely related chemical
compounds—estradiol, estrone, and estriol. The most
potent is estradiol. It is metabolized to estrone, which
is half as potent. Estrone is further metabolized to es-
triol, which is considerably less potent. Estrogens are
responsible for development of the sex organs during
growth in utero and for maturation at puberty. They
are also responsible for characteristics such as growth
of hair, texture of skin, and distribution of body fat.
Estrogens affect the release of pituitary gonadotropins;
cause capillary dilation, uid retention, and protein
metabolism; and inhibit ovulation and postpartum
breast engorgement.
Uses
Estrogen products are used for relief of hot ash symp-
toms (vasomotor) of menopause; for contraception; for
hormone replacement therapy after an oophorectomy,
in conjunction with appropriate diet, calcium, and
physical therapy; for the prevention of osteoporosis; for
treatment of severe acne in female patients (contained
in oral contraceptives); and to slow the disease progress
(and minimize discomfort) in patients with advanced
prostatic cancer and certain types of breast cancer.

Postmenopausal women with an intact uterus are at
an increased risk of developing endometrial cancer with
the use of estrogens alone. If estrogen therapy is indicat-
ed, it should be accompanied by progestin therapy to re-
duce the risk of endometrial cancer. There is no evidence
that “natural” estrogens are more or less hazardous than
“synthetic” estrogens at equiestrogenic dosages.
Results of a controlled study, the Women’s Health
Initiative (WHI), have indicated that hormone replace-
ment therapy is associated with a small increase in the
risk of coronary artery disease (CAD). Follow-up stud-
ies reafrm that hormone therapy is effective for relief
of vasomotor symptoms associated with menopause,
and that the risk of CAD tended to be reduced in wom-
en close to menopause compared with increased risk in
women more distant from menopause. Based on WHI
data, use of hormone replacement therapy for fewer
than 5 years is a reasonable option for relief of moderate
to severe vasomotor symptoms; however, before initia-
tion of therapy the patient should have a baseline risk
assessment (family history of CAD, age, body weight,
diabetes, smoking) and then should be monitored an-
nually. Long-term use of hormone replacement therapy
is not recommended because of the risk of stroke, ve-
nous thromboembolism, and breast cancer that has been
documented in studies completed since 2002.
Therapeutic Outcomes
The primary therapeutic outcomes expected from es-
trogen therapy are as follows:
1. Contraception (see Chapter 40)
2. Hormonal balance
3. Prevention of osteoporosis
4. Palliative treatment of prostate and breast cancer
5. Treatment of severe acne in females
Nursing Implications for Estrogen Therapy
Premedication assessment
1. Determine whether the patient is pregnant before
starting estrogen therapy; hold the medication and
consult the prescriber if there is a possibility of
pregnancy.
2. Obtain baseline weight and vital signs, especially
accurate blood pressure readings.
3. Ask whether the individual has a history of throm-
boembolic disorders or cancer of the reproduc-
tive organs; if so, hold medication and contact the
healthcare provider.
Availability, dosage, and administration
See Table 38.1
Medication Safety Alert
The use of estrogens during early pregnancy is contraindi-
cated. Serious birth defects have been reported, and it has
been found that the female offspring have an increased risk
of developing vaginal or cervical cancer later in life.
Gonadal Hormones CHAPTER 38 617
Common adverse effects
Neurologic
Headache, migraine, dizziness, insomnia, anxiety, nervous-
ness, emotional lability. These symptoms tend to be mild
and resolve with continued therapy. If they do not re-
solve or become particularly bothersome, the patient
should consult the healthcare provider.
Endocrine
Weight gain, edema, breast tenderness, nausea. These
symptoms tend to be mild and resolve with continued
therapy. If they do not resolve or become particularly
bothersome, the patient should consult the healthcare
provider.
Serious adverse effects. The following are all compli-
cations associated with estrogen therapy. It is extremely
important that the patient be evaluated by her healthcare
provider for any of the following symptoms or other
symptoms that the patient recognizes to be of concern.
Cardiovascular. Hypertension, thrombophlebitis,
and thromboembolism.
Metabolic. Hyperglycemia.
Gynecologic. Breakthrough bleeding may occur.
Long-term exposure to estrogens can increase the risks
of breast, endometrial, and vaginal cancers in women.
Too much estrogen aggravates endometriosis, a painful
growth of the uterine lining outside the uterus, where-
as too little estrogen weakens bones (osteoporosis).
Drug interactions
Warfarin. This medication may diminish the anti-
coagulant effects of warfarin. Monitor the prothrom-
bin time (international normalized ratio [INR]) and
increase the dosage of warfarin if necessary.
Lamotrigine. Estrogens contained in contraceptives
may decrease the serum concentration of lamotrigine.
This may increase the risk of seizures. Monitor serum
concentrations of lamotrigine.
Phenytoin. Phenytoin enhances the metabolism of
estrogens. Spotting or bleeding may be an indication of
reduced estrogen levels and reduced contraceptive ac-
tivity with estrogen-containing contraceptives. Using
alternative forms of birth control is recommended.
Thyroid hormones. Patients who have no thyroid
function (and therefore prescribed thyroid replacement
therapy) and who start estrogen therapy may require
an increase in thyroid hormone dosage. Estrogens in-
crease thyroid-binding globulin levels, which reduce
the level of circulating free thyroxine (T4). The total
level of T4 is normal or increased. Do not adjust the
thyroid hormone dosage until the patient shows clini-
cal signs of hypothyroidism.
DRUG CLASS: PROGESTINS
Actions
Progesterone and its derivatives (the progestins) inhib-
it the secretion of pituitary gonadotropins, preventing
618 UNIT VII Drugs Affecting the Endocrine System

Table 38.1 Estrogens

GENERIC NAME BRAND NAME AVAILABILITY USES DOSAGE RANGE
conjugated Premarin Tablets: 0.3, 0.45, Menopause, atophic PO: 0.3–1.25 mg daily cyclicallya
estrogens Do not confuse 0.625, 0.9, vaginitis Intravaginal cream: 0.5–2 g
Premarin with 1.25 mg intravaginally daily cyclicallya
Prevacid. IV: 25 mg in 5-mL Female hypogonadism PO: 0.3–0.625 mg daily cyclicallya
C.E.S. vial
Ovarian failure or PO: 1.25 mg daily cyclicallya
Cream: 0.625 mg/g
postoophorectomy
Osteoporosis (prevention) PO: 0.3 mg initially daily cyclicallya;
dose may be titrated; use lowest
effective dose
Breast carcinoma PO: 10 mg three times daily for at
least 3 mo
Prostatic carcinoma PO: 1.25–2.5 mg three times daily
conjugated Duavee Tablet: conjugated Menopause (moderate PO: 1 tablet daily
estrogens estrogens to severe vasomotor
and 0.45 mg, symptoms); prevention
bazedoxifene bazedoxifene of postmenopausal
20 mg osteoporosis
esteried Menest Tablets: 0.3, 0.625, Menopause, atrophic PO: 0.3–1.25 mg daily cyclicallya
estrogen 1.25 mg vaginitis
Female hypogonadism, PO: 1.25–7.5 mg daily cyclicallya
postoophorectomy,
ovarian failure
Breast carcinoma PO: 10 mg three times daily
Prostatic carcinoma PO: 1.25–2.5 mg three times daily
estradiol Estrace Tablets: 0.5, 1, 2 mg Menopause, atrophic PO: 0.5–2 mg daily or cyclicallya
Do not Do not confuse Injections: valerate vaginitis, hypogonadism, IM: valerate 10–20 mg q4 wk
confuse Estrace with in oil: 10, 20, 40 postoophorectomy, IM: cypionate: 1–5 mg monthly
estradiol with Evista. mg/mL ovarian failure
Risperdal. Cypionate: 5 mg/mL Prostatic carcinoma PO: 1–2 mg three times daily
Cream, vaginal: 0.1 IM: valerate 30 mg q1–2 wk
mg/g
Breast carcinoma PO: 10 mg three times daily for at
least 3 mo
Alora, Vivelle-Dot, Transdermal Menopause, female Transdermal system: patch should
Dotti, Minivelle, patch applied hypogonadism, be placed on clean, dry area of
Lyllana twice weekly: primary ovarian failure, skin on trunk (usually abdomen
0.025, 0.0375, atrophic vaginitis, or buttock) on cyclic schedule;
0.05, 0.075, postoophorectomy, rotate application site; interval of
0.1 mg/24 hr osteoporosis prevention 1 wk between uses of same site
Climara Transdermal patch Menopause, female Transdermal system: patch should
applied once hypogonadism, be placed on clean, dry area of
weekly: 0.025, primary ovarian failure, skin on trunk (usually abdomen
0.0375, 0.05, atrophic vaginitis, or buttock) on cyclic schedule;
0.06, 0.075, postoophorectomy, rotate application site; interval of
0.1 mg/24 hr osteoporosis prevention 1 wk between uses of same site
Menostar Transdermal Prevention of Apply one patch weekly to clean,
patch applied postmenopausal dry area of the lower abdomen;
once weekly: osteoporosis rotate site weekly; remove old
0.014 mg/24 hr patch and discard appropriately
Divigel Transdermal gel: Menopause 0.25 g applied once daily; may
0.25 mg/0.25 g; apply 0.25–1 g daily based on
0.5 mg/0.5 g; symptoms
0.75 mg/0.75 g;
1 mg/g; 1.25 mg/
1.25 g
 Gonadal Hormones CHAPTER 38 619

Table 38.1 Estrogens—cont’d

GENERIC NAME BRAND NAME AVAILABILITY USES DOSAGE RANGE
Elestrin Transdermal gel: Menopause 0.87 g applied once daily; may
0.06% apply 0.87–1.7 g daily based on
symptoms
EstroGel Topical gel: 0.06% in Menopause, vaginal atrophy Topical: apply contents of
pump one pump daily to one arm,
spreading from wrist to upper
arm on all sides; allow to
dry; wash hands with soap
and water; if uterus is intact,
progestin should also be taken
to prevent endometrial cancer;
alcohol gel is ammable until dry,
so avoid re, ame, or smoking
until dry
Evamist Transdermal spray: Menopause Topical: 1 spray once every
1.53 mg/spray morning
May apply 1–3 sprays daily based
on symptoms
Femring Vaginal ring: 0.05/24 Menopause 0.05 mg intravaginally; adjust dose
hr, 0.1 mg/24 hr Vaginal atrophy based on clinical response; ring
should remain in place for 3
months
Available in Canada.
Do not confuse.
aCyclically = 3 weeks of daily estrogen followed by 1 week off; 25 days daily and 5 days off.

maturation of ovarian follicles and thus inhibiting organs; if so, withhold medication and contact the
ovulation. healthcare provider.

Uses Availability, dosage, and administration

Progestins are used primarily to treat secondary amen-
orrhea, breakthrough uterine bleeding, and endome-
triosis, but they may also be used in combination with
estrogens as contraceptives (see Chapter 40).
Therapeutic Outcomes
The primary therapeutic outcomes expected from pro-
gestin therapy are as follows:
1. Contraception
2. Relief of symptoms of endometriosis
3. Hormonal balance to relieve amenorrhea or abnor-
mal uterine bleeding
Nursing Implications for Progestins
Premedication assessment
1. Determine whether the patient is pregnant before
starting progestin therapy; hold the medication and
consult the healthcare provider if there is a possibil-
ity of pregnancy.
2. Obtain baseline weight and vital signs, especially
accurate blood pressure readings.
3. Ask whether the individual has a history of throm-
boembolic disorders or cancer of the reproductive
See Table 38.2
Medication Safety Alert
The use of progestins in early pregnancy has been associat-
ed with birth defects. If pregnancy is suspected, the health-
care provider should be consulted immediately.
Common adverse effects. These symptoms tend
to be mild and resolve with continued therapy. If
they do not resolve or become particularly bother-
some, instruct the patient to consult the healthcare
provider.
Endocrine. Weight gain, edema, tiredness, oily scalp,
acne.
Gastrointestinal. Nausea, vomiting, diarrhea.
Serious adverse effects. The following are complica-
tions associated with progestin therapy. If these com-
plications occur, it is extremely important that the
patient be evaluated by the healthcare provider to con-
sider therapeutic alternatives.
620 UNIT VII Drugs Affecting the Endocrine System

Table 38.2 Progestins

GENERIC NAME BRAND NAME AVAILABILITY USES DOSAGE RANGE
medroxyprogesterone Provera Tablets: 2.5, 5, Secondary PO: 5–10 mg daily for 5–10
Do not confuse Do not confuse 10 mg amenorrhea days; therapy may be started
medroxyprogesterone with Provera with at any time
methylprednisolone. Premarin or Abnormal uterine PO: 5–10 mg daily for 5–10
Parlodel. bleeding days, beginning on day 16 or
21 of menstrual cycle
norethindrone acetate Aygestin Tablets: 5 mg Amenorrhea, PO: 2.5–10 mg starting on day
abnormal 20 and ending on day 25 of
uterine menstrual cycle
bleeding
Endometriosis PO: 5 mg for 2 wk; increase
in increments of 2.5 mg/
day q2wk until 5 mg/day is
reached
progesterone Progesterone, Tablets, capsules: Amenorrhea, Amenorrhea: PO: 400 mg at
Prometrium 100, 200 mg endometrial bedtime for 10 days
Transdermal cream: hyperplasia, IM: 5–10 mg for 6–8
10%, 20% functional consecutive days
Injection: 50 mg/mL uterine Functional uterine bleeding
Vaginal gel: 4%, 8% bleeding IM: 5–10 mg/day for 6 doses
Vaginal Endometrial hyperplasia,
suppositories: prevention: 200 mg once
100, 200 mg daily at bedtime for 12 days
sequentially per 28-day cycle
Do not confuse.

Gynecologic
Breakthrough bleeding, amenorrhea, breast enlargement,
teratogenicity. Because of the possibility of birth defects,
a healthcare provider should be consulted immediate-
ly if the patient becomes pregnant.
Neurologic. Continuing headache, depression.
Gastrointestinal. Cholestatic jaundice.
Drug interactions
Rifampin. Rifampin may enhance the metabolism of
norethindrone. The dosage of norethindrone may need
to be increased to provide therapeutic benet.
DRUG CLASS: ANDROGENS
Actions
Testosterone and androstenedione are the principle
androgens. The dominant male sex hormone is testos-
terone. It is the primary natural androgen produced by
the testicles. Androgens are responsible for the normal
growth and development of male sex organs and for
maintenance of secondary sex characteristics. These
effects include the growth and maturation of the pros-
tate, seminal vesicles, penis, and scrotum; the develop-
ment of male hair distribution; laryngeal enlargement
(Adams apple); vocal cord thickening; alterations in
body musculature; and fat distribution.
Uses
Androgens are used to treat hypogonadism, androgen
deciency, delayed puberty in male patients and is
used for palliation of breast cancer in postmenopausal
women with certain cell types of cancer. When andro-
gens are used for palliation of cancer in women, they
suppress cancer cell growth. In addition, androgens
may be used to treat wasting syndrome associated
with acquired immunodeciency.
Therapeutic Outcomes
The primary therapeutic outcomes expected from an-
drogen therapy are as follows:
1. Restoration of hormonal balance in androgen
deciency
2. Reduced discomfort associated with breast cancer
3. Increased muscle mass when used to treat wasting
syndrome
4. Stimulation of puberty in carefully selected male
patients with delayed puberty
Nursing Implications for Androgens
Premedication assessment
1. Obtain baseline vital signs and weight, and assess
mental status.
2. Check baseline electrolyte values; report abnormal
ndings. Be especially alert for hypercalcemia.
 Gonadal Hormones CHAPTER 38 621

Table 38.3 Androgens

GENERIC NAME BRAND NAME AVAILABILITY USES DOSAGE RANGE
SHORT-ACTING AGENTS
testosterone gel AndroGel, Topical gel: 1%, Male hypogonadism Topical: open one or more hormone
Testim, 1.62%, 2% packets (depending on dosage);
Fortesta squeeze entire contents onto palm of
Vogelxo hand; apply to clean, dry, intact skin of
shoulders, upper arms, and abdomen;
allow to dry before dressing; wash
hands with soap and water; do not
apply to genitals
testosterone USP in Androderm Transdermal patch: Male hypogonadism Transdermal system: 1–3 patches
gel base 2, 4 mg applied to skin on hips, abdomen,
thighs, or buttocks nightly for 24 hr;
replace q24h; do not apply to scrotum
LONG-ACTING AGENTS
testosterone pellets for Testopel Pellets: 25, 50, 75, Male hypogonadism Subcutaneous: 2–6 pellets implanted
implantation 100, 200 mg Delayed puberty q3–6 mo
testosterone enanthate Xyosted Subcutaneous: 50, Male hypogonadism Subcutaneous: 50–100 mg
75, 100 mg/0.5 once weekly
mL autoinjector
testosterone cypionate IM: 100, 200 mg/ As for testosterone As for testosterone enanthate
mL enanthate
ORAL PRODUCTS
methyltestosterone Methitest Tablets: 10 mg Delayed puberty PO: 10–50 mg daily
Breast carcinoma PO: 50–200 mg daily, in 1–4 doses

3. Identify baseline glucose levels for those initiating
androgen therapy who are taking insulin or oral
hypoglycemic agents, because the use of androgens
may cause hypoglycemia.
Availability, dosage, and administration
See Table 38.3
Medication Safety Alert
Testosterone has been subject to abuse, typically at doses
higher than recommended for the approved indication and
in combination with other anabolic androgenic steroids.
Anabolic androgenic steroid abuse can lead to serious
cardiovascular and psychiatric adverse reactions.
Common adverse effects
Gastrointestinal
Gastric irritation. If gastric irritation occurs, adminis-
ter drug with food or milk. If symptoms persist or in-
crease in severity, report this to the healthcare provider
for evaluation.
Genitourinary. Androgen therapy may increase pros-
tate specic antigen (PSA) levels and increase the risk
of benign prostatic hyperplasia. PSA levels should be
monitored and a prostate examination obtained before
treatment and at 3 to 12 months in men aged 55 to 69
years or at 40 years or older for those men at increased
risk for prostate cancer. Monitor patients with benign
prostatic hyperplasia (BPH) for worsening of signs and
symptoms of BPH.
Serious adverse effects
Cardiovascular
Hypertension. Increased blood pressure has been as-
sociated with testosterone. Blood pressure should be
monitored before treatment, at 3 to 6 weeks and then
periodically.
Venous thromboembolism. Venous thromboembolic
events, including deep vein thrombosis (DVT) and
pulmonary embolism (PE), have been reported with
testosterone products. Monitor patients with symp-
toms of pain, edema, warmth, and erythema in the
lower extremity for DVT and those with acute short-
ness of breath for PE.
Hematologic
Increased hematocrit and hemoglobin. Hematocrit and
hemoglobin should be monitored before treatment, at
3 to 6 months, and then annually.
Metabolic
Electrolyte imbalance, edema. The most commonly al-
tered electrolytes are potassium (K+), sodium (Na+),
and chloride (Cl ); hyperkalemia is most likely to occur.
Many symptoms associated with altered uid and elec-
trolyte balance are subtle and interspersed with general
symptoms of drug toxicity or the disease process itself.
622 UNIT VII Drugs Affecting the Endocrine System
Gather data about changes in the patient’s mental status
(e.g., alertness, orientation, confusion), muscle strength,
muscle cramps, tremors, nausea, and general appear-
ance (e.g., drowsy, anxious, lethargic). Always check
the electrolyte reports for early indications of electrolyte
imbalance. Keep accurate records of intake and output,
daily weights, and vital signs. Patients should report
weight gains of more than 2 pounds per week. Diuretic
therapy, with or without dietary reduction of salt, may
be prescribed if edema is signicant.
Hypercalcemia. In immobilized patients and patients
with breast cancer, androgen therapy may cause hy-
percalcemia. Monitor patients for nausea, vomiting,
constipation, poor muscle tone, and lethargy. These
are indications of hypercalcemia and are indications
for discontinuation of androgen therapy. Force uids
to minimize the possibility of renal calculi. Encourage
the patient to drink 8 to 12 eight-ounce glasses of water
daily. The patient should perform weight-bearing and
active and passive exercises to the degree tolerated to
minimize loss of calcium from bones.
Endocrine
Masculinization. Women receiving high doses of an-
drogens may develop signs of masculinization. Women
should be monitored for signs of masculinization (e.g.,
deepening of the voice, hoarseness, growth of facial
hair, clitoral enlargement, and menstrual irregulari-
ties) during androgen therapy. The drug should usu-
ally be discontinued when mild masculinization is
evident because some adverse androgenic effects (e.g.,
voice changes) may not reverse with discontinuation
of therapy. In consultation with the healthcare provid-
er, the woman may decide that some masculinization
is acceptable during treatment for breast cancer. Help
patients adjust to a possible change in self-image or
self-esteem caused by the effects of masculinization.
Men should be carefully monitored for the de-
velopment of gynecomastia, priapism, or excessive
sexual stimulation. These are indications of androgen
overdose.
Gastrointestinal
Hepatotoxicity. The symptoms of hepatotoxicity
include anorexia, nausea, vomiting, jaundice, hepa-
tomegaly, splenomegaly, and abnormal liver func-
tion test results (e.g., elevated bilirubin, aspartate
aminotransferase [AST], alanine aminotransferase
[ALT], gamma-glutamyltransferase [GCT], and alka-
line phosphatase levels [ALP]; increased prothrombin
time [INR]).
Life Span Considerations
Androgens
Male children receiving androgens must have the effects of
the drug on long bones monitored by periodic radiographs of
long bones. Usually, radiographs of long bones are obtained
every 3 to 6 months to check the status of the epiphyseal
line. Androgens may prematurely close the epiphyseal line,
preventing bone elongation.
Drug interactions
Warfarin. Androgens may enhance the anticoagu-
lant effects of warfarin. Observe for the development
of petechiae; ecchymoses; nosebleeds; bleeding gums;
dark, tarry stools; and bright red or coffee-ground em-
esis. Monitor the prothrombin time (INR), and reduce
the dosage of warfarin if necessary.
Oral antidiabetic agents, insulin. Monitor for hypo-
glycemia; symptoms include headache, weakness, de-
creased coordination, general apprehension, diaphore-
sis, hunger, and blurred or double vision. The dosage
of the hypoglycemic agent or insulin may need to be
reduced. Notify the healthcare provider if any of these
symptoms appear.
Corticosteroids. Concurrent use may increase the
possibility of electrolyte imbalance and uid retention.

Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• The gonadal hormones are necessary for the body to grow
and mature into the adult form and for reproduction.
• Male and female gonads secrete hormones. The male
testes secrete predominantly androgens, and the female
ovaries secrete primarily estrogens and progesterone.
• These hormones are responsible for the shape and
secondary sex characteristics associated with the male
and female body forms.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX exam and include both NGN (Next Generation) and
traditional questions. See Chapter 1 for further information re-
garding question types.
Scenario
A male patient diagnosed with hypogonadism came into the
clinic for a routine check on his progress with treatment. The
nurse obtained his vital signs and weight and after checking
his recent lab results noted the blood glucose was 70 mg/dL.
1. When androgens are administered to a female patient with breast
cancer, the nurse may expect the development of which adverse
effect? (Select all that apply.)
1. Hypotension
2. Weight gain and edema
3. Masculinization
4. Hypercalcemia
5. Increased hematocrit and hemoglobin
Objective: Compare the adverse effects seen with the use of
estrogen hormones with those seen with androgens.
NCLEX item type: Multiple response
Cognitive skill: Application
Gonadal Hormones CHAPTER 38 623
2. The nurse is educating a female patient on the use of estrogens
for a newly diagnosed condition. Which of the statements by the
nurse indicate appropriate therapeutic outcomes for the use of
estrogens? (Select all that apply.)
1. “Estrogens are used for postmenopausal women to
provide hormonal balance and reduce hot ashes.”
2. “One of the important uses for estrogens is prevention of
osteoporosis.”
3. “I know that patients who take estrogens have reported
relief of headaches and decreased insomnia.”
4. “Estrogens have been found to help treat severe acne.”
5. “For patients who are at risk, the use of estrogens has
been found to prevent coronary artery disease.”
Objective: Identify the uses of estrogens and progestins.
NCLEX item type: Multiple response
Cognitive skill: Application
3. The nurse recognizes that progestin is used to treat which of the
following conditions in women? (Select all that apply.)
1. Prevention of ovulation for contraceptive use
2. Treatment of breakthrough uterine bleeding
3. Relief of symptoms of endometriosis
4. Treatment of breast cancer symptoms
5. Treatment of hypogonadism
Objective: Identify the uses of estrogens and progestins.
NCLEX item type: Multiple response
Cognitive skill: Application
4. The patient in the scenario diagnosed with hypogonadism who is
on testosterone pellets subcutaneously is newly diagnosed with
diabetes and has been started on an oral hypoglycemic agent.
Which adverse effects will the nurse monitor with this combination
of medications?
1. Hypoglycemia
2. Hyperglycemia
3. Hypokalemia
4. Hypocalcemia
Objective: Compare the adverse effects seen with the use of
estrogen hormones with those seen with androgens.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
Unit VIII Drugs Affecting the Reproductive System

39 Drugs Used in Obstetrics

https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify appropriate nursing assessments during normal
labor and delivery.
2. Discuss potential complications of preterm labor and when
uterine relaxants and magnesium sulfate are used.
3. Describe assessments needed for uterine stimulants
administered for induction of labor, augmentation of labor,
and postpartum atony and hemorrhage.
4. Discuss education needed for care of the neonate,
including erythromycin ophthalmic ointment.

Key Terms
pregnancy hypertension
disorders (PRĔG-nĕn-sē hī-pĕr-TĔN-
shŭn) (p. 626)
lochia (LŌ-kē-ă) (p. 627)
precipitous labor and delivery dysfunctional labor (dĭs-FŬNK-shŭn-
(prē-SĬP-ĭ-tŭs LĀ-bŭr) (p. 636) ăl LĀ-bŭr) (p. 636)
augmentation (ŏg-mĕn-TĀ-shŭn)
(p. 636)

OBSTETRICS
Obstetrics is the eld of healthcare practice associat-
ed with pregnancy, the health of the mother and the
child, and the process of birth. The current culture is
for mothers who are expecting to deliver a child to be
admitted to a hospital or birthing center and have the
baby under controlled conditions. The labor and deliv-
ery process is unpredictable to some extent, and hav-
ing trained clinicians present during the birth provides
a sense of control. Nurses working in obstetrics are
trained in assessment of the mother during the trimes-
ters of fetal growth and the baby on delivery.
NURSING IMPLICATIONS FOR OBSTETRICS
Assessment
Prenatal assessment. Obtain basic historical informa-
tion about the woman and family concerning acute or
chronic conditions, surgeries, and deaths.
• Has the patient been treated for kidney or bladder
problems; high blood pressure; heart disease; rheu-
matic fever; hypothyroidism or hyperthyroidism;
diabetes mellitus; allergies to any foods, drugs, or
environmental substances; or sexually transmitted
infections (STIs)?
• Has the patient been exposed to any communicable
diseases since becoming pregnant?
• Has the patient received blood or blood products?
If the woman answers yes to any of these questions,
nd out which healthcare provider made the diag-
nosis, when the condition occurred, and how the
624
condition was treated. Request the approximate
date of the last Papanicolaou (Pap) test and results.
Gather data about menstrual pattern (e.g., age of ini-
tial onset, duration and frequency of monthly peri-
ods, date of last full menstrual cycle, any bleeding
since the last full menstrual period) and contracep-
tive use (e.g., condoms, foam, diaphragm, sponge,
oral contraceptives, intrauterine devices).
Take an obstetric history. Ask the woman if she
has had any previous live births, stillbirths, or
spontaneous or therapeutic abortions. If any of
the deliveries were premature, obtain additional
information about the infant’s gestational age,
survival of the child, suspected causes of pre-
maturity, and infections. Ask whether any of the
births required a cesarean delivery. If yes, ask
why. Ask if Rho(D) immune globulin (RhoGAM)
has been given for Rh factor incompatibility.
Nutritional history
• What is the patient’s usual or prepregnant weight?
How much weight has she gained or lost in the past
3 months?
• What are the woman’s favorite foods? Are there any
foods that she avoids? How often does she eat? What
has she eaten in the past 3 days? Does she normally
take daily vitamins, minerals, or herbal products?
• Are there any cultural food practices to be main-
tained during the pregnancy?
Elimination pattern
• What is the patient’s elimination pattern?

• How often does she have bowel movements?
• What is the stool consistency and color?
• Is there any bleeding?
• Are laxatives ever needed? If so, how often?
Psychosocial cultural history
• Determine how the woman feels about this pregnancy
(e.g., excited, nervous, or if the baby is not intended).
• Determine cultural patterns regarding prenatal care
(e.g., language spoken, activities that she cannot do
while pregnant, whether she prefers a female care-
giver). Ask the pregnant woman what specic cultural
practices she would like to follow during the pregnancy.
• Who makes up her support group: husband, boy-
friend, friends, partner, family, tribal healer?
• Ask about her employment status and what type of
work she performs.
• Determine the woman’s level of education, eco-
nomic status, and general interest in learning more
about effective management of the pregnancy.
• Ask if patient feels safe in the home, to determine
potential domestic violence/abuse. Will referral to
social services agencies be necessary?
Medication history. Ask the woman if she takes any
prescribed medications, over-the-counter medications,
or herbal remedies. If she is not currently taking any
medications, ask whether she has taken any over the
past 6 months. Determine which have been prescribed
and for what purpose.
Alcohol and tobacco history. The pregnant woman
should be encouraged to abstain from smoking, chew-
ing, or vaping tobacco products; using nicotine patches;
or drinking alcohol during pregnancy. Numerous data
indicate that use of tobacco products and drinking are
dangerous to the fetus. Increased incidences of neona-
tal mortality, low birth weight, and prematurity have
been well reported (see Chapter 48). Determine the use
of alcohol and street or recreational drugs of any type,
including what, how much, and how frequent.
Physical examination. Assist the woman to undress
and prepare for examination, including a pelvic exami-
nation and Pap test.
• Height and weight: Record height and weight. (See an
obstetrics textbook for a detailed guide to all aspects of
a prenatal visit and the initial assessments performed.)
• Hypertension: Take the blood pressure. Ask if any
treatment has been given for high blood pressure. If
so, inquire about the onset, treatment, and degree of
control achieved.
• Heart rate: At prenatal visits, count the pulse for 1
full minute. Report irregularities in rate, rhythm, or
volume. On subsequent visits, anticipate an increase
in rate of approximately 10 beats/min during the
course of the pregnancy.
• Respirations: Record the rate of respirations. As the
pregnancy progresses, observe for hyperventilation
and thoracic breathing.
• Temperature: If the temperature is elevated, ask
about any signs of infection or exposure to people
with known communicable diseases.
Drugs Used in Obstetrics CHAPTER 39 625
• Laboratory and diagnostic studies: Obtain a urine spec-
imen using the clean-catch method.
• Blood tests: Testing for complete blood count (CBC),
hemoglobin, hematocrit, hemoglobin electrophore-
sis, rubella titer, Rh factor, and STIs (e.g., syphilis,
gonorrhea, chlamydia) may be ordered at this initial
visit. These may include antibody, sickle cell, and
thalassemia screens; folic acid level; and, as appro-
priate, puried protein derivative, human immuno-
deciency virus (HIV), hepatitis B, and toxicology
screens. With a history of diabetes, hypertension, or
renal disease, additional laboratory testing may be
ordered (e.g., 1-hour glucose tolerance, creatinine
clearance, total protein excretion).
Assessment during rst, second, and third trimesters.
Assessment done at routine visits during the preg-
nancy includes weight; measurement of blood pres-
sure, pulse, and respirations; and examination of the
abdomen, with measurement of fundal height and fe-
tal heart sounds. Any problems or concerns should be
discussed. Hemoglobin and hematocrit may be peri-
odically rechecked.
The pregnant woman who is not experiencing
complications is usually examined monthly for the
rst 6 months, every 2 weeks in the seventh and
eighth months, and weekly during the last month.
Vaginal examinations are usually performed on the
initial visit and are not repeated until 2 to 3 weeks
before the estimated date of delivery or estimated
date of birth (due date), at which time the cervical
status, degree of engagement, and fetal presentation
are evaluated. A sonogram may be obtained in early
pregnancy.
Assessment of the pregnant patient at risk. Assess for
signs and symptoms of potential obstetric complica-
tions (see an obstetrics textbook for further details of
each complication): infection, hyperemesis gravidar-
um, spontaneous abortion, preterm labor, premature
rupture of membranes (PROM), gestational diabetes,
preeclampsia, HELLP (hemolysis, elevated liver en-
zymes, and low platelet count) syndrome, and intra-
uterine fetal death.
• Infection: Record the patient’s temperature. Report
any elevations to the healthcare provider immedi-
ately for further evaluation. As appropriate, obtain
urine for urinalysis.
• Hyperemesis gravidarum: Obtain details of persistent,
severe vomiting.
• Early pregnancy loss, placental separation, abortion:
Assess for signs of bleeding. Gather specic infor-
mation about the onset, duration, volume (number
of pads used), and color, and report any clots or
tissue.
• Ask the patient to describe any pain experienced us-
ing a scale of 0 to 10. Has she had any backache or
pelvic cramping, sharp abdominal pain, faintness,
or pain in the shoulder area?
626 UNIT VIII Drugs Affecting the Reproductive System
• Vital signs should be taken and compared with base-
line data whenever bleeding is suspected. Assess
for development of shock—restlessness, perspira-
tion, pallor, clammy skin, dyspnea, tachycardia, and
blood pressure changes. Record fetal heart tones at
regular intervals to determine any fetal distress.
• Preterm labor: Preterm labor is dened as:
 • Labor occurring after 20 and before 37 completed
weeks of gestation plus
 • Clinically documented uterine contractions (4/20
minutes or 6/60 minutes) plus
 • Ruptured membranes or
 • Intact membranes and cervical dilation greater
than 2 cm or
 • Intact membranes and cervical effacement great-
er than 80% or
 • Intact membranes and cervical change during
observation
These can be measured by changes in dilation or ef-
facement, or by changes in cervical length measured
clinically, or by ultrasound.
A fetal bronectin (FFN) test may be ordered to as-
sess the presence of preterm labor in patients whose
presenting symptoms are questionable so that early
intervention (e.g., tocolytic therapy, corticosteroids,
transport to a tertiary care center) can be initiated
when indicated or, if negative, unnecessary interven-
tions can be avoided. The FFN test is for women with
intact membranes and cervical dilation of less than 3
cm. This test may detect the probability of preterm la-
bor from 24 to 34 weeks’ gestation. If the test is nega-
tive, the patient is unlikely to experience preterm de-
livery in the next 7 to 14 days (Fig. 39.1). Home uterine
activity monitoring using a tocodynamometer may be
used to detect excessive uterine contractions.
• PROM: Assess for and obtain specics of any signs
of leakage of amniotic uid from the vagina.
• Gestational diabetes: Review urinalysis reports for
glycosuria. Review history of symptoms, especially
during previous pregnancies. Review 1- and 3-hour
glucose tolerance blood test results.
• Pregnancy hypertension disorders: Assess for and report
sudden hypertension (an elevation of systolic pressure
30 mm Hg or more above prior readings, systolic blood
pressure of 140 mm Hg or more, or diastolic pressure
of 90 mm Hg or more). Pregnancy hypertension disor-
ders include preeclampsia (elevated blood pressure;
proteinuria as a result of hypoperfusion secondary to a
vasospastic process that affects the fetus, the placenta,
and maternal organs and vasculature) and eclampsia
(convulsions accompanying preeclampsia).
• Assess for edema of any body parts (e.g., ngers,
hands, face, legs, ankles). Assess hydration status,
and, in particular, obtain daily weights.
• Review laboratory reports for indications of abnormal
electrolytes, elevated uric acid or hematocrit levels,
and thrombocytopenia in the blood and for the pres-
ence of red blood cells (RBCs) and protein in the urine.
• Assess for signs and symptoms of seizure activity.
• Monitor fetal heart rate and movements (fetal
distress).
• Assess for start of labor or signs of other compli-
cations, such as pulmonary edema, disseminated
intravascular coagulation, heart failure, abruptio
placentae, or cerebral hemorrhage.
• When giving magnesium sulfate for preeclampsia,
assess deep tendon reexes, respiratory status (re-
port depression), sedation level, intake and output,
seizure precautions, and cardiac status. (Always
have calcium gluconate, the antidote for magne-
sium sulfate, available.)
Life Span Considerations
The status of the fetus may be assessed by fetal movement
counts, contraction stress testing, biophysical prole, and
ultrasonography for placental placement and measurement
of maturity indicators. Amniocentesis may be performed to
assess fetal lung maturity and detect fetal disorders.
Assessment during normal labor and delivery
History of pregnancy. On admission of the preg-
nant woman to the hospital, obtain the following
information:
• Name and age
• Obstetric history (gravida, para, abortions, fetal
deaths, birth weight of previous children, and com-
plications during previous deliveries)
• Estimated due date, estimated gestational age, and
day of last menstrual period
• Prenatal care (type and amount, any signicant
problems)
• Prenatal education (type and extent of childbirth
preparation)
• Plan for infant feeding
• Status of membranes (intact, ruptured, time rup-
tured, amount, and color of uid that escaped)
• Status of labor (time of onset of contractions; fre-
quency, duration, and intensity; how patient is cop-
ing with contractions)
• Time of last meal
Physical examination. The physical examination
should include the following:
• Height, weight, vital signs (temperature, blood
pressure, pulse, and respirations)
• State of hydration, including presence of edema
• Size and contour of abdomen and fundus
• Frequency of contractions
• Fetal heart rate
• Vaginal examination: cervical dilation and efface-
ment, status of membranes, and presentation and
position of fetus
Assessment after delivery and during postpartum care
• The vital signs should be checked every 15 minutes
during the rst hour after delivery or until the woman
is stable, then every 30 minutes for the next 2 hours.
 Drugs Used in Obstetrics CHAPTER 39 627

Regular uterine contractions

More than 4/hr
EGA 24–33 wk

Rule out

PPROM
Delivery Placental abruption
Placenta previa Transcervical bleeding
Fetal distress Ruptured membranes
Fetal death
Chorioamnionitis

Obtain mother’s vital signs

Continuous EFM
Obtain laboratory tests
Admit to labor and
and swabs for FFN, GBS delivery department
Amniocentesis NPO
IV Fluid
Restrict activity

Cervical changes

Consider tocolytic
treatment:
1. magnesium sulfate
>3 cm 2. nifedipine
Or 80% effaced 3. indomethacin
<2 cm

Get TV Administer
ultrasound No tocolysis or GBS antenatal
prophylaxis unless active corticosteroids:
labor betamethasone,
dexamethasone

Fig. 39.1 Alternatives to the treatment of preterm labor. EFM, External fetal monitor; EGA, estimated gestational age;
FFN, fetal bronectin (indicates probability of preterm labor); GBS, group B streptococcus (if positive, treat with penicillin
during labor); NPO, nothing by mouth; PPROM, preterm premature rupture of membranes; TV, transvaginal. Note:
Tocolysis indicates use of medications to stop preterm labor.

• Inspect the perineum and note any abnormal swell-
ing or bruising.
• Assess fundal height and rmness every 15 min-
utes for 1 hour, then every 30 minutes for the next
4 hours. Continue to assess fundal height and posi-
tion until the woman is discharged.
• Describe the amount of lochia (vaginal discharge af-
ter delivery) and the color and the presence of clots
every 15 minutes for 1 hour, every 30 minutes for
4 hours, and at least every 4 hours for the next 12
hours or as needed (PRN).
• Assess breasts for redness, softness, and nipple condi-
tion. Encourage early feedings with normal newborns as
allowed. Check for breast engorgement and discomfort.
Assessment of the neonate
• Ensure a patent airway.
• Observe umbilical cord until pulsations cease, then
clamp or ligate it.
• Assess neonate’s health status at 1 minute and 5
minutes after delivery using the Apgar scoring sys-
tem (Table 39.1).
• Perform rapid estimation of gestational age (Fig. 39.2).
628 UNIT VIII Drugs Affecting the Reproductive System

Table 39.1 Apgar Scoring System

SIGN SCORE
0 1 2
Heart rate (beats/min) Absent Slow (<100) >100
Respiratory effort Absent Slow, irregular Good, crying
Muscle tone Flaccid Some exion of extremities Active motion
Reex irritability No response Grimace Cry
Color Blue, pale Body pink, extremities blue Completely pink

A
Fig. 39.2 Estimation of gestational age. (A) New Ballard Score for newborn maturity rating. Expanded scale includes
extremely premature infants and has been rened to improve accuracy in more mature infants. (B) Intrauterine growth:
birth weight percentiles based on live single births at gestational ages 20 to 44 weeks. (A, From Ballard JL, Khoury JC,
Wedig K, etal. New Ballard score expanded to include extremely premature infants. J Pediatr. 1991;119[3]:417.
Continued
 Drugs Used in Obstetrics CHAPTER 39 629

5000
4750
4500 90th percentile
50th percentile
4250
10th percentile
4000
3750 Large for gestational age
3500 Average for gestational age
Small for gestational age
3250
3000
Birth weight (g)

2750
2500
2250
2000
1750
1500
1250
1000
750
500
250
0
20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44
B Gestational age (weeks)

Fig. 39.2_Cont’d B, Data from Alexander GR, Himes JH, Kaufman RB, etal. A United States national reference for fetal
growth. Obstet Gynecol. 1996;87[2]:163–168.)

Implementation bleeding is present, blood studies for hemoglobin,

Prenatal
• Collect information relating to the mother’s health
status and the pregnancy. Observe for signs of po-
tential complications of pregnancy.
• Assist with routine prenatal examinations and diag-
nostic procedures.
• Review laboratory and diagnostic studies per-
formed; report abnormal ndings to the healthcare
provider.
• During the rst trimester, initiate discussion of in-
fant feeding options available; provide information
needed for parents to make a decision.
Complications of pregnancy
• Infection: Monitor for infections and intervene ac-
cording to the healthcare provider’s orders when an
infection is conrmed.
• Hyperemesis gravidarum (see Chapter 33): Monitor
hydration status, daily weight, and vital signs.
Provide for dietary needs through intravenous (IV)
therapy, nutritional supplements, and gradual pro-
gression of diet as tolerated.
• Bleeding, spontaneous abortion: Ensure that the patient
adheres to bed rest and give sedatives as prescribed.
Monitor maternal vital signs, fetal heart rate and
activity, and the volume (frequency of change and
number of pads used) of bleeding present. When
hematocrit, white blood cells, human chorionic go-
nadotropin titer, and blood type and crossmatch
may be ordered. Other diagnostic procedures, such
as culdoscopy, sonography, laparoscopy, fetoscopy,
and pregnancy tests, may be performed.
Preterm labor
• Monitor uterine contractions and continue external
fetal and uterine monitoring.
• Position the mother on her side, increase uid in-
take, and start an IV infusion as ordered. Monitor
hydration, maintain accurate intake and output re-
cords, and take daily weights.
• Assist with obtaining cervical and vaginal cultures,
as ordered.
• Perform cervical examination to determine dilation
and effacement. Assess for leakage of amniotic uid.
• Take maternal vital signs. Record fetal heart rate
and frequency and intensity of uterine contractions.
• Administer prescribed uterine relaxants (toco-
lytic agents), such as indomethacin, nifedipine, or
magnesium sulfate. (See the magnesium sulfate
drug monograph later in this chapter for adminis-
tration information and monitoring parameters.)
Glucocorticoids, usually betamethasone or dexa-
methasone, may be administered by the intramus-
cular (IM) route to accelerate lung maturation to
630 UNIT VIII Drugs Affecting the Reproductive System
minimize fetal respiratory distress syndrome. Either
glucocorticoid may be used in cases in which it is
anticipated that premature labor should be stopped
for only 36 to 48 hours, such as with PROM. There is
no evidence to support one glucocorticoid over an-
other. Review available laboratory studies (e.g., FFN,
electrolyte studies, CBC with differential, platelets,
uric acid level, hematocrit, serum estriol, lecithin-
to-sphingomyelin ratio) and report ndings to the
healthcare provider.
• All patients in preterm labor are considered to be at
high risk for neonatal group B streptococcal infection
and therefore often receive prophylactic antibiotics.
Commonly used antibiotics include penicillin G and
ampicillin, or clindamycin for patients allergic to
penicillins.
• Provide appropriate psychological support. Involve
supportive pastoral care as appropriate.
Premature rupture of membranes
• Check fetal heart tones and fetal activity.
• Describe the color, characteristics, and amount of
amniotic uid leakage.
• Check maternal vital signs; report elevated temper-
ature, chills, or malaise to the healthcare provider
immediately.
• Continue to monitor for any leakage of uid.
• Limit number of cervical exams to prevent infection.
Gestational diabetes mellitus
• Assist with the performance of glucose tolerance
testing.
• Perform blood glucose testing four times daily, and
assist the patient in administering prescribed insu-
lin. While reviewing the self-monitoring blood glu-
cose levels, ensure that the patient understands her
individualized insulin dosage adjustment.
• Encourage adherence to diet and exercise pre-
scribed to achieve tight glucose control to maintain
desired weight gain during the pregnancy and to
prevent complications (e.g., neonatal hypoglycemia
or stillbirth).
• Women with gestational diabetes mellitus (GDM)
have twice the risk of developing hypertension
as other pregnant women, so the blood pressure
should be monitored regularly.
• Monitor for development of hypoglycemia and hy-
perglycemia. Consult current American Diabetes
Association (ADA) guidelines for monitoring GDM.
• During labor, monitor glucose level every 2 hours;
maintain adequate hydration.
• During the postpartum period, continue to monitor
glucose levels. (Usually with GDM, the mother’s
glucose reverts to normal during the postpartum
period. Therefore careful monitoring of glucose and
adjustment of insulin dosages are required.)
The patient with diabetes should have multiple
laboratory tests, including glycosylated hemoglobin
(hemoglobin A1c), serum creatinine, urine microalbu-
min, and other tests consistent with the history. The
woman with diabetes must understand the importance
of having a sustained record of preconception glycemic
control to prevent maternal and fetal complications.
Pregnancy hypertension disorders (preeclampsia, ec-
lampsia)
• Monitor maternal vital signs, fetal heart tones, and
fetal movement at appropriate intervals consistent
with presenting symptoms. Maintain the patient on
bed rest in a lateral position to promote uteropla-
cental circulation and to reduce compression of the
vena cava.
• Maintain hydration by the oral or IV route (usually
1000 mL plus the amount of urine output over the
past 24 hours). Maintain accurate intake and output,
and obtain daily weights. Salt intake is generally
maintained at a normal level, although heavy use
should be discouraged.
• Test the urine for protein and specic gravity every
hour. Report a steady decrease in hourly output
or output of less than 30 mL/hr to the healthcare
provider.
• Review available laboratory studies and report nd-
ings to the healthcare provider (e.g., electrolyte lev-
els, CBC with differential, platelets, liver enzyme
levels, uric acid level, hematocrit, serum estriol,
lecithin-to-sphingomyelin ratio).
• Monitor deep tendon reexes and for signs of sei-
zure activity (e.g., increased drowsiness, hyper-
reexia, visual disturbances, and development of
severe pain). If symptoms are present, report to the
healthcare provider immediately.
• If seizures occur, give supportive care, provide a
nonstimulating environment, and have oxygen and
suction available. Institute seizure precautions.
• Be alert for complications (e.g., start of labor, pulmo-
nary edema, disseminated intravascular coagulation,
heart failure, abruptio placentae, cerebral edema).
• Administer prescribed drugs (e.g., diazepam or
phenobarbital, antihypertensives). The vasodila-
tor hydralazine is usually administered to control
blood pressure. It may be administered orally or
intravenously, depending on the severity of the
condition. If given intravenously, monitor the ma-
ternal and fetal heart rates and the mother’s blood
pressure every 2 to 3 minutes after the initial dose
and every 10 to 15 minutes thereafter. The diastolic
pressure is usually maintained at 90 to 100 mm Hg.
Anticonvulsants such as magnesium sulfate or phe-
nytoin may be given for seizure activity (see drug
monograph for hydralazine for administration and
monitoring of the patient during drug therapy).
Termination of pregnancy
• If bleeding occurs near the estimated date of deliv-
ery, the infant may be delivered by cesarean birth. If
 Drugs Used in Obstetrics CHAPTER 39 631

Table 39.2 Prostaglandins in Obstetrics (Uterine Stimulants)

DINOPROSTONE
Dinoprostone (prostaglandin E2) is a natural chemical in the body that causes uterine and gastrointestinal smooth muscle
stimulation. It also plays an active role in cervical softening and dilation (cervical ripening) unrelated to uterine muscle
stimulation. When used during pregnancy, dinoprostone produces cervical softening and dilation and, in higher doses,
increases the frequency and strength of uterine contractions.
Dinoprostone is used to start and continue cervical ripening at term. In larger doses, it is also used to expel uterine contents in
cases of intrauterine fetal death, benign hydatidiform mole, missed spontaneous miscarriage, and second-trimester abortion.
Occasionally, oxytocin and dinoprostone are used together to shorten the duration of time required to expel uterine contents.
DRUG USE DOSAGE
Cervidil vaginal insert (slab) Cervical ripening and initiation of The 10-mg slab is inserted transversely into the
10 mg labor posterior fornix of the vagina. The patient should remain
supine for 2 hr but may become ambulatory thereafter.
The slab is removed on the onset of labor or 12 hr after
insertion.
Prepidil vaginal gel 0.5 mg/3 Cervical ripening Using the prelled syringe and technique recommended
gm in prelled applicator by the manufacturer, the gel is inserted into the cervical
canal just below the internal cervical os. Depending on
response, the dose may be repeated in 6 hr. Maximum
dose is 1.5 mg (7.5 g) in a 24-hr period.
MIFEPRISTONE AND MISOPROSTOL
Mifepristone (also known as RU-486) is a steroid that binds to the progesterone receptors of the pregnant uterus, blocking the
effects of the hormone progesterone. Blocking this receptor during pregnancy leads to contractions of the uterine muscle
with expulsion of fetal contents.
Misoprostol is a synthetic prostaglandin E used to induce uterine contractions in the pregnant uterus. It is used as a
cervical ripening agent, for induction of labor, and for treatment of serious postpartum hemorrhage in the presence of
uterine atony. Mifepristone followed by misoprostol may be used to terminate an intrauterine pregnancy through 70 days’
gestation.
mifepristone (Mifeprex 200- Medical termination of intrauterine Day 1: mifepristone (Mifeprex) 200 mg as a single dose.
mg tablets) pregnancy through 70 days’ Day 2 and 3: misoprostol 800 mcg buccally 24–48 hr after
and misoprostol (Cytotec gestation, in combination with mifepristone administration. Dose is administered as two
100- and 200-mcg misoprostol 200-mcg tablets in each cheek pouch, held in place for
tablets) 30 min. Any remnants may be swallowed with water or
other liquid.
Day 7–14: Patients should follow up with their
healthcare provider 1–2 wk after the administration
of the mifepristone to conrm that complete
termination of pregnancy has occurred and to evaluate
degree of bleeding. If the pregnancy is not ongoing but
complete expulsion has not occurred, another dose
of 800 mcg misoprostol in the buccal pouches may
be administered. The patient should follow up with
the healthcare provider in approximately 7 days for
assessment.

it appears that a spontaneous abortion (i.e., miscar- intraamniotically, intramuscularly, or by vaginal

riage) is occurring, the woman may be hospitalized
for observation and bed rest, diagnosis for possible
causes (e.g., infection), and uid replacement.
• If a pregnancy is to be terminated (i.e., induced
abortion), the following methods may be used:
 • Before 12 weeks’ gestation: Suction curettage or di-
lation and evacuation
 • From 12 to 20 weeks’ gestation: Intraamniotic in-
stillation of hypertonic saline (20% solution)
or prostaglandin (see Table 39.2), administered
suppository
 • Intrauterine fetal death after 20 weeks’ gestation:
Prostaglandin suppositories with or without
oxytocin augmentation (see the section on uter-
ine stimulants later in this chapter)
• Encourage the persons involved in the loss of an in-
fant to talk about their feelings of grief, sadness, or
anger. Create memories of the experience through
photographs and mementos as appropriate. Have
chaplains involved in supportive processes as
632 UNIT VIII Drugs Affecting the Reproductive System

Table 39.3 Rho(D) Immune Globulin (human)

Rho(D) immune globulin (human) is used to prevent Rh immunization of the Rh-negative patient (mother) exposed to Rh-positive
blood as the result of a transfusion accident, during termination of a pregnancy, or as the result of a delivery of an Rh-positive
infant. An RhD-incompatible pregnancy is assumed present if the fetus/baby is either RhD positive or RhD unknown, or if the
father is either RhD positive or RhD unknown. If the baby or father are known to be RhD negative, Rho(D) immune globulin
injection is not indicated. Rho(D) immune globulin injection 300 mcg is referred to as “full-dose” (Rhophylac, HyperRHO S/D
Full Dose, WinRho SDF); 50-mcg doses are referred to as “minidoses” (HyperRHO S/D Mini-Dose, MICRhoGAM). Dosage
may also be expressed in International Units: 1 mcg = 5 IU. The following refers to use of Rho(D) immune globulin injection
relating to obstetrics
DRUG USE DOSAGE
WinRho SDF: 300, 500, 1000, Transfusion accident Rh-negative, premenopausal women
3000 mcg in single-dose vials who receive Rh-positive red cells
by transfusion should receive one
standard-dose (300 mcg) for each 15
mL of transfused packed red cells.
HyperRHO S/D Full Dose, RhoGAM, Antepartum prophylaxis—Used when First dose: 300 mcg IM at approximately
Rhophylac, WinRho SDF there has been a transfusion accident, 28 weeks’ gestation. (Note:
during termination of a pregnancy Rhophylac and WinRho SD can be
more than 12 weeks’ gestation, or administered IM or IV.)
as the result of a delivery of an Rh- Second dose: Another 300 mcg IM
positive infant within 72 hr of delivery.
HyperRHO S/D Full Dose, RhoGAM, Postpartum prophylaxis 300 mcg IM should be administered
Rhophylac, WinRho SDF within 72 hours of delivery. WinRho
SDF is 120 mcg IM or IV. The dose
should be administered within 72
hr of delivery. (Note: Rhophylac and
WinRho SD can be administered IM
or IV.)
HyperRHO S/D Mini-Dose; MICRhoGAM Postpartum prophylaxis—RhD 50 mcg IM within 72 hr of termination of
prophylaxis after spontaneous or pregnancy.
induced abortion up to 12 weeks’
gestation.

appropriate. Listen and allow feelings to be vented.
Give answers (if known) regarding future preg-
nancies. Refer for other counseling as appropriate.
Anticipate that depression may develop over the
next few weeks and that the patient may need treat-
ment for depression.
• Administer Rho(D) immune globulin to an Rh-
negative mother within 72 hours of the termination
of pregnancy (Table 39.3). Also check the patient’s
rubella titer; if low, obtain an order for inoculation
immediately after pregnancy.
Normal labor and delivery
• Perform routine admission procedures (e.g., vital signs,
fetal heart rate monitoring, birth plan). Determine
whether there will be someone present during the de-
livery process who will provide emotional support.
• Follow institutional guidelines regarding activity
level of the mother; some permit ambulation during
early stages of labor.
• During labor, provide pain relief, alternate side-
to-side positioning (avoid lying at on back), and
intervene with comfort measures (e.g., back rub,
pelvic rocking, efeurage, warm shower, music).
Encourage leg extension and dorsiexion of the foot
to relieve spasms and cramping.
• Provide privacy, and support the woman and coach
when necessary.
• Check for bladder distention. Have patient void ev-
ery 2 hours.
• Maintain adequate hydration by giving ice chips or
clear liquids. Check hydration status throughout
labor by observing mucous membranes, dryness of
lips, and skin turgor. Give oral hygiene frequently.
Do not give solid foods unless specically approved
by the healthcare provider.
• As labor progresses, continue to monitor the mater-
nal and fetal vital signs and the frequency, duration,
and intensity of uterine contractions.
• Report contractions of 90 seconds or more and those
not followed by complete uterine relaxation. Report
abnormal patterns on the fetal monitor, such as de-
creased variability, late decelerations, and variable
decelerations of the fetal heart rate.
• Continue to coach when necessary.
• As vaginal discharge increases, wash the perineum
with warm water, then dry the area. Change the bed
sheets, pad, and gown when necessary.

• Monitor the temperature every 4 hours while mem-
branes are intact and temperature remains within
normal range. Monitor every 2 hours if the tempera-
ture is elevated or if the membranes have ruptured.
• After delivery, record the time of delivery and po-
sition of the infant; the type of tear or episiotomy
and type of suture used in repair, if appropriate; any
anesthetic or analgesic used during repair; the time
of placental delivery; and any complications (e.g.,
additional bleeding, postpartum hemorrhage, or
neonatal distress).
• Administer and record oxytocic agent, as ordered.
Immediate neonatal care. Before delivery, the mater-
nal history through the current stage of labor should
be reviewed to identify potential complications that
may arise for the neonate. Although a complete physi-
cal examination of the neonate will be performed later,
a preliminary assessment and recording of data must
be completed at the time of birth. The following proce-
dures must be completed by the healthcare provider or
nurse immediately after delivery.
Airway. Ensure that the airway remains open. As
soon as the head is delivered, suction the orophar-
ynx and nasal passages with a small bulb syringe.
Immediately after delivery, hold the newborn with the
head lowered at a 10- to 15-degree angle to help drain
amniotic uid, mucus, and blood. Resuction with the
bulb syringe as necessary.
Clamping the umbilical cord. Consult with the mother
before delivery if she is participating in cord blood
banking. If so, special containers must be used for
blood storage and registration. When the airway is
opened and the respirations have stabilized, the neo-
nate should be held at the same level as the uterus un-
til cord pulsations cease. The cord is then clamped or
ligated.
Health status. The health status of the neonate is es-
timated at 1 minute and 5 minutes after delivery using
the Apgar scoring system (see Table 39.1). Rapid esti-
mation of gestational age is also performed (see Fig.
39.2).
Temperature maintenance. The neonate should be
dried immediately and body temperature maintained
with the use of prewarmed blankets, a heated infant
warmer. If the neonate is term and in stable condition
as assessed by the Apgar score, temperature may be
maintained by skin-to-skin contact with the mother.
Eye prophylaxis. It is a legal requirement that every
newborn baby’s eyes be treated prophylactically for
Neisseria gonorrhoeae. Another rapidly emerging neo-
natal conjunctival infection is chlamydial ophthalmia
neonatorum, which is caused by Chlamydia trachomatis.
The neonate may have become infected during birth
if the mother is infected. Ophthalmic erythromycin
is used for prophylactic treatment of neonatal con-
junctivitis caused by N. gonorrhoeae or C. trachomatis
(see drug monograph on erythromycin ophthalmic
Drugs Used in Obstetrics CHAPTER 39 633
ointment later in this chapter). Instillation of the oph-
thalmic agent may be delayed up to 1 hour to facilitate
parent-child bonding.
Other procedures. While the parents are bonding with
the newborn infant, the nurse should prepare an infant
identication bracelet and place it on the baby, with a
duplicate placed on the mother. Examine the placenta
and cord for anomalies and verify the presence of one
vein and two arteries. Samples of cord blood may be
collected for analysis of the Rh factor, blood grouping,
and hematocrit. The baby may be held by the parents
as long as the infant’s condition is stable. Breastfeeding
should be initiated. The newborn is cared for in the
presence of the family in most institutions while the
weight, measurements, and physical examinations are
completed. Some healthcare providers also order an
IM injection of vitamin K as prophylaxis against hem-
orrhage along with an IM injection of hepatitis B vac-
cine. Evaluation of the infant’s vital signs and color is
performed on a continuum. Alterations from baseline
are evaluated and reported.
Postpartum care. Postpartum is dened as the time be-
tween delivery and return of the reproductive organs
to prepregnancy status.
• An Rh-negative mother may receive Rho(D) im-
mune globulin within 72 hours of the completion of
the pregnancy.
• If the mother’s rubella titer is low, an appropriate
time for inoculation is immediately after delivery.
• Continue to assess the fundal height, position, and
lochia until the woman is discharged. The lochia nor-
mally progresses from blood red (bright) to darker
red with some small clots (1 to 3 days postpartum),
to pinkish, thin, watery consistency (4 to 10 days),
to a yellowish or creamy color (11 to 21 days). The
odor should be similar to that of a normal menstrual
ow; a foul-smelling odor should be reported to the
healthcare provider. Pads should be changed at fre-
quent regular intervals or with each voiding rather
than waiting for them to become heavily soiled.
• On delivery, the breasts secrete a thin yellow uid
called colostrum. Within the rst few days, breast
milk becomes available. This may produce some
discomfort for the mother as the breasts become
full. Engorgement in the breastfeeding mother can
be minimized by having the infant nurse more fre-
quently (every 60 to 90 minutes) or massaging and
hand-expressing or pumping milk to empty the
breasts completely. A warm shower or application
of warm, moist heat may also provide relief.
• The quantity of breast milk varies among moth-
ers. Diet, uid intake, and level of anxiety all affect
lactation.
• Monitor and record the number of infant voidings
(one wet diaper per day of age until 5 days old and
then six to eight wet diapers per day is average) and
stools (usually one in 24 hours).
634 UNIT VIII Drugs Affecting the Reproductive System
• Weigh the infant daily. It is normal for an infant to
lose up to 7% of their body weight over the rst 3
days. A weight gain of 0.75 to 1 ounce daily indi-
cates that the infant is receiving adequate nutrition-
al intake.
• Help the mother hold the baby correctly and pro-
vide instruction and guidance on the correct tech-
nique of breastfeeding, bottle feeding, and burping
the baby.
• Suppression of lactation in the nonnursing mother
includes having the woman wear a supportive,
well-tting bra within 6 hours of delivery. The bra
is removed only during bathing. Ice packs may be
applied to the axillary area of the breast for 15 to
20 minutes four times daily. Teach the mother to
avoid any stimulation of her breasts until the feel-
ing of fullness has subsided (usually 5 to 7 days).
The mother should not use a breast pump and when
showering should allow the warm water to run
down her back to avoid stimulating lactation.
• Encourage the mother who is breastfeeding or for-
mula feeding to eat a well-balanced diet with ad-
equate protein, vitamins, and uids to help restore
the body to the optimal level.
• Continue to provide emotional support to the new
mother and father.
• Afterpains often require a mild analgesic. For the
breastfeeding mother who is experiencing after-
pains, administering a mild analgesic approximately
40 minutes before nursing may relieve discomfort.
• Check on voiding and return of normal bowel elimi-
nation during the postpartum period.
• Check vital signs every shift or more frequently
when indicated.
• Monitor laboratory reports during the postpartum
period. The hematocrit may rise during the initial
period after childbirth; white blood cells, mainly
neutrophils, may be elevated as well, making it dif-
cult to diagnose an infection.
• Monitor for thromboembolisms during the postpar-
tum period. Clotting factors and brinogen are in-
creased during pregnancy and the immediate post-
partum period.
Patient Education
• Prenatal pregnancy education starts with open
communication with the expectant family. They
must be guided to understand the need for prenatal
care. Keep emphasizing what the family can do to
optimize the chances for a healthy baby, including
maintaining general health, nutritional needs, ade-
quate rest, and appropriate exercise and continuing
prescribed medication therapy.
• The amount of information provided to the expect-
ant mother or parents is individualized. The follow-
ing health teaching is an overview of information
that may be given (refer to a maternity textbook to
cover the areas not addressed).
Adequate rest and relaxation. Assist the individual to
plan for adequate rest periods throughout the day to
prevent fatigue, irritability, and exhaustion. Advise the
mother to avoid long periods of standing in one place
and to perform some daily activities while sitting.
Activity and exercise. Usually the woman can contin-
ue to perform common activities of daily living and
her usual exercise regimen. As pregnancy continues,
she will need to consult with her healthcare provider
regarding exercise limits. New attempts at strenuous
exercise (such as jogging or aerobics) should not be
started during pregnancy. Daily walks in fresh air are
encouraged.
Encourage good posture and participation in pre-
natal classes in which exercises are taught to strength-
en the abdominal muscles and relax the pelvic oor
muscles.
The woman should avoid lifting heavy objects and
anything that might cause physical harm, especially as
the pregnancy progresses, because pregnancy may af-
fect balance.
Employment. Advice about continued employment
should be based on the type of job; working condi-
tions; amount of lifting, standing, or exposure to toxic
substances; and the individual’s state of health.
General personal hygiene. Encourage maintenance
of general hygiene through daily tub baths or show-
ers. The pregnant woman should avoid soaking in a
hot tub or whirlpool because of the danger of slipping
and falling while getting in and out of the tub. Tub
baths should not be taken once the membranes have
ruptured.
Encourage the use of plain soap and water to
cleanse the perineum and prevent odors. Deodorant
sprays should not be used because of possible irrita-
tion. Tell the pregnant woman that an increase in vagi-
nal discharge is common. Discharge that is yellowish
or greenish, is foul smelling, or causes irritation and
itching should be reported for further evaluation.
Clothing. Encourage the mother to dress in noncon-
stricting clothing. As the pregnancy progresses, the
mother may be more comfortable with a maternity
girdle to support the abdomen. Encourage the mother
to wear a well-tting bra to provide proper breast sup-
port. The pregnant woman should avoid any restric-
tive clothing that would limit lower leg circulation.
Oral hygiene. Encourage the pregnant patient to have
a thorough dental examination at the beginning of the
pregnancy. She should tell the dentist that she is preg-
nant at the time of the examination.
Sexual activity. Refer to an obstetrics textbook for dis-
cussion of alterations in sexuality during pregnancy.

The wide range of feelings, needs, and intervention
deserve more consideration than can be presented in
this text.
Smoking and alcohol. The pregnant woman should
be encouraged to abstain from smoking, chewing, or
vaping tobacco products; using nicotine patches; or
drinking alcohol during pregnancy. Numerous data
indicate that use of tobacco products and drinking
are dangerous to the fetus. Increased incidences of
neonatal mortality, low birth weight, and prematurity
have been well reported (see Chapter 48).
Nutritional needs. Balanced nutrition is always to be
encouraged, but it is especially important throughout
the course of the pregnancy. Recommended daily al-
lowances vary based on the individual’s age, weight at
the time of pregnancy, and daily activity level.
Encourage eliminating caffeine from the diet dur-
ing pregnancy. Limit the consumption of coffee, tea,
cola beverages, and cocoa. Discuss with the woman
to avoid highly spiced foods and any foods that she
knows have caused heartburn and to eat all foods in
moderation.
Usual weight gain is 3.5 to 5 pounds during the rst
trimester, followed by an average gain of 1 pound per
week during the second and third trimesters. The rate
of weekly weight gain may be slightly higher for an un-
derweight woman and slightly lower for overweight
women. Stress the need to report a weight gain of 2 or
more pounds in any 1 week for further evaluation.
Bowel habits. Assess the individual’s usual pattern of
elimination and anticipate its continuance until later
in pregnancy. Pressure on the lower bowel from the
presenting part of the fetus may cause constipation
and hemorrhoids. Stool softeners or a bulk laxative
may be prescribed if problems persist. Encourage the
consumption of fresh fruits and vegetables and whole
grains and an adequate intake of six to eight 8-ounce
glasses of uid daily.
Douching. Discourage any type of douching because it
is contraindicated during pregnancy.
Discomforts of pregnancy. Use assessment data as
pregnancy progresses to determine individualized
teaching needed to deal with discomforts such as back-
ache, leg cramps, hemorrhoids, and edema.
Complications of pregnancy. Individualize health
teaching to deal with complications as they arise. The
woman should always immediately report loss of
uid vaginally; decreased fetal movement; dizziness;
double or blurred vision; severe headache; abdominal
pain or persistent vomiting; fever; edema of the face,
ngers, legs, or feet; and weight gain in excess of 2
pounds weekly.
Drugs Used in Obstetrics CHAPTER 39 635
At discharge
• Review instructions on self-care (e.g., breast care,
fundal height, lochia, incisional or perineal care,
bowel and bladder expectations, nutritional and
uid intake, activity). Stress signs of problems that
should be reported to the healthcare provider.
• Contraceptives: Discuss appropriate sexual activity
and limitations. Remind the woman that breastfeed-
ing is not a form of contraception. Alternative meth-
ods of contraception should be used if the patient
does not wish to become pregnant immediately.
• Review infant care needs, bathing, vital signs, fon-
tanel assessment, care of the umbilical cord and
circumcision, normal sleep pattern, and feeding.
Assess the breastfeeding process and assist with ed-
ucation and a public health nurse referral as needed.
• Stress the need for follow-up care of the mother and
infant. Provide the specic date and time of health-
care provider appointments. The mother usually re-
turns for a follow-up examination at the healthcare
provider’s ofce 6 to 8 weeks after delivery.
Fostering health maintenance
• Discuss any medications prescribed for the mother
or infant and how they will benet the course of
treatment to produce optimal response.
• Seek cooperation and understanding of the following
points so that medication adherence is increased: name
of medication; dosage, route, and times of administra-
tion; and common and serious adverse effects.
Patient self-assessment. Enlist the mother’s help in
developing and maintaining a written record of moni-
toring parameters (e.g., blood pressure, pulse, daily
weight, presence and relief of discomfort, exercise tol-
erance, fetal movement). See Patient Self-Assessment
Forms for Prenatal Care and Postpartum Care on the
Evolve website. Complete the Premedication Data
column for use as a baseline to track response to drug
therapy, progression of the pregnancy, and postpartum
recovery. Ensure that the patient understands how to
use the form, and instruct the patient to take the com-
pleted form to follow-up visits. During follow-up vis-
its, focus on issues that will foster adherence with the
therapeutic interventions prescribed.
DRUG THERAPY IN PREGNANCY
DRUG CLASS: UTERINE STIMULANTS
Uses
There are four primary clinical indications for the use of
uterine stimulants: (1) induction or augmentation of la-
bor; (2) control of postpartum atony and hemorrhage; (3)
control of postsurgical hemorrhage (as in cesarean birth);
and (4) induction of therapeutic (induced) abortion.
Induction of labor. Uterine stimulants, primarily
oxytocin, may be prescribed in cases in which, in the
636 UNIT VIII Drugs Affecting the Reproductive System
healthcare provider’s judgment, continuation of the
pregnancy is considered to be a greater risk to the
mother or fetus than the risk associated with drug-
induced induction of labor. A history of precipitous la-
bor and delivery (rapid labor and delivery lasting less
than 3 hours), postterm pregnancy (pregnancy last-
ing longer than 40 weeks), prolonged pregnancy with
placental insufciency, PROM, or preeclampsia may
indicate the need to induce labor. Vaginal inserts and
gels and oral dosage forms of prostaglandins are being
tested as adjunctive therapy to help ripen the cervix
(see Table 39.2).
Augmentation of labor. With regard to augmentation of
labor, in general, oxytocin should not be used to has-
ten labor. The type and force of contraction induced
by the oxytocin may be harmful to the mother and fe-
tus. In occasional cases of dysfunctional labor, there is
a prolonged latent phase of cervical dilation or arrest
of descent through the birth canal. Oxytocin infusions
starting with low dosages and continuous fetal moni-
toring may be benecial in these cases.
Postpartum atony and hemorrhage. After delivery of
the fetus and the placenta, the uterus sometimes remains
accid and “boggy.” Continued IV infusions of low-dose
oxytocin or IM injections of methylergonovine (see next
monograph) may be used to stimulate rm uterine con-
tractions to reduce the risk of postpartum hemorrhage
from an atonic uterus or postsurgical hemorrhage.
Occasionally, doses of methylergonovine are ad-
ministered orally for a few days after delivery to assist
in uterine involution.
Therapeutic (induced) abortion. Pharmacologic agents
are usually not effective in evacuating uterine con-
tents until several weeks into the second trimester of
pregnancy. Various dosage forms of prostaglandins
(mifepristone and misoprostol; see Table 39.2) and
hypertonic sodium chloride (20%) may be effective.
Uterine smooth muscle is not very responsive to ox-
ytocin stimulation until late in the third trimester, so
even large doses of oxytocin are not indicated in thera-
peutic abortion. Regardless of the stage of pregnancy,
stimulants such as methylergonovine may be pre-
scribed after the uterus is emptied to control bleeding
and maintain uterine muscle tone.
oxytocin (ŏk-sē-TŌ-sĭn)
Pitocin (pĭ-TŌ-sĭn)
Actions
Oxytocin is a hormone produced in the hypothala-
mus and stored in the pituitary gland. When released,
it stimulates the smooth muscle of the uterus, blood
vessels, and the mammary glands. When administered
during the third trimester of pregnancy, active labor
may be initiated.
Uses
Oxytocin is the drug of choice for inducing labor at
term and for augmenting uterine contractions during
the rst and second stages of labor. Oxytocin is rou-
tinely administered immediately postpartum to con-
trol uterine atony and hemorrhage.
Therapeutic Outcomes
The primary therapeutic outcomes associated with
oxytocin therapy are as follows:
1. Initiation of labor
2. Support of uterine contractions during the rst and
second stages of labor
3. Control of postpartum bleeding
Nursing Implications for Oxytocin
Premedication assessment. Never leave a patient re-
ceiving an oxytocin infusion unattended. Ensure that
the IV site is functional before adding oxytocin; use an
infusion pump.
1. Monitor maternal vital signs, especially blood pres-
sure and pulse rate.
2. Obtain baseline assessment data of the mother’s hy-
dration status. Continue to monitor intake and out-
put throughout drug therapy.
3. Monitor characteristics of uterine contractions (e.g.,
frequency, rate, duration, and intensity).
4. Monitor fetal heart rate and rhythm. Be alert for
signs of fetal distress.
5. Check amount and characteristics of vaginal discharge.
Availability. IV: 10 units/mL in 1-mL, 10-mL, 30-mL,
and 50-mL vials.
Dosage and administration
• Starting the infusion: Establish records of baseline vi-
tal signs and intake and output. Oxytocin adminis-
tered IV should be added to the solution after the IV
is shown to be patent and running.
• Rate: Careful monitoring of the prescribed rate of
infusion is imperative. Should the IV line suddenly
open, the resulting severe contractions could be ex-
tremely dangerous to the mother and fetus.
• Infusion pump: A constant infusion pump is essen-
tial to controlling the rate of administration. Keep in
mind that a pump can fail.
• Induction of labor: IV: Initial rate: 0.5 to 1 milliunit
(mU). May increase by 1 to 2 mU/min every 15 to 60
minutes. It is absolutely necessary that an infusion
pump be used to help control the rate of oxytocin in-
fusion. Most pregnancies that are close to term will
respond well to 2 to 10 mU/min. Rarely will a patient
require more than 20 mU/min. Those patients at 32 to
36 weeks’ gestation often require 20 to 30 mU/min or
more to develop a laborlike contraction pattern. Rates
of infusion should not be altered more frequently
than every 15 to 30 minutes. It is often necessary to
reduce or discontinue the infusion as spontaneous
uterine activity develops and labor progresses.

• Augmentation of labor: IV: Occasionally, labor that
started spontaneously may not progress satisfacto-
rily. Labor may be augmented by oxytocin infusions
at rates of 0.5 to 2 mU/min.
• Postpartum hemorrhage: IM: 3 to 10 units given after
delivery of the placenta. IV: 10 to 40 units may be
added to 1000 mL of normal saline solution and run
at a rate necessary to control uterine atony.
Medication Safety Alert
Before starting an oxytocin infusion, establish records of
baseline vital signs and intake and output. A constant infu-
sion pump is recommended for controlling the rate of ad-
ministration. If the infant develops sudden distress, reduce
the oxytocin infusion to the slowest possible rate according
to hospital policy, turn the mother to the left lateral position,
administer oxygen by nasal cannula or face mask, and call
the healthcare provider immediately.
Common adverse effects
Gynecologic
Uterine contractions. Oxytocin infusions should be
monitored by both a tocodynamometer, or “toco” (an
instrument that measures uterine contractions), and a
fetal heart monitor. Maintain an ongoing record of the
frequency, duration, and intensity of uterine contrac-
tions. Contractions longer than 90 seconds require that
the ow rate of the oxytocin be slowed or discontinued.
Gastrointestinal
Nausea, vomiting. Although uncommon, these ad-
verse effects may occur. Reduction in dosage may con-
trol symptoms.
Serious adverse effects
Fetal heart rate
Fetal distress. Fetal heart rate should be monitored
continuously and especially closely during uterine
contractions. Normal fetal heart rate is 120 to 160
beats/min. Indications of fetal distress may be mani-
fested by tachycardia (>160 beats/min) followed by
bradycardia (<120 beats/min). As the degree of dis-
tress progresses, bradycardia occurs more frequently
and lasts longer than 15 seconds after contractions. If
the infant develops sudden distress, reduce the oxy-
tocin infusion to the slowest possible rate according to
hospital policy, turn the mother to the left lateral posi-
tion, administer oxygen by nasal cannula or face mask,
and call the healthcare provider immediately.
Cardiovascular
Hypertension, hypotension. Check the mother’s blood
pressure and pulse rate at least every 30 minutes dur-
ing oxytocin infusion. Report trends upward or down-
ward to the healthcare provider because oxytocin may
cause hypertension or hypotension.
Endocrine
Water intoxication. Oxytocin can alter uid balance by
stimulating antidiuretic hormone, causing the body to
Drugs Used in Obstetrics CHAPTER 39 637
accumulate water. This is particularly likely to occur
if oxytocin is administered with electrolyte solutions.
Symptoms of water intoxication include drowsiness,
listlessness, headache, confusion, anuria, edema, and,
in extreme cases, seizures.
Metabolic
Dehydration. Because mothers are routinely placed on
nothing by mouth (NPO) status during labor, an occa-
sional patient may develop dehydration, even though
an IV is running. Monitor urine output; dry, crusted
lips; and requests for water. Report to the healthcare
provider and request ice chips and additional IV uids
if appropriate.
Medication Safety Alert
Overdosage of oxytocin may cause hyperstimulation of the
uterus, resulting in severe contractions with possible abrup-
tio placentae, cervical lacerations, impaired uterine blood
ow or rupture, and fetal trauma.
Postpartum hemorrhage. Early postpartum hemor-
rhage occurs within the rst 24 hours after delivery
and is usually dened as a blood loss of 500 mL or
more. The hemorrhage may be caused by uterine at-
ony, retained fragments of placenta, or lacerations of
the vaginal tract. Less common causes include defec-
tive blood clotting mechanisms, uterine eversion, and
uterine infections.
Oxytocin is routinely administered after delivery of
the placenta to cause the uterus to contract and to de-
crease blood loss. Always check the height of the fun-
dus of the uterus (usually at umbilical level) every 5
minutes after delivery. Report if the uterus is not rm
or the height is rising. (This may be an indication of
urinary retention or a uterus lling with blood.) When
the uterus becomes boggy, uterine massage is neces-
sary until it becomes rm.
Check the vaginal ow rate on each perineal pad at
least every 30 minutes. With uterine atony or retained
placental fragments, the uterus becomes boggy and
dark vaginal bleeding is present; with a laceration of
the cervix or vagina, the bleeding is bright red and the
uterus is rm. Regardless of the cause of postpartum
hemorrhage, the woman must be observed carefully
for signs of hypovolemic shock.
Monitor vital signs as ordered by the healthcare pro-
vider or every 15 minutes until stable, every 30 minutes
for 2 hours, and then every hour until denitely stable.
Report an increasing respiratory rate; pulse rate that
increases and becomes thready; a pulse decit; blood
pressure that indicates hypotension; skin that is pale,
cold, and clammy; or nail beds, lips, and mucous mem-
branes that are pale or cyanotic. Monitor urine output
and report an output of 30 mL/hr or less. Observe for
restlessness and complaints of thirst and for any de-
crease in level of consciousness.
638 UNIT VIII Drugs Affecting the Reproductive System
Drug interactions
Anesthetics. Monitor the blood pressure and heart
rate and rhythm closely. Report signicant changes.
For those patients receiving a local anesthetic contain-
ing epinephrine, immediately report any complaints
of diaphoresis, fever, chest pain, palpitations, or severe
throbbing headache.
methylergonovine maleate (mĕth-ĭl-ŭr-GŎN-ō-vēn MĂL-
ē āt)
Actions
Methylergonovine directly stimulates uterine contrac-
tions. Small doses produce contractions with normal
resting muscle tone, intermediate doses cause more
forceful and prolonged contractions with an elevated
resting muscle tone, and large doses cause severe, pro-
longed contractions. Because of this sudden, intense
uterine activity, which is dangerous to the fetus, this
agent cannot be used for induction of labor.
Uses
Methylergonovine produces more sustained con-
tractions than oxytocin and is used in small doses in
postpartum patients to control bleeding and maintain
uterine rmness. Methylergonovine may be used in
patients who wish to breastfeed because it will not
inhibit stimulation of milk production by prolactin.
Hypertension and headaches may develop in patients
who have received caudal or spinal anesthesia fol-
lowed by a dose of methylergonovine. Monitor the pa-
tient’s blood pressure and heart rate and rhythm.
Therapeutic Outcome
The primary therapeutic outcome associated with
methylergonovine therapy is reduced postpartum
blood loss.
Nursing Implications for Methylergonovine
Premedication assessment
1. Ask for a medical history, especially of kidney disease,
liver disease, high blood pressure, heart disease (e.g.,
mitral valve stenosis, chest pain, recent heart attack),
diabetes, high cholesterol, smoking/tobacco use, blood
vessel disease (e.g., Raynaud disease), or complications
during pregnancy (e.g., preeclampsia or eclampsia).
2. Obtain baseline vital signs, especially blood pres-
sure and pulse.
3. Assess amount and characteristics of vaginal dis-
charge and fundal height and contractility.
Availability. PO: 0.2-mg tablets.
Injection: 0.2 mg/mL in 1-mL ampules.
Dosage and administration. Adult: PO: 0.2 mg three or
four times daily for up to 1 week.
IM/IV: 0.2 mg; repeat as necessary every 2 to 4 hours.
Medication Safety Alert
Use methylergonovine with extreme caution in patients with
hypertension, preeclampsia, heart disease, mitral valve ste-
nosis, sepsis, or hepatic or renal impairment.
Common adverse effects
Gastrointestinal
Nausea, vomiting. These adverse effects are usu-
ally mild and tend to resolve with continued therapy.
Encourage the patient not to discontinue therapy with-
out rst consulting the healthcare provider.
Abdominal cramping. This is normally an indication of
therapeutic activity, but, if severe, reduction or discon-
tinuation of medication may be necessary.
Serious adverse effects
Cardiovascular
Hypertension. Certain patients, especially those who
are eclamptic or were previously hypertensive, may be
particularly sensitive to the hypertensive effects of this
agent. These patients have a higher incidence of devel-
oping generalized headaches, severe dysrhythmias, and
strokes. Monitor the patient’s blood pressure and pulse
rate and rhythm. Inform the healthcare provider immedi-
ately if the patient complains of headache or palpitations.
Drug interactions. Drugs that may enhance therapeutic
and toxic effects of methylergonovine include macrolide
antibiotics (e.g., erythromycin, clarithromycin), HIV
protease or reverse transcriptase inhibitors (e.g., delavir-
dine, indinavir, nelnavir, ritonavir), and azole antifun-
gal agents (e.g., itraconazole, voriconazole). The dose of
methylergonovine should be reduced to prevent toxicity.
DRUG CLASS: UTERINE RELAXANTS
Uterine relaxants, also known as tocolytic agents,
are used primarily to delay or prevent preterm la-
bor and delivery in selected patients (see the section
Assessment of the Pregnant Patient at Risk earlier in
the chapter). Tocolytic agents act by inhibiting uter-
ine muscle contractions. According to the American
College of Obstetricians and Gynecologists, they are
used to inhibit labor up to 48 hours, enabling cortico-
steroids to be administered to mature fetal lungs and
transport of the mother to a hospital with a neonatal
intensive care unit. Agents used are beta-2 agonists
(e.g., terbutaline), calcium channel blockers (e.g., nife-
dipine), magnesium sulfate, and nonsteroidal anti-
inammatory drugs (e.g., indomethacin).
magnesium sulfate
Actions
Magnesium is an ion normally found in the blood in
concentrations of 1.8 to 3 mEq/L. When administered

parenterally in doses sufcient to produce levels high-
er than 4 mEq/L, the drug may depress the central ner-
vous system and block peripheral nerve transmission,
producing anticonvulsant effects and smooth muscle
relaxation.
Uses
Magnesium sulfate is an option in obstetrics to inhibit
premature labor, control maternal seizure activity as-
sociated with preeclampsia or eclampsia and to pro-
vide neuroprotection in preventing cerebral palsy to
preterm infants. When used as an anticonvulsant or to
inhibit labor, blood levels should be maintained at 4
to 8 mEq/L. Clinical trials have not demonstrated that
use of magnesium sulfate for tocolysis is any more ef-
fective than placebo, and calls are being made for dis-
continuation of its use for inhibiting preterm labor. If
being prescribed for neuroprotection, a 24-hour infu-
sion before delivery is adequate. It is recommended
that magnesium sulfate not be used beyond 5 to 7 days
for the treatment of preterm labor because it has been
shown to cause low calcium levels and bone changes
(osteopenia) in the baby. There is positive evidence of
human fetal risk, but the potential benets from using
the drug in pregnant women may be acceptable in cer-
tain situations despite its risks.
Patients maintained at a magnesium serum level be-
tween 3 and 5 mEq/L rarely show any adverse effects
from hypermagnesemia. At a level of approximately 5
to 8 mEq/L, patients begin to show increasing signs of
toxicity that correlate fairly well to serum levels. Early
signs of maternal toxicity are complaints of “feeling hot
all over” and “being thirsty all the time,” ushed skin,
and diaphoresis. Patients may then become hypotensive
and have depressed patellar, radial, and biceps reexes
and accid muscles. Later signs of hypermagnesemia
are central nervous system depression shown rst by
anxiety and then confusion, lethargy, and drowsiness.
If serum levels continue to increase, cardiac depression
and respiratory paralysis may result. Magnesium sul-
fate should be administered with extreme caution to
patients with impaired renal function and whose urine
output is less than 100 mL over the past 4 hours.
Therapeutic Outcomes
The primary therapeutic outcomes associated with
magnesium sulfate therapy are as follows:
1. Arrest of preterm labor
2. Elimination of maternal seizure activity
3. Possible neuroprotection against the development
of cerebral palsy in the newborn.
Nursing Implications for Magnesium Sulfate
Premedication assessment
1. Obtain baseline vital signs, especially blood pres-
sure, pulse, and respirations.
2. Perform a mental status examination: level of con-
sciousness, orientation, and anxiety level.
Drugs Used in Obstetrics CHAPTER 39 639
3. Check deep tendon reexes; report hyporeexia or
absence of reexes.
4. Review intake and output record; report declining
output.
5. Have calcium gluconate or calcium chloride and
equipment for IV administration available in case
they are needed.
6. Obtain baseline laboratory values (e.g., serum mag-
nesium level).
7. Monitor fetal heart rate and uterine activity; report
distress.
Availability. Injection: solutions: 1% (0.081 mEq/mL),
2% (0.162 mEq/mL), 4% (0.325 mEq/mL), 8% (0.65
mEq/mL), and 50% (4 mEq/mL).
Dosage and administration. IM: Intramuscular injec-
tion is extremely painful. Avoid, if possible, or admin-
ister in conjunction with a local anesthetic.
IV: It is essential that an infusion pump be used to
help control infusion of the loading dose and continu-
ous drip.
Seizures in preeclampsia/eclampsia. IV: Loading dose:
4 g of magnesium sulfate is added to 250 mL of 5%
dextrose in water (D5W) and infused slowly at a rate
of 10 mL/min. (The IV loading dose is usually admin-
istered at the same time as a 10-g IM loading dose.)
Maintenance dose: 1 to 2 g/hr by continuous infusion.
Preterm labor. IV: Loading dose: 4 g of magnesium
sulfate is added to 250 mL of D5W or 0.9% sodium
chloride solution and infused IV over 30 minutes.
Maintenance dose: 1 to 3 g/hr by continuous infusion.
Medication Safety Alert
Deep tendon reexes, uid intake and output, vital signs, and
orientation to the environment must be monitored on a regu-
lar, ongoing basis during the administration of magnesium
sulfate.
Serious adverse effects
Neurologic
Deep tendon reexes. The presence or absence of the
patellar reex (knee-jerk reex), biceps reex, or radial
reex is a primary monitoring parameter for magne-
sium sulfate therapy.
The patellar reex should be monitored hourly if
the patient is receiving a continuous IV infusion or
before every dose if being administered intermittently
IM or IV. If the reex is absent, further doses should be
withheld until it returns. If the patellar reex cannot
be used because of epidural anesthesia, the biceps or
radial reex may be used.
Confusion. Perform a baseline assessment of the pa-
tient’s degree of alertness and orientation to name,
place, and time before initiating therapy. Make regu-
larly scheduled mental status evaluations to ensure
that the patient is oriented.
640 UNIT VIII Drugs Affecting the Reproductive System
Metabolic
Intake and output. Magnesium toxicity is more likely
to occur in patients with reduced renal output. Report
urine outputs of less than 30 mL/hr or less than 100
mL over 4 hours. Observe the urine color and meas-
ure the specic gravity. Note any other uid and elec-
trolyte loss, such as vaginal bleeding, diarrhea, or
vomiting.
Cardiovascular
Vital signs. Vital signs (blood pressure, heart rate and
rhythm) should be measured every 15 to 30 minutes
when a patient is receiving a continuous IV infusion.
Take vital signs before and after each administration
for patients receiving intermittent therapy. The res-
piratory rate should be at least 16 breaths/min before
the administration of further doses of magnesium sul-
fate. Do not administer additional doses if there is a
reduced respiratory rate, a drop in blood pressure or
fetal heart rate, or other signs of fetal distress.
Overdose. The antidote for magnesium intoxication
(shown by respiratory depression and heart block) is
calcium gluconate. A 10% solution of calcium gluco-
nate should be kept ready for use at the patient’s bed-
side. The dosage is 5 to 10 mEq (10 to 20 mL) IV over
3 minutes or 0.5 to 2 g (5 to 20 mL) of a 10% solution
of calcium gluconate IV at 200 mg/min. Administer
cardiopulmonary resuscitation until the patient re-
sponds appropriately.
Neonatal effects. Infants born of mothers who receive
magnesium sulfate must be monitored for hypoten-
sion, hyporeexia, and respiratory depression.
Drug interactions
Central nervous system depressants. Central nerv-
ous system depressants, including analgesics, gen-
eral anesthetics, and alcohol, will potentiate the cen-
tral nervous system depressant effects of magnesium
sulfate.
Medication Safety Alert
Periodically check orientation to make sure the patient is
not suffering from magnesium toxicity. Early signs of mater-
nal toxicity are complaints of “feeling hot all over” and “be-
ing thirsty all the time,” ushed skin color, and diaphoresis.
Patients may then become hypotensive; have depressed
patellar, radial, and biceps reexes; and have accid mus-
cles. Later signs of hypermagnesemia are central nervous
system depression, shown rst by anxiety, followed by con-
fusion, lethargy, and drowsiness. If serum levels continue to
increase, cardiac depression and respiratory paralysis may
result. The patellar reex should be monitored hourly if the
patient is receiving a continuous IV infusion or before every
dose if administered intermittently IM or IV. If the reex is ab-
sent, further doses should be withheld until it returns. If the
patellar reex cannot be used because of epidural anesthe-
sia, the biceps or radial reex may be used.
Neuromuscular blockade. Concurrent use of neuro-
muscular blocking agents and magnesium sulfate will
further depress muscular activity. Monitor the patient
closely for depressed reexes and respiration.
DRUG THERAPY FOR NEONATAL CARE
erythromycin ophthalmic ointment (ĕ-rĭth-rō-MĪ-sĭn)
Actions and Uses
Erythromycin is a macrolide antibiotic used prophy-
lactically to prevent ophthalmia neonatorum caused
by N. gonorrhoeae and chlamydial ophthalmia caused
by C. trachomatis.
Therapeutic Outcome
The primary therapeutic outcome associated with eryth-
romycin ophthalmic ointment therapy is prevention of
postpartum gonorrhea or chlamydia eye infection.
Nursing Implications for erythromycin Ophthalmic
Ointment
Premedication assessment. Describe any drainage
present in the eye or on the lids; cleanse thoroughly.
Availability. Ophthalmic ointment: 5 mg/g in 1-g tube.
Dosage and administration
• Ointment: A new tube should be started for each
infant.
• Wash hands: Wash hands immediately before admin-
istration to prevent bacterial contamination. Apply
clean gloves.
• Cleanse the eyes: Using a separate sterile absorbent
cotton or gauze pad for each eye, wash the un-
opened lids from the nose outward until free of
blood, mucus, or meconium.
• Open the eyes and instill medication: For each eye,
separate the eyelids and instill a ¼-inch ribbon of
erythromycin ointment along the lower conjuncti-
val surface; begin at the inner canthus and move to
the outer aspect of the eye. Administer medication
within 2 hours of birth.
• Irrigation: DO NOT irrigate the eyes after instillation.
Common adverse effects
Sensory
Mild conjunctivitis. Mild conjunctival inammation
occurs in the neonate and may interfere with the abil-
ity to focus. This adverse effect generally disappears
in 1 to 2 days. Assure the family that the redness is
temporary.
Drug interactions. No signicant drug interactions
have been reported.
 Drugs Used in Obstetrics CHAPTER 39 641

Nursing Implications for Phytonadione

phytonadione (fī-tō-nă-DĪ ōn)
Premedication assessment. No assessment is required.

Availability. Injection: 1 mg in 0.5-mL ampule and pre-

Actions
lled syringe.
Vitamin K (phytonadione) is a fat-soluble vitamin
necessary for the production of the blood-clotting
Dosage and administration. IM: 0.5 to 1 mg in the lat-
factors prothrombin (factor II), proconvertin (factor
eral aspect of the thigh within 1 hour of birth.
VII), plasma thromboplastin component (factor IX),
and Stuart factor (factor X) in the liver. Vitamin K is
absorbed from the diet and is normally produced by Medication Safety Alert
the bacterial ora in the gastrointestinal tract, from DO NOT administer phytonadione intravenously! Severe re-
which it is absorbed and transported to the liver for actions, including hypotension, cardiac dysrhythmias, and
clotting factor production. Because bacteria have not respiratory arrest, have been reported.
yet colonized the colon, newborns are often decient
in vitamin K. They also may be decient in these
Serious adverse effects
clotting factors and are therefore more susceptible
Hematologic
to hemorrhagic disease in the rst 5 to 8 days after
Bruising, hemorrhage. Observe for bleeding (usually
birth.
occurring on the second or third day). Bleeding may be
seen as petechiae; generalized ecchymoses; or bleeding
Uses
from the umbilical stump, circumcision site, nose, or
Phytonadione is routinely administered prophylacti-
gastrointestinal tract. Assess results of serial prothrom-
cally to protect against vitamin K deciency bleeding
bin times.
(VKDB) of the newborn (formerly known as hemor-
rhagic disease of the newborn).
Drug interactions. No signicant drug interactions
have been reported.
Therapeutic Outcome
The primary therapeutic outcome associated with
phytonadione therapy is prevention of VKDB of the
newborn.
642 UNIT VIII Drugs Affecting the Reproductive System

Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions

Key Points the NCLEX exam and include both NGN (Next Generation) and
traditional questions. See Chapter 1 for further information re-
• Today’s healthcare system is placing more emphasis on garding question types.
self-care for the mother and her newborn. Shortened
hospital stays have heightened the healthcare
professional’s awareness of the need to provide more
Scenario
education to the mother and signicant others, not only A young mother of two children under the age of 3 arrived
for the care needs of the mother but also for those of the at the emergency department (ED) in labor. It was established
newborn. that she was at only 28 weeks’ gestation.
• Every encounter with the mother is an opportunity to
enhance her learning and preparation for parenting. Use of 1. The nurse’s assessment of the pregnant patient in the scenario
community resources for prenatal and parenting classes who is in the early stages of labor includes which of the following?
should be encouraged. (Select all that apply.)
• The prenatal examination provides a basis for establishing 1. Vital signs
the future healthcare needs of the mother and infant. 2. Apgar score
Psychosocial and cultural aspects of care must be 3. Cervical dilation
incorporated into the assessments and interventions 4. Frequency of uterine contractions
planned for self-care. At subsequent prenatal visits, 5. A history of the pregnancy
relevant information must be provided on all aspects of 6. Checking the fundus
self-care to enhance the normal growth and development 7. Fetal heart rate
of the fetus and to prevent or manage potential 8. Effacement
complications of pregnancy. Objective: Identify appropriate nursing assessments during normal
• After delivery, the mother should be provided with the labor and delivery.
pertinent discharge information through one-on-one NCLEX item type: Extended multiple response
teaching or through discharge classes and be provided Cognitive skill: Recognize cues
with telephone follow-up, home visitations, and referrals to
available community resources to meet the care needs of 2. The nurse caring for the patient in the scenario who is estimated
the mother and newborn at home. to be 28 weeks and in preterm labor expects that in addition to
starting an IV for hydration and ruling out any complications, in
• Dinoprostone can be used for cervical ripening or
order to delay delivery, which of the following medications may be
termination of intrauterine pregnancy depending on the
administered? (Select all that apply.)
product used.
• Mifepristone and misoprostol must be used together for 1. Magnesium sulfate
medical termination of intrauterine pregnancy. 2. Nifedipine
3. Dinoprostone
• Oxytocin is used for induction of labor by stimulating
4. Indomethacin
uterine contractions and to control postpartum bleeding
5. Misoprostol
• Magnesium sulfate is used for treatment of preterm labor,
seizures associated with preeclampsia/eclampsia and Objective: Discuss potential complications of preterm labor and
possible prevention of cerebral palsy in infants. when uterine relaxants and magnesium sulfate are used.
NCLEX item type: Multiple response
• Vitamin K deciency is common in the newborn. If vitamin
Cognitive skill: Application
K deciency is not treated, the infant is at risk for vitamin
K deciency bleeding (VKDB), previously known as 3. Choose the most likely options for the information missing from
hemorrhagic disease of the newborn. the sentence below by selecting from the lists of options provided.
• Erythromycin ophthalmic ointment is the only approved
The nurse will assess for __________1_________ and
agent available in the United States for prevention of
___________1__________ when the patient is receiv-
ophthalmia neonatorum.
ing oxytocin for _________2______________ and
__________2__________.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
OPTIONS 1 OPTION 2
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap- Boggy, accid uterus Postpartum hemorrhage
ter content. Excessive thirst Induction of labor
Number and frequency of Postpartum atony
Go to your Evolve website (https://evolve.elsevier.com/Willihng
contractions
anz) for additional online resources.
Increase in number of Augmentation of labor
Clinical Judgment and Next-Generation NCLEX® Exam- perineal pads required
ination-Style Questions The following questions are typical of
 Drugs Used in Obstetrics CHAPTER 39 643

Objective: Describe assessments needed for uterine stimulants 5. The new mother asks the nurse why they had to give her new
administered for induction of labor, augmentation of labor, and baby medication in the eyes. Which response by the nurse would
postpartum atony and hemorrhage. need to be corrected?
NCLEX item type: Cloze 1. “The medication erythromycin ointment is used for all
Cognitive skill: Analyze cues newborns to prevent postpartum eye infections.”
4. The nurse caring for the patient in the scenario who is estimated 2. “Your baby needs to have this eye ointment to be able
to be 28 weeks and in preterm labor expects that in addition to develop proper vision in the future.”
to starting an IV for hydration and in order to delay delivery, 3. “The eye ointment is an antibiotic that prevents
magnesium sulfate was started. The nurse needs to observe for ophthalmia neonatorum.”
what complications that can develop during this phase of labor? 4. “We need to give your baby this medication to prevent
(Select all that apply.) any infections in the eye from birth.”
1. Premature rupture of membranes Objective: Discuss education needed for care of the neonate,
2. Fetal distress including erythromycin ophthalmic ointment.
3. Gestational diabetes NCLEX item type: Multiple choice
4. Preeclampsia Cognitive skill: Comprehension
5. Hyperemesis gravidarum
Objective: Discuss potential complications of preterm labor and
when uterine relaxants and magnesium sulfate are used.
NCLEX item type: Multiple response
Cognitive skill: Application
40 Drugs Used in Men’s and Women’s Health

https://evolve.elsevier.com/Willihnganz

Objectives
1. Describe the major adverse effects and contraindications 4. Describe pharmacologic treatments of benign prostatic
to the use of oral contraceptive agents. hyperplasia.
2. Identify the patient teaching necessary with the 5. Describe the pharmacologic treatment of erectile
administration of the transdermal contraceptive and the dysfunction.
intravaginal hormonal contraceptive.
3. Discuss osteoporosis and its risk factors, as well as
preventative measures and the pharmacologic treatment
used.

Key Terms
leukorrhea (lŭ-kō-RĒ-ă) (p. 644)
sexually transmitted infections
(SĔK-shū-ăl-ē trănz-MĬT-ĕd ĭn-
FĔK-shŭnz) (p. 644)
dysmenorrhea (dĭs-mĕn-ō-RĒ-ă)
(p. 651)
osteoporosis (ŏs-tē-ō-pō-RŌ- erectile dysfunction (ĕ-RĔK-tīl dĭs-
sĭs) (p. 657) FŬNK-shŭn) (p. 665)
benign prostatic hyperplasia (bē-
NĪN prō-STĀT-ĭc hī-pŭr-PLĀ-
zhă) (p. 661)

VAGINITIS
Scrins frm h vagina usually rprsn a nrmal
physilgic prcss, bu if h discharg bcms x-
cssiv, i is knwn as leukorrhea, an abnrmal, usu-
ally whiish, vaginal discharg ha may ccur a any
ag. I affcs alms all fmals a sm im in hir
livs. Lukrrha is n a disas bu a sympm f an
undrlying disrdr. Th ms cmmn caus is an in-
fcin f h lwr rprduciv rac, bu hr physi-
lgic and nninfcius causs f vaginal discharg
ar wll knwn (Bx 40.1).
Th ms cmmn rganisms causing h infcius
yp f lukrrha ar Candida albicans, Trichomonas vag-
inalis, and Gardnerella vaginalis (Bx 40.2). Occasinally,
C. albicans infcins f h muh, gasrinsinal
rac, r vagina may dvlp as scndary infcins
during h us f brad-spcrum anibiics, such as
pnicillins, racyclins, and cphalsprins.
Pahgns ha ar cmmnly ransmid by sx-
ual cnac ar calld sexually transmitted infections
(STIs). In sm disass, such as gnrrha, syphilis,
chlamydia, gnial hrps simplx virus, and human
papillmavirus (HPV) infcin, sxual ransmissin is
h primary md f ransmissin. Th mdicains usd
 ra hs infcins ar fund in Tabl 40.1. In hr
disass, such as giardiasis, shigllsis, and infcins
644
wih h hpaiis viruss, hr impran nnsxual
mans f ransmissin als xis. Unfrunaly, h ru
incidnc f STIs is n knwn in h Unid Sas b-
caus f larg numbrs f unrprd cass.
DRUG THERAPY FOR LEUKORRHEA AND
GENITAL INFECTIONS
S Tabl 40.1
NURSING IMPLICATIONS FOR MEN’S AND
WOMEN’S HEALTH
Assessment
Th fllwing assssmn qusins apply  all ag
grups.
Female reproductive history. Assss fr h fllwing:
• Ag f mnarch
• Usual parn f mnss: durain, numbr f pads
usd, las mnsrual prid
• Pain, discmfr, sping bwn prids, r x-
ndd im f mnsrual w
• Numbr f prgnancis, liv birhs, miscarriags, r
abrins
• Vaginal dischargs, infcins, gnial lsins,
r wars. Dscrib clr, dr, and amun f
 Drugs Used in Men’s and Women’s Health CHAPTER 40 645

Box 40.1 Causes of Vaginal Discharge Box 40.2 Sexually Transmitted Infections
PHYSIOLOGIC BACTERIA
• Ovulation • Neisseria gonorrhoeae
• Coitus • Gardnerella vaginalis
• Oral contraceptives • Treponema pallidum
• Pregnancy • Klebsiella granulomatis
• Premenstruation
CHLAMYDIAE
• Premenarche
• Chlamydia trachomatis
• Intrauterine device
ECTOPARASITES
INFECTIOUS
• Sarcoptes scabiei
• Vaginal
• Phthirus pubis
 • Candida
 • Trichomonas FUNGUS
 • Gardnerella • Candida albicans
 • Toxic shock syndrome
MYCOPLASMA
• Vulvar
• Ureaplasma urealyticum
 • Herpes
• Mycoplasma hominis
 • Condylomata acuminata
 • Syphilis PROTOZOA
 • Bartholinitis • Trichomonas vaginalis
 • Lymphogranuloma venereum • Entamoeba histolytica
 • Granuloma inguinale • Giardia lamblia
 • Urethritis
VIRUSES
 • Pyoderma
• Herpes simplex virus
• Cervical
• Hepatitis A, B, C
 • Gonorrhea
• Cytomegalovirus
 • Chlamydial or bacterial cervicitis
• Human papillomavirus (HPV)
 • Chronic cervicitis
• Poxvirus
 • Pelvic inammatory disease
• Human immunodeciency virus (HIV)
NONINFECTIOUS • Norlyda
• Atrophic vaginitis • Norlyroc
• Foreign body
• Vaginal adenosis
• Allergic vulvovaginitis
• Vulvar, vaginal carcinoma • Ag f mnpaus
• Cervical polyps • Psmnpausal wmn: Has hr bn any vagi-
• Cervical erosions, ulcers nal blding?
• Uterine carcinoma • Hisry and frquncy f Papaniclau (Pap)
• Endometrial myoma ss
• Vesicovaginal stula • Rprduciv prblms (.g., ndmrisis, var-
• Enterovaginal stula
ian cyss, and urin brids)
• Hisry f STIs (.g., chlamydia, syphilis, gnrrha,
yas infcins, gnial hrps, human immun-
discharg; dscrib lsins r any iching. Is hr dcincy virus [HIV], gnial wars [HPV]). If s,
pain wih urinain r sxual inrcurs? whn and wha was h ramn?
• Cnracpiv mhds usd (.g., ral cnracp- • If a prscripin fr ral cnracpiv hrapy is
ivs, inraurin dvic, cndms, r sprmicidal bing rqusd, ask abu any indicain f hypr-
prducs) nsin, har r livr disas, hrmbmblic
• If aking ral cnracpivs, wha yps? Hw lng disrdrs, smking hisry, r cancr f h rpr-
hav ral cnracpivs bn usd? Ar hy akn duciv rgans.
rgularly? Wha, if any, advrs ffcs hav bn
xprincd? Male reproductive history. Assss fr h fllwing:
• Hisry f mulipl sxual parnrs—mal, fmal, • Parn f urinain. Has hr bn a rcn chang
r bh. Wha yp f prcin is usd during sx- in h parn f urinain (.g., difculy iniiaing
ual inrcurs? urin sram, nd  srain  mpy h bladdr,
• Is bras slf-xaminain prfrmd rgularly? frquncy f ncuria, pain n urinain, frquncy,
Hav any abnrmal ndings bn nd, such as urgncy, hmauria, incninnc, dribbling, r uri-
lumps r discharg? nary rnin)?
646 UNIT VIII Drugs Affecting the Reproductive System

Table 40.1 Causative Organisms and Products Used to Treat Genital Infections a
CAUSATIVE ORGANISM GENERIC NAME BRAND NAME
VULVOVAGINITIS
Candida albicans (fungus) butoconazole vaginal cream Gynazole-l
clotrimazole vaginal cream Gyne-Lotrimin
uconazole oral tablets Diucan
miconazole vaginal cream, suppositories Monistat 1, Monistat 3,
Monistat 7
terconazole vaginal cream, suppositories —
Trichomonas vaginalis (protozoa) metronidazole oral tablets Flagyl
tinidazole oral tablets (alternative) Tindamax
Bacterial vaginosis (formerly Metronidazole oral tablets, vaginal gel Flagyl; MetroGel-Vaginal
known as Gardnerella vaginalis secnidazole oral packet (alternative) Solosec
[bacteria])
tinidazole oral tablets (alternative) Tindamax
clindamycin vaginal cream Cleocin
GONORRHEA
Neisseria gonorrhea (bacteria) ceftriaxone —
Gentamicin + azithromycin or Cexime Gentamicin +Zithromax or
(alternative regimens if Ceftriaxone is Suprax
unavailable)
SYPHILIS
Treponema pallidum (spirochete) penicillin G benzathine Bicillin L-A
tetracyclineb —
Doxycyclineb Vibramycin
GENITAL HERPES
Herpes simplex genitalis (virus) acyclovir oral capsules Zovirax
famciclovir oral tablets —
valacyclovir oral tablets Valtrex
CHLAMYDIAE
Chlamydia trachomatis (chlamydia) doxycycline Vibramycin
azithromycin (alternative) Zithromycin

Levooxacin--alternative —

Data from Workowski KA, Bachmann LH, Chan PA; Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2021. MMWR
Recomm Rep. 2021
aSee Chapter 45 for individual drug monographs.
bTetracycline and doxycycline are alternatives to Penicillin G Benzathine if penicillin allergy is present. Guidelines recommend desensitization of penicillin allergy, then use

penicillin G Benzathine. If penicillin allergy is not reasonable, use tetracycline or doxycycline.

• Prsnc f a urhral discharg r gnial r pri-
anal lsins. Is hr any swlling f h pnis?
• Is hr pain in h lwr back, prinum, r
plvis?
• Hisry f prsaiis, bnign prsaic hyprplasia,
r prsaic cancr
• Is sicular slf-xaminain prfrmd rgularly?
Hav any abnrmal ndings bn nd, such as
lumps r masss?
• Hisry f STIs (.g., chlamydia, syphilis, gnr-
rha, yas infcins, gnial hrps, HIV, gnial
wars [HPV]). If hr is a hisry, whn and wha
was h ramn?
• Hisry f mulipl sxual parnrs—mal, fmal,
r bh. Wha yp f prcin is usd during sx-
ual inrcurs?
• Hisry f arhralgia, fvr, chills, malais, pharyn-
giis, r ral lsins
• Hisry f prir illnsss
• Hisry f rcil dysfuncin (ED) and dscripin
f parn f alrd rcil funcining
• If ED has ccurrd, ask spcically abu vascular
disrdrs ha may lad  changs in bld w
 h pnis (.g., srk). Ask abu smking and
h us f drugs ha may affc h vascular sysm
(.g., anihyprnsiv agns).
 Drugs Used in Men’s and Women’s Health CHAPTER 40
• Has h individual had prsa surgry? If s, was
h ns f h ED bfr r afr h surgry?
• Ohr nurlgic disrdrs (.g., Parkinsn disas
and spinal crd injuris) may caus prblms wih
sxual funcining.
• Has h individual had any hr gniurinary
cndiins (.g., sicular injury) ha may b ass-
ciad wih sxual dysfuncin?
• Endcrin disrdrs such as hyrid disas, adr-
nal disrdrs, and diabs mllius ar als assci-
ad wih sxual dysfuncin. Ds h pain hav
any f hs illnsss?
History of current symptoms. Ask h pain  d-
scrib h currn prblm r prblms ha iniiad
his visi. Hw lng hav h sympms xisd? Is
hr a rcurrnc f sympms ha wr rad
prviusly?
Medication history
• Has h individual akn srids r anibiics
rcnly? If s, wha cndiin was bing rad
and fr hw lng? Hw lng ag was hrapy
discninud?
• Ar vr-h-cunr, hrbal, prscribd, r rcr-
ainal drugs bing akn? If s, wha, why, and fr
hw lng?
• Ar hr any allrgis  mdicains (.g.,
anibiics)?
• If having a rcurrnc f an STI, wha was h prvi-
us ramn?
In h prsnc f ED, a numbr f drugs may cn-
ribu  h prblm (.g., anihyprnsivs, ani-
psychics, ricyclic anidprssans, mnamin
xidas inhibirs, hrmns, sdaiv-hypnics,
simulans, hrmnal chmhrapuics, pias,
srids, and rcrainal drugs); hrfr a mdi-
cain hisry is xrmly impran.
Psychosocial. STIs caus a high dgr f anxiy. Th
inima naur f h qusining rquird  bain
a sxual hisry may b mbarrassing. Vaginal r ur-
hral discharg may als b alarming  h pain
sking halhcar. Whn an STI diagnsis is suspc-
d, xplain h cndnialiy plicy f h faciliy b-
fr asking abu sxual parnrs. (Many individuals
d n rurn fr fllw-up appinmns; hr may
b nly n chanc  bain rlvan infrmain
abu cnacs.)
Ask abu lifsyl rinain (.g., hrsxual,
bisxual, r hmsxual and numbr f parnrs). Has
hr bn knwn cnac wih ppl wih STIs? Ar
prcauins usd during sxual cnacs?
Assss h lvl f anxiy prsn and adapiv r-
spnss and cping mchanisms usd.
647
Laboratory and diagnostic studies
• Rviw rprs n Gram sains and culurs
frm h anus, hra, and urhra fr gnrrha;
Vnral Disas Rsarch Labrary, rapid plas-
ma ragin, and urscn rpnma anibdy
absrpin ss fr syphilis; issu culurs fr
hrps simplx virus yp 2; HIV sing (anibd-
is agains HIV-1 and HIV-2 saring wih nzym
immunassay; cnrm by using h Wsrn bl
s r an immunurscnc assay). HIV sing
shuld b ffrd  vryn valuad fr any
yp f STI.
• Diagnsic sudis ar individualizd  h suspc-
d caus f h signs and sympms (.g., cmpl
bld cun, culurs f prsa scrins, urin
culurs, lvls f prsa-spcic anign, bld
ura nirgn, crainin) fr prsaic disrdrs.
Physical examination
• Prfrm ruin physical xaminain f h wm-
an, including plvic xaminain, Pap s, culurs,
and bras xaminain.
• Prfrm ruin physical xaminain f h man,
including sicular xaminain (rcal xamina-
in wih palpain f prsa afr ag 40). An
anrcal xaminain and xaminain f hra,
nsils, and muh shuld b cmpld fr mn f
hmsxual r bisxual rinain.
Implementation
• Rcrd basic pain daa (.g., high, wigh, vial
signs).
• Prpar h pain fr, and assis wih, a physical
xaminain.
• Obsrv disribuin f bdy hair and prsnc
f any scars, lsins, bdy rashs, pubic lic, r
mis.
• Assis wih spcimn cllcin (.g., vaginal
smars, culurs f discharg).
• Inspc h pnis and scrum fr swlling r abnr-
maliis; bsrv fr urhral discharg.
• Prvid psychlgical suppr and rfr fr avail-
abl cunsling, as apprpria.
Patient Education
Instructions for adolescents. Th ra f STIs is high
in his ag grup, s i is impran  d a hrugh
assssmn f sxual aciviy and pracics. Fr hs
wh ar sxually aciv, cunsling rgarding saf
sx pracics and vlunary sing and ramn
shuld b ffrd. Mdical car fr STIs can b pr-
vidd wihu parnal cnsn r knwldg. Chck
individual sa laws fr hs ha allw sing and
cunsling fr HIV. All adlscns shuld b augh
hrughly abu alrnaivs fr absinnc and
abu saf sx pracics.
648 UNIT VIII Drugs Affecting the Reproductive System
Instructions for women
• Warm siz bahs may hlp rliv vaginal r pri-
nal irriain.
• Duching shuld b avidd unlss spcically pr-
scribd by h halhcar prvidr. Duching alrs
h pH f h vagina and may ncurag h grwh
f pprunisic rganisms.
• Prsnal hygin shuld includ wiping frm frn
 back afr viding and dfcain, viding bfr
and afr inrcurs, clansing gnials hrughly
bfr and afr inrcurs, and changing mn-
srual ampns r pads frqunly. Avid waring
undrwar mad f synhic marials; cn ma-
rials hlp prvn misur accumulain.
• Cnracpiv mhds (.g., ral and hr hr-
mnal cnracpivs, inraurin dvics) r sur-
gical prcdurs such as hysrcmy d n pr-
vid any prcin agains HIV r hr STIs. I
is ncssary  us physical and chmical barrirs
(.g., cndms, fam sprmicids).
• Srss h nd fr an annual Pap s  dc cr-
vical cancr ha riginas frm crvical inrapi-
hlial nplasia.
Instructions for men
• Pracic gd prsnal hygin. Kp h pnis,
scrum, and prianal ara hrughly clansd.
Wash aras bfr and afr inrcurs. Urina af-
r inrcurs. Wash hands wll.
• Prsaiis is rad wih anibiics, aniinammary
agns, and sl sfnrs. Th lcal applicain f
ha wih a siz bah, drinking plny f uids, and
adqua rs ar als usually usd fr rlif f h
sympms f prsaiis.
• Mn nd annual physical xaminains afr ag
40, which includs a rcal xaminain  palpa
h prsa.
• Discuss apprpria inrvnins fr mn wih al-
rd sxual funcin ha may b rad wih mdi-
cains such as phsphdisras inhibirs (.g.,
Viagra, Cialis) r surgical inrvnin (.g., pnil
prshsis). Rmind h pain f h nd fr cn-
sulain wih a halhcar prvidr bfr using
phsphdisras inhibirs. Alhugh hs drugs
ar radily availabl vr h Inrn, ppl wih
cardivascular disrdrs ar paricularly suscpibl
 lif-hraning cnsquncs wih hir us.
• Lax cndms can b ffciv in rducing sxual
ransmissin f HIV and sm hr STIs (.g., gn-
rrha, richmnas, chlamydia), bu cndms ar
n as ffciv agains STIs ransmid by skin--
skin cnac, such as hrps simplx virus, HPV, and
syphilis.
• Mn having hmsxual rlainships and ppl
wh injc drugs shuld b vaccinad fr hpaiis
A virus. Th frqun us f nnxynl-9 sprmi-
cid during anal inrcurs irrias h pihlial
lining f h rcum, prviding a pral f nry fr
HIV and hr STIs.
Instructions for women and men
• Whn infcins ar prsn, absain frm sxual
inrcurs. Srss h nd  prvn rinfcin.
Whn sxual pracics ar rsumd, us lax cn-
dms. Rsarch dmnsras ha vaginal sprmi-
cids cnaining nnxynl-9 may n b ffciv in
prvning crvical gnrrha, chlamydia, r HIV in-
fcin. Accrding  h Cnrs fr Disas Cnrl
and Prvnin, h rl f sprmicids, spngs, and
diaphragms fr prvning ransmissin f HIV has
n bn valuad. On sudy indicas ha h fr-
qun us f nnxynl-9 may acually incras h
risk f HIV infcin during vaginal inrcurs b-
caus f irriain f vaginal issus.
• Us sxual absinnc during h cmmunicabl
phas f any disas. Rmmbr ha whn having
sx wih an individual, n is als having sx wih
all prvius sxual parnrs, and hus h infcius
pssibiliis shuld b cnsidrd.
• If having sx wih a parnr wih an unknwn saus
r n infcd wih HIV r anhr STI, a nw cn-
dm shuld b usd fr ach insriv inrcurs.
• I is advisd ha bh parnrs b sd fr STIs,
including HIV, bfr h rs sxual ncunr.
• Pracic saf sx, if n absinnc. Us lax cn-
dms. Discuss prpr chniqus fr applying, us-
ing, rmving, and discarding cndms.
• Arrang fr fllw-up appinmns wih h halh-
car prvidr and apprpria rfrrals fr cunsl-
ing r wih h scial srvics dparmn as ndd.
• All sxual parnrs nd  undrsand h impr-
anc f “parnr srvics,” h dcumnain f all
sxual parnrs fr h purps f prviding valu-
ain and ramn  anyn wh may hav bn
xpsd  an STI bfr h infcd individual b-
cam clinically sympmaic. Cass f syphilis, gn-
rrha, chlamydia, and acquird immundcincy
syndrm ar rprd in vry sa.
Medications
For women. Tach h pain h prpr way  ap-
ply mdicains pically r inravaginally using in-
mns r suppsiris. I is impraiv ha prpr
clansing f h gnial ara b dn rgularly using
sap and war; rins and dry wll. Hands shuld b
washd bfr and afr h applicain r insrin
f mdicains and bfr and afr iling. Afr
vry us, h vaginal applicar shuld b hrughly
washd wih sap and war and hn drid. Afr in-
sring a vaginal mdicain (cram r suppsiry),
h wman shuld rmain in a rcumbn psiin fr
30 minus  allw im fr drug absrpin. A mini-
pad can b wrn  cach rmaining drainag. (S Fig.
7.14 fr prpr adminisrain f vaginal mdicain.)
 Drugs Used in Men’s and Women’s Health CHAPTER 40 649

Wih ral cnracpiv hrapy, ach n nly h Table 40.2 Monophasic Oral Contraceptives a
mdicain schdul and dsag, bu als wha  d
PRODUCT PROGESTIN ESTROGEN
if a ds is missd, frquncy f fllw-up car, and
cmmn and srius advrs ffcs. Aviane levonorgestrel ethinyl estradiol
(0.1 mg) (20 mcg)
For men and women. Tach h mdicain rgimn
and wh mus ak h mdicains—bh parnrs in Apri desogestrel ethinyl estradiol
a sxual rlainship. (0.15 mg) (30 mcg)
Yaz drospirenone ethinyl estradiol
Fostering health maintenance (3 mg) (20 mcg)
• Thrughu h curs f ramn, discuss mdi- Necon 0.5/35 norethindrone ethinyl estradiol
cain infrmain and hw i will bn h pa- (0.5 mg) (35 mcg)
in. Srss h impranc f nnpharmaclgic Cryselle norgestrel ethinyl estradiol
inrvnins such as mainaining gnral halh (0.3 mg) (30 mcg)
and prpr nuriin and hygin. Srss h nd Altavera levonorgestrel ethinyl estradiol
fr adhrnc wih h ramn rgimn. (0.15 mg) (30 mcg)
• Prvid h pain and signican hrs wih im- Junel 1/20 norethindrone ethinyl estradiol
pran infrmain cnaind in h spcic drug acetate (1 mg) (20 mcg)
mngraphs fr h drugs prscribd. Addiinal Kelnor 1/35 ethynodiol ethinyl estradiol
halh aching and nursing inrvnins fr cm- diacetate (1 mg) (35 mcg)
mn and srius advrs drug ffcs ar fund in Nymyo norgestimate ethinyl estradiol
ach mngraph. (0.25 mg) (35 mcg)
• Sk cprain and undrsanding f h fl- Setlakinb levonorgestrel ethinyl estradiol
lwing pins s ha mdicain adhrnc is in- (91 tablets) (0.15 mg) (30 mcg)
crasd: nam f mdicain; dsag, ru, and
aThere are more than 80 monophasic oral contraceptive products available.
ims f adminisrain; and cmmn and srius This table is a representative list of estrogen-progestin combinations available
advrs drug ffcs. under a variety of brand names. Unless otherwise listed, monophasic
contraceptives contain 21 active tablets followed by 7 inactive tablets.
bExtended- or continuous-cycle oral contraceptive. Contains 84 active tablets

Patient self-assessment. Enlis h pain’s hlp in
dvlping and mainaining a wrin rcrd f mni-
ring paramrs (.g., bld prssur, puls, wigh,
dgr f rlif frm mnsrual pain, mnsrual cycl
infrmain fr wmn n ral cnracpivs). S
Appndix B: Tmpla fr Dvlping a Wrin Rcrd
fr Pains  Mnir Thir Own Thrapy. Fr pains
wih STIs, a lising f h sympms prsn and dgr
f rlif baind may b apprpria. Cmpl h
Prmdicain Daa clumn fr us as a baslin  rack
rspns  drug hrapy. Ensur ha h pain undr-
sands hw  us h frm, and insruc h pain 
bring h cmpld frm  fllw-up visis. During
fllw-up visis, fcus n issus ha will fsr adhr-
nc wih h hrapuic inrvnins prscribd.
Health Promotion
The consistent use of male latex condoms signicantly re-
duces the risk of HIV infection, gonorrhea and chlamydia,
herpes simplex virus in men and women, and HPV in wom-
en, but male condoms may be less effective in protecting
against STIs transmitted by skin-to-skin contact (e.g., genital
herpes, syphilis) because the infected areas may not be cov-
ered by the condom.
DRUG THERAPY FOR CONTRACEPTION
Oral (hrmnal) cnracpivs (birh cnrl pills)
bcam availabl in 1960. Thy nw rprsn n f
and 7 inert tablets. A menstrual period occurs only during the time the inert
tablets are taken.
h ms cmmn frms f aricial birh cnrl in h
Unid Sas. I is simad ha apprximaly n-
hird f all wmn bwn ags 18 and 44 yars us
ral cnracpivs
DRUG CLASS: ORAL CONTRACEPTIVES
Actions
Esrgns, and prgsins  sm xn, induc cn-
racpin by inhibiing vulain. Th srgns blck
piuiary rlas f fllicl-simulaing hrmn (FSH),
prvning h varis frm dvlping a fllicl frm
which h vum is rlasd. Prgsins inhibi piuiary
rlas f luinizing hrmn (LH), h hrmn r-
spnsibl fr rlasing an vum frm a fllicl. Ohr
mchanisms play a cnribury rl in prvning cn-
cpin. Esrgns and prgsins alr crvical mucus
by making i hick and viscus, inhibiing sprm migra-
in. Hrmns als chang h ndmrial wall, im-
pairing implanain f h frilizd vum.
Uses
Thr ar w yps f ral cnracpivs: h cm-
binain pill, which cnains bh an srgn and
a prgsin, and h minipill, which cnains nly
a prgsin. Th cmbinain pills ar subdividd
in xd cmbinain r mnphasic (Tabl 40.2),
650 UNIT VIII Drugs Affecting the Reproductive System

Table 40.3 Biphasic Oral Contraceptives a

PRODUCT PROGESTIN ESTROGEN OTHER INGREDIENTS
Amethia (91 tablets)b levonorgestrel ethinyl estradiol —
84 white tablets (0.15 mg) 84 white tablets (30 mcg)
7 blue tablets (10 mcg)
Lo Loestrin FE (28 tablets) norethindrone ethinyl estradiol ferrous fumarate (75 mg)
24 blue tablets (1 mg) 24 blue tablets (10 mcg) (2 brown tablets)
2 white tablets (10 mcg)
Mircette (28 tablets)c desogestrel ethinyl estradiol —
21 white tablets (0.15 mg) 21 white tablets (20 mcg)
5 yellow tablets (10 mcg)
aThere are more than 18 biphasic oral contraceptive products available. This table is a representative list of estrogen-progestin combinations available under a variety of
brand names.
bActive for 84 days, followed by a menstrual period.
cOne white tablet is taken daily for 21 days, followed by one green (inert) tablet for 2 days, then one yellow (active) tablet daily for 5 days.

Table 40.4 Triphasic Oral Contraceptives a

PRODUCT PROGESTIN ESTROGEN (MCG) OTHER INGREDIENTS
Aranelleb norethindrone ethinyl estradiol —
7 tablets (0.5 mg) 35 mcg
9 tablets (1 mg) 35 mcg
5 tablets (0.5 mg) 35 mcg
Caziantb desogestrel ethinyl estradiol —
7 tablets (0.1 mg) 25 mcg
7 tablets (0.125 mg) 25 mcg
7 tablets (0.15 mg) 25 mcg
Enpresse-28b levonorgestrel ethinyl estradiol —

6 tablets (0.05 mg) 30 mcg

5 tablets (0.075 mg) 40 mcg
10 tablets (0.125 mg) 30 mcg
Estrostep Fe (28 tablets) norethindrone acetate ethinyl estradiol ferrous fumarate (75 mg)
5 tablets (1 mg) 20 mcg 7 brown tablets
7 tablets (1 mg) 30 mcg
9 tablets (1 mg) 35 mcg
aThere are more than 34 triphasic oral contraceptive products available. This table is a representative list of estrogen-progestin combinations available under a variety of
brand names.
bSeven inert tablets.

biphasic (Tabl 40.3), riphasic (Tabl 40.4), and quad-
riphasic (Tabl 40.5) prducs. Th mnphasic cm-
binain pills cnain a xd rai f srgn and
prgsin givn daily fr 21 days, bginning n day
5 f h mnsrual cycl. Th biphasic prduc cn-
ains a xd ds f srgn and a prgsin ds
n days 1  10 ha is lwr han ha n days 11 
21 f h mnsrual cycl. Th riphasic cmbinain
pills prvid hr cncnrains f srgn and
prgsin, and h quadriphasic pills prvid fur
cncnrains f hrmns. Th purps f h vari-
abl cncnrains is  prvid cnracpin wih
h lws ncssary ds f hrmns. Ms f h
cmbinain pills ar als packagd in 28-abl cn-
ainrs. Th las 7 abls ar inr bu ar supplid
s ha hr is n brak in h ruin f aking 1
abl daily. Th prgsin-nly prducs (Tabl 40.6)
ar packagd in unis f 28 abls. All abls cnain
aciv hrmn; 1 abl shuld b akn daily a ap-
prximaly h sam im ach day. Thr is n cyclic
brak.
Th prgsin-nly pills, r minipills, rprsn a
cmmn frm f ral cnracpiv hrapy. Many ad-
vrs ffcs f cmbinain-yp cnracpivs ar
causd by h srgn cmpnn f h abl. Fr
hs wmn paricularly suscpibl  advrs ffcs
 Drugs Used in Men’s and Women’s Health CHAPTER 40 651

Table 40.5 Quadriphasic Oral Contraceptive a placb; Amhys). A primary purps fr hs cn-
racpiv prducs is  shrn h durain f mn-
PRODUCT PROGESTIN ESTROGEN
ss, dcrasing h frquncy  fur ims pr yar,
Natazia Phase 1: 2 dark yellow estradiol valerate r cmplly liminaing mnss. Wih susaind hr-
tablets (no progestin) (3 mg)
mn us, hr is grar supprssin f ndmrial
Phase 2: 5 medium red estradiol valerate grwh, rducing prgnancy risk, and a lighr prid,
tablets dienogest (2 mg) (2 mg) if any, lasing abu 2 days during h 7 days ff h ac-
Phase 3: 17 light yellow estradiol valerate iv abls (84/7 rgimn). Ohr advanags  hs
tablets dienogest (3 mg) (2 mg) prducs, in addiin  fwr prids, is a lwr cu-
Phase 4: 2 dark red tablets estradiol valerate mulaiv ds f hrmns akn cmpard wih ral
(no progestin) (1 mg) cnracpivs cycld mnhly, and h allviain f
aOther quadriphasic oral contraceptives are: Fayosim, Quartette, and Rivelsa. sympms f cxising mdical cndiins ha may
b xacrbad during mnss (.g., anmia).
Clinical rials indica ha xndd- and cninuus-
Table 40.6 Progestin-Only Contraceptives cycl ral cnracpivs ar as ffciv in prvning
NORETHINDRONE prgnancy as mnhly ral cnracpivs. Ths prd-
PRODUCT (PROGESTIN) (MG) DROSPIRENONE ucs hav similar advrs ffc prls; h nly signi-
Camila 0.35 canly diffrn advrs ffc cmpard wih mnhly
Deblitane 0.35 ral cnracpivs is a chang in blding parn. Ths
Errin 0.35 ral cnracpivs ar assciad wih mr brak-
Heather 0.35 hrugh blding and sping han h mnhly ral
cnracpiv pills.
Incassia 0.35
Cigar smking incrass h risk f srius ad-
Jencycla 0.35 vrs cardivascular ffcs (.g., bld cls) in prsns
Lyza 0.35 wh bh smk and us cmbinain ral cnracp-
Nora-BE 0.35 ivs. This risk incrass wih ag and havy smking
Norlyda 0.35 (a las 15 cigars daily) and is qui signican in
Norlyroc 0.35 wmn ldr han 35 yars. Wmn wh us ral cn-
racpivs ar srngly ncuragd n  smk.
Sharobel 0.35
Slynd 4 mg Therapeutic Outcome. Th primary hrapuic u-
Tulana 0.35 cm assciad wih ral cnracpiv hrapy is
prvnin f prgnancy.

Nursing Implications for Oral Contraceptives

f srgn hrapy, h minipill prvids an alrnaiv.
Wmn wh migh prfr h minipill ar hs wih a
hisry f migrain hadachs, hyprnsin, mnal
dprssin, wigh gain, and bras ndrnss and
hs wh wan  brasfd psparum. Th mini-
pill is n wihu is disadvanags, hwvr. Bwn
30% and 40% f wmn aking h minipill cninu 
vula. Dysmenorrhea, manifsd by irrgular pri-
ds, infrqun prids, and sping bwn prids,
is cmmn in wmn aking h minipill. Birh cnrl
is mainaind by prgsin aciviy n crvical mucus,
urin and fallpian ranspr, and implanain. Thr
is a slighly highr incidnc f bh urin and ubal
prgnancis.
Alrnaiv dsag frms fr ral cnracpivs ar
availabl ha ar knwn as xndd-cycl and cn-
inuus-cycl ral cnracpivs. Ths mnphasic
cmbinain ral cnracpivs ar givn in h fl-
lwing rgimns: 24 days, fllwd by placb fr 4
days (24/4 rgimn; .g., Yaz, Lsrin 24 F, Gianvi);
84 days, fllwd by placb fr 7 days (84/7 rgi-
mn; .g., Jlssa, Slakin); r cninuusly (wihu
Premedication assessment
1. Rviw h mdical hisry. If hr is a hisry f
bsiy, smking, hyprnsin, gallbladdr disas,
diabs mllius, svr varics vins, sizur dis-
rdrs, ligmnrrha r amnrrha, rhumaic
har disas, hrmbmblic disas, srk, ma-
lignancy f bras r h rprduciv sysm, r-
nal r livr disas, svr mnal dprssin, sus-
pcd prgnancy, r rpad cnracpiv failur,
cnsul wih a halhcar prvidr bfr dispns-
ing birh cnrl pills.
2. Tak a baslin bdy wigh masurmn, alng
wih bld prssur masurmn in h supin and
siing psiins.
3. Ensur ha a prgnancy s has bn givn and
ha h pain is n prgnan.
Availability
S Tabls 40.2, 40.3, 40.4, 40.5, and 40.6
Dosage and administration. Th srgnic cmpnn
f h cmbinain-yp pills is rspnsibl fr ms
652 UNIT VIII Drugs Affecting the Reproductive System
f h advrs ffcs assciad wih hrapy. Th
US Fd and Drug Adminisrain (FDA) has rcm-
mndd ha hrapy b iniiad wih a prduc cn-
aining a lw ds f srgn. Advrs ffcs mus
b rviwd in rlain  individual cas hisris and
may b adjusd basd n h incidnc and yp f
advrs ffcs.
Before initiating therapy. Th pain shuld hav
a cmpl physical xaminain ha includs
bld prssur, bdy wigh, plvic and bras x-
aminains, Pap s, urinalysis, and hmglbin r
hmacri.
Instructions for using combination oral contracep-
tives. Sar h rs pill n h rs Sunday afr h
mnsrual prid bgins. Tak n pill daily, a h
sam im, unil h pack is gn. If using a 21-day
pack, wai 1 wk and rsar n h nx Sunday. If us-
ing a 28-day pack, sar a nw pack h day afr nish-
ing h las pack. Full prcin by h pill during h
rs mnh may n ccur, s h us f an addiinal
frm f birh cnrl (cndms, fam) during h rs
mnh is advisd. If h prduc prscribd als cn-
ains an irn supplmn, b sur  ak h 7 inr
abls mnhly. Th irn supplmn is in h 7 inr
abls, n h 21 abls cnaining hrmns. (Many
wmn skip h inr abls ach mnh, hinking ha
hy hav n bn.)
• Severe diarrhea or vomiting: If svr diarrha r vm-
iing ccur wihin 3  4 hurs afr aking an aciv
abl, i shuld b cnsidrd a missd ds; addi-
inal cnracpiv masurs ar rcmmndd.
• Missed pills: Tak h pill as sn as a missd pill
is rmmbrd; ak h nx pill a h rgularly
schduld im. If w pills ar missd, ak w
pills as sn as rmmbrd and w pills h nx
day. Sping may ccur whn w pills ar missd.
Us anhr frm f birh cnrl (cndms, fam)
unil h pack f pills is nishd. If three or more
pills ar missd, sar using anhr frm f birh
cnrl immdialy. Sar a nw pack f pills n
h nx Sunday vn if mnsruaing. Discard h
ld pack f pills. Us hr frms f birh cnrl
hrugh h nx mnh afr missing hr r mr
pills.
• Missed pills and skipped periods: Rurn  h halh-
car prvidr fr a prgnancy s.
• Skipping one period but not missing a pill: I is n un-
cmmn fr a wman  miss a prid ccasinally
whn n h pill. Sar h nx pack n h appr-
pria Sunday.
• Spotting for two or more cycles: S h halhcar pr-
vidr. A dsag adjusmn may b ncssary.
• Periodic examinations: A yarly xaminain shuld
includ bld prssur ss, plvic xaminain,
urinalysis, bras xaminain, and Pap s.
• Discontinuing the pill for conception: Bcaus f
a pssibiliy f birh dfcs, h pill shuld b
discninud 3 mnhs bfr amping prgnan-
cy. Us hr mhds f cnracpin fr hs 3
mnhs.
• Duration of oral contraceptive therapy: Many halh-
car prvidrs prfr  hav pains discninu
h pill fr 3 f vry 28 mnhs. This allws h
bdy  rurn  a nrmal cycl. B sur  us hr
frms f cnracpin during his im. Lng-rm
us (3 r mr yars) mus b drmind n an in-
dividual basis.
• Serious adverse effects to be reported as soon as pos-
sible: Svr hadachs, dizzinss, blurrd visin,
lg pain, shrnss f brah, and chs pain,.
Alhugh hs advrs ffcs ar usually f mi-
nr cnsqunc, a mr srius cndiin mus b
ruld u.
Note: Whn bing sn by a halhcar prvidr r
a dnis fr hr rasns, b sur  mnin aking
ral cnracpivs.
Instructions for using the minipill. Sar using h mini-
pill n h rs day f mnsruain. Tak n abl
daily, vry day, rgardlss f whn h nx prid
is. Tabls shuld b akn a apprximaly h sam
im vry day.
• Missed pills: If n pill is missd, ak i as sn as
rmmbrd, and ak h nx pill a h rgularly
schduld im. Us anhr frm f birh cnrl
unil h nx prid. If w pills ar missd, ak
n f h missd pills immdialy and ak h
rgularly schduld pill fr ha day n im. Th
nx day, ak h rgularly schduld pill and h
hr missd pill. Us anhr mhd f birh cn-
rl unil h nx prid.
• Missed periods: Sm wmn n changs in h
im as wll as durain f hir prids whil us-
ing minipills. This is  b xpcd. If mnss is
vry 28  30 days, vulain may sill b ccur-
ring. Fr maximal safy, us alrnaiv frms f
cnracpin n days 10 hrugh 18. If irrgular
blding ccurs vry 25  45 days, vulain is
prbably n rgular. If all abls ar akn cr-
rcly bu n prid has rsuld fr mr han
60 days, spak  h halhcar prvidr abu a
prgnancy s.
Note: Rpr suddn, svr abdminal pain, wih
r wihu nausa and vmiing,  h halhcar pr-
vidr immdialy. Thr is a highr incidnc f c-
pic prgnancy wih h minipill bcaus i ds n
inhibi vulain in all wmn.
• Serious adverse effects to be reported as soon as pos-
sible: Svr hadachs, dizzinss, blurrd visin,
lg pain, shrnss f brah, chs pain, and acu
abdminal pain. Alhugh hs advrs ffcs ar
usually f minr cnsqunc, a mr srius cn-
diin mus b ruld u.
• Duration of oral contraceptive therapy: Many halhcar
prvidrs prfr  hav hir pains discninu
 Drugs Used in Men’s and Women’s Health CHAPTER 40
h pill fr 3 f vry 28 mnhs. This allws h
bdy  rurn  a nrmal cycl. B sur  us hr
frms f cnracpin during his im. Lng-rm
us (3 r mr yars) mus b drmind n an in-
dividual basis.
• Discontinuing the pill for conception: Bcaus f a ps-
sibiliy f birh dfcs, discninu h pill 3 mnhs
bfr amping prgnancy. Us hr mhds f
cnracpin fr hs 3 mnhs.
Common adverse effects. Ths ar h ms cmmn
advrs ffcs f hrmnal cnracpiv hrapy. If
hs sympms ar n rslvd afr 3 mnhs f hr-
apy, h wman shuld rurn  hr halhcar prvidr
fr rvaluain and a pssibl chang in prscripin.
Gastrointestinal. Nausa.
Gynecologic, hormonal. Wigh gain, sping,
changd mnsrual w, missd prids, chlasma
(facial pigmnain).
Psychological, neurologic. Dprssin, md chang-
s, hadachs.
Serious adverse effects. Th fllwing sympms
rprsn h dvlpmn f scndary disrdrs.
Examinain, a chang in ral cnracpiv, and
pssibl ramn wih hr mdicains may b
ncssary.
Gynecologic. Vaginal discharg, brakhrugh bld-
ing, yas infcin.
Neurologic
Blurred vision, severe headaches, dizziness. Rpr as
sn as pssibl. Ths advrs ffcs ar usually f
minr cnsqunc, bu hy may b arly indicains
f srius advrs ffcs.
Cardiovascular
Venous thromboembolism. Rpr as sn as pssibl
any lg pain, chs pain, shrnss f brah.
Drug interactions
Drugs that reduce therapeutic effects
• Carbamazpin, xcarbazpin, phnyin, primi-
dn, pirama, S. Jhn’s wr, and h aniviral
pras inhibirs (.g., saquinavir, rinavir, indi-
navir, nlnavir, amprnavir) may incras h ra
f mablism f h ral cnracpiv hrmns in
h livr, pssibly dcrasing hir cnracpiv f-
fc. An alrnaiv r addiinal frm f birh cn-
rl is advisabl during cncurrn us.
• Anibacrial agns (.g., pnicillins, racyclins,
rifampin, isniazid, grisfulvin) apparnly alr
mablism f hrmns in h gu, making h cn-
racpiv lss ffciv. An alrnaiv r addiinal
frm f birh cnrl is advisabl during cncurrn
us.
Reduced therapeutic effects of drugs by oral contraceptives.
• Oral cnracpivs rduc lamrigin bld lv-
ls. Mnir lamrigin bld lvl and bsrv fr
653
sizur aciviy. An incras in h ds f lamrig-
in migh b rquird  prvn sizurs.
Herbal Interactions
ST. JOHN’S WORT
St. John’s wort may increase the liver’s metabolism of oral
contraceptive hormones, possibly resulting in decreased
contraceptive effect. An alternative or additional form of birth
control is advisable during concurrent use.
Drugs that enhance therapeutic and toxic effects.
Iracnazl and kcnazl may inhibi h mab-
lism f ral cnracpivs. Mnsrual irrgulariis
als may b nd. Adjusmn f hrmn dsag
may b ncssary.
Warfarin. Oral cnracpivs may diminish r n-
hanc h anicagulan ffcs f warfarin. Mnir
h prhrmbin im and h inrnainal nr-
malizd rai, and adjus h dsag f warfarin if
ncssary.
Phenytoin. Mnir pains wih cncurrn hrapy
fr signs f brakhrugh sizurs r phnyin xic-
iy—nysagmus, sdain, and lhargy. Srum lvls
may b rdrd, and a chang in dsag f phnyin
may b rquird.
Thyroid hormones. Pains wh hav n hyrid
funcin and wh sar srgn hrapy may rquir
an incras in hyrid hrmn dsag. Esrgns in-
cras hyrid-binding glbulin lvls, which rduc
h lvl f circulaing fr hyrxin (T4). Th al
lvl f T4 is ihr nrmal r incrasd. D n adjus
h hyrid hrmn dsag unil h pain shws
clinical signs f hyphyridism.
Benzodiazepines. Oral cnracpivs appar 
hav a variabl ffc n h mablism f bnzdi-
azpins. Ths ha hav rducd mablism wih
an incras in hrapuic rspns and xic ffc ar
alprazlam, clrazpa, chlrdiazpxid, diazpam,
and urazpam. Bnzdiazpins ha hav nhancd
mablism and rducd hrapuic aciviy whn
akn wih ral cnracpivs ar lrazpam, xaz-
pam, and mazpam. Adjus h dsag f h bn-
zdiazpin accrdingly.
DRUG CLASS: TRANSDERMAL CONTRACEPTIVE
norelgestromin–ethinyl estradiol transdermal system
(nōr-ĕl-JĔS-trō-mĭn–ĔTH-ĭ-nĕl ĕs-trĕ-DĪ-ŏl)
Xulane (ZŪ-lān)
Actions
Ehinyl sradil, an srgn, and nrlgsrmin, a
prgsin, wrk ghr as a cnracpiv by inhib-
iing vulain. Esrgns blck piuiary rlas f
FSH, prvning h varis frm dvlping a fllicl
654 UNIT VIII Drugs Affecting the Reproductive System
ha rlass an vum. Prgsins inhibi piuiary r-
las f LH, h hrmn rspnsibl fr rlasing an
vum frm a fllicl. Ohr mchanisms play a cn-
ribury rl in prvning cncpin. Esrgns and
prgsins alr crvical mucus by making i hick and
viscus, inhibiing sprm migrain. Hrmns als
chang h ndmrial wall, impairing implanain
f h frilizd vum.
Uses
Th ransdrmal cnracpiv sysm wrks vry
much lik h cmbinain ral cnracpivs, x-
cp ha h srgn and prgsin hrmns ar in a
ransdrmal pach dsag frm ha is applid wkly
fr 3 wks. During h furh wk f h mnsru-
al cycl, n pach is wrn and wihdrawal blding
(mnss) shuld bgin.
In Nvmbr 2005 h FDA issud a cauinary n
abu cncrn fr grar xpsur  srgns frm
h pach cmpard wih aking a similar ral cnra-
cpiv abl prduc. In gnral, incrasd srgn
xpsur incrass h risk f bld cls. Alhugh
h FDA blivs ha h ransdrmal cnracpiv
sysm is a saf and ffciv mhd f cnracpin,
h FDA ncurags wmn  discuss h issu wih
hir halhcar prvidr, paricularly if hy ar a
highr risk fr cardivascular disass basd n h
prsnc f hyprnsin, bsiy, diabs, smking,
and/r ldr ag.
Cigar smking incrass h risk f srius ad-
vrs cardivascular ffcs (.g., bld cls) in hs
wh bh smk and us cmbinain cnracpivs.
This risk incrass wih ag and havy smking (a
las 15 cigars pr day) and is signican in wmn
ldr han 35 yars. Wmn wh us cmbinain cn-
racpivs such as h ransdrmal pach ar srngly
ncuragd n  smk.
Therapeutic Outcome
Th primary hrapuic ucm assciad wih
ransdrmal cnracpiv hrapy is prvnin f
prgnancy.
Nursing Implications for Transdermal
Contraceptives
Premedication assessment
1. Rviw h mdical hisry. If hr is a hisry
f hyprnsin, gallbladdr disas, diabs
mllius, svr varics vins, sizur disr-
drs, ligmnrrha r amnrrha, rhumaic
har disas, hrmbmblic disas, srk,
malignancy f bras r h rprduciv sysm,
rnal r livr disas, svr mnal dprssin,
suspcd prgnancy, r rpad cnracpiv
failur, r if h pain smks, cnsul wih h
halhcar prvidr bfr dispnsing birh cn-
rl pachs.
2. Tak a baslin bld prssur in h supin and si-
ing psiins.
3. Ensur ha a prgnancy s has bn givn and
ha h pain is n prgnan.
Availability. Transdermal patch: 4.86 mg nrlgsr-
min and 0.53 mg hinyl sradil pr pach. Th pach
rlas 150 mcg f nrlgsrmin and 35 mcg f hi-
nyl sradil pr 24 hurs.
Implementation
Before initiating therapy. Th pain shuld hav a
cmpl physical xaminain ha includs bld
prssur, plvic and bras xaminains, Pap s, uri-
nalysis, and hmglbin r hmacri. A prgnancy s
shuld b prfrmd n sxually aciv fmal pains.
Instructions for using transdermal contraceptives. A
nw pach shuld b applid n h sam day f h
wk. This day is knwn as “pach chang day.” Th
pach shuld b applid  clan, dry, inac, halhy
skin n h buck, abdmn, uppr ur arm, r
uppr rs in a plac whr i will n b rubbd by
igh clhing. Pachs shuld n b placd n rd irri-
ad skin r n h brass. Pachs shuld n b cu.
Tpical prducs such as makup, pwdr, lins, r
crams shuld n b applid  h skin r  h pach
ara bcaus h pach may n adhr prprly and
absrpin f h hrmns may b impaird.
Slc n f h fllwing mhds  sar
cnracpin:
• First day start: Apply h rs pach during h rs
24 hurs f h mnsrual prid. N n a calndar
h day f h wk as a rmindr f pach chang
day. If h pach is sard afr h rs 24 hurs
f h mnsrual cycl, a nnhrmnal backup cn-
racpiv (cndms, sprmicidal fam, diaphragm)
shuld b usd cncurrnly fr h rs 7 cnscu-
iv days f h rs cycl.
• Sunday start: Sar h rs pach n h rs Sunday
afr mnss bgins. A nnhrmnal backup cnra-
cpiv (cndms, sprmicidal fam, diaphragm)
shuld b usd cncurrnly fr h rs 7 cnscu-
iv days f h rs cycl.
• Switching from oral contraceptives to the patches: Apply
a pach n h rs day f h mnss. If hr is n
wihdrawal blding wihin 5 days f h las ac-
iv hrmn abl (afr day 21), a prgnancy s
shuld b cmpld  nsur ha hr is n prg-
nancy bfr h pach is sard.
Medication Safety Alert
When removing the patch, dispose of it properly. Fold the
used patch over on itself and place in a sturdy container,
preferably with a child-resistant cap, and discard in a waste
receptacle out of reach of children and pets. It still contains
active hormone residual. Do not ush down the toilet.
 Drugs Used in Men’s and Women’s Health CHAPTER 40
If a pach is parially r cmplly dachd:
• For less than 24 hours: Try  rapply h pach in h
sam plac r rplac i wih a nw pach immdi-
aly. N backup cnracpin is ncssary. Pach
chang day will rmain h sam. D n ry  r-
apply h pach if h adhsiv will n adhr 
h skin. D n us hr adhsivs r ap  hld
a pach in plac. Apply a nw pach in a diffrn
lcain.
• For more than 24 hours or if not sure how long since
detachment: Bcaus hr may b a lack f prc-
in frm prgnancy, sp h currn cnracpiv
cycl and sar a nw cycl immdialy by applying
a nw pach. This is a “nw day 1” and a nw pach
chang day. A nnhrmnal backup cnracpiv
(cndms, sprmicidal fam, diaphragm) shuld b
usd cncurrnly fr h rs 7 cnscuiv days f
h nw cycl.
If a wman frgs  chang h pach:
• At the start of any patch cycle (week 1/day 1): Thr may
b a lack f prcin frm prgnancy. Apply h
nw pach as sn as i is rmmbrd. This is a nw
day 1 and a nw pach chang day. A nnhrmnal
backup cnracpiv (cndms, sprmicidal fam,
diaphragm) shuld b usd cncurrnly fr h
rs 7 cnscuiv days f h nw cycl.
• In h middl f h pach cycl (wk 2/day 8 r
wk 3/day 15):
 • For up to 48 hours: Apply a nw pach immdia-
ly. Th nx pach shuld b applid n h usual
pach chang day. N backup cnracpin is
ndd.
 • For more than 48 hours: Bcaus hr may b a lack
f prcin frm prgnancy, sp h currn cn-
racpiv cycl and sar a nw 4-wk cycl im-
mdialy by applying a nw pach. This is a nw
day 1 and a nw pach chang day. A nnhrmnal
backup cnracpiv (cndms, sprmicidal fam,
diaphragm) shuld b usd cncurrnly fr h
rs 7 cnscuiv days f h nw cycl.
• At the end of the patch cycle (week 4/day 22): Th pach
shuld b rmvd as sn as h wman rmm-
brs  rmv i. Th nw cycl shuld b sard
n h usual pach chang day, which is h day af-
r day 28. N backup cnracpin is ndd.
Ohr impran pins:
• Missed patches and skipped periods: Rurn  h
halhcar prvidr fr a prgnancy s.
• Skipping one period but not missing a patch: I is n
uncmmn fr a wman  ccasinally miss a p-
rid whn rciving hrmn hrapy. Sar h nx
cycl n h sam pach chang day. If w cnscu-
iv prids ar missd, a prgnancy s is in rdr.
Cnracpiv hrapy shuld b discninud if
prgnancy is cnrmd.
• Spotting for two or more cycles: S h halhcar pr-
vidr  hav hr causs f blding assssd.
655
• Periodic examinations: A yarly xaminain shuld
includ bld prssur ss, plvic xaminain,
urinalysis, bras xaminain, and Pap s.
• Serious adverse effects to be reported as soon as pos-
sible: Svr hadachs, dizzinss, blurrd visin,
lg pain, shrnss f brah, chs pain, and acu
abdminal pain. Alhugh hs advrs ffcs ar
usually f minr cnsqunc, absnc f srius
advrs ffcs such as hrmbmblism r cpic
prgnancy mus b cnrmd.
Note: Whn bing sn by a halhcar prvidr r
a dnis fr hr rasns, b sur  mnin ha hr-
mnal cnracpivs ar bing akn.
Common and serious adverse effects. S Cmmn
Advrs Effcs and Srius Advrs Effcs fr Oral
Cnracpivs arlir in his scin.
Drug interactions. S Drug Inracins fr Oral
Cnracpivs arlir in his scin.
DRUG CLASS: INTRAVAGINAL HORMONAL
CONTRACEPTIVES
etonogestrel–ethinyl estradiol vaginal ring (ē-tŏn-ō-
GĔS-trĕl–ĔTH-ĭ-nĕl ĕs-trĕ-DĪ-ŏl VĂ-gĭ-năl RĬNG)
NuvaRing (NŪ-vă-rĭng)
EluRyng (el’ ue ring)
segesterone–ethinyl estradiol vaginal ring (sedg-est-
rohn)
Annovera (ahn-ov-rah)
Actions
An srgn (hinyl sradil) and a prgsin (n-
gsrl r sgsrn) wrk ghr as a cnracp-
iv by inhibiing vulain. Esrgns blck piuiary
rlas f FSH, prvning h varis frm dvlping
a fllicl ha rlass an vum. Prgsins inhibi piu-
iary rlas f LH, h hrmn rspnsibl fr rlas-
ing an vum frm a fllicl. Ohr mchanisms play a
cnribury rl in prvning cncpin. Esrgns
and prgsins alr crvical mucus by making i hick
and viscus, inhibiing sprm migrain. Hrmns
als chang h ndmrial wall, impairing implana-
in f h frilizd vum.
Uses
Th NuvaRing and Annvra vaginal rings wrk vry
much lik h cmbinain ral cnracpivs, xcp
ha h srgn and prgsin hrmns ar in a plasic
ring dsag frm ha h wman insrs in hr vagina
fr 3 wks. Th ring is rmvd fr a 1-wk brak, dur-
ing which wihdrawal blding (mnss) shuld bgin.
Cigar smking incrass h risk f srius ad-
vrs cardivascular ffcs (.g., bld cls) in prsns
wh bh smk and us cmbinain cnracpivs.
656 UNIT VIII Drugs Affecting the Reproductive System
This risk incrass wih ag and havy smking (a
las 15 cigars pr day) and is qui signican in
wmn ldr han 35 yars. Wmn wh us hrmn
cnracpivs ar srngly ncuragd n  smk.
Therapeutic Outcome
Th primary hrapuic ucm assciad wih in-
ravaginal hrmn cnracpiv hrapy is prvn-
in f prgnancy.
Nursing Implications for Intravaginal Hormonal
Contraceptive
Premedication assessment
1. Rviw h mdical hisry. If hr is a hisry f
hyprnsin, gallbladdr disas, diabs ml-
lius, svr varics vins, sizur disrdrs, li-
gmnrrha r amnrrha, rhumaic har dis-
as, hrmbmblic disas, srk, malignancy
f bras r h rprduciv sysm, rnal r livr
disas, svr mnal dprssin, suspcd prg-
nancy, r rpad cnracpiv failur, r if h pa-
in smks, cnsul wih h halhcar prvidr
bfr dispnsing h birh cnrl ring.
2. Tak a baslin bld prssur in h supin and si-
ing psiins.
3. Ensur ha a prgnancy s has bn givn and
ha h pain is n prgnan.
Availability. NuvaRing and EluRyng ach rlas 0.12
mg ngsrl and 0.015 mg hinyl sradil pr day
(3-wk durain).
Annvra rlass 0.15 mg sgsrn and 0.013
mg hinyl sradil pr day (3-wk durain).
Implementation
Before initiating therapy. Th pain shuld hav a
cmpl physical xaminain ha includs bld
prssur, plvic and bras xaminains, Pap s, uri-
nalysis, and hmglbin r hmacri.
Instructions for using the intravaginal hormonal
contraceptive
• Insertion: Slcing a cmfrabl psiin, cmprss
h ring and insr in h vagina. Th xac psi-
in insid h vagina is n criical fr is funcin
bu shuld b bhind h plvic bn. Insr n
h apprpria day, as dscribd lar, and lav
in plac fr 3 cnscuiv wks. Chck rgularly
(such as bfr and afr inrcurs)  nsur ha
h ring is in plac  prvid pimal prcin.
• Removal: Rmv h ring 3 wks lar n h sam
day f h wk as i was insrd and a abu h
sam im. Rmv by hking h indx ngr un-
dr h frward rim r by grasping h rim bwn
h indx and middl ngrs and pulling i u.
• NuvaRing: Plac h usd ring in h fil puch and
discard in a was rcpacl u f rach f childrn
and ps. I sill cnains aciv hrmn rsidual.
D n ush dwn h il. Insr a nw ring n
day 7 (h sam day and im f h wk) ha h
ld ring was rmvd.
• Annvra: Afr rmval, wash wih warm war
and mild sap, dry wih a clan clh r papr w-
l, and sr in h cas prvidd. Rinsr h sam
ring n day 7 (h sam day and im f h wk)
ha h ring was rmvd, washd, and srd).
Slc n f h fllwing mhds  sar
cnracpin:
• If no hormonal contraceptive was in use in the past
month: Cuning h rs day f mnsruain as day
1, insr h cnracpiv ring n r prir  day 5
f h cycl, vn if mnss is cninuing. N n
a calndar h day f h wk as a rmindr f h
rmval day 3 wks lar. A nnhrmnal backup
cnracpiv (.g., cndms, sprmicidal fam, di-
aphragm) shuld b usd cncurrnly fr h rs 7
cnscuiv days f cninuus ring us.
• Switching from a combination oral contraceptive: Insr
h ring any im wihin 7 days afr h las aciv
cmbind ral cnracpiv abl and n lar han
h day ha a nw cycl f pills wuld hav bn
sard. N backup cnracpin is ncssary.
• Switching from a progestin-only minipill: Insr h
ring h fllwing day afr discninuing h mini-
pill. A nnhrmnal backup cnracpiv (.g.,
cndms, sprmicidal fam, diaphragm) shuld b
usd cncurrnly fr h rs 7 cnscuiv days f
cninuus ring us.
If h ring is xplld r rmvd, r hr is a pr-
lngd ring-fr inrval during h aciv 3 wks:
• For less than 2 hours: Rins h ring in cl r luk-
warm (n h) war and rinsr as sn as
pssibl.
• For longer than 2 hours or if not sure how long since
expelled: If h ring has bn u fr lngr han 2
hurs, hr may b a lack f prcin frm prg-
nancy. Rinsr h ring, bu us a nnhrmnal
backup cnracpiv (.g., cndms, sprmicidal
fam, diaphragm) fr h nx 7 cnscuiv days f
cninuus ring us.
If a wman frgs  chang h ring:
• If left in place for up to 1 extra week (4 weeks total):
Rmv i and insr a nw ring afr a 1-wk ring-
fr inrval. Us a nnhrmnal backup cnracp-
iv (.g., cndms, sprmicidal fam, diaphragm)
fr h nx 7 cnscuiv days f cninuus ring
us.
• If left in place for more than 4 weeks: Rmv h ring.
Rul u prgnancy. Insr a nw ring afr a 1-wk
ring-fr inrval if n prgnan. Us a nnhrmn-
al backup cnracpiv (.g., cndms, sprmicidal
fam, diaphragm) fr h nx 7 cnscuiv days f
cninuus ring us.
Ohr impran pins:
• Missing one period but being adherent to the program: I
is n uncmmn fr a wman  ccasinally miss
a prid whn rciving hrmn hrapy. Sar h
 Drugs Used in Men’s and Women’s Health CHAPTER 40
nx cycl n h sam insrin day (i.., n h 29h
day). If w cnscuiv prids ar missd, a prg-
nancy s is in rdr. Cnracpiv hrapy shuld
b discninud if prgnancy is cnrmd.
• Missd n prid and h ring was u fr mr
han 2 hurs r was lf in fr mr han 4 wks:
Rurn  h halhcar prvidr fr a prgnancy
s.
• Spotting for two or more cycles: S h halhcar pr-
vidr  hav hr causs f blding assssd.
• Periodic examinations: A yarly xaminain shuld
includ bld prssur ss, plvic xaminain,
urinalysis, bras xaminain, and Pap s.
• Serious adverse effects to be reported as soon as pos-
sible: Svr hadachs, dizzinss, blurrd visin,
lg pain, shrnss f brah, chs pain, and acu
abdminal pain. Alhugh hs advrs ffcs ar
usually f minr cnsqunc, absnc f srius
advrs ffcs such as hrmbmblism r cpic
prgnancy mus b cnrmd.
Note: Whn bing sn by a halhcar prvidr r
a dnis fr hr rasns, b sur  mnin ha hr-
mnal cnracpivs ar bing akn.
Common and serious adverse effects. S Cmmn
Advrs Effcs and Srius Advrs Effcs fr Oral
Cnracpivs arlir in his scin.
Drug Interactions. S Drug Inracins fr Oral
Cnracpivs arlir in his scin.
DRUG CLASS: INTRAVAGINAL NONHORMONAL
CONTRACEPTIVE
Phxxi, a vaginal gl (lacic acid, ciric acid, and p-
assium biarra), was apprvd as a vaginal rgu-
lar (lwrs pH) fr h prvnin f prgnancy
fr us as an n-dmand mhd f cnracpin. I
is usd inravaginally (n prlld singl-ds ap-
plicar) up  1 hur bfr ach pisd f vaginal
inrcurs. An addiinal applicarful shuld b
insrd if inrcurs ds n ccur wihin 1 hur
f iniial insrin. I is n hugh  b as ffciv
if adminisrd afr inrcurs. Us ds n pr-
c agains STIs r HIV. I may b usd a any im
during h mnsrual cycl. Phxxi may b usd wih
hrmnal cnracpivs, mal and fmal cndms,
and vaginal diaphragms bu shuld n b usd wih
vaginal ring cnracpivs. A prmarking sudy
dmnsrad a cumulaiv prgnancy ra f 13%
vr 7 cycls f ypical us.
Th ms cmmn advrs racins ar a burning
snsain, vulvvaginal prurius, vulvvaginal myc-
ic infcin, urinary rac infcin, vulvvaginal dis-
cmfr, bacrial vaginsis, vaginal discharg, gni-
al discmfr, dysuria, and vulvvaginal pain. Mal
parnrs may xprinc lcalizd burning, iching, r
pain.
657
OSTEOPOROSIS
Osteoporosis is h ms cmmn bn disas. I is
characrizd by lw bn minral dnsiy (BMD) (i..,
lw bn mass) and micrarchicural alrains ha
rsul in bn fragiliy and incrasd risk f fracurs.
Th bns ms cmmnly affcd by sprsis
includ h hip, spin, and wris. Mr han 50 mil-
lin mn and wmn in h Unid Sas hav s-
prsis r spnia (lw BMD). Abu n f vry
w ppl in h Unid Sas ldr han 50 yars is
a risk fr an spric fracur.
Bn is living issu ha is cnsanly bing brkn
dwn and rplacd (bn rmdling). Th prcss f
bn rmdling mainains a halhy skln. Bn
rmdling ccurs a spcic sis wihin h skln
and prcds in an rdrly fashin; bn rsrpin is
always fllwd by bn frmain. Osclass ar
rspnsibl fr bn rsrpin, whras sblass
ar rspnsibl fr bn frmain. Bh yps f clls
ar dpndn n ach hr fr h prcss f bn
rmdling. In spnia and sprsis, h bal-
anc is alrd bwn sclass and sblass,
rsuling in grar bn rmval han rplacmn.
Osclass rquir wks  rsrb bn, whras s-
blass nd mnhs  prduc nw bn. Thrfr
any prcss ha incrass h ra f bn rmdling
rsuls in n bn lss vr im.
Risk facrs assciad wih sprsis and frac-
urs includ (bu ar n limid ) incrasing ag,
fmal sx, psmnpausal saus, hypgnadism
(dcrasd sx hrmns), lw bdy wigh, hisry
f parnal hip fracur, rac and hniciy (whi pr-
sns ar a highr risk han black prsns), prsnc f
rhumaid arhriis, currn smking, alchl inak
(3 r mr drinks daily), lw BMD, viamin D d-
cincy, and lw calcium inak. Anhr risk facr fr
spric fracur is lng-rm us f crain mdi-
cains; h ms cmmnly implicad drugs ar glu-
ccricids, anicagulans, anipilpics, armaas
inhibirs, anicancr drugs, and gnadrpin-rlas-
ing hrmn agniss.
Osprsis is fn diagnsd afr h ccur-
rnc f fragiliy fracur (a yp f fracur ha c-
curs as rsul f nrmal aciviis, such as a fall frm
sanding high r lss). In pains wihu fragiliy
fracur, sprsis is fn diagnsd by lw BMD.
Dual-nrgy x-ray absrpimry (DEXA) is h cur-
rn gld sandard s fr diagnsing sprsis
in ppl wihu an spric fracur. Rsuls f
DEXA ar scrd as h numbr f sandard dviains
(SDs) frm a yung, halhy nrm (usually fmal)
and rprd as T scrs. Fr xampl, a T scr f −2
indicas a BMD ha is 2 SDs lss han h cmparaiv
nrm. A T scr f −2.5 r lss indicas h prsnc
f sprsis. Th inrnainal rfrnc sandard
fr h dscripin f sprsis in psmnpausal
wmn and in mn agd 50 yars r ldr is a fmral
658 UNIT VIII Drugs Affecting the Reproductive System
nck BMD f 2.5 SDs r mr blw h yung fmal
adul man T scr f 2; hwvr, lw BMD as ma-
surd by DEXA is an imprfc prdicr f fracur
risk, idnifying lss han n-half f h ppl wh
g n  hav an spric fracur.
Svral inrvnins  prsrv bn srngh ar
rcmmndd  h gnral ppulain. Ths in-
clud an adqua inak f calcium and viamin D,
liflng paricipain in rgular wigh-baring and
muscl-srnghning xrciss, cssain f bacc
us, idnicain and ramn f alchlism, and
idnicain f risk facrs fr falling.
DRUG THERAPY FOR OSTEOPOROSIS
Accrding  h guidlins f h Amrican Cllg
f Physicians and f h Amrican Assciain f
Clinical Endcrinlgiss and Amrican Cllg f
Endcrinlgiss, h bisphsphnas (alndrna,
risdrna, and zldrnic acid) and dnsumab ar
apprpria as iniial hrapy fr ms pains wih
sprsis. Thy all rduc hip, nnvrbral, and
vrbral (spin) fracurs. Ohr ramns includ
abalparaid, ibandrna, ralxifn, rmszumab,
and riparaid. Abalparaid, riparaid, and r-
mszumab shuld b rsrvd fr pains wih a
high risk fr fracurs. Abalparaid and riparaid
ar rcmbinan frms f parahyrid hrmn. Thy
simula sblas funcin, incras gasrinsi-
nal calcium absrpin, and incras rnal ubular r-
absrpin f calcium. Abalparaid and riparaid
rsuls in incrasd bn minral dnsiy, bn mass,
and srngh, rmszumab binds and inhibis sclrs-
in, wih a dual ffc f incrasing bn frmain and
dcrasing bn rsrpin. Diary and supplmnal
calcium and viamin D ar als usd fr ramn.
NURSING IMPLICATIONS FOR OSTEOPOROSIS
Assessment
History of risk factors
Smoking. Obain a hisry f h numbr f ciga-
rs r cigars ha h pain smks daily; includ
hr surcs f nicin, such as chwing bacc
and rplacmn hrapy. Hw lng has h prsn
smkd? Has h prsn vr rid  sp smking?
Ask if h pain undrsands h ffc f smking n
bn halh. Hw ds h individual fl abu mdi-
fying hir smking habi?
Dietary habits. Obain a diary hisry. Ask spcic
qusins  bain daa rlaing  h amun f cal-
cium- and viamin D–rich fds, such as milk, ha ar
cnsumd n a daily basis.
Psychomotor functions
• Drmin h pain’s yp f lifsyl. Hav h
pain dscrib xrcis lvl in rms f amun
(.g., walking 3 mils), innsiy (.g., walking 3
mph), and frquncy (.g., walking vry hr
day). Is h pain’s jb physically dmanding r f
a sdnary naur?
• Drmin h pain’s lvl f psychlgical srss.
Ask h individual  sima h amun f srss
in hir lif. Hw ds h prsn cp wih srss-
ful siuains a hm and in h wrkplac?
Alcohol. Drmin whhr h pain cnsums al-
chl grar han hr drinks daily, and cunsl h
nd  dcras cnsumpin r sp alghr.
Dentition. Nurss shuld prvid ducain rgarding
h nd fr dnal xaminain prir  iniiain f
mdicain. Cmplicains frm h us f hs drugs
hav bn assciad wih dnal wrk, such as h
xracins, dnal implans, dnal surgry, and pr
ral hygin. Gd ral hygin nds  b srssd.
Pain. Assss fr and rpr incrasd pain in hips,
grin, r highs wih lng-rm us f mdicain.
Implementation
• Prfrm nursing assssmns n a schduld basis.
• Mak rfrrals as indicad fr srss managmn,
smking cssain, and diary cunsling and fr
an xrcis prgram apprpria fr h individu-
al’s nds.
• Prc h pain frm pssibl falls by assising
during ambulain.
Patient Education
Suggs ha pains sp smking if hy d smk.
Prvid ducainal marials fr smking cssain.
Smking has bn linkd  sprsis bcaus
sudis hav indicad ha nicin inrfrs wih
h funcin and grwh f h sblass. Thrfr
ncurag a drasic rducin in—and prfrably al
absinnc frm—smking. Includ infrmain abu
smking cssain and availabl suppr rsurcs.
Fostering health maintenance
• Thrughu h curs f ramn, discuss mdica-
in infrmain and hw i will bn h pain.
• Tach pain hw  manag sympms f s-
prsis, spcically pain.
• Explain h nd  mainain an xrcis prgram
and mdify diary habis  incras calcium and
viamin D in h di. Cssain f smking and min-
imal alchlic inak ar srngly rcmmndd.
• Prvid h pain and signican hrs wih
h impran infrmain cnaind in h sp-
cic drug mngraphs fr h drugs prscribd.
Addiinal halh aching and nursing inrvn-
ins fr cmmn and srius advrs ffcs will
b fund in ach drug mngraph.
• Sk cprain and undrsanding f h fl-
lwing pins s ha mdicain cmplianc is
 Drugs Used in Men’s and Women’s Health CHAPTER 40
incrasd: nam f mdicain; dsag, rus, and
ims f adminisrain; and cmmn and srius
advrs ffcs.
Patient self-assessment. Enlis h pain’s hlp
in dvlping and mainaining a wrin rcrd f
mniring paramrs (.g., bld prssurs, wigh,
xrcis). S h Pain Slf-Assssmn Frm fr
Osprsis Agns n h Evlv wbsi. Cmpl
h Prmdicain Daa clumn fr us as a baslin
 rack rspns  drug hrapy. Ensur ha h pa-
in undrsands hw  us h frm, and insruc
h pain  bring h cmpld frm  fllw-up
visis. During fllw-up visis, fcus n issus ha will
fsr adhrnc wih h hrapuic inrvnins
prscribd.
DRUG CLASS: BISPHOSPHONATES
Actions
Bisphsphnas (alndrna, risdrna, and zl-
drnic acid) inhibi bn rsrpin by acins n s-
class. Dcrasing h ra f bn rsrpin lads
 an indirc incras in BMD.
Uses
Alndrna is usd in h ramn and prvnin f
sprsis in psmnpausal wmn, h ramn
f sprsis in mn, and h ramn f gluccr-
icid-inducd sprsis in mn and wmn wih
lw BMD wh ar rciving a daily dsag f 7.5 mg
r mr f prdnisn.
Risdrna is usd in h ramn and prvnin
f sprsis in psmnpausal wmn, h ra-
mn f sprsis in mn, and h ramn and
prvnin f gluccricid-inducd sprsis.
Zldrnic acid is usd in h ramn and pr-
vnin f sprsis in psmnpausal wmn,
h ramn f sprsis in mn, and h ra-
mn and prvnin f gluccricid-inducd s-
prsis in mn and wmn wh ar iniiaing r
cninuing sysmic gluccricids in a daily dsag
quivaln  7.5 mg r mr f prdnisn and wh
ar xpcd  rmain n gluccricids fr a las
12 mnhs.
Therapeutic Outcome
Th primary hrapuic ucm fr bisphsphnas
is  rduc fracurs in pains wih sprsis.
Nursing Implications for Bisphosphonates
Premedication assessment
1. Obain h pain’s baslin vial signs and n
any bn pain prsn prir  ramn.
2. Encurag an adqua calcium and viamin D in-
ak in h di whil aking hs drugs.
3. Prvid ducain rgarding h nd fr a dnal
xaminain prir  iniiain f mdicain.
659
4. Chck labrary valus fr calcium, magnsium,
and phspha.
Availability, dosage, and administration
S Tabl 40.7
Medication Safety Alert
Administer bisphosphonates in the morning 30 minutes or
more before the rst food, beverage (except plain water), or
other medication(s) of the day. Do not take with mineral water
or with other beverages. Patients should be instructed to sit
or stand upright (not to lie down) for at least 30 minutes after
administration and until after rst food of the day (to reduce
esophageal irritation).
Oral solution: Mus b fllwd wih a las 2
uncs f plain war.
Tablets: Mus b akn wih 6  8 uncs f plain
war. Th abl shuld b swallwd whl.
Effervescent tablet: Disslv n abl in 4 uncs
f rm-mpraur plain war nly; nc ffrvs-
cnc sps, wai 5 minus r mr and sir h slu-
in fr apprximaly 10 scnds  rmv bubbls
and hn drink.
Common adverse effects
Neurologic
Headache. Tll h pain ha a hadach may c-
cur bu nds b slf-limiing.
Gastrointestinal
Abdominal pain, gastroesophageal reux disease, dyspep-
sia, constipation, diarrhea. Ths advrs ffcs ar ms
cmmn and ar usually mild and nd  rslv
wih cninud hrapy. If advrs ffcs bcm
mr svr, h pain shuld cnac h halhcar
prvidr.
Musculoskeletal pain. This is a cmmn advrs f-
fc. I is usually mild and nds  rslv wih cnin-
ud hrapy. If advrs ffcs bcm mr svr, h
pain shuld cnac h halhcar prvidr
Serious adverse effects
Dysphagia, gastritis, gastric ulcers. Bisphsphnas
givn rally may caus lcal irriain f h uppr
gasrinsinal mucsa. Us cauin in pains wih
aciv uppr gasrinsinal prblms such as dys-
phagia, gasriis, r ulcrs. Pains shuld b insruc-
d  discninu hrapy and alr h halhcar pr-
vidr if difculy in swallwing, pain n swallwing,
chs pain, r nw r wrsning harburn dvlps.
Musculoskeletal pain. Incapaciaing bn, jin, and
r muscl pain has bn rprd. Th ns f symp-
ms varis frm 1 day  svral mnhs. Pains
shuld b insrucd  discninu hrapy and cnac
h halhcar prvidr if svr sympms dvlp.
Nephrotoxicity. Bisphsphnas ar cnraindicad
in pains wih a crainin claranc f lss han 35
mL/min.
660 UNIT VIII Drugs Affecting the Reproductive System
Table 40.7 Bisphosphonates
GENERIC NAME BRAND NAME AVAILABILITY
alendronate Fosamax Solution: 70 mg/75 mL
Binosto Tablets: 5, 10, 35, 70 mg
Effervescent tablet: 70 mg
risedronate Actonel Tablets: 5, 35, 150 mg
Atelvia Tablets, Delayed Release: 35 mg
zoledronic acid Reclast IV Solution: 5 mg/100 mL
Aclasta
Available in Canada.
Zldrnic acid shuld b usd wih cauin in pains
wih chrnic rnal impairmn, spcially in pains
wih prxising rnal cmprmis, and in pains wih
advancd ag, cncmian nphrxic mdicains,
cncmian diuric hrapy, r svr dhydrain.
Osteonecrosis of the jaw. Osncrsis f h jaw is
gnrally assciad wih h xracin. Risk facrs
includ h xracins, dnal implans, dnal sur-
gry, diagnsis f cancr, and pr ral hygin. Th
risk incrass wih durain f ramn.
Atypical femoral fractures. Aypical fmral fracurs
may ccur wih minimal r n rauma  h affcd
ara. Pains shuld rpr any high r grin pain.
Spping h bisphsphnas shuld b cnsidrd
afr discussin wih h halhcar prvidr.
Drug interactions
Calcium supplements/antacids. Cadminisrain wih
calcium and anacids will inrfr wih h absrpin
f ral bisphsphnas. Pains shuld wai a las 30
minus afr aking bisphsphnas bfr aking cal-
cium r anacids.
Aspirin and nonsteroidal antiinammatory drugs. Th
incidnc f uppr gasrinsinal advrs ffcs is
incrasd wih daily ral dss f aspirin r nnsri-
dal aniinammary drugs whil aking bisphsph-
nas. Us cauin bcaus adminisrain f nn-
sridal aniinammary drugs is assciad wih
gasrinsinal irriain.
Nephrotoxic drugs. Us cauin whn aking zl-
drnic acid wih hr pnially nphrxic drugs
such as nnsridal aniinammary drugs and
aminglycsids.
DOSAGE
Glucocorticoid-induced osteoporosis: PO: 5 mg once daily
Postmenopausal women not receiving estrogen PO: 10 mg
once daily
Osteoporosis in men: PO: 70 mg once weekly or 10 mg
once daily
Osteoporosis in postmenopausal women:
Prevention: PO: 35 mg once weekly or 5 mg once daily
Treatment: PO: 70 mg once weekly or 10 mg once daily
Glucocorticoid-induced osteoporosis: PO: 5 mg daily
Osteoporosis in men: PO: 35 mg once weekly
Osteoporosis in postmenopausal women: PO: 5 mg daily
or 35 mg once weekly or 150 mg once monthly
Osteoporosis in postmenopausal women: PO: 35 mg once
weekly
Osteoporosis treatment: 5 mg IV infusion over no less than
15 min once yearly
Osteoporosis prevention:
Reclast: IV: 5 mg once every 2 yr
Aclasta: IV: 5 mg as a single (one-time) dose
Glucocorticoid-induced osteoporosis: 5 mg IV infusion over
no less than 15 min once yearly
denosumab (dĕn-Ō-sū-măb)
Prolia (PRO-lee-a)
Actions
Dnsumab is a mnclnal anibdy ha prvns
sclas frmain, lading  dcrasd bn r-
srpin and incrasd bn mass in pains wih
sprsis.
Uses
Dnsumab is usd in h ramn f sprsis in
psmnpausal wmn and mn a high risk f frac-
ur and in gluccricid-inducd sprsis.
I is als usd as ramn fr bn lss in mn
rciving andrgn dprivain hrapy (.g., lupr-
lid) fr nnmasaic prsa cancr and ramn
f bn lss in wmn rciving armaas inhibir
hrapy (.g., anasrzl) fr bras cancr.
Therapeutic Outcome
Th hrapuic ucms fr dnsumab ar a r-
ducin in fracurs in pains wih sprsis and
prvnin f bn lss in mn rciving andrgn
dprivain hrapy and wmn rciving armaas
inhibirs fr bras cancr.
Nursing Implications for Denosumab
Premedication assessment
1. Obain baslin mpraur, bld prssur, and
har ra.
2. Chck labrary valus fr calcium, magnsium,
and phspha.
 Drugs Used in Men’s and Women’s Health CHAPTER 40
Availability. Subcutaneous solution: Prlia: 60 mg/mL in
1-mL prlld syring
Dosage and administration. Dnsumab shuld b
adminisrd subcuanusly in h uppr arm, uppr
high, r abdmn by a halhcar prfssinal.
Insruc pains  ak 1000 mg calcium daily and
a las 400 IU viamin D daily.
Treatment of androgen deprivation–induced bone loss
in men with prostate cancer: Subcutaneous: 60 mg as a
singl ds, nc vry 6 mnhs.
Treatment of aromatase inhibitor–induced bone loss in
women with breast cancer: Subcutaneous: 60 mg as a
singl ds, nc vry 6 mnhs.
Treatment of osteoporosis in men or in postmenopausal
women: Subcutaneous: 60 mg as a singl ds, nc v-
ry 6 mnhs.
Treatment of glucocorticoid-induced osteoporosis:
Subcutaneous: 60 mg as a singl ds, nc vry 6
mnhs.
Common adverse effects
Dermatologic. Drmaiis (4%  11%), czma (4% 
11%), skin rash (3%  11%).
Cardiovascular. Hyprnsin, hyprchlsrlmia
in wmn.
Musculoskeletal. Arhralgia (7%  14%), limb pain
(10%  12%), back pain (8%  12%).
Urinary. Cysiis may ccur in wmn. Insruc h
pain  cnac h halhcar prvidr.
Serious adverse effects. Insruc h pain  cnac
h halhcar prvidr rgarding h fllwing symp-
ms r cndiins.
Hypersensitivity. Anaphylacic racins may ccur.
Dnsumab may b discninud prmannly if a sig-
nican racin ccurs.
Hypocalcemia. Obain calcium lvl bfr iniiaing
hrapy; a dcin lvl mus b crrcd bfr ini-
iaing dnsumab hrapy. Adqualy supplmn
pains wih calcium and viamin D.
Osteonecrosis of the jaw. Mnir fr sympms f
jaw pain, difculy in chwing.
Atypical femoral fractures. Evalua pains wih
high r grin pain  rul u a fmral fracur.
Infections. Th pain may dvlp signs r symp-
ms f infcin such as fvr, ndrnss and inam-
main, r muscl r jin pain.
Dermatologic reactions. Svr sympms f drmai-
is, rashs, and czma may dvlp.
Drug interactions. N drug inracins hav bn
rprd.
BENIGN PROSTATIC HYPERPLASIA
Th prsa gland funcins as par f h mal rpr-
duciv sysm. I is a rm rgan, wighing abu 20
661
g, h siz f a walnu. I is lcad a h bas f h
urinary bladdr and cmplly surrunds h prxi-
mal urhra. As par f h mal rprduciv sysm,
i prducs a uid during jaculain ha mixs wih
sprm frm h ss and uid frm h sminal vsi-
cls  frm smn. Th gland may als prc agains
urinary rac infcins hrugh scrin f prsaic
anibacrial facr. Tw hr chmicals scrd by
h prsa gland ar acid phsphaas and prsa-
spcic anign (PSA). An lvad PSA lvl may in-
dica h prsnc f prsa cancr.
Enlargmn f h prsa gland as mn ag is an
alms univrsal phnmnn. A cndiin calld en-
larged prostate, prostatism, r benign prostatic hyperpla-
sia (BPH) is cmmn lar in lif, affcing mr han
50% f mn in hir 60s and as many as 90% in hir 70s
and 80s. Many mn wih BPH will nd sm yp f
ramn. Alhugh an nlargd prsa is an appar-
nly nrmal par f aging, prblms wih urinain
ha fn accmpany his nlargmn ar n nrmal.
BPH is much mr cmmn han prsa cancr;
hwvr, an nlargd prsa gland can b causd by
prsa cancr. Bcaus h signs f nlargd prs-
a ar fn h sam as h signs and sympms f
prsa cancr, i is impran  bain a halhcar
prvidr’s pinin s ha h prpr diagnsis can b
mad. Th halhcar prvidr may als nd  rul
u prsa infcin and hr pssibl causs f h
pain’s sympms.
Th pahgnsis f BPH is n wll undrsd,
bu i appars  invlv h prsnc f incras-
ing lvls f dihydrssrn (DHT), causd by a
slw incras in prducin, rducd mablism, r
bh, ha simula h grwh f nw prsa clls.
Dihydrssrn is frmd in h prsa gland
frm ssrn prducd in h ss. Th cnvr-
sin f ssrn  DHT is caalyzd by h nzym
5-alpha rducas.
Th sympms f BPH ar highly variabl and pain
spcic and ar dividd in w cagris: bsruciv
and irriaiv (Bx 40.3). Obsruciv sympms rsul
Box 40.3 Symptoms of Benign Prostatic Hyperplasia
OBSTRUCTIVE
• Reduced force of urinary stream
• Resistance to initiation of voiding
• Prolonged dribbling after urination
• Sensation of incomplete bladder emptying
• Decreased or interrupted stream
• Double voiding
• Straining or pushing to urinate
IRRITATIVE
• Increased frequency
• Nocturia
• Difcult or painful urination (dysuria)
• Sudden urgency
• Urge incontinence
662 UNIT VIII Drugs Affecting the Reproductive System
dircly frm narrwing f h bladdr nck and ur-
hra. Irriaiv sympms rsul frm incmpl blad-
dr mpying r urinary rac infcin scndary 
prsaic bsrucin. As h prsa gland nlargs,
i cmprsss h urhra, parially r cmplly b-
srucing urin w frm h bladdr. Ovr im, symp-
ms bcm prgrssivly wrs, rquiring mdical a-
nin. Whn ncssary h hyprplasic issu may b
rmvd surgically  rduc h urinary bsrucin.
Transurhral rscin r lasr hrapy may b usd 
ra glands smallr han 60 g, whras largr glands ar
rmvd surgically (prsacmy). Inrmin cah-
rizain svral ims daily r placmn f a prma-
nn indwlling cahr may b usd if h pain is
n a candida fr surgry.
DRUG THERAPY FOR BENIGN
PROSTATIC HYPERPLASIA
BPH may als b rad succssfully wih mdica-
in. Th alpha-1 adrnrgic blcking agns alfuzsin,
sildsin, r amsulsin ar usd  rlax h smh
muscl f h bladdr and prsa. Ohr alpha-1 ad-
rnrgic blcking agns (.g., dxazsin, razsin)
ar als usd  ra hyprnsin (s Chapr 22).
Aniandrgn agns, such as nasrid and duas-
rid, slcivly blck andrgns a h prsa cllu-
lar lvl and caus h prsa gland  shrink. Sudis
indica ha a cmbinain f an alpha blckr wih a
5-alpha rducas inhibir is mr ffciv in slwing
h prgrssin f BPH han ihr agn aln. Th
phsphdisras inhibir adalal has als bn ap-
prvd fr h ramn f BPH.
DRUG CLASS: ALPHA-1 ADRENERGIC BLOCKING
AGENTS
Actions
Alpha-1 adrnrgic blcking agns hav slciviy
fr h alpha-1A rcpr subyp fund n h prs-
a gland. Apprximaly 70% f h alpha-1 rcp-
rs in h human prsa ar f h alpha-1A subyp.
Alfuzsin, sildsin, and amsulsin ar alpha-1A–
spcic adrnrgic blcking agns, whras dxa-
zsin and razsin ar nnspcic alpha-1 blcking
agns. Ths agns blck alpha-1 rcprs n h
prsa gland and crain aras f h bladdr nck,
causing muscl rlaxain and allwing grar uri-
nary uw in mn wih an nlargd prsa gland.
Alpha-1 blcking agns d n rduc prsa siz r
inhibi ssrn synhsis as d h 5-alpha rduc-
as inhibirs, nr d hy affc PSA lvls.
Uses
Alpha-1 blcking agns ar usd  rduc mild 
mdra urinary bsrucin manifsains (.g.,
hsiancy, rminal urin dribbling, inrrupd
sram, impaird siz and frc f sram, snsain f
incmpl bladdr mpying) in mn wih BPH. Thy
prduc a 20%  30% incras in urin w ra in
up  50% f mn wih urinary sympms. Sympms
shw imprvmn afr 1 wk f hrapy, bu 2  3
mnhs f cninud hrapy ar rquird  assss full
ffc. Alpha-1A–spcic drugs (i.., alfuzsin, amsu-
lsin, sildsin) ar n usd  ra hyprnsin.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm al-
pha-1 blckr hrapy ar rducd sympms and
imprvmn in urin w assciad wih prsa
gland nlargmn.
Nursing Implications for Alpha-1 Adrenergic
Blocking Agents
Premedication assessment
1. Obain baslin bld prssur radings in supin
and sanding psiins.
2. Chck if h pain has a hisry f svr crbral
r crnary arrisclrsis, gasriis, r ppic ulcr
disas. (Rducin f bld prssur may dimin-
ish bld w  hs rgins, causing hrapy 
wrsn h cndiin.)
Availability, dosage, and administration
S Tabl 40.8
Medication Safety Alert
The initial doses of the alpha-1 blocking agents may cause
dizziness (6% to 7%) and hypotension with tachycardia and
fainting (<0.5%) in patients starting therapy. This effect may be
minimized by giving the rst doses with food. Patients should
be warned that this adverse effect might occur, it is transient,
and they should lie down immediately if symptoms develop.
Common adverse effects
Neurologic
Drowsiness, headache, dizziness, weakness, lethargy. Tll
h pain ha hs advrs ffcs may ccur bu
nd  b slf-limiing. Th pain shuld n sp
aking h mdicain and shuld cnsul h halh-
car prvidr if h prblm bcms unaccpabl.
Cardiovascular
Dizziness, tachycardia, fainting. Dizzinss may ccur in
mr han 2% f pains, and rhsaic hypnsin
ccurs in lss han 0.5% f pains whn hrapy is
iniiad. Sympms dvlp 15  90 minus afr h
rs ds is akn. T dcras h incidnc, adminis-
r h rs ds wih fd. Insruc h pain  li
dwn immdialy if hs sympms ccur. Prvid
fr h pain’s safy.
Drug interactions
Drugs that enhance therapeutic and toxic effects. Diurics,
cimidin, ranquilizrs, alchl, anihisamins, ba-
adrnrgic blcking agns (.g., prpranll, anll),
 Drugs Used in Men’s and Women’s Health CHAPTER 40 663

Table 40.8 Alpha-1 Blocking Agents Used for Benign Prostatic Hyperplasia
GENERIC NAME BRAND NAME AVAILABILITY DOSAGE
alfuzosin Uroxatral Tablets, extended-release PO: 10 mg daily to be taken immediately after the same meal
(24 hr): 10 mg each day
Tablets should not be crushed or chewed
doxazosin Cardura Tablets: 1, 2, 4, 8 mg PO: 1–8 mg once daily
Cardura XL Tablets, extended-release
(24 hr): 4, 8 mg
silodosin Rapao Capsules: 4, 8 mg PO: 8 mg daily; 4 mg daily for patients with renal impairment
tamsulosin Flomax Capsules: 0.4 mg PO: 0.4 mg daily, taken approximately 30 min after the same
meal each day
If symptoms are not adequately controlled after 2–4 wk of
therapy, the dose may be increased to 0.8 mg once daily
If administration is discontinued or interrupted for several
days, at either the 0.4- or 0.8-mg dose, start therapy again
with the 0.4-mg once-daily dose
terazosin — Capsules: 1, 2, 5, 10 mg PO: Initial: 1 mg daily at bedtime
Increase stepwise to 2 mg, 5 mg, or 10 mg daily to achieve
desired response of symptoms and ow rate
Maximum dose is 20 mg/day in 1 or 2 divided doses.

and hr anihyprnsiv agns shuld n b usd Uses

wih alfuzsin. Mnir h bld prssur rspns
 h cumulaiv ffcs f anihyprnsiv agns.
Tak h pain’s bld prssur in supin and rc
psiins.
Kcnazl, iracnazl, rinavir, diliazm,
and hr pn cychrm P-450 cmpnn 3A4 in-
hibirs inhibi h mablism f alfuzsin and sild-
sin and shuld n b usd cncurrnly wih alfuzsin
and sildsin.
Mnir fr an incras in svriy f advrs sid
ffcs such as sdain, hypnsin, and bradycardia
r achycardia.
Avanal, sildenal, tadalal, vardenal. Ths drugs
ar usd  ra ED. Thy may aggrava hypn-
siv ffcs f dxazsin and razsin, causing dizzi-
nss and achycardia. Adjus by rducing h ds f
h drugs usd  ra ED.
Duasrid inhibis 5-alpha rducas yps 1 and 2.
I is usd  ra h sympms assciad wih BPH,
rduc h risks assciad wih urinary rnin, and
minimiz h nd fr surgry assciad wih BPH.
Mr han 6  12 mnhs f ramn may b nc-
ssary  assss whhr a hrapuic rspns has
bn achivd. Pains wh rspnd  hrapy hav
fwr sympms assciad wih parial bsrucin,
imprvd urinary w ras, and a smallr prsa
gland. Duasrid is n apprvd by h FDA  ra
mal parn baldnss.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm
duasrid hrapy ar as fllws:
• Rducd sympms and imprvmn in urin w
assciad wih prsaic nlargmn
• Rducd nd fr surgry fr BPH

DRUG CLASS: ANTIANDROGEN AGENTS Nursing Implications for Dutasteride

dutasteride (dŭ-TĂS-tĕr-īd)
Avodart (ĂV-ō-dărt)
Actions
Duasrid is an andrgn hrmn inhibir ha
acs by inhibiing h nzym 5-alpha rducas. Th
cnvrsin f ssrn  DHT is caalyzd by 5-al-
pha rducas yps 1 and 2. Rducin in DHT lvls
rducs h hyprplasic cll grwh assciad wih
prsaic hyprplasia.
Premedication assessment. Obain a baslin PSA
bld lvl. Duasrid causs a dcras in srum
PSA lvls by abu 50% in pains wih BPH, vn
in h prsnc f prsa cancr. Any susaind in-
cras in PSA lvls whil a pain is rciving du-
asrid shuld b invsigad, including cnsid-
rain f prsa cancr and nncmplianc wih
hrapy.
Availability. PO: 0.5-mg capsuls.
Dosage and administration. PO: 0.5 mg nc daily,
wih r wihu fd.
664 UNIT VIII Drugs Affecting the Reproductive System
Medication Safety Alert
Dutasteride is contraindicated in women who are or may
become pregnant because it may cause abnormalities of
the external genitalia of a male fetus of a pregnant woman
who received the drug. Dutasteride is absorbed through hu
man skin. A woman who is pregnant or who may become
pregnant should not handle crushed or broken dutasteride
capsules.
Men treated with dutasteride should not donate blood
until at least 6 months after stopping therapy to avoid
introducing the drug to a pregnant woman.
Common adverse effects
Reproductive
Impotence, decreased libido, decreased volume of ejacu-
late. Ths advrs ffcs appar in small numbrs
f mn rciving highr dss f duasrid. Tll h
pain ha hs advrs ffcs may ccur bu nd 
b slf-limiing. Th incidnc f impnc, dcrasd
libid, and jaculain disrdr dcrass wih incras-
ing durain f ramn. Dcrasd vlum f jacu-
la ds n appar  inrfr wih nrmal sxual
funcin. Th pain shuld n sp aking h mdi-
cain and shuld cnsul his halhcar prvidr if h
prblm bcms unaccpabl.
Drug interactions
Drugs that enhance toxic effects. Kcnazl, ira-
cnazl, rinavir, diliazm, vrapamil, cimidin,
and ciprxacin inhibi h mablism f duas-
rid. Duasrid shuld b givn wih xrm cau-
in  mn aking any f hs mdicains.
nasteride (fĭn-ĂS-tĕr-īd)
Proscar (PRŌ-skăr), Propecia (prō-PĒ-shē ă)
Actions
Finasrid is an andrgn hrmn inhibir ha acs
by inhibiing h nzym 5-alpha rducas. Th cn-
vrsin f ssrn  DHT is caalyzd by 5-alpha
rducas. Rducin in DHT lvls rducs h hy-
prplasic cll grwh assciad wih prsaic hypr-
plasia. Elvad DHT lvls als induc andrgnic
alpcia, mr cmmnly knwn as male pattern bald-
ness (vrx and anrir midscalp).
Uses
Finasrid inhibis 5-alpha rducas yp 2. Prscar
is usd  ra h sympms assciad wih BPH, r-
duc h risks assciad wih urinary rnin, and
minimiz h nd fr surgry assciad wih BPH.
Mr han 6  12 mnhs f ramn may b nc-
ssary  assss whhr a hrapuic rspns has
bn achivd. Pains wh rspnd  hrapy hav
fwr sympms assciad wih parial bsrucin,
imprvd urinary w ras, and a smallr prsa
gland.
Prpcia is usd  ra andrgnic alpcia.
Afr a las 3 mnhs f daily us, nasrid main-
ains hair cun and simulas nw hair grwh in
hs wh rspnd. Cninud us is ncssary  sus-
ain h rsuls. Wih discninuain f ramn, h
ffcs ar rvrsd wihin 1 yar. Finasrid ds n
appar  affc nnscalp bdy hair.
Therapeutic Outcomes
Th primary hrapuic ucms xpcd frm n-
asrid hrapy ar as fllws:
• Rducd sympms and imprvmn in urin w
assciad wih prsaic nlargmn
• Rvrsal f mal parn hair lss
• Rducd nd fr surgry fr BPH
Nursing Implications for Finasteride
Premedication assessment. Obain a baslin PSA
bld lvl. Finasrid causs a dcras in srum
PSA lvls by abu 50% in pains wih BPH, vn in
h prsnc f prsa cancr. Any susaind incras
in PSA lvls whil rciving nasrid shuld b in-
vsigad, including cnsidrain f prsa cancr
and nncmplianc wih hrapy.
Availability. PO: Prscar: 5-mg abls; Prpcia: 1-mg
abls.
Dosage and administration. BPH: PO: 5 mg nc daily,
wih r wihu fd.
Androgenetic alopecia: PO: 1 mg nc daily, wih r
wihu fd.
Medication Safety Alert
Finasteride is contraindicated in women who are or may be-
come pregnant because it may cause abnormalities of the
external genitalia of a male fetus of a pregnant woman who
received the drug. Finasteride is absorbed through human
skin. A woman who is pregnant or who may become preg-
nant should not handle crushed or broken nasteride tablets.
Tablets are coated and will prevent contact with the active
ingredient during normal handling.
Common adverse effects
Reproductive
Impotence, decreased libido, decreased volume of ejacu-
late. Ths advrs ffcs appar in small numbrs
f mn rciving highr dss f nasrid. Tll h
pain ha hs advrs ffcs may ccur bu nd
 b slf-limiing. Th dcrasd vlum f jacula
ds n appar  inrfr wih nrmal sxual func-
in. Th pain shuld n sp aking h mdicain
and shuld cnsul his halhcar prvidr if h prb-
lm bcms unaccpabl.
 Drugs Used in Men’s and Women’s Health CHAPTER 40
Drug interactions. N clinically signican drug inr-
acins hav bn rprd  da.
ERECTILE DYSFUNCTION
Erectile dysfunction (ED) is h cnsisn inabiliy 
achiv r mainain an rcin sufcin fr saisfac-
ry sxual aciviy. Thr has bn a signican in-
cras in discussin abu ED, smims calld impo-
tency, bcaus f h availabiliy and high fcacy f
ral mdicin usd  ra crain yps f cass f ED.
Th prvalnc f ED incrass wih ag, alhugh i
is n an inviabl ucm f aging. Apprximaly
5% f mn xprinc h prblm a h ag f 40, and
15%  25% f mn agd 65 yars r ldr ar affcd.
ED usually is h rsul f a cmbinain f vas-
cular, nurlgic, and psychlgical facrs. Vascular
and nurgnic causs f ED incras wih ag. Risk
facrs includ cigar smking, hyprlipidmia, hy-
prnsin, diabs mllius, crnary arry disas,
and priphral vascular disas. Ohr causs f ED
ar psychlgical (.g., srss, dprssin, inrpr-
snal rlainships), damag  nurlgic pahways
(.g., rauma frm bicycl sas, prsacmy, rans-
urhral rscin f h prsa, diabs mllius,
alchl abus). A cmmn caus f ED is h us f
mdicins fr hr mdical cndiins (Bx 40.4). I
is fn difcul  drmin whhr ED is causd
by mdicins, h cndiin fr which h mdicin is
usd, r bh.
Th diagnsis f ED is basd n a mdical and sxual
hisry, physical xaminain, and labrary sudis.
An abrup ns and inrmin parn f difculy
achiving r mainaining an rcin may suggs a
psychlgical caus, whras a gradual ns in ED is
mr likly h rsul f a vascular r nurlgic caus.
Th caus f ED is usually mulifacrial. A variy f
ramns hav bn dvlpd fr ED, ach wih
advanags and disadvanags: psychhrapy, inra-
cavrnsal injcin wih prsaglandins, inraurhral
prsaglandin, vacuum cnsricin dvics, vascular
surgry, hrmnal hrapy, pnil prshss, and ral
phsphdisras inhibir hrapy.
DRUG THERAPY FOR ERECTILE DYSFUNCTION
DRUG CLASS: PHOSPHODIESTERASE
INHIBITORS
Actions
Phsphdisras inhibirs ar slciv inhibirs
f h phsphdisras 5 (PDE5) nzym. Rsarch
indicas ha niric xid, a naurally ccurring nur-
ransmir fund in nrv ndings and ndhlial
clls, acivas h nzym guanyla cyclas, which
cnvrs guansin riphspha  cyclic guansin
mnphspha (cGMP) in smh muscl clls. Th
incras in cGMP causs smh muscl rlaxain. In
h crpus cavrnsum f h pnis, smh muscl
665
Box 40.4 Drugs That May Cause Erectile Dysfunction
ANTIHYPERTENSIVE AGENTS
• Thiazide diuretics (most common)
• Beta-adrenergic blocking agents (especially propranolol
and nonselective agents; less so with beta-1 selective
agents)
• Alpha-adrenergic blocking agents (e.g., prazosin,
terazosin)
• Sympatholytic agents (e.g., clonidine, methyldopa,
reserpine)
• Spironolactone (antiandrogen effect)
CENTRAL NERVOUS SYSTEM DEPRESSANTS
• Phenothiazine antipsychotic agents (e.g., uphenazine,
thioridazine)
• Butyrophenones (e.g., haloperidol)
• Monoamine oxidase inhibitors
• Tricyclic antidepressants
• Selective serotonin reuptake inhibitors (e.g., sertraline,
paroxetine)
• Lithium
CARDIOVASCULAR AGENTS
• Digoxin (estrogen effect)
• Clobrate
• Gembrozil
MISCELLANEOUS AGENTS
• Substances of abuse (e.g., smoking, alcohol, cocaine,
marijuana)
• Chemotherapy agents (e.g., chlorambucil,
cyclophosphamide, methotrexate)
• Anabolic steroids
• Estrogens
• Corticosteroids
• Cimetidine (antiandrogen effect)
• 5-Alpha reductase inhibitors (nasteride, dutasteride)
• Interferon-α
Data from Koeneman KS, Mulhall JP, Goldstein I. Sexual health for the man at
midlife: in-ofce workup. Geriatrics. 1997;52:76-86; Brock GB, Lue TF. Drug-
induced male sexual dysfunction, an update. Drug Saf. 1993;8:414-426; and
McVary KT. Erectile dysfunction. N Engl J Med. 2007;357:2472-2481.
rlaxain allws bld inw  ll h many small
sinusidal spacs, rsuling in an rcin. In h cr-
pus cavrnsum, h nzym PDE5 inacivas cGMP.
Th phsphdisras inhibirs nhanc h rlax-
an ffc f niric xid rlasd in rspns  sxual
simulain by incrasing cGMP cncnrain in h
crpus cavrnsum, rsuling in smh muscl rlax-
ain and grar bld w in h crpus cavrn-
sum, which prducs an rcin.
Uses
Sildnal was apprvd in 1998 as h rs ral hra-
py  ra mal ED. Thr hr prducs, vardnal,
adalal, and avanal, hav sinc bn apprvd.
Sxual simulain is rquird fr an rcin bcaus
h phsphdisras inhibirs d n hav a di-
rc rlaxan ffc n h smh muscl f h cr-
pus cavrnsum. In h absnc f sxual simulain,
hs agns hav n pharmaclgic ffc. Thy ar
666 UNIT VIII Drugs Affecting the Reproductive System
Table 40.9 Phosphodiesterase Inhibitors Used for Erectile Dysfunction
GENERIC NAME BRAND NAME AVAILABILITY
avanal Stendra Tablets: 50, 100, 200 mg
sildenal Viagra Tablets: 25, 50, 100 mg
tadalala Cialis Tablets: 2.5, 5, 10, 20 mg
vardenal — Tablets: 2.5, 5, 10, 20 mg
aTadalal is also approved for treatment of benign prostatic hyperplasia (5 mg once daily).
n an aphrdisiac; hy d n incras sxual dsir
r sxual simulain r affc h frquncy f sxual
inrcurs. Sildnal and vardnal ar akn a any
pin frm 30 minus  4 hurs bfr sxual aciviy.
Avanal is apprvd  b akn 15 minus bfr sx-
ual aciviy. Tadalal als sars  wrk wihin 30 min-
us, bu may las fr up  36 hurs. Tadalal has als
bn apprvd as a nc-daily ds ha, whn akn
daily, may signicanly rduc h ns f acin, al-
lwing mr spnaniy in sxual rlains. Tadalal
is als apprvd fr h ramn f BPH.
Sxual simulain is rquird wih all fur agns
fr rcin. Th rcin lass fr an hur r s, al-
hugh i is highly variabl, basd n cninud sxual
simulain, aainmn f rgasm, and h individu-
al pain. Th phsphdisras inhibirs shuld
n b akn mr fn han nc vry 24 hurs.
Th phsphdisras inhibirs hav bn sd in
wmn  ra sxual dysfuncin, bu h rsuls 
da hav bn incnclusiv, s phsphdisras in-
hibirs ar n rcmmndd fr wmn.
Phsphdisras inhibirs ar als nding a nw
hrapuic us in a rar lung cndiin knwn as pul-
monary arterial hypertension. By mchanisms in lung
issu similar  hs in pnil issu as dscribd
arlir, phsphdisras inhibirs caus an incras
in cGMP in pulmnary issu, lading  rlaxain f
smh muscl and vasdilain f h pulmnary ar-
rial bd, rducing hyprnsin. Sildnal (Rvai)
and adalal (Adcirca) hav bn apprvd fr us in
pulmnary arrial hyprnsin.
Therapeutic Outcome
Th primary hrapuic ucm xpcd frm phs-
phdisras inhibir hrapy is imprvd rcil
funcin and vrall sxual saisfacin in mn wih
DOSAGE
Initial: 100 mg
Maintenance: 50–100 mg
Maximum: 200 mg/24 hr
Initial: 50 mg
Maintenance: 25–50 mg
Maximum: 100 mg/24 hr
Intermittent use: initial, 10 mg
Maintenance: 5–10 mg
Maximum: 20 mg/24 hr
Daily use: initial, 2.5 mg; maximum for daily use, 5 mg
Initial: 10 mg; older than 65 yr, 5 mg
Maintenance: 5–10 mg
Maximum: 20 mg/24 hr
ED. Tadalal may als b usd  rduc sympms
and imprv urinary w assciad wih prsaic
nlargmn.
Nursing Implications for Phosphodiesterase
Inhibitors
Premedication assessment. Obain baslin vial signs
and a hisry f rcn us f mdicins, including rc-
rainal drugs. Pains wih cardivascular disas
shuld sk hir halhcar prvidr’s apprval b-
fr saring phsphdisras inhibir hrapy.
Availability, dosage, and administration. S Tabl
40.9. Phsphdisras inhibirs d n prc
agains STIs, HIV, r prgnancy. Us f a cndm
and a sprmicid cnaining nnxynl-9 will hlp
prc agains sm STIs and unwand prgnancy.
Phsphdisras inhibirs d n affc sprm
cun r miliy and d n rduc friliy.
Common adverse effects
Vascular
Headache, ushing of the face and neck. Ths advrs
ffcs appar in small numbrs f mn rciving
highr dss f phsphdisras inhibirs. Tll h
pain ha hs advrs ffcs may ccur bu nd
 b slf-limiing. If hy cninu  b a prblm, a
rducd dsag may limina h advrs ffcs. Th
pain shuld cnsul his halhcar prvidr if h
prblm bcms unaccpabl.
Sensory
Color vision impairment. Mild, ransin rvrsibl im-
pairmn f blu r grn clr inrprain may c-
cur. This is hugh  b causd by inhibiin f h
phsphdisras 6 nzym, which plays a rl in
phransducin in h rina. If his cninus  b
 Drugs Used in Men’s and Women’s Health CHAPTER 40
prblm, a rducd dsag may limina h advrs
ffc. Tll h pain  cnsul a halhcar prvidr
if h prblm bcms unaccpabl.
Serious adverse effects
Cardiovascular
Hypotension, dizziness, angina. Pains wih har
disas, angina, diabs mllius, and hyprnsin
shuld sk hir halhcar prvidr’s apprval bfr
using phsphdisras inhibirs. Pains rciving
nirglycrin r issrbid shuld n ak phsphdi-
sras inhibirs bcaus f a pnially faal inrac-
in. If hypnsin, dizzinss, r angina dvlps, h
pain shuld li dwn, discninuing sxual aciviy.
Do not take nitroglycerin for angina. I may wrsn h
sympms. Sk mdical anin, as ndd.
Sensory
Loss of vision. A small numbr f cass f suddn
visin lss causd by nnarriic ischmic pic nu-
rpahy (NAION) hav bn rprd. This is a cndi-
in in which bld w  h pic nrv is blckd.
Ppl suffring suddn rducin in visin r visin
lss shuld sp aking hs mdicins and sk md-
ical anin quickly. Pains wh ar cnsidring
aking hs mdicins shuld infrm hir halhcar
prvidr if hy hav vr had svr lss f visin,
which migh rc a prir pisd f NAION. A his
im, i is n knwn whhr hs mdicins fr ED
ar h caus f h lss f visin r whhr h prb-
lm is rlad  hr mdical cndiins, such as high
bld prssur, diabs, r a cmbinain f hs
prblms.
Sudden decrease or loss of hearing. Suddn dcras
r lss f haring has bn rprd rarly; haring
changs may b accmpanid by innius and dizzi-
nss. Insruc pains  sk mdical assisanc fr
suddn dcras in haring r lss f haring
Reproductive
Sustained erection. Priapism is an rcin ha will
n g away. If an rcin lass mr han 4 hurs,
Clinical Judgment and Next-Generation NCLEX ® Examination-Style Questions
Key Points
• There is a great need for counseling about contraception
and about modes of transmission of STIs for all those
who are sexually active. One age group that often does
not receive adequate counseling on safe sex practices is
adolescents, many of whom are sexually active.
• Nurses must be leaders in encouraging people to report
STIs and seek healthcare as soon as an STI is suspected.
• Nurses must be leaders in promoting health and
wellness, encouraging men and women to complete
annual physical examinations that could detect the early
onset of disease.
667
mdical anin shuld b sugh quickly. Priapism
mus b rad as sn as pssibl r lasing damag
can happn  h pnis, including h inabiliy  hav
rcins.
Drug interactions
Nitroglycerin patches, nitroglycerin ointment, amyl ni-
trate. Niras incras h prducin f niric xid,
pnially causing hypnsin and arrhyhmias. I is
hugh ha niras inhald fr rcrainal us dur-
ing sxual aciviy (“ppprs” such as buyl nira,
amyl nira, r amyl niri) will hav h sam ffc
whn cmbind wih phsphdisras inhibirs.
Niras frm fd surcs d n rac wih phsph-
disras inhibirs.
Cimetidine, erythromycin, ketoconazole, itraconazole, ritona-
vir, indinavir, saquinavir. Ths agns inhibi h mab-
lism f phsphdisras inhibirs, pnially caus-
ing an incrasd incidnc f advrs ffcs such as
ushing, hypnsin, and dizzinss. A lwr dsag
f h phsphdisras inhibir may b ncssary.
Alcohol. Alchl and phsphdisras inhibirs
ar bh mild vasdilars. Excssiv cnsumpin f
alchl in cmbinain wih phsphdisras inhibi-
rs may caus dcrasd bld prssur, dizzinss,
and rhsaic hypnsin. Us cauin whn cm-
bining phsphdisras inhibirs and alchl.
Alpha-adrenergic blocking agents. Us f phsphdis-
ras inhibirs in cnjuncin wih alpha-adrnrgic
blcking agns (.g., amsulsin, alfuzsin, razsin,
dxazsin, prazsin) may rsul in signican hyp-
nsin. Mnir bld prssur; rpr pisds f
dizzinss. Dsag rducin f h phsphdisras-
5 inhibir r a chang  anhr phsphdisr-
as inhibir may b ncssary  prvn xcssiv
hypnsin.
Rifampin. This drug may nhanc h mablism
f sildnal and adalal, rducing hir durain f
acin. An incras in dsag r arlir sxual aciviy
may rslv h prblm.
• It is important for the consumer to be aware that hormonal
contraceptives have reduced effectiveness when taken in
combination with many other medications or when doses are
missed, thus requiring an alternative form of contraception.
• Osteoporosis affects both men and women and is
considered a part of aging. Bone loss can be managed
with proper exercise, diet, and pharmacologic agents.
• The bisphosphonates (alendronate, risedronate, and
zoledronic acid) are the gold standard for treating
osteoporosis. Atypical femur fracture is a rare complication
of chronic bisphosphonate therapy. Patients should be
told to report any dull or aching pain in the groin or thigh.to
their healthcare provider.
668 UNIT VIII Drugs Affecting the Reproductive System
• Benign prostatic hyperplasia and erectile dysfunction
are the two most common male reproductive
system conditions that are treated successfully with
pharmacotherapy.
• When treating benign prostatic hyperplasia, the alpha-
adrenergic blocking agents provide symptom improvement
after 1 week, whereas 5-alpha-reductase inhibitors require
6 to 12 months before symptoms improve.
• When treating erectile dysfunction, the
phosphodiesterase-5 inhibitors in conjunction with alpha-
adrenergic blocking agents (e.g., tamsulosin, alfuzosin,
terazosin, doxazosin) may result in signicant hypotension.
Monitor for dizziness and hypotension. Reduction in the
dose of the phosphodiesterase inhibitor or a change to
another phosphodiesterase inhibitor product may be
necessary to reduce hypotension.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX exam and include both NGN (Next Generation) and
traditional questions. See Chapter 1 for further information re
garding question types.
Scenario
A woman came into the clinic seeking information regarding
oral contraception.
1. It is important for the nurse to get a thorough history on the
woman in the scenario who wishes to start oral contraceptives,
because the increased estrogen exposure may increase the risk
for developing which complication? (Select all that apply.)
1. Weight gain
2. Breakthrough bleeding
3. Nausea
4. Blood clots
5. Hypothyroidism
6. Yeast infections
7. Depression
8. Hypertension
Objective: Describe the major adverse effects and
contraindications to the use of oral contraceptive agents.
NCLEX item type: Extended multiple response
Cognitive skill: Recognize cues
2. The nurse reviewed the patient instructions regarding the
administration of transdermal versus intravaginal contraceptive
before instructing the patient and recognized it was necessary to
include in the teaching which of the following?
1. Transdermal contraception is more effective than
intravaginal.
2. Intravaginal contraception is more effective than
transdermal.
3. Transdermal patches are changed every week and
intravaginal rings are changed every 3 weeks.
4. Transdermal patches are changed every 3 weeks and
intravaginal rings are changed every week.
Objective: Identify the patient teaching necessary with the
administration of the transdermal contraceptive and the intravaginal
hormonal contraceptive.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
3. The nurse giving instructions to the patient in the scenario about
the use of the minipill realizes that further education is needed
after the patient made which statement?
1. “I will need to use condoms for the rst month while on
the pill to provide birth control.”
2. “I know that if I get a bad headache, dizziness, or blurred
vision, I will need to contact this clinic as soon as possible.”
3. “I know I should switch to some other form of birth
control for 3 months before I try to get pregnant.”
4. “I think I can remember to take the pill every day, but if I
do forget, I can simply skip it and wait until the next day
to take the pill again.”
Objective: Describe the major adverse effects and
contraindications to the use of oral contraceptive agents.
NCLEX item type: Multiple choice
Cognitive skill: Comprehension
4. The nurse is reviewing the drugs approved for use to reduce the
symptoms of benign prostatic hyperplasia. Match the drug with
the expected outcome. (Select all that apply.)
DRUG USED FOR BPH THERAPEUTIC OUTCOME
alfuzosin (Uroxatral) Reduce need for surgery for BPH
tamsulosin (Flomax) Reversal of male pattern hair loss
dutasteride (Avodart) Improvement in urine ow
associated with BPH
nasteride (Proscar)
Objective: Describe pharmacologic treatments of benign prostatic
hyperplasia.
NCLEX item type: Extended drag and drop
Cognitive skill: Recognize cues
 Drugs Used in Men’s and Women’s Health CHAPTER 40 669

5. Choose the most likely options for the information missing from 6. The patient taking alendronate (Fosamax) for osteoporosis asks
the sentence below by selecting from the lists of options provided. the nurse how it works. What is the most appropriate response by
the nurse? (Select all that apply.)
The nurse is completing a patient history on a man who pres-
ents with erectile dysfunction. The treatment may include 1. “This medication acts on the osteoclasts (responsible
_________1___________ and __________1_________, for bone resorption) by inhibiting their action, thus
which will have the effect of _________2_____________ decreasing the rate at which bone is broken down and
and ___________2_____________. reabsorbed into the bloodstream.”
2. “This medication increases the rate at which bone
remodeling takes place, which causes new bone to be
OPTION 1 OPTION 2 laid down.”
sildenal (Viagra) Improved urinary ow 3. “This medication increases the rate at which bone is
broken down and reabsorbed into the bloodstream.”
alfuzosin (Uroxatral) Improved hair loss
4. “This medication works with the calcium in your body to
dutasteride (Avodart) Improved erectile function build new bone.”
avanal (Stendra) Improved overall sexual satisfaction 5. “With this medication we encourage you to take oral
calcium and vitamin D.”
Objective: Discuss osteoporosis and its risk factors, as well as
Objective: Describe the pharmacologic treatment of erectile
preventative measures and the pharmacologic treatment used.
dysfunction.
NCLEX item type: Multiple response
NCLEX item type: Cloze
Cognitive skill: Application
Cognitive skill: Evaluate cues
Unit IX Drugs Affecting Other Body Systems

41 Drugs Used to Treat Disorders of the Urinary

System
https://evolve.elsevier.com/Willihnganz

Objectives
1. Discuss the adverse effects of the drugs used to treat 3. Identify the symptoms, treatment, and medications used
disorders of the urinary tract. for urinary tract disorders.
2. Identify important nursing interventions associated with the
drug therapy and treatment of diseases of the urinary system.

Key Terms
pyelonephritis (pī-ă-lō-nĕ-FRĪ-tĭs) (p. 670)
cystitis (sĭs-TĪ-tĭs) (p. 670)
prostatitis (prŏs-tă-TĪ-tĭs) (p. 670)
urethritis (yū-rĕ-THRĪ-tĭs) (p. 670)
overactive bladder (OAB)
syndrome (ō-vĕr-ĂK-tĭv BLĂ-dĕr SĬN-
drōm) (p. 675)
frequency (FRĒ-kwĕn-sē) (p. 675)
urgency (ĔR-jĕn-sē) (p. 675)
incontinence (ĭn-KŌN-tĭ-nĕns)
(p. 675)
urge incontinence (ĔRJ ĭn-KŌN-tĭ-nĕns)
(p. 675)
stress incontinence (p. 675)
overow incontinence (p. 676)
nocturia (nŏk-TŪ-rē-ă) (p. 676)
urinary antispasmodic agents
(YĔR-ĭn-ăr-ē ăn-tī-spăz-MŎD-ĭk
Ā-jĕnts) (p. 676)

considered to be colicated UTIs. The athogens tend

URINARY TRACT INFECTIONS
Urinary tract infections (UTIs) are aong the ost
coon infectious diseases in huans, accounting for
ore than 11 illion healthcare roviders’ ofce visits
yearly. UTIs are second only to uer resiratory tract
infections as a cause of orbidity fro infection. UTIs
encoass several different tyes of infection of local
tissue: pyelonephritis (the kidneys), cystitis (the blad-
der), prostatitis (the rostate gland), and urethritis (the
urethra) (Fig. 41.1).
The incidence of UTIs in woen is aroxiately
10 ties higher than in en. The urethra is shorter in
feales than it is in ales, so bacteria have a shorter
distance to travel to the bladder. Proxiity of the ure-
thral eatus to the vagina and rectu can also ake it
easier for bacteria to cause an infection. The incidence
increases in woen with age, so that by age 60 u to
20% of woen will have suffered fro at least one UTI
in their lives.
Gra-negative aerobic bacilli fro the gastro-
intestinal tract cause ost UTIs. Escherichia coli accounts
for about 80% of non–institutionally acquired unco-
licated UTIs. Other coon infecting organiss
are Staphylococcus saprophyticus, Klebsiella pneumoniae,
Enterobacter secies, Proteus mirabilis, and Pseudomonas
aeruginosa. Healthcare-associated UTIs and those asso-
ciated with urinary tract athologic abnoralities are
670
to be the sae tyes of bacteria, but they are frequently
ore resistant to the antibiotics coonly used. This
requires the use of ore otent antibiotics for longer
courses of theray, lacing the atient at a greater risk
for colications secondary to drug theray.
The use of an indwelling urinary catheter should
be avoided if ossible. When used, adherence to strict
asetic technique and attachent to a closed drainage
syste are necessary to reduce the rate of infection.
NURSING IMPLICATIONS FOR URINARY SYSTEM
DISEASE
The inforation the nurse gains through assessent of
the atient’s clinical signs and sytos is iortant
to the healthcare rovider when analyzing data for di-
agnosis and for evaluation of the atient’s resonse to
rescribed treatent.
Assessment
History of urinary tract symptoms
• Does the individual have a history of a congenital
disorder of the urinary tract, sexually transitted
infections, recent delivery of a baby, rostatic dis-
ease, recent catheterization, urologic instruenta-
tion or surgical rocedure, renal calculi, gout, UTI,
or bladder dysfunction of neurologic origin? Obtain
details alicable to the atient’s resonses.
 Drugs Used to Treat Disorders of the Urinary System CHAPTER 41
Bladder
Prostate
gland
Fig. 41.1 The urinary system. (Modied from Gould B. Pathophysiology
for the Health Professions. 3rd ed. Philadelphia: Saunders; 2006.)
• Is there a roble with defecation? When was the
last bowel oveent?
History of current symptoms
• Has the individual had any chills, fever, general
alaise, or a change in ental status? New con-
fusion in an older atient ay be the only sign of
a UTI. Ask questions relating to ersonal hygiene
ractices and sexual intercourse to evaluate for the
ossibility of bacterial containation as an underly-
ing cause of cystitis. Has the erson been catheter-
ized or on rolonged bed rest for any reason?
• Pattern of urination: Ask the individual to describe
the sytos that affect their ability to void. What
is the current urination attern, and have there been
recent changes? Such details as frequency, dysuria
(ainful urination), changes in the urine strea,
hesitancy in starting to void, heaturia (blood in
the urine), nocturia (awaken at night with the desire
to urinate and, if so, how any ties does this oc-
cur during an average night?), and urgency are all
of signicance. Ask about the ability to sit through a
2-hour eeting or ride in a car for 2 hours without
urinating. State the onset, course of rogression of
the sytos, and any self-treatent that has been
atteted and resonse achieved. Is it difcult to
ostone urination when the urge to urinate is felt?
Is there incontinence (leaking) of urine? If so, when
does this haen and what causes it? Does the in-
continence occur when coughing, walking, running,
lifting a heavy object, or if one is unable to reach a
toilet iediately?
• Pattern of pain: Record the details of any ain the a-
tient describes—frequency, intensity, duration, and
location. Use a ain rating scale (0 to 10: 0 for no
671
ain; 10 for severe ain). Pain associated with renal
athologic conditions usually occurs at the groin,
back, ank, and suraubic area, and uon urina-
tion (dysuria). Does the ain radiate? If so, obtain
details.
• Intake and output: Ask secically about the indi-
Kidney vidual’s usual daily uid intake. How frequently
does the atient usually void? What is the aount
of each voiding?
Ureter
Life Span Considerations
Urinary Tract Infections
In children and men, UTIs may have a serious underlying
cause and must be thoroughly investigated to identify the
cause.
Urethra
Medication history. Ask for a list of all rescribed over-
the-counter edicines and herbal suleents being
taken. Many haracologic agents (e.g., anticholinergic
agents, antihistaines, antihyertensives, decongest-
ants, oioid analgesics, and tricyclic antideressants)
can induce urinary retention, an altered urinary elii-
nation attern, or urologic sytos. Has the erson
recently been on edications to revent or treat
a UTI?
Nutritional history
• Has the individual been fasting for any rolonged
eriod?
• How uch alcoholic beverage has been consued?
• Are vitains, inerals, or other dietary sule-
ents taken regularly?
• What kinds of uids are taken daily: water, coffee,
soft drinks, energy drinks?
• How any dairy roducts, chocolate foods, sicy
foods, or eat roducts are consued daily?
Laboratory and diagnostic studies. Review diagnostic
and laboratory reorts, such as urinalysis, renal func-
tion tests, voiding evaluation rocedures (e.g., urody-
naic studies), cystoscoy, and colete blood count
with differential, urine culture, and sensitivity results.
Urinalysis is a hysical, cheical, and icrosco-
ic exaination of the urine and is the ost routine
test that the nurse encounters. The color, aearance
(e.g., clear, foay, cloudy), and odor of the urine are
noted, and the H, rotein, glucose, and ketones are
deterined with reagent disticks. Secic gravity
is easured with a refractoeter, and a icroscoic
exaination of the urinary sedient is erfored
to detect the resence of red and white blood cells,
bacteria, casts, and crystals. An understanding of the
signicant data that this basic test can reveal is iera-
tive to onitoring the atient. Refer to Table 41.1 for a
descrition of the data. See a general edical-surgical
text for details of collecting urine sales correctly.
672 UNIT IX Drugs Affecting Other Body Systems

Table 41.1 Urinalysis

PROPERTY NORMAL DATA ABNORMAL DATA
Color, Straw, clear Dark smoky color, reddish, or brown may indicate blood; white or cloudy may indicate UTI
appearance yellow, or or chyluria; dark yellow to amber may indicate dehydration; green, deep yellow, or brown
amber may indicate liver or biliary disease
Some drugs or foods also alter urine color: red or red-brown (beets, rhubarb), reddish
orange (phenazopyridine [Pyridium]), dark yellow or brown (nitrofurantoin), blue
(methylene blue), bright yellow (vitamin B complex), reddish orange (rifampin)
Odor Ammonia-like Foul smell may indicate infection; dehydrated patient’s urine is concentrated, with ammonia
on standing smell resulting from urea breakdown by bacteria; sweet or fruity odor associated with
starvation or diabetic acidosis (ketoacidosis)
Protein 0 to trace Foamy or frothy-appearing urine may indicate protein in urine; proteinuria associated with
kidney disease, toxemia of pregnancy; also found in leukemia, lupus erythematosus,
cardiac disease
Glucose 0 to trace Presence usually associated with diabetes mellitus or low renal threshold with glucose
“spillage”; also seen at times of severe stress (e.g., major infection) or after high
carbohydrate intake
Ketones 0 Associated with dehydration, starvation, ketoacidosis, diet high in protein and low in
carbohydrates
pH 4.5–8.0 pH <4.5 indicates metabolic acidosis, respiratory acidosis, diet high in meat protein and/or
cranberries
Medications can be prescribed to produce alkaline or acidic urine pH >8.0 associated with
bacteriuria (UTI from Klebsiella or Proteus spp.), diet high in fruits and/or vegetables
Red blood cell 0–3/HPF Indicative of bleeding at some location in the urinary tract; infection, obstruction, calculi,
count renal failure, tumors, anticoagulants, excess aspirin, menstrual contamination
White blood 0–5/HPF Increase indicates infection somewhere in urinary tract; may also be associated with lupus
cell count nephritis, strenuous exercise
Casts 0 May indicate dehydration, possible infection within renal tubules, other types of renal
disease
Bacteria 0 May indicate UTI or contaminated specimen collection
Specic gravity 1.003–1.029 Used as indicator of hydration (in absence of renal pathologic condition); sp gr >1.018
(sp gr) is early sign of dehydration; sp gr <1.010 is “dilute urine” and may indicate uid
accumulation; xed sp gr ≅1.010 may indicate renal disease; sp gr <1.005 may indicate
diabetes insipidus, excess uid intake, overhydration; sp gr >1.026 may indicate
decreased uid intake, vomiting, diarrhea, diabetes mellitus
HPF, High-power eld; UTI, urinary tract infection.

Implementation • Monitor the ain level and rovide aroriate

• Individualize the care lan to address the tye of
urinary tract disorder (e.g., retention, incontinence,
or cystitis).
• Adinister edications rescribed and listed on
the edication adinistration record or in the elec-
tronic edical record.
• Monitor laboratory studies (e.g., urinalysis, co-
lete blood count with differential, and creatinine
clearance).
• Note dietary orders; indicate the aount of uid to
be taken every shift to aintain an adequate intake.
• Note daily weights as aroriate to diagnosis;
indicate whether bladder training, Kegel exer-
cises, or other easures should be taught and
encouraged.
• Indicate the level of activity or exercise eritted.
• Perfor focused assessent of sytos (e.g., re-
tention, urinary frequency, and ain).
suortive and haracologic interventions.
• Adinister rescribed edications; onitor re-
sonse and adverse effects.
• Maintain adequate uid intake and an accurate in-
take and outut record. Instruct the atient to avoid
foods known to be bladder irritants, such as sicy
foods, citrus juices, alcohol, and caffeine.
• For inability to void, institute techniques to stiu-
late voiding (e.g., roer ositioning to void, run-
ning water in sink, and ouring war water over
erineu).
• For incontinence, establish a regular toileting sched-
ule and initiate bladder training easures as a-
roriate and as ordered. Start easures to revent
erineal irritation. Aly external urinary diversion
devices as ordered, such as an external condo
catheter. Use incontinence ads as needed. Kee the
urinal or bedan readily available.
 Drugs Used to Treat Disorders of the Urinary System CHAPTER 41
• Facilitate odications of the environent that ro-
ote regular, easy access to toilet facilities, and ro-
ote the atient’s safety with features such as better
lighting, abulatory assistance equient, clothing
alterations, tied voiding, and toileting equient,
such as an elevated toilet seat or coode.
• Ileent easures to aintain the individual’s
dignity and rivacy and to revent ebarrassent
when incontinence is resent.
• Maintain the activity and exercise level rescribed.
Patient Education
For incontinence
• Teach ersonal hygiene easures to kee the skin
clean and dry and revent erineal breakdown.
Exlore aliances and incontinence roducts
available for ersonal use.
• Teach Kegel exercises and bladder training, and stress
the iortance of resonding to the urge to void.
For urinary tract infections
• Teach woen the following easures to avoid fu-
ture UTIs: avoid nylon underwear (use cotton)
and tight, constrictive clothing in the erineal area;
avoid frequent use of bubble baths; wash the eri-
neal area iediately before and after sexual inter-
course; and urinate iediately after intercourse.
• Teach woen the roer ethod of wiing after
defecation or urination (front to back) to revent
bacterial containation. Exlain the correct roce-
dure for obtaining a clean-catch urine sale and
the iortance of having follow-u urine cultures
collected as requested by the healthcare rovider.
• Teach cofort easures, such as the use of a sitz bath.
• Stress the iortance of adequate uid intake and
its effect of diluting the urine, decreasing bladder
irritability, and heling reove organiss resent
in the bladder. Dene “adequate intake of uid” to
the individual in ters of the nuber and size of
glasses of liquid to be consued during the day.
• Exlain the signs of iroveent or worsening of
the urinary condition aroriate to the individu-
al’s diagnosis. Ehasize sytos that should be
reorted to the healthcare rovider.
For urinary retention. Teach self-exaination to assess
for bladder distention, Credé aneuver (anual co-
ression of the bladder through ressure on the lower
abdoen) to aid in etying the bladder, and, as a-
roriate, self-catheterization.
Medications
• For urinary retention, exlain adverse effects to an-
ticiate with the rescribed edications.
• For the urinary analgesic henazoyridine hydro-
chloride, exlain that the urine will be reddish or-
ange. If discoloration of the skin or sclera occurs, the
atient should contact the healthcare rovider.
673
• For UTIs, instruct atients to take the edicines ex-
actly as rescribed for the entire course of edica-
tion. Discontinuing the antiicrobial agent when
the sytos irove ay result in another infec-
tion after aroxiately 2 weeks that will be resis-
tant to antiicrobial treatent.
• See individual drug onograhs regarding treat-
ent of acute attacks and how long before re-
sonse can be anticiated. Stress the need for
follow-u laboratory results to evaluate resonse
to theray.
Fostering health maintenance
• Discuss edication inforation and how it will
benet the course of treatent to roduce an oti-
al resonse. Stress aintenance of adequate urine
volue as a art of the overall treatent of urinary
tract disorders.
• Seek cooeration and understanding of the fol-
lowing oints so that edication adherence is in-
creased: nae of edication; dosage, route, and
ties of adinistration; and coon and serious
adverse effects. See individual drug onograhs
for additional teaching.
Patient self-assessment. Enlist the atient’s hel
in develoing and aintaining a written record of
onitoring araeters for urinary antiicrobial
agents. See the Patient Self-Assessent For for
Urinary Antibiotics on the Evolve website. Colete
the Preedication Data colun for use as a baseline
to track resonse to theray. Ensure that the atient
understands how to use the for, and instruct the
atient to take the coleted for to follow-u vis-
its. During follow-u visits, focus on issues that will
foster adherence with the theraeutic interventions
rescribed.
DRUG THERAPY FOR URINARY TRACT
INFECTIONS
DRUG CLASS: URINARY ANTIMICROBIAL AGENTS
Actions
Urinary antiicrobial agents are substances that are
secreted and concentrated in the urine in sufcient
aounts to have an antisetic effect on the urine and
urinary tract.
Uses
Selection of the roduct to be used is based on identi-
cation of the athogens by Gra staining or by urine
culture in severe, recurrent, or chronic infections.
Fosfoycin and nitrofurantoin are used only for
UTIs. Exales of other antibiotics that are also used
to treat urinary infections are cotrioxazole, ciro-
oxacin, levooxacin, ceftriaxone, cehalexin, and
gentaicin. These agents are effective in a variety of
674 UNIT IX Drugs Affecting Other Body Systems
tissue infections against any different icro-
organiss. Because of their use in ultile organ sys-
tes, they are discussed in detail (with nursing ro-
cesses) in Chater 45
Fluid intake should be encouraged so that there will
be at least 2000 L of urinary outut daily. Duration of
treatent deends on whether the infection is unco-
licated or colicated; whether the infection is acute,
chronic, or recurrent; the athogen being treated; the
antiicrobial agent being used for treatent; and
whether a follow-u culture can be collected to assess
the success of the theray.
DRUG CLASS: FOSFOMYCIN ANTIBIOTIC
fosfomycin (fŏs-fō-MĪ-sĭn)
Monurol (MŎN-ĕr-ŏl)
Actions
Fosfoycin is a hoshonic acid derivative.
Fosfoycin acts by inhibiting bacterial cell wall syn-
thesis and by reducing adherence of bacteria to eithe-
lial cells of the urinary tract.
Uses
Fosfoycin is the rst antibiotic agent to be aroved
as a single-dose treatent for UTIs. It is used to treat
uncolicated acute cystitis in woen caused by sus-
cetible strains of E. coli and Enterococcus faecalis. It is
not indicated for the treatent of kidney infections
such as yelonehritis.
Therapeutic Outcome
The riary theraeutic outcoe associated with fos-
foycin theray is resolution of the UTI.
Nursing Implications for Fosfomycin
Premedication assessment
1. Record voiding characteristics (e.g., frequency,
aount, color, odor, and associated sytos such
as burning and ain) to serve as a baseline for oni-
toring theray.
2. Assess for and record any existing gastrointestinal
colaints before initiating theray.
3. Record baseline vital signs.
Availability. PO: Single-dose 3-g ackets of fosfoycin
granules.
Dosage and administration. Adult: PO: Pour the entire
contents of a single-dose acket of fosfoycin into 90
to 120 L (3 to 4 ounces) of water and stir to dissolve.
Do not use hot water. Take iediately after dissolv-
ing in water. Fosfoycin ay be taken with or without
food. Do not take additional ackets of edicine with-
out aroval fro the healthcare rovider. Additional
adverse effects develo with ultile doses, but there
is little theraeutic gain. Do not take in its dry for;
always ix fosfoycin with water before ingesting.
Common adverse effects
Gastrointestinal
Nausea, diarrhea, abdominal cramps, atulence. These
adverse effects are usually ild and tend to resolve
without need for theray because only one dose of fos-
foycin is adinistered.
Serious adverse effects
Genitourinary
Perineal burning, dysuria. Burning with urination ay
be roduced by the infection itself. Sytos should
irove in 2 to 3 days after taking fosfoycin; if not
iroved, the atient should contact their healthcare
rovider.
Drug interactions
Metoclopramide. Metocloraide has been reorted
to lower the seru concentration and urinary excre-
tion of fosfoycin by enhancing gastric otility.
DRUG CLASS: OTHER URINARY ANTIBACTERIAL
AGENT
nitrofurantoin (nī-trō-fŭ-RĂN-tō-ĭn)
Macrodantin (măk-rō-DĂN-tĭn)
Macrobid (MĂK-rō-bĭd)
Actions
Nitrofurantoin is an antibiotic that acts by interfering
with several bacterial enzye systes.
Uses
This antibiotic is not effective against icroorganiss
in the blood or in tissues outside the urinary tract.
It is active against any gra-ositive and gra-
negative organiss, such as E. faecalis, E. coli, and Proteus
secies. It is not active against P. aeruginosa or Serratia
secies.
Therapeutic Outcome
The riary theraeutic outcoe associated with ni-
trofurantoin theray is resolution of the UTI.
Nursing Implications for Nitrofurantoin
Premedication assessment
1. Record voiding characteristics (e.g., frequency,
aount, color, odor, and associated sytos such
as burning and ain) to serve as a baseline for oni-
toring theray.
2. Assess for and record any gastrointestinal co-
laints resent before initiating drug theray.
3. When using nitrofurantoin, check for history of
glucose-6-hoshate dehydrogenase deciency; if
 Drugs Used to Treat Disorders of the Urinary System CHAPTER 41
resent, withhold the drug and contact the health-
care rovider.
4. To serve as a baseline, assess the atient for the res-
ence of eriheral neuroathies before initiating
theray.
5. Record baseline vital signs.
Availability. PO: 25-, 50-, and 100-g casules;
25-g/5-L susension.
Dosage and administration. Adult: PO: Macrodantin
50 to 100 g four ties daily or Macrobid 100 g two
ties a day for 7 days or at least 3 days after obtaining
sterile urine. Adinister with food or ilk to reduce
gastrointestinal adverse effects. To aintain adequate
urine concentrations, sace the doses at even intervals
around the clock. According to the Infectious Diseases
Society of Aerica, nitrofurantoin onohydrate/ac-
rocrystals can be dosed 100 g twice daily for 5 days
in woen.
Pediatric: Do not adinister to infants younger
than 1 onth. PO: 5 to 7 g/kg/24 hr in four divided
doses. Suspension: Store in a dark aber container
away fro bright light.
Medication Safety Alert
Nitrofurantoin must be in the bladder in a sufcient concen-
tration to be therapeutically effective. Nitrofurantoin therapy
is not recommended for use in patients who have a creati-
nine clearance lower than 60 mL/min; however, according to
the 2015 Beers Criteria, nitrofurantoin can be used in indi-
viduals with a creatinine clearance of 30 mL/min or greater,
but prolonged use should be avoided.
Common adverse effects
Gastrointestinal
Nausea, vomiting, anorexia. Adinister with food or
ilk to reduce gastric irritation.
Urinary
Urine discoloration. Tell the atient that urine ay be
tinted rust brown to yellow and that this discoloration
should not be a cause for alar.
Serious adverse effects
Hypersensitivity, immune system
Dyspnea, chills, fever, erythematous rash, pruritus. These
sytos are the early indications of an allergic re-
action to nitrofurantoin. Acute reactions usually occur
within 8 hours in reviously sensitized individuals
and within 7 to 10 days in atients who develo sen-
sitivity during the course of theray. Discontinue the
drug and notify the healthcare rovider.
Neurologic
Peripheral neuropathies. Nitrofurantoin ay cause e-
riheral neuroathies, articularly in atients with renal
iairent, aneia, diabetes, electrolyte ibalance, or
675
vitain B deciency. Nitrofurantoin should be dis-
continued at the rst sign of nubness or tingling in the
extreities.
Inammation, immune system
Second infection. Infor the healthcare rovider i-
ediately if dysuria, ungent-selling urine, or fever
develos. These sytos ay be the early indica-
tion of a second infection by an organis resistant to
nitrofurantoin.
Pulmonary. Nitrofurantoin used for ore than 6
onths ay cause interstitial neuonitis or brosis.
Monitor for alaise, dysnea, cough, or fever.
Drug interactions
Probenecid. Probenecid ay inhibit the excretion of
nitrofurantoin fro the renal tubules. Monitor atients
for the develoent of adverse effects of nitrofuran-
toin and for signs of incoletely treated UTI.
Eplerenone, spironolactone. Nitrofurantoin ay en-
hance the hyerkaleic effects of these two agents.
Monitor seru otassiu levels and for the develo-
ent of dysrhythias.
Antacids. Discourage the atient fro taking rod-
ucts containing agnesiu trisilicate (e.g., Gaviscon-2)
concurrently with nitrofurantoin because the antacid
ay inhibit absortion of the nitrofurantoin.
DRUG THERAPY FOR OVERACTIVE
BLADDER SYNDROME
Overactive bladder (OAB) syndrome is a coon
roble affecting any adults, esecially those
older than 65 years. It is dened by the International
Continence Society as “urgency, with or without urge
incontinence, usually with frequency and nocturia”
(Urology, 2001). These sytos are thought to be a
result of the detrusor uscle (of the bladder) beco-
ing overactive but can also be to the result of other
urinary robles. The diagnosis of OAB can be ade
if there is no roven infection or other obvious atho-
logic condition. OAB without urge incontinence is
ore coon in en than in woen; however, it is
not uncoon for atients with OAB also to have
stress incontinence.
The three riary sytos of OAB syndroe
are frequency, urgency, and urinary incontinence.
Frequency is the need to void eight or ore ties
daily. Urgency, the ost coon syto associat-
ed with OAB, is a sudden, coelling desire to ass
urine that is very difcult to ignore. Incontinence is
the inability to control urine fro assing fro the
bladder. Incontinence can be subdivided into urge
incontinence, stress incontinence, and overow in-
continence. Urge incontinence is the involuntary leak-
age of urine accoanied or iediately receded
by urgency. Stress incontinence is the brief burst of
incontinence brought on by exercise, running, lifting,
676 UNIT IX Drugs Affecting Other Body Systems
sneezing, or coughing. Predisosing factors are age,
regnancy, childbirth, cognitive iairent, and
obesity. Overow incontinence, also known as chronic
urinary retention, is urinary leakage resulting fro
an overlled and distended bladder that is unable to
ety, causing urine to leak fro the distended blad-
der. This ay be caused by the inability to feel the
urge to urinate, and therefore the bladder is never
etied. This occurs in en with benign rostatic
hyerlasia (BPH). Nocturia is the need to void at
night. Nocturia usually accoanies urgency, with or
without urge incontinence, and is the colaint that
the individual has to wake at night one or ore ties
to void.
In ales, an overlaing and often confusing rob-
le is BPH (see Chater 40). Patients with BPH are
also suscetible to frequent urination but, unlike OAB,
BPH can cause hesitancy and decreased ow during
urination. Many en have sytos of OAB and
BPH and can be treated for both at the sae tie.
OAB syndroe cannot be cured, but a variety of
nonharacologic and haracologic treatents can
be used to reduce the sytos associated with the
disease. The goals of theray are to decrease frequency
by increasing voided volue, to decrease urgency, and
to reduce incidents of urinary urge incontinence. A di-
ary to record the attern and tye of urinary leakage
and frequency and the volue of uid consution
(“ins and outs”) can be very helful in develoing an
awareness of contributors and iroveent or dete-
rioration of sytos over tie. Lifestyle changes—
such as sacing uid consution throughout the
day instead of a large intake at one tie; avoiding
diuretic-like stiulants, such as alcohol, caffeine, and
sicy foods; and avoiding uid intake after 6 pm—can
hel with sytos.
Sources of caffeine that are resent in drugs such
as Excedrin, Midol, Vanquish, and Anacin should be
noted. Kegel exercises are recoended to strength-
en external shincter function and increase resistance
when there is sudden urinary urgency. Bladder train-
ing—the atient is initially taught to void every hour
on the hour, then asked to increase the duration be-
tween voids by 15 inutes each week—can hel in-
crease volue and control urgency. A cobination of
bladder training and Kegel exercises hels the atient
regain bladder control, increasing voided volues and
the tie interval between voids. Absorbent under-
garent roducts are helful in allowing social obil-
ity and aintaining dry skin. They also hel roote
self-condence and dignity.
The rst lines of haracologic treatent of OAB
are anticholinergic agents and irabegron (Myrbetriq),
a beta-3 adrenergic agonist. Anticholinergic agents
with ore selective action on the bladder are darifena-
cin, fesoterodine, oxybutynin, solifenacin, tolterodine,
and trosiu.
DRUG CLASS: ANTICHOLINERGIC AGENTS FOR
OVERACTIVE BLADDER SYNDROME
Actions
Anticholinergic agents, also known as urinary anti-
spasmodic agents, block the cholinergic (uscarinic)
recetors of the detrusor uscle of the bladder, caus-
ing relaxation. They decrease involuntary contractions
of the detrusor uscle and irove bladder volue
caacity.
Uses
The anticholinergic agents are used to reduce the ur-
gency and frequency of bladder contractions and
delay the initial desire to void in atients with OAB.
Cholinergic recetors are found throughout the body,
articularly in the salivary glands, eyes, colon, and
brain. Thus inhibition of these recetors can lead to
adverse effects, including dry outh, blurred vision,
constiation, confusion, and sedation. Each of these
agents has soe degree of selectivity for the choliner-
gic recetors in the bladder, but the agents are variable
in whether they also block recetors in other arts of
the body, leading to ore adverse effects. They should
not be used for atients with narrow-angle glaucoa,
yasthenia gravis, gastric retention, or bowel disease
such as ulcerative colitis, or atients with urinary
retention caused by an obstructive uroathy such as
rostatitis.
Therapeutic Outcome
The riary theraeutic outcoe exected fro uri-
nary anticholinergic agents is control of incontinence
associated with OAB.
Nursing Implications for Urinary Anticholinergic
Agents
Premedication assessment
1. Record voiding characteristics (e.g., frequency,
aount, color, odor, associated sytos such as
burning and ain) to serve as a baseline for onitor-
ing theray.
2. Obtain baseline vital signs.
Availability, dosage, and administration. See Table 41.2.
Common adverse effects
Neurologic
Dry mouth, urinary hesitancy, retention, sedation. These
adverse effects are usually dosage related and resond
to a reduction in dosage. Sedation often resolves with
continued use. Instruct the atient to relieve dry outh
by sucking on ice chis or hard candy or by chewing
gu.
Gastrointestinal
Constipation, bloating. Encourage balanced nutrition
and inclusion of fresh fruits and vegetables for ber
 Drugs Used to Treat Disorders of the Urinary System CHAPTER 41
and an adequate uid intake to hel alleviate these
colications. If this aroach is unsuccessful, sug-
gest a stool softener or bulk-foring suleent.
Avoid stiulant laxatives, which ay have cholinergic
effects, counteracting the anticholinergic roerties.
Sensory
Blurred vision. Caution atients not to drive or oer-
ate ower equient until they have adjusted to this
adverse effect.
Serious adverse effects. If any of the aforeentioned
adverse effects intensies, it should be reorted to the
rescribing healthcare rovider for evaluation.
Drug interactions
Anticholinergic agents. The concurrent use of the uri-
nary anticholinergic agents with other anticholinergic
agents ay increase the frequency and severity of dry
outh, blurred vision, constiation, and other anticho-
linergic haracologic effects.
Fluoxetine, erythromycin, clarithromycin, itraconazole,
ritonavir. These agents inhibit the etabolis of
tolterodine, darifenacin, and solifenacin. It is reco-
ended that dosages not be raised above the initial
starting dosage in atients taking these edicines
concurrently.
DRUG CLASS: BETA-3 ADRENERGIC AGENT FOR
OVERACTIVE BLADDER SYNDROME
mirabegron (mĭr-ă-BĔG-rŏn)
Myrbetriq (mēr-BĔH-trĭk)
Actions
Mirabegron is a beta-3 adrenergic agonist. It relaxes
the detrusor uscle during the storage hase of blad-
der lling, which increases bladder caacity.
Uses
Mirabegron is used for the treatent of OAB with
sytos of urge incontinence, urgency, and urinary
frequency. Because irabegron relaxes the detrusor
uscle, atients with bladder outlet obstruction (e.g.,
enlarged rostate) and atients taking anticholinergic
drugs for OAB ay be at risk of urinary retention.
Therapeutic Outcome
The riary theraeutic outcoe exected fro ira-
begron is control of incontinence associated with OAB.
Nursing Implications for Mirabegron
Premedication assessment
1. Record voiding characteristics (e.g., frequency,
aount, color, odor, associated sytos such as
burning and ain) to serve as a baseline for onitor-
ing theray.
2. Obtain baseline vital signs.
677
Availability. PO: 25- and 50-g tablets, extended re-
lease (24 hours). lso available as 8 g/L Extended-
Release Granules for susension.
Liquid: 8 g/L in 100 L bottle.
Dosage and administration. PO: Initial: 25 g once
daily; efcacy is observed within 8 weeks for 25-g
dose. May increase to 50 g once daily based on indi-
vidual atient efcacy and tolerability.
Common adverse effects
Gastrointestinal
Constipation, diarrhea, dry mouth. About 1.5% of atients
being treated with irabegron reorted constiation or
diarrhea. Theray usually does not need to be discon-
tinued, but eating foods that add bulk to the diet ay
be helful for both constiation and diarrhea. Patients
with constiation ay also benet fro the use of a
stool softener. Encourage adequate uid intake.
Mouth dryness ay be alleviated by sucking hard
candy or ice chis or by chewing gu. Encourage ad-
equate uid intake.
Urinary
Urinary retention. Urinary retention is ore likely to
be reorted by atients who already have soe degree
of bladder outlet obstruction (ost coonly ros-
tatic enlargeent) and in those atients already taking
anticholinergic agents for OAB. Start theray with the
lower dose available.
Urinary tract infection. Aroxiately 4% of atients
being treated with irabegron develoed a UTI. If
sytos of OAB becoe ore severe, or burning on
urination is reorted, infor the healthcare rovider.
Mirabegron usually does not need to be discontinued
but the UTI should be treated.
Serious adverse effects
Hypertension. Monitor the atient’s blood ressure
eriodically. Notify the healthcare rovider if this effect
starts to occur, because this haens riarily with
individuals already being treated for hyertension.
Drug interactions
Metoprolol, digoxin, nebivolol, fesoterodine. Mirabe-
gron inhibits the etabolis of etorolol, digoxin,
ecainide, nebivolol, and fesoterodine. When any of
these drugs is adinistered with irabegron, start the
drug with the lowest dose available to deterine the
effect of the alteration of its etabolis by irabegron.
Alternatively, change to edicines whose etabolis
is not inhibited by irabegron.
Anticholinergic agents. The concurrent use of ira-
begron with anticholinergic agents used for OAB ay
enhance the risk of urinary retention and other an-
ticholinergic adverse/toxic effects (e.g., constiation,
dry outh). Initiate anticholinergic agent theray with
low doses to assess tolerance of the atient to otential
adverse effects.
678 UNIT IX Drugs Affecting Other Body Systems

Table 41.2 Urinary Anticholinergic Agents

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE
darifenacin — Tablets, extended Initial dose: 7.5 mg once daily
release (24 hr): Based on individual response, the dosage may be increased to
7.5, 15 mg 15 mg once daily as early as 2 wk after starting therapy
May be taken without regard to food
oxybutynin Tablets: 5 mg Initial dose: 5 mg (tablets or syrup) two or three times/day
Do not confuse Syrup: 5 mg/5 mL Maximum dose: 20 mg daily
oxybutynin with Ditropan XL Tablets, extended Initial dose: 5 mg once daily
OxyContin. release (24 hr): Dosage may be adjusted at weekly intervals in 5-mg increments
5, 10, 15 mg Maximum dose: 30 mg daily
May be administered with or without food and must be
swallowed whole with the aid of liquids; do not crush or chew
Pediatric (6 yr and older): PO: 5 mg once daily; adjust dose as
needed in 5 mg increments at weekly intervals; maximum
dose, 20 mg daily
Gelnique Topical gel: 10% Apply the contents of one sachet once daily to clean, dry, intact
skin on abdomen, thighs, or upper arms/shoulder
Rotate site; do not apply to same site on consecutive days
Wash hands after use
Cover treated area with clothing after gel has dried to prevent
transfer of medication to others
Do not bathe, shower, or swim until 1 hr after gel is applied
Oxytrol Transdermal Initial dose: Apply one patch every 3–4 days to dry, intact skin
patch: 36 mg on abdomen, hip, or buttock
(3.9 mg/day Select a new application site with each new patch to avoid
release) reapplication to the same site within 7 days
fesoterodine Toviaz Tablets, extended 4–8 mg daily; 4 mg daily for patients taking potent CYP3A4
release (24 hr): inhibitors or with renal impairment
4, 8 mg
solifenacin VESIcare Tablets: 5, 10 mg Initial dose: 5 mg once daily
If well tolerated, dosage may be increased to 10 mg once daily
May be taken without regard to food.
tolterodine Detrol Tablets: 1, 2 mg Initial dose: 1–2 mg twice daily based on individual response and
Do not confuse Do not confuse tolerance
tolterodine with Detrol with Capsules, Initial dose: 2–4 mg once daily taken with liquids and swallowed
tolcapone. Datril. extended whole
Detrol LA release (24 hr):
2, 4 mg
trospium — Tablets: 20 mg Initial dose: 20 mg twice a day at least 1 hr before meals on an
empty stomach
For patients with renal impairment (CrCl <30 mL/min),
recommended dose is 20 mg once daily at bedtime
— Capsules, Initial dose: 60 mg daily in the morning; should be taken with
extended water on an empty stomach at least 1 hr before food
release (24 hr): Not recommended for patients with renal impairment (CrCl <30
60 mg mL/min)
Creatinine clearance; CYP3A4, cytochrome P450 component 3A4.
Do not confuse.

MISCELLANEOUS URINARY AGENTS the bladder, usually resulting in urination. It ay also
stiulate gastric otility, increase gastric tone, and re-
store iaired rhythic eristalsis.
bethanechol chloride (bĕ-THĂN-ĕ-kŏl)
Uses
Actions Bethanechol is used in cases of nonobstructive uri-
Bethanechol is a arasyathetic nerve stiulant that nary retention, articularly in ostoerative and
causes contraction of the detrusor urinae uscle in ostartu atients, to restore bladder tone and
urination.
 Drugs Used to Treat Disorders of the Urinary System CHAPTER 41
Therapeutic Outcome
The riary theraeutic outcoe associated with
bethanechol theray is restoration of bladder tone and
urination.
Nursing Implications for bethanechol
Premedication assessment
1. Record voiding characteristics (e.g., frequency,
aount, color, odor, and associated sytos such
as burning and ain) to serve as a baseline for oni-
toring theray.
2. Record any gastrointestinal sytos resent to
serve as a baseline for onitoring theray.
Availability. PO: 5-, 10-, 25-, and 50-g tablets.
Dosage and administration. Adult: PO: 10 to 50 g
three to four ties a day.
Common adverse effects
Vascular
Flushing of skin, headache. A haracologic roerty
of the drug results in dilated blood vessels.
Serious adverse effects
Gastrointestinal
Nausea, vomiting, sweating, colicky pain, abdominal cramps,
diarrhea, belching, involuntary defecation. These effects are
caused by a haracologic roerty of the drug. Consult
the healthcare rovider; a dosage adjustent ay con-
trol these adverse effects. Provide suort for the atient
who develos diarrhea or involuntary defecation.
Drug interactions
Beta-adrenergic blocking agents. Beta blockers ay
enhance the adverse effects of bethanechol. Esecially
of concern is the otential for cardiac conduction ab-
noralities and bronchoconstriction. Monitor for ar-
rhythias, bradycardia, and resiratory difculty.
Reort to the healthcare rovider if resent.
phenazopyridine hydrochloride (fĕn-ā-zō-PĬR-ă-dēn)
Pyridium (pī-RĬD-ē-ŭm)
Actions
Phenazoyridine is an agent that, as it is excreted
through the urinary tract, roduces a local anesthetic
679
effect on the ucosa of the ureters and bladder. It acts
within about 30 inutes after oral adinistration.
Uses
Phenazoyridine relieves burning, ain, urgency, and
frequency associated with UTIs. It also reduces bladder
sas, which relieves the resulting urinary retention
and urgency. Phenazoyridine is also used for re-
oerative and ostoerative surface analgesia in urologic
surgical rocedures and after diagnostic tests in which
instruentation is necessary. It is occasionally used to
relieve the discofort caused by an indwelling catheter.
Therapeutic Outcome
The riary theraeutic outcoe associated with
henazoyridine theray is relief of burning, frequen-
cy, ain, and urgency associated with UTI.
Nursing Implications for Phenazopyridine
Premedication assessment
1. Record voiding characteristics (e.g., frequency,
aount, color, odor, and associated sytos such
as burning and ain) to serve as a baseline for oni-
toring theray.
2. Record skin color before initiating theray.
Availability. PO: 95-, 99.5-, 100-, and 200-g tablets.
Dosage and administration. Adult: PO: 190 to 200 g
three ties daily for two days.
Common adverse effects
Urinary
Reddish-orange urine discoloration. Be certain that the
atient understands that the color of the urine will be-
coe reddish orange when this drug is used and that
this discoloration is no cause for alar.
Serious adverse effects
Integumentary, sensory
Yellow sclera or skin. The atient should reort any
yellowish tinge develoing in the sclera (white or-
tion) of the eye.
Drug interactions
Urine colorimetric procedures. Phenazoyridine inter-
feres with colorietric diagnostic tests erfored on
urine. Consult the hosital laboratory for alternative
easures.
680 UNIT IX Drugs Affecting Other Body Systems

Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions

Key Points
OPTION 1 OPTION 2 OPTION 3
• UTIs are some of the most common types of infections
and are found in all patient care settings. Frequency Practicing Kegel bethanechol
• For UTIs, instruct patients to take the medicines exercises (Urecholine)
exactly as prescribed for the entire course of Painful urination Avoiding public fosfomycin
medication. Discontinuing the antimicrobial agent places (Monurol)
when the symptoms improve may result in another Frequent Taking liquids oxybutynin
infection that may be resistant to antimicrobial infections after 6 pm (Ditropan)
treatment. Urgency Avoiding alcohol mirabegron
and caffeine (Myrbetriq)
• The nurse can provide signicant care by understanding
and reporting the early symptoms associated with Incontinence nitrofurantoin
acute and chronic infections and assisting patients (Macrodantin)
who have difculty with urinary retention and
incontinence.
Objective: Identify the symptoms, treatment, and medications used
• Overactive bladder syndrome has three primary for urinary tract disorders.
symptoms. A combination of bladder training and Kegel NCLEX item type: Cloze
exercises helps the patient regain bladder control, Cognitive skill: Evaluate cues
increasing voided volumes and the time interval between
voids. Anticholinergic agents or mirabegron are used to 2. The nurse caring for the patient in the scenario with overactive
reduce the symptoms of OAB. bladder who also suffers from frequent bladder infections can
expect which medications to be ordered for the infection? (Select
all that apply.)
Additional Learning Resources 1. Nitrofurantoin (Macrodantin)
2. Fosfomycin (Monurol)
SG Go to your Study Guide for additional Review Questions 3. Tolterodine (Detrol)
for the NCLEX® Examination, Critical Thinking Clinical Situa-
4. Mirabegron (Myrbetriq)
tions, and other learning activities to help you master this chap-
5. Phenazopyridine hydrochloride (Pyridium)
ter content.
Objective: Identify the symptoms, treatment, and medications used
Go to your Evolve website (https://evolve.elsevier.com/ for urinary tract disorders.
Willihnganz) for additional online resources. NCLEX item type: Multiple response
Cognitive skill: Application
Clinical Judgment and Next-Generation NCLEX® Exam-
3. The nurse was administering an anticholinergic agent for the patient
ination-Style Questions The following questions are typical of
in the scenario with an overactive bladder, and knows which side
the NCLEX exam and include both NGN (Next Generation)
effects can be expected from these agents? (Select all that apply.)
and traditional questions. See Chapter 1 for further information
regarding question types. 1. Dry mouth
2. Blurred vision
3. Constipation
Scenario 4. Urinary frequency
5. Diarrhea
A patient admitted to the hospital with appendicitis had surgery Objective: Discuss the adverse effects of the drugs used to treat
and developed symptoms of an overactive bladder postopera- disorders of the urinary tract.
tively. NCLEX item type: Multiple response
1. Choose the most likely options for the information missing Cognitive skill: Application
from the sentence below by selecting from the lists of options 4. The nurse was administering bethanechol chloride (Urecholine) for
provided. the treatment of which urinary disorder?
The nurse caring for the patient in the scenario who was di- 1. Overactive bladder syndrome
agnosed with an overactive bladder knows that the symp- 2. Acute cystitis
toms of an overactive bladder include ______1__________ 3. Nonobstructive urinary retention
and ______1_________and _______1________ which 4. Urinary tract infection
can be treated with ________2__________ and
Objective: Identify the symptoms, treatment, and medications used
________2__________. as well as the medication such as
for urinary tract disorders
_______3__________ and _________3_________ used to
NCLEX item type: Multiple choice
help control the syndrome.
Cognitive skill: Comprehension
 Drugs Used to Treat Disorders of the Urinary System CHAPTER 41 681

5. The nurse implemented important interventions to help a patient Objective: Identify important nursing interventions associated with
with the treatment of various urinary tract disorders. Indicate with the drug therapy and treatment of diseases of the urinary system.
an X the nursing actions that are indicated and those that are NCLEX item type: Matrix
nonessential for the patient care of urinary tract disorders. Cognitive skill: Generate solutions

NON-
NURSING INTERVENTION INDICATED ESSENTIAL
For a patient with overactive
bladder educate to avoid
bubble baths
Teach the Credé maneuver
to aid emptying bladder for
urinary retention
Promote safety with elevated
toilet seats or commodes
Determine specic gravity of
the urine
Keep skin clean and dry to
prevent breakdown secondary
to incontinence
Determine whether patient
has any allergies to
medications ordered
Educate patients with frequent
infections the importance of
adequate uid intake
42 Drugs Used to Treat Glaucoma and Other Eye
Disorders
https://evolve.elsevier.com/Willihnganz

Objectives
1. Explain patient assessments needed for eye disorders. 3. Discuss the medications used in the management of
2. Identify patient teaching needs for patients with glaucoma. open-angle glaucoma.

Key Terms
cornea (KŎR-nē-ă) (p. 682)
sclera (SKLĀR-ă) (p. 682)
iris (Ī-rĭs) (p. 682)
sphincter muscle (SFĬNK-tĕr MŬS-ŭl)
(p. 682)
miosis (mī-Ō-sĭs) (p. 682)
dilator muscle (DĪ-lā-tŭr) (p. 682)
mydriasis (mī-DRĪ-ă-sĭs) (p. 682)
lens (LĔNZ) (p. 682)
near point (NĒR PŌYNT) (p. 682)
zonular fibers (ZŎN-yū-lăr) (p. 682)
cycloplegia (sī-klō-PLĒ-jē-ă) (p. 682)
lacrimal canaliculi (LĂ-krĭ-măl kăn-ă-
LĬK-yū-lī) (p. 683)
intraocular pressure (IOP) (ĭn-tră-
ŎK-yū-lăr) (p. 684)
closed-angle glaucoma (KLŌZD ĂN-
gŭl glŏ-KŌ-mă) (p. 684)
open-angle glaucoma (ō-PĒN ĂN-gŭl
glŏ-KŌ-mă) (p. 684)

relaxation of the sphincter muscle, which causes the

ANATOMY AND PHYSIOLOGY
OF THE EYE
The eyeball has three coats, or layers: the protective ex-
ternal, or corneoscleral coat; the nutritive middle vas-
cular layer, called the choroid; and the light-sensitive
inner layer, or retina (Fig. 42.1).
The cornea, or outermost sheath of the anterior
eyeball, is transparent so that light can enter the eye.
The cornea has no blood vessels; it receives its nutri-
tion from the aqueous humor and its oxygen supply by
diffusion from the air and surrounding vascular struc-
tures. There is a thin layer of epithelial cells on the ex-
ternal surface of the cornea that is resistant to infection.
An abraded cornea, however, is highly susceptible to
infection. The cornea has sensory bers, and any dam-
age to the corneal epithelium will cause pain. Seriously
injured corneal tissue is replaced by scar tissue that is
usually not transparent. The sclera is the eye’s white
portion that is continuous with the cornea and is not
transparent. The pupil is the center black portion of the
eye, which is actually a hole in the iris that allows light
to reach the retina.
The iris is a diaphragm that surrounds the pupil and
gives the eye its color—blue, green, hazel, brown, or
gray. The sphincter muscle within the iris encircles the
pupil and is innervated by the parasympathetic ner-
vous system. Miosis is contraction of the iris sphincter
muscle, which causes the pupil to narrow. The dilator
muscle, which runs radially from the pupillary mar-
gin to the iris periphery, is sympathetically innervat-
ed. Mydriasis is contraction of the dilator muscle and
pupil to dilate (Fig. 42.2).
Constriction of the pupil normally occurs with light
or when the eye is focusing on nearby objects. Dilation
of the pupil normally occurs in dim light or when the
eye is focusing on distant objects.
The lens is a transparent gelatinous mass of bers
encased in an elastic capsule situated behind the iris.
Its function is to ensure that the image on the retina is
in sharp focus. It does this by changing shape (accom-
modation). This occurs readily in youth, but with age
the lens becomes more rigid and the ability to focus
close objects is lost. The near point, the closest point
that can be seen clearly, recedes. With age, the lens may
lose its transparency and become opaque, forming a
cataract. Blindness can occur unless the cataract can be
treated or surgically removed.
The lens has ligaments around its edge, called zonu-
lar fibers, that connect with the ciliary body. Tension on
the zonular bers helps change the shape of the lens.
In the unaccommodated eye, the ciliary muscle is re-
laxed and the zonular bers are taut. For near vision,
the ciliary muscle bers contract, relaxing the pull on
the ligaments and allowing the lens to become thick.
Accommodation depends on two factors: (1) the ability
of the lens to assume a more biconvex shape when ten-
sion on the ligaments is relaxed, and (2) ciliary muscle
contraction. Paralysis of the ciliary muscle is termed
cycloplegia The ciliary muscle is innervated by para-
sympathetic nerve bers.
The ciliary body secretes aqueous humor, which
bathes and feeds the lens, posterior surface of the

682
 Drugs Used to Treat Glaucoma and Other Eye Disorders CHAPTER 42 683

cornea, and iris. After it is formed, the uid ows for- sclera into a meshwork that leads into the Schlemm
ward between the lens and the iris into the anterior canal and the venous system of the eye.
chamber. It drains out of the eye through drainage Eyelids, eyelashes, tears, and blinking all protect
channels located near the junction of the cornea and the eye. There are about 200 eyelashes for each eye.
The eyelashes cause a blink reex whenever a foreign
Lateral body touches them, closing the lids for a fraction of a
rectus second to prevent the foreign body from entering the
muscle
eye. Blinking, which is bilateral, occurs every few sec-
Choroid
Ciliary onds during waking hours. It keeps the corneal surface
body
free from mucus and spreads the lacrimal uid evenly
Sclera Iris over the cornea. Tears are secreted by lacrimal glands
Fovea and contain lysozyme, a mucolytic lubrication for lid
centralis Cornea movements. They wash away foreign objects and form
Optic a thin lm over the cornea, providing it with a good
nerve Lens Pupil optical surface. Tear uid is lost by drainage into two
Aqueous small ducts, the lacrimal canaliculi, at the inner corners
humor of the eyelids and by evaporation.
Suspensory
Retinal ligaments
blood
Ciliary
GENERAL CONSIDERATIONS FOR
vessels
Retina muscle TOPICAL OPHTHALMIC DRUG THERAPY
Medial The most common route of administration for ophthal-
rectus
muscle mic drugs is topical application. Advantages include
Fig. 42.1 Cross-section of the eye. convenience, simplicity, noninvasive nature, and the
ability of the patient to self-administer. Topically ad-
ministered medications do not penetrate adequately
for use with posterior eye diseases, such as diseases of
the optic nerve or retina, so topical administration is
not used for such diseases.
Proper administration of ophthalmic drugs is essen-
Sympathetic tial to optimal therapeutic response. The administra-
motor nerve fiber; tion technique used often determines drug safety and
contraction efcacy (see Chapter 7, Fig. 7.7).
caused by dim
light or
• Based on the volume that the eye can retain, use of
mydriatic agents more than 1 drop per administration is questionable.
• If more than one drug is to be administered at about
the same time, separate the administration of the
Radially arranged different medications by at least 5 minutes. This en-
dilator muscle
sures that the rst medication is not washed away
fibers of the iris
by the second, or that the second medication is not
Sphincter muscle diluted by the rst.
fibers of the iris • Minimize systemic absorption of ophthalmic drops
by compressing the tear duct at the inner canthus
Pupil
of the eye for 3 to 5 minutes after instillation. This
Parasympathetic reduces the passage of medication via the nasolacri-
motor nerve fiber; mal duct into areas of absorption, such as the nasal
contraction and pharyngeal mucosa.
caused by bright • Eyecup use is discouraged because of the risk of
light or miotic
agents contamination, which can cause infection.
• Ophthalmic ointments may impede delivery of oth-
er ophthalmic drugs to the affected site by serving
as a barrier to contact. Administer drops before ap-
plying ointments. Try not to administer drops for a
few hours after the use of ointment. The ointment
should be administered beginning at the inner can-
thus and moving to the outer aspect of the eye.
• Ointments may blur vision during the waking
Fig. 42.2 Effect of light or ophthalmic agents on the iris of the eye. hours. Use with caution in conditions in which
684 UNIT IX Drugs Affecting Other Body Systems

visual clarity is critical (e.g., operating motor equip- obstruction of the trabecular network in the iridocor-
ment, reading). neal angle (Fig. 42.5). This occurs in patients who have
• Observe expiration dates closely. Do not use out- narrow anterior chamber angles. Symptoms develop
dated medication. gradually and appear intermittently for short periods,
• Solutions and ointments are frequently misused. Do especially when the pupil is dilated. (Dilation of the
not assume that patients know how to effectively pupil pushes the iris against the trabecular meshwork,
use these agents. causing the obstruction.) Symptoms often reported are
• In an effort to enhance safety of ophthalmic medi- blurred vision, halos around white lights, frontal head-
cations, the ophthalmic medicine industry recom- ache, and eye pain. Patients often associate the symp-
mends the use of standard colors for drug labels and toms with stress or fatigue. An attack can also be pre-
bottle caps (see the following chart). Ophthalmic cipitated by administration of a mydriatic agent, such
drug labels include “For Ophthalmic Use.” The as atropine or scopolamine, for eye examination.
nurse should become familiar with these colors and
types of ophthalmic medications to help prevent
DRUG THERAPY FOR GLAUCOMA
inadvertently picking up and administering the
wrong solution. The treatment of open-angle glaucoma is maintenance
of IOP at normal levels to prevent blindness. Treatment
options include surgery, laser surgery, and drug
THERAPEUTIC CLASS CAP AND LABEL COLOR
Antiinfectives Brown or tan
Beta-adrenergic blocking agents Yellow, blue, or both Retina Iridocorneal
angle
Miotics Green
Mydriatics and cycloplegics Red Iris
Nonsteroidal antiinammatory Gray Vitreous Anterior
agents cavity chamber

GLAUCOMA
Optic
Glaucoma is an eye disease characterized by abnormal- nerve
ly elevated intraocular pressure (IOP), which may result Aqueous
from excessive production of the aqueous humor or pathway
from diminished ocular uid outow. Increased pres- Canal of
sure, if persistent and sufciently elevated, may lead Schlemm
to permanent blindness. There are three major types Posterior
of glaucoma: primary, secondary, and congenital. chamber
Primary includes closed-angle glaucoma (also known Fig. 42.3 Anterior and posterior chambers of the eye. Arrows indicate
as narrow-angle glaucoma) and open-angle glaucoma. the pathway of aqueous ow.
These are diagnosed by determination of the irido-
corneal angle of the anterior chamber, where aqueous
humor reabsorption takes place. Secondary glaucoma
may result from previous eye disease or may occur af-
ter a cataract extraction and may require drug therapy
for an indenite period. Congenital glaucoma requires
surgical treatment.
Open-angle glaucoma develops insidiously over
the years as pathologic changes at the iridocorneal
angle prevent the outow of aqueous humor through
the trabecular network to the Schlemm canal and into
the veins of the eye (Fig. 42.3). In cases of open-angle Iris
glaucoma, there is reduced outow of aqueous humor
Open angle
through the trabecular network and Schlemm canal 20-40 degrees
because of resistance of the aqueous humor outow;
Iridocorneal
the iridocorneal angle is open (Fig. 42.4). Canal of angle
IOP builds up and, if not treated, will damage the Schlemm
Trabecular
optic disk. Initially the patient has no symptoms, but network
over the years there is a gradual loss of peripheral vi-
Fig. 42.4 Open-angle glaucoma. Obstruction to the ow of the
sion. If untreated, total blindness may result. aqueous humor is caused by reduced outow at the Schlemm canal
Acute closed-angle glaucoma occurs when there in the trabecular network. There is no obstruction from closure of the
is a sudden increase in IOP caused by a mechanical iridocorneal angle.
 Drugs Used to Treat Glaucoma and Other Eye Disorders CHAPTER 42
Access to canal of Schlemm
Canal of is obstructed, stopping
Schlemm fluid from escaping
Trabecular
network
Fig. 42.5 Closed-angle glaucoma. Obstruction to the ow of aqueous
uid to the Schlemm canal causes closed-angle glaucoma.
therapy. A prostaglandin analog (e.g., latanoprost) is
often the initial drug used to treat open-angle glaucoma.
Other agents that may also be used are beta-adrenergic
blocking agents (e.g., timolol), alpha-adrenergic agents
(e.g., brimonidine), carbonic anhydrase inhibitors (e.g.,
dorzolamide), and netarsudil, a rho kinase inhibitor.
The selection of the drug is determined to a great ex-
tent by the requirements of the individual patient and
response to therapy.
Acute closed-angle glaucoma requires immediate
treatment to reduce IOP. Intravenous mannitol, an
osmotic diuretic, may be administered to draw aque-
ous humor from the eye. Topical corticosteroids may
be used to reduce ocular inammation. Other medica-
tions used to reduce formation of aqueous humor in-
clude a beta blocker, prostaglandin, an alpha-adrenergic
agent, or a carbonic anhydrase inhibitor
NURSING IMPLICATIONS FOR GLAUCOMA AND
OTHER EYE DISORDERS
The nurse has an important role in educating the pub-
lic and promoting safety measures to protect the eye
from potential sources of injury. Healthcare profession-
als can participate in this role during their daily con-
tacts with people in the community. The use of safety
glasses in potentially hazardous situations, prevention
of chemical burns from common household cleaning
items or other agents at home or work, proper cleaning
and wearing of contact lenses or glasses, and selection
of safe toys and play activities for children are some ar-
eas about which the nurse can teach the public. These
safety measures can signicantly reduce the number of
injuries that occur annually.
Nurses play an important role in detecting eye dis-
orders and implementing treatment plans. An example
of this is in patients with diabetes mellitus. Encourage
685
annual, or more frequent, eye examinations to detect
and prevent complications associated with the disease.
The primary delivery of eye care is through self-
administration of drugs. One of the greatest challenges
in the care of chronic eye disorders such as glaucoma is
convincing the patient of the need for long-term treat-
ment and adherence to the therapeutic regimen.
Assessment
Eye examination
• When an eye injury has occurred, document visual
acuity by screening vision with the Snellen chart.
Comparison screenings should be performed at
each subsequent visit.
• Observe for eyelid edema. It may be an indication
of a systemic disease process or tumor. Report if
present.
• Assess pupils for equality of size, roundness, and
response to light. Report irregular contour, unequal
size, or decreased response to light.
• Observe for and report nystagmus.
• Observe for any redness or drainage in the eyes.
• Observe for complete closure of the eyelid. This is
essential for protection of the cornea. Patients who
have received corneal anesthesia, have had fth
cranial nerve surgery, have exophthalmos, or are
unconscious must have the cornea protected to pre-
vent damage.
• Ask whether glasses or contact lenses are worn.
• Inspect the eye dressings and report immediately
for evaluation if any drainage is observed. Never re-
move the surgical dressing after surgery to inspect
the eye.
History of symptoms
• Ask the patient to describe the symptoms for which
treatment is being sought. How do symptoms affect
daily life? Do visual problems affect ability to read?
• Is there a family history of cataracts, glaucoma, or
macular degeneration?
• Are activities limited in any way by any vision
problem?
• Do any leisure activities have the potential for eye
injury?
• Has the person had any noticeable pain, burning,
foreign body sensation, blurred or halo vision, or
loss of vision?
• Ask whether there is any difculty in adjusting vi-
sion when going from a dark to a brightly lighted
area or vice versa.
• Are colors clear and crisp, or do they lack clarity?
• Has there been an increase in tearing or discharge
from the eye? If so, ask for details of appearance and
amount of drainage.
• Has there been any recent nausea or vomiting?
Psychological. What type of response is the patient
exhibiting to the disturbance in visual acuity? Is the
686 UNIT IX Drugs Affecting Other Body Systems
patient withdrawing socially? Identify a support sys-
tem available for at-home care and assistance. Plan a
specic time to meet with the patient and signicant
others to discuss at-home care and community re-
sources available if assistance is indicated.
Life Span Considerations
Diminished Visual Acuity
Diminished visual acuity affects most aspects of a person’s
life, so it is imperative to evaluate an individual’s ability to per-
form the usual activities of daily living when visual impairment
develops. Many medications used to treat other disorders
can reduce visual acuity; this adverse effect should be antici-
pated and its consequences monitored. Every attempt must
be made to help the patient adapt to the visual impairment
and provide for personal safety.
Diagnostics. Ask the patient to describe what eye di-
agnostic procedures have been completed before ad-
mission (e.g., visual acuity measurement, tonometry,
slit-lamp examination, visual elds). A tonometer is
used to measure the IOP inside the eye to evaluate a
patient’s risk for glaucoma and to assess the success or
failure of ongoing treatment. There are several types
of tonometers available (e.g., applanation, Goldmann,
noncontact, ocular response analyzer), the use of
which ranges from quick screening for increased IOP
to very precise measurement of IOP. Most tonometers
measure pressure in units of millimeters of mercury
(mm Hg).
Medications. Ask for a list of all prescribed and over-
the-counter medications and herbal products be-
ing taken. Ask for details on medications, dosage,
schedule, and degree of compliance. List all ordered
medications on the medication administration re-
cord (MAR). If beta blockers are being taken, list the
pulse and blood pressure on the MAR as a preas-
sessment to administration of the ophthalmic drops.
Note parameters relating to the prevention of injury,
the activity and exercise level permitted, and diet
orders.
Implementation
• Perform assessments every shift consistent with the
patient’s status and diagnosis.
• Prepare the patient for eye examinations, diagnos-
tics, or eye surgery.
• Administer cycloplegic and mydriatic medications
prescribed for dilation of the eye before an eye ex-
amination or ophthalmic surgery.
• Administer miotic medication to produce constric-
tion of the eye after eye examination or diagnostic
procedures, as prescribed.
• Administer all ophthalmic medications prescribed
while maintaining aseptic technique to prevent the
transfer of infection from one eye to the other.
• Protect the cornea from damage during anesthesia
or in an unconscious patient through the use of oph-
thalmic ointment or articial tears to prevent cor-
neal drying.
• Assist with diagnostic procedures (e.g., visual elds,
tonometry, visual acuity).
• Take baseline vital signs.
• Institute appropriate comfort measures.
• If eye surgery has been performed (e.g., trabecu-
lectomy), institute routine postoperative care mea-
sures. Position the patient as ordered, usually on
the back or on the unoperated side. With the scleral
buckling procedure, positioning orders may be ex-
tremely specic.
• Ensure that an eye patch and shield are applied
properly to protect the eye from further injury.
• Explain and enforce activity and exercise restric-
tions. To prevent an increase in IOP, instruct the pa-
tient to avoid heavy lifting, straining on defecation,
coughing, or bending and placing the head in a de-
pendent position.
• A blind or disoriented patient or a patient with both
eyes patched may experience effects of sensory
deprivation.
• Always speak before touching a person with im-
paired vision.
• Check on the patient at frequent intervals; initiate
conversations and regularly orient the patient to
date, time, and place.
• If the patient is agitated, contact the prescribing
healthcare provider; it may be necessary to obtain an
order to remove one eye patch or sedate the patient.
• Provide emotional support.
Health Promotion
 • Perform hand hygiene thoroughly each time the area is
touched (before or after eye treatments or instillation of
medications).
 • Use only sterile medications or dressings on the eye.
 • Wipe the eye from the inner canthus outward; discard the
tissue used; perform hand hygiene before proceeding to
the second eye.
 • When an infection is present, prevent cross-
contamination; always use a separate source of
medication and dropper for each eye.
 • Never touch the eyeball or face with the tip of the dropper
or opening of the ointment container. Demonstrate the
proper way to set the medication lid down so that the
inside is not contaminated.
 • When inserting or removing contact lenses, perform hand
hygiene rst and then follow the manufacturer’s instructions
regarding the cleansing and care of the lenses.
 • Report any persistent redness or drainage from the eyes.
Patient Education
After eye surgery
• Teach the patient and family proper hygiene and
eye care techniques to ensure that medications,
 Drugs Used to Treat Glaucoma and Other Eye Disorders CHAPTER 42
dressings, and/or surgical wounds are not contami-
nated during necessary eye care.
• Teach the patient and family about signs and symp-
toms of infections and when and how to report them
to allow early recognition and treatment of possible
infection.
• Instruct the patient to comply with postoperative
restrictions on head positioning, bending, cough-
ing, and the Valsalva maneuver to optimize visual
outcomes and prevent increased IOP.
• Instruct the patient to instill the eye medications us-
ing aseptic techniques and to comply with the pre-
scribed eye medication routine to prevent infection
(see Chapter 7, Fig. 7.7). In general, using more than
1 drop per dose of medication does not improve
response but increases the frequency of adverse ef-
fects and the cost of therapy. Instruct the patient on
how to block the nasolacrimal duct during instilla-
tion to minimize systemic effects.
• When using more than one medication, separate
drop instillation of each agent by at least 5 min-
utes to provide optimal ocular contact for each
medication.
• Instruct the patient to monitor pain and take pre-
scribed pain medication as directed; report pain not
relieved by prescribed medications.
• Instruct the patient about the importance of contin-
ued follow-up as recommended to maximize poten-
tial visual outcomes.
Disease or disorder
• Reinforce the teaching of pertinent facts regarding
the diagnosis and disease process.
• If the patient is being treated for glaucoma, stress
the need for lifelong treatment and use of medica-
tions. Explain that adherence with the drug regimen
can help prevent blindness.
• If an infectious process is present, teach personal
hygiene measures to prevent introduction of an
infection.
Visual acuity
• Provide for patient safety.
• Assess whether diminished visual acuity will re-
duce the ability of the patient to perform their usual
activities of daily living. Teach adaptation methods
appropriate to the situation.
• Restrict the operation of tools or power equipment
as appropriate to the degree of alteration present.
Medications
• Review the details of medication administration.
• Ensure that directions are printed in large, bold
print that the individual can read.
• Have the patient store all medications in an area
separate from other containers so that they cannot
inadvertently put things other than medication into
the eye.
687
• Have the person demonstrate the ability to self-
administer the eye medications to ensure manual
dexterity to perform the procedures.
• Keep an extra bottle of eye medications on hand,
particularly those used to reduce IOP.
Fostering health maintenance
• Discuss medication information and how it will
benet the course of treatment (e.g., reduction of
IOP, elimination of an infection).
• Seek cooperation and understanding of the fol-
lowing points so that medication compliance is
increased: name of medication; dosage, route, and
times of administration; and common and serious
adverse effects. Verify ability to self-administer all
medications. Additional health teaching is included
in the individual drug monographs.
• Encourage the patient to discuss any adverse ef-
fects that the medications may produce with the
healthcare provider to plan mutually for ways to
minimize these effects or make adaptations rather
than reduce the frequency or eliminate the use of
the medications.
Patient self-assessment. Enlist the patient’s help in
developing and maintaining a written record of moni-
toring parameters (e.g., blood pressure and pulse with
adrenergic and beta-adrenergic blocking agents, de-
gree of visual disturbance, progression of impairment)
and response to prescribed therapies for discussion
with the primary healthcare provider. See Patient Self-
Assessment Form for Eye Medications on the Evolve
website. Complete the Premedication Data column for
use as a baseline to track response to therapy. Ensure
that the patient understands how to use the form and
instruct the patient to take the completed form to all
follow-up visits. During follow-up visits, focus on is-
sues that will foster adherence with the therapeutic in-
terventions prescribed.
DRUG CLASS: CARBONIC ANHYDRASE INHIBITORS
Actions
These agents are inhibitors of the enzyme carbonic an-
hydrase. Inhibition of this enzyme results in a decrease
in the production of aqueous humor, thus lowering IOP.
Uses
These agents are used in conjunction with other treat-
ments to control IOP in cases of intraocular hyper-
tension and closed-angle and open-angle glaucoma.
Dorzolamide and brinzolamide have the advantage of
intraocular administration, with less potential for sys-
temic adverse effects.
Therapeutic Outcome
The primary therapeutic outcome expected from car-
bonic anhydrase inhibitors is reduced IOP.
688 UNIT IX Drugs Affecting Other Body Systems
Nursing Implications for Carbonic Anhydrase
Inhibitors
Premedication assessment
1. Establish whether the patient is pregnant; if preg-
nancy is suspected, withhold the medication and
contact the healthcare provider.
2. Check for allergy to sulfonamide antibiotics; with-
hold the medication and contact the healthcare pro-
vider if allergy is present.
3. Ensure that contact lenses have been removed be-
fore the instillation of dorzolamide or brinzolamide
drops.
4. If acetazolamide or methazolamide tablets are used
ensure that baseline electrolyte laboratory studies
have been drawn as ordered.
5. If acetazolamide or methazolamide tablets are used
assess and record baseline weight, hydration data,
vital signs, and mental status.
6. Record premedication IOP readings and visual acu-
ity data.
7. If acetazolamide or methazolamide tablets are used
assess for signs of gastric symptoms before initiat-
ing drug therapy. If present, schedule medications
for administration with milk or food.
Availability, dosage, and administration
See Table 42.1
Common adverse effects with ophthalmic eyedrop
preparations. Brinzolamide and dorzolamide may
cause ocular adverse effects including transient burn-
ing and stinging (less with dorzolamide), ocular dis-
comfort and transient blurred vision (more common
with brinzolamide), and, rarely, conjunctivitis, lid re-
actions, and photophobia. A supercial punctate ker-
atitis occurs in 10% to 15% of patients. In supercial
punctate keratitis, the eyes are usually painful, watery,
sensitive to bright light, and bloodshot, and vision
may be slightly blurred.
Table 42.1 Carbonic Anhydrase Inhibitors
GENERIC NAME BRAND NAME AVAILABILITY
acetazolamide — Tablets: 125, 250 mg
Capsules, extended release (12 hr):
500 mg
Powder for injection: 500 mg
brinzolamide Azopt Ophthalmic solution: 1% in 10- and
15-mL dropper bottles
dorzolamide Trusopt Ophthalmic solution: 2% in 10-mL
dropper bottle
methazolamide — Tablets: 25, 50 mg
Serious adverse effects with ophthalmic eyedrop
preparations. Brinzolamide and dorzolamide are sul-
fonamide derivatives; although administered ocularly,
systemic absorption may occur and could result in
hypersensitivity reaction if the patient is allergic to
sulfonamides (see later).
Common adverse effects with oral administration of
tablets (acetazolamide or methazolamide)
Gastric irritation. If gastric irritation occurs, admin-
ister the medication with food or milk. If symptoms
persist or increase in severity, report to the healthcare
provider for evaluation.
Serious adverse effects
Hematologic
Electrolyte imbalance, dehydration. Although infre-
quent, treatment with carbonic anhydrase inhibitors
may lead to excessive diuresis, resulting in water
dehydration and electrolyte imbalance. The electro-
lytes most commonly altered are K+, Na+, and Cl .
Hypokalemia is most likely to occur. Many symp-
toms associated with altered uid and electrolyte bal-
ance are subtle and resemble general symptoms of
drug toxicity or the disease process itself. Gather data
about changes in the patient’s mental status (e.g., alert-
ness, orientation, confusion), muscle strength, muscle
cramps, tremors, nausea, and general appearance (e.g.,
drowsy, anxious, lethargic). Always check the electro-
lyte reports for early indications of electrolyte imbal-
ance. Keep accurate records of intake and output, daily
weight, and vital signs.
Sulfonamide-like reactions
Dermatologic, hematologic, neurologic reactions. Carbonic
anhydrase inhibitors are sulfonamide derivatives and
thus have the potential to cause adverse effects simi-
lar to those associated with sulfonamide antimicrobial
therapy. These adverse effects, although rare, include
dermatologic, hematologic, and neurologic reactions.
DOSAGE
PO: 250 mg one to four times daily or 500-
mg extended release twice daily
Intraocular: 1 drop in affected eye(s) three
times daily
If more than one ophthalmic agent is to be
administered in the same eye, separate
the administration by at least 10 min
Intraocular: 1 drop in affected eye(s) three
times daily
If more than one ophthalmic agent is to be
administered in the same eye, separate
the administration by at least 10 min
PO: 50–100 mg, two or three times daily
 Drugs Used to Treat Glaucoma and Other Eye Disorders CHAPTER 42 689

(For further discussion, see the section on sulfona-
mides in Chapter 45.) Do not administer to patients
who are allergic to sulfonamide antibiotics without
healthcare provider approval. Observe closely for the
development of hypersensitivity.
Neurologic
Confusion. Perform a baseline assessment of the pa-
tient’s degree of alertness and orientation to name,
place, and time before initiating therapy. Make regu-
larly scheduled subsequent mental status evaluations
and compare ndings. Report changes in the patient’s
mental status.
Drowsiness. This adverse effect is usually mild and
tends to resolve with continued therapy. Encourage
the patient not to discontinue therapy without rst
consulting the healthcare provider. The patient who
works with machinery, operates a motor vehicle, ad-
ministers medications, or performs other duties that
require mental alertness should not take these medica-
tions while working.
Drug interactions
Digoxin. Patients receiving these orally administered
diuretic drugs may excrete excess potassium, which
leads to hypokalemia. If the patient is also receiving
digoxin, monitor closely for signs of digoxin toxicity
(e.g., anorexia, nausea, fatigue, blurred or colored vi-
sion, bradycardia, dysrhythmias).
Corticosteroids (prednisone, others). Corticosteroids
may enhance the loss of potassium. Check potassium
levels and monitor more closely for hypokalemia when
these two agents are used concurrently.
DRUG CLASS: ALPHA-ADRENERGIC AGENTS
Actions
Alpha-adrenergic agents have several uses in ophthal-
mology. Sympathomimetic agents cause pupil dilation,
increased outow of aqueous humor, vasoconstriction,
relaxation of the ciliary muscle, and a decrease in the
formation of aqueous humor.
Uses
Alpha-adrenergic agents are used to lower IOP in
open-angle glaucoma, relieve congestion and hyper-
emia, and produce mydriasis for ocular examinations.
Use with caution in patients with hypertension, dia-
betes mellitus, hyperthyroidism, heart disease, arterio-
sclerosis, or long-standing bronchial asthma.
Therapeutic Outcomes
The primary therapeutic outcomes expected from alpha-
adrenergic agents are as follows:
1. Mydriasis for ophthalmic examination
2. Reduced IOP in open-angle glaucoma
3. Reduced redness of the eyes from irritation
Nursing Implications for Alpha-Adrenergic Agents
Premedication assessment
1. Obtain baseline vital signs, including blood pres-
sure and pulse.
2. Record premedication IOP readings and visual acu-
ity data.
Availability, dosage, and administration. See Table 42.2
Common adverse effects
Sensory
Sensitivity to bright light. The mydriasis produced al-
lows excessive amounts of light into the eyes, which
causes the patient to squint. Sunglasses will help re-
duce the brightness. Caution the patient to temporarily
avoid tasks that require visual acuity, such as driving
or operating power machinery.
Conjunctival irritation, lacrimation. These adverse
effects are usually mild and tend to resolve with

Table 42.2 Alpha-Adrenergic Agents

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE COMMENTS
apraclonidine Iopidine Solution: 0.5%, 0.5% - 1 to 2 drops in affected An alpha-2 adrenergic agent used to:
1% eye(s) 3 times daily -lower IOP in open-angle glaucoma;
1% - 1 drop 1 hr before -control IOP after laser surgery
surgery and 1 drop
immediately after surgery
brimonidine Alphagan P Solution: 0.1%, 1 drop q8h in affected An alpha-2 adrenergic agent used
0.15%, 0.2% eye(s) to lower IOP in open-angle
glaucoma or ocular hypertension
phenylephrine Altafrin Solution: 2.5%, 1 drop every 3 to 5 minutes 2.5% and 10% solutions used for
10% as needed, up to 3 drops pupil dilation in uveitis, open-
per eye; does may be angle glaucoma, and diagnostic
repeated if needed procedures
tetrahydrozoline Visine Advanced Solution: 0.05% 1–2 drops two to four times Used as a topical vasoconstrictor
hydrochloride Relief daily
Good Sense Eye
Drops
IOP, Intraocular pressure.
690 UNIT IX Drugs Affecting Other Body Systems
continued therapy. Encourage the patient not to dis-
continue therapy without rst consulting the health-
care provider.
Serious adverse effects
Cardiovascular
Systemic adverse effects. Systemic effects from oph-
thalmic instillation are uncommon and minimal;
however, systemic absorption may occur via the lac-
rimal drainage system into the nasopharyngeal pas-
sages. Systemic effects are manifested by palpitations,
tachycardia, dysrhythmias, hypertension, faintness,
trembling, and diaphoresis. These are indications of
overdose or excessive administration. Report to the
healthcare provider for treatment and dosage adjust-
ment. Prevent systemic effects by carefully blocking
the inner canthus for 3 to 5 minutes after instilling the
medication to prevent absorption via the nasolacrimal
duct. Monitor the pulse rate and blood pressure, and
instruct the patient to continue to do this at home; re-
port signicant changes from the baseline data.
Diaphoresis, trembling. Touch the patient and bed-
ding to assess for diaphoresis, particularly when these
medications are used in surgery in which the patient
is under sterile drapes, anesthetized, and unable to re-
spond to verbal questioning.
Drug interactions
Tricyclic antidepressants. Tricyclic antidepressants (e.g.,
amitriptyline, imipramine, doxepin) may cause additive
hypertensive effects. Monitor carefully for poor blood
pressure control or a gradually increasing blood pressure.
DRUG CLASS: BETA-ADRENERGIC BLOCKING
AGENTS
Actions
Beta-adrenergic blocking agents are used in ophthal-
mology to reduce elevated IOP. Their exact mechanism
Table 42.3 Beta-Adrenergic Blocking Agents
GENERIC NAME BRAND NAME AVAILABILITY
betaxolol Betoptic S Solution: 0.5% in 5-, 10-,
hydrochloride 15-mL dropper bottles
Suspension: 0.025% in
5, 10,15-ml dropper bottles
carteolol — Solution: 1% in 5-, 10-, 15-
mL dropper bottles
levobunolol ___ Solution: 0.5% in 5-, mL
hydrochloride dropper bottles
metipranolol — Solution: 0.3% in 5-, 10-mL
dropper bottles
timolol maleate Timoptic Solution: 0.25%, 0.5% in 5-, 1 drop of 0.25%
10-, 15-mL dropper bottles
Solution, gel-forming: 0.25%, daily; 1 drop of gel
0.5%
of action is not known, but it is thought that they re-
duce the production of aqueous humor.
Uses
Beta blockers are used to reduce IOP in patients
with chronic open-angle glaucoma or ocular hyper-
tension. Unlike anticholinergic agents, there is no
blurred or dim vision or night blindness because IOP
is reduced with little or no effect on pupil size or vi-
sual acuity.
Therapeutic Outcome
The primary therapeutic outcome expected from beta-
adrenergic blocking agents is reduced IOP.
Nursing Implications for Beta-Adrenergic Blocking
Agents
Premedication assessment
1. Obtain baseline vital signs, including pulse and
blood pressure; hold the medication and contact the
healthcare provider if bradycardia, hypertension, or
respiratory disorders are present.
2. Record the premedication IOP readings and visual
acuity data.
Availability, dosage, and administration. See Table42.3
Common adverse effects
Sensory
Conjunctival irritation, lacrimation. These adverse ef-
fects are usually mild and tend to resolve with con-
tinued therapy. Encourage the patient not to discon-
tinue therapy without rst consulting the healthcare
provider.
Serious adverse effects
Cardiovascular
Bradycardia, hypotension. Systemic effects are un-
common but may be manifested by bradycardia,
INITIAL DOSAGE COMMENTS
1–2 drops twice Beta-1 blocking agent; onset in
daily 30 min, duration is 12 hr; several
weeks of therapy may be required
to determine optimal dosage
1 drop twice daily Beta-1, beta-2 blocking agent;
duration is up to 12 hr
1 drop once or twice Beta-1, beta-2 blocking agent; onset
daily within 60 min, duration is up to 24 hr
1 drop twice daily in Beta-1, beta-2 blocking agent; onset
affected eye(s) within 30 min, duration is 12–24 hr
Beta-1, beta-2 blocking agent; onset
solution twice within 30 min, duration is up to
24 hr; gel may be used once daily
solution once daily
 Drugs Used to Treat Glaucoma and Other Eye Disorders CHAPTER 42 691

dysrhythmias, hypotension, faintness, and bronchos-
pasm. These adverse effects are more commonly observed
in patients requiring higher dosages of beta-adrenergic
blocking agents and in patients with hypertension, dia-
betes mellitus, heart disease, arteriosclerosis, or long-
standing bronchial asthma. Report to the healthcare pro-
vider for treatment and dosage adjustment. Record the
blood pressure and pulse rate at specic intervals.
Availability, dosage, and administration. See Table 42.4.
If more than one drug is to be instilled in the same eye,
administer the drugs at least 5 minutes apart.
Medication Safety Alert
Do not administer prostaglandin agonists into the eyes when
the patient is wearing contact lenses. Lenses may be rein-
serted 15 minutes after administration.

Drug interactions
Nonophthalmic beta-adrenergic blocking agents. Non-
ophthalmic beta blockers (e.g., propranolol, atenolol,
metoprolol) may enhance the systemic therapeutic
and toxic effects of ophthalmic beta-adrenergic block-
ing medications. Monitor for an increase in severity of
adverse effects such as fatigue, hypotension, bronchos-
pasm, and bradycardia.
DRUG CLASS: PROSTAGLANDIN AGONISTS
Actions
Prostaglandin agonists reduce IOP by increasing the
outow of aqueous humor.
Uses
The prostaglandin agonists are used to reduce IOP in
patients with chronic open-angle glaucoma or ocular
hypertension who have not responded well to other
IOP-lowering agents.
Therapeutic Outcome
The primary therapeutic outcome expected from pros-
taglandin agonists is reduced IOP.
Common and serious adverse effects
Sensory
Conjunctival irritation, burning and stinging, lacrima-
tion. These adverse effects are usually mild and tend to
resolve with continued therapy. Encourage the patient
not to discontinue therapy without rst consulting the
healthcare provider.
Eye pigment changes. The prostaglandin agonists
may gradually cause changes to pigmented tissues,
including change to eye color, increasing the amount
of brown pigment in the iris. The change may take sev-
eral months to years to develop and is thought to be
permanent. Iris pigmentation changes may be more
evident in patients with green-brown, blue-brown,
gray-brown, or yellow-brown irises. The eyelids may
also develop color changes. There may also be an in-
creased growth of eyelashes.
Drug interactions
Thimerosal. A precipitate occurs when eyedrops
containing thimerosal (a commonly used preservative
in ophthalmic solutions) are mixed with latanoprost.
Administer eyedrops at least 5 minutes apart.

Nursing Implications for Prostaglandin Agonists DRUG CLASS: RHO KINASE INHIBITOR
Premedication assessment
1. Obtain baseline vital signs.
netarsudil (ne-TAR-soo-dil)
2. Record the premedication IOP readings and visual
Rhopressa (ro-PRESS-ah)
acuity data.

Table 42.4 Prostaglandin Agonists

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE COMMENTS
bimatoprost Lumigan Solution: 0.01%, 0.03% 1 drop in each Do not exceed dosage because it may
in 2.5-, 5-, 7.5-mL affected eye in the reduce IOP-lowering effect.
dropper bottles evening
latanoprost Xalatan Solution: 0.005% in 1 drop in each Do not exceed dosage because it may
2.5-mL dropper affected eye in the reduce IOP-lowering effect.
bottle evening
tauprost Zioptan Solution: 0.0015% 1 drop in each Do not exceed dosage because it may
in 0.3-mL pouch affected eye in the reduce IOP-lowering effect.
packaged in 10, evening If used with other ophthalmic agents,
30-count containers separate administration by at least 5 min.
travoprost Travatan Z Solution: 0.004% in 1 drop in each Do not exceed dosage because it may
2.5-, 5-mL dropper affected eye in the reduce IOP-lowering effect.
bottles evening
IOP, Intraocular pressure.
692 UNIT IX Drugs Affecting Other Body Systems
Actions
Netarsudil, a rho kinase inhibitor, is a new class of
medications that reduces IOP by increasing trabecular
meshwork outow.
Uses
Netarsudil is used to reduce elevated IOP in patients
with open-angle glaucoma or ocular hypertension. The
role of netarsudil has not been established, but will
likely be used (individually or in combination) in pa-
tients inadequately responding to or intolerant of other
agents used to treat increased IOP. Netarsudil is also
available in combination with latanoprost (Vyzulta).
Therapeutic Outcomes
The primary therapeutic outcome expected from rho
kinase inhibitor use is reduced IOP.
Nursing Implications for Rho Kinase Inhibitors
Premedication assessment
1. Obtain baseline vital signs.
2. Record the premedication IOP readings and visual
acuity data.
3. View the patient’s corneas for any discoloration or
staining from previously used medications. Note
normal or abnormal discoloration in patient records.
Availability. Ophthalmic: 0.02% solution in 2.5 mL
bottles.
Storage. Containers should be stored refrigerated at
36 to 46°F until ready for application. After opening
and applying, store at room temperature (up to 77°F)
for up to 6 weeks before discarding.
Dosage and administration. Elevated IOP: 1 drop into
affected eye(s) daily in the evening. If used in conjunc-
tion with other ophthalmic preparations, wait at least
5 minutes between administration of each medication.
Remove contact lenses before administration and wait
at least 15 minutes after administration before reinsert-
ing contact lenses.
Common adverse effects
Sensory
Conjunctival irritation, hyperemia, lacrimation, blurred vi-
sion, pain during application. These adverse effects are
usually mild and tend to resolve with continued use.
Encourage the patient not to discontinue therapy with-
out rst visiting with the healthcare provider.
Serious adverse effects
Conjunctival hemorrhage, corneal deposits. These ad-
verse effects need to be brought to the attention of the
healthcare provider. Most corneal deposits resolve
with discontinuation of therapy.
Drug interactions. There are no clinically signicant
drug interactions reported.
OTHER OPHTHALMIC AGENTS
DRUG CLASS: ANTICHOLINERGIC AGENTS
Actions
Anticholinergic agents cause the smooth muscle of the
ciliary body and iris to relax, producing mydriasis (ex-
treme dilation of the pupil) and cycloplegia (paralysis
of the ciliary muscle).
Uses
Ophthalmologists use anticholinergic agents for their
pharmacologic effects to examine the interior of the
eye, measure the proper strength of lenses for eye-
glasses (refraction), and rest the eye in inammatory
conditions of the uveal tract.
Therapeutic Outcomes
The primary therapeutic outcomes expected from anti-
cholinergic ophthalmic use are as follows:
1. Visualization of intraocular structures
2. Reduced uveal tract inammation
Nursing Implications for Anticholinergic Agents
Premedication assessment
1. Check for the diagnosis of increased IOP. If pres-
ent, hold the medication and contact the healthcare
provider for approval before instillation of the anti-
cholinergic agent.
2. Take vital signs; if the patient has hypertension, con-
tact the healthcare provider for approval before in-
stilling the anticholinergic agent.
Availability, dosage, and administration
See Table 42.5
Medication Safety Alert
The pharmacologic effects of anticholinergic agents cause
an increase in IOP. Use these agents with extreme caution in
patients with narrow anterior chamber angle; in infants, chil-
dren, and older adults; and in patients with hypertension, hy-
perthyroidism, and diabetes. Discontinue therapy if signs of
increased IOP (i.e., blurred vision, halos around white lights,
frontal headaches and eye pain) or systemic effects develop.
Common adverse effects
Sensory
Sensitivity to bright light. The mydriasis produced al-
lows excessive light into the eyes, causing the patient
to squint. Sunglasses will help reduce the brightness.
Caution the patient to temporarily avoid tasks that re-
quire visual acuity, such as driving or operating power
machinery.
Conjunctival irritation, lacrimation. These adverse effects
are usually mild and tend to resolve with continued
therapy. Encourage the patient not to discontinue ther-
apy without rst consulting the healthcare provider.
 Drugs Used to Treat Glaucoma and Other Eye Disorders CHAPTER 42 693

Table 42.5 Anticholinergic Agents

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE COMMENTS
atropine sulfate Isopto-Atropine Ointment: 1% Uveitis: 1–2 drops up Onset of mydriasis and cycloplegia is
Solution: 1% to three times daily 30–40 min, duration is 7–12 days.
Do not use in infants.
cyclopentolate Cyclogyl Solution: 0.5%, 1%, Refraction: 1 drop For mydriasis and cycloplegia
hydrochloride 2% followed by another necessary for diagnostic procedures;
drop in 5–10 min 1–2 drops of 1%–2% pilocarpine
allows full recovery within 6–24 hr.
CNS disturbances of hallucinations,
loss of orientation, restlessness,
and incoherent speech have been
reported in children.
homatropine Homatropaire Solution: 5% Uveitis: 1–2 drops Onset of mydriasis and cycloplegia is
hydrobromide q3–4h 40–60 min; duration is 1–3 days.
tropicamide Mydriacyl Solution: 0.5%, 1% Refraction: 1–2 drops, Onset of mydriasis and cycloplegia is
repeated in 5 min 20–40 min; duration is 6 hr.
CNS disturbances such as
hallucinations, loss of orientation,
restlessness, and incoherent speech
have been reported in children.
CNS, Central nervous system.

Serious adverse effects species, and Fusarium species. It is effective in treating

Neurologic
Systemic adverse effects. Prolonged use may result
in systemic effects manifested by ushing and dry-
ness of the skin, dry mouth, blurred vision, tachycar-
dia, dysrhythmias, urinary hesitancy and retention,
vasodilation, and constipation. These are indications
of overdose or excessive administration. Report to the
healthcare provider for treatment and dosage adjust-
ment. Prevent systemic effects by carefully blocking the
inner canthus for 3 to 5 minutes after instilling the med-
ication to prevent absorption via the nasolacrimal duct.
Monitor the pulse rate and blood pressure, and instruct
the patient to continue to do this at home; report sig-
nicant changes from the baseline data. Children are
particularly prone to developing systemic reactions.
Drug interactions. No clinically signicant drug inter-
actions have been reported.
DRUG CLASS: ANTIFUNGAL AGENTS
fungal blepharitis, conjunctivitis, and keratitis caused
by susceptible organisms. If little or no improvement is
noted after 7 to 10 days of treatment, resistance to the
antifungal agent may have developed. Topical admin-
istration does not appear to result in systemic effects.
Therapeutic Outcome
The primary therapeutic outcome expected from nata-
mycin is eradication of fungal infection.
Nursing Implications for Natamycin
Premedication assessment
1. Collect ordered cultures or slide smears before initi-
ating drug therapy.
2. Record baseline data relating to symptoms accom-
panying the fungal infection and the degree of
visual impairment.
Availability. Ophthalmic: 5% suspension in 15 mL
bottle.

Dosage and administration. Fungal keratitis: One drop

natamycin (nă-tă-MĪ-sĭn)
Natacyn (NĂT-ă-sĭn)
Actions
Natamycin acts by altering the cell wall of the fungus
to prevent it from serving as a selective barrier, there-
fore causing loss of uids and electrolytes.
Uses
Natamycin is an antifungal agent that is effective against
a variety of yeasts, including Candida species, Aspergillus
in the conjunctival sac at 1- or 2-hour intervals for the
rst 3 to 4 days. The dosage may then be reduced to 1
drop every 3 to 4 hours. Continue therapy for 14 to 21
days.
Fungal blepharitis or conjunctivitis: One drop in the
conjunctival sac every 4 to 6 hours.
Common adverse effects
Sensory
Sensitivity to bright light. The slight mydriasis pro-
duced allows an excessive amount of light into the
694 UNIT IX Drugs Affecting Other Body Systems

Table 42.6 Antiviral Agents

GENERIC
NAME BRAND NAME AVAILABILITY DOSAGE
acyclovir Avaclyr Ointment: 3% Apply a ½ inch ribbon of ointment in the lower cul-de-sac of the affected
eye(s) ve times daily (about every 3 hr while awake) until the corneal
ulcer heals, then three times daily for 7 days
ganciclovir Zirgan Gel: 0.15% Initial dosage: 1 drop in affected eye ve times daily (about q3h while
awake) until the corneal ulcer heals
Maintenance dosage: 1 drop three times daily for 7 days
triuridine — Solution: 1% Intraocular: Place 1 drop onto the cornea of the affected eye q2h during
in 7.5-mL waking hours; do not exceed 9 drops daily
dropper bottle Continue for 7 more days to prevent recurrence, using 1 drop q4h (5 drops
daily)

eyes, causing the patient to squint. Sunglasses will
help reduce the brightness. Caution the patient to
avoid tasks temporarily that require visual acuity, such
as driving or operating power machinery.
Blurred vision, lacrimation, redness. Provide for patient
safety during temporary visual impairment. Instruct
the patient not to rub the eyes forcefully while tear-
ing. These adverse effects are usually mild and tend to
resolve with continued therapy. Encourage the patient
not to discontinue therapy without rst consulting the
healthcare provider.
Serious adverse effects
Sensory
Eye pain. If eye pain develops, discontinue use and
consult an ophthalmologist immediately.
Therapeutic effect. If, after several days of therapy,
the symptoms do not improve or if they gradually
worsen, consult the prescribing healthcare provider
treating the patient.
Drug interactions. No signicant drug interactions
have been reported.
DRUG CLASS: ANTIVIRAL AGENTS
Actions
The ophthalmic antiviral agents act by inhibiting viral
replication.
Uses
Acyclovir, ganciclovir, and triuridine are used to
treat acute herpetic keratitis (dendritic ulcers), kerato-
conjunctivitis, and epithelial keratitis caused by herpes
simplex virus types 1 and 2. Acyclovir is available as an
ointment, ganciclovir as a gel, and triuridine as a solution
for optimal treatment based on location of the infection
in the eye area. These antiviral agents are not effective
against infections caused by bacteria, fungi, or Chlamydia
organisms.
Therapeutic Outcome
The primary therapeutic outcome expected from anti-
viral agents is eradication of the viral infection.
Nursing Implications for Antiviral Agents
Premedication assessment. Record baseline data
concerning the symptoms and the degree of visual
impairment.
Availability, dosage, and administration
See Table 42.6
Storage. Triuridine should be stored in the
refrigerator.
Medication Safety Alert
If signicant improvement has not occurred 7 to 14 days af-
ter initiating treatment with triuridine, other therapy should
be considered. Do not exceed 21 days of continuous thera-
py because of potential ocular toxicity.
Common adverse effects
Sensory
Visual haze, lacrimation, redness, burning. Patients may
notice a mild, transient stinging, burning, and red-
ness of the conjunctiva and sclera on instillation.
Provide for patient safety during temporary visual
impairment. Instruct the patient not to rub the eyes
forcefully while tearing. These adverse effects are
usually mild and tend to resolve with continued
therapy. Encourage the patient not to discontinue
therapy without rst consulting the healthcare
provider.
Sensitivity to bright light. The slight mydriasis pro-
duced allows excessive light into the eyes, causing
the patient to squint. Sunglasses will help reduce the
brightness. Caution the patient to temporarily avoid
tasks that require visual acuity, such as driving or op-
erating power machinery.
Serious adverse effects
Immune system
Allergic reactions. Discontinue therapy and consult
an ophthalmologist immediately.
Drug interactions. No signicant drug interactions
have been reported.
 Drugs Used to Treat Glaucoma and Other Eye Disorders CHAPTER 42 695

DRUG CLASS: OPHTHALMIC ANTIBIOTICS DRUG CLASS: OPHTHALMIC ANTIINFLAMMATORY

Uses
Ophthalmic antibiotics (Table 42.7) are used to treat
supercial eye infections and for prophylaxis against
gonorrhea infection in the eyes of newborn infants
(ophthalmia neonatorum). Prolonged or frequent in-
termittent use of topical antibiotics should be avoided
because of the possibility of hypersensitivity reactions
and the development of resistant organisms, including
fungi. If hypersensitivities or new infections appear
during use, consult an ophthalmologist immediately.
Refer to Chapter 45 for a discussion of these antibiotics.
DRUG CLASS: CORTICOSTEROIDS
Uses
Corticosteroid therapy (Table 42.8) is used for allergic
reactions of the eye and other acute, noninfectious in-
ammatory conditions of the conjunctiva, sclera, cor-
nea, and anterior uveal tract. Corticosteroid therapy
must not be used for bacterial, fungal, or viral infec-
tions of the eye because corticosteroids decrease de-
fense mechanisms and reduce resistance to pathologic
organisms. This therapy should be used only for a lim-
ited time and the eye should be checked frequently for
an increase in IOP. Prolonged ocular steroid therapy
may cause glaucoma and cataracts. Refer to Chapter 37
for further discussion of the corticosteroids.
AGENTS
Flurbiprofen sodium, ketorolac tromethamine, brom-
fenac, nepafenac, and diclofenac sodium are topical
nonsteroidal antiinammatory drugs for ophthal-
mic use. These agents have been shown to have anti-
inammatory, antipyretic, and analgesic activity by
inhibiting the biosynthesis of prostaglandins that are
responsible for an increase in intraocular inammation
and pressure. They also inhibit prostaglandin-mediat-
ed constriction of the iris (miosis) that is independent of
cholinergic mechanisms. Flurbiprofen is used primar-
ily to inhibit miosis during cataract surgery. Diclofenac
sodium, nepafenac, and bromfenac are used to treat
postoperative inammation after cataract extraction.
AVAILABILITY AND DOSAGE
See Table 42.9
DRUG CLASS: ANTIHISTAMINES
Alcaftadine, azelastine, bepotastine, cetirizine, eme-
dastine, epinastine, ketotifen, and olopatadine are
histamine-1 antagonists that act by inhibiting release
of histamine from mast cells. They are used for relief of
signs and symptoms and prevention of itching associ-
ated with allergic conjunctivitis. For best results, they
should be instilled in the eyes before exposure to aller-
gens such as pollen (Table 42.10).

Table 42.7 Ophthalmic Antibiotics DRUG CLASS: ANTIALLERGENIC AGENTS

ANTIBIOTIC BRAND NAME AVAILABILITY Uses
azithromycin AzaSite Drops Cromolyn sodium, lodoxamide, and nedocromil are
bacitracin — Ointment stabilizing agents that inhibit the release of histamine
besioxacin Besivance Drops and the slow-reacting substance of anaphylaxis from
ciprooxacin Ciloxan Drops, ointment mast cells after exposure to specic antigens. They are
used to treat allergic ocular disorders such as vernal
erythromycin — Ointment
keratoconjunctivitis, vernal keratitis, and allergic kera-
gatioxacin Zymaxid Drops toconjunctivitis. Cromolyn sodium is available as a 4%
gentamicin Gentak Drops, ointment
levooxacin — Drops
Table 42.8 Corticosteroids
moxioxacin Moxeza, Vigamox Drops
GENERIC NAME BRAND NAME AVAILABILITY
ooxacin Ocuox Drops
dexamethasone Maxidex Suspension
sulfacetamide Bleph-10 Drops, ointment
— Solution
tobramycin Tobrex Drops, ointment
Ozurdex Implant
ophthalmic
diuprednate Durezol Emulsion
COMBINATION PRODUCTS
uocinolone Retisert Intravitreal implant
trimethoprim- Polytrim Drops
polymyxin B ophthalmic uorometholone FML Ointment
polymyxin Polycin Ointment FML Liquilm Suspension
B-bacitracin loteprednol Lotemax Suspension;
neomycin-polymyxin Neo-Polycin Ointment ointment; gel
B-bacitracin ophthalmic prednisolone Pred Mild Suspension
neomycin-polymyxin Neosporin Solution triamcinolone Triesence Suspension for
B-gramicidin ophthalmic intravitreal injection
696 UNIT IX Drugs Affecting Other Body Systems

solution; 1 or 2 drops are applied in each eye four to six
times daily at regular intervals. Lodoxamide (Alomide)
is available as a 0.1% solution; 1 or 2 drops are ap-
plied in each affected eye four times daily. Nedocromil
(Alocril) is available as a 2% solution; 1 or 2 drops are
applied in each eye twice daily at regular intervals.
DRUG CLASS: DIAGNOSTIC AGENT
uorescein (ŭ-RĔS-ēn)
Uses
Fluorescein is used in tting hard contact lenses and as
a diagnostic aid in identifying foreign bodies in the eye
and abraded or ulcerated areas of the cornea. It is also
useful for evaluating retinal vasculature for abnormal
circulation.
When uorescein is instilled in the eye, it stains the
pathologic tissues green if observed under normal
light and bright yellow if viewed under cobalt blue
light. Fluorescein is available in 0.6- and 1-mg strips
for topical application, and 10% and 25% solutions
for injection into the aqueous humor. The strips have
the advantage of being used once and then discarded.
Product names include Fluorescite, AK-Fluor, BioGlo,
and Ful-Glo.
DRUG CLASS: ARTIFICIAL TEAR SOLUTIONS
Uses
Articial tear solutions mimic natural secretions of the
eye. They provide lubrication for dry eyes and may
be used as lubricants for articial eyes. Most products
contain variable concentrations of methylcellulose,
polyvinyl alcohol, and polyethylene glycol. The dosage

Table 42.9 Ophthalmic Antiinammatory Agents

Generic Name Brand Name Availability Dosage
bromfenac Prolensa 0.07% solution One drop is instilled in the operated eye once or twice daily
BromSite 0.075% and 0.09% (depending on product) beginning 24 hr after cataract surgery for
solution up to 2 wk to treat postoperative pain and inammation.
diclofenac — 0.1% solution One drop is applied to the affected eye four times daily beginning 24
hr after surgery and continuing for 2 wk.
urbiprofen — 0.03% solution Instill 1 drop in the appropriate eye every 30 min, beginning 2 hr
before surgery (for a total of 4 drops).
ketorolac Acular LS 0.4% solution One drop is applied to each eye four times daily to relieve ocular
Acular 0.5% solution itching associated with seasonal allergic conjunctivitis.
This same dose may be applied to the operated eye for pain and
photophobia for up to 3 days after surgery.
nepafenac Nevanac 0.1% suspension Nevanac: One drop is applied to the affected eye(s) three times daily.
Ilevro 0.3% suspension Ilevro: One drop is applied to the affected eye(s) daily.
Both agents should be used beginning 1 day before cataract
surgery; continue the day of surgery and through the rst 2 wk of
the postoperative period for pain and inammation.

Table 42.10 Ophthalmic Antihistamines

GENERIC NAME BRAND NAME AVAILABILITY DOSAGE
alcaftadine Lastacaft Solution: 0.25% in 3-mL dropper bottle Instill 1 drop in each eye once daily.
azelastine — Solution: 0.05% in 6-mL dropper bottle Instill 1 drop in each affected eye twice daily.
bepotastine Bepreve Solution: 1.5% in 5 and 10-mL dropper Instill 1 drop in each affected eye twice daily.
bottle
cetirizine Zerviate Solution: 0.24% in 7.5-, 10-mL dropper Instill 1 drop in affected eye twice daily (∼8 hr
bottle apart).
epinastine — Solution: 0.05% in 5-mL dropper bottles Instill 1 drop in each eye twice daily.
ketotifen Zaditor Solution: 0.025% in 5-, 10-mL dropper Instill one drop in each eye q8–12h.
bottles
olopatadine — Solution: 0.1% in 5-ml dropper bottle;0.2% Instill 1–2 drops in each affected eye twice
in 2.5 mL dropper bottle; 0.7% in 2.5 daily at interval of 6–8 hr.
mL dropper bottle
olopatadine Pataday Solution: 0.2% in 2.5-mL dropper bottle Instill 1 drop in each affected eye once daily.
 Drugs Used to Treat Glaucoma and Other Eye Disorders CHAPTER 42
is 1 to 3 drops in each eye three or four times daily, as
needed. Product names include Systane Ultra, Refresh,
Tears Naturale Free, Articial Tears, and HypoTears.
DRUG CLASS: VASCULAR ENDOTHELIAL GROWTH
FACTOR ANTAGONISTS
Macular degeneration is a deterioration of the macula,
a small area in the retina at the back of the eye that
is required to see ne details clearly (e.g., reading or
threading a needle) or to judge distances (e.g., when
driving an automobile). With macular degeneration,
central vision is affected by blurriness, dark areas, and
distortion. Peripheral vision is usually not affected.
Many older people develop macular degeneration
as part of the body’s natural aging process. The most
common is age-related macular degeneration (AMD).
Why it develops is unknown. Macular degeneration is
the leading cause of severe vision loss in white people
older than 65 years.
The two most common types of AMD are “dry”
(atrophic or nonexudative) and “wet” (neovascular or
exudative).
• Dry macular degeneration (atrophic) is caused by the
aging and thinning of the tissues of the macula.
Vision loss is usually gradual. Most people have the
dry form of AMD.
• Wet macular degeneration (exudative) accounts for
about 10% of all AMD cases. It results when abnor-
mal blood vessels form underneath the retina at the
back of the eye. These new blood vessels leak uid
or blood and blur central vision. Vision loss may be
rapid and severe.
Treatment for both dry and wet AMD consists of
encouraging patients to quit chewing, smoking or
Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• The nurse has an important role to educate the patient
about glaucoma management.
• The nurse is instrumental in educating the public and
promoting safety measures to protect the eyes from
sources of injury.
• Examples of areas in which the nurse can teach the public
are the use of safety glasses in hazardous situations,
prevention of chemical burns from common household
cleaning items or other agents at home or work, proper
cleaning and wearing of contact lenses or glasses, and the
selection of safe toys and play activities for children. These
safety measures can signicantly reduce the number of
injuries that occur annually.
• Nurses instruct patients on proper administration of eye
medications.
• Nurses need to determine that the patient understands how
to prevent eye infections and how eye infections are treated.
697
vaping with nicotine-containing products to avoid
the increased risk of progression to advanced AMD.
For patients with moderate to advanced dry AMD
and patients with wet AMD in one or both eyes, a dai-
ly oral eye vitamin supplement containing vitamin C
500 mg, vitamin E 400 international units, lutein 10
mg, zeaxanthin 2 mg, zinc 80 mg, and copper 2 mg
(e.g., PreserVision) is recommended. It may be effec-
tive for reducing the risk of progression to advanced
AMD.
Pegaptanib (Macugen), aibercept (Eylea), beva-
cizumab, brolucizumab (Beovu), and ranibizumab
(Lucentis) are selective vascular endothelial growth
factor (VEGF) antagonists used to treat wet AMD.
VEGF is secreted and binds to its receptors, which
are located primarily on the surface of endothe-
lial cells of blood vessels. VEGF induces new blood
vessel growth and increases vascular permeability
and inammation, all of which are thought to con-
tribute to the progression of the wet form of AMD.
Pegaptanib, aibercept, bevacizumab, brolucizumab,
and ranibizumab are antagonists that bind to extra-
cellular VEGF, preventing it from binding to VEGF
receptors and thus preventing it from forming new
blood vessels. Pegaptanib is injected into the vitreous
humor of the affected eye once every 6 weeks; aiber-
cept is administered every 4 weeks for the rst 12
weeks, then every 8 weeks thereafter. Bevacizumab,
brolucizumab, and ranibizumab are administered
once monthly. In the days after administration of an
agent, patients are at risk for the development of en-
dophthalmitis. Instruct the patient to seek immediate
care from their ophthalmologist if the eye becomes
red, sensitive to light, or painful or if a deterioration
of vision is noted.
• The prostaglandin agonists bimatoprost, latanoprost,
tauprost, and travoprost are often the initial drugs used
to treat open-angle glaucoma. The prostaglandin agonists
may gradually cause changes to pigmented tissues,
including change to eye color, increasing the amount of
brown pigment in the iris.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
The following questions are typical of the NCLEX exam and in-
clude both NGN (Next Generation) and traditional questions.
See Chapter 1 for further information regarding question types.
698 UNIT IX Drugs Affecting Other Body Systems

Scenario 4. Choose the most likely options for the information missing from the
following sentence by selecting from the lists of options provided.
A patient made an appointment to see the eye doctor related
to gradual loss of peripheral vision. After the examination the The nurse will instruct the patient in the scenario, who
patient was diagnosed with open-angle glaucoma and was was started on a second agent, on adverse effects of
prescribed an eyedrop medication for use. ________1________and ______1________while taking
dorzolamide (Trusopt) and timolol (Timoptic) for glaucoma
1. The nurse explained the proper technique for instilling eyedrops which are from the drug class ________2_______ and
for the patient in the scenario with open-angle glaucoma. Which _______2__________, respectively.
statements by the nurse are appropriate for teaching the patient
about proper administration of eye drops? (Select all that apply.)
1. “You will need to tilt your head back so that the eyedrop OPTION 1 OPTION 2
can be properly administered.” hypertension carbonic anhydrase inhibitor
2. “After the eye drop had been administered you will need
to keep your eyes closed.” hypokalemia prostaglandin agonists
3. “If you provide gentle pressure at the inner canthus to hyperthyroidism beta-adrenergic blocking
block the tear duct the medication stays in your eye.” agents
4. “If you wear contact lenses you will need to put them in bronchospasms alpha-adrenergic agents
before administration.”
5. “When you have more than one agent to use for
glaucoma, you will need to space the drops by at least 5 Objective: Identify patient teaching needs for patients with
minutes to provide proper absorption.” glaucoma.
Objective: Identify patient teaching needs for patients with NCLEX item type: Cloze
glaucoma. Cognitive skill: Analyze cues
NCLEX item type: Multiple response 5. The nurse providing postoperative instructions for a patient after
Cognitive skill: Application eye surgery will include which of these statements? (Select all that
2. The nurse is instructing the patient in the scenario who is being apply.)
started on timolol maleate (Timoptic). Which statement by the 1. “You will need to notify your healthcare provider when
nurse is appropriate? any eye pain is not relieved by pain medication.”
1. “This medication will inhibit the release of histamine so 2. “You can resume normal activities but be careful with
you will not have itchy eyes.” operating power tools or driving if there is still some
2. “These eyedrops are used to treat your glaucoma by decreased vision.”
reducing the formation of aqueous humor.” 3. “You need to use aseptic technique when changing
3. “These drops can be used for examination purposes dressings or administering medications.”
because they will cause the pupil to dilate.” 4. “Please be sure to call your healthcare provider with any
4. “This medication can reduce redness of the eyes caused signs of infection in your eye.”
by irritation.” 5. “Remember to store your eyedrops with other containers
that look alike, so you do not lose them.”
Objective: Discuss the medications used in the management of
open-angle glaucoma. Objective: Identify patient teaching needs for patients with
NCLEX item type: Multiple choice glaucoma.
Cognitive skill: Comprehension NCLEX item type: Multiple response
Cognitive skill: Application
3. Before administering a beta-adrenergic blocking agent to the
patient in the scenario for reduction of intraocular pressure, the
nurse should assess the patient for a history of which disorders?
(Select all that apply.)
1. Peptic ulcer disease
2. Diabetes mellitus
3. Hypertension
4. Urinary retention
5. Dysrhythmia
6. Hyperlipidemia
7. Asthma
8. Bradycardia
9. Psoriasis
10. Hyperthyroidism
Objective: Explain patient assessments needed for eye disorders.
NCLEX item type: Extended multiple response
Cognitive skill: Recognize cues
Drugs Used to Treat Cancer
Objectives
1. Discuss the goals of chemotherapy.
2. Describe the role of targeted anticancer agents in treating
cancer.
3. Identify how chemoprotective agents are used in treating
cancer.
Key Terms
cancer (KĂN-sŭr) (p.699) malignant (mă-LĬG-nănt) (p. 699)
metastases (mĕ-TĂS-tă-sēz) (p. 699) palliation (păl-ē-Ā-shŭn) (p. 701)
neoplastic disease (nē-ō-PLĂS-tĭk combination therapy (kŏm-bĭ-NĀ-
dĭs-ĒZ) (p. 699) shŭn THĀR-ŭ-pē) (p. 701)
CANCER AND THE USE OF
ANTINEOPLASTIC AGENTS
Cancer is a group of more than 100 different diseases
that are characterized by uncontrolled cellular growth,
local tissue invasion, and distant metastases (Chabner,
2010). It is a group of once-normal cells that have mu-
tated to abnormal cells that generally multiply more
rapidly than normal cells, lose the ability to perform
specialized functions, invade surrounding tissues, and
develop growths in other tissues distant to the site of
original growth (metastases). Cancer is also referred
to as a neoplasm, neoplastic disease, or new growth. The
new growth may be subdivided into benign or ma-
lignant cells. Because benign cells do not metastasize,
they are generally not as life threatening as the malig-
nant cells. Malignant cells often metastasize to other or-
gans of the body, making treatment and survival sub-
stantially less likely.
The American Cancer Society reported that the rates
of cancer occurrences and deaths have decreased from
an all-time high in the year 1991. As of 2017 the rate
has dropped by 29% as a result of reductions in smok-
ing and improvements in detection and treatment.
Cancer is the second most common cause of death
in the United States, exceeded only by heart disease
(Fig. 43.1). In 2020 it was estimated that there were
1.8 million new cancer cases and almost 606,000
deaths from cancer, which is about 1660 deaths per
day.
43
https://evolve.elsevier.com/Willihnganz
4. Discuss bone marrow stimulants and their effect and use.
5. Describe the nursing assessments and interventions
needed to help alleviate the adverse effects of
chemotherapy.
targeted anticancer agents (TĂR-
gĕt-ĕd ăn-tē-KĂN-sŭr) (p. 703)
chemoprotective agents (kē-mō-
prō-TĔK-tĭv) (p. 703)
Cancers can occur anywhere in the body: within
organs (e.g., liver, colon, lungs); within blood compo-
nents (e.g., lymphatic system) causing lymphoma; and
within bone marrow, causing leukemias. Treatment
of cancer often requires a combination of surgery, ra-
diation, chemotherapy, targeted drug therapy, and
biologic therapy. Targeted agents are small molecules
that inhibit enzymes (enzymes are proteins that cause
chemical reactions in living cells) responsible for the
activation of various proteins that form intracellular
signaling cascades. These agents treat cancer by cor-
recting a dysregulated signaling pathway. Biologic
therapies are made from a living organism or its by-
products and include antibodies, vaccines, growth fac-
tors, and cytokines. The biologic therapies classied
as antibodies recognize an antigen that is expressed
preferentially on cancer cells or immune cells or tar-
gets growth factors responsible for cancer growth.
Surgery and radiation are considered to be local thera-
py, whereas chemotherapy, targeted drug therapy, and
biologic therapies use the systemic circulation to treat
the primary tumor and metastases. Recent advance-
ments in understanding carcinogenesis, cellular and
molecular biology, genetics, and tumor immunology
have enhanced the role that antineoplastic agents may
play in treatment. It is beyond the scope of this chapter
to delve into the interrelationships of chemotherapy
and neoplastic disease; however, a short discussion of
the concepts of cancer chemotherapy will be presented.
699
700 UNIT IX Drugs Affecting Other Body Systems

Male Female
Prostate 164,690 19% Breast 266,120 30%
Lung & bronchus 121,680 14% Lung & bronchus 112,350 13%
Estimated New Cases

Colon & rectum 75,610 9% Colon & rectum 64,640 7%

Urinary bladder 62,380 7% Uterine corpus 63,230 7%
Melanoma of the skin 55,150 6% Thyroid 40,900 5%
Kidney & renal pelvis 42,680 5% Melanoma of the skin 36,120 4%
Non-Hodgkin lymphoma 41,730 5% Non-Hodgkin lymphoma 32,950 4%
Oral cavity & pharynx 37,160 4% Pancreas 26,240 3%
Leukemia 35,030 4% Leukemia 25,270 3%
Liver & intrahepatic bile duct 30,610 4% Kidney & renal pelvis 22,660 3%
All sites 856,370 100% All sites 878,980 100%

Male Female
Lung & bronchus 83,550 26% Lung & bronchus 70,500 25%
Prostate 29,430 9% Breast 40,920 14%
Colon & rectum 27,390 8% Colon & rectum 23,240 8%
Estimated Deaths

Pancreas 23,020 7% Pancreas 21,310 7%

Liver & intrahepatic bile duct 20,540 6% Ovary 14,070 5%
Leukemia 14,270 4% Uterine corpus 11,350 4%
Esophagus 12,850 4% Leukemia 10,100 4%
Urinary bladder 12,520 4% Liver & intrahepatic bile duct 9,660 3%
Non-Hodgkin lymphoma 11,510 4% Non-Hodgkin lymphoma 8,400 3%
Kidney & renal pelvis 10,010 3% Brain & other nervous system 7,340 3%
All sites 323,630 100% All sites 286,010 100%
Estimates are rounded to the nearest 10, and cases exclude basal cell and squamous cell skin cancers and in situ carcinoma except urinary bladder. Ranking is based on
modeled projections and may differ from the most recent observed data.
©2018, American Cancer Society, Inc., Surveillance Research

Fig. 43.1 Leading sites of new cancer cases and deaths—2020 estimates. (Data from American Cancer Society. Cancer
Facts & Figures 2020. Atlanta: American Cancer Society; 2020. Retrieved from Siegel RL, Miller KD, Cancer statistics,
2020. https://doi.org/10.3322/caac.21590)

again when the cell is divided into two daughter

S cells. The daughter cells may advance again into the
G1
G0
(resting phase)
M
Fig. 43.2 The cell cycle. G0, Resting phase; G1, gap 1 phase; G2, gap
2 phase; M, mitosis; S, synthesis.
As a result of rapidly changing approaches to the treat-
ment of specic malignancies and the changing nature
of chemotherapeutic regimens, specic agents and
dosages will not be discussed.
All cells, whether normal or malignant, pass
through a similar series of phases during their lifetime,
although duration of time spent in each phase differs
with the type of cell (Fig. 43.2). The cell cycle involves
ve stages: DNA replication (S phase), cell division (M
phase), two resting phases (G1 and G2), and a resting
(nondividing state [G0]) phase. The cell cycle begins
same cycle. The time required to complete one cycle is
termed the generation time.
Many antineoplastic agents are cell cycle specic
G2 (i.e., the drug is selectively toxic when the cell is in a
specic phase of growth and therefore is schedule de-
pendent). Malignancies most amenable to cell cycle–
specic chemotherapy are those that proliferate or
grow very rapidly. Cell cycle–nonspecic drugs are
active throughout the cell cycle and may be more ef-
fective against slowly proliferating neoplastic tissue.
These agents are not schedule dependent but are dose
dependent. One implication of cell cycle specicity is
the importance of correlating the dosage schedule of
anticancer therapy with the known cellular kinetics of
that type of neoplasm. Drugs are usually administered
when the cell is most susceptible to the cytotoxic ef-
fects of the agent for a higher “kill rate” of neoplastic
cells.
DRUG THERAPY FOR CANCER
The overall goal of cancer chemotherapy is to give a
dose large enough to be lethal (cytotoxic) to the cancer
cells but small enough to be tolerable for normal cells.
It is hoped that a long-term survival or cure can be
achieved by this means. A second goal may be control

of the disease (arresting tumor growth). When a cancer
is beyond control, the goal of treatment may be pallia-
tion (alleviation) of symptoms (e.g., administration of
chemotherapy to reduce tumor size for easier breathing
in a patient with lung cancer). Finally, in some types of
cancer in which no tumor is detectable yet the patient
is known to be at risk of developing a particular cancer
or having recurrence of a cancer, prophylactic surgery
and/or chemotherapy may be administered.
Chemotherapy is most effective when the tumor
is small and the cell replication is rapid. Cancer cells
are the most sensitive to chemotherapy when the
cells are dividing rapidly. This is when phase-specic
drugs are most effective. As a tumor enlarges, more of
the cells are in the resting phase. These cells respond
better to phase-nonspecic chemotherapeutic agents.
Combination therapy, using cell cycle–specic and cell
cycle–nonspecic agents, is superior in therapeutic ef-
fect than the use of single-agent chemotherapy. The
use of combination drug therapy allows for cell death
during different phases of the cell cycle, but the agents
often have toxic effects on different organs at different time
intervals after administration. The choice of chemo-
therapeutic agents depends on the type of tumor cells,
their rate of growth, and the size of the tumor.
The traditional major groups of chemotherapeutic
agents have been classied as alkylating agents, anti-
metabolites, mitotic inhibitors, antineoplastic anti-
biotics, hormones, and topoisomerase inhibitors but
now include the small molecule targeted agents (tyro-
sine kinase inhibitors, polyadenosine diphosphate ri-
bose polymerase [PARP] inhibitors, cyclin-dependent
kinases 4 and 6 inhibitors, and proteasome inhibi-
tors), checkpoint inhibitors, and the biologic therapies
(Table 43.1).
ALKYLATING AGENTS
Alkylating agents are highly reactive chemical com-
pounds that bond with DNA molecules, causing
cross-linking of DNA strands. The interstrand bind-
ing prevents the separation of the double-coiled
DNA molecule that is necessary for cellular division.
Alkylating agents are cell cycle nonspecic, which
means that they are capable of combining with cellular
components at any phase of the cell cycle. Generally,
the development of resistance to one alkylating agent
imparts cross-resistance to other alkylators. Examples
of alkylating agents are busulfan, cisplatin, and
cyclophosphamide.
ANTIMETABOLITES
Antimetabolites (subclassied as folic acid, purine, and
pyrimidine antagonists) inhibit key enzymes in the
biosynthetic pathways of DNA and RNA synthesis.
These agents interfere with the ability of the neoplastic
cell to multiply. Many of the antagonists are cell cycle
specic, killing cells during the S phase of cell matu-
ration. Unfortunately, these agents are not selective to
Drugs Used to Treat Cancer CHAPTER 43 701
cancer cells, killing rapidly growing normal cells as
well. Their most common side effects are secondary
to injury to normal cells, such as bone marrow cells
and hair follicle cells. Examples of antimetabolites are
6-mercaptopurine, capecitabine, methotrexate, and
uorouracil.
MITOTIC INHIBITORS
Mitotic inhibitors are cell cycle–specic agents that
block the formation of the mitotic spindle during mi-
tosis, thus inhibiting cell division. Even though there
is close structural similarity, cross-resistance does not
usually develop between the two agents. Vincristine
and vinblastine are examples of natural derivatives of
the periwinkle plant. Other commonly used mitotic in-
hibitors include docetaxel and paclitaxel.
ANTINEOPLASTIC ANTIBIOTICS
Antineoplastic antibiotics bind to DNA, inhibiting DNA
or RNA synthesis; this eventually inhibits protein syn-
thesis, preventing cell replication. They also inhibit
topoisomerase II, daunorubicin, and doxorubicin that
are cell cycle–nonspecic antineoplastic antibiotics.
HORMONES
Hormones play a major role in cancer chemotherapy.
Corticosteroids (usually prednisone) may be benecial
in treating lymphomas and acute leukemia because of
their lympholytic effects and ability to suppress mito-
sis in lymphocytes. Steroids are also used to help re-
duce inammation and edema secondary to radiation
therapy. As palliative therapy, corticosteroids are used
to temporarily suppress fever, diaphoresis, and pain
and to restore—to some degree—appetite, weight,
strength, and a sense of well-being in critically ill pa-
tients. With symptomatic relief, it is hoped that the
patient’s general physical condition may be improved
sufciently to permit further denitive therapy.
Although estrogens and androgens may be used
for breast or prostate cancer, they are seldom used.
Agents such as aromatase inhibitors (e.g., anastro-
zole) or tamoxifen are now used for breast cancer.
Antiandrogens (e.g., enzalutamide) and luteinizing
hormone–releasing hormone agonists (e.g., leuprolide)
are used for prostate cancer.
TOPOISOMERASE INHIBITORS
Topoisomerase inhibitors interfere with enzymes
called topoisomerases, which help separate the strands
of DNA so they can be copied. Irinotecan and etopo-
side are examples of topoisomerase inhibitors.
TYROSINE KINASE INHIBITORS
Tyrosine kinase inhibitors compete with adenosine
5-triphosphate (ATP) and inhibit tyrosine kinase, an
enzyme that can transfer a phosphate group from ATP
to a protein in a cell. There are several examples of
these drugs such as getinib, erlotinib, and sorafenib.
702 UNIT IX Drugs Affecting Other Body Systems

Table 43.1 Selected Chemotherapy and Immunotherapy Medications

CLASS AGENT SELECTED CLINICAL USE
Alkylating agents busulfan CML
cisplatin Bladder, breast, lung, ovarian, testicular cancers, non-
Hodgkin lymphoma
cyclophosphamide Breast, CLL, ALL, non-Hodgkin lymphoma
Antimetabolites 6-mercaptopurine ALL
capecitabine Breast, colorectal cancer
uorouracil Breast, colorectal, and skin cancer
methotrexate ALL, breast, bladder cancer, lymphoma, osteosarcoma
Mitotic inhibitors docetaxel Breast, NSCLC, prostate cancer
paclitaxel Breast, ovarian, NSCLC
vinblastine Hodgkin lymphoma, Kaposi sarcoma
vincristine ALL, Hodgkin’s Lymphoma, neuroblastoma
Antineoplastic antibiotics daunorubicin ALL, AML
doxorubicin Breast, ovarian cancer, ALL, AML
Hormones anastrozole Breast cancer
enzalutamide Prostate cancer
leuprolide Prostate cancer
tamoxifen Breast cancer
Topoisomerase inhibitors etoposide SCLC, testicular cancer
irinotecan Colorectal cancer
Tyrosine kinase inhibitors erlotinib NSCLC
getinib NSCLC
sorafenib Renal cell carcinoma, mantle cell lymphoma
Polyadenosine diphosphate ribose olaparib Breast, ovarian, pancreatic, prostate cancer
polymerase inhibitors (PARP inhibitors) rucaparib Ovarian, prostate cancer
Cyclin-dependent kinases 4/6 inhibitors palbociclib Breast cancer
ribociclib Breast cancer
Proteasome inhibitors bortezomib Multiple myeloma, mantle cell lymphoma
carlzomib Multiple myeloma
ixazomib Multiple myeloma
Checkpoint inhibitors atezolizumab SCLC, NSCLC, breast cancer
ipilimumab Colorectal cancer, melanoma, NSCLC
nivolumab Melanoma, NSCLC, esophageal cancer
pembrolizumab Melanoma, NSCLC, gastric cancer
ALL, Acute lymphocytic leukemia; AML, acute myeloid leukemia; CLL, chronic lymphocytic leukemia; CML, chronic myeloid leukemia; NSCLC, non–small cell lung
cancer; SCLC, small cell lung cancer.

POLYADENOSINE DIPHOSPHATE RIBOSE
POLYMERASE INHIBITORS
PARP inhibitors are the enzymes responsible for cell
activity such as DNA repair, genomic stability, and
programmed cell death. These inhibitors are used for
treatment of ovarian, pancreatic, prostate and breast
cancer. Olaparib and rucaparib are examples of PARP
inhibitors.
CYCLIN-DEPENDENT KINASES 4/6 INHIBITORS
Cyclin-dependent kinases 4 and 6 are enzymes im-
portant in the cell cycle as it moves from the G1 to the
S phase. The inhibitor drugs stop the cell cycle from
progressing. These inhibitors are used for treatment
of metastatic breast cancer. Palbociclib and riboci-
clib are examples of cyclin-dependent kinases 4/6
inhibitors.
PROTEASOME INHIBITORS
Proteasome inhibitors are drugs that block the action
of proteasomes, which are part of cellular complexes
that break down proteins. Bortezomib, carlzomib,
and ixazomib are proteasome inhibitors approved to
treat multiple myeloma.

CHECKPOINT INHIBITORS
Immune checkpoints are proteins on immune cells
called T cells that need to be activated (or inactivated)
to start an immune response. Cancers cells can send an
“off” signal to the T cells and can prevent the immune
system from destroying the cancer. Checkpoint inhibi-
tors target these checkpoint proteins (programmed cell
death protein 1 [PD-1], programmed death ligand 1
[PD-L1], and cytotoxic T-lymphocyte-associated pro-
tein 4 [CTLA-4]). Nivolumab and pembrolizumab
blocks PD-1, atezolizumab blocks PD-L1, and ipilim-
umab blocks CTLA-4. They are used to treat several
types of cancers, such as melanoma, non–small lung
cancer, and small cell lung cancer.
BIOLOGIC THERAPIES
Biologic therapies, also known as targeted antican-
cer agents, include cytokines, monoclonal antibodies,
growth factors, and vaccines. They evolved from re-
search indicating that cell membrane receptors control
cell proliferation, cell migration, angiogenesis (new
blood vessel growth), and cell death that are integral to
the growth and spread of cancer. Many of the biologic
therapies act on receptors, such as epidermal growth
factor receptors (EGFRs) (e.g., human epidermal
growth factor receptor-2 [HER-2]), platelet-derived
growth factor, and vascular endothelial growth factor
(VEGF). Targeted anticancer agents are noncytotoxic
drugs that target the key pathways (e.g., EGFR, VEGF)
that provide growth and survival advantages for can-
cer cells, while not assaulting normal cells. These path-
ways are relatively specic for cancer cells; theoretical-
ly, targeted agents are not associated with the severe
toxicities common with cytotoxic chemotherapy, but
allergic reactions are more common because many of
the products are derived from foreign proteins.
OTHER AGENTS
As new pathways of tumor cell metabolism are identi-
ed, however, not all agents will t into these classes.
The mechanisms whereby these agents cause cell death
have not been fully determined in all cases.
Two other groups of medicines, chemoprotective
agents and bone marrow stimulants, have become
available to help protect normal human cells from
chemotherapy and help stimulate the normal body de-
fense mechanism. Chemoprotective agents (Table 43.2)
help reduce the toxicity of chemotherapeutic agents to
normal cells. Both targeted agents (described earlier)
and chemoprotective agents allow the use of full thera-
peutic doses of chemical chemotherapies to attack the
cancer. Bone marrow stimulants (Table 43.3) are also
used in supporting persons undergoing cancer treat-
ment and in bone marrow transplantation of healthy
cells. Several types of cancer (e.g., leukemias, lympho-
mas) are treated by chemotherapeutic agents that kill
bone marrow cells while killing the cancer cells. The
bone marrow stimulants trigger the recovery of the
Drugs Used to Treat Cancer CHAPTER 43 703
bone marrow cells several days earlier than would
happen in the natural course of recovery. The major
benet to this earlier recovery is that patients’ immune
systems are able to respond to and stop infections from
being pathologic, and thus patients can be released
from isolation rooms several days earlier. Cancers and
other diseases (chronic renal failure, anemia of chronic
disease) also cause anemia, which can be very debili-
tating to the patient. Darbepoetin and epoetin stimu-
late the bone marrow to produce red blood cells to
treat anemia.
A routine complication of chemotherapy is nausea
and vomiting. See Chapter 33 for more information.
SAFETY WHEN USING CHEMOTHERAPY
Guidelines for the safe handling of chemotherapeutic
agents by healthcare providers include measures to
prevent inhalation of aerosols, prevention of drug
absorption through the skin, safe disposal, and pre-
vention of contamination of body uids. Many chemo-
therapeutic agents may induce cancers in healthy
individuals. Chemotherapy should only be mixed in
the pharmacy department using vertical-ow laminar
hoods and other sterile precautions.
Chemotherapy is individualized to the patient and
is often prescribed according to the patient’s calculated
body surface area (m2) and type of cancer.
NURSING IMPLICATIONS FOR CHEMOTHERAPY
Assessment
History of risk factors
• Ask for age, gender, and race. Take a family history
of the incidence of cancer.
• Ask about job-related exposure to known chemical
carcinogens (e.g., benzene, vinyl chloride, asbestos,
soot, tars, oils).
• Ask about exposure to chewing, smoking or vap-
ing tobacco products and tobacco smoke. Obtain a
history of the use of smokeless tobacco or the num-
ber of cigarettes or cigars smoked daily. How long
has the person smoked? Has the person ever tried
to stop smoking? How does the person feel about
modifying their smoking habit? Is there chronic ex-
posure to secondhand smoke at home or at work?
• Ask about a drug history to obtain information on
pharmacologic agents that have the potential to
become carcinogens (e.g., diethylstilbestrol, cyclo-
phosphamide, melphalan, azathioprine).
• Ask about a history of viral diseases suspected of
being associated with carcinogenesis (e.g., Epstein-
Barr virus, hepatitis B virus, human immuno-
deciency virus, human papillomavirus).
• Is there a history of exposure to, or treatment with,
radiation?
Dietary habits
• Take a dietary history. Ask specic questions to
obtain data relating to foods eaten that are high in
704 UNIT IX Drugs Affecting Other Body Systems

Table 43.2 Chemoprotective Agents

GENERIC NAME BRAND NAME MAJOR INDICATIONS
amifostine Ethyol Amifostine is a prodrug that is metabolized by enzymes in tissues to a free
thiol metabolite that can reduce the toxic effects of cisplatin. Normal tissue
has a higher afnity for the free thiol. The higher concentration of free thiol in
normal tissues is available to bind to and detoxify the reactive metabolites of
cisplatin, reducing damage to normal tissues. Amifostine is used to reduce the
cumulative renal toxicity associated with the repeated administration of cisplatin
in patients with advanced ovarian cancer and non–small cell lung cancer. It
is also used to reduce the incidence of xerostomia in patients undergoing
postoperative radiation treatment for head and neck cancer.
dexrazoxane Totect Dexrazoxane is an intracellular chelating agent used in conjunction with
doxorubicin. It is used to reduce the incidence and severity of cardiomyopathy
associated with doxorubicin in women with metastatic breast cancer who have
received a cumulative doxorubicin dose of 300 mg/m2 and who would benet
from continuing doxorubicin therapy.
glucarpidase Voraxaze Glucarpidase is used in the treatment of toxic plasma methotrexate
concentrations. It breaks down methotrexate into inactive metabolites that are
then eliminated from the body.
leucovorin — Leucovorin is administered hours after high-dose methotrexate chemotherapy
to prevent methotrexate toxicity (commonly referred to as leucovorin rescue).
Leucovorin may also be administered as an antidote to an inadvertent
overdose of methotrexate, pemetrexed, or pralatrexate chemotherapy.
mesna Mesnex Mesna is a prodrug that is metabolized by enzymes in kidney tissue to a
free thiol metabolite that can reduce the toxic effects of ifosfamide and
cyclophosphamide. The free thiol binds and deactivates the toxic metabolites
of ifosfamide and cyclophosphamide. Mesna is used as a prophylactic agent
to reduce the incidence of ifosfamide- and cyclophosphamide-induced
hemorrhagic cystitis.

Table 43.3 Bone Marrow Stimulants

GENERIC NAME BRAND NAME MAJOR INDICATIONS
darbepoetin alfa Aranesp Darbepoetin stimulates erythropoiesis (production of red blood cells [RBCs]).
Do not confuse It is used to treat anemia in patients receiving chemotherapy and anemia
Aranesp with Aricept associated with chronic kidney disease. Increased hemoglobin levels are not
or Arimidex. generally observed until 2–6 wk after initiating treatment with darbepoetin.
Darbepoetin is administered by weekly subcutaneous injection.
epoetin alfa Procrit, Epogen Epoetin alfa stimulates production of RBCs. It is used to treat anemia in
patients with chronic renal failure or those receiving chemotherapy. Epoetin is
administered by subcutaneous or IV injection three times weekly.
lgrastim Neupogen Filgrastim is also known as a human granulocyte colony-stimulating factor
(G-CSF). It stimulates production of neutrophilic white blood cells. It is
used to reduce the neutropenia interval in bone marrow transplantation, to
stimulate white blood cell production in patients receiving myelosuppressive
chemotherapy, and to treat neutropenia in acute myelogenous leukemia. It
is also used to increase the yield of peripheral blood progenitor cells prior to
bone marrow ablation; lgrastim is administered, and peripheral progenitor
cells are harvested and then readministered after bone marrow ablation for a
more rapid recovery of the bone marrow.
peglgrastim Neulasta Peglgrastim and lgrastim have the same mechanism of action. Peglgrastim
has reduced renal clearance and prolonged duration of action compared with
lgrastim.
sargramostim Leukine Sargramostim is also known as granulocyte-macrophage colony-stimulating
factor (GM-CSF). It stimulates production of granulocytes and macrophages,
increases the cytotoxicity of monocytes toward certain neoplastic cell lines,
and activates polymorphonuclear neutrophils to inhibit the growth of tumor
cells. Sargramostim is used to accelerate bone marrow transplant recovery,
correct neutropenia in patients with aplastic anemia, and stimulate bone
marrow recovery in patients receiving myelosuppressive chemotherapy.
Do not confuse.

fat or in animal protein (especially red meats; salt-
cured, smoked, or charcoaled foods; and nitrate and
nitrite additives). Are whole grains included in the
diet? How many servings of fruits and vegetables
are eaten daily? What types of vegetables are eaten
daily? Estimate the number of calories consumed
per day.
• Ask the patient about normal eating patterns, food
likes and dislikes, and elimination pattern.
• Ask whether certain foods cause bloating, indiges-
tion, or diarrhea, and how much seasoning and
spices are put on food.
• What is the usual uid intake daily? How much
coffee, tea, soda (soft drinks), and fruit juice is con-
sumed? Determine the frequency and volume of al-
coholic beverages consumed.
• Is the person experiencing anorexia, nausea, and
vomiting? If so, what measures are being used to
control these symptoms?
• Obtain a baseline height and weight. Has there been
a weight gain or loss in the past year?
• Obtain details of any symptoms that are affecting
the individual’s ability to eat (e.g., anorexia, vomit-
ing, diarrhea, smells that deter eating, pain).
Preexisting health problems. Ask about any pre-
existing health problems for which the patient is, or
has been, receiving treatment. Continue treatment of
any preexisting health problems (e.g., angina, heart
failure, asthma).
Understanding of the diagnosis
• Ask the patient to explain their understanding of
the current diagnosis and plan of treatment.
• Review the admission notes or old charts to deter-
mine the details relating to the diagnostic test data,
type of cancer, staging of the disease, laboratory val-
ues, and treatments to date (Box 43.1).
Adaptation to the diagnosis
• Determine whether this is the initial or a subsequent
cycle of chemotherapy. Gather data regarding the
patient’s and signicant others’ understanding of
the disease and the planned course of treatment.
• Ask how the patient normally copes with stressful
situations. Does the patient have a condante who
is supportive and understanding?
• Observe both the verbal and nonverbal messages
conveyed during the interview. Take note of the pa-
tient’s general appearance, tone of voice, inections,
and gestures. Try to pick up on subtle clues and con-
rm their meanings with the patient.
• Inquire regarding psychological issues that the pa-
tient is perceiving, such as loss of control, loss of
self-esteem, loss of body parts, change in lifestyle,
and/or guilt.
• Review the healthcare provider’s progress notes for
information being given to the patient and family
throughout the course of treatment.
Drugs Used to Treat Cancer CHAPTER 43 705
Box 43.1 Cancer Care
Nursing assessments that apply to the patient undergoing
chemotherapy include the following:
1. Pain management: Work with the healthcare provider
to manage pain.
2. Ability to perform activities of daily living: Encourage
self-care as tolerated.
3. Activity tolerance: Whether bedbound or chairbound.
4. Appetite: Encourage small amounts and favorite foods.
5. Oral care: Use soft brush or soft cloth, mouthwash
with viscous lidocaine. Use a mucositis scale for
oral assessment. If dry mouth is present, consider
lubricating and moisturizing agents, sugarless gum,
Campho-Phenique, and protect from trauma (see
Chapter 31 for further discussion).
6. Allow rest periods: Fatigue is common with normal
activities.
7. Determine IV access: Implanted infusion ports such as
tunneled Hickman catheter or Port-A-Cath implantable
infusion port (see Chapter 11 for further discussion).
8. Observe for any impaired skin integrity: From pressure
injuries to excoriation from diarrhea.
Psychomotor functions
• Ask the patient to describe exercise levels in terms
of amount tolerated, the degree of fatigue pres-
ent, and the ability to perform activities of daily
living.
• Is the patient having difculty performing normal
roles (e.g., homemaker, provider, mother, father)?
• Refer the patient and family to social services for
needed guidance and support personnel to assist
in the management of problems such as inability to
work and need for home care.
Safety. Assess for weakness, confusion, orthostatic
hypotension, or similar symptoms that could signal
impending potential for injury.
Symptoms of pharmacologic adverse effects. Ask
specic questions to determine whether the individual
has been or is experiencing symptoms associated with
the type of drugs being administered, such as myelo-
suppression, anemia, bleeding, stomatitis (mucositis),
altered bowel patterns (e.g., diarrhea, constipation),
alopecia, neurotoxicity, anorexia, nausea, or vomiting.
Physical assessment
• Perform a baseline physical, psychosocial, and spir-
itual assessment of the individual to serve as the
database for ongoing assessments throughout the
course of care.
• Throughout the course of therapy, perform daily as-
sessments of the physical, psychosocial, and spiri-
tual needs of the individual and family. Perform a
focused assessment on the body systems affected by
the disease process and those likely to be affected by
metastasis (e.g., lungs, brain, bone, liver).
706 UNIT IX Drugs Affecting Other Body Systems
Sexual assessment. Discuss birth control and repro-
ductive counseling issues at the time of initiation of
therapy. Male patients may wish to use a sperm bank.
Female patients may wish to harvest eggs. A contra-
ceptive method should be discussed.
Smoking. Discuss tobacco product use (smoking,
chewing, vaping) with the patient and plan a mutually
agreeable way to handle this habit, both while hospital-
ized and when at home. Does the patient wish to modi-
fy the habit? Provide smoking cessation education.
Pain. Ask whether the person is having any pain and
what interventions are being used to manage the pain.
Obtain a rating of pain level and the degree of relief
being gained from current medications and supportive
practices (e.g., relaxation or guided imagery).
Implementation
• Implement planned interventions consistent with
assessment data and identied individual needs of
the patient (e.g., nutritional support, blood compo-
nent therapy, growth factor therapy, fatigue, alope-
cia, anemia, constipation, diarrhea, nausea and vom-
iting, neutropenia, pain, and thrombocytopenia).
• Assess body weight and height, because dosages of
many chemotherapeutic agents are based on body
surface area.
• Examine laboratory data on a continuum. Monitor
for the development of cancer emergencies (e.g.,
hypercalcemia, superior vena cava syndrome, dis-
seminated intravascular coagulation).
• Administer intravenous (IV) medications (see
Chapter 11 for IV administration principles, ad-
ministration of drugs via venous access devices,
and care and handling of venous catheters). It is
essential to wear nitrite gloves and disposable non-
permeable fabric when handling any body uids.
• Monitor vital signs, including temperature, pulse,
respirations, and blood pressure, at least every shift
or more frequently depending on recommended
monitoring parameters of specic drugs prescribed.
• Hydration: Monitor the patient’s state of hydration.
Check skin turgor, mucous membranes, and softness
of the eyeballs. Electrolyte reports require vigilant ob-
servation; report abnormal ndings to the healthcare
provider. Fluid replacement via IV administration or
total parenteral nutrition may be appropriate in some
cases. Some chemotherapeutic agents require hydra-
tion before administration to prevent damage to the
kidneys or bladder. Prehydration is also planned for
highly emetogenic chemotherapy (see Chapter 33,
Table 33.2) to prevent dehydration from vomiting.
Regardless of the agents administered, always moni-
tor 24-hour urine output and read the urinalysis to
detect abnormalities. Chemotherapy administration
should be performed by qualied registered nurses or
prescribers with specic skills in the correct handling
and administration techniques for chemotherapeutic
agents. For more information on advanced education
required for administering chemotherapeutic agents,
consult Oncology Nursing Society guidelines, avail-
able at https://www.ons.org/.
• Infection: Report even the slightest sign of infection
for evaluation (e.g., elevating temperature, chills,
malaise, hypotension, pallor).
• Nausea, vomiting: There are three patterns of em-
esis associated with antineoplastic therapy: acute,
delayed, and anticipatory. (See Chapter 33 for the
treatment of nausea and vomiting associated with
chemotherapy.) The goal of treatment is to prevent
nausea and vomiting. Many chemotherapy regi-
mens require prechemotherapy administration of
an antiemetic followed by as-needed (PRN) orders
for breakthrough nausea and vomiting.
1. Chart the degree of effectiveness achieved when
antiemetics are given.
2. Report poor control to the prescriber.
3. Changing the antiemetic medication ordered or
the route of administration may improve control.
4. Patients experiencing nausea and vomiting must
be weighed daily and monitored for electrolyte
values and accurate intake and output.
• Positioning: Position changes should be scheduled to
prevent alterations in skin integrity.
• Diarrhea: Record the color, frequency, and consis-
tency of stool. Include an estimate of the volume of
watery stools in the output record. Check for occult
blood. Provide for adequate hydration and admin-
ister any drugs ordered to relieve the symptoms.
1. Encourage adequate uid intake and dietary al-
terations, such as eliminating spicy foods and
foods high in fat content. It may be necessary to
switch to a clear liquid diet followed by a diet
low in ber. Diarrhea may require high-protein
foods with high caloric value and vitamin and
mineral supplements. Patients with diarrhea
should be weighed daily and monitored for uid
intake and output and electrolyte values.
2. Check the anal area for irritation, provide for
hygiene measures, and protect from excoriation
with products such as A+D Ointment or zinc ox-
ide ointment.
• Constipation: Compare this symptom with the pa-
tient’s usual pattern of elimination. Many people do
not normally defecate daily. Perform daily assess-
ment of bowel sounds when the patient is hospital-
ized. When a patient is constipated, the prescriber
usually orders stool softeners or laxatives, uids,
and a diet that enhances normal defecation. Observe
carefully for signs of an impaction (the urge to def-
ecate with little to no stool or seepage of watery
stool).
• Stomatitis (mucositis): Use meticulous oral hygiene
measures (see Chapter 31). Schedule oral hygiene
measures using prescribed local anesthetic and

antimicrobial solutions. Perform oral hygiene be-
fore and after meals and at bedtime if symptoms are
mild. With moderate lesions, increase the frequency
to every 2 hours. In patients with severe symptoms,
the mouth is rinsed hourly while the patient is
awake.
• Bleeding: Observe and report signs and symptoms
of bleeding (e.g., epistaxis; hematuria; bruises;
petechiae; dark, tarry stools; coffee-ground em-
esis; or blurred vision). Instruct female patients to
report menstrual ow that is excessive, is bright
colored, or lasts for a prolonged period. Check
laboratory reports for indications of, for example,
changes in hematologic status and electrolytes;
report abnormal or changing values to the health-
care provider.
• Pain: Administer pain medications prescribed at
scheduled intervals to maintain a constant blood
level of the analgesic and thereby promote maxi-
mum pain control. Maintain a record of pain medi-
cations administered and the patient’s rating of the
degree of pain relief achieved (see Chapter 19).
1. Report insufcient pain relief.
2. Obtain orders for the treatment of the pain, or
institute PRN analgesics prescribed for break-
through pain episodes.
• Neurotoxicity: Monitor for disorientation, confusion,
ne-motor activity alterations, gait alterations, and
paresthesias.
• Anxiety: Monitor the degree of anxiety being exhib-
ited and intervene appropriately to alleviate. Give
prescribed medications; discuss issues about which
the patient or signicant others are concerned (e.g.,
possible depression, thoughts of suicide). Keep the
patient involved in making appropriate decisions
regarding self-care to give some degree of control
over the situation; discuss when prescribed treat-
ments are to be performed.
1. Implement relaxation techniques (use of biofeed-
back, visual imagery) as prescribed.
2. Deal with stress-related issues that arise in the
support or family group.
Patient Education
Nutrition
• Teach the patient specic ways to implement di-
etary needs (e.g., ways to support increased protein
and caloric intake, such as adding powdered milk to
puddings, creamed soups). Suggest using nutrition-
al supplements such as Ensure or Boost (see Chapter
46). Suggest the patient try different brands and add
freshly squeezed orange or lemon juice to help alter
the aftertaste frequently cited by postchemotherapy
patients who are using nutritional supplements.
• If the patient is receiving enteral tube feedings, pe-
ripheral parenteral nutrition, or total parenteral nu-
trition, arrange for necessary at-home support for
administration and monitoring of therapy. Suggest
Drugs Used to Treat Cancer CHAPTER 43 707
obtaining educational materials from the American
Cancer Society on dietary interventions during the
treatment of cancer.
Diagnosis and adaptation to diagnosis
• Encourage the patient and support group to dis-
cuss concerns about the disease, prognosis, and
treatment.
• Present the patient with appropriate choices that al-
low involvement in the decisions concerning selec-
tion of care. Encourage the patient to maintain the
best health possible. Include the patient in selecting
the diet, planning activities, scheduling rest periods,
and attending to personal care. Stress what the pa-
tient can do, not what the patient cannot do.
• Emphasize the prevention of complications through
maintenance of nutrition and hydration and com-
mitment to hygiene practices.
Sexual needs. Patients should discuss methods of
birth control to be used during chemotherapy and/or
sperm storage and fertilization counseling.
Vascular access devices. The need for frequent injec-
tion of chemotherapeutic agents intravenously neces-
sitates the use of implanted vascular access devices,
which include Hickman catheters, Port-A-Cath im-
plantable infusion ports, and peripherally inserted cen-
tral catheter (PICC) lines (see Chapter 11 for more in-
formation regarding care of these devices). Instruction
should be provided on the self-care and frequency of
required follow-up care for central lines or ports.
Skin care
• Have the patient bathe in lukewarm water and use
mild soap. Gently pat the skin dry. Discuss the use
of skin moisturizer with the prescriber.
• Instruct the patient to report rashes or areas that ap-
pear sunburned or blistered.
• Stress the need to avoid sunlight for patients re-
ceiving drugs that may produce a photosensitivity
reaction.
• Teach personal hygiene measures to provide for
skin care and to prevent skin breakdown.
Psychomotor
• Discuss activities the patient is able to perform inde-
pendently and those requiring assistance.
• Provide for patient safety on a continuum.
• Include the support group in the development of a
plan to provide for self-care at home.
• Arrange appropriate referrals to support the self-
care needs of the person in the home environment.
Nausea and vomiting
• Teach the patient when and how to take prescribed
antiemetics. Have the patient verbalize their under-
standing with teach-back.
708 UNIT IX Drugs Affecting Other Body Systems
• Make suggestions for comfort measures to mini-
mize nausea (e.g., rinsing the mouth frequently, us-
ing a cool cloth to wash the face, employing relax-
ation and distraction techniques).
• Teach the patient to take their weight daily and ex-
plain parameters of weight loss that must be report-
ed to the healthcare provider.
Diarrhea or constipation
• Teach the patient the proper use of PRN medica-
tions prescribed to treat constipation or diarrhea.
• Explain measures to prevent constipation, such as
drinking sufcient uids daily, eating high-ber
foods, and avoiding foods that cause constipation.
Instruct the individual to report failure to have stools
in a usual pattern of elimination or the presence of
seeping, loose, watery stools while feeling the need
to defecate (may be an indication of an impaction).
• When diarrhea is present, instruct the patient to
avoid foods that irritate or stimulate peristalsis—
for example, coffee, tea, and hot or cold beverages.
Encourage the increased intake of potassium-con-
taining foods.
Neutropenia
• Explain the measures that the individual should ini-
tiate to minimize the chance of infection when neu-
tropenia is present (e.g., handwashing; avoidance of
exposure to individuals known to have an infection;
no fresh owers, vegetables, or receptacles with
free-standing water such as denture cups or humid-
iers; and avoidance of pets and patients receiving
immunizations, especially live vaccines).
• Teach signs and symptoms of infection and when to
report symptoms. Be certain that the person under-
stands how to take her or his temperature and that
even minor elevations should be reported.
• Teach self-care of central lines, when present, con-
sistent with the patient’s or signicant others’ abili-
ty to perform the procedure while maintaining strict
aseptic technique. Arrange for referral to a commu-
nity or home care agency as indicated.
• See Table 43.3 for bone marrow stimulants used to
treat neutropenia.
Pain
• Discuss beliefs about pain with the patient and
signicant others as a baseline for health teaching
needed.
• Instruct the patient to record the intensity of the
pain experienced and degree of pain relief obtained
from prescribed medications (see Chapter 19 for a
pain scale).
• Emphasize the need to report both pain that is not
being controlled and new symptoms of pain being
felt.
• Stress the importance of taking pain medications at
prescribed intervals to obtain maximum relief.
• Determine whether the patient has access to medica-
tions for pain. (Does the patient have sufcient mon-
ey to purchase or obtain prescribed medication?)
• Stress the need for the patient to start stool softeners
and to take them regularly to prevent constipation
when opioid analgesics are used.
• Oral medications are often used to provide pain
relief. Several analgesics are also available as rec-
tal suppositories. Pain control must be achieved.
When oral and rectal forms of pain management
no longer sufce, patients may require hospitaliza-
tion for stabilization on parenteral forms of opioid
analgesics. Infusion pumps are frequently used,
and spinal morphine may be delivered effectively
via epidural or intrathecal catheters; transdermal
and sublingual pain control methods may also be
used. Patients must understand that they can be
kept comfortable.
Anemia
• Teach the patient the possible causes and related
self-care needed when anemia is present (e.g., man-
agement of fatigue by spacing of activities and pre-
vention of orthostatic hypotension by rising slowly,
sitting and resting, and then standing).
• Instruct the patient not to drive or operate power
equipment for safety reasons.
• See Table 43.3 for bone marrow stimulants used to
treat anemia.
Thrombocytopenia
• Teach self-monitoring for other blood-related symp-
toms (e.g., bleeding, bruising, hematuria, epistaxis,
coffee-ground emesis, or excessive or prolonged
menstrual ow).
• Suggest safety measures when at home (e.g., avoid-
ing use of sharp knives, shaving with an electric ra-
zor, wearing a thimble when sewing).
• Stress that the patient should not take any aspirin
or aspirin-containing products that may increase
bleeding should it occur.
Home care
• While the patient is receiving chemotherapy, soiled
linens should be washed separately from other
household linens; the soiled linens should be placed
in washable pillowcases and washed twice.
• Because most chemotherapeutic agents are excreted
in the urine and feces, it is best to ush the toilet two
or three times after each voiding or defecation.
• If emesis occurs, dump waste in toilet and ush two
or three times.
Anxiety
• Assist the patient to practice stress reduction tech-
niques, and make the patient aware of cancer sup-
port resources available, such as the American
Cancer Society (https://www.cancer.org/).

Fostering health maintenance
• Throughout the course of treatment, discuss medi-
cation information and how the medication will
benet the patient.
• Drug therapy will be individualized for the patient
and type of cancer being treated. The need to fol-
low the established regimen precisely must be em-
phasized to obtain maximum cytotoxic effects while
minimizing adverse effects. Adverse effects to the
drug therapy should be expected, and the patient
and signicant others must be educated in the man-
agement of the common and serious adverse effects.
Additional teaching must be individualized to the
patient for equipment used to administer drug ther-
apy or nutritional support.
• Seek cooperation and understanding of the fol-
lowing points so that medication compliance is
increased: name of medication; dosage, route, and
times of administration; and common and serious
Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• Nurses play a crucial role in the treatment of patients with
cancer. No other disease seems to evoke fear and anxiety
in the same way that the diagnosis of cancer has on the
patient and family. Nurses are often the contact between
the healthcare provider, patient, and family in helping with
adaptation to the diagnosis and entry into the healthcare
system for treatment.
• Nurses are often the rst to identify complications of
therapy; for example, they are often the rst to recognize
and report early symptoms of infection in
an immunocompromised patient. Early recognition
and prompt action often reduce the severity of the
complications.
• It is important for nurses caring for cancer patients to
research all drugs prescribed for the patient and to perform
focused assessments on body systems known to be
affected by the specic agents administered.
• Health teaching for the patient and signicant others is
essential to achieving the best response to the therapeutic
regimen prescribed. Everyone involved in the patient’s
care needs to understand the purpose of the medications
prescribed and when to contact the healthcare provider
for any problems encountered. The patient and signicant
others must feel like integral parts of the team, whose
members desire the best possible quality of life for those
affected by the disease.
• Nurses are active providers of public information on
wellness. They also coordinate screening programs for the
early detection of cancer.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
Drugs Used to Treat Cancer CHAPTER 43 709
adverse effects. Patients should be encouraged to
maintain basic good health practices throughout
treatment (e.g., adequate rest, exercise consistent
with abilities, stress management or stress reduc-
tion techniques, and maintenance of usual spiritual
beliefs).
Patient self-assessment. Enlist the patient’s help in
developing and maintaining a written record of moni-
toring parameters (e.g., nausea, vomiting, pain relief,
constipation, diarrhea). See Patient Self-Assessment
Form for Antineoplastic Agents on the Evolve website.
Complete the Premedication Data column for use as a
baseline to track response to drug therapy. Ensure that
the patient understands how to use the form, and in-
struct the patient to take the completed form to follow-
up visits. During follow-up visits, focus on issues that
will foster adherence with the therapeutic interven-
tions prescribed.
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX exam and include both NGN (Next Generation) and
traditional questions. See Chapter 1 for further information re-
garding question types.
Scenario
A patient being seen in the oncology clinic was recently diag-
nosed with lymphoma. The patient had no family history of any
cancer and no experience with healthcare. The patient asked
the nurse what to expect for treatment.
1. The nurse understands that the goals of chemotherapy may be
different for individual patients and include which of the following?
(Select all that apply.)
1. Chemotherapy’s goal is to give a dose large enough to
kill cancer cells but preserve normal cells.
2. One of the goals of chemotherapy is to kill all the fast-
growing cells without harmful adverse effects.
3. Chemotherapy has the goal of controlling the progression
of the disease.
4. One of the goals of chemotherapy is to alleviate symptoms
of cancer in cases in which no cure is available.
5. Chemotherapy has the goal of preventing cancer from
developing in patients at risk.
Objective: Discuss the goals of chemotherapy.
NCLEX item type: Multiple response
Cognitive skill: Application
710 UNIT IX Drugs Affecting Other Body Systems

2. The nurse is caring for the patient in the scenario with lymphoma, 4. “The drug lgrastim is used to stimulate the production of
who will be receiving prednisone. The patient asks the nurse what white blood cells to reduce neutropenia.”
effect this medicine will have. What would be an appropriate Objective: Discuss bone marrow stimulants and their effect and
response by the nurse? use.
1. Prednisone is used to prevent nausea and hair loss.” NCLEX item type: Multiple choice
2. “You are taking prednisone to prevent further occurrence Cognitive skill: Comprehension
of your cancer.”
3. “The mechanism of action is unknown, but it seems to 6. The nurse caring for the patient in the scenario discussed the
work by reducing the need for more chemotherapy.” types of assessments and interventions that may be necessary to
4. “Prednisone has a lympholytic effect, which means it can treat the adverse effects of chemotherapy.
suppress mitosis in lymphocytes.” Which nursing intervention/assessment listed in the far left
Objective: Describe the role of targeted anticancer agents in column is appropriate for alleviating the adverse effect of
treating cancer. chemotherapy. More than one intervention/assessment
NCLEX item type: Multiple choice may apply. Note: Not all interventions will be used.
Cognitive skill: Comprehension
3. The nurse is teaching the patient in the scenario, who will be taking
APPROPRIATE
methotrexate, which may cause thrombocytopenia. What must the INTERVENTION
nurse include in the teaching? (Select all that apply.) OR ASSESSMENT
1. Avoid fresh owers, vegetables, or fruit. NEEDED FOR
2. Use an electric shaver and practice safe handling of NURSING EACH ADVERSE
sharp objects, such as kitchen knives. ASSESSMENT/ ADVERSE EFFECTS OF EFFECT OF
INTERVENTION CHEMOTHERAPY CHEMOTHERAPY
3. Report hematuria, epistaxis, or coffee-ground emesis.
4. Obtain adequate daily exercise. Analysis of Diarrhea
5. Avoid taking any aspirin or aspirin-containing products. platelet count
Objective: Describe the nursing assessments and interventions Assess appetite Nausea and
needed to help alleviate the adverse effects of chemotherapy. vomiting
NCLEX item type: Multiple response Perform oral care Thrombocytopenia
Cognitive skill: Application
Analysis of Anemia
4. The nurse is explaining to the patient in the scenario the use of hemoglobin
chemoprotective agents for treating cancer;. Which statements Apply A&D Neutropenia
should the nurse include in the discussion? (Select all that apply.) ointment
1. “Chemoprotective agents include bone marrow Determine activity
stimulants and targeted agents.” tolerance
2. “The drug glucarpidase (Voraxaze) is used for patients Perform daily
taking methotrexate to prevent toxic concentrations by weights
helping break it down to be eliminated.”
3. “Chemoprotective agents are used to prevent allergic Teach signs and
reactions that are common responses to foreign symptoms of
proteins.” infection
4. “Mesna (Mesnex) is used to reduce the toxic effects of Assess pain
certain chemotherapy agents that can cause hemorrhagic Take vital signs
cystitis.”
Allow for rest
5. “Chemoprotective agents are used in cancer treatment to
periods
reduce the toxicity of chemotherapeutic agent to normal
cells.” Teach personal
hygiene measures
Objective: Identify how chemoprotective agents are used in
treating cancer. Analyze white
NCLEX item type: Multiple response blood cell count
Cognitive skill: Application with differential

5. The nurse educated the patient in the scenario on the bone marrow
stimulants used to reduce the toxic effects of chemotherapeutic Objective: Describe the nursing assessments and interventions
agents. Which statement by the nurse needs to be corrected? needed to help alleviate the adverse effects of chemotherapy.
NCLEX item type: Extended drag and drop
1. “These drugs are used to trigger the recovery of the bone Cognitive skill: Generate solutions
marrow several days earlier than it would normally happen.”
2. “The drug epoetin alfa is used to stimulate the production
of red blood cells to treat anemia.”
3. “These drugs are used to reduce the severity of
thrombocytopenia after chemotherapy.”
Drugs Used to Treat Musculoskeletal Disorders
Objectives
1. Describe the therapeutic effect of centrally acting skeletal
muscle relaxants on the central nervous system and the
common and serious adverse effects.
Key Terms
cerebral palsy (sĕ-RĒ-brăl PŎL-zē) hypercapnia (hī-pĕr-KĂP-nē-ă)
(p. 711) (p. 712)
multiple sclerosis (MŬL-tĭ-pŭl sklĕ- spasticity (spăs-TĬS-ĭ-tē) (p. 714)
RŌ-sĭs) (p. 711) muscle spasms (MŬ-sŭl SPĂ-zĭmz)
gout (p. 711) (p. 714)
The skeletal system includes the bones of the skeleton
and the cartilages, ligaments, and other connective tis-
sue that stabilize or connect the bones. In addition to
supporting the weight of the body, bones work togeth-
er with muscles to maintain body position and to pro-
duce controlled, precise movements. Without the skel-
eton to pull against, contracting muscle bers could
not make us sit, stand, walk, or run. Common disor-
ders that affect the musculoskeletal system are gout,
cerebral palsy, multiple sclerosis and stroke syndrome.
Gout is a common and treatable form of inamma-
tory arthritis. Gout develops as a result of excessive
uric acid in the blood (hyperuricemia). Uric acid, the
end product of purine metabolism, is a waste product
that has no physiologic role. Humans lack uricase, an
enzyme that breaks down uric acid into a more water-
soluble product (allantoin). The amount of uric acid
in the body depends on the balance between dietary
intake purines, synthesis, and the rate of excretion.
Gout results from overproduction (10% of cases) or
underexcretion (90% of cases) of uric acid. Excess uric
acid crystallizes in soft tissues and in particularly in
joints. This initiates an inammatory reaction leading
to swelling, heat, and intense pain.
Cerebral palsy is a neurologic disorder in which
movement of the extremities is marked by any combi-
nation of the following: exaggerated reexes, abnormal
posture, involuntary movements, and walking difcul-
ties. Cerebral palsy can be caused by an injury or a birth
defect.
Multiple sclerosis is an autoimmune neurologic dis-
ease that affects the brain and spinal cord. Symptoms
44
https://evolve.elsevier.com/Willihnganz
2. Describe the physiologic effects of neuromuscular blocking
agents and the common and serious adverse effects.
3. Identify the therapeutic response and the common and
serious adverse effects from gout medications.
neuromuscular blocking
agents (nyū-rō-MŬS-kyū-lăr BLŎK-
ĭng Ā-jĕnts) (p. 717)
may be mild, such as numbness in the limbs, or
severe, such as paralysis or loss of vision. The pro-
gression, severity, and specic symptoms of multiple
sclerosis are unpredictable and highly variable be-
tween persons.
Stroke syndrome is a condition of sudden onset of
vertigo, numbness, aphasia, and dysarthria, marked
by hemiplegia or hemiparesis caused by vascular le-
sions of the brain, embolism, thrombosis, or ruptured
aneurysm. The spasticity caused by the syndrome is
treatable with muscle relaxants.
MUSCLE RELAXANTS,
NEUROMUSCULAR BLOCKING AGENTS,
AND GOUT AGENTS
NURSING IMPLICATIONS FOR SKELETAL
MUSCLE RELAXANTS, NEUROMUSCULAR
BLOCKING AGENTS, AND GOUT AGENTS
Assessment
Assessment for skeletal muscle disorders. Musculo-
skeletal disorders may produce varying degrees of
pain and immobility, impairing the individual’s ability
to perform the activities of daily living. The nursing
assessments performed are individualized to the mus-
cles affected and the underlying disease.
Current history
• What is the reason for seeking treatment now?
Request a brief history of any symptoms present.
• What is the degree of impairment present (e.g.,
strength, gait, conservation effect, compensatory
711
712 UNIT IX Drugs Affecting Other Body Systems
action)? What is the effect on usual daily activities
(e.g., dressing, preparing meals, eating, performing
basic hygiene, maintaining home)?
• Assess the pain level and extent, frequency of an-
algesic use, precipitating factors, and any measures
the patient has identied that alleviate pain.
• Assess the extent of muscle spasticity and the mus-
cle groups affected. Are there impairments that af-
fect the patient’s self-care, activities of daily living,
or ability to fulll work responsibilities?
History
• Ask the patient to describe the degree of disorder
caused by the musculoskeletal impairment (e.g.,
scoliosis, poliomyelitis, rickets, osteoarthritis, cere-
bral palsy, multiple sclerosis, muscular dystrophy,
spinal cord injury, stroke).
• Have there been any injuries to, or surgeries on, the
musculoskeletal system (e.g., dislocations, sprains,
fractures, joint replacements)? If so, obtain details.
• Ask the patient if there is a family history of difcul-
ties or abnormal responses to neuromuscular block-
ing agents during anesthesia.
Medication history
• Ask the patient to list all prescribed and over-the-
counter medications taken within the past 6 months.
Are any herbal medicines being taken? Ask speci-
cally about antiinammatory or corticosteroid use.
• What has been the response to the medications
taken (e.g., antiinammatories, analgesics, skeletal
muscle relaxants)?
• What are the medications most recently taken and
when were they taken?
• What nonpharmacologic treatments are being used
(e.g., heating pad, massage therapy, acupuncture,
cupping)?
Activity and exercise
• What is the extent of usual daily exercise?
• Determine which activities of daily living can
be performed independently and which require
assistance.
• Ask about any assistive devices used (e.g., cane,
walker).
Sleep and rest
• Does the pain of repositioning at night awaken the
patient? Seek further information regarding the po-
sitions that initiate pain and the type of padding
or additional pillows or devices being used for
positioning.
Elimination
• Ask specically about the ability to toilet indepen-
dently. Does mobility interfere with this function? Is
constipation, diarrhea, or incontinence a problem?
If so, how is it managed?
Nutrition
• Take a diet history. Is the diet consistent with the
recommended diet? Are supplemental vitamins and
minerals (e.g., calcium) taken daily?
• Weigh the individual and ask whether there has
been a weight gain or loss over the past 6 months. If
so, obtain details.
Physical examination
• Gently inspect the affected limb or joint for swell-
ing, edema, bruises, redness, localized tenderness,
deformities, or malalignments.
• During examination, note differences in circumfer-
ence, symmetry, or length of limbs.
• Record any abnormalities present (e.g., scoliosis,
contractures, atrophy).
• Record range of motion present in joints, gait, and
degree of mobility.
• Evaluate capillary rell and check for presence of
paresthesia (numbness and tingling).
Laboratory and diagnostic studies
• Review diagnostic studies performed (e.g., radi-
ography, magnetic resonance imaging, computed
tomography, arthroscopic reports, bone scan, bone
mass measurements, endoscopy).
• Examine laboratory ndings associated with the
disease process present (e.g., calcium, phosphorus,
lupus testing, rheumatoid factor, uric acid level,
C-reactive protein, human leukocyte antigen, aldol-
ase [high levels can be a sign of muscle damage],
aspartate, creatine kinase).
Assessment for neuromuscular blocking agents
• Assessment of the patient’s vital signs, mental sta-
tus, and in particular, respiratory function is man-
datory for people having received neuromuscular
blocking agents. The adverse effects associated with
these drugs may occur 48 hours or more after ad-
ministration. Close observation of respiratory func-
tion, ability to swallow secretions, and the presence
of a cough reex is necessary. Suction, oxygen, me-
chanical ventilators, and resuscitation equipment
should be available in the immediate area.
• Monitor blood pressure, pulse, and respirations.
Review the baseline readings of the patient’s vital
signs before administration of anesthetic and neuro-
muscular blocking agents. Generally, changes from
the baseline should be reported.
• Monitor the patient closely for clinical signs of
hypoxia and hypercapnia (symptoms of elevated
carbon dioxide levels, including tachycardia, hy-
potension, and cyanosis). Arterial blood gas levels
(see Chapter 30, Table 30.1) may conrm the clinical
observations.
Detection of respiratory depression
• Early signs of diminished ventilation are difcult to
detect, particularly after the patient leaves the im-
mediate postoperative area when continuous moni-
toring with pulse oximetry is discontinued. Often
the signs of restlessness, anxiety, lethargy, decreased
mental alertness, and headache are early subtle
clues to respiratory distress.
 Drugs Used to Treat Musculoskeletal Disorders CHAPTER 44
• Use of the abdominal, intercostal, or neck muscles is
an indication of respiratory distress. Flaring of the
nostrils may be present in severe cases.
• As respiratory distress progresses, respirations be-
come shallow and rapid. Assess for asymmetric
chest movements.
• The development of cyanosis is a late sign of respi-
ratory complications. Respiratory distress should
be detected early through close observation before
cyanosis develops.
• Assess muscle strength by asking the patient to lift
their head off the pillow and hold a few seconds.
Pain assessment. Assess the degree of pain present
because neuromuscular blocking agents paralyze the
muscles but do not relieve pain.
Implementation
Nursing interventions with musculoskeletal disorders
• Assist with physical examination, drawing of blood
samples, and obtaining vital signs and weight in
preparation for diagnostic procedures.
• Adapt procedures to meet the self-care abilities of
the individual patient.
• Administer prescribed medications (e.g., anti-
inammatory drugs, analgesics, muscle relaxants).
• Provide specic instructions on the application
of hot or cold packs. Generally, ice packs alleviate
swelling for the rst 48 hours after muscle injury.
• Elevating the extremity immediately after injury
decreases swelling and, to some degree, alleviates
pain.
• Maintain the activity level prescribed (e.g., bed rest,
immobilization of muscle group or limb). During
the initial phase of treatment, immobilizing the af-
fected limb or joint will decrease muscle spasms
and therefore decrease pain. Maintenance of proper
alignment of the affected limb or joint will also re-
lieve pain and swelling. Various approaches may
be used for immobilization, including elastic ban-
dages, splinting, casts, bed rest, or modied activity
levels.
• Range-of-motion exercises may be prescribed to
maintain joint function and prevent muscle atrophy
and contractures. The activity plan prescribed must
be individualized to the diagnosis and should be
carefully followed for maximum effectiveness.
• Increased anxiety produces stress on the body’s
muscles. Implement measures to produce relax-
ation and provide for the psychological needs of the
individual.
Nursing interventions with neuromuscular blocking
agents
• Neuromuscular blocking agents are used during
anesthesia and surgery to relax muscle groups,
and during the use of mechanical ventilation to im-
prove airow and oxygenation of the patient. See
713
a critical care nursing text for a detailed discussion
of nursing care while the patient is receiving me-
chanical ventilation. Generally, a relatively short-
acting neuromuscular blocking agent is used to
facilitate endotracheal intubation. The patient will
be intubated and receiving mechanical ventilation
before administration of neuromuscular blocking
agents.
• Monitor airway patency, respiratory rate, and tidal
volume in accordance with hospital policy.
• The histamine release caused by these drugs may
produce increased salivation. In patients who are
paralyzed or who have incomplete return of control
over swallowing, coughing, and deep breathing,
these secretions may obstruct the airway. Have suc-
tioning equipment by the bedside.
• Assess for dyspnea and loud or gurgling sounds
with respirations. Suction secretions according to
hospital policies and procedures. If qualied, pal-
pate for coarse chest wall vibrations and auscultate
for crackles.
• Deep-breathing exercises allow the opportunity to
assess the patient’s cough reex. Assist the patient
by splinting any abdominal or thoracic incisions.
Have the patient take three or four deep breaths and
then cough. During this process, assess the patient’s
ability to breathe deeply.
• Patients can usually cough better in a semi-Fowler
or high Fowler position; therefore depending on the
situation and stability of the patient’s vital signs,
elevating the head of the bed may assist coughing
and breathing. For unconscious or semiconscious
patients, position on the side, using good body
alignment. Keep the bed’s side rails up.
• People still paralyzed by the effects of neuromuscular
blocking agents may experience pain and be unable
to speak to request medication. Ensure that analge-
sics are scheduled on a regular basis and adminis-
tered on time.
• Deal calmly with the patient experiencing respira-
tory dysfunction. The inability to breathe may cause
the patient to panic. Provide reassurance while initi-
ating measures to assist the patient.
• Question antibiotic orders that prescribe amino-
glycosides or tetracycline when neuromuscular
blocking agents have been used. These drugs may
potentiate the neuromuscular blocking activity.
Patient Education
Pain relief
• The degree of musculoskeletal pain relief with and
without activity should be discussed. Make modi-
cations appropriate to the diagnosis and degree of
impairment.
• Teach procedures designed to relieve pain (e.g.,
application of cold or heat, elevation of body part,
proper body alignment).
714 UNIT IX Drugs Affecting Other Body Systems
Activities and exercise. The patient should resume ac-
tivities of daily living within the boundaries set by her
or his healthcare provider. Activities such as regular
moderate exercise, meal preparation, resumption of
usual sexual activities, and social interaction should be
encouraged once specic orders have been obtained.
Psychosocial. For chronic disorders, encourage the
patient to express feelings regarding chronic illness.
The adjustment to this situation involves working
through great personal fears, frustrations, hostilities,
and resentments associated with the loss of personal
control in one’s life.
Medications. Many of the medications used in the
treatment of musculoskeletal disorders produce seda-
tion. Teach the patient about safety precautions such as
avoiding the use of power equipment or driving while
taking these medications.
Fostering health maintenance
• Throughout the course of treatment, discuss medi-
cation information and the individual’s expectations
of therapy. Ensure that the individual understands
the activity level prescribed, pain relief methods,
and safety precautions to ensure personal safety
during mobility.
• Seek cooperation and understanding of the fol-
lowing points so that medication compliance is
increased: name of medication; dosage, route, and
times of administration; and common and serious
adverse effects.
Patient self-assessment. Enlist the patient’s help in
developing and maintaining a written record of moni-
toring parameters (e.g., level, location, and duration of
pain; areas or muscles affected; degree of impairment
with improvement in mobility; exercise tolerance). See
Patient Self-Assessment Form for Muscle Relaxants
on the Evolve website. Complete the Premedication
Data column for use as a baseline to track response to
drug therapy. Episodes of nausea, vomiting, or diar-
rhea should be reported for the prescriber’s evaluation
if it is a new symptom. Ensure that the patient under-
stands how to use the form, and instruct the patient
to take the completed form to follow-up visits. During
follow-up visits, focus on issues that will foster adher-
ence with the therapeutic interventions prescribed.
DRUG THERAPY FOR
MUSCULOSKELETAL DISORDERS
Skeletal muscle relaxants are used to treat musculo-
skeletal conditions such as low back pain and spastic
muscle conditions associated with cerebral palsy, mul-
tiple sclerosis, and spinal cord injuries. Approximately
2 million people in the United States use skeletal mus-
cle relaxants annually, primarily for low back pain.
Skeletal muscle relaxants are often divided into anti-
spasticity medicines and antispasmodic medicines.
Spasticity is dened as an upper motor neuron dis-
order, possibly caused by a conduction interruption
in the nerve pathway. It is characterized by muscle
hypertonicity and involuntary jerks, which produce
stiff, awkward movements. Spasticity is often a com-
plication in patients with multiple sclerosis or cerebral
palsy. Antispasticity agents include tizanidine, dan-
trolene, baclofen, and diazepam.
Muscle spasms are often associated with musculo-
skeletal trauma or inammation (e.g., strains, sprains,
sciatica, herniated disks). Spasms are sudden alternat-
ing contractions and relaxations or sustained contrac-
tions of muscle. Antispasmodic agents used to treat
muscle spasms are the benzodiazepines (diazepam),
cyclobenzaprine, carisoprodol, metaxalone, chlorzoxa-
zone, methocarbamol, tizanidine, and orphenadrine.
Diazepam and tizanidine have both antispastic and
antispasmodic activity. The centrally acting skeletal
muscle relaxants act within the brainstem, basal gan-
glia, and spinal cord to induce muscle relaxation (Table
44.1). Dantrolene is a muscle relaxant that acts directly
on the skeletal muscle to reduce the force of muscle
contractions.
Medications used in the management of gout vary
in their actions. Some agents are used to treat acute at-
tacks to relieve pain and inammation, such as colchi-
cine. Other drugs alter the production or excretion of
uric acid.
DRUG CLASS: CENTRALLY ACTING SKELETAL
MUSCLE RELAXANTS
Actions
The centrally acting skeletal muscle relaxants belong
to a class of compounds used to relieve acute muscle
spasm. The exact mechanism of action of the cen-
trally acting skeletal muscle relaxants is not known,
except that they act by central nervous system de-
pression. Baclofen (see next drug monograph), a
gamma-aminobutyric acid derivative, works by in-
terrupting polysynaptic reexes at the spinal cord
level.
The centrally acting skeletal muscle relaxants do not
have any direct effect on muscles, nerve conduction, or
neuromuscular junctions. All of these muscle relaxants
produce some degree of sedation, and most healthcare
providers think that the benets of these agents, other
than baclofen, come from their sedative effects rather
than from actual muscle relaxation.
Uses
The centrally acting skeletal muscle relaxants are used
in combination with physical therapy, rest, and anal-
gesics to relieve muscle spasm associated with acute,
painful musculoskeletal conditions. They should not
be used in muscle spasticity associated with cerebral
 Drugs Used to Treat Musculoskeletal Disorders CHAPTER 44 715

Table 44.1 Centrally Acting Skeletal Muscle Relaxants

GENERIC NAME BRAND NAME AVAILABILITY ADULT DOSAGE RANGE (PO) COMMENTS
carisoprodol Soma Tablets: 250, 350 mg 250–350 mg four times Onset of action:
Do not confuse daily 30 min; duration:
Soma with Senna. 4–6 hr
chlorzoxazone Lorzone Tablets: 250, 375, 500, 250–750 mg three or four Commonly causes
750 mg times daily gastrointestinal
discomfort; may be
hepatotoxic
cyclobenzaprine Amrix, Tablets: 5, 7.5, 10 mg Tablets: 5-10 mg three Recommended only for
Do not confuse Teva-Cycloprine Capsules, extended times daily; do not short-term treatment
cyclobenzaprine with release (24 hr): 15, exceed 30 mg daily (2–3 wk) of painful
cyproheptadine. 30 mg Capsules, extended musculoskeletal
Suspension: 1 mg/mL release: 15–30 mg conditions; very
in 250 mL bottles once daily; do not sedating
exceed 30 mg daily
metaxalone Skelaxin Tablets: 400, 800 mg 800 mg three or four Use with caution in
Do not confuse times daily patients with liver
metaxalone with disease
metolazone.
methocarbamol Robaxin, Tablets: 500, 750 mg 1–1.5 g four times daily Mechanism unknown;
Methocarbamol Injection: 100 mg/mL in does not directly
Omega 10-mL vials relax tense skeletal
muscles
orphenadrine citrate — Tablets, extended 100 mg two times daily Also has analgesic
release (12 hr): properties; do not
100 mg use in patients
Injection: 30 mg/mL in 60 mg IV or IM; may be with glaucoma or
2-mL vials repeated every 12 hours. prostatic hyperplasia
tizanidine Zanaex Tablets: 2, 4 mg 4–8 mg q6–8h; do not Peak effects at 1–2 hr
Do not confuse Do not confuse Capsules: 2, 4, 6 mg exceed 36 mg daily and dissipates
tizanidine with Zanaex with between 3 and
nizatidine or Xanax or Anaex. 6 hr; used for
tiagabine. Gen-Tizanidine management of
increased muscle
tone associated with
spasticity
Available in Canada.
Do not confuse.

or spinal cord disease because they may reduce the
strength of remaining active muscle bers, causing
further impairment and debilitation.
Therapeutic Outcome
The primary therapeutic outcome expected from cen-
trally acting skeletal muscle relaxant therapy is relief
from muscle spasm.
Nursing Implications for Centrally Acting Skeletal
Muscle Relaxants
Premedication assessment
1. Review allergies and obtain baseline vital signs and
mental status of patient.
2. Have ordered laboratory studies carried out (e.g.,
liver function studies [bilirubin, aspartate ami-
notransferase [AST], alanine aminotransferase
[ALT] and alkaline phosphatase [ALP], increased
prothrombin time [PT] international normalizing
ratio [INR], complete blood cell count [CBC]).
Availability, dosage, and administration. See Table 44.1
Common adverse effects. These adverse effects are
usually mild and tend to resolve with continued
therapy. Encourage the patient not to discontinue
therapy without rst consulting with the healthcare
provider.
Neurologic
Sedation, weakness, lethargy, dizziness. Provide for
patient safety for the duration of these symptoms; re-
port to the healthcare provider for further evaluation.
Patients must avoid operating power equipment or
driving.
Gastrointestinal. Report any gastrointestinal com-
plaints to the healthcare provider for further evaluation.
716 UNIT IX Drugs Affecting Other Body Systems
Serious adverse effects
Gastrointestinal
Hepatotoxicity. The symptoms of hepatotoxicity are
anorexia, nausea, vomiting, jaundice, hepatomegaly,
splenomegaly, and abnormal liver function test results
(e.g., elevated bilirubin, AST, ALT, ALP, and PT/INR).
Hematologic
Blood dyscrasias. Routine laboratory studies (e.g., red
blood cell [RBC], white blood cell [WBC], and differ-
ential counts) are scheduled for patients taking these
agents for 30 days or longer. Stress the importance of
returning for this laboratory work. Monitor for the
development of sore throat, fever, purpura, jaundice,
and/or excessive progressive weakness.
Drug interactions
Central nervous system depressants. Central nervous
system depressants, including alcohol, opioid agonists,
antiepileptics, sedative-hypnotics, benzodiazepines,
phenothiazines, and antidepressants, potentiate the
sedative effects of centrally acting skeletal muscle re-
laxants. People who work around machinery, drive a
car, administer medicines, or perform other duties that
require mental alertness should not take these medica-
tions while working.
baclofen (BĂK-lō-fĕn)
Lioresal (lī ŌR-ĕ-sŏl)
Actions
Baclofen is a centrally acting skeletal muscle relaxant
that acts somewhat differently from the other centrally
acting agents. It is a gamma-aminobutyric acid deriva-
tive that interrupts polysynaptic reexes at the level of
the spinal cord.
Uses
Baclofen is used in the management of muscle spas-
ticity resulting from multiple sclerosis, spinal cord in-
juries, cerebral palsy, and other spinal cord diseases.
It is not recommended for use in spasticity associated
with Parkinson disease, stroke, or rheumatic disorders.
Use of baclofen to treat cerebral palsy usually requires
intrathecal infusion using a pump. Use baclofen with
caution for all patients who must use spasticity to
maintain an upright posture and balance in moving.
Therapeutic Outcome
The primary therapeutic outcome expected from ba-
clofen therapy is relief from muscle spasm.
Nursing Implications for Baclofen
Premedication assessment
1. Check history for any spastic disorders (e.g.,
Parkinson disease, stroke, rheumatic disorders).
If present, withhold medication and check with
healthcare provider.
2. Perform a baseline mental status examination.
Availability. PO: 5-, 10-, and 20-mg tablets, oral sus-
pension 1 mg/mL and 5 mg/mL.
Intrathecal: 0.05-, 0.5-, 1-, and 2-mg/mL ampules/
vials.
Dosage and administration. Adult: PO: Initially 5 mg
three times daily. Increase the dosage by 5 mg every 3
to 7 days based on response. Optimum effects are usu-
ally noted at dosages of 40 to 80 mg daily but may take
several weeks to achieve. Intrathecal administration
with the use of a pump has become common.
Medication Safety Alert
Do not abruptly discontinue baclofen therapy. Severe exac-
erbation of spasticity and hallucinations may result.
Common adverse effects. These adverse effects are
usually mild and tend to resolve with continued ther-
apy. Encourage the patient not to discontinue therapy
without rst consulting with the healthcare provider.
Gastrointestinal. Nausea.
Neurologic
Fatigue, headache, drowsiness, dizziness. Provide for
patient safety during episodes of dizziness; report to
the healthcare provider for further evaluation.
Drug interactions
Central nervous system depressants. Central nervous
system depressants, including sleep aids, analgesics,
benzodiazepines, and alcohol, potentiate the sedative
effects of baclofen. Persons who work around ma-
chinery, drive a car, administer medicines, or perform
other duties in which they must remain mentally alert
should not take these medications while working.
DRUG CLASS: DIRECT-ACTING SKELETAL MUSCLE
RELAXANTS
dantrolene (DĂN-trō-lēn)
Dantrium (DĂN-trē-ŭm)
Actions
Dantrolene is a muscle relaxant that acts directly on
skeletal muscle. This medication produces generalized
mild weakness of skeletal muscles and decreases the
force of reex muscle contractions, hyperreexia, clo-
nus, muscle stiffness, involuntary muscle movements,
and spasticity.
Uses
Dantrolene is used to control the spasticity of chronic
disorders such as cerebral palsy, multiple sclerosis, spi-
nal cord injury, and stroke syndrome. Dantrolene is also
approved by the US Food and Drug Administration to
treat neuroleptic malignant syndrome associated with
 Drugs Used to Treat Musculoskeletal Disorders CHAPTER 44
the use of antipsychotic agents (see Chapter 17) and
unusual reactions to neuromuscular agents used with
balanced anesthesia.
Therapeutic Outcome
The primary therapeutic outcome expected from dan-
trolene therapy is relief from muscle spasm.
Nursing Implications for Dantrolene
Premedication assessment
1. When used for neuroleptic malignant syndrome,
perform a baseline assessment of vital signs, espe-
cially temperature.
2. Establish a baseline of degree of muscle symptoms
present.
Availability. PO: 25-, 50-, and 100-mg capsules. IV:
Solution: 20-mg/vial; suspension: 250 mg/vial.
Dosage and administration. Adult: PO: Initially, 25
mg daily for 7 days. Increase to 25 mg three times
daily for 7 days; then increase to 50 mg three times
daily for 7 days, with a nal dosage of 100 mg three
times daily; some patients may require 100 mg four
times daily.
Response to therapy. Tell the patient that effectiveness
of the drug may not be apparent for 1 week or longer.
Encourage the patient not to discontinue therapy with-
out rst consulting with the healthcare provider.
Common adverse effects. These adverse effects are
usually mild and tend to resolve with continued ther-
apy. They can often be minimized by starting therapy
with low doses. Encourage the patient not to discon-
tinue therapy without rst consulting with the health-
care provider.
Neurologic
Weakness, drowsiness, dizziness, lightheaded-
ness. Provide for patient safety during episodes of
dizziness; report to the healthcare provider for further
evaluation.
Gastrointestinal. Diarrhea.
Serious adverse effects
Sensory
Photosensitivity. The patient should be cautioned
to avoid exposure to sunlight and ultraviolet light.
Suggest wearing long-sleeved clothing, a hat, and sun-
glasses while exposed to sunlight. The patient must not
use tanning lamps. The patient should not discontinue
therapy without notifying the healthcare provider.
Gastrointestinal
Hepatotoxicity. The symptoms of hepatotoxicity are
anorexia, nausea, vomiting, jaundice, hepatomegaly,
splenomegaly, and abnormal liver function test results
(e.g., elevated bilirubin, AST, ALT, and ALP; increased
PT/INR).
717
Drug interactions
Central nervous system depressants. Central nervous
system depressants, including sleeping aids, analgesics,
benzodiazepines, and alcohol, will potentiate the seda-
tive effects of dantrolene. The patient who works with
machinery, operates a motor vehicle, administers medica-
tions, or performs other duties that require mental alert-
ness should not take these medications while working.
DRUG CLASS: NEUROMUSCULAR BLOCKING
AGENTS
Actions
Neuromuscular blocking agents act by interrupting
transmission of impulses from motor nerves to muscles
at the skeletal neuromuscular junction. Neuromuscular
blocking agents have no effect on consciousness, mem-
ory, or the pain threshold. Reassurance by nursing
personnel is essential to paralyzed patients (e.g., those
on ventilators), and analgesics and sedatives must be
administered on schedule. These patients may suffer
extreme pain and may be unable to ask for analgesics.
Uses
Neuromuscular blocking agents are important skeletal
muscle relaxants. These agents are used to produce ad-
equate muscle relaxation during anesthesia to reduce
the use (and adverse effects) of general anesthetics,
ease endotracheal intubation and prevent laryngo-
spasm, decrease muscular activity in electroshock ther-
apy, and aid in reducing the muscle spasms associated
with tetanus.
Therapeutic Outcome
The primary therapeutic outcome expected from neuro-
muscular blocking therapy is smooth and skeletal mus-
cle relaxation.
Nursing Implications for Neuromuscular Blocking
Agents
Premedication assessment
1. These drugs are administered by an anesthetist or
anesthesiologist during surgical anesthesia or by a
critical care nurse when a patient is placed or be-
ing maintained on a ventilator. Check hospital or
institutional policy to determine who may admin-
ister these drugs and what the specic monitoring
parameters are.
2. Check history for hepatic, pulmonary, and renal
disease or neurologic disorders such as myasthenia
gravis, spinal cord injury, or multiple sclerosis. If
present, tag the chart appropriately before adminis-
tration of anesthesia.
3. Have oxygen, suction, and articial respiration
equipment available in the immediate area when-
ever these drugs are to be used. Also have antidotes
(e.g., neostigmine methylsulfate [Bloxiverz], pyr-
idostigmine bromide [Regonol]) available.
718 UNIT IX Drugs Affecting Other Body Systems

Availability. See Table 44.2
Administration. These agents are usually given by
the intravenous (IV) route but may also be given by
the intramuscular (IM) route. Because they are potent
drugs, they should be used only by those thoroughly
familiar with their effects, such as an anesthetist or an-
esthesiologist, and under conditions in which the pa-
tient can receive constant, close attention for signs of
respiratory failure. Adequate equipment for articial
respiration, antidotes, and other measures for prompt
treatment of toxicity must be readily available.
Patients with hepatic, pulmonary, or renal disease
or neurologic disorders such as myasthenia gravis, spi-
nal cord injury, or multiple sclerosis must be fully eval-
uated to assess their ability to tolerate neuromuscular
blocking agents. Much smaller doses are often neces-
sary when these diseases are present. Neonates and
older patients also require adjustments in dosage
because of the insensitivity of their neuromuscular
junctions.
Treatment of overdose. Treatment of overdose in-
cludes articial respiration with oxygen and antidotes
such as neostigmine methylsulfate (Bloxiverz) and
pyridostigmine bromide (Regonol). Atropine sulfate is
usually administered with neostigmine or pyridostig-
mine to block bradycardia, hypotension, and salivation
induced by these agents. Another available antidote,
sugammadex (Bridion), is the rst selective relaxant
binding agent used to reverse neuromuscular block-
ade after administration of the nondepolarizing neuro-
muscular blocking agents vecuronium or rocuronium.
There is no antidote for the early blockade induced by
succinylcholine. Fortunately, it is of short duration and
does not require reversal.
Common adverse effects
Histamine release. Neuromuscular blocking agents
cause histamine release, which may cause bronchos-
pasm, bronchial and salivary secretions, ushing,
edema, and urticaria. Ensure that the airway is patent
and that secretions are suctioned regularly to prevent
obstruction. Report evidence of bronchospasm, edema,
and urticaria immediately.
Neurologic
Mild discomfort. Mild to moderate discomfort, par-
ticularly in the neck, upper back, and lower intercostal
and abdominal muscles, will be noted when the pa-
tient rst ambulates after use.
Serious adverse effects
Respiratory
Signs of respiratory distress. Monitor vital signs for
a prolonged period after administration of neuro-
muscular blocking agents.
Diminished cough reex, inability to swallow. Assess deep
breathing and coughing at regular intervals. Have suc-
tion and oxygen equipment available, and be familiar
with institutional emergency code practices.
Drug interactions
Drugs that enhance therapeutic and toxic ef-
fects. General anesthetics (e.g., ether, enurane), ami-
noglycoside antibiotics (e.g., gentamicin, neomycin,
streptomycin, tobramycin, amikacin), clindamycin,
tetracycline, procainamide, lidocaine, beta-adrenergic
blocking agents (e.g., propranolol, timolol, pindolol,
nadolol), aprotinin, metoclopramide, lithium, and
agents that deplete potassium (e.g., thiazide diuret-
ics, furosemide, torsemide, bumetanide, ethacrynic
acid, chlorthalidone, amphotericin B, corticosteroids)
inhibit neuromuscular transmission, which results in
prolonged neuromuscular blockade.
Label charts of patients scheduled for surgery who
are taking any of these agents. These combinations
may potentiate respiratory depression. Check the
anesthetist’s records of surgical patients. Monitor post-
operative patients for respiratory depression for a pro-
longed period. This may occur 48 hours or more after
drug administration.

Table 44.2 Neuromuscular Blocking Agents

GENERIC NAME
atracurium besylate
cisatracurium besylate
pancuronium bromide
rocuronium bromide
succinylcholine
vecuronium bromide
Do not confuse vecuronium with
vancomycin.
Do not confuse.
BRAND NAME AVAILABILITY
— 10 mg/mL in 5- and 10-mL vials
Nimbex 2 mg/mL in 5- and 10-mL vials; 10 mg/mL in
Do not confuse Nimbex with Niferex, 20-mL vials
Bumex
— 1 mg/mL in 10-mL vials
— 10 mg/mL in 5- and 10-mL vials; 5 mL syringes
Anectine, Quelicin 20 mg/mL in 10-mL vials, 5-, 10-mL syringes
— 10, 20 mg/vial; 1 mg/mL in 10-mL syringes
 Drugs Used to Treat Musculoskeletal Disorders CHAPTER 44
Drugs that reduce therapeutic effects. These include
neostigmine methylsulfate and pyridostigmine bro-
mide. These agents are used as antidotes in case of
overdosage of the neuromuscular blocking agents.
Carbamazepine. Carbamazepine hastens recovery
time from neuromuscular blocking agents. Higher or
more frequent doses of the neuromuscular blocking
agent may be necessary.
Respiratory depressants. Analgesics, sedatives, and
benzodiazepines used in combination with muscle re-
laxants may potentiate respiratory depression. Check
the anesthetist’s records of surgical patients. Monitor
postoperative patients for respiratory depression for a
prolonged period. This may occur 48 hours or more
after drug administration.
DRUG CLASS: GOUT AGENTS
colchicine (KŌL-chĭ-sēn)
Actions
The exact mechanism of action is not known, but col-
chicine interrupts the cycle of urate crystal deposition
in the tissues that results in an acute attack of gout. It
does not affect the amount of uric acid in the blood or
urine; therefore it is not a uricosuric agent.
Uses
Colchicine is used to prevent and treat acute gout ares
when taken at the rst sign of a are up. Joint pain and
swelling begin to subside within 12 hours and are usu-
ally gone within 48 to 72 hours after initiating therapy.
Therapeutic Outcome
The primary therapeutic outcome expected from col-
chicine therapy is elimination of joint pain secondary
to acute gout attack.
Nursing Implications for Colchicine
Premedication assessment
1. Assess for and record any gastrointestinal com-
plaints present before initiation of drug therapy.
2. Assess for a history of allergy to colchicine. If pres-
ent, withhold the drug and consult with the health-
care provider.
3. Obtain baseline complete blood count and differen-
tial, uric acid level, blood urea nitrogen (BUN), cre-
atinine, AST, ALT, and other values as requested by
the healthcare provider for future comparison and
for monitoring for development of blood dyscrasias,
renal dysfunction, and liver impairment, as well as
tracking progress in control of uric acid level.
4. Assess the patient’s level and location of pain using
the pain rating scale (0 to 10); assess affected area
for signs of inammation—erythema, edema, and
mobility.
719
Availability. PO: Tablets and capsules: 0.6 mg. Solution:
0.6 mg/5 mL.
Dosage and administration. Adult: PO: Acute gout:
1.2 mg at rst sign of gout are, followed by 0.6 mg 1
hour later; do not exceed 1.8 mg over 1 hour. Therapy
should start within 36 hours of attack onset. After the
acute attack, 0.6 mg should be administered two times
daily to prevent relapse for up to 6 months. Do not ex-
ceed 1.2 mg/day.
Medication Safety Alert
Use with extreme caution in older adults or debilitated pa-
tients and in patients with impaired renal, cardiac, or gastro-
intestinal function.
Fluid intake. Monitor intake and output during ther-
apy. Maintain uid intake at 8 to 12 eight-ounce glasses
daily.
Common adverse effects
Gastrointestinal
Nausea, vomiting, diarrhea. These are common ad-
verse effects of colchicine therapy. Discontinue therapy
when gastrointestinal symptoms develop. Always re-
port bright red blood in vomitus, coffee-ground vomi-
tus, or dark, tarry stools.
Serious adverse effects
Hematologic
Blood dyscrasias. Serious, potentially fatal, blood
dyscrasias, including anemia, agranulocytosis, and
thrombocytopenia, have been associated with colchi-
cine therapy. Although the development of blood dys-
crasias is rare, periodic differential blood counts are
recommended if the patient requires prolonged treat-
ment. Routine laboratory studies (e.g., RBC, WBC, and
differential counts) should be scheduled. Stress to the
patient the importance of returning for this laboratory
work. Monitor for the development of sore throat, fe-
ver, purpura, jaundice, or excessive and progressive
weakness and report any such development immedi-
ately to the healthcare provider.
Neuromuscular toxicity. Colchicine-induced neuro-
muscular toxicity and rhabdomyolysis have been re-
ported with chronic treatment in therapeutic doses.
Patients with renal dysfunction and elderly patients,
even those with normal renal and hepatic function, are
at increased risk. Monitor for signs and symptoms of
muscle pain, tenderness, or weakness, and monitor
creatine phosphokinase kinase.
Drug interactions
Drugs that enhance the toxic effects. Clarithromycin,
diltiazem, itraconazole, ranolazine, and verapamil
reduces the metabolism or enhances the exposure of
720 UNIT IX Drugs Affecting Other Body Systems
colchicine. Concomitant use of atorvastatin, simvas-
tatin, pravastatin, uvastatin, lovastatin, gembrozil,
and fenobrate, may potentiate the development of
myopathy.
probenecid (prō-BĔN-ĕ-sĭd)
Actions
Uricosuric agents act on the tubules of the kidneys to
enhance the excretion of uric acid. Probenecid pro-
motes renal excretion of a number of substances, in-
cluding uric acid. It inhibits the reabsorption of urate
in the kidney, which results in reduction of uric acid in
the blood.
Uses
Probenecid is used to treat hyperuricemia and chronic
gouty arthritis. It is not effective for acute attacks of
gout and is not an analgesic.
Therapeutic Outcome
The primary therapeutic outcome expected with pro-
benecid therapy is prevention of acute attacks of gouty
arthritis.
Nursing Implications for Probenecid
Premedication assessment
1. Inquire about the time of onset of the last gout at-
tack; do not administer medication during or within
2 to 3 weeks of an acute attack.
2. Assess for and record any gastrointestinal com-
plaints before initiating drug therapy.
3. Ask about any history of blood dyscrasias or kid-
ney stones; if present, withhold drug and contact a
healthcare provider.
4. Obtain baseline blood studies as requested (e.g.,
uric acid and serum creatinine levels) to assess ap-
propriateness and to monitor response to therapy.
Medication Safety Alert
 • Do NOT start probenecid therapy during an acute attack
of gout; wait 2 to 3 weeks.
 • Do NOT administer to patients with histories of blood
dyscrasias or uric acid kidney stones.
 • Do NOT administer to patients with a creatinine clearance
lower than 50 mL/min.
Availability. PO: 500-mg tablets.
Dosage and administration. Adult: PO: Initially 250
mg twice daily for 1 week, then 500 mg twice daily.
The dosage may be increased by 500 mg every few
weeks to goal. Administer with food or milk to di-
minish gastric irritation. Maintain uid intake at 2 to
3 L daily.
Common adverse effects
Metabolic
Acute gout attacks. Patients should be told that the
incidence of gout attacks may increase for the rst few
months of therapy and that they should continue ther-
apy without changing the dosage during the attacks.
Serious adverse effects
Gastrointestinal
Nausea, anorexia, vomiting. Use probenecid with cau-
tion in patients with a history of peptic ulcer disease.
Individuals who experience symptoms of ulcers and
are still undiagnosed should be encouraged to report
gastrointestinal symptoms if they increase in intensity
or frequency. Always report bright red blood in vomi-
tus, coffee-ground vomitus, or dark, tarry stools.
Hypersensitivity, immune system
Hives, pruritus, rash. These are signs of hypersensitivity;
notify the healthcare provider. Therapy may have to be
discontinued.
Drug interactions
Oral hypoglycemic agents. Monitor for hypoglycemia
(e.g., headache, weakness, decreased coordination,
general apprehension, diaphoresis, hunger, blurred or
double vision). The dosage of the hypoglycemic agent
may need to be reduced. Notify the healthcare provid-
er if any of these symptoms appear.
Acyclovir, famciclovir, valacyclovir, indomethacin, ri-
fampin, sulfonamides, naproxen, penicillins, cephalosporins,
methotrexate. Probenecid blocks the renal excretion of
these agents. See individual drug monographs of the
drugs listed for serious adverse effects that may indi-
cate development of toxicity.
Salicylates. Although occasional use of aspirin will
not interfere with the effectiveness of probenecid,
regular use of aspirin or aspirin-containing products
should be discouraged. If analgesia is required, sug-
gest acetaminophen.
Antineoplastic agents. Because of the potential de-
velopment of renal uric acid stones, probenecid is not
recommended for increased uric acid levels caused by
antineoplastic therapy.
DRUG CLASS: XANTHINE OXIDASE INHIBITORS
Actions
Xanthine oxidase inhibitors block the terminal path-
ways in uric acid formation by inhibiting the enzyme
xanthine oxidase. The two drugs currently available
are allopurinol and febuxostat.
Uses
Allopurinol is used to treat primary hyperuricemia in
patients with gout or gout secondary to antineoplastic
therapy. It is not effective for treating acute attacks of
gouty arthritis. Allopurinol has an advantage over uri-
cosuric agents (probenecid) in that gouty nephropathy
 Drugs Used to Treat Musculoskeletal Disorders CHAPTER 44
Table 44.3 Xanthine Oxidase Inhibitors
GENERIC NAME BRAND NAME AVAILABILITY
allopurinol Zyloprim, PO: 100-, 300-mg tablets
AG-Allopurinol IV: 500 mg/vial
febuxostat Uloric PO: 40-, 80-mg tablets
JAMP
Febuxostat
Available in Canada.
and the formation of urate stones are less likely because
the drug inhibits the production of uric acid. It may
also be used in patients with renal failure. Uricosuric
agents should not be used in this case.
Febuxostat is approved for the chronic man-
agement of hyperuricemia in patients with gout.
Febuxostat is not approved for use in asymptomatic
hyperuricemia.
Therapeutic Outcome
The primary therapeutic outcome associated with
xanthine oxidase inhibitor therapy is reduced serum
uric acid levels with a lower frequency of acute gout
attacks.
Nursing Implications for Xanthine Oxidase
Inhibitors
Premedication assessment
1. Inquire about the time of onset of gout attack; do not
start the medication during an acute attack.
2. Assess for and record any gastrointestinal com-
plaints before initiating drug therapy.
3. Obtain baseline blood studies, blood counts, and re-
nal and liver function studies as requested.
Availability, dosage, and administration. See Table 44.3
Allopurinol. Adult: IV: Chemotherapy-induced tumor
lysis syndrome: 200 to 400 mg/kg/day, maximum dose
is 600 mg/day. Infuse at a concentration no greater
than 6 mg/mL. When possible, allopurinol therapy
should be started 24 to 48 hours before chemotherapy
known to cause tumor lysis. Dosage must be reduced
in patients with a creatinine clearance of 20 mL/min
or lower.
Febuxostat. Dosage must be reduced in patients
with a creatinine clearance of 30 mL/min or lower.
Medical Safety Alert
Patients with gout with established cardiovascular (CV) dis-
ease treated with febuxostat had a higher rate of CV death
compared with those treated with allopurinol.
Fluid intake. Maintain uid intake at 8 to 12 eight-
ounce glasses daily.
721
DAILY DOSAGE MAXIMUM DAILY DOSAGE
PO: 300 mg 800 mg
PO: Initially, 40 mg 120 mg
Dosage adjustment: If serum uric
acid level is not <6 mg/dL after
2 wk therapy, raise the dosage
to 80 mg
Common adverse effects
Metabolic
Acute gout attacks. Patients should be told that the
frequency of gout attacks may increase for the rst few
months of therapy with xanthine oxidase inhibitors.
The patient should continue therapy without changing
the dosage during the attacks. Patients may be treated
with nonsteroidal antiinammatory agents or colchi-
cine to prevent acute gout areups.
Gastrointestinal
Gastric irritation. If gastric irritation occurs, admin-
ister with food or milk. If symptoms persist or in-
crease in severity, report to the healthcare provider for
evaluation.
Nausea, vomiting, diarrhea. These adverse effects
are usually mild and tend to resolve with continued
therapy. Encourage the patient not to discontinue
therapy without rst consulting with the healthcare
provider.
Neurologic
Dizziness, headache. These adverse effects are usu-
ally mild and tend to resolve with continued therapy.
Encourage the patient not to discontinue therapy with-
out rst consulting with the healthcare provider.
Serious adverse effects
Gastrointestinal
Hepatotoxicity. The symptoms of hepatotoxicity are
anorexia, nausea, vomiting, jaundice, hepatomegaly,
splenomegaly, and abnormal liver function test results
(e.g., elevated bilirubin, AST, ALT, ALP; increased PT/
INR). Periodic measurement of liver function tests is
appropriate when initiating therapy and in patients
with hepatic impairment.
Hematologic
Bone marrow suppression. Routine laboratory studies
(RBC, WBC, and differential counts) should be sched-
uled. Stress the importance of the patient returning
for this laboratory work. Monitor for sore throat, fe-
ver, purpura, jaundice, or excessive and progressive
weakness.
Hypersensitivity
Fever, pruritus, rash. Report symptoms for further
evaluation by the healthcare provider. Pruritus may be
relieved by adding baking soda to the bathwater.
722 UNIT IX Drugs Affecting Other Body Systems
Drug interactions
Theophylline derivatives. Xanthine oxidase inhibitors,
when given with theophylline derivatives, may cause
theophylline toxicity. Observe for vomiting, dizziness,
restlessness, and cardiac arrhythmias. The dosage of
theophylline may need to be reduced.
Azathioprine, mercaptopurine. Xanthine oxidase inhibi-
tors inhibit the metabolism of these agents. When initiat-
ing therapy with azathioprine or mercaptopurine, start at
one-fourth to one-third of the normal dosage and adjust
subsequent dosages according to the patient’s response.
Clinical Judgment and Next-Generation NCLEX® Examination-Style Questions
Key Points
• Skeletal muscular disorders such as cerebral palsy, multiple
sclerosis, and gout cause pain and varying degrees of
immobility, limiting a patient’s ability to perform activities of
daily living.
• Nurses can play an important role in providing counseling
and guidance to patients and family members in
understanding muscle spasticity and pain and how to
maintain an appropriate balance between daily activities
and timing of analgesics to optimize quality of life.
• Nurses also play a crucial role in providing comfort and
monitoring to patients who have received neuromuscular
blocking agents. It is mandatory that nurses know how
to recognize and respond quickly when respiratory
emergencies arise.
• Colchicine is used for acute gout attack (ares) and
to prevent attacks. Allopurinol is used to treat primary
hyperuricemia in patients with gout.
Additional Learning Resources
SG Go to your Study Guide for additional Review Questions
for the NCLEX® Examination, Critical Thinking Clinical Situa-
tions, and other learning activities to help you master this chap-
ter content.
Go to your Evolve website (https://evolve.elsevier.com/Willihng
anz) for additional online resources.
Clinical Judgment and Next-Generation NCLEX® Exam-
ination-Style Questions The following questions are typical of
the NCLEX exam and include both NGN (Next Generation) and
traditional questions. See Chapter 1 for further information re-
garding question types.
Scenario
A patient previously diagnosed with cerebral palsy came to the
clinic to have the baclofen pump relled. The patient had been
managed with the skeletal muscle relaxant for several years,
and its use allowed the patient to remain mobile with the use
of canes.
Ampicillin, amoxicillin. There is a high incidence of
rash when patients are taking both allopurinol and
ampicillin or amoxicillin. Do not consider the patient
allergic to either drug until sensitivity tests identify a
hypersensitivity reaction.
Cyclophosphamide. There is a greater incidence of
bone marrow depression in patients receiving allopu-
rinol and cyclophosphamide concurrently. Monitor for
sore throat, fever, purpura, jaundice, or excessive and
progressive weakness.
1. The nurse is administering a centrally acting skeletal muscle
relaxant (other than baclofen) to another patient not in the scenario
and knows that these drugs are used for patients with which
diagnoses? (Select all that apply.)
1. Muscle spasms
2. Cerebral palsy
3. Spinal cord injury
4. Pulled back muscles (acute injury)
5. Gout
Objective: Describe the therapeutic effect of centrally acting
skeletal muscle relaxants on the central nervous system and the
common and serious adverse effects.
NCLEX item type: Multiple response
Cognitive skill: Application
2. The nurse reviewed the common and serious adverse effects
of baclofen (Lioresal) with the patient in the scenario. Which
statement by the patient indicates an adequate understanding of
these effects? (Select all that apply.)
1. “I understand that I need to watch out for headaches.”
2. “If I start to get drowsy, I need to stop what I am doing so
I don’t make a mistake.”
3. “Baclofen caused some nausea when I rst started on
it, but I am used to it now, so I don’t get nauseated
anymore.”
4. “If I get dizzy I know I need to tell my healthcare provider.”
5. “Sometimes this med will cause pain, but it goes away
with movement.”
Objective: Describe the therapeutic effect of centrally acting
skeletal muscle relaxants on the central nervous system and the
common and serious adverse effects.
NCLEX item type: Multiple response
Cognitive skill: Application
 Drugs Used to Treat Musculoskeletal Disorders CHAPTER 44 723

3. The nurse was discussing the common and serious adverse effects 4. The nurse is preparing to administer allopurinol (Zyloprim) to an
of a neuromuscular blocking agent that will be used with a patient elderly patient and instructed the patient on the adverse effects.
who was undergoing a surgical procedure. Indicate with an X the Which statement by the patient indicates an understanding of the
statement by the nurse that refers to a common adverse effect or teaching?
a serious adverse effect. 1. “I will discontinue this medication if I start to get a
headache.”
COMMON ADVERSE SERIOUS ADVERSE 2. “As I understand it, this medication will decrease how
EFFECTS EFFECTS often I get gout attacks.”
“If you experience 3. “If I get nauseated and vomit, I need to discontinue this
ushing, edema medication because it will not get better.”
and itching, this 4. “I am taking this for my gout, and it will treat any gout
may be caused areups.”
by histamine Objective: Identify the therapeutic response and the common and
release.” serious adverse effects from gout medications.
“We monitor NCLEX item type: Multiple choice
you closely Cognitive skill: Comprehension
for respiratory 5. When monitoring for adverse effects, the nurse will recognize
depression when which of the following as reportable symptoms related to
these medicines colchicine? (Select all that apply.)
are administered.”
1. Nausea
“There is
2. Nasal congestion
always suction
3. Dark, tarry stools
equipment and
4. Diarrhea
oxygen available
5. Vomiting
in case you
6. Constipation
nd you cannot
7. Headaches
swallow for a time
8. Sore throat
after receiving
these medicines.” Objective: Identify the therapeutic response and the common and
serious adverse effects from gout medications.
“Sometimes there
NCLEX item type: Extended multiple response
will be some neck
Cognitive skill: Recognize cues
and upper back
discomfort after
the administration
of these types of
medications.”

Objective: Describe the physiologic effects of neuromuscular

blocking agents and the common and serious adverse effects.
NCLEX item type: Matrix
Cognitive skill: Evaluate cues
45 Drugs Used to Treat Infections
https://evolve.elsevier.com/Willihnganz
Objectives
1. Explain the major actions of classes of drugs used to treat
infectious diseases.
2. Describe the signs and symptoms of the common adverse
effects of antibiotic therapy.
3. Describe the nursing assessments and interventions for
the common adverse effects associated with antimicrobial
Key Terms
pathogenic (păth-ō-JĔN-ĭk) (p. 724) gram-positive
antibiotics (ăn-tī-bī-Ŏ-tĭks) (p. 724) microorganisms (GRĂM PŎ-zĭ-tĭv
gram-negative mī-krō-ŌR-găn-ĭz-ĕmz) (p. 724)
microorganisms (GRĂM NĔG-ĭ-tĭv) prophylactic antibiotics (prō-fĭ-LĂK-
(p. 724) tĭk) (p. 725)
nephrotoxicity (nĕf-rō-tŏks-ĬS-ĭ-tē)
(p. 726)
AntimicrobiAl Agents
Animicrbial agns ar chmicals ha limina liv-
ing micrrganisms ha ar pathogenic (xic)  h
pain. Animicrbial agns may b f chmical ri-
gin, such as h sulfnamids, r hy may b drivd
frm hr living rganisms. Ths drivd frm
hr living micrrganisms ar calld antibiotics; fr
xampl, pnicillin was rs drivd frm h mld
Penicillium notatum. Ms anibiics usd day ar
harvsd frm larg clnis f micrrganisms,
which ar hn purid and chmically mdid
in smisynhic animicrbial agns. Th chmi-
cal mdicain maks h anibiic mr ffciv
agains spcic pahgnic rganisms. Animicrbial
agns ar fn rs classid accrding  h yp f
pahgn  b dsryd, such as bacria (anibac-
rial agns), fungus (anifungal agns), r virus (an-
iviral agns). Th animicrbial agns ar hn sub-
dividd by chmical familis in drug classs such
as h pnicillins, racyclins, and aminglycsids.
Th slcin f h animicrbial agn mus b
basd n h snsiiviy f h pahgn and h ps-
sibl xiciy  h pain. If a all pssibl, infc-
ing rganisms shuld rs b islad and idnid.
Culur and snsiiviy ss shuld b cmpld 
idnify h infciv rganism and drmin h ani-
biic  which h infcing rganism is ms snsiiv.
Bacria ar classid as gram-negative microorganisms
724
agents: allergic reaction, nephrotoxicity, ototoxicity, and
hepatotoxicity.
4. Discuss the primary uses for antitubercular, antifungal, and
antiviral agents.
ototoxicity (ō-tō-tŏks-ĬS-ĭ-tē) (p. 727)
hypoprothrombinemia (hī-pō-prō-
thrŏm-bĭn-Ē-mē-ă) (p. 734)
penicillinase-resistant
penicillins (pĕn-ĭ-SĬL-ĭn-ās rē-ZĬS-
tĕnt pĕn-ĭ-SĬL-ĭnz) (p. 740)
(.g., Acinetobacter spp., Citrobacter spp., Enterobacter
spp., Escherichia coli, Klebsiella spp., Providencia spp.,
Pseudomonas spp., Salmonella spp., and Shigella spp.) r
gram-positive microorganisms (.g., Staphylococcus au-
reus, Staphylococcus epidermidis, Streptococcus pyogenes,
Streptococcus pneumoniae); hwvr, if clinically indi-
cad, a pain may b sard n a brad-spcrum
anibiic rgimn unil h infcing rganism is idn-
id and is drug snsiiviy is drmind. Th ani-
micrbial hrapy is hn sard basd n h snsiiv-
iy rsuls and h clinical judgmn f h halhcar
prvidr. In h inpain sing, hwvr, i is ruin
 bain spcimns f h infcing rganism frm in-
fcd sis (.g., bld, urin, wund) and hn sar
hrapy immdialy wih n r mr animicrbial
agns ha ar ms likly  sp h infcin. This is
knwn as empirical treatment. Whn h culurs idni-
fy h pahgn and h snsiiviy ss indica which
animicrbial agn will b ms ffciv, ha ani-
micrbial agn is sard and all hr animicrbial
agns ar discninud. Discninuain f hrapy f
unndd animicrbial agns hlps prvn h d-
vlpmn f rsisan rganisms and rduc halh-
car css.
Th Amrican Har Assciain and Amrican
Cllg f Cardilgy (Nishimura  al, 2017) guid-
lins rcmmnd prphylacic anibiic ramn
fr pains wih cardiac cndiins ha pu hm a

highs risk fr infciv ndcardiis (IE) and a high
risk f xprincing advrs ucms frm IE. Ths
cardiac cndiins includ prshic cardiac valv;
prvius IE; cngnial har disas; unrpaird, cy-
anic cngnial har disas, including palliaiv
shuns and cnduis; cngnial har dfcs cm-
plly rpaird wih prshic marial r a prsh-
ic dvic—whhr placd by surgry r by cahr
inrvnin—during h rs 6 mnhs afr h pr-
cdur; rpaird cngnial har dfcs wih rsidual
dfcs a h si r adjacn  h si f a prshic
pach r prshic dvic; and cardiac ransplanain.
Fr pains a risk fr dvlping IE, h us f pro-
phylactic antibiotics is rcmmndd bfr dnal
prcdurs and prcdurs n rspirary rac r in-
fcd skin, skin srucurs, r musculsklal issu
NursiNg implicatioNs for aNtimicrobial
therapy
Nurss mus cnsidr h nir pain whn admin-
isring and mniring animicrbial hrapy. I is
ssnial ha h nurs b knwldgabl abu h
drugs, including physilgic paramrs fr mnir-
ing xpcd hrapuic aciviy and advrs ffcs.
I is impran  ach h individual wih an infcin
h basic principls f slf-car, which will nhanc h
rcvry prcss, and masurs  prvn h sprad
f infcin. Wih cmmunicabl disass, xpsd in-
dividuals mus b cnacd fr fllw-up sing and
apprpria ramn.
an
History of current infection. Wha sympms ar d-
scribd by h pain? Which f h sympms d-
scribd pnially rla  an infcius prcss?
Exnd qusining  hlp h pain fcus—fr
xampl, whn did h sympms bgin? Hav hy
wrsnd? Is hr fvr, nigh swas, malais,
chrnic faigu, wigh lss, arhralgia, cugh (yp f
scrins), diarrha, painful urinain, nausa, vm-
iing, lsins r skin rash, discharg, r drainag? Is
hr any swlling, pain, r ha in a paricular ara
r discharg frm a si? Has h pain bn ra-
d prviusly fr a similar infcin? Ask qusins
spcic  h bdy sysms affcd by h infcin
(.g., pain and burning wih urinain fr a urinary
rac infcin [UTI]). Drmin h pain’s currn
living nvirnmn and rviw h insiuinal pli-
cy. Many pains rsiding in lng-rm car faciliis
ar scrnd fr mhicillin-rsisan Staphylococcus
aureus (MRSA) and vancmycin-rsisan Enterococcus
faecium (VRE).
Halhcar-assciad infcins ar cmmn ra-
sns fr admissin  hspials, as wll as rasns fr
xndd says. Ths infcins ccur whn pains
wh ar bing rad fr hr cndiins dvlp an
addiinal infcin whil bing card fr by halh-
car wrkrs. Th cmmn yps f halhcar-ass-
Drugs Used to Treat Infections CHAPTER 45 725
ciad infcins ar halhcar-assciad pnumnia
(HCAP) and UTIs.
Whn raing pains wih sxually ransmid
infcins (STIs), ask abu h numbr f sxual par-
nrs, sxual rinain, and us f prcauins during
inrcurs. (S Chapr 40 fr furhr dails.)
Medication history
• Ask h pain  lis all currn prscribd and
vr-h-cunr (OTC) mdicains r hs akn
in h pas 6 mnhs. Ask spcically abu any
mdicins, such as cricsrids, chmhrapy,
r ransplan immunsupprssans, ha may affc
h immun saus f h individual.
• Ds h prsn ak any yp f allrgy injcins
r mdicains?
• Is h prsn immunizd agains childhd
disass?
• Has h prsn bn rad fr an infcin rcn-
ly? If ys, wha mdicains wr akn and wr
hr any allrgic rspnss? If s, ask fr dails f
h sympms f h allrgic racin.
• Has h pain akn his mdicain bfr? If
s, wha sympms (.g., nausa, vmiing, diar-
rha, rash, iching, r hivs) dvlpd whn ak-
ing i ha ld h pain  sa ha hr was an
allrgy? Ask h pain  dscrib h apparanc
f a rash, whr i sard, and h curs f rcv-
ry. Hw sn afr saring h mdicain did h
sympms dvlp?
• Ask if h pain has vr dvlpd a scnd-
ary infcin (black, hairy ngu; whi pachs
[hrush] in muh; vaginal infcin) whn aking
an anibiic. Fr xampl, wmn aking ani-
biics may dvlp a vaginal infcin bcaus f
supprssin f nrmal ra.
Physical examination
• Prfrm a had-- bdy r funcinal assss-
mn, fcusing n h aras prinn  h admi-
ing diagnsis.
• Assss fr risk facrs ha may cnribu  d-
vlpmn f infcin, such as xnsiv surgical
prcdurs, bsiy, undrlying cnribury cndi-
ins (.g., chrnic bsruciv pulmnary disas,
diabs), immunhrapy drugs, malnuriin, and
ag xrms (infans r ldr aduls).
Psychosocial. Fr an individual wih a srius cm-
municabl disas, assss h rspns and adap-
iv prcsss usd  cp wih h disas and is
ramns.
Assessments during antimicrobial therapy. Rad ach
drug mngraph fr spcic cmmn and srius ad-
vrs ffcs, and individualiz h assssmns fr
h drugs prscribd. Nausa, vmiing, diarrha, al-
lrgis, anaphylaxis, nphrxiciy, hpaxiciy,
726 UNIT IX Drugs Affecting Other Body Systems
xiciy, hmalgic dyscrasias, scndary infc-
in, and phsnsiiviy ar fund wih rcurring
frquncy in h animicrbial drug mngraphs.
Nasa, on, and daha. Ths cndiins ar
h “big hr” advrs ffcs assciad wih ani-
micrbial drug hrapy. Whn hy ccur, gahr daa
such as h fllwing:
1. Did h pain hav a hisry f nausa, vmiing,
r diarrha bfr saring h drug hrapy?
2. Hw sn afr saring h mdicain did h
sympms sar?
3. Sinc saring h mdicain, has h di r war
surc changd in any way?
4. Was h pain aking hr drugs, ihr prscrip-
in r OTC mdicains, bfr iniiaing anibiic
hrapy?
5. Hw much uid is h pain cnsuming whn
aking mdicains? Inadqua uid inak sm-
ims causs gasriis manifsd by nausa.
6. Fr diarrha, wha was h parn f liminain
bfr drug hrapy? Rpr diarrha and h char-
acr and frquncy f sls, as wll as any abdm-
inal pain, prmply. Nausa, vmiing, and diarrha
ar fn ds rlad and rsul frm changs in
nrmal bacrial ra in h bwl, irriain, and
scndary infcin. Sympms rslv wihin a
fw days, and discninuain f hrapy is rarly
rquird.
Whn drug hrapy causs nausa and vmiing,
h halhcar prvidr may lc  giv h ani-
biic wih fd  dcras irriain, vn hugh
absrpin may b slighly dcrasd, r may chs
 swich  a parnral dsag frm. Whn rpr-
ing any incidnc f nausa and vmiing, all signi-
can daa shuld b cllcd and rprd. Adminisr
prscribd animics r anidiarrhal agns (s als
Chaprs 33 and 34).
Sconda ncon. Assss fr sympms f sc-
ndary infcin such as ral infcin. Obsrv fr a
black, hairy ngu; whi pachs (hrush) in h ral
caviy; cld srs; cankr srs; and glssiis. Thr
may b lsins and iching in h vaginal and anal
aras. Scndary infcin f h insin, such as
Clostroides difcile, can prduc svr, lif-hraning
diarrha. Scndary infcin may ccur in pains r-
civing brad-spcrum anibiic hrapy, paricularly
in hs wh ar immunsupprssd. Mnir fr h
dvlpmn f sympms f scndary infcin, and
nify h halhcar prvidr if his ccurs. Insruc
h pain  minimiz xpsur  ppl knwn 
hav an infcin and  pracic gd prsnal hy-
gin masurs.
As and anaphas. Th svriy f an allrgic
racin rangs frm a mild rash  faal anaphylaxis.
Allrgic racins may dvlp wihin 30 minus f
adminisrain f mdicains (.g., anaphylaxis, la-
ryngal dma, shck, dyspna, skin racins) r may
ccur svral days afr discninuing hrapy (.g.,
skin rashs, fvr). All pains mus b qusind fr
prvius allrgic racins, and allrgy-prn pains
mus b bsrvd clsly. I is impran ha a pain
n b labld “allrgic”  a paricular mdicain
wihu adqua dcumnain. Pains wh rpr
gasrinsinal (GI) sympms f nausa, vmiing,
and/r diarrha wih n hr sympms (.g., skin
rash, facial dma, dyspna, hypnsin) shuld n
b labld allrgic  h mdicin. Th mdicain 
which a pain claims an allrgy may b a lifsaving
drug fr ha pain in h fuur.
Clsly mnir all pains—paricularly hs
wih hisris f allrgis, ashma, r rhiniis and hs
wh ar aking mulipl drug prparains—fr an al-
lrgic rspns during animicrbial hrapy. All pa-
ins shuld b wachd carfully fr pssibl allrgic
racins fr a las 20  30 minus afr adminis-
rain f a mdicain. Hwvr, sm drug racins
may n ccur fr svral days. Hld h prscribd
animicrbial mdicain if h prsn rprs a ps-
sibl allrgy. In h vn f suspcd anaphylaxis,
summn h halhcar prvidr and h mrgncy
car immdialy.
Alhugh a srius racin may ccur wih h
rs adminisrain f a drug, rpad xpsurs  a
prviusly snsiizd subsanc can b faal. Rspnd
immdialy  any signs f racin, including swll-
ing, rdnss, r pain a h si f injcin; hivs; na-
sal cngsin and discharg; whzing prgrssing
 dyspna; pulmnary dma; sridr; and srnal
rracins.
Nphooc. Assss nephrotoxicity hrugh an in-
crasing bld ura nirgn (BUN) and crainin,
dcrasing urin upu, dcrasing urin spcic
graviy, cass r prin in h urin, frank bld r
smky-clrd urin, r rd bld clls (RBCs) in x-
css f 0  3 RBCs/high-pwr ld (HPF) (Tabl 41.1)
n h urinalysis rpr.
Medication Safety Alert
Maintain an accurate intake and output record; report declin-
ing output or output less than 30 mL/hr in the adult patient.
Many antimicrobial agents are potentially nephrotoxic (e.g.,
aminoglycosides, tetracyclines, vancomycin). Concomitant
therapy with diuretics enhances the likelihood of toxicity, par-
ticularly in the older or debilitated patient. When renal func-
tion is impaired, most drug dosages must be decreased or
alternative drug therapy used.
Hpaooc. Assss fr prxising hpaic disas
such as cirrhsis r hpaiis. Rviw labrary sud-
is (.g., bilirubin, aspara aminransfras [AST],
alanin aminransfras [ALT], and alkalin phs-
phaas lvls [ALP]; inrnainal nrmalizd rai
[INR]) and rpr abnrmal ndings  h halhcar
prvidr. Svral drugs  b sudid in his chapr ar
pnially hpaxic (.g., isniazid, sulfnamids).
Th livr is aciv in h mablism f many drugs,

and drug-inducd hpaiis may ccur. Th acual livr
damag may ccur shrly afr xpsur  h phar-
maclgic agn, r may n appar fr svral wks
afr iniial xpsur. Th sympms f hpaxiciy
ar anrxia, nausa, vmiing, jaundic, hpamg-
aly, splnmgaly, and abnrmal livr funcin s r-
suls (.g., lvad bilirubin, AST, ALT, ALP; incrasd
INR). Pains wih prxising hpaic disas such
as cirrhsis r hpaiis will rquir lwr dsags f
drugs mablizd by h livr.
Oooc. Damag  h ighh cranial nrv (oto-
toxicity) can ccur frm drug hrapy, paricularly
frm aminglycsids. This may iniially b manifs-
d by dizzinss, innius, and prgrssiv haring lss.
Assss h pain fr difculy in walking unaidd,
and assss h lvl f haring daily. Inninally
spak  pains sfly; n if hy ar awar ha yu
said anyhing. Tak paricular nic f h pain
wh rpadly asks, “Wha did yu say?” r wh
sars alking mr ludly r prgrssivly incrass
h vlum n h lvisin r radi. Rpr pr-
xising haring impairmn r sympms f dvl-
ping haring dcis  h halhcar prvidr and
iniia rdrs prscribd. Prvid fr pain safy
if innius r dizzinss accmpanis h sympms f
haring impairmn.
Bood dscasas
• Ask spcically abu any hisry f bld disr-
drs diagnsd and ramns prscribd.
• Ask spcically abu any yps f anmia (.g.,
aplasic, hmlyic, mgalblasic) r dcincis
f flic acid, viamin B12, r glucs-6-phspha
dhydrgnas.
• Ask whhr h individual has rcivd chm-
hrapy, radiain hrapy, r ransplan hrapy, all
f which may induc an immuncmprmisd sa
and changs in h bld.
• Has h pain rcivd bld cll simular
drugs, such as pin alfa (Epgn) r lgrasim
(Nupgn)?
• Ds h pain hav any blding disrdrs, such
as hmphilia r hrmbcypnia?
• Obsrv fr blding gums, prlngd bld-
ing a an injcin si, pchia, and pisaxis
(nsblds).
• Rviw admissin labrary sudis and rpr ab-
nrmaliis (.g., cmpl bld cun [CBC] wih
diffrnial, incrasd BUN r crainin lvls).
• Individualiz car  h yp f bld dyscrasia
prsn. Whn hypprhrmbinmia is prsn,
h usual ramn is adminisrain f viamin
K. Srius and pssibly faal bn marrw sup-
prssin may ccur afr hrapy is iniiad wih
sm anibiics (.g., chlramphnicl). Mnir
fr signs and sympms such as sr hra, faigu,
lvad mpraur, small pchial hmrrhags,
and bruiss n h skin, and if prsn, rpr hs
sympms immdialy.
Drugs Used to Treat Infections CHAPTER 45 727
Phoosns. Assss fr h dvlpmn f dr-
malgic sympms such as xaggrad sunburn,
iching, rash, uricaria, prurius, and scaling, paricu-
larly afr xpsur  sunligh. Phsnsiiviy is
sldm vidn during hspializain. I is mr cm-
mnly sn in ambulary pracic.
Whn h drug mngraph liss his as a pnial
srius advrs ffc, h nurs shuld prvid halh
aching  prvn is ccurrnc. Insruc h pain
 avid xpsur  sunligh and ulravil ligh
(.g., sun lamps, sunanning bds); war lng-slvd
clhing, a ha, and sunglasss; and apply sunscrn 
xpsd skin whn ging u in h sunligh.
inn
• Ruin mniring f all individuals rciving ani-
micrbial hrapy shuld includ saus f hydra-
in, mpraur, puls, rspirains, and bld
prssur. Mnir a las vry 4 hurs and mr
frqunly as h pain’s clinical saus warrans.
• Us h Cnrs fr Disas Cnrl and Prvnin
(CDC) rcmmndd prcauins fr infcin
ransmissin—sandard prcauins and apprpri-
a guidlins fr islain. Cnsul h CDC’s wb-
si, as wll as clinical plicis and prcdurs, 
prvn ransmissin f infcin. Always rmm-
br h impranc f adqua handwashing.
• Always mnir fr phlbiis whn animicrbials
ar adminisrd inravnusly.
• Adminisr animicrbials as prscribd n h im
schdul sablishd.
• In sm cass, a scnd drug (.g., prbncid) may
b adminisrd cncurrnly  inhibi h xcr-
in f h anibiic (.g., pnicillin, cphalsp-
rin). Whn his is dn, mnir clsly fr advrs
ffcs.
Medication history
• Ask h pain  lis all prscribd mdicains,
OTC mdicains, and hrbal prducs bing ak-
n. Ask spcically abu h rcn us f cric-
srids, chmhrapy, r ransplan supprssans.
• Ds h pain hav any allrgis? If s, bain
dails f mdicains and acual sympms ha
ccur during an allrgic racin. Wha ramn
was usd fr any pas allrgic rspnss? Wha ani-
biics hav bn akn? Wr hr any prblms
during anibiic hrapy?
pn edn
Th fllwing basic principls f pain car shuld
n b vrlkd whn raing pains wih
infcins:
• Adqua rs wih as lil srss as pssibl. Rs
dcrass mablic nds and nhancs h physi-
lgic rpair prcss.
• Nuriinal managmn, including anin  hy-
drain, prins, fas, carbhydras, minrals, and
728 UNIT IX Drugs Affecting Other Body Systems
viamins,  suppr h bdy’s nds during an in-
ammary rspns. Adqua nurins  m
h nrgy nds, spcially during ims f fvr,
ar ssnial s ha h bdy will n brak dwn
is prin srs  m nrgy rquirmns. Th
diary aching mus b individualizd  h pa-
in’s diagnsis and pin f rcvry. Unlss cnra-
indicad by cxising disas, ncurag adqua
uid inak f 2000  3000 mL/24 hr and simula-
nusly mnir h pain fr signs and sympms
f uid vlum dci r uid vlum vrlad.
• Exnsiv aching, individualizd  h circum-
sancs and md f ransmissin f h disas,
shuld b givn  hs wih cmmunicabl in-
fcin. This shuld includ cnacing xpsd
individuals in accrdanc wih insiuinal pli-
cis fr disas scrning, ramn, and fllw-up
cunsling.
• Explain prsnal hygin masurs, such as hand-
washing chniqus, managmn f xcrins
such as spuum, wund car, and h impranc f
n sharing prsnal hygin ims wih hrs.
• Insruc h pain  rfrain frm sxual inr-
curs during hrapy fr STIs.
Medications
• Drug hrapy spcic fr h yp f micrrganism
causing h infcin shuld b xplaind in dail
s ha h pain will raliz h nd fr adhr-
nc  h prscribd rgimn.
• Examin ach drug mngraph  idnify suggs-
ins  h pain n hw  handl h cmmn
advrs ffcs assciad wih animicrbial hr-
apy. Th pain als mus b augh h signs and
sympms ha mus b rprd  h halhcar
prvidr. Srss  h pain h impranc f n
discninuing h prscribd mdicain unil h
advrs ffcs hav bn discussd wih h halh-
car prvidr.
• Dvlp a mdicain schdul wih h pain fr
a-hm mdicains prscribd. Mak sur ha
h pain undrsands why i is impran  ak
animicrbials fr h nir curs f drug hrapy
and n  discninu hm whn fling br.
Cmpling ramn is criical  prvning mi-
crbial rsisanc  anibiics. In addiin, pains
mus knw slf-mniring paramrs fr h pr-
scribd drug hrapy.
• Nursing mhrs shuld rmind hir halhcar
prvidr ha hy ar bras fding s ha ani-
biics may b slcd ha will hav n ffc n h
infan.
• Afr an allrgic racin, h pain and family
shuld infrm anyn raing h pain in h
fuur f h allrgy  a spcic drug. Waring an
allrgy bracl r ag may b apprpria. A wall
card dscribing h yp f allrgy can b hlpful 
fuur halhcar prvidrs.
• Fllw rcmmndains fr annual inunza vac-
cin and pnumcccal vaccin fr high-risk indi-
viduals (.g., childrn; pains wih diabs, ash-
ma, r pulmnary disas; ldr aduls; halhcar
wrkrs; ppl wih chrnic r dbiliaing disas-
s). Always chck wih h halhcar prvidr if in
dub abu advisabiliy f adminisring vaccin.
Fostering health maintenance
• Thrughu h curs f ramn, discuss mdi-
cain infrmain. Cninu  mphasiz hs
facrs ha h pain can cnrl  alr h pr-
grssin f h disas: mainnanc f gnral
halh and nuriinal nds, adqua rs and ap-
prpria xrcis, and aking h prscribd mdi-
cain unil h nir curs f hrapy has bn
cmpld.
• Discuss xpcains f hrapy s ha h pain
undrsands whhr a saisfacry rspns 
drug hrapy is bing achivd, such as h rlif
f sympms fr which ramn was sugh (.g.,
rlif f burning wih urinain and frquncy f
urinain, rlif f cugh, r nd f drainag and
haling f a wund).
Patient self-assessment. Enlis h pain’s hlp in
dvlping and mainaining a wrin rcrd f mn-
iring paramrs (.g., lis prsning sympms:
cugh wih a larg amun f phlgm, wund drain-
ag, mpraur, xrcis lranc). S Pain Slf-
Assssmn Frm fr Anibiics n h Evlv wb-
si. Cmpl h Prmdicain Daa clumn fr
us as a baslin  rack rspns  drug hrapy.
Ensur ha h pain undrsands hw  us h
frm, and insruc h pain  ak h cmpld
frm  fllw-up visis. During fllw-up visis,
fcus n issus ha will fsr adhrnc  h hra-
puic inrvnins prscribd.
Drug therApy for infectious
DiseAse
Drug ClASS: AmiNOglyCOSiDeS
an
Aminglycsid anibiics kill bacria primarily by
inhibiing prin synhsis. Ohr mchanisms f ac-
in hav n y bn fully dnd.
u
Th aminglycsids ar usd primarily agains gram-
ngaiv micrrganisms ha caus UTIs, mningiis,
wund infcins, and lif-hraning spicmias.
Thy ar h mainsays in h ramn f halhcar-
assciad gram-ngaiv infcins (.g., Acinetobacter
spp., Citrobacter spp., Enterobacter spp., E. coli, Klebsiella
spp., Providencia spp., Pseudomonas spp., Salmonella

spp., and Shigella spp.). Nmycin may als b usd
bfr surgry  rduc h nrmal ral cnn f
h insinal rac.
t o
Th primary hrapuic ucm xpcd frm
aminglycsid hrapy is liminain f bacrial
infcin.
Nn in  and
Premedication assessment
1. Obain baslin assssmns f h prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr any allrgis and sympms f haring
lss r rnal disas. If prsn, wihhld drug and
rpr ndings  h halhcar prvidr.
4. If h pain has had anshsia wihin h pas 48
 72 hurs, chck  s if sklal muscl rlaxans
wr adminisrd. If usd, wihhld h drug and
nify h halhcar prvidr.
5. Chck fr schduld im f labrary amin-
glycsid srum lvl sing. Afr lvls hav bn
drmind, assss whhr rsuls ar nrmal r
xic. Cnac h halhcar prvidr as apprpria.
6. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, BUN, cr-
ainin, culur and snsiiviy).
Availability, dosage, and administration
S Tabl 45.1.
Ad copabs. Do not mix hr drugs in
h sam syring wih aminglycsid anibiics r
infus ghr wih hr drugs. S Drug Inracins
lar in his scin fr incmpaibiliis.
ra o nson. Chck wih h hspial labra-
ry rgarding iming f aminglycsid bld lvl
ss. Th ra f infusin is qui impran fr amin-
glycsid anibiics, spcially if prinfusin and ps-
infusin srum lvls ar bing masurd. Cnsul
wih a pharmacis r rviw h individual packag li-
raur fr prpr infusin ra. Afr lvls hav bn
drmind, assss whhr rsuls ar nrmal r xic.
Serious adverse effects
Snso
Ototoxicity. Damag  h ighh cranial nrv can
ccur as a rsul f aminglycsid hrapy. Cninu
 bsrv pains fr xiciy afr hrapy has
bn discninud. Ths advrs ffcs may appar
svral days lar.
gnona
Nephrotoxicity. Mnir urinalysis and kidny func-
in ss fr abnrmal rsuls. Rpr incrasing BUN
and crainin lvls, dcrasing urin upu r d-
crasing spcic graviy (dspi amun f uid in-
ak), cass r prin in h urin, frank bld r
Drugs Used to Treat Infections CHAPTER 45 729
smky-clrd urin, r RBCs in xcss f 0  3 RBCs/
HPF (s Tabl 41.1) n h urinalysis rpr.
Drug interactions
Nphooc pona. Cphalsprins, amphricin-
B, vancmycin, and lp diurics, whn cmbind
wih aminglycsids, may incras h nphrxic
pnial. Mnir h urinalysis and kidny funcin
s ndings fr abnrmal rsuls.
Oooc pona. Aminglycsids, whn cmbind
wih rsmid, bumanid, and fursmid, may in-
cras xiciy. Thrfr nursing assssmns fr
innius, dizzinss, and dcrasd haring shuld b
dn rgularly vry shif.
mashna as. Aminglycsids shuld b
avidd in pains wih myashnia gravis if pssibl.
Thy may inrfr wih nurmuscular ransmissin
and lad  wrsning muscl waknss.
Nosca bockad. Taking aminglycsid ani-
biics in cmbinain wih sklal muscl rlaxans
may prduc rspirary dprssin. Chck h ans-
hsia rcrds f pspraiv pains  drmin
whhr sklal muscl rlaxans such as succinylch-
lin r pancurnium brmid wr adminisrd dur-
ing surgry.
Th nurs shuld mnir and assss h rspira-
ry ra, dph f rspirains, and chs mvmn
and rpr apna immdialy. Bcaus hs ffcs
may b sn fr up  48 hurs afr adminisrain
f sklal muscl rlaxans, cninu mniring rs-
pirains, puls, and bld prssur bynd h usual
pspraiv vial signs ruin.
Hpan. Th aminglycsid gnamicin and hpa-
rin ar physically incmpaibl. Do not mix ghr
bfr infusin.
Ba-aca–p anbocs (pncns, cphaospo-
ns). Ths drugs rapidly inaciva aminglycsid
anibiics. Do not mix ghr r adminisr ghr
a h sam inravnus (IV) si.
Drug ClASS: CArBAPeNemS
an
Th carbapnms ar xrmly pn brad-spcrum
anibiics rsisan  ba-lacamas nzyms scr-
d by bacria. Thy ac by inhibiing bacrial cll wall
synhsis.
u
• Imipnm-cilasain (Primaxin) is a cmbina-
in prduc cnaining a carbapnm anibiic
calld imipnm and cilasain, an inhibir f
h rnal dippidas nzym dhydrppidas
I. Cilasain has n animicrbial aciviy; i pr-
vns h inacivain f imipnm by h rnal
nzym. I is usd fr h ramn f lwr r-
spirary rac and inraabdminal infcins;
infcins f h urinary rac, bns, jins, and
730 UNIT IX Drugs Affecting Other Body Systems

Table 45.1 Aminoglycosides

geNeriC NAme BrAND NAme AvAilABility ADult DOSAge rANge
amikacin — Injection: IM, IV: 15 mg/kg/24 hr
Do not confuse 500 mg/2 mL in 2-mL vial (max 1.5 g/day)
amikacin with Anakinra. 1 g/4 mL in 4-mL vial
gentamicin — Injection: IM, IV: 3–5 mg/kg/day in
10 mg/mL in 2- mL vials two or three doses or
40 mg/mL in 2- and 20-mL vials 5–7 mg/kg once daily
40-, 60-, 80-, 100-, 120-mg single-dose containers
neomycin — Tablets: 500 mg PO: 4–12 g daily in four
divided doses
plazomicin Zemdri Injection: 500 mg/ 10 mL IV: 15 mg/kg once daily;
adjust dose for obesity
streptomycin — Injection: 1-g vials IM: 15 mg/kg/day once daily
tobramycin — Injection: IM, IV: 3–5 mg/kg/day in
10 mg/mL in 2-mL vials two or three doses or
80 mg/2 mL in 2-mL vials 5 mg/kg once daily
1.2 g in 30-mL bulk vials
2 g in 50-mL bulk vials
Inhalation: 300-mg/4-mL and 300-mg/5-mL
nebulizer solution
Inhalation: 28-mg capsules in boxes of 8 or 56
Do not confuse.

skin; gynclgic infcins; ndcardiis; and
bacrial spicmia causd by gram-ngaiv r
gram-psiiv rganisms. A primary hrapuic
rl f imipnm-cilasain is in h ramn f
svr infcins causd by mulirsisan rgan-
isms and in mixd anarbic-arbic infcins,
primarily hs invlving inraabdminal and
plvic spsis in which Bacteroides fragilis is a cm-
mn pahgn. I shuld b usd in cmbinain
wih anipsudmnal agns bcaus f rsis-
anc f Pseudomonas cepacia and Pseudomonas ae-
ruginosa  imipnm.
• Imipnm/cilasain/rlbacam (Rcarbri).
Rlbacam is a ba-lacamas inhibir ha
prcs imipnm frm dgradain by crain
ba-lacamass. Rcarbri is usd in cmbina-
in wih imipnm and cilasain (rnal dhy-
drppidas inhibir)  ra hspial-acquird
bacrial pnumnia (HABP) and vnilar-
assciad bacrial pnumnia (VABP) causd
by Acinetobacter calcoaceticus-baumannii cmplx,
Enterobacter cloacae, Escherichia coli, Haemophilus
inuenzae, Klebsiella aerogenes, Klebsiella oxytoca,
Klebsiella pneumoniae, Pseudomonas aeruginosa, and
Serratia marcescens in pains a las 18 yars ld.
I is als usd fr cmplicad UTIs, including py-
lnphriis and cmplicad inraabdminal in-
fcins (cIAI) in pains wh hav limid r n
alrnaiv ramn pins.
• Mrpnm is a carbapnm anibiic ha
has a chmical srucur ha prcs i agains
dhydrppidas I, s ha cilasain is n nc-
ssary. I has a brad spcrum f aciviy similar
 ha f imipnm, bu i is mr aciv agains
Enrbacriaca and lss aciv agains gram-
psiiv bacria. I is usd aln by h IV ru
fr h ramn f inraabdminal infcins
causd by E. coli, Klebsiella pneumoniae, P. aerugi-
nosa, B. fragilis, and Peptostreptococcus spp. I is als
usd aln inravnusly  ra bacrial mnin-
giis causd by Strep. pneumoniae, Haemophilus in-
uenzae, and Neisseria meningitidis. Vabrbacam
is a ba-lacamas inhibir ha prcs mrp-
nm frm dgradain by crain ba lacamass.
Vabrbacam is usd in cmbinain wih mrp-
nm (Vabmr)  ra cmplicad UTIs, includ-
ing pylnphriis causd by E. coli, K. pneumoniae,
and Enterobacter cloacae spcis in pains a las
18 yars ld.
• Erapnm is a carbapnm anibiic ha has a
chmical srucur ha prcs i agains dhydr-
ppidas I, s ha cilasain is n ncssary. I has
a brad spcrum f aciviy and is apprvd  ra
infcins causd by arbic and anarbic gram-ps-
iiv and gram-ngaiv bacria causing cmplicad
inraabdminal infcins, skin and skin srucur in-
fcins, cmmuniy-acquird pnumnia, UTIs (in-
cluding pylnphriis), and acu plvic infcins.
I is ffciv agains suscpibl srains f S. aureus, S.
agalactiae, Strep. pneumoniae, S. pyogenes, E. coli, K. pneu-
moniae, Moraxella catarrhalis, H. inuenzae, Bacteroides
spp., Clostridium spp., and Peptostreptococcus spp

t o
Th primary hrapuic ucm xpcd frm car-
bapnm hrapy is liminain f bacrial infcin.
Nn in  cn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis. Ask spcically abu pni-
cillin and cphalsprin allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
6. Prfrm a baslin assssmn f h pain’s d-
gr f alrnss and rinain  nam, plac, and
im bfr bginning hrapy.
7. Ask whhr hr is a hisry f sizur aciviy b-
fr iniiaing hrapy.
Availability, dosage, and administration
S Tabl 45.2.
Hpsns. Alhugh hs anibiics ar
carbapnms rahr han pnicillins r cphalspr-
ins, hy als cnain a ba-lacam nuclus. Crss-
hyprsnsiiviy may dvlp bwn hs classs.
Cmpl a hisry f hyprsnsiiviy bfr saring
hrapy. If an allrgic racin  a carbapnm ccurs,
discninu h infusin. Srius racins may rquir
pinphrin and hr mrgncy masurs.
Ad copabs. Do not mix hr drugs in
h sam syring wih carbapnms r infus ghr
wih hr drugs. S Drug Inracins lar in his
scin fr incmpaibiliis.
Th carbapnms rquir spcial car rgarding
mixing and adminisrain:
• Imipnm-cilasain shuld n b mixd wih r
physically addd  hr anibiics, bu i may b
adminisrd cncmianly wih hr anibiics,
such as aminglycsids.
• Mrpnm shuld n b mixd wih r physically
addd  sluins cnaining hr mdicins.
• Erapnm fr IV us shuld b rcnsiud wih
bacrisaic war r 0.9% sdium chlrid (nr-
mal salin) fr injcin. D n rcnsiu r di-
lu wih dxrs sluins.
• Erapnm fr IM us shuld b rcnsiud wih 1%
lidcain injcin (wihu pinphrin). Adminisr
h injcin wihin 1 hur f rcnsiuin.
Common adverse effects
gasonsna
Severe diarrhea. Svr diarrha may dvlp frm
using carbapnms. Bld and mucus in h sl
may als b prsn. This may b an indicain f
Drugs Used to Treat Infections CHAPTER 45 731
drug-inducd psudmmbranus cliis and shuld
b rprd immdialy. Wihhld h nx ds f an-
ibiic unil h halhcar prvidr givs apprval fr
adminisrain.
Nooc
Dizziness. Prvid fr pain safy during pisds
f dizzinss; rpr fr furhr valuain.
Confusion, seizures. Sizur aciviy—including my-
clnic aciviy, fcal rmrs, cnfusin, and hr si-
zurs—has bn rprd wih h carbapnms. Ths
pisds ccur ms cmmnly in pains wih his-
ris f prvius sizur aciviy and rnal impairmn.
Prfrm a baslin assssmn f h pain’s d-
gr f alrnss and rinain  nam, plac, and
im bfr iniiaing hrapy. Mak rgularly schd-
uld subsqun mnal saus valuains, and cm-
par ndings. Rpr alrains in cnsciusnss.
Implmn sizur prcauins. Mak sur ha h
pain cninus wih anicnvulsan hrapy. If si-
zurs dvlp, prvid fr pain safy and hn r-
crd h xac im f sizur ns and durain f
ach phas, a dscripin f h spcic bdy pars
invlvd, and any prgrssin in h affcd pars.
Dscrib aumaic rspnss during h clnic phas:
alrd, jrky rspirains r frhy salivain, dilad
pupils and any y mvmns, cyansis, diaphrsis,
r incninnc.
vasca
Phlebitis. Carfully assss pains fr hrmbphl-
biis. Inspc h IV ara frqunly using a phlbiis
scal and rpr rdnss, warmh, ndrnss  uch,
and dma in h IV si.
Drug interactions
Pobncd. Prbncid inhibis h urinary xcr-
in f carbapnms. D n adminisr prbncid
cncurrnly.
vapoc acd. Carbapnm anibiics may prduc
clinically signican rducins in valpric acid lv-
ls, which may lad  a lss f sizur cnrl. If any
carbapnm is adminisrd wih valpric acid, srum
valpric acid lvls shuld b mnird frqunly.
gancco. Cncurrn adminisrain f ganci-
clvir and imipnm-cilasain has rsuld in an in-
crasd incidnc f sizurs. Avid cncurrn us if
a all pssibl.
Drug ClASS: CePHAlOSPOriNS
an
Th cphalsprins ar chmically rlad  h pni-
cillins and hav a similar mchanism f aciviy. Th
cphalsprins ac by inhibiing cll wall synhsis
in bacria. Th cphalsprins may b dividd in
grups, r “gnrains,” basd primarily n ani-
micrbial aciviy. Th rs-gnrain cphalsprins
hav ffciv aciviy agains gram-psiiv micrr-
ganisms (Staph. aureus, Staph. epidermidis, Strep. pyogenes,
732 UNIT IX Drugs Affecting Other Body Systems
Table 45.2 Carbapenems
geNeriC NAme BrAND NAme AvAilABility
ertapenem Invanz Injection: 1-g vials
imipenem- Primaxin IV Injection:
cilastatin Do not confuse IV: 250-,
Primaxin with 500-mg vials
Premarin.
meropenem — Injection: 500-mg,
1-g vials
meropenem- Vabomere Injection: 2-g vials
vaborbactam
Do not confuse.
Strep. pneumoniae) and rlaivly mild aciviy agains
gram-ngaiv micrrganisms (E. coli, K. pneumoni-
ae, Proteus mirabilis). Scnd-gnrain cphalsp-
rins hav smwha incrasd aciviy agains gram-
ngaiv bacria bu ar much lss aciv han h
hird-gnrain agns, which ar gnrally lss aciv
han rs-gnrain agns agains gram-psiiv ccci,
alhugh hy ar much mr aciv agains pnicillin-
as-prducing bacria. Sm f h hird-gnrain
cphalsprins als ar aciv agains P. aeruginosa, a p-
n gram-ngaiv micrrganism. Furh-gnrain
cphalsprins ar brad-spcrum agns wih bh
gram-ngaiv and gram-psiiv cvrag. Cfarlin,
a fh-gnrain agn, is h nly cphalsprin wih
aciviy agains MRSA. I is currnly apprvd  ra
suscpibl skin infcins and cmmuniy-acquird
bacrial pnumnia. Cdrcl is a sidrphr cph-
alsprin ha nly has aciviy agains gram-ngaiv
arbic bacria. I is currnly usd  ra cmplicad
UTIs, including pylnphriis and hspial acquird
and vnilar assciad bacrial pnumnia causd
by h fllwing suscpibl gram-ngaiv micr-
rganisms: E. coli, K. pneumoniae, P. mirabilis, P. aerugino-
sa, and Enterobacter cloacae cmplx, in pains 18 yars
r ldr wh hav limid r n alrnaiv ramn
pins.
u
Cphalsprins may b usd wih cauin as alrna-
ivs whn pains ar allrgic  h pnicillins unlss
hy ar als allrgic  h cphalsprins. Th cph-
alsprins ar usd fr crain urinary and rspira-
ry rac infcins, abdminal infcins, bacrmia,
mningiis, and smyliis.
t o
Th primary hrapuic ucm xpcd frm cph-
alsprin hrapy is liminain f bacrial infcin.
DOSAge rANge
IM, IV: 1 g daily
Infuse IV solution over 30 min for up to 14 days
Limit IM injection to 7 days
IV: 50 mg/kg/day up to 4 g/day in two to four doses;
125, 250, or 500 mg by IV infusion over 20–30 min
Infuse 750-mg or 1-g dose over 40–60 min; if nausea
develops, slow the infusion rate
IM: 500–750 mg q12h, depending on severity of
infection; do not exceed 1500 mg/day
IV: 1 g IV q8h; infuse over 15–30 min or as a bolus over
3–5 min
IV: 4 g q8h for up to 14 days; infuse over 3 hr
Nn in  cn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr any allrgis, sympms f rnal disas,
r blding disrdrs. If prsn, wihhld drug and
rpr ndings  h halhcar prvidr.
4. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability, dosage, and administration
S Tabl 45.3.
Common adverse effects
gasonsna
Diarrhea. Cphalsprins caus diarrha by alr-
ing h bacrial ra f h GI rac. Th diarrha is
usually n svr nugh  warran discninuing
mdicain. Encurag h pain n  discninu
hrapy wihu cnsuling h halhcar prvidr.
Whn diarrha prsiss, mnir h pain fr signs
f dhydrain.
Hepatotoxicity. Transin lvains f livr func-
in s rsuls (.g., AST, ALT, alkalin phsphaas)
hav bn rprd. Mnir rurning labrary
daa and rpr abnrmal ndings  h halhcar
prvidr.
in ss (opponsc ncons)
Secondary infections. Oral hrush, gnial and anal
prurius, vaginiis, and vaginal discharg may ccur
wih cphalsprin hrapy. Rpr  h halhcar
prvidr prmply bcaus hs infcins ar rsis-
an  h riginal anibiic usd. Tach h impranc
f miculus ral and prinal prsnal hygin.
 Drugs Used to Treat Infections CHAPTER 45 733

Table 45.3 Cephalosporins

geNeriC NAme BrAND NAme geNerAtiON AvAilABility ADult DOSAge rANge
cefaclor — 2 Capsules: 250, 500 mg PO: 250–500 mg q8h; do not
Tablets, extended release (12 hr): 500 exceed 4 g/day
mg
Oral suspension: 125, 250, 375 mg/5
mL
cefadroxil — 1 Capsules: 500 mg PO: 1–2 g daily in one or two
Tablets: 1000 mg doses
Suspension: 250, 500 mg/5 mL
cefazolin — 1 Injection: 500-mg and 1-, 10-, 100-, IM, IV: dose depends on
300-g vials organism being treated
cefdinir — 3 Capsules: 300 mg PO: 300 q12h and 600 mg
Oral suspension: 125, 250 mg/5 mL once daily
cefepime — 4 Injection: 1-, 2-g vials IM, IV: 0.5–2 g q8–12h
cederocol Fetroja — Injection: 1 g IV: 2 g q8h for 7–14 days
cexime Suprax 3 Tablets, chewable: 100, 200 mg PO: 200 mg q12h or 400 mg
Do not Capsules: 400 mg once daily
confuse Suspension: 100, 200, 500 mg/5 mL
Suprax
with
Surfak.
cefotaxime — 3 IV: 500-mg and 1-, 2-g vials IV: 1–2 g q4–12h; do not
exceed 12 g/day
cefotetan Cefotan 2 Injection: 1-, 2-g vials IM, IV: 1–3 g q12h; do not
exceed 6 g/day
cefoxitin — 2 Injection: 1-, 2-, 10-g vials IM, IV: 1–2 g q4–6h or 2–3 g
q6–8h; do not exceed 12 g/
day
cefpodoxime — 3 Tablets: 100, 200 mg PO: 200 mg q12h for 7–14 days
Suspension: 50, 100 mg/5 mL
cefprozil — 2 Tablets: 250, 500 mg PO: 250–500 mg q12h for 10
Suspension: 125, 250 mg/5 mL days
ceftaroline Tearo 5 (MRSA IV: 400-, 600-mg vials IV: 600 mg q12h for 5–14 days
active)
ceftazidime Fortaz Tazicef 3 Injection: 500-mg and 1-, 2-, 6-g vials IM, IV: 1–2 g q12h
ceftriaxone — 3 Injection: 250-, 500-mg and 1-, 2-, 10-, IM, IV: 1–2 g once daily; do not
100-g vials exceed 4 g daily
cefuroxime — 2 Tablets: 250, 500 mg PO: 250–500 mg q12h
Do not IV: 750-mg and 1.5-, 7.5-g vials IV: 750 mg–1.5 g q8h
confuse
cefuroxime
with
deferoxamine.
cephalexin — 1 Tablets: 250, 500 mg PO: 250–1000 mg q6h or 500
Capsules: 250, 500, 750 mg mg q12h
Suspension: 125, 250 mg/5 mL
COmBiNAtiON PrODuCtS
ceftazidime/ Avycaz Injection: 2 g ceftazidime; 500 mg IV: 2.5 mg ceftazidime q8h
avibactam avibactam
ceftolozane/ Zerbaxa Injection: 1 g ceftolozane; 500 mg IV: 1.5 g ceftolozane q8h
tazobactam tazobactam
Do not confuse.
734 UNIT IX Drugs Affecting Other Body Systems
rna
Nephrotoxicity. Transin lvains f rnal s r-
suls (.g., BUN, srum crainin) hav bn rprd.
Rnal xiciy, as vidncd by prinuria, hmauria,
cass, dcrasd crainin claranc, and dcrasd
urin upu, als has bn rprd. Mnir rurn-
ing labrary daa and rpr abnrmal ndings 
h halhcar prvidr.
Haooc
Hypoprothrombinemia. Hypoprothrombinemia, a r-
ducin in circulaing prhrmbin, wih and wihu
blding, has bn rprd. This rar ccurrnc is
ms frqun in ldr adul, dbiliad, r hrwis
cmprmisd pains wih brdrlin viamin K d-
cincy. Tramn wih brad-spcrum anibiics
liminas nugh GI ra  caus a furhr rducin
in viamin K synhsis.
Assss h pain fr cchymsis afr minimal
rauma; prlngd blding a an infusin si r frm
a surgical wund; r h dvlpmn f pchia,
blding gums, r nsblds. Nify h halhcar
prvidr f any f h signs f hypprhrmbinmia.
Th usual ramn is adminisrain f viamin K.
Electrolyte imbalance. If a pain dvlps hypr-
kalmia r hyprnarmia, cnsidr h lcrly
cnn f h anibiics. Ms cphalsprins hav a
high lcrly cnn.
vasca
Thrombophlebitis. Phlbiis and hrmbphlbiis, r
inammain f h vin wih a bld cl r hrm-
bus, ar rcurrn prblms assciad wih IV admin-
israin f cphalsprins. Us small IV ndls in
larg vins and alrna infusin sis, if pssibl, 
minimiz irriain. Carfully assss pains rciving
IV cphalsprins fr h dvlpmn f hrmb-
phlbiis. Inspc h IV infusin ara frqunly whn
prviding car; inspc during drssing changs and
whn h infusin is changd  a nw si. Always in-
vsiga pain a h IV si. Rpr rdnss, warmh,
ndrnss  uch, and dma in h affcd par.
Drug interactions
Nphooc pona. Pains rciving cphalspr-
ins, aminglycsids, vancmycin, and lp diurics
cncurrnly shuld b assssd fr signs f nphr-
xiciy. Mnir urinalysis and kidny funcin ss
fr abnrmal rsuls. Rpr incrasing BUN and cr-
ainin lvls, dcrasing urin upu r dcrasing
spcic graviy (dspi amun f uid inak), cass
r prin in h urin, frank bld r smky-clrd
urin, r RBCs in xcss f 0  3 RBCs/HPF (s Tabl
41.1) n h urinalysis rpr.
Anacds. Anacids inhibi h absrpin f cfaclr,
cfdinir, and cfpdxim. If anacids mus b akn,
h anibiic shuld b akn 2 hurs bfr r afr
h anacid.
Hsan-2 anaonss. Hisamin-2 (H2) an-
agniss (.g., cimidin, famidin, nizaidin,
raniidin) inhibi h absrpin f cfpdxim and
cfurxim, dcrasing h anibiic ffc. Bcaus
f h lng durain f acin f h H2 anagniss, i
is rcmmndd ha hy n b adminisrd whn
hs cphalsprins ar prscribd.
ion sppns. Irn supplmns and fd fri-
d wih irn inhibi h absrpin f cfdinir. If irn
supplmns mus b akn, h anibiic shuld b
akn 2 hurs bfr r afr h irn supplmn.
Pobncd. Pains rciving prbncid in cm-
binain wih cphalsprins ar mr suscpibl 
xiciy bcaus f h inhibiin f xcrin f h
cphalsprins by prbncid. Mnir clsly fr ad-
vrs ffcs.
Acoho. Insruc h pain  avid alchl cn-
sumpin during cfan hrapy. Pains ingsing
alchl during, and fr 24  72 hurs afr, adminis-
rain f cfan will bcm ushd, rmulus,
dyspnic, achycardic, and hypnsiv. Als, ll h
pain n  us OTC prparains cnaining alc-
hl, such as muhwash (.g., Cēpacl, Lisrin) r
cugh prparains.
Oa conacps. Cphalsprins may inrfr
wih h cnracpiv aciviy f ral cnracpivs.
Oral cnracpivs shuld n b discninud, bu
cunsling rgarding us f addiinal mhds f
cnracpin (.g., cndms and fam) shuld b
plannd.
Drug ClASS: glyCOPePtiDeS
an
Glycppids ar a class f anibiics ha prvns
h synhsis f bacrial cll walls. This si f acin is
diffrn frm h sis f hr anibiics inrfring
wih cll wall synhsis.
u
• Dalbavancin is usd in h ramn f adul pa-
ins wih acu bacrial skin and skin srucur
infcins causd by suscpibl islas f h fl-
lwing gram-psiiv micrrganisms: Staph. aureus
(including mhicillin-suscpibl and mhicillin-
rsisan srains), Strep. pyogenes, Streptococcus
agalactiae, Streptococcus dysgalactiae, Streptococcus an-
ginosus grup, and Enterococcus faecalis (vancmy-
cin-suscpibl srains).
• Oriavancin is usd in h ramn f adul pa-
ins wih acu bacrial skin and skin srucur
infcins causd by suscpibl islas f h fl-
lwing gram-psiiv micrrganisms: Staph. aureus
(including mhicillin-suscpibl and mhicillin-
rsisan srains), Strep. pyogenes, Strep. agalactiae,
Strep. dysgalactiae, Strep. anginosus grup, and E. fae-
calis (vancmycin-suscpibl srains).
• Tlavancin is usd in h ramn f cmplicad
skin and skin srucur infcins (cSSSIs) causd
by suscpibl gram-psiiv rganisms including
 Drugs Used to Treat Infections CHAPTER 45 735

Table 45.4 Glycopeptides

geNeriC NAme BrAND NAme AvAilABility DOSAge rANge
dalbavancin Dalvance IV: 500 mg/vial 1500 mg as a single dose or 1000 mg as a single dose
initially, followed by 500 mg as a single dose 1 wk later
oritavancin Orbactiv IV: 400 and 1200 mg as a single dose
Kimyrsp 1200 mg/vial
telavancin Vibativ IV: 750 mg/vial 10 mg/kg q24h
vancomycin Vancocin PO: 125- and Adult:
Do not confuse PMS_Vancomycin 250-mg capsules; PO: 500–2000 mg daily in divided doses q6h (not
vancomycin with 25-, 50-mg/mL appropriate for systemic infections because of low
vecuronium, oral solution absorption)
Vibramycin, IV: 0.5-, 0.75-, 1-, IV: 15 mg/kg q12h is a usual starting dose in most
azithromycin, or 1.25-, 1.5-, 5-, nonobese patients with normal renal function or
gentamicin. 10-, 100-g 15–20 mg/kg/dose q8–12h with normal renal
powder/vial function
Pediatric:
PO: 40 mg/kg/day in three or four divided doses for
7–10 days (maximum: 2000 mg/day)
IV: 40 mg/kg/day in three or four divided doses for
7–10 days (maximum: 2000 mg/day)
Available in Canada.
Do not confuse.

mhicillin-suscpibl r -rsisan Staph. aureus, 4. Assss fr any allrgis.

vancmycin-suscpibl E. faecalis, and Strep. pyo-
genes, Strep. agalactiae, r Strep. anginosus grup. I is
als usd  ra hspial-acquird and vnilar-
assciad bacrial pnumnia causd by suscp-
ibl islas f Staph. aureus whn alrnaiv ra-
mns ar n apprpria.
• Vancmycin is ffciv agains nly gram-psiiv
bacria such as srpccci, saphylccci, C. dif-
cile, Listeria monocytogenes, and Corynebacterium ha
may caus ndcardiis, smyliis, mningiis,
pnumnia, r spicmia. I may b usd rally
agains saphylcccal nrcliis and anibiic-
assciad psudmmbranus cliis prducd by
C. difcile. Bcaus f pnial advrs ffcs, van-
cmycin hrapy is rsrvd fr pains wih p-
nially lif-hraning infcins wh cann b
rad wih lss xic agns such as pnicillins r
cphalsprins.
t o
Th primary hrapuic ucm xpcd frm all
h glycppid hrapis is liminain f bacrial
infcin.
Nn in  gd
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr nrmal rnal funcin and haring bfr
iniiaing hrapy.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability, dosage, and administration
S Tabl 45.4.
S s. Srum rugh lvls f vancmycin
shuld b ruinly rdrd  minimiz advrs f-
fcs. Nify h halhcar prvidr f any abnrmal
srum lvls rprd s ha dsag adjusmns may
b mad. Cnsul labrary rprs fr nrmal rang.
Srum lvls ar n ncssary fr lavancin, dalba-
vancin, r riavancin.
Medication Safety Alert
Rapid IV administration of vancomycin, telavancin, or
dalbavancin may result in a severe hypotensive episode.
Patients develop a red neck syndrome, or red man syn-
drome, characteristic of vancomycin. It is manifested by
a sudden and profound hypotension, with or without a
maculopapular rash over the face, neck, upper chest, and
extremities. The rash generally resolves within a few hours
after terminating the infusion. In rare cases, the adminis-
tration of uids, antihistamines, or corticosteroids may be
necessary. For vancomycin and telavancin, administer the
solution over at least 60 minutes. For dalbavancin, ad-
minister over 30 minutes. Monitor blood pressure during
infusion.
Oritavancin should be infused over 3 hours. If an infusion-
related reaction (pruritus, urticaria, ushing) occurs, consider
slowing or interrupting the infusion.
736 UNIT IX Drugs Affecting Other Body Systems
Serious adverse effects
Snso
Ototoxicity. Vancmycin may caus xiciy. This
may iniially b manifsd by dizzinss, innius, high
n haring lss, and prgrssiv vrall haring lss.
Oldr pains ar paricularly suscpibl  dafnss.
Assss pains fr difculy in walking unaidd, and
assss h lvl f haring daily. Inninally spak
 pains sfly; n if hy ar awar ha anyhing
was said. Tak paricular nic f h pain wh r-
padly asks, “Wha did yu say?” r wh sars alk-
ing mr ludly r prgrssivly incrass h vlum
n h lvisin r radi.
una
Nephrotoxicity. Mnir urinalysis and kidny func-
in ss fr abnrmal rsuls. Rpr incrasing BUN
and crainin lvls, dcrasing urin upu r d-
crasing urin spcic graviy (dspi amun f uid
inak), cass r prin in h urin, frank bld r
smky-clrd urin, r RBCs in xcss f 0  3 RBCs/
HPF (s Tabl 41.1) n h urinalysis rpr.
Cadoasca
QT interval prolongation. Avid lavancin in pains
wih cngnial lng QT syndrm, knwn prlnga-
in f h crrcd QT (QTc) inrval, uncmpnsa-
d har failur, r svr lf vnricular hyprrphy.
Coaaon. Alhugh lavancin and riavancin
d n inrfr wih cagulain, hy can inrfr
wih crain ss usd  mnir cagulain, such as
prhrmbin im r INR, acivad parial hrmb-
plasin im, and acivad cling im.
Hpac cs. ALT lvains hav bn rprd
wih dalbavancin.
in ss (opponsc ncons)
Secondary infections. Oral hrush, gnial and anal
prurius, vaginiis, and vaginal discharg may ccur.
Rpr prmply bcaus hs infcins ar rsisan
 h riginal anibiic usd. Tach h impranc f
miculus ral and prinal prsnal hygin.
Drug interactions
Nphooc, oooc. Cncurrn and squnial
us f vancmycin wih hr xic r nphrxic
agns such as h aminglycsids (.g., gnamicin,
bramycin, amikacin), cisplain, fursmid, rsm-
id, and bumanid rquirs carful mniring.
Nosca bockad. Vancmycin in cmbinain
wih sklal muscl rlaxans may prduc rspirary
dprssin. Chck h anshsia rcrd in pspra-
iv pains  drmin whhr sklal muscl rlax-
ans such as succinylchlin r pancurnium brmid
wr adminisrd during surgry. Th nurs shuld
mnir and assss h rspirary ra, dph f rspi-
rains, and chs mvmn and rpr apna imm-
dialy. Bcaus hs ffcs may b sn fr up  48
hurs afr adminisrain f sklal muscl rlaxans,
cninu mniring rspirains, puls, and bld prs-
sur bynd h usual pspraiv vial signs ruin.
Hpan. Avid h us f IV hparin wih lavancin
and riavancin. Bh may aricially incras h r-
suls f labrary ss cmmnly usd  mnir IV
hparin ffcivnss (.g., acivad parial hrmb-
plasin im).
Drug ClASS: glyCylCyCliNeS
n (tī-gĕ-SĪ-klēn)
t (TĪG-ă-sĭl)
an
Tigcyclin is h rs f h animicrbial agns knwn
as h glycylcyclins. Tigcyclin is chmically rlad
 h racyclins bu is n suscpibl  h mcha-
nisms ha caus rsisanc  h racyclins. I acs
by binding  h 30S ribsm, prvning prin syn-
hsis. I is a bacrisaic anibiic ffciv agains a
brad spcrum f gram-psiiv, gram-ngaiv, and
anarbic micrrganisms. I is n ffciv agains
viruss.
u
Tigcyclin is usd  ra cSSSIs causd by E. coli,
Enterococcus faecalis, Staph. aureus (mhicillin-
suscpibl and mhicillin-rsisan islas),
Strep. agalactiae, and B. fragilis. I may als b
usd  ra cmplicad inraabdminal infc-
ins causd by Citrobacter freundii, Enterobacter
cloacae, E. coli, Klebsiella oxytoca, K. pneumoniae,
Enterococcus faecalis, Staph. aureus (mhicillin-
suscpibl islas nly), B. fragilis, B. vulgatus,
Clostridium perfringens, and Peptostreptococcus mi-
cros. In an ffr  slw h dvlpmn f srains
f bacria rsisan  igcyclin, i shuld b
usd nly whn h pahgn is rsisan  hr
availabl anibiics.
Tigcyclin is n apprvd fr us in ppl yung-
r han 18 yars. As wih racyclins, igcyclin ad-
minisrd during h ags f h dvlpmn (h
las half f prgnancy hrugh ag 8 yars) may caus
naml hypplasia and prmann yllw, gray, r
brwn saining f h h.
t o
Th primary hrapuic ucm xpcd frm ig-
cyclin hrapy is liminain f bacrial infcin.
Nn in  tn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis.

5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability. IV: 50-mg vials.
Dosage and administration. IV: Iniial: 100 mg fl-
lwd by 50 mg vry 12 hurs. Adminisr by IV in-
fusin vr 30  60 minus. Thrapy is cninud fr
5  14 days, dpnding n h svriy and si f h
infcin and h pain’s clinical prgrss.
Common adverse effects
gasonsna
Gastric irritation. Th ms cmmn advrs ffcs f
igcyclin hrapy ar nausa and vmiing (30% and
20%, rspcivly). Ths advrs ffcs ar usually
mild  mdra in h rs 1  2 days f hrapy and
nd  rslv wih cninud hrapy.
Severe diarrhea. Rarly, svr diarrha may dvlp
frm h us f igcyclin. Rpr diarrha f v r
mr sls daily  h halhcar prvidr. This may
b an indicain f drug-inducd psudmmbranus
cliis. Bld r mucus in h sl als shuld b r-
prd  h halhcar prvidr. Warn patients not to
treat diarrhea themselves when taking this drug. Th
us f diphnxyla, lpramid, r pargric may
prlng r wrsn h cndiin.
inna
Photosensitivity. Phsnsiiviy rsuling in an x-
aggrad sunburn afr shr xpsur has bn r-
prd. Th pain shuld b cauind  avid xp-
sur  sunligh and ulravil ligh. Suggs waring
lng-slvd clhing, a ha, and sunglasss whn u-
drs. Discurag h us f anning lamps. Cnsul
h halhcar prvidr abu h advisabiliy f dis-
cninuing hrapy.
Drug interactions
Waan. Tigcyclin may nhanc h ani-
cagulan ffcs f warfarin. Obsrv fr pchia;
cchymss; nsblds; blding gums; dark, arry
sls; and brigh rd r cff-grund msis. Mnir
h INR and rduc h dsag f warfarin if ncssary.
Oa conacps. Tigcyclin may inrfr wih
h aciviy f ral cnracpivs. Oral cnracpivs
shuld n b discninud, bu cunsling rgarding
us f addiinal mhds f cnracpin (.g., cn-
dms and fam) shuld b plannd.
Drug ClASS: mACrOliDeS
an
Th macrlid anibiics ac by inhibiing prin
synhsis in suscpibl bacria. Thy ar bacri-
saic and bacricidal, dpnding n h rganism
and drug cncnrain prsn. Eryhrmycin is ffc-
iv agains gram-psiiv micrrganisms and gram-
ngaiv ccci. Azihrmycin is lss aciv agains
Drugs Used to Treat Infections CHAPTER 45 737
gram-psiiv rganisms han ryhrmycin bu has
grar aciviy agains gram-ngaiv rganisms ha
ar rsisan  ryhrmycin. Clarihrmycin has a
spcrum f aciviy similar  ha f ryhrmycin bu
has cnsidrably grar pncy.
u
Th macrlids ar usd fr rspirary, GI rac, skin,
and sf issu infcins and fr STIs, spcially whn
pnicillins, cphalsprins, and racyclins cann
b usd. Fidaxmicin is a macrlid anibiic usd 
ra C. difcile–assciad diarrha. I shuld b usd
nly fr C. difcile infcins.
t o
Th primary hrapuic ucm xpcd frm mac-
rlid hrapy is liminain f bacrial infcin.
Nn in  md
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability, dosage, and administration
S Tabl 45.5.
PO: Azihrmycin and ryhrmycin shuld b ad-
minisrd a las 1 hur bfr r 2 hurs afr mals.
Clarihrmycin may b akn wihu rgard  mals.
IM: Bcaus f pain n injcin and h pssibil-
iy f sril abscss frmain, IM adminisrain
f ryhrmycin is gnrally n rcmmndd fr
mulipl-ds hrapy.
IV: Dilu h dsag f ryhrmycin in 100  250
mL f salin sluin r 5% dxrs and adminisr
vr 20  60 minus. Thrmbphlbiis afr IV infu-
sin is a rlaivly cmmn advrs ffc.
Common adverse effects
gasonsna
Gastric irritation. Th ms cmmn advrs ffcs f
ral macrlid hrapy ar diarrha, nausa and vm-
iing, and abnrmal as. Ths advrs ffcs ar
usually mild and nd  rslv wih cninud hr-
apy. Encurag h pain n  discninu hrapy
wihu rs cnsuling h halhcar prvidr.
Serious adverse effects
gasonsna
Severe diarrhea. Svr diarrha may dvlp frm
h us f ryhrmycin. Rpr diarrha f v r
mr sls daily  h halhcar prvidr. This may
738 UNIT IX Drugs Affecting Other Body Systems

Table 45.5 Macrolides

geNeriC NAme BrAND NAme AvAilABility ADult DOSAge rANge
azithromycin Zithromax Tablets: 250, 500, 600 mg PO: 500 mg as a single dose on day 1,
Packets: 1 g followed by 250 mg once daily on days
Suspension: 100, 200 mg/5 mL 2–5 for a total dose of 1.5 g
Injection: 500 mg in 10-mL vial IV: 500 mg daily. Dilute powder to a
concentration of 1–2 mg/mL; infuse
1-mg/mL concentration over 3 hr or
2-mg/mL concentration over 1 hr
Do not administer as an IV bolus or IM
clarithromycin — Tablets: 250, 500 mg PO: 250–500 mg q12h for 7–14 days
Suspension: 125, 250 mg/5 mL
Tablets, extended release (24 hr): 500, mg
erythromycin Erythrocin Tablets: 250, 400, 500 mg PO: 250 mg four times daily for 10–14
EryPed, EryTab Tablets, delayed release: 250, 333, 500 mg days
Capsules, delayed release particles: 250 IV: 15–20 mg/kg/24 hr; up to 4 g/24 hr
mg
Suspension: 200, 400 mg/5 mL
IV: 500-mg vials for reconstitution
daxomicin Dicid Tablets: 200 mg 200 mg twice daily for 10 days
Suspension: 40 mg/mL in 136 ml bottle

b an indicain f drug-inducd psudmmbranus Oa conacps. Macrlids may inrfr wih

cliis. Bld r mucus in h sl shuld als b r- h aciviy f ral cnracpivs. Oral cnracpivs
prd  h halhcar prvidr. Warn patients not to shuld n b discninud, bu cunsling rgarding
treat diarrhea themselves when taking this drug. Th us f addiinal mhds f cnracpin (.g., cn-
us f diphnxyla, lpramid, r pargric may dms and fam) shuld b plannd.
prlng r wrsn h cndiin.
vasca Drug ClASS: OxAzOliDiNONeS
Thrombophlebitis. Carfully assss pains rciving
IV ryhrmycin fr hrmbphlbiis. Inspc h IV
nzd (lĭn-ā-ZŌ-lĭd)
infusin ara frqunly whn prviding car; inspc
Zvx (ZĪ-vŏks)
during drssing changs and whn h infusin is
Do not confuse Zyvox with Zosyn or Zovirax.
changd  a nw si. Always invsiga pain a h dzd (tĕd-ī-ZŌ-lĭd)
IV si. Rpr rdnss, warmh, ndrnss  uch, svx (siv-EX-troh)
and dma in h affcd par.

Drug interactions an

toc casd b acods. Macrlid anibiics
may inhibi h mablism f svral drugs, causing
accumulain and pnial xiciy. Ths drugs ar al-
fnanil, bnzdiazpins (.g., alprazlam, diazpam,
midazlam, riazlam), buspirn, carbamazpin,
cyclsprin, digxin, fldipin, hydrxymhylglu-
aryl cnzym A (HMG-CA) rducas inhibirs
(.g., arvasain, lvasain, simvasain), mpra-
zl, acrlimus, hphyllins, vinblasin, warfarin,
and hr drugs mablizd by h cychrm P450
(CYP) CYP3A nzym sysm. Rad individual drug
mngraphs fr mniring paramrs f xiciy
frm hs agns.
Pod. Cadminisrain f a macrlid ani-
biic wih pimzid is cnraindicad. Dah has
rsuld frm his cmbinain f drug hrapy.
rapn, abn. Th cadminisrain f a mac-
rlid anibiic wih rifampin r rifabuin may caus
a rducin in animicrbial ffc whil incrasing h
frquncy f GI advrs ffcs.
Linzlid and dizlid ar bh oxazolidinones. Thy ac
by inhibiing prin synhsis in bacrial clls. Thy ar
bacricidal in crain srains f bacria and bacri-
saic in hrs. Unrlad  anibacrial aciviy, hy
ar rvrsibl mnamin xidas inhibirs, inhibiing
h acin f mnamin xidas yp A, an nzym r-
spnsibl fr mablizing srnin in h brain.
u
Linzlid is usd in h ramn f srius r lif-
hraning infcins causd by gram-psiiv micr-
rganisms. I is apprvd fr us wih VRE bacria
and uncmplicad and cSSSIs causd by mhicillin-
suscpibl and mhicillin-rsisan Staph. aureus,
Strep. pyogenes, r Strep. agalactiae. I may als b usd
 ra cmmuniy-acquird pnumnia causd by
pnicillin-suscpibl Strep. pneumoniae. I is n indi-
cad fr ramn f gram-ngaiv infcins. Ohr
apprpria anibiics  prvid gram-ngaiv cv-
rag shuld b usd cncurrnly. Linzlid shuld
 Drugs Used to Treat Infections CHAPTER 45 739

b rsrvd fr hs cass in which hr anibiics IV: Infus h ds vr 30  120 minus. D n
such as vancmycin ar inffciv, s ha rsisan adminisr cncurrnly wih hr mdicins. If h
srains f bacria d n rapidly dvlp. sam IV lin is usd fr squnial infusin f hr
Tdizlid is usd in ramn f adul pains wih mdicins, ush h lin bfr and afr infusin f
acu bacrial skin and skin srucur infcins causd linzlid wih 5% dxrs, nrmal salin, r laca-
by suscpibl islas f h fllwing gram-psiiv d Ringr sluin. Kp h linzlid infusin in is
micrrganisms: mhicillin-rsisan and mhicillin- wrappr unil rady fr adminisrain. Linzlid may
suscpibl Staph. aureus, Strep. pyogenes, Strep. agalac- xhibi a yllw clr ha may innsify vr im bu
tiae, Strep. anginosus grup, and Enterococcus faecalis. wihu a lss f pncy.
N dsag adjusmn is ncssary whn swiching
t o frm IV  ral adminisrain using h abl r ral
Th primary hrapuic ucm xpcd frm lin- suspnsin dsag frm.
zlid and dizlid hrapy is liminain f bacrial tdod. Adults: Acu bacrial skin and skin
infcin. srucur infcins: PO, IV: 200 mg nc daily fr 6
days.
Nn in  lnzd nd tdzd IV: Infus h ds vr 1 hur. If h sam IV lin
Premedication assessment is  b usd fr squnial infusin f hr drugs
• Obain baslin assssmns f prsning r sluins, h lin shuld b ushd wih nrmal
sympms. salin bfr and afr dizlid infusin.
• Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus. Common adverse effects
• Assss fr and rcrd any gasric and visual symp- gasonsna
ms bfr iniiaing hrapy. Gastric irritation. Th ms cmmn advrs ffcs f
• Assss fr any allrgis. bh agns ar nausa and vmiing (9% and 11%, r-
• Obain baslin labrary sudis rdrd and r- spcivly). Ths advrs ffcs ar usually mild and
viw rsuls (.g., CBC wih diffrnial, plals, mdra in h rs fw days f hrapy and nd 
bld glucs, lcrlys, culur and snsiiviy). rslv wih cninud hrapy.
Nooc
Availability Headaches. Hadachs wr rprd in 1%  11%
lnod. PO: 600-mg abls; 100-mg/5-mL ral f pains aking bh agns. Hadachs wr n
suspnsin in 150 mL. IV: 200- and 600-mg prlld svr nugh  discninu hrapy and ndd 
cnainrs a 2 mg/mL. rslv wih cninud hrapy.
tdod. PO: 200-mg abls; IV: 200 mg/vial.
Serious adverse effects
Dosage and administration gasonsna
lnod. Adults: Severe diarrhea. Rarly, svr diarrha may dvlp
frm h us f bh agns. Rpr diarrha f v r
mr sls daily  h halhcar prvidr. This may
DOSe AND rOute Of b an indicain f drug-inducd psudmmbranus
tyPe Of iNfeCtiON ADmiNiStrAtiON DurAtiON (DAyS)
cliis. Bld r mucus in h sl shuld als b r-
Skin 400 mg PO q12h 10–14 prd  h halhcar prvidr. Warn patients not to
(uncomplicated) treat diarrhea themselves when taking this drug. Th
Skin (complicated) 600 mg PO or IV 10–14 us f diphnxyla, lpramid, r pargric may
q12h
prlng r wrsn h cndiin.
Community- 600 mg PO or IV 10–14
acquired q12h
Haooc
pneumonia Bone marrow suppression. Srius and pssibly faal
Methicillin-resistant 600 mg PO or IV Determined bn marrw supprssin may ccur afr hrapy is
Staphylococcus q12h clinically iniiad wih bh agns. Early signs includ sr
aureus (MRSA) hra, faigu, lvad mpraur, and small p-
infections chial hmrrhags and bruiss n h skin. If pains
Vancomycin- 600 mg PO or IV 14–28 dscrib any f hs sympms, rpr hm  h
resistant q12h halhcar prvidr immdialy. Ruin labrary
infections sudis (RBC and whi bld cll cuns, diffrnial
Hospital-acquired 600 mg PO or IV 10–14 cuns, plals) ar schduld fr pains aking lin-
pneumonia q12h
zlid fr 14 days r lngr. Srss h impranc f
Urinary tract 600 mg IV q 12 h Determined
infection clinically
rurning fr his labrary wrk. Mnir fr h d-
(complicated) vlpmn f sr hra, fvr, purpura, jaundic, r
xcssiv r prgrssiv waknss.
740 UNIT IX Drugs Affecting Other Body Systems
in ss (opponsc ncons)
Secondary infections. Oral hrush, gnial and anal pru-
rius, vaginiis, and vaginal discharg may ccur. Rpr
 h halhcar prvidr prmply bcaus hs infc-
ins ar rsisan  h riginal anibiic usd. Tach
h impranc f miculus ral and prinal hygin.
maboc
Lactic acidosis. Lacic acidsis has bn rprd in
cnjuncin wih linzlid hrapy. Pains wh d-
vlp rcurrn nausa r vmiing, unxplaind aci-
dsis, r a lw bicarbna lvl shuld b rprd 
h halhcar prvidr as sn as pssibl.
Nooc
Seizures. Sizurs hav bn rprd in pains r-
civing bh agns. Pains shuld b mnird fr
h dvlpmn f sizurs, paricularly hs wih a
hisry f sizur aciviy r hs pains whs clini-
cal cndiin (.g., hypxia) may mak hm mr sus-
cpibl  sizurs.
Visual neuropathy. Changs in visin frm blurrd vi-
sin  lss f visin hav bn rprd wih bh agns.
Pains shuld b askd  rpr, and shuld b mni-
rd fr, changs in visual acuiy, clr visin, r visual
ld and blurrd visin. Ths sympms shuld b r-
prd  h halhcar prvidr fr furhr valuain.
Drug interactions
monoan odas nhbos. Bh agns inhibi mn-
amin xidas A and shuld n b usd in pains ak-
ing hr mnamin xidas inhibirs (.g., phnlzin,
iscarbxazid, ranylcyprmin, mpridin, slgilin,
rasagilin, ramadl, mhadn) r wihin 2 wks f
aking such prducs. Alhugh n rprd wih ihr
agn, faal drug inracins hav bn rprd bwn
mnamin xidas inhibirs and h agns lisd hr.
Adnc ans. Bh agns ar mnamin
xidas inhibirs ha will rduc h mablism f
adrnrgic agns (.g., dpamin, pinphrin, nr-
pinphrin, phdrin, psudphdrin, phnylpr-
panlamin), pnially rsuling in achycardia and
hyprnsin. Iniial dss f h adrnrgic agns
shuld b rducd  s hw h pain rspnds b-
fr using nrmal dss.
Soonc ans. As mnamin xidas A inhibi-
rs, bh agns hav h pnial  inrac wih sr-
nrgic agns (.g., uxin, parxin, srralin;
ricyclic anidprssans; buspirn; ripans)  induc
a srnin syndrm. Pains dvlping signs and
sympms f srnin syndrm, such as hyprrxia
(wiching) and incrdinain, fvr, xcssiv swaing,
shivring r shaking, diarrha, and cnfusin, shuld b
rprd  h halhcar prvidr fr furhr valuain.
Drug ClASS: PeNiCilliNS
an
Pnicillins wr h rs ru anibiics  b grwn
and usd agains pahgnic bacria in humans. Thy
currnly rmain n f h ms widly usd classs
f anibiics.
Th pnicillins ac by inrfring wih h synhsis
f bacrial cll walls. Th rsuling cll wall is wak-
nd bcaus f dfciv srucur, and h bacria
ar subsqunly dsryd by smic lysis. Th pni-
cillins ar ms ffciv agains bacria ha muliply
rapidly. Thy d n hindr grwh f human clls b-
caus human clls hav prciv mmbrans bu n
cll wall.
Many bacria ha ar iniially snsiiv  pnicillins
dvlp a prciv mchanism and bcm rsisan
 pnicillin hrapy. Ths bacria prduc h nzym
pnicillinas (ba-lacamas), which can dsry h an-
ibacrial aciviy f ms pnicillins. Pnicillinas in-
acivas h pnicillin anibiics by spliing pn h
ba-lacam ring f h pnicillin mlcul. Rsarchrs
hav dvlpd w mchanisms  prvn his inaci-
vain. Th rs is  mdify h pnicillin mlcul 
“prc” h ring srucur whil raining animicr-
bial aciviy. This mchanism culminad in h dvl-
pmn f h penicillinase-resistant penicillins (.g., naf-
cillin, xacillin, diclxacillin). Th scnd mhd is 
add anhr chmical wih a similar srucur ha will
mr radily bnd  h pnicillinas nzyms han
h pnicillin, laving h fr pnicillin  inhibi cll
wall synhsis. Passium clavulana is nw addd 
amxicillin (Augmnin)  bnd  pnicillinass ha
wuld nrmally dsry his anibiic. Sulbacam has
bn addd  ampicillin (Unasyn) and azbacam 
pipracillin (Zsyn) fr similar rasns.
u
Pnicillins ar usd  ra middl ar infcins (iis
mdia), pnumnia, mningiis, UTIs, and syphilis, and
as a prphylacic anibiic bfr surgry r dnal pr-
cdurs fr pains wih hisris f rhumaic fvr.
t o
Th primary hrapuic ucm xpcd frm pni-
cillin hrapy is liminain f bacrial infcin.
Nn in  pnn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any allrgis, sympms f
diarrha, and abnrmal livr r rnal funcin s
rsuls. If prsn, wihhld drug and rpr nd-
ings  h halhcar prvidr.
4. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability, dosage, and administration
S Tabl 45.6.
 Drugs Used to Treat Infections CHAPTER 45 741

Table 45.6 Penicillins

geNeriC NAme
amoxicillin
ampicillin
dicloxacillin
Do not confuse dicloxacillin
with doxycycline.
nafcillin
oxacillin
penicillin G, potassium or
sodium
penicillin V potassium
COmBiNAtiON PrODuCtS
amoxicillin and potassium
clavulanate (co-amoxiclav)
ampicillin and sulbactam
sodium
piperacillin and tazobactam
Available in Canada.
Do not confuse.
BrAND
NAme AvAilABility ADult DOSAge rANge
— Tablets: 500, 875 mg PO: 250–875 mg q8–12h
Tablets, chewable: 125, 250 mg
Capsules: 250, 500 mg
Suspension: 125, 200, 250, 400 mg/5
mL
— Capsules: 500 mg IM, IV: 0.5–1 g q4–6h
Injection: 0.125-, 0.25-, 0.5-, 1-, 2-, 10-g PO: 250–500 mg q6h
vials
— Capsules: 250, 500 mg PO: 250–500 mg q6h
— IV: 1-, 2-, 10-g powder for reconstitution IV: 500–1000 mg q4h
— Injection: 1-, 2-, 10-g vials IM, IV: 0.5–1 g q4–6h
Pzerpen Injection: 0.02, 0.04, 0.06, 5, 20 million IM, IV: 600,000–30 million units daily
units mg/5 mL
— Tablets: 250, 500 mg PO: 125–500 mg q6h
Suspension: 125, 250 mg/5 mL
Augmentin Tablets, chewable: 200, 400 mg PO: 250 mg q8h or 500–875 mg
Clavulin Tablets: 250, 500, 875 mg q12h
Tablets, extended release (12 hr): 1000 Extended release: 2000 mg q12h
mg Extra strength suspension: 600 mg
Suspension: 125, 200, 250, 400, 600 q12h
mg/5 mL
Unasyn Injection: 1.5-, 3-, 15-g bottles and vials IM, IV: 1.5–3 g q6h
Zosyn IV: 2.25-, 3.375-, 4.5-, 13.5-, 40.5-g vials 3.375–4.5 g q6h; Maximum dose:
18 g/day

Ad copabs. Do not mix wih hr rna

drugs in h sam syring wih pnicillins r infus
wih hr drugs. S h Drug Inracins lar in his
scin fr incmpaibiliis.
Common adverse effects
gasonsna
Diarrhea. Pnicillins caus diarrha by alring h
bacrial ra f h GI rac. Th diarrha is usu-
ally n svr nugh  warran discninuain.
Encurag h pain n  discninu hrapy
wihu rs cnsuling h halhcar prvidr. If
diarrha prsiss, mnir h pain fr signs f
dhydrain.
Severe adverse effects
gasonsna
Hepatotoxicity. Transin lvains f livr funcin
s rsuls (.g., AST, ALT, alkalin phsphaas lv-
ls) hav bn rprd. Mnir rurning labrary
daa and rpr abnrmal ndings  h halhcar
prvidr.
Nephrotoxicity. Transin lvains f rnal s r-
suls (.g., BUN, srum crainin lvls) hav bn
rprd. Rnal xiciy, as vidncd by prinu-
ria, hmauria, cass, dcrasd crainin claranc,
and dcrasd urin upu, als has bn rprd.
Mnir rurning labrary daa and rpr abnr-
mal ndings  h halhcar prvidr.
Haooc
Electrolyte imbalance. Th lcrly cnn f h
anibiics may caus hyprkalmia r hyprnarmia.
Sm f h pnicillins (.g., pnicillin G inravnusly,
pipracillin, icarcillin) hav a high lcrly cnn.
vasca
Thrombophlebitis. Carfully assss pains rciv-
ing IV pnicillins fr h dvlpmn f hrmb-
phlbiis. Inspc h IV infusin ara frqunly
whn prviding car; inspc during drssing chang-
s and whn h infusin is changd  a nw si.
Always invsiga pain a h IV si. Rpr rd-
nss, warmh, ndrnss  uch, and dma in h
affcd par.
742 UNIT IX Drugs Affecting Other Body Systems
Drug interactions
Pobncd. Pains rciving prbncid in cmbi-
nain wih pnicillins ar mr suscpibl  xic-
iy bcaus prbncid inhibis rnal xcrin f h
pnicillins. Mnir clsly fr advrs ffcs.
This cmbinain may b usd advanagusly
whn raing infcins in which high srum lvls f
pnicillin ar rquird.
Apcn, aocn, and aopno. Whn ampicil-
lin r amxicillin is usd cncurrnly wih allpuri-
nl, hr is a highr incidnc f a skin rash. D n
labl h pain as allrgic  pnicillins unil furhr
skin sing has vrid ha hr is a ru hypr-
snsiiviy  pnicillins.
Anacds. Excssiv us f anacids may diminish
h absrpin f ral pnicillins.
Oa conacps. Pnicillins may inrfr wih
h aciviy f ral cnracpivs. Oral cnracpivs
shuld n b discninud, bu cunsling rgarding
us f addiinal mhds f cnracpin (.g., cn-
dms and fam) shuld b plannd.
Drug ClASS: PleurOmutiliN
n ( fam  n)
Xn (zn--)
an
Lfamulin is h rs f h animicrbial agns
knwn as a plurmuilin. I acs by binding  h 23S
ribsmal RNA f h 50S subuni, inhibiing bacrial
prin synhsis.
u
Lfamulin is usd  ra f aduls wih cmmu-
niy-acquird bacrial pnumnia causd by Strep.
pneumoniae, Staph. aureus (mhicillin-suscpibl
islas), Haemophilus influenzae, Legionella pneu-
mophila, Mycoplasma pneumoniae, and Chlamydia
pneumoniae.
t o
Th primary hrapuic ucm xpcd frm l-
famulin hrapy is liminain f bacrial infcin.
Nn in  ln
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiain f hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
6. Ensur ha h pain is n prgnan.
Availability. IV: 150 mg/15 mL. Oral: 600 mg abls.
Dosage and administration. IV: 150 mg vry 12 hurs
vr 60 minus. Thrapy is cninud fr 5  7 days.
Culd swich  h abls and giv 600 mg vry 12
hurs  cmpl h ramn curs.
Oral: 600 mg vry 12 hurs fr 5 days. Th abls
shuld b adminisrd a las 1 hur bfr a mal r
2 hurs afr a mal. Tabls shuld n b crushd r
dividd and b akn wih 6  8 uncs f war.
Common adverse effects
gasonsna
Nausea, vomiting, and diarrhea. Th IV sluin and
abls may caus diarrha. Th abls may caus nau-
sa, and vmiing. Encurag h pain n  discn-
inu hrapy wihu rs cnsuling h halhcar
prvidr. If h pain bcms dbiliad, cnac h
halhcar prvidr.
maboc
Hypokalemia. Th IV sluin may caus hyp-
kalmia. Passium lvls may nd  b mnird.
Serious adverse effects
gasonsna
Hepatotoxicity. Transin lvains f livr funcin
s rsuls (.g., AST, ALT, alkalin phsphaas lv-
ls) hav bn rprd wih bh IV and ral hrapy.
Mnir rurning labrary daa and rpr abnr-
mal ndings  h halhcar prvidr.
Cadoasca
QT interval prolongation. Lfamulin may prlng h
QT inrval in sm pains. Avid us in pains
wih knwn prlngain f h QT inrval and in pa-
ins aking cncmian mdicains ha prlng h
QT inrval. Mnir ECG during ramn.
Drug interactions
Ds ha ncas ads cs. Clarihrmycin,
iracnazl, amidarn, ryhrmycin, diliazm,
and vrapamil may inhibi h mablism f lfamu-
lin ha will incras h bld lvls f lfamulin. This
nly applis  lfamulin abls.
Ds ha dcas hapc o-
cos. Carbamazpin, phnbarbial, phnyin,
rifampin, and S. Jhn’s wr may incras h m-
ablism f lfamulin and may rduc h hrapuic
ucm. Avid hs mdicain if pssibl.
Drug ClASS: QuiNOlONeS
an
Quinln anibiics ar an impran class f hra-
puic agns. Th subclass knwn as h urquin-
lns is ffciv agains a wid rang f gram-psiiv
and gram-ngaiv bacria, including sm anarbs.

Th urquinlns ac by inhibiing h aciviy f
DNA gyras, an nzym ssnial fr h rplicain f
bacrial DNA.
u
• Ciprxacin was h rs wll-lrad, brad-
spcrum ral anibiic in h quinln sris. I is
usd fr h ramn f UTIs, infcius diarrha,
and chrnic bacrial prsaiis causd by E. coli r
Proteus mirabilis. Alhugh ciprxacin is indicad
in adul pains fr ramn f lwr rspirary
rac infcins causd by E. coli, K. pneumoniae, P.
mirabilis, Pseudomonas aeruginosa, Haemophilus in-
uenzae, Haemophilus parainuenzae, r Strep. pneu-
moniae, i is n h rs chic in h ramn f
pnumnia scndary  Strep. pneumoniae. Bcaus
urquinlns hav bn assciad wih sri-
us advrs racins, rsrv urquinlns fr
ramn f uncmplicad UTIs and acu xacr-
bains f chrnic brnchiis in pains wh hav
n alrnaiv ramn pins.
• Dlaxacin is indicad in aduls wih acu bac-
rial skin and skin srucur infcins causd by cr-
ain gram-psiiv and gram-ngaiv pahgns,
including MRSA. I is als indicad fr aduls wih
cmmuniy-acquird bacrial pnumnia causd
by crain gram-psiiv, gram-ngaiv, and
aypical rganisms such as Pseudomonas aeruginosa,
Mycoplasma pneumoniae and Chlamydia pneumoniae.
I is h nly urquinln aciv agains MRSA.
• Lvflxacin has brad-spcrum aciviy agains
gram-ngaiv, gram-psiiv, and anarbic
bacria. I is usd  ra maxillary sinusiis,
acu bacrial xacrbains f chrnic brnchi-
is, cmmuniy-acquird pnumnia, skin and
sf issu infcins, chrnic bacrial prsai-
is, UTIs, acu pylnphriis, and inhalainal
anhrax. I has an advanag f nc-daily ral
dsing. Lvflxacin shuld b usd wih cauin
in ldr pains wh may b suscpibl  pr-
lngain f h QT inrval and h dvlpmn
f pnially lif-hraning dysrhyhmias.
Lvflxacin is cnraindicad in pains wih
hypkalmia r hs rciving amidarn, s-
all, and hr aniarrhyhmic agns.
• Mxixacin is aciv agains gram-psiiv micr-
rganisms such as Strep. pneumoniae and Staph.
aureus, gram-ngaiv rganisms such as H. inu-
enzae, and aypical causs f pnumnia such as C.
pneumoniae and M. pneumoniae. I is apprvd fr
us in pains wih acu bacrial sinusiis, acu
bacrial xacrbain f chrnic brnchiis, and
cmmuniy-acquird pnumnia causd by suscp-
ibl rganisms. Mxixacin shuld b usd wih
cauin in ldr pains wh may b suscpibl
 prlngain f h QT inrval and h dvlp-
mn f pnially lif-hraning dysrhyhmias.
Mxixacin is cnraindicad in pains wih
Drugs Used to Treat Infections CHAPTER 45 743
hypkalmia r hs rciving amidarn, s-
all, r hr aniarrhyhmic agns.
• Oxacin has brad-spcrum aciviy agains
gram-ngaiv, gram-psiiv, and anarbic bac-
ria. I diffrs frm ciprxacin in ha i has grar
aciviy agains STIs such as Chlamydia trachomatis
and gnial ureaplasma. Oxacin is als lss suscp-
ibl  drug inracins han ar hr urqui-
nlns. Oxacin is usd  ra UTIs, prsaiis,
skin infcins (.g., clluliis and impig), lwr
rspirary pnumnia, and STIs hr han syphilis
and gnrrha.
t o
Th primary hrapuic ucm xpcd frm qui-
nln hrapy is liminain f bacrial infcin.
Nn in  Qnn
Premedication assessment
• Obain baslin assssmns f prsning
sympms.
• Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
• Assss fr and rcrd any gasric sympms bfr
iniiain f hrapy.
• Assss fr any allrgis.
• Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
• Ensur ha h pain is n prgnan.
• Warn pains f pssibl phxiciy (s Srius
Advrs Effcs lar in his scin).
Availability, dosage, and administration
S Tabl 45.7.
Chdn and od ads, pans akn cocosods,
anspan pans. Flurquinlns shuld n b pr-
scribd fr pains yungr han 18 yars. Us in pdi-
aric pains has rsuld in an incrasd incidnc f
musculsklal disrdrs such as arhralgia, ndinp-
ahy, and gai abnrmaliy. This risk is furhr incrasd
in ldr pains (usually ldr han 60 yars), in pa-
ins aking cricsrids (.g., prdnisn, dxa-
mhasn), and in pains wih rgan ransplans.
Pnan won. Quinln hrapy is n rcm-
mndd during prgnancy unlss h bn f hr-
apy uwighs h risk. N sudis hav bn cm-
pld in human pains, bu animal sudis hav
dmnsrad varius ragnic ffcs.
Common adverse effects
gasonsna
Nausea, vomiting, diarrhea, abdominal discomfort. Ths
advrs ffcs ar usually mild and nd  rslv
wih cninud hrapy. Encurag h pain n
 discninu hrapy wihu rs cnsuling h
halhcar prvidr. If h pain bcms dbiliad,
cnac h halhcar prvidr.
744 UNIT IX Drugs Affecting Other Body Systems

Table 45.7 Fluoroquinolones

geNeriC NAme BrAND NAme AvAilABility DOSAge rANge
ciprooxacin Cipro Tablets: 100, 250, 500, 750 mg PO: 0.5–1.5 g daily in two
Do not confuse Suspension: 250, 500 mg/5 mL divided doses 2 hr after
ciprooxacin with Injection: 200 mg/100 mL and 400 meals
cephalexin. mg/200 mL in exible containers IV: 400–800 mg daily in two
divided doses q12h
delaoxacin Baxdela Injection: 300-mg vial IV: 300 mg; infuse over 60 min
Tablets: 450 mg q12h
PO: 450 mg q12h
levooxacin — Tablets: 250, 500, 750 mg PO: 250–750 mg once daily
Solution: 25 mg/mL IV: 250–750 mg infused
Injection: 250-, 500-, 750-mg containers slowly over at least 60 min
moxioxacin — Tablets: 400 mg IV, PO: 400 mg once daily;
Injection: 400 mg/250 mL may be taken with or
without food
ooxacin Tablets: 300, 400 mg PO: 400–800 mg daily in two
divided doses q12h, 1 hr
before or 2 hr after meals,
with a large glass of uid
Do not confuse.

Nooc
Dizziness, lightheadedness. Alhugh uncmmn, cip-
rxacin may caus hs disurbancs. Thy nd 
b slf-limiing, and hrapy shuld n b discnin-
ud unil h pain cnsuls h halhcar prvidr.
Cauin h pain agains driving r prfrming
hazardus asks unil adjusd  h ffcs f h
mdicain.
Serious adverse effects
maboc
Hypoglycemia. Flurquinlns hav bn assci-
ad wih h dvlpmn f srius, and smims
faal, hypglycmia. Ths vns hav ccurrd ms
fn in ldrly pains wih diabs bu hav als
bn rprd in pains wihu a prir hisry f
diabs. Prmp idnicain and ramn f hyp-
glycmia is ssnial. Individual quinlns may diffr
in hir pnial  caus his ffc.
inna
Phototoxicity. Phxic racins hav bn rpr-
d in pains rad wih urquinlns. Expsur
 dirc and indirc sunligh and h us f sun lamps
shuld b avidd. Ths racins hav ccurrd wih
and wihu h us f sunblcks and sunscrns and
wih singl dss f urquinlns. Th pain
shuld n ak addiinal dss and shuld cnac
h halhcar prvidr if a snsain f skin burning,
rdnss, swlling, blisrs, rash, iching, r drmaiis
dvlps. Suggs waring lng-slvd clhing, a
ha, and sunglasss whn xpsd  sunligh.
Rash. Rpr a rash r prurius immdialy and
wihhld addiinal dss pnding apprval by h
halhcar prvidr.
Cadoasca
Aortic aneurysm ruptures. Flurquinlns may
caus aric anurysm rupurs r disscin wihin 2
mnhs f us, paricularly in ldrly pains. Pains
wih priphral ahrsclric vascular disass,
hyprnsin, gnic disrdrs invlving bld vs-
sl changs (.g., Marfan syndrm), and ldrly pa-
ins shuld avid urquinlns unlss n hr
ramn pins ar availabl. Cninuing hrapy
bynd 14 days may als incras h risk.
gasonsna
Hepatotoxicity. Transin lvains f livr funcin
s rsuls (.g., AST, ALT, alkalin phsphaas lvls)
hav bn rprd. Mnir rurning labrary daa
and rpr abnrmal ndings  h halhcar prvidr.
rna
Nephrotoxicity. Transin lvains f rnal s r-
suls (.g., BUN, srum crainin lvls) hav bn
rprd. Rnal xiciy, as vidncd by prinu-
ria, hmauria, cass, dcrasd crainin claranc,
and dcrasd urin upu, als has bn rprd.
Mnir rurning labrary daa and rpr abnr-
mal ndings  h halhcar prvidr.
Nooc
Tinnitus, headache, dizziness, mental depression, drowsi-
ness, confusion. Quinln hrapy may caus hs
disurbancs. Cnsul wih h halhcar prvidr
whn hs ffcs ccur. Cauin h pain agains
driving r prfrming hazardus asks unil adjusd
 h ffcs f h mdicain.
Worsening symptoms for those with myasthenia
gravis. Quinlns may xacrba muscl waknss
in pains wih myashnia gravis. Avid in pains
wih knwn hisry f myashnia gravis.

Irreversible peripheral neuropathy (serious nerve dam-
age). Flurquinlns hav bn assciad wih an
incrasd risk f priphral nurpahy. Discninu
immdialy if h pain xprincs sympms f
priphral nurpahy (including pain, burning, in-
gling, numbnss, and/r waknss) r hr alra-
ins in snsains (including ligh uch, pain, m-
praur, psiin sns and vibrary snsain, and/
r mr srngh)  minimiz h dvlpmn f
an irrvrsibl cndiin. Avid urquinlns in
pains wh hav prviusly xprincd priphral
nurpahy.
Drug interactions
ion, anacds, scaa. Irn sals, zinc sals, sucral-
fa, and anacids cnaining magnsium hydrxid
r aluminum hydrxid dcras h absrpin f
quinlns. Adminisr a las 2 hurs bfr r 6
hurs afr ingsin f anacids, sucralfa, r irn-
cnaining prducs, dpnding n h quinln.
Nonsoda annaao ds. Th cncur-
rn adminisrain f nnsridal aniinamma-
ry drugs wih urquinlns (.g., lvxacin,
xacin) may incras h risk f cnral nrvus
sysm simulain wih sizurs. Us wih xrm
cauin. Cnsidr h us f hr analgsics r ani-
inammary agns.
thophn. Th urquinlns (.g., ciprxa-
cin, mxixacin, xacin), whn givn wih h-
phyllin, may prduc hphyllin xiciy. Obsrv
fr vmiing, dizzinss, rslssnss, and cardiac dys-
rhyhmias. Mnir hphyllin srum lvls. Th
dsag f hphyllin may nd  b rducd.
Drug ClASS: StrePtOgrAmiNS
qnn-dn (kwĭ-nyū-PRĬS-tĭn dăl-fō-PRĬS-tĭn)
snd (SĬN-ŭr-sĭd)
an
Quinuprisin-dalfprisin is h rs f a nw class f
animicrbial agns knwn as streptogramins. Ths
w agns wr dvlpd frm prisinamycin. Whn
usd in cmbinain, hy ar synrgisic and ac by
inhibiing prin synhsis in bacrial clls.
u
Quinuprisin and dalfprisin ar agns ha can b
usd in h ramn f srius r lif-hraning in-
fcins ha ar assciad wih VRE bacria and cSS-
SIs causd by mhicillin-suscpibl Staph. aureus r
Strep. pyogenes. Th us f quinuprisin-dalfprisin, a
rprsnaiv f a nw class f anibiics, shuld b
rsrvd fr hs cass in which hr anibiics such
as vancmycin ar inffciv, s ha rsisan srains
f bacria d n rapidly dvlp.
Drugs Used to Treat Infections CHAPTER 45 745
t o
Th primary hrapuic ucm xpcd frm
quinuprisin-dalfprisin hrapy is liminain f bac-
rial infcin.
Nn in  sn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, plals,
bld glucs, lcrlys, crain kinas, livr
funcin ss, culur and snsiiviy).
Availability. IV: 500 mg (150 mg quinuprisin and 350
mg dalfprisin) in 10-mL vial. All dsag rcmmn-
dains ar basd n al quinuprisin and dalfpris-
in, in milligrams.
Dosage and administration. Adult: IV: 7.5 mg/kg
vry 8 hurs fr h ramn f VRE bacrmia r
vry 12 hurs fr ramn f cSSSIs. Infus h ds
vr 60 minus.
Ad copab. Rcnsiu nly wih 5%
dxrs r sril war fr injcin and hn dilu
wih 5% dxrs  a nal cncnrain f 100 mg/
mL. A prcipia will frm if rcnsiud wih h-
r sandard diluns. If infusd in an IV lin bing
usd fr hr mdicins, ush h lin wih 5% dx-
rs. D n ush wih hparin r sdium chlrid.
Serious adverse effects
vasca
Pain, infusion site inammation. Th ms frqun
advrs vnus vns includ pain a h admin-
israin si, dma, infusin si racin, and
hrmbphlbiis.
gasonsna
Nausea, vomiting, anorexia, abdominal cramps, diar-
rhea. Ths advrs ffcs ar usually mild and nd
 rslv wih cninud hrapy.
Hepatotoxicity. Th sympms f hpaxiciy
ar anrxia, nausa, vmiing, jaundic, hpa-
mgaly, splnmgaly, and abnrmal livr funcin
ss (.g., lvad bilirubin, AST, ALT, gamma-
gluamylransfras [GGT], and alkalin phs-
phaas lvls; incrasd INR).
mscoska
Arthralgia, myalgia. Arhralgias and myalgias may
ccur during hrapy. Dcrasing h frquncy f
adminisrain  vry 12 hurs may minimiz
rcurrnc.
746 UNIT IX Drugs Affecting Other Body Systems
Table 45.8 Sulfonamides
geNeriC NAme BrAND NAme AvAilABility
sulfadiazine — Tablets: 500 mg
sulfasalazine Azuldine Tablets: 500 mg
Tablets, delayed release: 500 mg
sulfamethoxazole/ Bactrim, Bactrim DS Tablets: 400/80-, 800/160-mg
trimethoprim Do not confuse sulfamethoxazole/trimethoprim
Bactrim with Suspension: 200/40 mg
Biaxin. sulfamethoxazole/trimethoprim
Sulfatrim IV: 80/16 mg/mL
sulfamethoxazole, trimethoprim
Available in Canada.
Do not confuse.
Drug interactions
toc ndcd b qnpsn-daopsn. Quinu-
prisin-dalfprisin may dcras h mablism f
HMG-CA rducas inhibirs (.g., arvasain, l-
vasain, pravasain, uvasain, simvasain), cycl-
sprin, rinavir, vincrisin, pacliaxl, dcaxl, a-
mxifn, diazpam, midazlam, mhylprdnisln,
carbamazpin, nifdipin, vrapamil, diliazm, lid-
cain, and hr pn CYP3Anzym sysm inhibirs.
Srum cncnrains f hs agns shuld b mni-
rd clsly if usd cncurrnly wih quinuprisin-
dalfprisin.
Drug ClASS: SulfONAmiDeS
an
Th sulfnamids ar n ru anibiics bcaus hy
ar n synhsizd by micrrganisms; hwvr, hy
ar highly ffciv anibacrial agns. Sulfnamids
ac by inhibiing bacrial bisynhsis f flic acid,
which vnually rsuls in bacrial cll dah. Human
clls d n synhsiz flic acid and hrfr ar n
affcd.
u
Sulfnamids ar usd primarily  ra UTIs and i-
is mdia. Thy may als b usd  prvn srp-
cccal infcin r rhumaic fvr in hs allrgic 
pnicillin.
Bcaus f an incrasing incidnc f rganisms r-
sisan  sulfnamid hrapy and h unrliabiliy f
in vir sulfnamid snsiiviy ss, pains shuld
b mnird clsly fr cninud hrapuic r-
spns  ramn. This is paricularly impran fr
pains bing rad fr chrnic and rcurrn UTIs.
Th sulfnamid ms cmmnly usd day is ac-
ually a cmbinain f rimhprim (TMP) and sulfa-
mhxazl (SMX) (.g., crimxazl, TMP-SMX).
This cmbinain blcks w sps in h pahway f
flic acid prducin; hrfr fwr rsisan srains
f micrrganisms hav dvlpd. Crimxazl
ADult DOSAge rANge
PO: Initial dose: 2–4 g, then 2–4 g/day in three
to six divided doses
PO: Initial therapy: 3–4g daily in three to four
divided doses; maintenance dosage: 2g daily
PO: 2–4 tablets daily, depending on strength,
disease being treated
IV: 8–10 mg/kg/day (based on trimethoprim) in
two to four divided doses
Pneumocystis pneumonia: 15–20 mg/kg/24
hr (based on trimethoprim) in three or four
divided doses for up to 14 days
is fn usd fr ramn f UTIs, iis mdia in
childrn, ravlr’s diarrha, acu xacrbains f
chrnic brnchiis in aduls, and prphylaxis and ra-
mn f Pneumocystis jiroveci pnumnia in immun-
cmprmisd pains.
t o
Th primary hrapuic ucm xpcd frm sul-
fnamid hrapy is liminain f bacrial infcin.
Nn in  snd
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
bginning hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability, dosage, and administration
S Tabl 45.8.
Medication Safety Alert
Patients should be encouraged to drink water several times
daily while receiving sulfonamide therapy. In rare situations,
crystals form in the urinary tract if the patient becomes too
dehydrated.
Common adverse effects
gasonsna
Nausea, vomiting, anorexia, diarrhea. Ths advrs f-
fcs ar usually mild and nd  rslv wih cnin-
ud hrapy. Encurag h pain n  discninu
hrapy wihu rs cnsuling h halhcar pr-
vidr. If h pain bcms dbiliad, cnac h
halhcar prvidr.

inna
Dermatologic reactions. Rpr a rash r prurius im-
mdialy and wihhld addiinal dss pnding ap-
prval by h halhcar prvidr.
Photosensitivity. Th pain shuld b cauind 
avid xpsur  sunligh and ulravil ligh. Suggs
waring lng-slvd clhing, a ha, and sunglasss
whn udrs. Discurag h us f anning lamps.
Haooc
Hematologic reactions. Ruin labrary sudis
(.g., CBC wih diffrnial) ar schduld fr pains
aking sulfnamids fr 14 days r lngr. Srss h im-
pranc f rurning fr his labrary wrk. Mnir
fr h dvlpmn f a sr hra, fvr, purpura,
jaundic, r xcssiv and prgrssiv waknss.
Nooc
Neurologic effects. Rpr h dvlpmn f inni-
us, hadach, dizzinss, mnal dprssin, drwsi-
nss, r cnfusin.
Drug interactions
Oa hpocc ans. Sulfnamids may dis-
plac sulfnylura ral hypglycmic agns (.g.,
glipizid, glimpirid, glyburid) and mgliinid
ral hypglycmic agns (rpaglinid, naglinid)
frm prin-binding sis, rsuling in hypglycmia.
Mnir fr hypglycmia, hadach, waknss,
dcrasd crdinain, gnral apprhnsin, diaphr-
sis, hungr, and blurrd r dubl visin. Th dsag f
h hypglycmic agn may nd  b rducd. Nify
h halhcar prvidr if any f hs sympms appar.
Waan. Sulfnamids may nhanc h ani-
cagulan ffcs f warfarin. Obsrv fr pchia;
cchymss; nsblds; blding gums; dark, arry
sls; and brigh rd r cff-grund msis. Mnir
INR and rduc dsag f warfarin if ncssary.
mhoa. Sulfnamids may prduc mh-
rxa xiciy whn givn simulanusly. Mnir
pains n cncurrn hrapy fr ral smaiis and
fr signs f nphrxiciy (.g., liguria, hmauria,
prinuria, cass).
Phnon. Sulsxazl may displac phnyin
frm prin-binding sis, rsuling in phnyin x-
iciy. Mnir pains n cncurrn hrapy fr signs
f phnyin xiciy (.g., nysagmus, sdain, lh-
argy); srum lvls may b rdrd. A rducd dsag
f phnyin may b rquird.
Anonsn-conn n nhbos, anonsn -
cpo bocks, pnon, sponoacon. Wih cncur-
rn us f hs agns and TMP-SMX, rimhprim
may ac addiivly  supprss aldsrn, rsuling
in hyprkalmia ha may lad  cardiac arrhyhmias.
Mnir srum passium lvls.
Drug ClASS: tetrACyCliNeS
an
Tracyclins ar a class f anibiics ha ar ffc-
iv agains gram-ngaiv and gram-psiiv bacria.
Drugs Used to Treat Infections CHAPTER 45 747
Thy ac by inhibiing prin synhsis by bacrial
clls.
u
Th racyclins ar fn usd in pains allrgic
 pnicillins fr h ramn f crain STIs, UTIs,
uppr rspirary rac infcins, pnumnia, and
mningiis. Thy ar paricularly ffciv agains
skin (acn), ricksial, and mycplasma infcins.
Thr hav bn hr nw racyclins apprvd.
Eravacyclin is usd fr h ramn f cmplicad
inraabdminal infcins causd by E. coli, E. cloa-
cae, K. oxytoca, E. faecalis, Staph. aureus, Strep. angino-
sus, C. perfringens, and Bacteroides spp. in pains 18
yars r ldr. Omadacyclin is usd fr h ra-
mn f adul pains wih cmmuniy-acquird
bacrial pnumnia (CABP) and acu bacrial skin
and skin srucur infcins. Sarcyclin is usd 
ra inammary lsins f nnndular mdra
 svr acn vulgaris in pains 9 yars and ldr.
Tracyclins adminisrd during h ags f h
dvlpmn (las half f prgnancy hrugh ag 8
yars) may caus naml hypplasia and prmann
yllw, gray, r brwn saining f h. Tracyclins
ar scrd in bras milk, s nursing mhrs n -
racyclin hrapy ar advisd  fd hir infans fr-
mula r cw’s milk, as apprpria.
t o
Th primary hrapuic ucm xpcd frm -
racyclin hrapy is liminain f bacrial infcin.
Nn in  tn
Premedication assessment
1. Obain baslin assssmns f prsning sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms prsn
bfr bginning hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability, dosage, and administration. S Tabl 45.9.
PO: Emphasiz h impranc f aking mdicain 1
hur bfr r 2 hurs afr ingsing anacids, milk,
r hr dairy prducs, r prducs cnaining cal-
cium, aluminum, magnsium, r irn (.g., viamins).
Exception: Fd and milk d n inrfr wih h ab-
srpin f dxycyclin.
Common adverse effects
gasonsna
Nausea, vomiting, anorexia, abdominal cramps, diar-
rhea. Ths advrs ffcs ar usually mild and nd
 rslv wih cninud hrapy. Encurag h pa-
in n  discninu hrapy wihu rs cnsul-
ing h halhcar prvidr.
748 UNIT IX Drugs Affecting Other Body Systems

Table 45.9 Tetracyclines

geNeriC NAme BrAND NAme AvAilABility ADult DOSAge rANge
doxycycline Vibramycin Tablets: 20, 50, 75, 100, 150 mg PO: 100 mg twice daily
Do not confuse Do not confuse Tablets, delayed release: 50, 75, 80, IV: 100 mg twice daily or 200 mg once
doxycycline with Vibramycin with 100, 120, 150, 200 mg daily
dicloxacillin or vancomycin. Capsules: 50, 75, 100, 150 mg
dicyclomine. Doryx Capsules, delayed release: 40 mg
Atridox Suspension: 25 mg/5 mL
Syrup: 50 mg/5 mL
IV: 100-mg vials
eravacycline Xerava Injection: 50 and 100-mg vials IV: 1 mg/kg over 60 min q12h for 4–14
days
minocycline CoreMino Capsules: 50, 75, 100 mg PO, IV: 200 mg, followed by 100 mg
CO-Minocycline Tablets: 50, 75, 100 mg q12h
Tablets, extended release (24 hr): 45,
55, 65, 80, 90, 105, 115, 135 mg
Capsules, extended release (24 hr):
45, 90, 135 mg
Extended-release powder in dental
base: 1 mg
IV: 100-mg vial
omadacycline Nuzyra Tablets: 150 mg PO: Days 1 and 2, 450 mg daily, then
Injection: 100 mg/vial 300 mg daily for 7-14 days
IV: Day 1, 200 mg once or 100mg two
times daily for 1 day, then 100 mg
daily for 7-14 days
sarecycline Seysara Tablets: 60, 100 and 150 mg PO: based on weight, 60–150 mg
once daily
tetracycline — Capsules: 250, 500 mg PO: 250–500 mg four times daily
Available in Canada.
Do not confuse.

inna tooh dopn. D n adminisr racyclins

Photosensitivity. Phsnsiiviy rsuling in an x-
aggrad sunburn afr shr xpsur has bn r-
prd. Th pain shuld b cauind  avid xp-
sur  sunligh and ulravil ligh. Suggs waring
lng-slvd clhing, a ha, and sunglasss whn u-
drs. Discurag h us f anning lamps. Cnsul
h halhcar prvidr abu h advisabiliy f dis-
cninuing hrapy.
Drug and other interactions
Waan. Tracyclins may nhanc h ani-
cagulan ffcs f warfarin. Obsrv fr pchi-
a; cchymss; nsblds; blding gums; dark,
arry sls; and brigh rd r cff-grund msis.
Mnir h INR and rduc h dsag f warfarin if
ncssary.
ipad absopon. Irn, calcium-cnaining fds
(milk and dairy prducs), and calcium, aluminum, r
magnsium prparains (anacids) dcras absrp-
in f racyclins. Adminisr all racyclin prd-
ucs 1 hur bfr r 2 hurs afr ingsin f hs
fds r prducs. Exceptions: Fd and milk d n
inrfr wih h absrpin f dxycyclin.
Phnon, cabaapn. Ths agns rduc h
half-lif f dxycyclin. Mnir pains fr lack f
clinical imprvmn frm h infcin.
 prgnan pains r  childrn yungr han 8
yars. Th infan’s r child’s h naml may b pr-
mannly saind yllw, gray, r brwn.
lacaon. Nursing mhrs mus swich hir babis
 frmula whil aking racyclins bcaus racy-
clins ar prsn in bras milk.
Oa conacps. Tracyclins may inrfr wih
h aciviy f ral cnracpivs. Oral cnracpivs
shuld n b discninud, bu cunsling rgarding
us f addiinal mhds f cnracpin (.g., cn-
dms and fam) shuld b plannd.
Drug ClASS: ANtituBerCulAr AgeNtS
 (ĕth-ĂM-byū-tŏl)
an
Ehambul inhibis ubrculsis bacrial grwh
by alring cllular RNA synhsis and phspha
mablism.
u
Ehambul is an aniubrcular agn. I mus b
usd in cmbinain wih hr aniubrcular agns
 prvn h dvlpmn f rsisan rganisms.

t o
Th primary hrapuic ucm xpcd frm h-
ambul hrapy is liminain f ubrculsis.
Nn in  e
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis.
5. Prfrm baslin mnal saus assssmn (.g.,
rinain and alrnss), assss fr GI sympms,
and s clr visin (.g., rd-grn discriminain)
bfr iniiaing hrapy.
6. Rviw labrary daa f ubrculin sing and
culurs in h pain’s char.
Availability. PO: 100- and 400-mg abls.
Dosage and administration. Adult: PO: Iniial ramn:
15 mg/kg adminisrd as a singl ds vry 24 hurs.
Rramn: 25 mg/kg as a singl daily ds. Afr 60
days, rduc h dsag  15 mg/kg and adminisr
as a singl ds vry 24 hurs. Adminisr nc daily
wih fd r milk  minimiz gasric irriain.
Medication Safety Alert
The patient should be warned that omission of doses or in-
terrupted intake of ethambutol may result in bacterial drug
resistance, reversal of clinical improvement, and increased
susceptibility of family members and others to tuberculosis.
Common adverse effects
gasonsna
Nausea, vomiting, anorexia, abdominal cramps. Ths ad-
vrs ffcs ar usually mild and nd  rslv wih
cninud hrapy. Encurag h pain n  dis-
cninu hrapy wihu rs cnsuling h halh-
car prvidr. Adminisr h daily dsag wih fd
 minimiz nausa and vmiing.
Serious adverse effects
Nooc
Confusion, hallucinations. Prfrm a baslin assss-
mn f h pain’s dgr f alrnss and rina-
in  nam, plac, and im bfr iniiaing hrapy.
Mak rgularly schduld subsqun mnal saus
valuains and cmpar ndings. Rpr dvlp-
mn f alrains. Prvid fr pain safy during
pisds f alrd bhavir r prids f dizzinss.
Snso
Blurred vision, red-green vision changes. Bfr iniia-
ing hrapy, chck fr any visual alrains using a
clr visin char. Schdul subsqun valuains
n a rgular basis. Rpr h dvlpmn f visual
Drugs Used to Treat Infections CHAPTER 45 749
disurbancs fr h halhcar prvidr’s valuain.
Ths advrs ffcs disappar wihin a fw wks af-
r hrapy has bn discninud.
Drug interactions
Anacds. Aluminum sals may dlay and rduc ab-
srpin f hambul. Spara adminisrain by a
las 2 hurs.
nzd (ī-sō-NĪ-ă-zĭd)
iNh
an
Isniazid has bn a mainsay fr many yars in h
prvnin and ramn f ubrculsis. Dspi his,
is mchanism f acin is sill n fully knwn. I ap-
pars  disrup h Mycobacterium tuberculosis cll wall
and inhibi rplicain.
u
Isniazid is usd fr bh prphylaxis and ramn
f ubrculsis. I shuld b usd in cmbinain
wih hr aniubrcular agns fr hrapy f aciv
disas.
t o
Th primary hrapuic ucms xpcd frm is-
niazid hrapy ar as fllws:
• Prvnin f ubrculsis in ppl wih a psiiv
skin s
• Eliminain f ubrculsis in ppl wih aciv
disas
Nn in  inzd
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms, abnr-
mal livr funcin s rsuls, r parshsias prs-
n bfr iniiain f hrapy.
4. Assss fr any allrgis.
5. Chck mdicain rdrs fr cncurrn adminisra-
in f hr aniubrcular drugs and fr an rdr
fr pyridxin.
Availability. PO: 100- and 300-mg abls; 50-mg/5-mL
syrup. IM: 100 mg/mL in 10-mL vials.
Dosage and administration. Adult: PO: Treatment of
active tuberculosis: 5 mg/kg  a maximum f 300 mg
daily, r 15 mg/kg/day (900 mg maximum pr ds)
w r hr ims pr wk. Isniazid shuld b usd
in cnjuncin wih hr ffciv aniubrcular
agns. Prophylactic therapy: 300 mg daily in a singl
ds. Adminisr n an mpy smach fr maximum
ffcivnss. Pyridxin, 25  50 mg daily, is fn
750 UNIT IX Drugs Affecting Other Body Systems
givn cncurrnly wih isniazid  diminish priph-
ral nurpahis, dizzinss, and aaxia. IM: Sam as
fr PO adminisrain.
Pediatric: PO: 10  15 mg/kg/day (maximum ds
f 300 mg daily) in singl ds, r 20  40 mg/kg/
day (900 mg maximum pr ds) w r hr ims
wkly. Infans and childrn lra largr dsags
han aduls.
Common and serious adverse effects
gasonsna
Nausea, vomiting. Nausa and vmiing ar rlaivly
cmmn advrs ffcs f isniazid and ar ds r-
lad. Cncurrn us f pyridxin, 25  50 mg daily,
will usually prvn hs sympms.
Hepatotoxicity. Th incidnc f hpaxiciy in-
crass wih ag and wih h cnsumpin f alchl.
This racin usually ccurs wihin h rs 3 mnhs
f hrapy and is hugh  b an allrgic racin.
Th sympms f hpaxiciy ar anrxia, nausa,
vmiing, jaundic, hpamgaly, splnmgaly, and
abnrmal livr funcin s rsuls (.g., lvad bili-
rubin, AST, ALT, GGT, and alkalin phsphaas lv-
ls; incrasd INR).
Nooc
Tingling, numbness. Tingling and numbnss f h
hands and f ar rlaivly cmmn advrs ffcs
f isniazid and ar dsag rlad. Cncurrn us
f pyridxin, 25  50 mg daily, will usually prvn
hs sympms. Whn parshsias ar prsn, h
pain mus b cauind  inspc h xrmiis fr
any skin brakdwn bcaus f h diminishd snsa-
in. Cauin pains n  immrs f r hands in
war wihu rs sing h mpraur. Mnir
pains wih parshsias fr adqua nuriin.
Dizziness, ataxia. Prvid fr pain safy and assis-
anc in ambulain unil ihr a dsag adjusmn
r addiin f pyridxin prvids sympmaic rlif.
Drug interactions
Dsa. Pains rciving cncurrn hrapy
may xprinc changs in physical crdinain and
mnal affc and bhavir. Prvid fr pain safy
and mnir h pain’s mnal saus bfr and
during hrapy. If pssibl, avid cncmian hrapy.
Cabaapn. Isniazid may inhibi h mab-
lism f carbamazpin. Mnir pains rciving
cncurrn hrapy fr signs f carbamazpin xic-
iy (.g., aaxia, hadach, vmiing, blurrd visin,
drwsinss, cnfusin).
thophn. Isniazid may inhibi h mablism
f hphyllin. Mnir pains rciving cncurrn
hrapy fr signs f hphyllin xiciy (.g., anxiy,
achycardia, nausa, hadach, vmiing).
Phnon. Isniazid may inhibi h mablism f
phnyin. Mnir pains rciving cncurrn hr-
apy fr signs f phnyin xiciy (.g., nysagmus,
sdain, lhargy). Srum lvls may b rdrd and
h dsag f phnyin rducd.
znd (pī-rah-ZIN-a-mīd)
an
Pyrazinamid is cnvrd  pyrazinic acid in h
mycbacrium rganism, which lwrs h pH f h
nvirnmn, alhugh h xac mchanism f acin
is n knwn.
u
Pyrazinamid is usd in h ramn f ubrcul-
sis. I mus b usd in cmbinain wih hr ani-
ubrcular agns  prvn h dvlpmn f r-
sisan rganisms. Pyrazinamid may inhibi uric acid
xcrin; acu guy aacks hav bn rprd. Us
wih cauin in pains wih chrnic gu. Is us is
cnraindicad wih acu gu.
t o
Th primary hrapuic ucm xpcd frm pyra-
zinamid hrapy is liminain f ubrculsis.
Nn in  pznd
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis.
5. Prfrm baslin mnal saus assssmn (.g., ri-
nain and alrnss).
6. Rviw labrary daa f ubrculin sing and
culurs in h pain’s char.
Availability. PO: 500-mg abls.
Dosage and administration. Adult: PO: Dosage by
weight: 40  55 kg: 1000 mg nc daily; 56  75 kg:
1500 mg nc daily; 76  90 kg: 2000 mg nc daily.
Note: Th prfrrd frquncy f adminisrain is
nc daily.
Medication Safety Alert
The patient should be warned that omission of doses or
interrupted intake of pyrazinamide may result in bacte-
rial drug resistance, reversal of clinical improvement, and
increased susceptibility of family members and others to
tuberculosis.
Common adverse effects
gasonsna
Nausea, vomiting, anorexia. Ths advrs ffcs ar
usually mild and nd  rslv wih cninud hrapy.
Encurag h pain n  discninu hrapy wih-
u rs cnsuling h halhcar prvidr. Adminisr

h daily dsag wih fd  minimiz nausa and
vmiing.
Ska and nosca cs
Arthralgia, myalgia. Ths advrs ffcs ar usu-
ally mild and nd  rslv wih cninud hrapy.
Encurag h pain n  discninu hrapy wih-
u rs cnsuling h halhcar prvidr.
Serious adverse effects
gasonsna
Hepatotoxicity. Mnir livr funcin
pridically.
Drug interactions
Ccospon. Pyrazinamid may dcras h srum
cncnrain f cyclsprin.
n (rĭf-ĂM-pĭn)
Do not confuse rifampin with ramipril or rifabutin.
rdn (RĬF-ă-dĭn)
Do not confuse Rifadin with Rifater.
an
Rifampin prvns RNA synhsis in mycbacria by
inhibiing DNA-dpndn RNA plymras. This ac-
in blcks ky mablic pahways ndd fr myc-
bacrium clls  grw and rplica.
u
Rifampin is usd in cmbinain wih hr agns fr h
ramn f ubrculsis. Rifampin is als usd  limi-
na mningccci frm h naspharynx f asympm-
aic N. meningitidis carrirs and  limina H. inuenzae
yp b frm h naspharynx f asympmaic carrirs.
t o
Th primary hrapuic ucms xpcd frm ri-
fampin hrapy ar as fllws:
• Eliminain f ubrculsis
• Eradicain f mningccci r H. inuenzae yp b
frm asympmaic carrirs f hs disass
Nn in  rn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms prsn
bfr bginning hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, ubrculin
ss, chs radigraphy).
Availability. PO: 150- and 300-mg capsuls. 25 mg/mL
pr 120 mL bl suspnsin. IV: 600-mg vials.
Drugs Used to Treat Infections CHAPTER 45 751
Dosage and administration. Adult: PO: 10 mg/kg
(maximum 600 mg) nc daily, ihr 1 hur bfr r
2 hurs afr a mal. IV: sam as fr PO.
Pediatric: PO: 10 mg/kg/day, wih a maximum
daily ds f 600 mg. IV: sam as fr PO.
Medication Safety Alert
Patients should be warned that omission of doses or inter-
rupted intake of rifampin may result in bacterial drug resis-
tance, reversal of clinical improvement, and increased sus-
ss ceptibility of family members to tuberculosis.
Common adverse effects
eco
Reddish orange secretions. Urin, fcs, saliva, spu-
um, swa, and ars may b ingd rddish rang.
This ffc is harmlss and will disappar afr dis-
cninuing hrapy; hwvr, rifampin may prma-
nnly disclr sf cnac lnss.
Serious adverse effects
gasonsna
Nausea, vomiting, anorexia, abdominal cramps. Ths
advrs ffcs ar usually mild and nd  rslv
wih cninud hrapy. Encurag h pain n
 discninu hrapy wihu firs cnsuling h
halhcar prvidr. If hs sympms ar accm-
panid by fvr, chills, r muscl and bn pain,
r if unusual bruising r a yllwish disclrain
f h skin r ys appars, cnac h halhcar
prvidr.
Drug interactions
Waan. Rifampin may diminish h anicagulan
ffcs f warfarin. Mnir h INR and incras h
dsag f warfarin if ncssary.
isonad. Cncurrn hrapy may rarly rsul in
hpaxiciy. Pains n cmbind hrapy shuld
hav livr funcin ss mnird pridically.
Dcasd hapc cs ndcd b -
apn. Rifampin simulas h mablism f bn-
zdiazpins (.g., diazpam, midazlam, riazlam),
quinidin, amidarn, vrapamil, nifdipin, mxi-
lin, nalapril, hphyllin, ba-blcking agns
(.g., bisprll, mprll, prpranll), phn-
barbial, urquinlns, ndansrn, halpri-
dl, lsaran, pras inhibirs, sulfnyluras, and
many hr drugs. Lng-rm cmbind hrapy may
rquir an incras in dsags fr hrapuic ffc.
Koconao. Adminisrain f rifampin and k-
cnazl dcrass srum lvls f bh drugs. Avid
cncurrn us if pssibl.
Oa conacps. Rifampin inrfrs wih h
aciviy f ral cnracpivs. Cunsling rgard-
ing alrnaiv mhds f birh cnrl shuld b
plannd.
752 UNIT IX Drugs Affecting Other Body Systems
Drug ClASS: OtHer ANtiBiOtiCS
zn (ăz-TRĒ ō-năm)
Do not confuse aztreonam with azithromycin.
az (ăz-ĂK-tăm)
an
Azrnam is a mnbacam anibiic, acing by inhi-
biin f cll wall synhsis.
u
Th mnbacams hav a high dgr f aciv-
iy agains ba-lacamas–prducing arbic
gram-ngaiv bacria, including P. aeruginosa.
Azrnam has ssnially n aciviy agains an-
arbs r gram-psiiv micrrganisms. I is usd
 ra urinary rac, lwr rspirary rac, skin,
inraabdminal, gynclgic, and bacrmic in-
fcins and mningiids causd by P. aeruginosa,
Salmonella spp., Shigella spp., N. gonorrhoeae, and
ampicillin-rsisan H. inuenzae. I is rcmmndd
ha azrnam b cmbind wih a brad-spcrum
anibiic in h iniial ramn f an infcin f
unknwn caus  ra suscpibl anarbs r
gram-psiiv rganisms.
t o
Th primary hrapuic ucm xpcd frm az-
rnam hrapy is liminain f bacrial infcin.
Nn in  azn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability. IM, IV: 1- and 2-g/vial. Inhalation: 75
mg/vial fr rcnsiuin.
Dosage and administration. Adult: IM or IV:
Urinary tract infections: 0.5  1 g vry 8  12 hurs.
Moderately severe systemic infections: 1  2 g vry 8
 12 hurs. Life-threatening infections: 2 g vry 6 
8 hurs.
Inhalation: Usual dsag: 75 mg hr ims daily
using an Alra Nbulizr Sysm (PARI Rspirary
Equipmn, Midlhian, VA). Rcnsiu h pw-
dr using h supplid dilun jus bfr inhalain.
Pains shuld us a shr- r lng-acing brnchdi-
lar bfr adminisrain f azrnam.
Common adverse effects
gasonsna
Nausea, vomiting, diarrhea. Ths advrs ffcs
ar usually mild and nd  rslv wih cninud
hrapy.
Serious adverse effects
gasonsna
Severe diarrhea. Svr diarrha may dvlp frm
h us f azrnam. Rpr diarrha f v r mr
sls daily  h halhcar prvidr. This may b an
indicain f drug-inducd psudmmbranus cli-
is. Bld r mucus in h sl als shuld b rprd
 h halhcar prvidr. Warn patients not to treat
diarrhea themselves when taking this drug. Th us
f pargric, diphnxyla, r lpramid may pr-
lng r wrsn h cndiin.
vasca
Phlebitis. Avid IV infusin in h lwr xrmiis
r in aras wih varicsiis. Us prpr chniqu in
saring h IV sluin.
Carfully assss a rgularly schduld inrvals
fr signs f dvlping phlbiis. Inspc fr rdnss,
warmh, ndrnss  uch, dma, r pain. Always
assss cmplains f pain a h infusin si. If signs f
inammain accmpany cmplains, discninu and
rsar lswhr.
in ss (opponsc ncons)
Secondary infections. Oral hrush, gnial and anal
prurius, vaginiis, and vaginal discharg may ccur.
Rpr prmply bcaus hs infcins ar rsisan
 h riginal anibiic usd. Tach h impranc f
miculus ral and prinal hygin masurs.
Drug interactions
Ba-acaas anbocs. Ths anibiics (.g., c-
fxiin, imipnm) induc h prducin f ba-
lacamas in sm gram-ngaiv rganisms, rsuling in
pssibl anagnism wih a ba-lacam anibiic such
as azrnam. I is rcmmndd ha ba-lacamas–
simulaing anibiics n b usd cncurrnly wih
azrnam.
ndn (klĭn-dă-MĬ-sĭn)
cn (klē-Ō-sĭn)
an
Clindamycin is an anibiic ha acs by inhibiing
prin synhsis.
u
Clindamycin is usful agains infcins causd by
gram-ngaiv arbic rganisms and a variy f
gram-psiiv and gram-ngaiv anarbs.
t o
Th primary hrapuic ucm xpcd frm
clindamycin hrapy is liminain f bacrial infcin.

Nn in  cndn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Rcrd parn f bwl liminain bfr iniia-
ing drug hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability. PO: 75-, 150-, and 300-mg capsuls;
75-mg/5-mL suspnsin in 100 ML bls. IV: 150
mg/mL in 2-, 4-, and 6-mL ampuls.
Dosage and administration. Adult: PO: 150  450 mg
vry 6 hurs. Do not rfrigra h suspnsin. I is
sabl a rm mpraur fr 14 days. IM: 600  2700
mg/24 hr. Do not xcd 600 mg pr injcin. Pain,
indurain, and sril abscsss hav bn rprd.
Dp IM injcin is rcmmndd  hlp minimiz
his racin. IV: 600  2700 mg/24 hr. Dilu  lss
han 6 mg/mL and adminisr a a ra lss han 30 mg/
min. Adminisrain by IV push is n rcmmndd.
Pediatric: PO: Suspnsin: 8  25 mg/kg/24 hr in
hr r fur dividd dss. Capsuls: 8  20 mg/kg/24
hr in hr r fur dividd dss. Capsuls shuld b
akn wih a full glass f war  prvn sphagal
irriain. IM: 15  40 mg/kg/24 hr in fur dividd ds-
s. IV: sam as fr IM us. Dilu  lss han 6 mg/mL
and adminisr a a ra lss han 30 mg/min.
Common adverse effects
gasonsna
Diarrhea. This advrs ffc is usually mild and
nds  rslv wih cninud hrapy. Encurag
h pain n  discninu hrapy wihu rs
cnsuling h halhcar prvidr.
Serious adverse effects
gasonsna
Severe diarrhea. Svr diarrha may dvlp frm
h us f clindamycin. Rpr diarrha f v r mr
sls daily  h halhcar prvidr. This may b an
indicain f drug-inducd psudmmbranus cli-
is. Bld r mucus in h sl shuld als b rprd
 h halhcar prvidr. Warn patients not to treat
diarrhea themselves when taking this drug. Th us
f pargric, diphnxyla, r lpramid may pr-
lng r wrsn h cndiin.
Drug interactions
Nosca bockad. Labl chars f pains
schduld fr surgry wh ar aking clindamycin.
Whn cmbind wih surgical muscl rlaxans r
Drugs Used to Treat Infections CHAPTER 45 753
aminglycsids, nurmuscular blckad may rsul.
Ths cmbinains als may pnia rspirary
dprssin. Chck h anshsia rcrd f surgical pa-
ins. Mnir pspraiv pains fr rspirary
dprssin fr a prlngd prid. This can ccur 48
hurs r mr afr h drug adminisrain.
ehocn. Thrapuic anagnism has bn r-
prd bwn clindamycin and ryhrmycin. D
n adminisr cncurrnly.
dn (dăp-tō-MĪ-sĭn)
cn (KYŪ-bĭ-sĭn)
an
Dapmycin is in h class f anibiics knwn as cy-
clic lipopeptide antibiotics. I has a uniqu mchanism f
acin amng h anibiics. I binds  bacrial mm-
brans and causs a rapid dplarizain f mmbran
pnial, lading  inhibiin f prin, RNA, and
DNA synhsis, which lads  cll dah. Bcaus f
is uniqu mchanism f acin, dapmycin is ffc-
iv agains micrrganisms ha hav dvlpd r-
sisanc  hr cmmnly usd anibiics.
u
Dapmycin has bn apprvd fr h ramn f
cSSSIs causd by Staph. aureus, Strep. pyogenes, Strep.
agalactiae, and Enterococcus faecalis. I is paricularly
valuabl in cass f gram-psiiv rganisms bcm-
ing rsisan  h ba-lacam anibiics (pnicillins
and cphalsprins) and vancmycin. In an ffr 
slw h dvlpmn f srains f bacria rsisan 
dapmycin, i shuld b usd nly whn h pah-
gn is rsisan  hr availabl anibiics.
t o
Th primary hrapuic ucm xpcd frm dap-
mycin hrapy is liminain f bacrial infcin.
Nn in  Dn
Premedication assessment
1. Obain baslin assssmns f prsning sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr any allrgis.
4. Assss h bwl liminain parns and rcrd
bfr iniiaing hrapy.
5. Ensur ha bld fr a baslin crain phsph-
kinas (CPK) and crainin kinas sudy has bn
drawn and sn  h labrary bfr dapmycin
is sard. Als, inquir and rcrd whhr h pa-
in has any paricular muscl waknss r pains,
paricularly in h xrmiis.
6. Obain hr baslin labrary sudis rdrd
and rviw rsuls (.g., CBC wih diffrnial, cul-
ur and snsiiviy).
754 UNIT IX Drugs Affecting Other Body Systems
Availability. IV: 350-, 500-mg vials.
Dosage and administration. IV: Cmplicad skin and
skin srucur infcins: 4 mg/kg nc vry 24 hurs
fr 7  14 days.
Endocarditis: 6 mg/kg infusd vr 30 minus v-
ry 24 hurs fr 2  6 wks.
Pains wh hav rducd rnal funcin wih a
crainin claranc f lss han 30 mL/min shuld
hav h sam dss adminisrd vry 48 hurs.
Ad copab. Dapmycin is n cmpaibl
wih dxrs-cnaining diluns, and addiivs r hr
mdicains shuld n b addd  dapmycin r in-
fusd simulanusly hrugh h sam IV lin. If h sam
IV lin is usd fr squnial infusin f svral diffrn
drugs, h lin shuld b ushd wih a cmpaibl infu-
sin sluin bfr and afr infusins wih dapmycin.
Common adverse effects
gasonsna
Gastric irritation. Th ms cmmn advrs ffcs
f dapmycin hrapy ar diarrha, cnsipain,
nausa, and vmiing. Ths advrs ffcs ar usu-
ally mild and nd  rslv wih cninud hrapy.
Serious adverse effects
gasonsna
Severe diarrhea. Svr diarrha may dvlp frm h
us f dapmycin. Bld and mucus in h sl als may
b prsn. This may b an indicain f drug-inducd
psudmmbranus cliis and shuld b rprd im-
mdialy. Wihhld h nx ds f anibiic unil h
halhcar prvidr givs apprval fr adminisrain.
mscoska
Skeletal muscle weakness and pain. Pains shuld
b mnird fr h dvlpmn f muscl pain r
waknss, paricularly in h disal xrmiis. I is
rcmmndd ha CPK cncnrains b mnird
wkly in pains rad wih dapmycin and mr
frqunly in hs wh dvlp unxplaind lva-
ins f CPK lvls during hrapy.
Drug interactions
Hmg-CoA dcas nhbos. Th sains (.g., arv-
asain, lvasain, simvasain, hrs) may infrqun-
ly caus sklal muscl mypahy and pnially
rhabdmylysis whn adminisrd wih dapmycin.
I is hrfr suggsd ha sain hrapy b dis-
cninud in pains bing rad wih dapmycin.
Sain hrapy may b riniiad afr dapmycin
hrapy has bn cmpld.
ndz (mĕt-rō-NĪ-dă-zŏl)
Do not confuse metronidazole with metoclopramide,
metoprolol, miconazole, or methazolamide.
f (FLĂ-jĭl)
an
Mrnidazl is a nirimidazl. I is a smwha
unusual mdicain in ha i has bacricidal, rich-
mnacidal, and przacidal aciviy. Is mchanism
f acin is unknwn.
u
Mrnidazl is usd  ra richmniasis, giardia-
sis, ambic dysnry, ambic livr abscss, and anar-
bic bacrial infcins.
t o
Th primary hrapuic ucm xpcd frm m-
rnidazl hrapy is liminain f infcin.
Nn in  mndz
Premedication assessment
1. Obain baslin assssmns f h prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms, p-
riphral nurpahy, r sizur disrdrs bfr ini-
iaing hrapy.
4. Assss fr any allrgis.
5. Prfrm a baslin assssmn f h pain’s d-
gr f alrnss and rinain  nam, plac, and
im bfr iniiaing hrapy.
6. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability. PO: 250- and 500-mg abls; 375-mg
capsuls. Suspension: 50 mg/mL in 120 mL bls.
Injection: 500-mg pwdr/vial.
Dosage and administration. Adult: PO:
• Trichomoniasis: Mn and wmn: 500 mg wic daily
fr 7 days (CDC) or 250 mg hr ims daily r 375
mg wic daily fr 7 days (manufacurr). Sxual
parnrs mus b rad cncurrnly  prvn
rinfcin. Singl dss f 2 g r w dss f 1 g
ach adminisrd h sam day appar  prvid
adqua ramn fr richmniasis in mn and
wmn.
• Giardiasis: 250 mg hr ims daily fr 5  7 days.
• Amebic dysentery: 750 mg hr ims daily fr 5  10
days.
• Amebic liver abscess: 500–750 mg vry 8 hurs fr 5
 10 days.
• Anaerobic bacterial infections: Adminisr wih par-
nral hrapy iniially. Th usual ral dsag is
7.5 mg/kg vry 6 hurs. D n xcd 4 g/24 hr.
Th usual durain is 7  10 days. Infcins f h
bns and jins, lwr rspirary rac, and nd-
cardium may rquir lngr ramn.

Adult: IV: Anaerobic bacterial infections: Lading
ds: 15 mg/kg infusd vr 1 hur. Mainnanc ds-
ag: 7.5 mg/kg infusd vr 1 hur vry 6 hurs. D
n xcd 4 g/24 hr. Cnvr  ral dsags whn
clinical cndiin is sabl. Dsag rducin is ncs-
sary in pains wih hpaic impairmn bu n rnal
impairmn.
Pediatric: PO: Trichomoniasis: 15 mg/kg/24 hr
in hr dividd dss fr 7 days. Amebiasis: 35  50
mg/kg/24 hr in hr dividd dss fr 7  10 days.
Giardiasis: 15 mg/kg/24 hr in hr dividd dss
(maximum f 250 mg/ds) fr 5 days.
Common adverse effects
gasonsna
Nausea, vomiting, diarrhea, metallic taste. Ths advrs
ffcs ar usually mild and nd  rslv wih cn-
inud hrapy.
Serious adverse effects
Nooc
Dizziness. Prvid fr pain safy during pisds
f dizzinss; rpr  h halhcar prvidr fr fur-
hr valuain.
Confusion, seizures. Pains rciving high dss f
mrnidazl, hs wih hisris f sizur aciviy,
and hs wih signican hpaic impairmn ar a
grar risk f cnfusin and sizurs. Prfrm a bas-
lin assssmn f h pain’s dgr f alrnss and
rinain  nam, plac, and im bfr iniiaing
hrapy. Mak rgularly schduld subsqun mnal
saus valuains and cmpar ndings. Rpr h
dvlpmn f alrains.
Implmn sizur prcauins (paddd sid rails,
availabl xygn, and sucin ss). Mak sur ha h
pain cninus wih anicnvulsan hrapy. If sizurs
dvlp, prvid fr pain safy and hn rcrd h
xac im f sizur ns and durain f ach phas, a
dscripin f h spcic bdy pars invlvd, and any
prgrssin in h affcd pars. Dscrib h aumaic
rspnss sn during h clnic phas—alrd, jrky
rspirains; frhy salivain; dilad pupils and y
mvmns; cyansis; diaphrsis; r incninnc.
vasca
Thrombophlebitis. Carfully assss pains rciving IV
mrnidazl fr h dvlpmn f hrmbphlbiis.
Inspc h IV infusin ara frqunly whn prvid-
ing car; visually inspc during drssing changs and
whnvr h infusin is changd  a nw si. Always
invsiga pain a h IV si. Rpr rdnss, warmh,
ndrnss  uch, and dma in h affcd par.
Drug interactions
Acoho. Us f alchl and alchl-cnaining prp-
arains, such as OTC cugh mdicains and muh-
washs (.g., Lisrin, Cēpacl), shuld b avidd
during and up  48 hurs afr discninuain f
mrnidazl hrapy. Mrnidazl inhibis nzyms
Drugs Used to Treat Infections CHAPTER 45 755
rquird  mabliz alchl, rsuling in mild symp-
ms f abdminal cramping, ushing, hadach, nau-
sa, vmiing, and swaing.
Waan. Mrnidazl may nhanc h ani-
cagulan ffcs f warfarin. Obsrv fr h dvlp-
mn f pchia; cchymss; nsblds; blding
gums; dark, arry sls; and brigh rd r cff-
grund msis. Mnir h INR and rduc h ds-
ag f warfarin if ncssary.
Dsa. Cmbind us f disulram and mr-
nidazl may rsul in mnal cnfusin and psych-
ss. Cncurrn hrapy is n rcmmndd.
lh. Pains rciving highr dsags f lihi-
um ar mr suscpibl  lihium xiciy and pn-
ial rnal damag. Mrnidazl shuld b iniiad
nly if absluly ncssary. Frqunly mnir srum
lihium and crainin cncnrains whn mrni-
dazl and lihium ar adminisrd cncurrnly.
Phnon, osphnon. Mrnidazl inhibis ph-
nyin mablism. Mnir pains wih cncurrn
hrapy fr signs f phnyin xiciy: nysagmus, s-
dain, and lhargy. Srum lvls may b rdrd and
h dsag f phnyin rducd.
ndz (tĭn-Ĭ-dă-zōl)
an
Tinidazl is a nirimidazl similar  mrnida-
zl. Is mchanism f acin is unknwn.
u
Tinidazl is usd  ra parasiic infcins such as
richmniasis causd by Trichomonas vaginalis in f-
mal and mal pains, giardiasis causd by Giardia
lamblia, and insinal ambiasis and ambic livr ab-
scss causd by Entamoeba histolytica.
t o
Th primary hrapuic ucm xpcd frm ini-
dazl hrapy is liminain f parasiic infcin.
Nn in  tndz
Premedication assessment
1. Obain baslin assssmns f h prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms, p-
riphral nurpahy, r sizur disrdrs bfr ini-
iaing hrapy.
4. Assss fr any allrgis.
5. Prfrm a baslin assssmn f h pain’s d-
gr f alrnss and rinain  nam, plac, and
im bfr iniiaing hrapy.
6. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
756 UNIT IX Drugs Affecting Other Body Systems
Availability. PO: 250- and 500-mg abls.
Dosage and administration. PO: Trichomoniasis: Mn
and wmn: 2 g nc. Sxual parnrs mus b ra-
d cncurrnly  prvn rinfcin. Amebic dysen-
tery and amebic liver abscess: 2 g nc daily fr 3 days.
Giardiasis: 2 g nc.
Note: Tinidazl shuld b adminisrd wih fd
 rduc h incidnc f GI ffcs.
Common adverse effects
gasonsna
Nausea, vomiting, diarrhea. Ths advrs ffcs
ar usually mild and nd  rslv wih cninud
hrapy.
Serious adverse effects
Nooc
Dizziness. Prvid fr pain safy during pisds
f dizzinss; rpr fr furhr valuain.
Confusion, seizures. Pains rciving high dss
f inidazl, hs wih hisris f sizur aciviy,
and hs wih signican hpaic impairmn ar a
grar risk f cnfusin and sizurs. Prfrm a bas-
lin assssmn f h pain’s dgr f alrnss and
rinain  nam, plac, and im bfr iniiaing
hrapy. Mak rgularly schduld subsqun mnal
saus valuains and cmpar ndings. Rpr h
dvlpmn f alrains.
Implmn sizur prcauins (paddd sid rails,
availabl xygn, and sucin ss). Mak sur ha
h pain cninus wih anicnvulsan hrapy. If
sizurs dvlp, prvid fr pain safy and hn
rcrd h xac im f sizur ns and durain
f ach phas, a dscripin f h spcic bdy pars
invlvd, and any prgrssin in h affcd pars.
Dscrib h aumaic rspnss sn during h cln-
ic phas—alrd, jrky rspirains; frhy salivain;
dilad pupils and y mvmns; cyansis; diaph-
rsis; r incninnc.
Drug interactions
Acoho. Us f alchl and alchl-cnaining prp-
arains, such as OTC cugh mdicains and muh-
washs (.g., Lisrin, Cēpacl), shuld b avidd
during hrapy and fr 72 hurs afr discninuain
f inidazl hrapy. Tinidazl inhibis nzyms r-
quird  mabliz alchl, rsuling in mild symp-
ms f abdminal cramping, ushing, hadach, nau-
sa, vmiing, and swaing.
Waan. Tinidazl may nhanc h anicagulan
ffcs f warfarin during and up  8 days afr aking
inidazl. Obsrv fr h dvlpmn f pchia;
cchymss; nsblds; blding gums; dark, arry
sls; and brigh rd r cff-grund msis. Mnir
h INR and rduc h dsag f warfarin if ncssary.
lh. Pains rciving highr dsags f lihium
ar mr suscpibl  lihium xiciy and pnial
rnal damag. Tinidazl shuld b iniiad nly if
absluly ncssary. Frqunly mnir srum lihi-
um and crainin cncnrains whn inidazl and
lihium ar adminisrd cncurrnly.
Phnon, osphnon. Tinidazl inhibis phny-
in mablism. Mnir pains wih cncurrn
hrapy fr signs f phnyin xiciy: nysagmus, s-
dain, and lhargy. Srum lvls may b rdrd and
h dsag f phnyin rducd.
Drug ClASS: tOPiCAl ANtifuNgAl AgeNtS
an
Th xac mchanisms whrby anifungal agns ac
ar unknwn; hwvr, i is knwn ha cll mm-
brans ar alrd, rsuling in incrasd prmabiliy,
lakag f amin acids and lcrlys, and impaird
upak f ssnial nurins ndd fr cll grwh.
u
Th cmmn pical fungal infcins causd by sv-
ral diffrn drmaphys ar ina pdis (ahl’s
f), ina cruris (jck ich), ina crpris (ringwrm),
and ina vrsiclr. Candida albicans is h ms cm-
mn caus f ral candidiasis (hrush), cuanus can-
didiasis (.g., diapr rash), and vaginal candidiasis
(mniliasis [yas infcin]).
t o
Th primary hrapuic ucm xpcd frm pi-
cal anifungal hrapy is liminain f fungal infcin.
Nn in  t ann
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Assss fr any allrgis.
Availability, dosage, and administration
S Tabl 45.10.
topca. Apply clan glvs. Wash hands hrughly
bfr and immdialy afr applicain. Clans skin
wih sap and war and dry hrughly.
Fr ahl’s f, h pwdr is ms ffciv in
inrriginus aras and in pains fr whm a dry
nvirnmn may nhanc h hrapuic rspns.
Insruc pains  war cn scks (avid nyln)
if pssibl and chang hm w r hr ims daily.
Tramns may b rquird fr 6 wks r lngr wih
lng-sanding infcins and in aras f hicknd skin.
Fr jck ich r ringwrm, war wll-ing, nn-
cnsricing, vnilad clhing.
Fr all fungal infcins, insruc pains  avid
igh-ing clhing and cclusiv drssings unlss
hrwis insrucd by h halhcar prvidr.
e conac. Insruc pains  avid cnac wih
h ys and  wash hir ys immdialy if cnac
ccurs.
 Drugs Used to Treat Infections CHAPTER 45 757

Table 45.10 Topical Antifungal Agents

geNeriC NAme BrAND NAme AvAilABility ADult DOSAge rANge
butenane Lotrimin Ultra Cream: 1% For ringworm, jock itch, athlete’s foot: Apply
Mentax topically to affected area one or two times
daily for 1–4 wk
butoconazole Gynazole-1 Vaginal cream: 2% For vaginal candidiasis: Insert 1 applicatorful
intravaginally at bedtime once
ciclopirox Loprox Cream: 0.77% For ringworm, jock itch, athlete’s foot, cutaneous
Gel: 0.77% candidiasis, and tinea versicolor: Massage
Shampoo: 1% product into affected skin twice daily for at
Solution for nails: 8% least 4 wk; shampoo: twice weekly for 4 wk
Topical suspension: 0.77%
clotrimazole Gyne-Lotrimin Vaginal cream: 1, 2% For vaginal candidiasis: Insert 1 applicatorful at
bedtime for 3–7 nights
Desenex, Alevazol Cream and ointment: 1% For ringworm, jock itch, athlete’s foot: Apply
— Solution: 1% topically to affected skin morning and evening;
gently rub in
— Oral lozenges: 10 mg (troches) For oral candidiasis: Allow 1 lozenge to dissolve
slowly in mouth ve times daily for 14
consecutive days
econazole Cream: 1% For ringworm, jock itch, athlete’s foot, tinea
Ecoza Foam: 1% versicolor: Apply over affected area once daily
For cutaneous candidiasis: Apply twice daily
(morning and evening)
enaconazole Jublia Solution: 10% For fungal infections of the toes: Apply to
affected toenails once daily for 48 wk
ketoconazole — Cream: 2% For ringworm, jock itch, athlete’s foot, cutaneous
Ketodan Foam: 2% candidiasis, tinea versicolor: Massage cream
Xolegel Gel: 2% into affected and surrounding tissue once
Nizoral AD Shampoo: 1%, 2% daily; may require 2–4 wk of treatment
For seborrheic dermatitis:
Cream and foam: Massage into affected area
twice daily for 4 wk
Gel: Massage into affected area once daily for
2 wk
For dandruff: Moisten hair and scalp with water;
apply shampoo and lather gently for 1 min;
rinse and reapply, leaving lather on scalp for
3 min; rinse thoroughly and dry hair; apply
shampoo twice weekly for 4 wk with at least 3
days between shampooing
luliconazole Luzu Cream, external 1% For jock itch, truncal lesions: Apply once daily
for 1 wk
For athlete’s foot: Apply once daily for 2 wk
miconazole Monistat 3 Kit Vaginal suppositories: 200 mg For vaginal candidiasis:
Vaginal cream: 2% Monistat 3: Insert 1 suppository intravaginally at
Monistat 7 Vaginal suppositories: 100 mg bedtime for 3 days
Vaginal cream: 2% Monistat 7: Insert 1 applicatorful or 1
suppository intravaginally at bedtime for 7
days
Micatin Cream: 2% For ringworm, jock itch, athlete’s foot, cutaneous
Lotrimin AF Powder: 2% candidiasis, tinea versicolor: Cover affected
Azolen Solution: 2% areas twice daily (morning and evening);
Lotrimin AF Spray: 2% treatment may require 2–4 wk
Aloe Vesta Clear Ointment: 2%
naftine Naftin Cream: 1, 2% For ringworm, jock itch, athlete’s foot:
Gel: 1, 2% Cream: massage into affected area once daily
Gel: massage into affected area twice daily
758 UNIT IX Drugs Affecting Other Body Systems

Table 45.10 Topical Antifungal Agents—cont’d

geNeriC NAme BrAND NAme AvAilABility ADult DOSAge rANge
nystatin – Oral suspension: 100,000 units/ For oral candidiasis: Sip 4–6 mL four times daily;
mL retain in mouth as long as possible before
swallowing
Oral tablets: 500,000 units For nonesophageal mucous membrane GI
Oral capsules: candidiasis: 1 or 2 tablets or capsules one to
0.5-, 1-million units three times a day
Cream, ointment, powder For cutaneous candidiasis: Apply to affected
area two or three times daily
oxiconazole Oxistat Cream: 1% For ringworm, jock itch, athlete’s foot: Massage
nitrate Lotion: 1% into affected areas once to twice daily at
bedtime
sertaconazole Ertaczo Cream: 2% For athlete’s foot: Apply twice daily for 4 wk
sulconazole Exelderm Cream: 1% For ringworm, jock itch, athlete’s foot: Massage
Solution: 1% into affected area once or twice daily
tavaborole Kerydin Solution: 5% For onychomycosis of the toenail: Apply to
affected toenail(s) once daily for 48 wk
terbinane Lamisil AT Cream: 1% For tinea versicolor, athlete’s foot, jock rash,
Spray: 1% ringworm: Massage into affected area once or
Gel: 1% twice daily; treatment may require 2–4 wk
terconazole – Vaginal cream: 0.4% and 0.8% For vaginal candidiasis:
Vaginal suppository: 80 mg Insert 1 applicatorful intravaginally daily at
bedtime for 3 (0.8% cream) or 7 (0.4% cream)
consecutive days
Insert 1 suppository intravaginally once daily at
bedtime for 3 consecutive days
tolnaftate Tinactin Cream: 1% For ringworm, jock itch, athlete’s foot, cutaneous
Solution: 1% candidiasis, tinea versicolor: Cover affected
Spray: 1% areas twice daily (morning and evening);
Powder: 1% treatment may require 2–4 wk

inaana. Giv h pain h fllwing insruc-  discninu hrapy wihu rs cnsuling h
ins: halhcar prvidr.
1. Wash h applicar in warm sapy war afr ach Redness, swelling, blistering, oozing. Ths signs may
us s ha i ds n bcm a vhicl fr rinfcin. b an indicain f hyprsnsiiviy. Infrm h halh-
2. Cnsidr using a pad  prc clhing. car prvidr.
3. Us h numbr f dss prscribd vn if symp-
ms disappar r mnsruain bgins. Drug interactions. N clinically signican drug inr-
4. Rfrain frm sxual inrcurs during hrapy (r acins hav bn rprd.
h mal parnr shuld war a cndm  avid
rinfcin). Drug ClASS: SyStemiC ANtifuNgAl AgeNtS
5. Whn bing rad wih vaginal inmn (.g.,
Vagisa-1), us cnracpin hr han a diaphragm
n b d dx (--ter--
r cndm. Prlngd cnac wih prlaum-basd
n  dk--Ko-)
prducs may caus h diaphragm and cndm 
n b d x
drira. a
n b 
Common and serious adverse effects ab
inna
Irritation. Sm pains xprinc vulvar r vagi-
nal burning, vulvar iching, discharg, srnss, r an
swlling frm h inravaginal prducs. Ths ad- Amphricin B is a fungisaic agn ha disrups h
vrs ffcs ar usually mild and nd  rslv cll mmbran f fungal clls, rsuling in a lss f cl-
wih cninud hrapy. Encurag h pain n lular cnns.

u
Amphricin B is usd primarily in raing sysm-
ic lif-hraning fungal infcins. I shuld n b
usd  ra nninvasiv fungal infcins such as ral
hrush, vaginal candidiasis, and sphagal candidiasis
in immuncmpn pains wih nrmal nurphil
cuns. Thr ar hr dsag frms f amphricin B,
ach wih diffrn brand nams and smwha diffr-
n apprval fr us. Each has diffrn rquirmns
fr rcnsiuin, diluin, lrain, and adminisra-
in ra. Wrk clsly wih h pharmacy dparmn
 nsur ha h crrc dsag frm is bing rcnsi-
ud and dilud prprly, and ha prpr adminisra-
in chniqu, including h us f apprpria inlin
lrs and ra f infusin, is bing usd.
t o
Th primary hrapuic ucm xpcd frm am-
phricin B hrapy is liminain f fungal infcin.
Nn in  an b
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr nrmal rnal funcin and nrmal lc-
rlys bfr iniiaing hrapy.
4. Assss fr any allrgis.
5. Gahr baslin daa abu h pain’s mnal sa-
us (.g., alrnss, rinain, cnfusin), muscl
srngh, prsnc f muscl cramps, rmrs, nau-
sa, and gnral apparanc (.g., drwsy, anxius,
lhargic).
6. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability. IV:
• Amphricin B sdium dxychla (“cnvn-
inal” amphricin B): 50 mg/vial
• Amphricin B lipid cmplx (Ablc): 5 mg/mL
in 20-mL vial
• Amphricin B lipsm (AmBism): 50 mg/vial
Dosage and administration. Dsag varis dpnding
n h dsag frm and h rganism fr which h
mdicin is bing usd. Cnsul h halhcar prvid-
r, labrary rsuls, and h pharmacis  prvid
chcks n h apprpria ds and adminisrain f
h anifungal agn.
Common and serious adverse effects
gna
Malaise, fever, chills, headache, nausea, vomiting. Ths
advrs ffcs nd  b ds rlad and may b
minimizd by slw infusin, rducin f dsag,
and alrna-day adminisrain. Chck PRN and
Drugs Used to Treat Infections CHAPTER 45 759
sanding rdrs fr drugs (.g., anihisamins, aspirin,
animics) ha may allvia hs sympms.
una
Nephrotoxicity. Nphrxiciy may b manifsd by
incrass in xcrin f uric acid, passium, and mag-
nsium; liguria; granular cass in h urin; prinu-
ria; and incrasd BUN and srum crainin lvls.
Mnir urinalysis and kidny funcin ss fr ab-
nrmal rsuls. Rpr incrasing BUN and crainin
lvls, dcrasing urin upu r dcrasing urin
spcic graviy (dspi amun f uid inak), cass
r prin in h urin, frank bld r smky-clrd
urin, r RBCs in xcss f 0  3 RBCs/HPF (s Tabl
41.1) n h urinalysis rpr. Rpr inpu and upu,
as wll as a prgrssiv dcras in daily urin vlum
r changs in visual characrisics.
Haooc
Electrolyte imbalance. Th lcrlys ms cm-
mnly alrd ar passium (K+) and magnsium
(Mg2+). Hypkalmia is ms likly  ccur. Many
sympms assciad wih alrd uid and lcrly
balanc ar subl and rsmbl gnral sympms f
drug xiciy r h disas prcss islf. Gahr daa
abu changs in h pain’s mnal saus (.g., alr-
nss, rinain, cnfusin), muscl srngh, muscl
cramps, rmrs, nausa, and gnral apparanc (.g.,
drwsy, anxius, lhargic). Always chck h lcr-
ly rprs fr arly indicains f lcrly imbal-
anc. Kp accura rcrds f inpu and upu, daily
wighs, and vial signs.
vasca
Thrombophlebitis. Carfully assss pains rciv-
ing IV amphricin B fr h dvlpmn f hrm-
bphlbiis. Inspc h IV infusin ara fn whn
prviding car; inspc during drssing changs
and whnvr h infusin is changd  a nw si.
Always invsiga pain a h IV si. Rpr rdnss,
warmh, ndrnss  uch, and dma in h af-
fcd par.
Drug interactions
Cocosods. Th cncurrn us f amphricin
B and cricsrids (.g., prdnisn) may nhanc
h lss f passium. Chck passium lvls and
mnir mr clsly fr hypkalmia.
Nphooc pona. Cmbining amphricin B
wih hr nphrxic agns such as aminglycsids,
diurics, r cisplain shuld b dn wih xrm
cauin. Mnir clsly fr signs f nphrxiciy.
Don. Bcaus amphricin B may induc
hypkalmia, us cauiusly in pains rciving
digxin. Hypkalmia may induc digxin xic-
iy. Mnir pains fr dysrhyhmias, nausa, and
bradycardia.
Dcs. Thiazid and lp diurics may in-
duc hypkalmia. Mnir pains rciving am-
phricin B and diuric hrapy vry clsly fr
hypkalmia.
760 UNIT IX Drugs Affecting Other Body Systems
nz (ū-KŎN-ă-zōl)
Dn (DĪ-ū-kăn)
Do not confuse Diucan with Dilantin or Diprivan.
an
Flucnazl is an anifungal agn chmically rlad
 kcnazl and iracnazl. I acs by inhibiing
crain mablic pahways in fungi, hus inrfring
wih cll wall synhsis.
u
Flucnazl is usd fr ral and IV ramn f cryp-
cccal mningiis and rpharyngal, sphagal, vul-
vvaginal, r sysmic candidiasis. Flucnazl hrapy
is usually rsrvd fr pains in whm hr anifungal
hrapy was n lrad r was inffciv. Flucnazl
is als usd prphylacically  prvn candidiasis in
bn marrw ransplan pains wh ar rciving
radiain r chmhrapy ramn and in pains
wih human immundcincy virus (HIV) infcin.
Flucnazl is als apprvd as a singl-ds ramn
f vaginal candidiasis in immuncmpn pains.
t o
Th primary hrapuic ucms xpcd frm u-
cnazl hrapy ar as fllws:
• Prvnin f sysmic fungal infcins
• Eliminain f fungal infcin
Nn in  fnz
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms and
abnrmal livr and rnal funcin bfr iniiaing
hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy).
Availability. PO: 50-, 100-, 150-, and 200-mg abls; 10
and 40 mg/mL suspnsin in 35-mL bl. IV: 200-
and 400-mg vials.
Dosage and administration. PO: 100  400 mg daily;
dsag mus b individualizd  yp f infcin b-
ing rad. IV: sam as fr PO.
Common adverse effects
gasonsna
Nausea, vomiting, diarrhea. Ths advrs ffcs ar
usually mild and nd  rslv wih cninud hr-
apy. Encurag h pain n  discninu hrapy
wihu rs cnsuling h halhcar prvidr.
Serious adverse effects
inna
Rash. Rpr sympms fr furhr valuain by
h halhcar prvidr. D n adminisr any furhr
dss unil s rdrd by h halhcar prvidr.
gasonsna
Hepatotoxicity. Th sympms f hpaxiciy ar
anrxia, nausa, vmiing, jaundic, hpamgaly,
splnmgaly, and abnrmal livr funcin s rsuls
(.g., lvad bilirubin, AST, ALT, GGT, and alkalin
phsphaas lvls; incrasd INR).
Drug interactions
Cdn. Cimidin inhibis h absrpin f u-
cnazl. Cncurrn us is n rcmmndd.
Dcs. Diurics inhibi h xcrin f ucnazl.
Mnir pains fr an incras in frquncy f advrs
ffcs. Th dsag f ucnazl may nd  b d-
crasd if cncurrn hrapy wih diurics is rquird.
toc ndcd b conao. Flucnazl can incras
srum cncnrains f alfnanil, bnzdiazpins,
buspirn, cyclsprin, lsaran, phnyin, vincris-
in, zidvudin, zlpidm, ricyclic anidprssans,
HMG-CA rducas inhibirs (.g., simvasain, ar-
vasain), pras inhibirs (.g., rinavir, indinavir),
and ral sulfnylura hypglycmic agns (.g., glip-
izid, glyburid). Flucnazl can als pnia h
anicagulan ffcs f warfarin. Rad individual drug
mngraphs fr mniring paramrs f xiciy frm
hs agns.
vn z (grĭz-ē-ō-FŬL-vĭn)
vn z
an
Grisfulvin is a fungisaic agn ha acs by spping
cll divisin and nw cll grwh.
u
Grisfulvin is usd  ra ringwrm f h scalp,
bdy, nails, and f. Afr grisfulvin is absrbd, i
is incrprad in h krain f h nails, skin, and
hair in hrapuic amuns. Th infcing fungus is
n killd, bu is grwh in nw clls is prvnd.
Onc h clls ar shd r rmvd, hy ar rplacd
by nw clls ha ar fr frm h infcin. Bcaus f
slw nail grwh, ramn is fn rquird fr sv-
ral mnhs.
t o
Th primary hrapuic ucm xpcd frm gris-
fulvin hrapy is liminain f fungal infcin.
Nn in  gvn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.

2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms r ab-
nrmal hmalgic, livr, r rnal funcin ss b-
fr iniiaing hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur and
snsiiviy, livr and rnal funcin ss).
6. Rcrd rsuls f baslin mnal saus
xaminain.
Availability. PO: Microsize: 500-mg abls; 125-mg/5-
mL ral suspnsin in 120-mL bl. Ultramicrosize:
125- and 250-mg abls.
Dosage and administration. Adult: PO: Microsize:
dpnding n h spcic rganism and h lcain
f h infcin, 500 mg  1 g in singl r dividd
dss daily. Absrpin frm h GI rac may b in-
crasd by adminisring grisfulvin wih a high-
fa mal.
Adult: PO: Ultramicrosize: dpnding n h spcic
rganism and h lcain f h infcin, 375  750
mg daily in dividd dss. Absrpin frm h GI
rac may b incrasd by adminisring grisfulvin
wih a high-fa mal.
Common adverse effects
gasonsna
Nausea, vomiting, anorexia, abdominal cramps. Ths ad-
vrs ffcs ar usually mild and nd  rslv wih
cninud hrapy. Encurag h pain n  dis-
cninu hrapy wihu rs cnsuling h halh-
car prvidr.
Serious adverse effects
inna, hpsns
Urticaria, rash, pruritus. Hyprsnsiiviy racins,
manifsd by iching, uricaria, and rash, ar rlaiv-
ly cmmn. Rpr sympms fr furhr valuain
by h halhcar prvidr. Prurius may b rlivd by
adding baking sda  h bah war.
Photosensitivity. Th pain shuld b cauind
 avid xpsur  sunligh and ulravil ligh.
Suggs waring lng-slvd clhing, ha, and sun-
glasss whn udrs. Discurag h us f anning
lamps. Cnsul h halhcar prvidr abu h ad-
visabiliy f cninuing hrapy.
Nooc
Confusion. Prfrm a baslin assssmn f h pa-
in’s dgr f alrnss and rinain  nam, plac,
and im bfr iniiaing hrapy. Mak rgularly schd-
uld subsqun mnal saus valuains, and cmpar
ndings. Rpr h dvlpmn f alrains.
Dizziness. Prvid fr pain safy during pisds
f dizzinss; rpr  h halhcar prvidr fr fur-
hr valuain.
Drugs Used to Treat Infections CHAPTER 45 761
in ss (opponsc ncons)
Secondary infections. Wih grisfulvin, ral hrush,
gnial and anal prurius, vaginiis, and vaginal dis-
charg may ccur. Rpr prmply  h halhcar
prvidr bcaus hs infcins ar rsisan  h
riginal animicrbial agn. Tach h impranc f
miculus ral and prinal prsnal hygin.
Haooc. Ruin labrary sudis (.g., RBC,
whi bld cll, and diffrnial cuns) ar schduld
fr pains aking grisfulvin fr 30 days r lngr.
Srss h impranc f rurning fr his labrary
wrk. Mnir fr sr hra, fvr, purpura, jaundic,
r xcssiv and prgrssiv waknss.
rna
Nephrotoxicity. Mnir urinalysis and kidny func-
in ss fr abnrmal rsuls. Rpr incrasing BUN
and crainin lvls, dcrasing urin upu r d-
crasing urin spcic graviy (dspi amun f uid
inak), cass r prin in h urin, frank bld r
smky-clrd urin, r RBCs in xcss f 0  3 RBCs/
HPF (s Tabl 41.1) n h urinalysis rpr.
gasonsna
Hepatotoxicity. Th sympms f hpaxiciy ar
anrxia, nausa, vmiing, jaundic, hpamgaly,
splnmgaly, and abnrmal livr funcin s rsuls
(.g., lvad bilirubin, AST, ALT, GGT, and alkalin
phsphaas lvls; incrasd INR).
Drug interactions
Waan. Grisfulvin may diminish h anicagulan
ffcs f warfarin. Mnir h INR and incras h
dsag f warfarin if ncssary.
Phnobaba. Th absrpin f grisfulvin is
impaird whn cmbind wih phnbarbial. If cn-
currn hrapy cann b avidd, adminisr h gri-
sfulvin in dividd dss hr ims daily.
Oa conacps. Grisfulvin may caus amn-
rrha, incrasd brakhrugh blding, and ps-
sibly dcrasd cnracpiv fcacy whn usd
cncmianly wih ral cnracpivs. Ohr mh-
ds f cnracpin (.g., cndms and fam) shuld
b cnsidrd during grisfulvin hrapy.
nz (ĭt-ră-KŎN-ă-zōl)
snx (SPŌR-ă-nŏks)
an
Iracnazl is an anifungal agn chmically rlad 
ucnazl and kcnazl. I acs by inrfring wih
cll wall synhsis, causing lakag f cllular cnns.
u
Iracnazl is usd rally  ra candidiasis, chrnic
muccuanus candidiasis, ral hrush, nychmy-
csis, candiduria, cccidiidmycsis, hisplasmsis,
chrmmycsis, blasmycsis, and paracccidiid-
mycsis. I is als ffciv agains Aspergillus spp.
762 UNIT IX Drugs Affecting Other Body Systems
Medication Safety Alert
Do not administer itraconazole to patients with a history of
heart failure. Itraconazole is a negative inotropic agent and
may seriously aggravate heart failure.
Itraconazole has many drug interactions because it is a
potent inhibitor of CYP3A4-metabolizing enzymes in the liver
(see Drug Interactions later in this section). Coadministration
of itraconazole with pimozide, dofetilide, or quinidine is
contraindicated. Fatal reactions may result.
t o
Th primary hrapuic ucm xpcd frm ira-
cnazl hrapy is liminain f fungal infcin.
Nn in  inz
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms, abnr-
mal livr funcin ss, r har failur bfr b-
ginning hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., livr funcin ss).
Availability. PO: 65, 100-mg capsuls; 200-mg abls;
10 mg/mL ral sluin in 150-mL cnainrs.
Dosage and administration. Adult: PO: 100  400 mg
daily. Dsags f mr han 200 mg shuld b givn in
w dividd dss. Insruc h pain  ak wih a
full mal  nsur maximum absrpin.
Medication Safety Alert
Do not use itraconazole capsules and itraconazole oral so-
lution interchangeably. Capsules are used to treat systemic
fungal infections. The oral solution should only be used to
treat oral or esophageal candidiasis in adult HIV-positive or
other immunocompromised patients.
Common adverse effects
gasonsna
Nausea, vomiting. Ths advrs ffcs ar usu-
ally mild and nd  rslv wih cninud hrapy.
Encurag h pain n  discninu hrapy wih-
u rs cnsuling h halhcar prvidr. Adminisr
wih a full mal fr maximum absrpin.
Serious adverse effects
gasonsna
Hepatotoxicity. Livr funcin ss ar rcmmndd
bfr iniiaing hrapy, wih fllw-up ss biwk-
ly  mnhly. Th sympms f hpaxiciy ar
anrxia, nausa, vmiing, jaundic, hpamgaly,
splnmgaly, and abnrmal livr funcin ss (.g.,
lvad bilirubin, AST, ALT, GGT, and alkalin phs-
phaas lvls; incrasd INR).
Cadoasca
Heart failure. Mnir h six cardinal signs f har
disas—dyspna, chs pain, faigu, dma, sync-
p, and palpiains—and individualiz car  dal
wih h dgr f impairmn (s als Chapr 27).
inna
Pruritus, rash. Rpr sympms  h halhcar
prvidr fr furhr valuain. Prurius may b r-
livd by adding baking sda  h bah war.
Drug interactions
Hsan-2 anaonss, anacds, poas nhb-
os. H2 anagniss (.g., cimidin, famidin, ra-
niidin, nizaidin), anacids, indinavir, and rinavir
inhibi h absrpin f iracnazl. Cncurrn us
is n rcmmndd.
Cabaapn, phnon, apn. Cncurrn ad-
minisrain f iracnazl and hs agns has r-
suld in a signican dcras in iracnazl aciviy
and clinical failur. Th mchanism is unknwn, bu
i is suspcd ha hs agns simula h mab-
lism f iracnazl. If hs agns ar  b usd
cncurrnly, iracnazl lvls mus b mnird 
nsur hrapuic ffc.
toc ndcd b aconao. Iracnazl can in-
cras srum cncnrains f alfnanil, bnzdi-
azpins (.g., riazlam, midazlam, alprazlam),
buspirn, calcium channl blckrs (.g., fldipin,
nisldipin, nifdipin, vrapamil), carbamazpin,
cyclsprin, digxin, dfilid, halpridl, HMG-
CA rducas inhibirs (.g., arvasain, lvas-
ain), isniazid, pimzid, acrlimus, lrdin,
vincrisin, zlpidm, and ral sulfnylura hyp-
glycmic agns (.g., glipizid, glyburid) and hr
drugs mablizd by h CYP3A4-mablizing
nzyms. Iracnazl can als pnia h ani-
cagulan ffcs f warfarin. Rad individual drug
mngraphs fr mniring paramrs f xiciy
frm hs agns.
nn (tŭr-BĪN-ă-fēn)
an
Trbinan is an allylamin drivaiv ha acs by in-
hibiing squaln pxidas, a ky nzym rquird
in srl bisynhsis in fungi. This acin causs ac-
cumulain f squaln and a dcincy f rgsrl,
rsuling in fungal cll dah.
u
Trbinan is usd in h ramn f nychmycsis
f h nail r ngrnail causd by drmaphys.
Maximum clinical ffc is bsrvd mnhs afr
h fungus has bn radicad whn a nw nail has

grwn. Th granuls ar usd  ra ina capiis in
childrn 4 yars and ldr.
t o
Th primary hrapuic ucm xpcd frm r-
binan hrapy is liminain f fungal infcin in
nails and ngrnails.
Nn in  tnn
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., CBC wih diffrnial, culur,
livr funcin ss, and lcrly lvls).
Availability. PO: 250-mg abls.
Dosage and administration. Adult: PO: 250 mg daily
fr 6 wks  ra fungal infcins f h ngrnail
and 12 wks fr ramn f infcins f h nail.
Pediatric: PO: Dosage by weight: lss han 25 kg, 125
mg/day; 25  35 kg, 187.5 mg/day; mr han 35 kg,
250 mg/day.
Serious adverse effects
inna, n ss
Pruritus, rash, fever, chills. Rpr sympms  h
halhcar prvidr fr furhr valuain. Prurius may
b rlivd by adding baking sda  h bah war.
rna
Nephrotoxicity. Assss fr incrasing BUN and crai-
nin lvls, dcrasing urin upu, dcrasing urin
spcic graviy, cass r prin in h urin, frank
bld r smky-clrd urin, r RBCs in xcss f 0 
3 RBCs/HPF (s Tabl 41.1) n h urinalysis rpr.
gasonsna
Hepatotoxicity. Rviw labrary sudis (.g., bili-
rubin, AST, ALT, GGT, alkalin phsphaas lvls;
incrasd INR) and rpr abnrmal ndings  h
halhcar prvidr.
Haooc
Neutropenia, lymphopenia. Nurpnia (nurphil
cun <1000 clls/mm3) and lymphpnia hav bn
bsrvd in pains rciving rbinan. Mnir h
CBC wih diffrnial in pains rciving ramn
fr lngr han 6 wks.
Drug interactions
Sc soonn pak nhbos and ccc an-
dpssans. Trbinan can incras srum cncn-
rains f slciv srnin rupak inhibirs and
ricyclic anidprssans. Mnir pains fr signs f
Drugs Used to Treat Infections CHAPTER 45 763
xiciy such as cnral nrvus sysm simulain,
sizur aciviy, and arrhyhmias.
Ccospon. Trbinan can dcras srum cn-
cnrains f cyclsprin. Mnir pains fr signs
f ransplan rjcin. Chck rugh cyclsprin
lvls.
Can. Trbinan can incras srum cncnra-
ins f caffin. Mnir pains fr xciabiliy, agi-
ain, irriabiliy, and achycardia.
Dohophan. Trbinan can incras srum
cncnrains f dxrmhrphan. Mnir pains
fr dizzinss, drwsinss, GI disurbancs, alrd sn-
sry prcpin, aaxia, slurrd spch, and dysphria.
rapn. Rifampin rducs srum lvls f rbin-
an. Us f anhr anifungal agn whs mab-
lism is n inducd by rifampin may b ncssary.
Cdn. Cimidin may inhibi h mablism
f rbinan, incrasing h pnial fr xiciy frm
rbinan. Swiching  anhr H2 anagnis, such
as famidin, ha is n likly  inhibi mablism
may rslv h inracin. Cninu  mnir fr
rbinan xiciy.
Drug ClASS: ANtivirAl AgeNtS
v (ă-SĬK-lō-vĭr)
Zvx (ZŌ-vĭr-ăks)
Do not confuse Zovirax with Zyvox.
an
Acyclvir is an aniviral agn ha acs by inhibiing
viral cll rplicain.
u
Acyclvir is usd pically  ra iniial infcins
f hrps gnialis and nn–lif-hraning cass f
muccuanus hrps simplx virus infcins in pa-
ins wih supprssd immun sysms. Th ral frm
is usd  ra iniial pisds and fr managmn f
rcurrn pisds f gnial hrps in crain pains.
Th IV frm is usd  ra iniial and rcurrn mu-
csal and cuanus hrps simplx virus yps 1 and
2 infcins in immunsupprssd aduls and childrn
and  ra svr iniial clinical pisds f hrps
gnialis in pains wh ar n immunsupprssd.
t o
Th primary hrapuic ucm xpcd frm acy-
clvir hrapy is liminain f sympms f viral
infcin.
Nn in  av
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
764 UNIT IX Drugs Affecting Other Body Systems
3. Assss fr and rcrd any abnrmal rnal funcin
bfr bginning hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., rnal funcin ss).
6. Prfrm baslin mnal saus xaminain (.g.,
rinain).
Availability. Topical: 5% inmn and cram. PO: 200-
mg capsuls; 400- and 800-mg abls; 200-mg/5-mL
suspnsin. IV: 50 mg/mL in 10- and 20-mL vials.
Dosage and administration. Adult: Topical: Apply 
ach lsin vry 3 hurs, six ims daily fr 7 days. A
ngr c r rubbr glvs shuld b usd  avid h
sprad f virus  hr issus and ppl. Us m-
iculus hand hygin chniqu bfr and afr ap-
plying h inmn. Do not apply  h ys. I is n
an phhalmic inmn.
IV: Dsag fr pains wih nrmal rnal funcin: 5
 10 mg/kg vry 8 hurs fr 5  7 days. Acyclvir is
rcnsiud wih 10 mL f prsrvaiv-fr sril wa-
r fr injcin  prvid a sluin cncnrain f 50
mg/mL. Th sluin is sabl fr 12 hurs. This slu-
in shuld b furhr dilud by a glucs and lcr-
ly IV uid  a cncnrain f 1  7 mg/mL bfr
adminisrain (sabl fr 24 hurs). Infus vr a las
1 hur  wll-hydrad pains  prvn rnal dam-
ag. Obsrv fr phlbiis a h infusin si. Blus r
rapid IV infusins may rsul in rnal ubular damag.
PO: Initial treatment of genital herpes: 200 mg vry 4
hurs whil h pain is awak, fr a al f 1000 mg
daily fr 10 days. Chronic suppressive therapy for recurrent
disease: 400 mg wic daily fr up  12 mnhs. Sm pa-
ins rquir 200 mg v ims daily. Intermittent therapy:
200 mg vry 4 hurs whil h pain is awak, fr a -
al f 1000 mg fr 5 days. Thrapy shuld b iniiad a
h arlis sign r sympm (prdrm) f rcurrnc.
Pediatric: Topical: Sam as fr adul pains. IV:
Pains ldr han 12 yars: sam as fr adul pains.
Serious adverse effects
inna
Pruritus, rash, burning. Rpr sympms  h halh-
car prvidr fr furhr valuain. Prurius may b
rlivd by adding baking sda  h bah war.
Rash, hives. Assss, dscrib, and char h lcain
and xn f hs prsning sympms. Rpr 
h halhcar prvidr fr furhr valuain.
Diaphoresis. Diaphrsis can b srius if h pain
is n wll hydrad. Assss hydrain sa, mnir
lcrlys, and prvid nursing inrvnins (.g.,
clan, dry linns; adqua uid inak).
vasca
Intravenous therapy. Avid IV infusin in h lwr
xrmiis and aras wih varicsiis. Us prpr
chniqu whn saring h IV sluin. Carfully
assss a rgularly schduld inrvals fr signs f
dvlping phlbiis. Inspc fr rdnss, warmh, n-
drnss  uch, dma, r pain.
rna
Nephrotoxicity. Mnir urinalysis and kidny func-
in ss fr abnrmal rsuls. Rpr incrasing BUN
and crainin lvls, dcrasing urin upu r d-
crasing urin spcic graviy (dspi amun f uid
inak), cass r prin in h urin, frank bld r
smky-clrd urin, r RBCs in xcss f 0  3 RBCs/
HPF (s Tabl 41.1) n h urinalysis rpr.
Cadoasca
Hypotension. Rcrd h bld prssur in bh su-
pin and siing psiins bfr and during adminis-
rain f his drug. Cauin h pain  ris slwly
frm a supin r siing psiin.
Nooc
Confusion. Prfrm a baslin assssmn f h pa-
in’s dgr f alrnss and rinain  nam,
plac, and im before iniiaing hrapy. Mak rgu-
larly schduld subsqun mnal saus valuains
and cmpar ndings. Rpr dvlpmn f alra-
ins in cnsciusnss.
Drug interactions
Pobncd. Prbncid may rduc urinary xcr-
in f acyclvir. Mnir clsly fr signs f xiciy
frm acyclvir.
thophn. Acyclvir may incras hphyllin
lvls. Mnir hphyllin srum lvls.
Phnon, osphnon, apoc acd. Acyclvir may
dcras phnyin, fsphnyin, and valpric acid
lvls. Mnir srum lvls and bsrv fr incrasd
frquncy f sizur aciviy.
zdodn. Pains may cmplain f svr drwsi-
nss and lhargy whn acyclvir and zidvudin ar
usd cncurrnly. Obsrv fr pain safy.
xv (bah-LOX-A-veer)
Xz (zof-LU-zah)
an
Balxavir is an aniviral agn ha acs by inhibiing h
ndnuclas aciviy f a slciv plymras acidic
prin ha is rquird fr viral gn ranscripin, r-
suling in inhibiin f inunza virus rplicain.
u
Balxavir is usd rally in raing uncmplicad
acu illnss causd by inunza A and B. Sudis
shw ha h durain f sympms f inunza in-
fcin (.g., nasal cngsin, sr hra, cugh, my-
algia, faigu, hadach, chills, swas) will b rducd
by abu 1 day if h pain has bn sympmaic
fr n mr han 2 days whn ramn is sard.
Balxavir can b usd fr prvning inunza infc-
in. I shuld n b usd as a subsiu fr annual
inunza vaccinain.

t o
Th primary hrapuic ucm xpcd frm bal-
xavir hrapy is rducd sympms causd by inu-
nza virus infcin.
Nn in  bxv
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls.
Availability. PO: 20-, 40-, 80 mg abls
Dosage and administration. Adult: PO: Dosage by
weight: 80 kg r mr: 80 mg as a singl ds; 40  lss
han 80 kg: 40 mg as a singl ds. Tramn shuld
bgin wihin 2 days afr h ns f sympms f in-
unza. Pains may als ak dcngsans, analg-
sics, and anipyric agns  rduc sympms.
Common adverse effects
gasonsna
Diarrhea. Pains rciving balxavir may dvlp
diarrha. If diarrha cninus r wrsns, rpr 
h halhcar prvidr fr valuain f hr pn-
ial cmplicains.
in ss
Cough, sore throat, fever, continuing symptoms. If h
pain sars cughing up yllw r grn spuum,
if a sr hra wrsns and bcms svr, if fvr
rurns afr ging away, r if sympms las lngr
han 1 r 2 wks, rpr  h halhcar prvidr fr
valuain f hr pnial cmplicains.
Drug interactions
Ds ha a dcas h hapc oco.
Cadminisrain wih anacids, calcium, irn, magn-
sium, and zinc may dcras plasma cncnrains f
balxavir, which may rduc h hrapuic ucm.
Balxavir may diminish h hrapuic h ffc
f liv anuad inunza virus vaccin Avid ani-
inunza anivirals during h prid bginning 48
hurs bfr and nding 2 wks afr liv inunza
virus vaccin adminisrain.
v (făm-SĬK-lō-vĭr)
an
Famciclvir is a prdrug f pnciclvir, an aniviral
agn ha acs by inhibiing viral cll rplicain.
Drugs Used to Treat Infections CHAPTER 45 765
u
Famciclvir is usd rally  ra rcurrn infcins
f gnial hrps and fr h managmn f acu
hrps zsr (shingls). In pains wih gnial hr-
ps, famciclvir rducs h im f viral shdding,
h durain f sympms, and h im f haling
if sard wihin 6 hurs f h ns f sympms
and cninud fr 5 days. In pains wih shingls,
if hrapy is bgun wihin 72 hurs and cninud fr
7 days, famciclvir rducs h ims  full crusing,
lss f vsicls, lss f ulcrs, and lss f cruss mr
ffcivly han placb ramn. Early ramn
wih famciclvir can als rduc h durain f ps-
hrpic nuralgia.
t o
Th primary hrapuic ucm xpcd frm fam-
ciclvir hrapy is liminain f sympms f viral
infcin.
Nn in  fv
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any abnrmal rnal funcin
bfr iniiaing hrapy.
4. Assss fr any allrgis.
5. Prfrm baslin mnal saus xaminain (.g.,
rinain).
6. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., rnal funcin ss).
Availability. PO: 125-, 250-, and 500-mg abls.
Dosage and administration. Adult: PO: Treatment
of genital herpes: Rcurrn pisds: 1000 mg wic
daily fr 1 day. Thrapy shuld b sard wihin 6
hurs f h firs sign r sympm f hrps brak-
u. Treatment of herpes zoster (shingles): 500 mg
vry 8 hurs fr 7 days. T b ffciv, hrapy
mus b sard wihin 72 hurs f h ns f
sympms.
Common adverse effects
gasonsna
Nausea, vomiting. Ths advrs ffcs ar usu-
ally mild and nd  rslv wih cninud hrapy.
Encurag h pain n  discninu hrapy wih-
u rs cnsuling h halhcar prvidr. Adminisr
wih fd r milk  rduc irriain.
Nooc
Headache. This advrs ffc is usually mild and
nds  rslv wih cninud hrapy. Encurag
h pain n  discninu hrapy wihu rs
cnsuling h halhcar prvidr.
766 UNIT IX Drugs Affecting Other Body Systems
Serious adverse effects
Nooc
Confusion. Prfrm a baslin assssmn f h pa-
in’s dgr f alrnss and rinain  nam,
plac, and im bfr iniiaing hrapy. Mak rgu-
larly schduld subsqun mnal saus valuains
and cmpar ndings. Rpr h dvlpmn f al-
rains in cnsciusnss.
Drug interactions
Pobncd. Prbncid may rduc urinary xcr-
in f famciclvir. Mnir clsly fr signs f xiciy
frm famciclvir.
v (ō-sĕl-TĂM-ĭ-vĭr)
t (TĂM-ĭ-ū)
Do not confuse Tamiu with tamoxifen or Therau.
an
Oslamivir is an aniviral agn ha acs by inhibiing
nuraminidas, an nzym n h viral cll ca ncs-
sary fr rprducin and sprad f viral cll paricls.
u
Oslamivir was h rs nuraminidas inhibir ap-
prvd fr ral us in raing uncmplicad acu ill-
nss causd by inunza A and B. Sudis shw ha
h durain f sympms f inunza infcin (.g.,
nasal cngsin, sr hra, cugh, myalgia, faigu,
hadach, chills, swas) will b rducd by abu
1 day (4 days vrsus 5 days) if h pain has bn
sympmaic fr n mr han 2 days whn ramn
is sard. Th svriy f sympms and pnial fr
cmplicains frm scndary infcin ar als sig-
nicanly rducd. Oslamivir can b usd fr pr-
vning inunza infcin. I shuld n b usd as a
subsiu fr annual inunza vaccinain.
t o
Th primary hrapuic ucm xpcd frm s-
lamivir hrapy is rducd sympms causd by
inunza virus infcin. I may als rduc h inci-
dnc f pprunisic scndary infcins such as
pnumnia.
Nn in  ov
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any gasric sympms bfr
iniiaing hrapy.
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls.
Availability. PO: 30-, 45-, and 75-mg capsuls; 6 mg/
mL ral suspnsin in 60-mL cnainr.
Dosage and administration. Adult: PO: 75 mg wic
daily fr 5 days. Tramn shuld bgin wihin 2 days
afr h ns f sympms f inunza. Pains may
als ak dcngsans, analgsics, and anipyric
agns  rduc sympms.
Common adverse effects
gasonsna
Nausea, vomiting. Pains rciving slami-
vir may dvlp nausa and vmiing wihin h
rs 2 days f ramn. Adminisring wih fd
r milk will minimiz h incidnc f nausa and
vmiing. If hs sympms cninu, rpr  h
halhcar prvidr fr valuain f hr pnial
cmplicains.
in ss
Cough, sore throat, fever, continuing symptoms. If h
pain sars cughing up yllw r grn spuum,
if a sr hra wrsns and bcms svr, if fvr
rurns afr ging away, r if sympms las lngr
han 1 r 2 wks, rpr  h halhcar prvidr fr
valuain f hr pnial cmplicains.
Serious adverse effects
Nopschac ns. Oslamivir may caus rar
nurpsychiaric vns (including cnfusin, d-
lirium, hallucinains, and slf-injury) paricularly in
childrn. Mnir clsly fr signs r sympms f un-
usual bhavir, including amps a slf-injury, cn-
fusin, and dlirium. Hld h nx ds and cnac
h halhcar prvidr as sn as pssibl.
Drug interactions. Oslamivir may diminish h hr-
apuic ffc f liv anuad inunza virus vac-
cin. Avid aniinunza anivirals during h prid
bginning 48 hurs bfr and nding 2 wks afr
liv inunza virus vaccin adminisrain.
vv (văl-ă-SĬK-lō-vĭr)
Do not confuse valacyclovir with valganciclovir
Vx (VĂL-trĕks)
Do not confuse Valtrex with Valcyte.
an
Valacyclvir is a prdrug f acyclvir, an aniviral
agn ha acs by inhibiing viral cll rplicain.
u
Valacyclvir is usd rally in aduls  ra acu hr-
ps zsr (shingls) and hrps labialis (cld srs
and gnial hrps) in immuncmpn pains. I
is als apprvd  ra variclla virus (chicknpx) in
childrn ags 2 hrugh 18 yars.

t o
Th primary hrapuic ucm xpcd frm va-
lacyclvir hrapy is liminain f sympms f viral
infcin.
Nn in  Vv
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr and rcrd any abnrmal rnal funcin
bfr iniiaing hrapy.
4. Assss fr any allrgis.
5. Prfrm baslin mnal saus xaminain (.g.,
rinain).
6. Obain baslin labrary sudis rdrd and r-
viw rsuls.
Availability. PO: 500-mg and 1-g abls.
Dosage and administration. Adult: PO: Treatment of
herpes zoster (shingles): 1 g hr ims daily fr 7 days.
T b ffciv, hrapy mus b sard wihin 48
hurs f h ns f h zsr rash. Treatment of geni-
tal herpes—initial episode: 1 g wic daily fr 10 days.
Tramn is ms ffciv if sard wihin 48 hurs
f rs sympms. For recurrent episodes: 500 mg wic
daily fr 3 days, iniiaing ramn a h rs sign f
sympms f an pisd.
Pediatric: PO: Treatment of varicella virus (chicken-
pox): 20 mg/kg adminisrd hr ims daily fr 5
days. Sar a h arlis sign f sympms. D n x-
cd 1 g hr ims daily.
Serious adverse effects and drug interactions. S ar-
lir scin n acyclvir.
znv (zăn-ĂM-ĭ-vĭr)
rnz (rĕl-ĔN-ză)
an
Zanamivir is an aniviral agn ha acs by inhibiing
nuraminidas, an nzym n h viral cll ca ncs-
sary fr rplicain and sprad f viral cll paricls.
u
Zanamivir was h rs nuraminidas inhibir mar-
kd fr us fr h ramn f uncmplicad acu
illnss causd by inunza A and B. Sudis shw
ha h durain f sympms (nasal cngsin, sr
hra, cugh, myalgia, faigu, hadach, chills, and
swas) f inunza infcin will b rducd by abu
1 day (4 days vrsus 5 days) if h pain has bn
sympmaic fr n mr han 2 days whn ramn
is sard. Th svriy f sympms and pnial
fr cmplicains frm scndary infcin ar als
Drugs Used to Treat Infections CHAPTER 45 767
signicanly rducd. Zanamivir can b usd in pr-
vning inunza infcin. I shuld n b usd as a
subsiu fr annual inunza vaccinain. Zanamivir
is n rcmmndd fr us in pains wih undr-
lying rspirary disas, such as ashma r chrnic
bsruciv pulmnary disas, bcaus f a lack f
fcacy in inunza ramn and risk f srius
brnchspasm. If zanamivir is prscribd in such pa-
ins, clsly mnir rspirary funcin.
t o
Th primary hrapuic ucm xpcd frm zana-
mivir hrapy is rducd sympms causd by inun-
za virus infcin. I may als rduc h incidnc f
pprunisic scndary infcins such as pnumnia.
Nn in  Znv
Premedication assessment
1. Obain baslin assssmns f prsning
sympms.
2. Rcrd mpraur, puls, rspirains, bld prs-
sur, and hydrain saus.
3. Assss fr ashma r chrnic bsruciv pulmnary
disas
4. Assss fr any allrgis.
5. Obain baslin labrary sudis rdrd and r-
viw rsuls (.g., pulmnary funcin ss).
Availability. Inhaler: 5-mg blisrs f pwdr fr inha-
lain hrugh a Diskhalr.
Dosage and administration. Adult: Inhalation: Tw
inhalains (n 5-mg blisr pr inhalain fr a -
al f 10 mg) wic daily (apprximaly 12 hurs
apar) fr 5 days. Tramn shuld bgin wihin 2
days afr h ns f sympms f inunza. On
h rs day f ramn, w dss shuld b akn,
prvidd hr ar a las 2 hurs bwn dss.
On subsqun days, dss shuld b apprximaly
12 hurs apar a apprximaly h sam im ach
day.
Pains wh ar schduld  us an inhald brn-
chdilar shuld us h brnchdilar bfr aking
zanamivir. Pains may als ak dcngsans, an-
algsics, and anipyric agns  rduc sympms.
Serious adverse effects
rspao
Asthma, bronchospasm, diminishing pulmonary func-
tion. Prfrm baslin pulmnary funcin ss 
assss whhr h pain shws drirain afr
hrapy is sard. If saring inhalain ramn
appars  prduc suddn brnchspasm r d-
rirain f rspirary funcin, ramn shuld
b discninud immdialy and h halhcar
prvidr cnacd. Immdialy rpr cmplains
f chs srnss, shrnss f brah, r hr ad-
vrs ffcs.
768 UNIT IX Drugs Affecting Other Body Systems

in ss Drug interactions. Zanamivir may diminish h hra-

Cough, sore throat, fever, continuing symptoms. If h
pain sars cughing up yllw r grn spuum,
if a sr hra wrsns and bcms svr, if fvr
rurns afr ging away, r if sympms las lngr
han 1 r 2 wks, rpr  h halhcar prvidr fr
valuain f hr pnial cmplicains.
puic ffc f liv anuad inunza virus vac-
cin. Avid aniinunza anivirals during h prid
bginning 48 hurs bfr and nding 2 wks afr
liv inunza virus vaccin adminisrain. Consider
therapy modication.

cn Jdn nd Nx-gnn NcleX® exnn-s Qn

K Pons 1. The nurse is administering tobramycin, an aminoglycoside, to the

patient in the scenario with cellulitis and is alert for which adverse
• Antimicrobial agents are chemicals that eliminate living effects? (Select all that apply.)
microorganisms that are pathogenic to the patient.
1. Ototoxicity
• If at all possible, the infecting organisms should rst be
2. Nystagmus
isolated and identied. The antimicrobial therapy is then
3. Nephrotoxicity
started based on the sensitivity results and the clinical
4. Photosensitivity
judgment of the healthcare provider.
5. Dizziness
• Nurses must consider the entire patient when
administering and monitoring antimicrobial therapy. Obc: Describe the signs and symptoms of the common
adverse effects of antibiotic therapy.
• It is essential that the nurse be knowledgeable about the
NClex  p: Multiple response
drugs, including physiologic parameters for monitoring
Con sk: Application
expected therapeutic activity and potential adverse
effects. 2. The nurse reviewed the major actions of nine classications of
• Beginning nursing students need to focus on the antiinfectives.
commonality of the premedication assessments and
adverse effects that may occur with the various drugs Draw an arrow line from the Drug Class column to the best
prescribed for infectious disease. Because of the matching statement in the Major Actions column. Answers
numerous drug interactions listed in the drug monographs, are used only once.
it is essential to consult a drug reference before
administering a prescribed antimicrobial. Drug ClASS mAjOr ACtiONS
• It is important to teach the individual with an infection Aminoglycosides Inhibit bacterial biosynthesis of folic acid
basic principles of self-care that will enhance the recovery
process and measures to prevent the spread of the Carbapenems Inhibit the activity of DNA gyrase
infection. In the case of communicable diseases, exposed Cephalosporins Bacteriostatic or bactericidal,
individuals must be contacted for follow-up testing and depending on concentration; inhibit
appropriate treatment. protein synthesis
Glycopeptides Inhibit protein synthesis; may be used
Addona lann rsocs for patients allergic to penicillins
SG Go to your Study Guide for additional Review Questions Macrolides Interfere with the synthesis of bacterial
for the NCLEX® Examination, Critical Thinking Clinical Situa- cell walls
tions, and other learning activities to help you master this chap- Penicillins Related to penicillins, with similar
ter content. mechanism of action
Quinolones Prevents synthesis of bacterial cell
Go to your Evolve website (https://evolve.elsevier.com/Willihng
walls; used primarily for gram-positive
anz) for additional online resources.
skin infections
Clinical Judgment and Next-Generation NCLEX® Exam- Sulfonamides Bactericidal, inhibit protein synthesis;
ination-Style Questions The following questions are typical of used primarily against gram-negative
the NCLEX exam and include both NGN (Next Generation) and bacteria
traditional questions. See Chapter 1 for further information re- Tetracyclines Potent broad-spectrum; inhibit bacterial
garding question types. cell wall synthesis; used against bacteria
that secrete beta-lactamase enzymes
Scnao
An elderly patient was admitted with a cellulitis infection of the Obc: Explain the major actions and effects of classes of drugs
left lower leg. The patient has a history for diabetes, hyper- used to treat infectious diseases.
tension, chronic obstructive pulmonary disease (COPD), and NClex  p: Drag and drop
hypothyroidism. Con sk: Recognize cues
 Drugs Used to Treat Infections CHAPTER 45 769

3 A patient was complaining of nausea and vomiting after taking Obc: Describe the nursing assessments and interventions for
ampicillin. After reassuring the patient, the nurse responded with the common adverse effects associated with antimicrobial agents:
which appropriate statement? allergic reaction, nephrotoxicity, ototoxicity, and hepatotoxicity.
1. “I would not worry about feeling this way; these symptoms NClex  p: Matrix
will go away in a couple of hours.” Con sk: Evaluate cues
2. “Because the symptoms of nausea and vomiting are 5. The patient in the scenario was switched to ertapenem (Invanz)
common responses to antibiotics, it may be helpful to for treatment of the cellulitis. The nurse performs which of the
take ampicillin with food.” following assessments before administration? (Select all that
3. “This is a sign that you are allergic to the drug. I will notify apply.)
your primary healthcare provider.”
4. “The drug needs to be discontinued, and you will need to 1. Assess for any allergies.
be started on another drug.” 2. Record the patient’s temperature, pulse, respirations,
and blood pressure.
Obc: Describe the signs and symptoms of the common 3. Obtain baseline assessments of presenting symptoms.
adverse effects of antimicrobial therapy. 4. Assess for any respiratory symptoms before initiating
NClex  p: Multiple choice therapy.
Con sk: Explain 5. Assess for hearing deciency before administration.
4. The nurse reviewed the common adverse effects associated Obc: Describe the signs and symptoms of the common
with antimicrobial agents and understands the reasons for adverse effects of antimicrobial therapy.
the assessments needed. Indicate with an X which nursing NClex  p: Multiple response
assessment or interventions from the left column applies to the Con sk: Application
common adverse effect.
6. A nurse is caring for a patient receiving valacyclovir (Valtrex).
During the administration of the medication the patient asked
ASSeSSmeNt/ AllergiC HePAtO- OtOtOx- NePHrO- what the drug is for. Which statement by the nurse is appropriate?
iNterveNtiONS reACtiONS tOxiCity iCity tOxiCity (Select all that apply.)
Assess for hives, 1. “This drug is used to eliminate your bacterial infection
nasal congestion, symptoms.”
and discharge 2. “When you take this drug we have to make sure that you
Intentionally speak take it three times a day for 7 days.”
softly and note if 3. “This medication has been ordered for your herpes
patient is aware zoster infection, or in other words, your shingles.”
that you said 4. “We need to watch for the development of any rash or
anything hives.”
Monitor bilirubin, 5. “If you develop symptoms of vomiting and jaundice you
AST, ALT, and INR need to let us know.”
Assess for Obc: Discuss the primary uses of antitubercular, antifungal
wheezing, stridor, and antiviral agents.
and sternal NClex  p: Multiple choice
retractions Con sk: Interpret
Assess urine output 7. The nurse was instructing a patient who was diagnosed with
and urinalysis for tuberculosis on the medications that will be used to treat the
changes disease. The nurse knows further education is needed when the
Assess for patient makes which statement?
dizziness and 1. “The drugs that I need to take for tuberculosis are the
tinnitus isoniazid (INH) and the rifampin (Rifadin).”
Monitor increases 2. “One of the common effects that I should be aware of is
in blood urea the potential for nausea and vomiting.”
nitrogen and 3. “My urine and tears may turn bright yellow with these
creatinine drugs.”
Assess for anorexia, 4. “I understand I need to take these drugs consistently or
with nausea and the organism develops a resistance to the drugs.”
vomiting and
jaundice
770 UNIT IX Drugs Affecting Other Body Systems

Obc: Discuss the primary uses of antitubercular, antifungal, 3. “So you are saying that coffee will interact with the drug?”
and antiviral agents. 4. “Now that I am taking this medication my thumbnail will
NClex  p: Multiple choice be back to normal after I am nished with the doses.”
Con sk: Comprehension Obc: Discuss the primary uses of antitubercular, antifungal, and
antiviral agents.
8. The nurse was educating the patient on the use of terbinane NClex  p: Multiple choice
prescribed for treatment of onychomycosis of the thumbnail. The Con sk: Analysis
nurse knows that further education is needed when the patient
makes which statement?
1. “I understand that I need to take this for at least 6 weeks.”
2. “I am concerned that this drug will cause liver problems
so I will ask my healthcare provider to check my labs.”
Unit X Drugs Affecting the General Health of the Body

Nutrition 46
https://evolve.elsevier.com/Willihnganz

Objectives
1. Identify sources of dietary ber and dietary fats.
2. Differentiate between fat-soluble and water-soluble
vitamins and discuss their functions.
3. Discuss the functions of minerals in the body.
4. Describe physical changes associated with a malnourished
state.
5. Describe the advantages and disadvantages of providing
nutrition by parenteral nutrition and enteral nutrition.

Key Terms
macronutrients (măk-rō-NŪ-trē-ĕnts)
(p. 771)
Dietary Reference Intakes (DRIs)
(DĪ-ĕ-tār-ē RĔF-rĕns ĬN-tāks) (p. 775)
Estimated Average Requirement
(EAR) (ĔS-tĭ-mā-tĕd ĂV-ĕ-rĕj rē-KWĪ-
ŭr-mĕnt) (p. 776)
Recommended Dietary Allowances
(RDAs) (rĕk-ō-MĔN-dĕd DĪ-ĕ-tār-ē
ă-LŎ-ĕn-sĕz) (p. 776)
Adequate Intake (AI) (ĂD-ĕ-kwĕt ĬN-
tāk) (p. 776)
Tolerable Upper Intake Level
(UL) (TŎL-ŭr-ă-bŭl ŬP-ŭr ĬN-tāk LĔ-
vŭl) (p. 776)
kilocalories (kĭl-ō-KĂL-ŏ-rēz) (p. 776)
Estimated Energy Requirement
(EER) (ĔS-tĭm-ă-tĕd ĔN-ŭr-jē rē-KWĪ-
ŭr-mĕnt) (p. 777)
carbohydrates (kăr-bō-HĪ-drāts) (p. 778)
monosaccharides (mŏn-ō-SĂK-ă-
rīdz) (p. 777)
disaccharides (dī-SĂK-ă-rīdz) (p. 778)
polysaccharides (pŏ-lē-SĂK-ă-rīdz)
(p. 777)
fiber (FĪ-bĕr) (p. 777)
lipids (LĬ-pĭdz) (p. 777)
essential fatty acids (ĂS-ĭdz) (p. 778)
gluconeogenesis (glū-kō-nē-ō-JĔN-ĕ-
sĭs) (p. 778)
vitamins (VĪ-tă-mĭnz) (p. 778)
minerals (MĬN-ĭ-rŭlz) (p. 778)
physical exercise (FĬZ-ĭ-kŭl ĔKS-ŭr-
sīz) (p. 780)
marasmus (mă-RĂZ-mŭs) (p. 781)
kwashiorkor (kwăsh-ē-ŌR-kōr) (p. 781)
mixed kwashiorkor-marasmus
(p. 781)
enteral nutrition (ĔN-tĕr-ăl nū-TRĬ-
shŭn) (p. 781)
tube feedings (p. 781)
parenteral nutrition (pă-RĔN-tĕr-ŭl
nū-TRĬ-shŭn) (p. 781)
total parenteral nutrition (TPN)
(TŌ-tăl) (p. 781)
peripheral parenteral nutrition
(PPN) (pĕ-RĬF-ĕr-ăl) (p. 781)
central parenteral nutrition
(CPN) (SĔN-trŭl) (p. 781)

Clinical Goldmine chemicals must be supplied from external sources. For

“For the two out of three adult Americans who do not smoke
and do not drink excessively, one personal choice seems to
inuence long-term health prospects more than any other:
what we eat” (The Surgeon General’s Report on Nutrition
and Health, 1988; retrieved from https://proles.nlm.nih.go
v/NN/B/C/Q/G).
PRINCIPLES OF NUTRITION
It is no coincidence that eating is one of life’s greatest
pleasures. The body needs a regular source of energy to
sustain its various functions, including respiration, nerve
transmission, circulation, physical work, and mainte-
nance of core temperature. There are many environmen-
tal, cultural, and behavioral reasons for what and how
people eat, but the most basic is to sustain life. Because
the body cannot make most of the needed nutrients, these
the most part, they are supplied from the food people eat.
Other chemicals are supplied by air, such as oxygen; by
water; and by sunlight, which helps the body manufac-
ture vitamin D. The energy derived from external sources
is converted to chemical energy by the body, which sus-
tains the body’s functions. The heat produced during
these chemical reactions maintains body temperature.
Energy sources required for balanced metabolism are
the macronutrients—fats, carbohydrates, and proteins—
which are measured in calories (see Macronutrients sec-
tion later in this chapter). Other essential nutrients in-
clude vitamins, minerals, and water. Imbalances between
energy intake (food) and energy expenditure result in
gain or loss of body composition, primarily in the form of
fat, which determines changes in weight.
Nutritional requirements vary based on level of
activity, age of the individual (e.g., infant, preschool
child, adolescent, adult, and older adult), and gender.
771
772 UNIT X Drugs Affecting the General Health of the Body
For example, there are differences in nutritional re-
quirements for a pregnant teenager, an adult woman,
and a lactating mother. The presence of disease, wound
healing, and the degree of catabolism also can inu-
ence nutritional needs. Therefore the reader should
consult a reliable nutrition textbook for current de-
tailed information.
Nutritional needs are met primarily from foods.
Foods in nutrient-dense forms contain essential vi-
tamins and minerals and also dietary ber. In some
cases, fortied foods and dietary supplements may be
useful in providing one or more nutrients if necessary.
No one food source can meet all of the body’s basic nu-
tritional requirements. Foods from a variety of groups
are required to provide an optimal nutrient balance
and to minimize naturally occurring toxic substances
from a single food source.
METHODS FOR ASSESSING NUTRITION
Governmental Guidelines
Two federal agencies, the US Department of Agriculture
(USDA) and the US Food and Drug Administration,
collaborate to publish Dietary Guidelines for Americans
every 5 years. The latest edition is the 2020-2025 Dietary
Guidelines for Americans (9th edition). These guidelines
are based on research of nutrients in foods and recom-
mend how to make the best food choices to promote
good health (Box 46.1). These guidelines encourage
the consumption of a healthy overall dietary pattern
at every stage of life, from birth through adulthood, as
described in the Healthy US-Style Dietary Pattern and
the USDA’s primary Dietary Pattern. It is based on the
types and proportions of foods Americans of all ages,
genders, races, and ethnicities typically consume, but
in nutrient-dense forms and appropriate amounts. The
USDA’s website (https://www.choosemyplate.gov)
contains a wealth of information on how people can
become more informed and more calorie conscious
and plan nutrient-rich meals with suggested propor-
tions (Fig. 46.1).
The key recommendations in the 2020-2025 Dietary
Guidelines are to develop a healthy dietary pattern
across each life stage. A healthy dietary pattern can
benet all individuals regardless of age, race, or ethnic-
ity, or current health status. Healthy dietary patterns
can help reduce the risk of chronic disease throughout
periods of growth, development, and aging, as well as
during pregnancy. A dietary pattern represents the to-
tality of all foods and beverages consumed. All foods
consumed as part of a healthy dietary pattern t to-
gether like a puzzle to meet nutritional needs with-
out exceeding limits, such as those for saturated fats,
added sugars, sodium, and total calories. All forms of
foods, including fresh, canned, dried, and frozen, can
be included in healthy eating patterns.
With obesity, metabolic syndrome, and type 2 dia-
betes mellitus reaching epidemic proportions over the
past decade in the United States and recent research
Recommendations of Dietary Guidelines for
Box 46.1
Americans, 2020–2025
FOUR DIETARY GUIDELINES
1. Follow a healthy dietary pattern at every life stage
(infancy, childhood, adolescence, adulthood,
pregnancy, lactation, and older adulthood).
 • All food and beverage choices matter.
 • Choose a healthy dietary pattern at an appropriate
calorie level to help meet nutrient needs, achieve
and maintain a healthy body weight, and reduce the
risk of chronic disease.
2. Customize and enjoy nutrient-dense food and
beverage choices to reect personal preferences,
cultural traditions, and budgetary considerations.
 • A healthy dietary pattern can benet all individuals
regardless of age, race, or ethnicity, or current
health status.
3. Focus on variety, nutrient-dense foods and beverages,
and amounts.
 • To meet nutrient needs within calorie limits, choose
a variety of nutrient-dense foods across and within
all food groups in recommended amounts.
 • Shifts are needed within the protein foods group
to increase seafood intake, but the foods to be
replaced depend on the individual’s current intake
from the other protein subgroups.
 • Replacing processed or high-fat meats (e.g., hot
dogs, sausages, bacon) with seafood could help
lower intake of saturated fat and sodium and
replacing processed or high-fat meats with beans,
peas, and lentils would have similar benets, as well
as increasing dietary ber.
4. Limit foods and beverages higher in added sugars,
saturated fat, and sodium, and limit alcoholic
beverages.
 • A healthy dietary pattern does not have much room
for extra added sugars, saturated fat, or sodium—or
for alcoholic beverages.
 • Cut back on foods and beverages higher in these
components to amounts that t within healthy
dietary patterns.
 • Commonly used oils include canola, corn, olive,
cottonseed, sunower, soybean, and peanut oil.
Oils also are found in nuts, avocados, and seafood.
They provide essential fatty acids.
 • Coconut, palm, and palm kernel oils (tropical oils)
are not included in the oils category because they
contain a higher percentage of saturated fat than do
other oils.
Adapted from U.S. Department of Agriculture and U.S. Department of Health
and Human Services. Dietary Guidelines for Americans, 2020-2025. 8th ed.
Washington, DC: U.S. Government Printing Ofce; 2020.
ndings raising concerns, the Dietary Guidelines have
undergone substantial scrutiny. The 2020-2025 version
was revised and updated extensively to address issues
and trends related to nutrition and overall health. The
2020-2025 Dietary Guidelines encourage the intake of
whole grains and suggest that people limit sugar in-
take. Another concern in the average American diet is
 Nutrition CHAPTER 46 773

Box 46.2 Dietary Fat Sources

MONOUNSATURATED FATS
• Olives
• Olive oil
• Canola oil
• Peanut oil
• Cashews
• Peanuts
• Avocados
POLYUNSATURATED FATS
• Corn oil
• Soybean oil
• Safower oil
• Cottonseed oil
• Fish
SATURATED FATS
• Whole milk
Fig. 46.1 MyPlate Food Guide. (From U.S. Department of Health and
• Cheese
Human Services/U.S. Department of Agriculture, 2011.)
• Ice cream
• Red meat
the consumption of trans-fatty acids (also called hydro- • Chocolate
genated fats) and saturated fats, which have no known • Coconut
nutritional benet but increase cholesterol levels and • Coconut oil
the frequency of heart disease. The guidelines now TRANS FATS
emphasize that intake of trans fats should be as low as • Stick margarines
possible. As of January 2006, food labels are required • Vegetable shortening
to list trans-fat content to help consumers become • Deep-fried chips
aware of and reduce their intake. The primary sources • French fries
of trans fats are commercially fried foods, stick mar- • Many fast foods
garine, processed and ready-to-eat foods, and snack • Most commercial baked goods
foods. Research indicates that monounsaturated and
polyunsaturated fats have some health benets, so
the guidelines also recommend obtaining between
20% and 35% of daily calories from these types of fats. The guidelines also make recommendations for
Saturated fats should continue to be limited. Primary healthy dietary pattern limits, which include the
sources of saturated fats are red meats, butter, and following:
high-fat dairy products (e.g., whole milk) (Box 46.2; • Limiting saturated fats and trans fats, added sugars,
Fig. 46.2). and sodium
The 2020-2025 Dietary Guidelines for Americans are • Consuming less than 10% of calories per day from
recommending two variations of the Healthy US-Style added sugars
Eating Pattern as examples of additional healthy eat- • Consuming less than 10% of calories per day from
ing patterns—the Healthy Mediterranean-Style Eating saturated fats
Pattern and the Healthy Vegetarian Eating Pattern. • Consuming less than 2300 mg per day of sodium
Both of these patterns align with the 2020-2025 Dietary If alcohol is consumed, it should be consumed in
Guidelines. A healthy dietary pattern made under these moderation (two drinks or less in a day for men and
guidelines includes the following: one drink or less in a day for women) and only by
• A variety of vegetables from all of the subgroups— adults of legal drinking age.
dark green, red and orange, legumes (beans and Several nutrients are considered as being under-
peas), starchy and other vegetables consumed: vitamins A, D, E, and C; folate; calcium;
• Fruits, especially whole fruits magnesium; ber; and potassium. These shortfalls are
• Grains, at least half of which are whole grains identied as low intakes of vegetables, fruits, whole
• Fat-free or low-fat dairy, including milk, yogurt, grains, and dairy. The 2020-2025 Dietary Guidelines en-
cheese, and/or fortied soy beverages courage dietary patterns that are rich in vegetables,
• A variety of protein foods, including seafood, lean fruit, whole grains, seafood, legumes, and nuts; mod-
meats and poultry, eggs, legumes (beans and peas), erate in low- and nonfat dairy products and alcohol
and nuts, seeds, and soy products (among adults); lower in red and processed meat; and
• Oils, including vegetable oils and oils in food, such low in sugar-sweetened foods and beverages and re-
as seafood and nuts ned grains.
774 UNIT X Drugs Affecting the General Health of the Body

Canola oil 7% 21% 11% 61%

Safflower oil 10% 76% Trace 14%
Sunflower oil 12% 71% 1% 16%
Corn oil 13% 57% 1% 29%
Olive oil 15% 9% 1% 75%
Soybean oil 15% 54% 8% 23%
Peanut oil 19% 33% Trace 48%
Cottonseed oil 27% 54% Trace 19%
Lard 43% 9% 1% 47%
Beef tallow 48% 2% 1% 49%
Palm oil 51% 10% Trace 39%
Butterfat 68% 3% 1% 28%
Coconut oil 91% 2% 7%

0 20 40 60 80 100
Percentage

Saturated Linoleic acid Alpha-linolenic acid (an omega-3 fatty acid) Mono-unsaturated fat

Fig. 46.2 All plant oils used in food preparation contain saturated, monounsaturated, and polyunsaturated fatty acids. It
is recommended that the use of those oils higher in saturated fatty acids be minimized. (From Thomas DQ, Kotecki JE.
Physical Activity and Health: An Interactive Approach. 2nd ed. Sudbury, MA: Jones and Bartlett; 2007. Reprinted with
permission.)

Alternatives to Governmental Guidelines being consumed as a calcium source could be re-

Nutrition experts at the Harvard University School of
Public Health have proposed the Healthy Eating Plate
(Fig. 46.3), the Kid’s Healthy Eating Plate (Fig. 46.4),
and the Healthy Eating Pyramid (Fig. 46.5) to address
deciencies in the USDA’s MyPlate Food Guide (https:-
//www.hsph.harvard.edu/nutritionsource/healthy-
eating-plate/). Some of the highlights of the Healthy
Eating Pyramid are as follows:
• Daily activity and weight control serve as the foun-
dation for the pyramid.
• Whole-grain foods, fruits, and vegetables (sources
of ber, vitamins, and minerals) are emphasized.
• Vegetable oils and nuts (sources of unsaturated fats)
and legumes receive greater emphasis as sources of
protein, ber, vitamins, and minerals. Good sources
of healthy unsaturated fats include olive, canola,
soy, corn, sunower, and peanut oils.
• Red meat should be consumed sparingly because
of saturated fat content. Switching to sh or chick-
en several times a week can improve cholesterol
levels.
• Food sources high in rened carbohydrates (e.g.,
white rice, white bread, potatoes, pasta, sweets)
should be consumed only sparingly. They can cause
rapid increases in blood sugar levels that can lead
to weight gain, diabetes, and heart disease. Whole-
grain carbohydrates cause slower, steadier increases
in blood sugar that do not overwhelm the body’s
ability to metabolize sugars.
• Dairy products are deemphasized and placed in
their own category; it is believed that dairy products
placed with a calcium supplement to avoid unneed-
ed calories and saturated fats.
• Moderate daily alcohol may be a healthy op-
tion unless contraindicated for specic people.
A good balance for men is one or two drinks
daily. Women should limit alcohol consump-
tion to no more than one drink per day. (See
https://www.cdc.gov/alcohol/fact-sheets.htm.)
Cultural Considerations
Another excellent source of healthy nutritional information
is Oldways (https://www.oldwayspt.org), a nutritional food
think tank. Oldways develops education programs to help
consumers make informed choices about eating, drinking,
and lifestyle. Their principles are grounded in a combination
of science, strong social conscience, and culinary excel-
lence. Oldways promotes Asian, Latin, Mediterranean, and
vegetarian evidence-based food pyramids for healthy eating.
Counting Calories
Knowing daily calorie needs may be useful for deter-
mining whether the number consumed is appropriate
in relation to the number needed each day. The best
way to assess the appropriate number of calories is
to monitor body weight and adjust calorie intake and
participation in physical activity based on changes in
weight over time. A reduction of 500 calories or more
per day is a common initial goal for weight loss for
adults; however, maintaining a smaller decit can
have a meaningful inuence on body weight over

Use healthy oils (like
olive and canola oil)
for cooking, on salad,
HEALTHY
and at the table. Limit
OILS
butter. Avoid trans fat.
The more veggies— VEGETABLES
and the greater the
variety—the better.
Potatoes and french fries
don't count.
Eat plenty of fruits of
all colors.
STAY ACTIVE!
© Harvard University
Harvard School of Public Health
The Nutrition Source
www.hsph.harvard.edu/nutritionsource
Fig. 46.3 The Healthy Eating Plate. (As print in image and © Harvard University. For more information, visit https://www
.health.harvard.edu.)
Fig. 46.4 Kids Healthy Eating Plate. (As print in image and © Harvard
University. For more information, visit https://www.health.harvard.edu.)
time. The effect of calorie reduction on weight does
not depend on how the reduction is produced—by re-
ducing calorie intake, increasing caloric expenditure
(more exercise), or both—yet, in research studies, a
greater proportion of the calorie reduction is often the
result of decreasing calorie intake, with a relatively
smaller fraction resulting from increased physical
activity.
Nutrition CHAPTER 46 775
WATER
Drink water, tea, or coffee
(with little or no sugar).
Limit milk/dairy
(1-2 servings/day) and
juice (1 small glass/day).
WHOLE
Avoid sugary drinks.
GRAINS
Eat whole grains (like brown
rice, whole-wheat bread,
and whole-grain pasta).
Limit refined grains (like
HEALTHY white rice and white bread).
PROTEIN
FRUITS
Choose fish, poultry, beans,
and nuts; limit red meat;
avoid bacon, cold cuts, and
other processed meats.
Harvard Medical School
Harvard Health Publications
www.health.harvard.edu
Life Span Considerations
Food for Thought
Because a pound of stored fat represents about 3500 ex
cess kilocalories (kcal):
 • An average excess of only 10 kcal/day in energy intake
over energy expenditure can result in about a 1-pound
weight gain in 1 year (10 kcal/day × 365 days = 3650
kcal).
 • Cutting back on only 100 kcal/day (e.g., 1 soft drink)
results in approximately a 10-pound weight loss in 1 year
(100 kcal/day × 365 days = 36,500 kcal), or consuming
an extra 100 kcal/day will result in a 10-pound gain.
 • For weight gain, add 500 cal/day to gain approximately 1
pound/wk.
 • For weight loss, subtract 500 cal/day for a loss of
approximately 1 pound/wk.
DIETARY REFERENCE INTAKES
The National Academies of Sciences, Engineering, and
Medicine collect data and publish a series of tables
known as Dietary Reference Intakes (DRIs), which pro-
vide quantitative estimates of nutrient intakes for plan-
ning and assessing diets for healthy people. The DRIs
are actually a set of four reference values: Estimated
Average Requirement, Recommended Dietary
Allowances, Adequate Intake, and Tolerable Upper
Intake Level. Links to the DRIs updated in 2017 may
be retrieved at https://www.nap.edu/catalog/24828/
guiding-principles-for-developing-dietary-reference-
intakes-based-on-chronic-disease.
776 UNIT X Drugs Affecting the General Health of the Body
OPTIONAL: ALCOHOL IN MODERATION
(Not for everyone)
DAIRY (1−2 servings a day) OR
VITAMIN D/CALCIUM SUPPLEMENTS
DAILY MULTIVITAMIN
PLUS EXTRA VITAMIN D NUTS, SEEDS, BEANS & TOFU
(For most people)
VEGETABLES & FRUITS HEALTHY FATS/OILS
DAILY EXERCISE & WEIGHT CONTROL
Fig. 46.5 The Healthy Eating Pyramid. (As print in image and © Harvard University. For more information, visit https://w
ww.health.harvard.edu.)
The Estimated Average Requirement (EAR) is a
nutrient intake value that is estimated to meet the
requirement of half of the healthy individuals in a
group. The most widely known component of the
DRIs is the Recommended Dietary Allowances (RDAs)
table. It lists the average daily dietary intake level
that is sufcient to meet the nutrient requirements
of almost all (97% to 98%) healthy individuals in
a group. (Groups are based on gender, age, and, if
applicable, pregnancy or lactation.) Recommended
Dietary Allowances are goals in meeting nutritional
needs. They do not meet the nutritional needs of ill
patients and do not account for nutritional value that
may be lost in cooking.
The RDA is based on the EAR plus twice the stan-
dard deviation: the RDA for a nutrient is a value to be
used as a goal for dietary intake by healthy individu-
als. There is no established benet for healthy persons
if they consume nutrient intakes greater than the RDA
or Adequate Intake.
Adequate Intake (AI) is a value based on observed or
experimentally determined approximations of nutri-
ent intake by a group of healthy people. The AI is used
when the RDA cannot be determined.
USE SPARINGLY:
RED MEAT, PROCESSED MEAT & BUTTER
REFINED GRAINS: WHITE RICE, BREAD & PASTA
POTATOES
SUGARY DRINKS & SWEETS
SALT
HEALTHY FATS/OILS:
OLIVE, CANOLA, SOY, CORN,
FISH, POULTRY & EGGS
SUNFLOWER, PEANUT
& OTHER VEGETABLE OILS;
TRANS−FAT FREE MARGARINE
WHOLE GRAINS:
BROWN RICE,
WHOLE WHEAT PASTA,
OATS, ETC.
WHOLE GRAINS
Another category in the DRI tables is the Tolerable
Upper Intake Level (UL). This level is dened as the
highest level of daily nutrient intake that is likely to
pose no risk of adverse health effects to almost all
those in the general population. As intake increases to
greater than the UL, the risk of adverse effects increas-
es. The UL is not intended to be a recommended level
of intake. For many nutrients, there are insufcient
data on which to develop a UL. This does not mean
that there is no potential for adverse effects resulting
from high intake. Over time, these data will help es-
tablish the value of megadoses of vitamins and nutri-
ents and provide information about whether there are
therapeutic and toxic effects to ingestion of large doses
of these chemicals.
MACRONUTRIENTS
The metabolism of the macronutrients—carbo-
hydrates, fats, and proteins—provides energy for
the body to maintain life (respiration, circulation,
physical work, nerve transmission, core body tem-
perature) and to repair damage induced by illness or
injury. Energy is measured in kilocalories (kcal). The
heat generated during these processes is reected as

Calculation of Estimated Energy
Table 46.1 Requirements (EERs)
LIFESTYLE MENa WOMENb
Sedentary 1.00 1.00
Low active 1.11 1.12
Active 1.25 1.27
Very active 1.48 1.45
aMen
ages 19 years and older: EER = 662 − (9.53 × age [yr]) + PA × (15.91 ×
weight [kg] + 539.6 × height [m])
bWomen ages 19 years and older: EER = 354 − (6.91 × age [yr]) + PA × (9.36 ×
weight [kg] + 726 × height [m])
PA, Physical activity coefcient.
Data from Institute of Medicine, Food and Nutrition Board. Dietary Reference
Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein,
and Amino Acids. Washington, DC: National Academies Press; 2005:185.
Retrieved from http://www.nap.edu/catalog.php?record_id=10490
body temperature. Energy balance in an individual
depends on dietary energy intake and energy expen-
diture. An excess of energy (food) intake over that
which is burned results in weight gain. Body weight
is lost through burning more kilocalories than are
consumed. A pound of body weight is approximately
3500 kcal.
The Estimated Energy Requirement (EER) is dened
as the average dietary energy intake that is predicted
to maintain energy balance in a healthy adult of a de-
ned age, gender, weight, height, and level of physical
activity consistent with good health (Table 46.1).
The National Academy of Sciences published the
Dietary Reference Intakes for Energy, Carbohydrate, Fiber,
Fat, Fatty Acids, Cholesterol, Protein and Amino Acids
in 2005. This report on macronutrients was spon-
sored for both the United States and Canada by sev-
eral government agencies, including Health Canada,
the US Department of Health and Human Services,
the US Food and Drug Administration, the National
Institutes of Health, the Centers for Disease Control
and Prevention, the USDA, and private sources. These
guidelines are based on research of nutrients in foods
and how the body uses energy from foods. The re-
port recommends that to meet the body’s energy and
nutritional needs while minimizing risk for chronic dis-
ease, adults should obtain 45% to 65% of their calories
from carbohydrates, 20% to 35% from fat, and 10% to
35% from protein. (See Chapter 35 for the American
Diabetes Association recommendations for intake of
carbohydrates, fats, and proteins for a patient with
diabetes mellitus.)
Carbohydrates, often referred to as sugars because
many of them taste sweet, are the major source of en-
ergy for body activities and metabolism. They occur in
nature as simple and complex molecules and are wa-
ter soluble. The simple carbohydrates are also known
as monosaccharides and disaccharides. Monosaccharides
such as glucose (also known as dextrose), fructose, and
galactose are the only sugars that can be absorbed
directly from the gastrointestinal (GI) tract into the
blood. They are the most rapidly available sources of
Nutrition CHAPTER 46 777
energy and are the only sugars capable of being used
directly to produce energy for the body. Disaccharides
such as sucrose (common table sugar), maltose, and
lactose are the most common sugars in foods, but
they must be metabolized to monosaccharides before
being absorbed into the bloodstream. For example,
a molecule of lactose is metabolized by the enzyme
lactase into a molecule each of glucose and galactose,
which are then absorbed through the gut wall into the
blood. Complex carbohydrates such as starch, dextrin,
and ber are also known as polysaccharides Complex
carbohydrates must also be metabolized into simple
sugars in the intestine before being absorbed. The car-
bohydrates provide about 4 kcal of energy per gram.
Daily caloric needs from carbohydrates range from 3
to 5.5 g/kg/day, depending on energy requirements
for daily living, stress, and wound healing. Fruits,
grains, and vegetables are excellent sources of carbo-
hydrates. Candies and carbonated beverages are com-
monly used sources of calories but contain no other
nutrients. End products of carbohydrate metabolism
are carbon dioxide (excreted primarily through the
lungs) and water.
A by-product of some complex carbohydrate me-
tabolism is fiber. Until recently, ber was thought to
be only a by-product of carbohydrate metabolism that
needed to be eliminated from the body. It is recognized
now as a macronutrient, a separate factor necessary
for complete nutrition and wellness. Dietary ber is
derived from plant sources and consists of undigest-
ible carbohydrates and lignin and digestible macronu-
trients (carbohydrates, proteins) such as cereal brans,
sweet potatoes, and legumes that contribute to overall
nutrition. Another category of ber is functional ber,
which consists of undigestible carbohydrates that have
a benecial physiologic effect on humans. An excellent
example of a functional ber is psyllium, an undigest-
ible ber that adds bulk to fecal content, which helps
timely passage of fecal contents in the GI tract, pre-
venting constipation. Functional ber content may de-
lay gastric emptying, giving a sense of fullness, which
may contribute to weight control. Delayed gastric
emptying may also reduce postprandial blood glucose
concentrations, potentially preventing excessive insu-
lin secretion and insulin sensitivity. Fibers can reduce
the absorption of dietary fat and cholesterol, as well
as enterohepatic recirculation of cholesterol and bile
acids, which may also reduce blood cholesterol con-
centrations. Total ber is the sum of dietary ber and
functional ber.
Fats, also known as lipids, serve as the body’s ma-
jor form of stored energy and are key components of
membranes, prostaglandins, and many hormones.
They are not water soluble. Examples of lipids are
cholesterol, fatty acids, triglycerides, and phospho-
lipids. Excess dietary carbohydrates and proteins are
converted to fat for storage. When used as an energy
source, fats generate 9 kcal of energy per gram. Fat
778 UNIT X Drugs Affecting the General Health of the Body
intake usually constitutes 25% to 40% of total caloric
intake, although the DRIs recommend limits of 20%
to 35% from fat. Healthy adults require 1 to 1.5 g/kg/
day. Even when patients severely restrict intake for
dieting purposes, 4% to 10% of total calories must be
supplied in the form of fats to prevent essential fatty
acid deciency.
Essential fatty acids are not produced by the body
and must be obtained from dietary sources. The most
prominent essential fatty acids are omega-3 and
omega-6 fatty acids. They are polyunsaturated fatty
acids, also known as alpha-linolenic acid and linoleic
acid, respectively. Both fatty acids are required for
eicosanoid and prostaglandin production and cell
membrane structure.
Dietary fats can be subdivided into four catego-
ries: monounsaturated, polyunsaturated, saturated,
and trans fats (see Box 46.2 for sources of dietary
fats). Monounsaturated fats decrease low-density
lipoproteins (LDLs) and increase high-density
lipoproteins (HDLs) and are considered to be car-
dioprotective. Polyunsaturated fats also lower LDL
and raise HDL levels. Saturated fats raise both LDL
and HDL and are thought to increase atherosclerotic
plaque formation in the arteries. Only recently has
it been recognized that trans fats may induce more
heart disease than saturated fats because, in addition
to raising LDL cholesterol, trans fats decrease HDL
cholesterol and increase triglycerides, as well as an-
other undesirable blood fat, lipoprotein. Saturated
fats and trans fats have no known benecial nutri-
tional effect and should be eliminated as much as
possible from the diet. Note in Fig. 46.2 how all plant
oils used in food preparation contain saturated,
monounsaturated, and polyunsaturated fatty acids.
It is recommended that we minimize the use of those
oils higher in saturated fatty acids. (See also Chapter
21 for further discussion of lipoproteins and choles-
terol.) End products of fat metabolism are water and
carbon dioxide and insoluble substances excreted in
sweat, bile, and feces.
Proteins are complex molecules composed of ami-
no acid chains. Amino acids can be subclassied as
essential and nonessential. The essential amino acids
must be provided from external sources to sustain
life; nonessential amino acids can be synthesized
to meet metabolic requirements. Before absorption,
proteins must be metabolized in the gut to the indi-
vidual amino acids. Once absorbed, the amino acids
are used to build new proteins, such as muscle and
other vital tissues, or are used as an energy source
if other energy sources are depleted. Amino acids
generate 4 kcal of energy per gram, similar to car-
bohydrates. Sources of highest protein value are
dairy products (e.g., milk, eggs, cheese), sh, and
meat. Grains and beans have less protein value. End
products of amino acid metabolism are nitrogenous
products such as urea, uric acid and ammonium,
carbon dioxide, and water. Protein requirements for
healthy people are 0.5 to 1 g/kg/day. Depending on
the amount of stress that a patient is experiencing
and the amount of tissue building and wound heal-
ing required, protein requirements may range from
1.5 to 2.5 g/kg/day. Calories from proteins generally
constitute 12% to 20% of total calorie intake, but the
National Academy of Sciences recommends 10% to
35% for healthy nutrition.
It is crucial that calorie intake be balanced among
carbohydrates, proteins, and fats. If there is an inad-
equate amount of carbohydrates to provide energy
to break down the proteins, fats, and carbohydrates,
the body will actually metabolize body proteins
and fats through a process called gluconeogenesis
to provide glucose energy to use the incoming pro-
teins and fats. Even though patients are receiving
adequate total calories, they may develop a protein-
wasting condition.
VITAMINS
Vitamins, whose name derives from the term vital
amines, are a specic set of chemical molecules that
regulate human metabolism necessary to maintain
health. To be classied as a vitamin, a chemical must
be ingested, because the human body does not make
sufcient quantities to maintain health, and the lack
of a vitamin in the diet produces a specic vitamin
deciency disease (e.g., beriberi is a thiamine de-
ciency, and scurvy is an ascorbic acid deciency).
To date, 13 compounds have been identied as vita-
mins, 9 of which are classied as water soluble and
4 as fat soluble (Table 46.2). Vitamins were originally
named according to letters of the alphabet, but as
a result of the diversity of actions of different vita-
mins, they are commonly referred to by their generic
names (e.g., phytonadione is vitamin K, and thia-
mine is vitamin B1).
MINERALS
Minerals (Table 46.3) are inorganic chemicals found in
nature. Minerals are essential to life, serving as com-
ponents of enzymes, hormones, and bone and tooth
structure. They help regulate acid-base and water bal-
ance, osmotic pressure and cell membrane permeabil-
ity, nerve conduction, muscle contractility, metabolism
of nutrients in foods, oxygen transport, and blood clot-
ting, to name a few.
WATER
Water is another nutrient essential for life. As noted in
Table 3.2, water accounts for 60% to 83% of total body
weight and plays a crucial role in transport of nutri-
ents, temperature regulation, and metabolic reactions.
Normal water losses occur through urination, perspi-
ration, defecation, and vaporization through the lungs.
Normal daily intake is highly variable, depending on
climate, activity level, and presence of a fever, but
Table 46.2 Vitamins
TYPE OF VITAMIN
Fat-Soluble Vitamins
Vitamin A (retinol)
Vitamin D (ergocalciferol, D2;
cholecalciferol, D3)
Vitamin E (alpha-tocopherol)
Vitamin K (phytonadione)
Water-Soluble Vitamins
Vitamin C (ascorbic acid)
Niacin (nicotinic acid, vitamin B3)
Riboavin (vitamin B2)
Thiamine (vitamin B1)
Pyridoxine (vitamin B6)
Cyanocobalamin (vitamin B12)
Folic acid (folacin)
Biotin
Pantothenic acid (vitamin B5)
ACTIONS
Essential for proper vision, growth, cellular
differentiation, healthy skin and mucous
membranes, reproduction, and immune
system integrity; needed to maintain healthy
skin and mucous membranes
Deciency: Night blindness, conjunctival xerosis
Regulates calcium and phosphorus metabolism
Deciency: Rickets
Acts as antioxidant; protects essential cellular
components from oxidation
Used for synthesis of prothrombin and
coagulation factors VII, IX, and X needed for
blood coagulation
Antioxidant; aids in formation and maintenance
of intracellular cement substances
Deciency: Scurvy
Used to decrease cholesterol levels; regulates
energy metabolism; helps maintain health of
skin, tongue, and digestive system
Deciency: Pellagra
Affects fetal growth and development;
coenzyme for production of mitochondrial
energy
Coenzyme for carbohydrate metabolism; used
for nerve conduction and energy production
Deciency: Beriberi
Metabolism of amino acids and proteins; may
be important in red blood cell regeneration
and normal nervous system functioning
Deciency: Anemia, spotty hair loss,
paresthesias
Needed as coenzyme for red blood cell
synthesis
Deciency: Megaloblastic anemia
Essential for cell growth and reproduction,
synthesis of DNA in red blood cells
Deciency: Impaired development of central
nervous system; anencephaly, spina bida
Essential for gluconeogenesis, fatty acid
synthesis, metabolism of branched-chain
amino acids
Essential for fat, carbohydrate, protein
metabolism
SOURCES
Liver, sh liver oils, eggs, whole milk,
sweet potatoes, cantaloupe, carrots,
spinach, broccoli, raw apricots
Liver, cod liver oil, egg yolks, butter, and
oily sh; produced in skin by exposure
to sunlight
Wheat germ oil, sunower oil,
cottonseed oil, safower oil, corn oil,
soybean oil, almonds, peanuts, green
leafy vegetables
Kale, collard greens, spinach, broccoli,
asparagus, lettuce, soybeans, pickles,
pine nuts, blueberries; needs bile
salts to be adequately absorbed in
the intestines; malabsorptive disease
processes can lead to decreased
vitamin K absorption; vitamin K
synthesized by intestinal ora; severe
diarrhea or use of antibiotics that kill
intestinal ora may result in deciency;
deciency exists in newborn infants
Citrus fruits and juices, fruits, and
vegetables such as broccoli, cabbage
Organ meats, poultry, sh, meats, yeast,
bran cereal, peanuts, brewer’s yeast
Green leafy vegetables, fruit, eggs
and dairy products, enriched cereal
products, organ meats, peanuts and
peanut butter
Pork products, whole grains, wheat
germ, meats, peas, cereal, dry beans,
peanuts
Milk, meats, whole-grain cereals, sh,
vegetables
Seafood, egg yolks, organ meats, milk,
most cheeses
Liver, beans, green vegetables, yeast,
nuts, fruit
Soy our, cereals, egg yolk, liver; also
synthesized in lower gastrointestinal
tract by bacteria and fungi
Organ meats, beef, and egg yolk
780 UNIT X Drugs Affecting the General Health of the Body

Table 46.3 Essential Minerals

MINERAL ACTIONS SOURCES
Calcium Nerve transmission, bone and tooth formation, blood Milk, cheese, vegetables
clotting; most abundant mineral in body
Chlorine Acid-base balance, gastric acid Table salt
Chromium Glucose and energy metabolism Vegetables, oils, meats, fats, brewer’s yeast,
cheddar cheese, wheat germ
Cobalt Component of cyanocobalamin (vitamin B12) Meats, milk
Copper Component of enzymes needed for iron metabolism Meats, drinking water
Fluorine Bone and tooth structure Drinking water, seafood, tea
Iodine Component of thyroid hormones Seafood, vegetables, dairy products, iodized salt
Iron Component of hemoglobin for oxygen transport, Meats, legumes, grains, leafy vegetables, eggs,
enzymes for energy metabolism clams, prunes, raisins
Magnesium Component of bones, enzymes; protein synthesis, Grains, green leafy vegetables, nuts, legumes,
nerve transmission oysters, crab, cornmeal
Manganese Component of enzymes; fat synthesis, bone and Whole grains, cereals, green vegetables, tea,
connective tissue synthesis ginger, cloves
Molybdenum Component of enzymes; metabolize iron and uric Cereals, legumes, meat, sunower seeds, wheat
acid germ
Phosphorus Acid-base balance, bone and tooth structure, energy Milk, cheese, grains, meats, green leafy vegetables,
production sh
Potassium Acid-base balance, nerve conduction, body water Citrus fruits, meat, milk, bananas, liver
balance, muscle contractions
Selenium Antioxidant Seafood, meat, grains, liver, kidney
Sodium Water balance, membrane transport, muscle Table salt, soy sauce, cured meats
contraction, acid-base balance
Sulfur Component of many tissue types such as tendons Sulfur-containing amino acids (e.g., methionine,
and cartilage, metabolic pathways, blood clotting cystine), garlic, onion, seafood, asparagus
Ultratrace Minerals
Nickel Cofactor in enzyme reactions Chocolate, nuts, fruits
Silicon Bone calcication, collagen Chicken skin, whole grains
Tin Exact functions unknown General diet
Vanadium Cofactor in enzyme reactions Olives, shellsh, mushrooms
Zinc Component of enzymes required for digestion, wound Oysters, liver, milk, sh, meats, carrots, oatmeal,
healing, vision, sexual development peas

ranges from 1.5 to 3 L/day for the average adult. Intake
should slightly exceed losses so that the person main-
tains adequate urine output to help ush waste prod-
ucts through the kidneys and minimize constipation.
PHYSICAL ACTIVITY
Balanced nutrition plays a key role in health and
wellness, but another equally important component
is physical exercise and activity. Throughout history,
it was known that the intake of food was necessary
to meet the physical energy needs to sustain life.
The balance of dietary energy intake and energy ex-
penditure was accomplished almost subconsciously
by most individuals because of the need for manu-
al labor in everyday life. Since the beginning of the
Industrial Revolution in the mid-1800s, the inven-
tion of many labor-saving devices (e.g., manufactur-
ing assembly lines, telegraph, telephone, e-mail, cell
phones, automobile, remote control) and new forms
of entertainment (e.g., radio, television, the Internet)
has reduced energy expenditure for most people.
Today, despite common knowledge that regular ex-
ercise is healthful, more than 60% of Americans are
not regularly physically active and 25% are not ac-
tive at all. In the past 50 years, society has welcomed
an immense variety of new types of foods made from
basic food sources (animals, plants). Ease and conve-
nience of food preparation (e.g., fast food restaurants,
drive-throughs, use of a microwave versus a convec-
tion oven) and increases in portion sizes to increase
commercial market share have placed too many eas-
ily consumed calories on the tables of the American
public. Consequently, reduced physical activity and
increased caloric intake have resulted in a national
epidemic of obesity, causing metabolic syndrome (see
Chapter 20) and premature death.

The latest reports from the National Academies
of Sciences, Engineering, and Medicine (2017) focus
on combating obesity with food literacy and physi-
cal exercise. The Academies have stressed the im-
portance of balancing diet with physical activity for
years and make recommendations about daily maxi-
mum caloric intake of food to be consumed based on
height, weight, and gender for four different levels
of physical activity (sedentary, low active, active,
and very active). The reports illustrate how difcult
it is to lose weight based on reduction of calories
alone and how important it is to maintain a level of
physical activity to prevent reduction in lean body
mass (muscle or protein wasting). The reports now
recommend moderate physical activity of at least 30
minutes daily, such as brisk walking, to reduce risk
of heart attack, stroke, colon cancer, high blood pres-
sure, diabetes, and other medical problems. To man-
age weight and prevent gradual, unhealthy weight
gain, 60 to 90 minutes of moderate-intensity physi-
cal activity (e.g., walking at a rate of 4 to 5 miles/hr)
or high-intensity activity (e.g., jogging at a rate of 4
to 5 miles for 20 to 30 minutes) four to seven times
weekly, in addition to the activities of daily living, is
recommended to maintain body weight (in adults)
in the recommended body mass index range (18 to
25 kg/m2).
MALNUTRITION
Nutrition plays a vital role in helping a patient recover
from illness. Adequate intake of nutrients is critical to
restoring normal homeostasis and rebuilding dam-
aged tissue. If nutritional needs are not adequately
addressed, malnutrition results. Malnutrition is a ma-
jor source of morbidity and mortality in patients who
suffer from disease because they are much more sus-
ceptible to infections and organ failure. Malnutrition
generally results from inadequate intake of protein
and calories or from a deciency of one or more vita-
mins and minerals.
Malnutrition resulting from inadequate inges-
tion of proteins and calories may be subdivided into
three types—marasmus, kwashiorkor, and mixed
kwashiorkor-marasmus. Marasmus, the most com-
mon form of malnutrition in hospitalized patients,
results from a lack of both total energy calories and
protein. Marasmus occurs most commonly in pa-
tients who suffer from chronic disease and who do
not ingest or use adequate amounts of proteins and
calories. These patients, in essence, are starving, and
they have a cachectic appearance. Laboratory tests
indicate normal serum albumin and transferrin con-
centrations but delayed cutaneous hypersensitivity.
In severe cases, muscle function is diminished.
Kwashiorkor is a protein deciency that develops
when the patient receives adequate fats and carbo-
hydrates in the diet but little or no protein. These
Nutrition CHAPTER 46 781
patients are often difcult to recognize because they
appear well nourished. They are often edematous,
and laboratory tests may show hypoalbuminemia.
Mixed kwashiorkor-marasmus results from inad-
equate protein building combined with a wasting
of fat stores and skeletal muscle. This most often re-
sults in a patient with marasmus who is suddenly
stressed with a new insult, such as infection. The
additional stress causes a greater energy need, lead-
ing to a greater loss of fat stores, muscle mass, and
serum proteins. These patients often have lower
immunocompetence, are hypoalbuminemic, and
have wounds that heal very slowly.
A patient’s nutritional status must be assessed
to diagnose a nutritional deciency. Nutrition as-
sessment requires completion of a medical history,
dietary history, physical examination, and anthro-
pometric measurements (height, weight, skinfold
thickness, limb size, and wrist circumference) and
collection of laboratory data. Laboratory tests used to
assess lean body mass include albumin, prealbumin,
retinol binding protein, and transferrin levels. Tests
commonly used to assess immune function are total
lymphocyte count and delayed cutaneous hyper-
sensitivity reactions.
THERAPY FOR MALNUTRITION
During illness, patients may require partial or full
supplementation of their nutritional needs to pre-
vent metabolic imbalances and starvation. One of
two forms of supplementation is often used, depend-
ing on the patient’s requirements. Enteral nutrition is
administered orally, either by drinking or by instil-
lation into the stomach through a feeding tube (tube
feedings—nasogastric, nasoduodenal, or nasojejunal
tube) or feeding gastrostomy tube (see Chapter 8).
Administration of nutrients directly into veins is
known as parenteral nutrition Total parenteral nutri-
tion (TPN) may be subdivided into peripheral paren-
teral nutrition (PPN) and central parenteral nutrition
(CPN). PPN refers to solutions that are administered
using the peripheral veins, and CPN refers to solu-
tions administered using a central vein (see Chapter
11 for a discussion of central venous access and im-
plantable vascular access devices that may be used to
administer parenteral nutrition).
Clinical Pitfall
Total parenteral nutrition orders are formulated daily based
on the patient’s status, weight, and uid and electrolyte bal-
ance. It is essential to check all aspects of the healthcare
provider’s order against the actual container of TPN solution
with a second qualied nurse and initiate the ow rate speci-
ed using an infusion pump. Follow clinical practice guide-
lines for changing the TPN container and tubing, generally
every 24 hours.
782 UNIT X Drugs Affecting the General Health of the Body
NURSING IMPLICATIONS FOR NUTRITIONAL
SUPPORT
The purpose of enteral or parenteral nutrition is to
supply the patient with an adequate intake of nutri-
ents to meet the body’s metabolic needs. Enteral and
parenteral forms of nutritional support are undertaken
for individuals who are unable to eat, have altered ab-
sorptive processes, or are unable to meet the body’s re-
quired nutritional demands resulting from coexisting
disease.
Assessment
History of nutritional decit. Review the patient’s his-
tory to identify the rationale for use of nutritional
support (e.g., protein-calorie malnutrition [kwashior-
kor and marasmus], burn, surgery, cancer, acquired
immunodeciency syndrome, hyperemesis gravidar-
um, infection, radiation therapy, chemotherapy, mal-
absorptive disorders, anorexia).
Nutritional history
• Are socioeconomic factors inuencing the individu-
al’s dietary practices?
• Are cultural or religious practices affecting the indi-
vidual’s food intake pattern? What are the patient’s
food preferences and food customs?
• Ask the patient to describe the pattern of the devel-
oping nutritional problem (e.g., amount of weight
loss and period of time over which it has occurred;
any concurrent symptoms).
• Ask the patient to do a 24-hour recall of foods eaten
and uids ingested, including an estimate of serv-
ing sizes.
• As time permits and condition of the patient war-
rants, have the person keep a record of all foods eat-
en and uids ingested over a specic time, usually 3
days. It may be useful to have the patient record the
times of meals and any activities that coincide with
the food intake. This will help establish a pattern of
the daily eating cycle.
• Are there any physical conditions that alter the pa-
tient’s ability to ingest food? Examine the oral cavity
for dentition or chewing problems, observe swal-
lowing, and check history regarding any incidence
of aspiration.
• Ask whether patient has any food or drug allergies.
• Is the patient taking any prescription or nonpre-
scription medicines, especially corticosteroids
or anabolic steroids; medicines for diabetes,
hypertension, or heart disease; tetracycline; or
vitamins?
• Is the patient pregnant or planning to become
pregnant in the next several months? Is the patient
breastfeeding?
Physical changes related to a malnourished state
• Obtain height, weight, arm muscle circumference,
and triceps skinfold thickness.
• Check the skin integrity, skeletal muscle mass, and
subcutaneous fat distribution. When performing an
examination, take into consideration normal altera-
tions in fat distribution throughout the life cycle.
• Skin integrity, muscle mass, and fat distribution:
Starvation may be manifested by depletion of skel-
etal muscle mass; however, it may also be caused
by muscle atrophy from disease or lack of use.
Another indication of starvation is fat depletion in
the waist, arms, and legs. Dry, dull hair that can be
easily pulled from the scalp is associated with pro-
tein deciency. With advanced protein deciency,
known as kwashiorkor, the skin may become dry and
aky. Observe for edema in the abdomen and sub-
cutaneous tissues, another sign of possible protein
deciency.
• Cardiovascular alterations: Caloric deciencies over
a long period may cause hypotension, generalized
weakness, and low energy levels. A thiamine de-
ciency can increase heart rate and heart size and
may be recognized by a widened pulse pressure.
• Respiratory alterations: Obese patients may have an
increase in fat sufcient to restrict expansion and
contraction of the chest, thereby compromising pul-
monary function. Patients need to have lung sounds
assessed to detect crackling sounds (crackles), an
indication of overhydration and excessive uid
intake.
• Neurologic alterations: Vitamin B deciencies may be
related to abnormal ndings with accompanying
symptoms, such as decreased position sense and
diminished vibratory sense, decreased tendon re-
exes, weakness, paresthesias, or decreased tactile
sensations; therefore these patients require a more
thorough neurologic evaluation. Thiamine decien-
cy may result in neurologic decit.
• Abdominal alterations: Perform an examination of
the abdomen by inspection, auscultation, percus-
sion, light palpation, and deep palpation as dictated
by the nurse’s level of knowledge and assessment
skills.
• Obtain a history of GI symptoms such as diarrhea,
vomiting, constipation, and abdominal pain and
their relationship to food consumption; ask spe-
cically for details on how any of these conditions
have been self-treated or treated by a healthcare
provider.
• Thyroid function: The thyroid gland and its hormones
inuence all body cells. Be aware of the signs and
symptoms of hypothyroidism (e.g., weight gain, dry
brittle hair, facial edema, enlarged breasts, slowed
pulse, coarse dry skin, deepening of the voice, leth-
argy, slowed speech and impaired memory, muscle
weakness, altered reexes). Conversely, be aware of
the signs and symptoms of hyperthyroidism (e.g.,
goiter, hyperactive reexes, weight loss, increased
pulse rate, dysrhythmias, elevated blood pressure,
emotional lability, heat intolerance).

Implementation
• Implement orders for diet, nutritional supplements,
vitamins, minerals, tube feedings, intravenous (IV)
therapy, or TPN.
• Perform assessments for nutritional and uid de-
cits and excess.
• Implement proper administration and monitoring
for complications associated with enteral, parenter-
al, or total parenteral administration.
• Perform verication of tube placement, including
pH testing, in accordance with clinical site policies.
• Implement institutional policies for ushing and
administration of medications via feeding tubes.
• Document all aspects of patient care relating to
nutritional therapy and the patient’s response to
therapy.
• If the patient is to continue special feedings af-
ter discharge, assure that the patient understands
proper storage of nutritional products or parenteral
solutions.
Monitoring tube feedings
• Check tube placement and gastric pH according to
clinical practice guidelines or healthcare provider
orders.
• In general, check tube placement and residual
volumes before the administration of each bolus
tube feeding, or every 4 or 8 hours for continu-
ous feedings. When residual volumes exceed 100
mL or another limit is specied by the healthcare
provider’s order, hold further tube feeding and
recheck residual volume in 1 hour. Most clinical
settings then resume the prescribed ordered vol-
ume if the repeat residual volume is less than 100
mL. Because higher residual volumes may indicate
obstruction, the healthcare provider should be no-
tied if the residual amount has not diminished to
less than 100 mL.
• Follow the healthcare provider’s orders for the
amount, type, strength of solution, and rate of admin-
istration, as well as the method of administration pre-
scribed (e.g., continuous, intermittent, bolus, cyclic).
Enteral feedings are often initiated at half strength
to determine how well the patient’s GI tract toler-
ates the solution. If abdominal distention, nausea,
vomiting, diarrhea, or cramping starts, discontinue
administration and notify the healthcare provider for
further orders.
• Initiate enteral feeding at a lower rate of about 20
mL/hr. Every 12 to 24 hours, increase the rate by
about 10 mL/hr until the appropriate hourly vol-
ume has been attained.
• Perform daily weights and monitor for signs of de-
hydration or overhydration. Monitor blood glucose
and other laboratory or diagnostic test results (no-
tify healthcare provider of abnormal results).
• Change tube feeding apparatus in accordance with
clinical facility policy, usually every 24 hours.
Nutrition CHAPTER 46 783
• Handle enteral feedings carefully to prevent bacte-
rial contamination. Store in a clean, cool place and
wash lids before opening the ready-to-use prepara-
tions. Check manufacturer’s recommendations for
the length of time that a formula is considered safe
at room temperature (usually 12 hours). Many clini-
cal sites suggest placing only enough formula for 4
or 8 hours in the delivery apparatus; check individ-
ual clinical site guidelines.
Monitoring peripheral parenteral nutrition
• Observe IV site for signs of inltration, phlebitis, or
local reaction.
• Monitor actual IV infusion rate and all aspects of the
IV order (type and strength of solution, rate of ad-
ministration). Check date on IV container and tub-
ing for need to be changed, usually every 24 hours.
• Monitor the patient for signs and symptoms of u-
id overload (e.g., bounding pulse rate, hoarseness,
dyspnea, cough, venous distention).
• Monitor for pyrogenic reaction (e.g., fever, chills,
general malaise, vomiting), usually within 30 min-
utes of initiating therapy.
• Monitor for anaphylactic reaction to proteins (e.g.,
wheezing, itching, hypotension, tightness in chest).
Monitoring central parenteral nutrition
• Monitor daily weights and laboratory or diagnostic
test results (notify healthcare provider of abnormal
results).
• Check all aspects of the healthcare provider’s order
against the actual container of CPN solution and
initiate the ow rate specied using an infusion
pump. Follow clinical practice guidelines for chang-
ing of CPN container and tubing, generally every 24
hours.
• Provide site care for central venous access in accor-
dance with clinical site policy. Assess site for red-
ness, swelling or drainage, elevated temperature, or
fatigue (signs of infection).
• Perform glucose and urine ketone tests as specied
by the healthcare provider’s orders, and administer
regular insulin according to orders. Check patient
for signs of hypoglycemia (e.g., nausea, weakness,
thirst, rapid respirations, headache).
• Assess for signs of refeeding syndrome during the
rst 24 to 48 hours after initiation of CPN or tube
feeding (e.g., changes in electrolytes, respiratory de-
pression, confusion, weakness, irritability, general-
ized lethargy).
• Observe for uid and electrolyte imbalances and
hyperglycemia resulting from high glucose content
of solution. Do not speed up CPN solution to catch
up if the amount delivered is behind schedule. This
practice may overload the individual’s system with
glucose.
• Individuals are tapered from CPN by gradu-
ally slowing the infusion rate of the CPN while
784 UNIT X Drugs Affecting the General Health of the Body
simultaneously increasing oral intake over a few
days. This procedure ensures that the patient’s GI
system can tolerate adequate oral feedings without
diarrhea developing.
Clinical Pitfall
Do not speed up CPN solution infusion to “catch up” if the
amount delivered is “behind schedule.” This practice may
cause signicant hyperglycemia and metabolic imbalance.
Patient Education
• Patients being discharged with enteral nutrition for
home use require considerable education for them-
selves and family or signicant others.
• Give specic written instructions on the administra-
tion procedures, type, rate and frequency, storage,
and handling of tube feedings ordered. Include in
the description signs that indicate a need to call the
healthcare provider (e.g., diarrhea, nausea, vomit-
ing, signs of infection).
• Teach the patient or primary caregiver the proce-
dure used in the hospital to administer the enteral
or parenteral solutions.
• Ask the appropriate individual(s) to demonstrate
competency in performing the procedures before
discharge. As appropriate, request a referral to a
community agency, such as visiting nurses, for as-
sistance in the home with the feedings.
• Give specic instructions on changing tubing, and
the importance of adhering to the techniques taught
in the hospital to prevent infection.
• Have the patient role-play the resolution of common
problems associated with the prescribed nutritional
therapy (e.g., tube obstruction, cramping, diarrhea,
nausea).
• Teach the person with a central IV line the proper
care of the line and dressing changes, as permitted
by the employing institution.
• Teach the individual to perform daily weights at the
same time of day in similar clothing on the same
scale.
• Teach appropriate oral hygiene measures and in-
clude ways to alleviate thirst and mouth dryness
(e.g., rinsing the mouth frequently, use of hard can-
dy or sugarless gum).
• Give written instructions of what to do if the patient
aspirates or the tube comes out.
• Explain techniques that can be used to self-
administer tube feedings ordered for intermittent
administration.
• Explain the importance of having the prescribed
laboratory tests done as scheduled to evaluate the
response to the nutritional therapy.
• Teach the patient to maintain a record of tempera-
ture, pulse, respirations, blood pressure, and de-
ned monitoring parameters.
Fostering health maintenance
• Provide the patient and signicant others with im-
portant information for the specic medications
prescribed. For example, when an iron preparation
is prescribed, the patient should understand it is
best taken between meals; however, as a result of
stomach irritation, it may be best to take it with food
or immediately after meals. Liquid iron should be
taken with a straw placed well back on the tongue,
and the mouth should be rinsed immediately af-
ter administration to prevent staining of the teeth.
When vitamins and minerals are prescribed, it is
necessary to continue their use for the period speci-
ed by the healthcare provider and to adhere to the
prescribed dosage.
• Ensure that the patient understands the care, han-
dling, and storage of all enteral, supplemental, or
parenteral solutions, and the need to prevent in-
fection through use of the proper administration
techniques.
• Discuss ways that the individual who is to be main-
tained on enteral nutrition or TPN for a long time
can be involved, as appropriate, with other house-
hold members during mealtimes.
• Seek cooperation and understanding of the fol-
lowing points so that medication compliance is
increased: name of medication; dosage, route, and
time of administration; and common and serious
adverse effects. For all supplemental, enteral, or
TPN solutions, the individual must understand all
components of the healthcare provider’s orders.
Patient self-assessment. Enlist the patient’s help in
developing and maintaining a written record of moni-
toring parameters. See the Patient Self-Assessment
Form for Nutritional Therapy on the Evolve website.
Complete the Premedication Data column for use as a
baseline to track response to drug therapy. Ensure that
the patient understands how to use the form, and in-
struct the patient to take the completed form to follow-
up visits. During follow-up visits, focus on issues that
will foster adherence with the therapeutic interven-
tions prescribed.
ENTERAL NUTRITION
Actions
Enteral nutrition is the provision of nutrients through
the GI tract. Formulas may be administered orally or
by nasogastric, nasoduodenal, or nasojejunal tube;
feeding gastrostomy tube; or jejunostomy tube.
Uses
There is an adage often used in medicine: “When the gut
works, and can be safely used, use it.” Supplementation
with enteral food formulas is indicated when oral con-
sumption is inadequate. Examples of when tube feedings
 Nutrition CHAPTER 46 785

might be necessary are head and neck surgery, esopha-
geal obstruction, stroke resulting in inability to chew
or swallow food, and dementia. Advantages to enteral
nutrition, compared with parenteral nutrition, are that
it avoids risks associated with IV therapy, provides GI
stimulation, and is physiologic; protocols for administra-
tion are much less stringent because there is less risk of
infection; and enteral feeding is less expensive. Enteral
feedings are contraindicated when there is intractable
vomiting, a paralyzed ileum, or the presence of certain
types of stulas. See Table 46.4 for examples of oral
supplements, standard feeding tube formulas, pediatric
formulas, and formulas for special cases such as hepatic,
renal, or pulmonary failure or malabsorption syndrome.
Therapeutic Outcomes
The primary therapeutic outcomes expected from en-
teral nutrition are the following:
1. Stabilization of the patient’s weight within identi-
ed parameters
2. Sufcient intake of nutrients to maintain age-
appropriate growth and development
3. Improved results seen in laboratory assessments of
nutrition
Nursing Implications for Enteral Nutrition
Premedication assessment
1. Assess for underlying diseases such as heart disease
or renal or liver impairment that may limit the rate
of administration and type of enteral formula to be
used.
2. Assess for food allergies and lactose intolerance.
3. Review and record daily weights, changes in gastric
motility, and stool characteristics.
4. Review enteral formula for type ordered and expi-
ration date of formula.

Table 46.4 Enteral Formulasa

CALORIES PROTEIN
BRAND NAMES (KCAL/ML) CONTENT (G/L) OSMOLALITY (MOSM/KG WATER) COMMENTS
Oral Supplements
Ensure Liquid 1.06 37 140 These products are dietary
Ensure HN 1.06 44 470 supplements and are available
in a variety of avors for
Ensure Plus 1.50 54.2 690
oral use. They require full
Boost 1.0 42 Variable based on mix digestive capability by gut.
At recommended dosages,
these formulas provide 100%
of the RDA for vitamins and
minerals.
Standard Isotonic Formulas
Isocal HN 1.06 44 270 These products are standard
Osmolite Liquid 1.06 37 300 formulas used for tube
feeding. They are lactose
Osmolite HN 1.06 44 300
free to prevent bloating and
Nutren 1.0 1.00 40.0 300–390 atulence, and are of low
Isosource HN 1.20 53 — residue and low viscosity.
At recommended dosages,
these formulas provide 100%
of the RDA for vitamins and
minerals.
Pediatric Formulas
Similac Soy Isomil 0.67 16.6 -- Soy-based infant formula; for
infants with allergy to cow’s
milk or those with lactose
intolerance or galactosemia.
Similac Alimentum 0.67 18.6 ___ For patients with severe food
allergies, protein maldigestion,
and fat malabsorption.
Enfamil Pregestimil 0.67 18.7 - Predigested; for patients with
severe malabsorption.
Phenex-1 Dependent on 15.0 g per 370 per 100 g of powder Phenylalanine free; for patients
prepared; 100 g of with phenylketonuria.
480 cal/100 g powder
of powder
Continued
786 UNIT X Drugs Affecting the General Health of the Body
Table 46.4 Enteral Formulasa—cont’d
CALORIES
BRAND NAMES (KCAL/ML)
Specialized Formulas
Glucerna 1.0 Cal 1.00
Nutren Pulmonary 1.50
Peptamen - 40.0
NovaSource Renal 2.0
Nutri-Hep 1.5
aFormulaslisted are representative examples and are not intended to be a complete list.
RDA, Recommended Dietary Allowance.
5. Monitor for signs and symptoms of aspiration (e.g.,
respiratory rate and depth, lung sounds) and eleva-
tion in body temperature.
6. Check tube placement and residual volume present
according to policy (see Chapter 8).
7. Check all aspects of the healthcare provider’s order
for a tube feeding—type, amount, rate of adminis-
tration, method of administration (bolus or continu-
ous)—and for specic orders regarding additional
water intake.
8. Check to ensure that laboratory tests have been
completed before starting enteral therapy (e.g., se-
rum prealbumin, albumin, urea nitrogen, creatinine,
electrolytes, hemoglobin, hematocrit, lipids, liver
function studies, glucose, total lymphocyte count,
ferritin, transferrin, urine specic gravity, and urine
ketones).
9. Be prepared to monitor for potential signs and symp-
toms of enteral nutrition complications throughout
the shift (e.g., tube obstruction, skin and mucous
membrane breakdown, nausea, diarrhea, consti-
pation, pulmonary complications, hyperglycemia,
hypercapnia, uid volume excess or decits).
Availability. See Table 46.4
Dosage and administration. Tube feedings, especially
those that have an osmolality of 300 mOsm/L water
or higher, need to be started with a quarter- or half-
strength formula to prevent diarrhea from a hyper-
tonic solution. The patient is positioned in the high
Fowler position during administration and for a pe-
riod of 30 to 60 minutes after feeding.
PROTEIN
CONTENT (G/L) OSMOLALITY (MOSM/KG WATER) COMMENTS
41 375 High-fat, low-carbohydrate
formula for patients with
glucose intolerance.
34 - High-fat, low-carbohydrate
formula for patients with
pulmonary disorders; reduced
CO2 production.
- Predigested; for patients with
protein maldigestion.
74 700 Essential amino acids for
patients with renal failure.
20 High in branched-chain and
low in aromatic amino acids;
for patients with hepatic
encephalopathy.
Tube feedings are administered by one of the following
methods:
1. Intermittent or bolus feedings: Administer 200 mL or
more of formula over 20 to 30 minutes using a reser-
voir bottle or bag. Formula is advanced by gravity.
2. Continuous drip: Formula is slowly administered
continuously over 12 to 24 hours using an infusion
pump. This method is recommended when feeding
is infused into the jejunum.
Administration of medicines to the tube-fed patient
• Administer each drug separately; do not combine.
• Stop formula and ush tubing with 15 to 30 mL
water.
• Administer prescribed medication, one crushed tab-
let at a time, suspended in tepid water, followed by
5 to 10 mL of water.
• Flush tube with 15 to 30 mL of water.
• Reinitiate tube feeding and record total amount of
water used for ushes.
Medication Safety Alert
 • Do not add prescribed medications directly to the formula
being administered.
 • Do not crush and administer any enteric-coated,
chewable, or sublingual tablets via the feeding tube.
Obtain a liquid form of the medication when possible.
 • Do not crush slow-release tablets and give via the tube. If
the size of the tube is sufcient, the slow-release capsules
may be opened, added to water, and given via the tube
with adequate water to clear the tubing completely after
administration.

Common adverse effects
Metabolic
Hyperglycemia. Hyperglycemia may develop easily,
especially when feeding is started for a malnourished
person. Check healthcare provider’s orders for fre-
quency of blood glucose monitoring and whether insu-
lin has been ordered for elevated glucose levels.
Serious adverse effects
Respiratory
Pulmonary complications. Assess for symptoms of
aspiration.
Gastrointestinal
Diarrhea or constipation. Changes in bowel pattern
and consistency often develop when enteral nutrition
is initiated. If diarrhea starts, discontinue feedings im-
mediately and report ndings to the healthcare pro-
vider for further orders.
Nausea, vomiting, increased residual volumes. These signs
are an indication of bowel obstruction. Discontinue
feedings and report ndings to the healthcare provider
for further orders.
Hypersensitivity, immune system
Rash, chills, fever, respiratory difculty. These signs are
an indication of allergy to the formula. Provide emer-
gency care as needed. Immediately discontinue feed-
ings and report ndings to the healthcare provider for
further orders.
Drug interactions. Food can affect medicines by al-
tering absorption, metabolism, and excretion; con-
versely, medicines can affect nutrition by similar
pathways. Interactions between drugs and nutrients
are particularly signicant in older adult patients
who often have several chronic diseases requiring
long-term multiple drug therapy and who may often
have poor nutrition. The following entries provide a
synopsis of the more common potential food-drug
interactions.
Alcohol and disulram, metronidazole, and tinidazole.
Alcohol interacts with these three medicines, caus-
Nutrition CHAPTER 46 787
Itraconazole solution. Take at least 1 hour before or
2 hours after meals. Take on an empty stomach to in-
crease absorption and therapeutic effect.
Alendronate, risedronate, ibandronate. Alendronate
should be taken at least 30 minutes before the rst food,
beverage, or medication of the day (for risedronate and
ibandronate, at least 2 hours). The patient should take
the drug with a full glass of plain water and not lie
down for at least 30 minutes with alendronate or rise-
dronate or 60 minutes with ibandronate.
Monoamine oxidase inhibitors (tranylcypromine, phen-
elzine, isocarboxazid). A major potential complication
with monoamine oxidase inhibitor (MAOI) therapy
is hypertensive crisis, particularly with tranylcy-
promine. Because MAOIs block amine metabolism
in tissues outside the brain, patients who consume
foods or medications containing indirect sympa-
thomimetic amines are at considerable risk for a
hypertensive crisis. Foods containing signicant
quantities of tyramine include well-ripened cheeses
(e.g., Camembert, Edam, Roquefort, Parmesan, moz-
zarella, cheddar), yeast extract, red wines, pickled
herring, sauerkraut, overripe bananas, gs, avoca-
dos, chicken livers, and beer. Other foods containing
vasopressors include fava beans, chocolate, coffee,
tea, and colas. Common prodromal symptoms of
hypertensive crisis include severe occipital headache,
stiff neck, sweating, nausea, vomiting, and sharply
elevated blood pressure. This drug-food interaction
may occur for up to 2 weeks after discontinuation of
the MAOI.
Warfarin. Patients receiving warfarin should avoid
extreme changes in diet and daily consumption of
large amounts of dark green vegetables. Herbal med-
icines (e.g., ginseng, ginkgo biloba, garlic) inhibit
platelet aggregation. Monitor patients for signs of
bleeding.
Grapefruit juice. Fresh or frozen grapefruit juice
inhibits the metabolism of several drugs. The sever-
ity of the interaction varies among people, among
drugs, and with the quant