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ICU
QUICK DRUG GUIDE
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ICU
QUICK DRUG GUIDE

Editor
Jennifer Pai Lee, Pharm.D., BCPS
http://icuquickdrug.com
Elsevier
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899

ICU QUICK DRUG GUIDE, FIRST EDITION ISBN: 978-0-323-68047-9

Copyright © 2021 by Elsevier, Inc. All rights reserved.

Notice

Practitioners and researchers must always rely on their own experi-

ence 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
verification of diagnoses and drug dosages should be made. To the
fullest extent of the law, no responsibility is assumed by Elsevier,
authors, editors or contributors for any injury and/or damage to
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Printed in the United States of America

Last digit is the print number: 9 8 7 6 5 4 3 2 1
To my soul mate, Joseph, and endearing angels,
Jonathan and Joshua.
 Foreword

The use of multiple pharmacologic interventions in patients in

critical care scenarios requires an in-depth background and of-
ten a quick reference source. Working in the intensive care unit
(ICU) as a pharmacist for many years, Dr. Lee identified the
need for the quick reference to make our significant pharma-
cologic interventions as accurate and easy as possible. With this
goal in mind and as part of her need to help the patients and
their care providers, she created the ICU Quick Drug Guide
reference book.
The ICU Quick Drug Guide is remarkable in its scope and
detail. It is clearly organized and arranged to cover nearly all
possible scenarios of the critically ill patients who may cross
the doors of the ICU. The book is divided into six sections
covering 24 different specific critical scenarios. Each chapter
is divided into a brief discussion of drugs used for the specific
treatment of the condition and clinical scenario. It is presented
in an outline format accompanied by numerous clear descrip-
tive tables of drug dosing, alternative agents, their antidotes (if
available), potential complications, and drug interactions that
may be encountered.
For the ICU nurses, residents, and physicians alike, this
book will become an invaluable reference. For ICU teams
rounding together, it will answer questions rapidly and accu-
rately. I can find no other similar reference in medicine and be-
lieve that the ICU Quick Drug Guide will become a standard
in the industry.
On a personal note, it was my pleasure to assist Dr. Lee
in her pursuit of her career goals beyond her initial research
studies on drugs for critically ill patients, particularly those
involving renal failure and spinal cord injury. Jennifer has de-
voted her time and training toward the betterment of patients
vi
 Foreword vii

through education and understanding of how our drugs work,

in whom they best work, and in what circumstances prob-
lems with our drugs may be anticipated or avoided. I believe
all readers will find this book useful and a highly valuable
resource.

Morton J. Kern, MD, MSCAI, FAHA, FACC

Chief of Medicine, VA Long Beach Health Care System
Professor of Medicine, University of California, Irvine
 About the Author

Jennifer Pai Lee received her Doctorate of Pharmacy from

the University of Southern California School of Pharmacy
in 2001. Following graduation, she completed a residency
in Clinical Pharmacy Practice at the Long Beach Memorial
Medical Center in 2002. She is a Board Certified Pharmaco-
therapy Specialist and serves as an clinical faculty at University
of California San Francisco, University of the Pacific, and Uni-
versity of Southern California Schools of Pharmacy. She has
been teaching medical and pharmacy students and residents
for almost twenty years as a clinical pharmacist in critical care.
Her practice interests include pharmacokinetics, critical care
medicine, and cardiology.
Jennifer is currently the Program Manager for Critical
Care/Emergency Services at Veterans Affairs Long Beach
Healthcare System. She has developed numerous guidelines
and protocols that are essential in taking care of critical care
patients to the present day. Furthermore, she has received a
research grant and has been actively involved in conducting
research studies as a principal investigator. She has given sev-
eral invited presentations at conferences, and has authored
many publications in peer-reviewed journals including New
England Journal of Medicine and Nephron as a primary and
corresponding author.

viii
 Preface

As a clinical pharmacist working and teaching for almost

20 years in the intensive care unit (ICU), I have needed to
look to different references for different challenging situations.
For example, how does one convert opioid dosing when tran-
sitioning from home oral oxycodone to intravenous (IV) hy-
dromorphone or IV morphine to transdermal fentanyl? How
do we select an anticonvulsant according to a validated clinical
practice guideline for a patient in refractory status epilepticus
with multiple drug allergies and interactions? What do we
choose for an optimal formulary agent within the class of many
similar drugs tailored to an individual patient? What source do
we use when we are seeking a novel antibiotic for a multidrug-
resistant pathogen for a specific type of infection?
Now more than ever, there is overwhelming medical
information available as reference books, articles, and online
resources. However, they may not be readily available or may
be too extensive and complex to search for answers while tend-
ing to a critically ill patient at bedside. In my experience, there
is no single reference that meets the needs of a clinician who
seeks urgently precise and accurate, evidence-based medical in-
formation while treating patients in the acute care setting. This
fact compelled me to write a pocket book that provides the
most current ICU drug information based on practice guide-
lines, along with expert opinions readily available at hand.
Each chapter is uniquely designed to provide a brief dis-
cussion of the disease state, followed by treatment algorithms
and drug tables that compare and contrast vital information
including pharmacokinetics, pharmacodynamics, drug inter-
actions, adverse effects, contraindication, and hepatic/renal
dosing along with clinical pearls to help clinicians decide on
optimal drug therapy at glance without a delay.
ix
x Preface

This book is divided into six sections containing the ma-

jor clinical ICU areas of practice. Section I highlights phar-
macotherapy in cardiovascular critical care, including acute
coronary syndromes, acutely decompensated heart failure,
adult advanced cardiac life support, anticoagulation for atrial
fibrillation/flutter, and hypertensive crisis. Section II addresses
management of endocrine emergencies such as diabetic keto-
acidosis, hyperosmolar hyperglycemic state, and adrenal and
thyroid dysfunction. In addition, treatment strategies for acute
pancreatitis, hepatic failure, and gastrointestinal complications
such as fistulas, postoperative ileus/nausea/vomiting, and
bleeding are depicted.
Section III presents empiric and definitive antimicrobial
therapy for infections involving the brain, lung, bloodstream,
abdomen, urinary tract, and skin and soft tissue. Section IV re-
views pharmacotherapeutic interventions in neurocritical care,
including, but not limited to, acute ischemic stroke, status
epilepticus, and intracranial hemorrhage. Section V discusses
treatment pathways for pulmonary disorders such as asthma
and chronic obstructive pulmonary disease exacerbations and
pulmonary hypertension. Section VI examines pharmacologic
therapies for acute poisoning, anaphylaxis, drug-induced hy-
perthermia, rapid sequence intubation, venous thromboem-
bolism, fluids and electrolytes, and pain, agitation/sedation,
and delirium.
I hope this book becomes a valuable resource for all entry-
level clinicians including physicians, pharmacists, nurses, and
other healthcare professionals needing a fundamental drug
sourcebook while working in ICU, emergency departments,
or acute care settings. Furthermore, it can serve as a quick
reference that provides a summary or refresher to experienced
clinicians working in the hospital setting.
I thank Dr. Morton J Kern for being a magnificent mentor
who inspired and advised me throughout the long journey to
completion of this book. In addition, I’d like to acknowledge
the following invaluable experts for reviewing the chapters:
 Preface xi

Ali K. Ashtiani, MD: Chapters 1–5

Ellis R. Levin, MD: Chapters 6 and 7
Timothy R. Morgan, MD: Chapters 8 and 9
Karen Tan, PharmD: Chapters 10 and 11
An T. Tran, MD: Chapters 13–15
Marius C. Viseroi, MD:
Chapters 12, 16–19, 21–22, and 24
Syeda A. Quadri, MD: Chapters 20 and 23
Morton J Kern, MD: All chapters

Jennifer P. Lee, Pharm.D., BCPS

Department of Pharmacy
VA Long Beach, Long Beach, California
 Contents

SECTION 1: CARDIOVASCULAR CRITICAL CARE

1 Acute Coronary Syndromes 3
2 Acutely Decompensated Heart Failure (ADHF) 18
3 Adult Advanced Cardiovascular Life Support 29
4 Anticoagulation for Atrial Fibrillation or Atrial Flutter 41
5 Hypertensive Crisis 48

SECTION 2: ENDOCRINE, GASTROINTESTINAL,

AND HEPATIC DISORDERS
6 Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic
State (HHS) 59
7 Other Endocrine Emergencies 65
8 Gastroenterology 73
9 Severe Acute Pancreatitis and Liver Failure 87

SECTION 3: INFECTIOUS DISEASES

10 Abdominal Infections 97
11 Other Infections 110
12 Sepsis and Septic Shock 164

SECTION 4: NEUROCRITICAL CARE

13 Acute Ischemic Stroke (AIS) 181
14 Other Neurocritical Care 189
15 Status Epilepticus 195

SECTION 5: PULMONARY DISORDERS

16 Asthma and Chronic Obstructive Pulmonary Disease (COPD)
Exacerbation 207

xii
 Contents xiii

17 Pulmonary Arterial Hypertension (Group 1 Pulmonary

Hypertension) 219

SECTION 6: MISCELLANEOUS
18 Acute Alcohol and Drug Poisoning 237
19 Anaphylaxis 259
20 Drug-Induced Hyperthermia 263
21 Fluids and Electrolyte Disorders 268
22 Pain, Agitation, Delirium, and Neuromuscular Blockade in
the Intensive Care Unit (ICU) 282
23 Rapid Sequence Induction 298
24 Venous Thromboembolism (VTE) 303
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SECTIONONE
Cardiovascular
Critical Care

1
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1
Acute Coronary
Syndromes

This chapter will review the pharmacologic management

of acute coronary syndromes (ACS) according to the 2013
American College of Cardiology Foundation/American
Heart Association (AHA) ST-Elevation Myocardial Infarction
(STEMI) and 2014 AHA/American College of Cardiology
Non-ST-Elevation Acute Coronary Syndromes (NSTE-ACS)
guidelines.

3
4 ICU Quick Drug Guide

CLINICAL SIGNS AND SYMPTOMS OF

ACS (FIG. 1.1)

Clinical signs and symptoms of ACS:

Chest pain/discomfort radiating to neck, jaws, or

shoulders; shortness of breath, nausea/vomiting,
indigestion, or new weakness/malaise

12-Lead ECG with 12-Lead ECG with

non-ST elevation ST elevation

Negative cardiac Positive cardiac Positive cardiac

enzymes enzymes enzymes

Unstable angina NSTEMI STEMI

Figure 1.1 ​Presentation and Diagnosis of Acute Myocardial Infarctions.

Data from Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/
ACC guideline for the management of patients with non–ST-elevation
acute coronary syndromes: executive summary: a report of the American
College of Cardiology/American Heart Association Task Force on Practice
Guidelines. Circulation. 2014;130:2354–2394. ACS, Acute coronary syndromes;
ECG, Electrocardiogram; NSTEMI, Non-ST-elevation myocardial infarction;
STEMI, ST-elevation myocardial infarction.
 CHAPTER 1 Acute Coronary Syndromes 5

CAUSES OF TROPONIN ELEVATIONS (BOX 1.1)

Box 1.1 Causes of Troponin Elevations

Acute decompensated heart failure Early post–cardiac surgery
Acute MI Heart transplantation
Acute pulmonary embolism Myocarditis
Aortic stenosis Pericarditis
Cardiac amyloidosis Post-PCI
Cardiotoxic chemotherapy Rhabdomyolysis
Chest compressions Sepsis
Chest wall trauma Severe strenuous exercise
Chronic heart failure Tachyarrhythmia
Direct current cardioversion/defibrillation Type A dissection
MI, Myocardial infarction; PCI, Percutaneous coronary intervention

ACUTE MANAGEMENT OF ACS

Goals of Care (Box 1.2)

Box 1.2 Goals of Care

NSTE-ACS: PREVENT TOTAL
STEMI: REPERFUSION THERAPY OCCLUSION OF THE VESSEL
Primary PCI recommended if Revascularization within 24–72 h vs.
possible within 90 min of medical management depending
presentation on risk stratification, symptom
If primary PCI impossible within resolution, and indicators of
120 min of medical contact, ongoing myocardial damage/
thrombolytic recommended ischemia
within 30 min of presentation
unless contraindicated
Surgical revascularization may be
indicated

NSTE-ACS, Non-ST-elevation acute coronary syndromes; PCI, Percutaneous coronary intervention;

STEMI, ST-elevation myocardial infarction
Data from O’Gara PT, Kushner FG, Ascheim DD, et al. ACCF/AHA guideline for the management
of ST-elevation myocardial infarction: a report of the American College of Cardiology Founda-
tion/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362–
e425; Amsterdam EA, Wenger NK, Brindis RG, et al. AHA/ACC guideline for the management of
patients with non–ST-elevation acute coronary syndromes: executive summary: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation. 2014;130:2354–2394.
6 ICU Quick Drug Guide

Initial Interventions on Presentation of ACS (Box 1.3)

Box 1.3 Initial Interventions on Presentation of ACS

Morphine 2–4 mg IV q5min prn chest pain
Provides analgesia and decreases pain-induced
sympathetic tone
Morphine may induce vasodilation and preload
reduction
Oxygen 2–4 L/min by nasal cannula or face mask if hypoxemia
(SaO2 ,90%), HF, or dyspnea
Use cautiously because it may promote coronary
vasoconstriction and generate toxic O2 metabolites
Aspirin 162–325 mg (non-EC) chewed and swallowed
immediately, then 81 mg (EC) daily
Inhibit platelet activation
Nitroglycerin Facilitate coronary vasodilation
(NTG) NTG 0.4 mg sublingually or spray q5min 33. If
continuous ischemic pain, HF, or htn, IV NTG 10 mcg/
min increased by 5 mcg/min q5min to desired effect
(NTE 200 mcg/min)
Avoid NTG if:
• SBP ,90 mm Hg or SBP #30 mm Hg below baseline
• Severe bradycardia with HR #50
• HR 100 in the absence of symptomatic HF, or RV
infarction
• Oral phosphodiesterase inhibitor within the past
24–48 h
b-Blockers Metoprolol 5 mg IV q5min up to 33 then 25–50 mg
PO q6–12h, transitioned to metoprolol tartrate BID or
metoprolol succinate daily
Decreases risk of ventricular arrhythmias and sudden
cardiac death post-MI
Improves oxygen flow through the coronary arteries
Initiate within first 24 h of ACS except for:
• Signs of HF or low-output state
• Increased risk of cardiogenic shock (SBP ,120, HR
.110 or ,60, age .70)
• Other CI to b-blockade (i.e., active asthma,
reactive airway disease, heart block)
 CHAPTER 1 Acute Coronary Syndromes 7

Box 1.3 Initial Interventions on Presentation of ACS—cont’d

Acronym Morphine
MONA 6 Oxygen
b-Blockers Nitroglycerin
Aspirin
b-Blocker

ACS, Acute coronary syndromes; BID, Twice daily; CI, Contraindication; EC, Enteric coated; HF,
Heart failure; HR, Heart rate; htn, Hypertension; MI, Myocardial infarction; NTE, Not to exceed;
PO, Orally; RV, Right ventricular; SBP, Systolic blood pressure
Data from Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the
management of patients with non–ST-elevation acute coronary syndromes: executive sum-
mary: a report of the American College of Cardiology/American Heart Association Task Force
on Practice Guidelines. Circulation. 2014;130:2354–2394.
8 ICU Quick Drug Guide

Additional Intervention in ACS

Management of NSTE-ACS (Fig. 1.2)

NSTE-ACS:
Definite or likely

Ischemia-guided strategy Early invasive strategy

Initiate DAPT and anticoagulant Initiate DAPT and anticoagulant

therapy therapy
1. ASA (Class I; LOE: A) 1. ASA (Class I; LOE: A)
2. P2Y12 inhibitor (in addition to ASA) 2. P2Y12 inhibitor (in addition to ASA)
(Class I; LOE: B): (Class I; LOE: B):
• Clopidogrel or • Clopidogrel or
• Ticagrelor • Ticagrelor
3. Anticoagulant: 3. Anticoagulant:
• UFH (Class I; LOE: B) or • UFH (Class I; LOE: B) or
• Enoxaparin (Class I; LOE: A) or • Enoxaparin (Class I; LOE: A) or
• Fondaparinux† (Class I; LOE: B) • Fondaparinux† (Class I; LOE: B)
• Bivslirudin (Class I; LOE: B)

Can consider GPI in addition to ASA

and P2Y12 inhibitor in high-risk
(e.g., troponin positive) pts
(Class IIB; LOE: B)
• Eptifibatide
• Tirofiban

Medical therapy
chosen based on cath
findings

Therapy Therapy
effective ineffective
 CHAPTER 1 Acute Coronary Syndromes 9

PCI with stenting CABG

Initiate/continue antiplatelet and
anticoagulant therapy
1. ASA (Class I; LOE: B)
2. P2Y12 inhibitor (in addition to
ASA):
• Clopidogrel (Class I; LOE: B) or
• Prasugrel (Class I; LOE: B) or
• Ticagrelor (Class I; LOE: B)
3. GPI (if not treated with bivalirudin
at time of PCI)
• High-risk features, not
adequately pretreated with
clopidogrel (Class I; LOE: A)
• High-risk features adequately
pretreated with clopidogrel
(Class IIa; LOE: B)
4. Anticoagulant:
• Enoxaparin (Class I; LOE: A) or
• Bivalirundin (Class I; LOE: B) or
• Fondaparinux† as the sole
anticoagulant (Class III: Harm;
LOE: B) or
• UFH (Class I; LOE: B)
Initiate/continue ASA therapy
and discontinue P2Y12 and/or
GPI therapy
1. ASA (Class I; LOE: B)
2. Discontinue clopidogrel/
ticagrelor 5 days before, and
prasugrel at least 7 days before
elective CABG
3. Discontinue clopidogrel/
ticagrelor up to 24 h before
urgent CABG (Class I; LOE: B).
May perform urgent CABG <5
days after clopidogrel/ticagrelor
and <7 days after prasugrel
discontinued
4. Discontinue eptifibatide/tirofiban
at least 2–4 h before, and
abciximab ≥12 h before CABG
(Class I; LOE: B).
Late hospital/posthospital care
1. ASA indefinitely
(Class I; LOE: A)
2. P2Y12 inhibitor (clopidogrel or
ticagrelor), in addition to ASA,
up to 12 months if medically
treated (Class I; LOE: B)
3. P2Y12 inhibitor (clopidogrel,
prasugrel, or ticagrelor), in
addition to ASA, at least 12
months if treated with coronary
stenting (Class I; LOE: B)

Figure 1.2 ​Management of Non-ST-Elevation Acute Coronary Syndrome.

From Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline
for the management of patients with non–ST-elevation acute coronary
syndromes: executive summary: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation. 2014;130:2354–2394. †Additional UFH or bivalirudin should
be given at the time of PCI because of the risk of catheter thrombosis.
ASA, Aspirin; CABG, Coronary artery bypass graft; DAPT, Dual antiplatelet
therapy; GPI, Glycoprotein IIb/IIIa inhibitor; NSTE-ACS, Non-ST-elevation
acute coronary syndromes; PCI, Percutaneous coronary intervention;
UFH, Unfractionated heparin. Class I, Strong recommendation; Class IIa,
Reasonable recommendation; Class IIb, May be considered; Class III, No befit;
LOE: A, Multiple populations evaluated; LOE: B, Limited populations evaluated.
Oral Antiplatelets (Table 1.1)

10 ICU Quick Drug Guide

Table 1.1 Oral Antiplatelet Therapy
DRUG ASPIRIN CLOPIDOGREL PRASUGREL TICAGRELOR

Mechanism of action Inhibits thromboxane Inhibits ADP-mediated platelet activation at P2Y12 receptor
A2-mediated platelet
activation
Loading dose 162–325 mg 600 mga 60 mg 180 mg
Maintenance dose 81 mg daily 75 mg daily 10 mg dailyb 90 mg BID
Prodrug No Yes Yes No
Reversible platelet No No No Yes
binding
Onset 30 min 2–6 h 30 min 30 min
Platelet inhibition 10–20% 30–40% 60–70% 60–70%
Hold before CABG Do not hold 5 days 7 days 5 days
Comments Non-EC formulation for load- Pharmacogenomic CI: history of stroke/TIA; Avoid concomitant
ing then EC formulation for variability (CYP2C19) bleeding risk ASA .100 mg daily
maintenance in response Caution: age 75 yr, (lack of efficacy)
weight ,60 kg
Notes:

CHAPTER 1 Acute Coronary Syndromes

• Aspirin plus P2Y12 for up to 12 months for patients treated initially with an invasive or ischemia-guided strategy
• Aspirin plus P2Y12 for at least 12 months for patients treated with coronary stents
ADP, Adenosine diphosphate; ASA, Aspirin; BID, Twice daily; CABG, Coronary artery bypass grafting; CI, Contraindication; CYP, Cytochrome P450 enzymes; EC, Enteric coated;
TIA, Transient ischemic attack
a
300 mg loading for #75 yr and no loading for .75 yr receiving fibrinolytic
b
Patients with weight ,60 kg should receive 5 mg daily
Data from O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362–e425; Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC
guideline for the management of patients with non–ST-elevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines. Circulation. 2014;130:2354–2394; Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI guideline for percutaneous coronary
intervention: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiogra-
phy and Interventions. J Am Coll Cardiol. 2011;58:e44–e122; Wijeyeratne YD, Heptinstall S. Anti-platelet therapy: ADP receptor antagonists. Br J Clin Pharmacol. 2011;4:647–657.

11
 12 ICU Quick Drug Guide
Parenteral Antithrombotics for Percutaneous Coronary Intervention (Table 1.2)
Table 1.2 Parenteral Antithrombotics for PCI
RETURN OF PLT
DRUG LD (IV) MD (IV) FUNCTION AFTER DC ELIMINATION DIALYZABLE

Indirect Thrombin Inhibitor

UFH With GP IIb/IIIa inhibitor: Rebolus to maintain goal — Hepatic and No
50–70 units/kg ACT during procedure RES
Without GP IIb/IIIa inhibi- With GP IIb/IIIa inhibitor:
tor: 70–100 units/kg 200–250 s
Without GP IIb/IIIa
inhibitor: 250–300 s
Direct Thrombin Inhibitor
Bivalirudin 0.75 mg/kg 1.75 mg/kg/h 1h 80% plasma Partial
(Angiomax) Additional 0.3 mg/kg if CrCl ,30: 1 mg/kg/h proteolysis
needed With or without UFH 20% renal
GP IIa/IIIa Inhibitors
Abciximab 0.25 mg/kg 0.125 mcg/kg/min 24–72 h; RES No
(ReoPro) Max: 10 mcg/min Up to 7 days
Not in U.S.
Eptifibatide 180 mcg/kg q10min 32 2 mcg/kg/min 4–8 h 50% renal Yes
(Integrilin) CrCl ,50: 1 mcg/kg/min
HD: avoid
Tirofiban 25 mcg/kg 0.15 mcg/kg/min 4–8 h 65% renal Yes
(Aggrastat) CrCl ,60: 0.075
mcg/kg/min
Direct P2Y12 Platelet Receptor Inhibitor

CHAPTER 1 Acute Coronary Syndromes

Cangrelor 30 mcg/kg 4 mcg/kg/min 1h Plasma N/A
(Kengreal) dephos-
phorylation
ACT, Activated clotting time; CrCl, Creatinine clearance; DC, Discontinuation; GP, Glycoprotein; HD, Hemodialysis; IV, Intravenously; LD, Loading dose; MD, Maintenance dose;
N/A, Not applicable; PCI, Percutaneous coronary intervention; PLT, Platelet; RES, Reticuloendothelial system; UFH, Unfractionated heparin
Data from O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362–e425; Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC
guideline for the management of patients with non–ST-elevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines. Circulation. 2014;130:2354–2394; Wijeyeratne YD, Heptinstall S. Anti-platelet therapy: ADP receptor antagonists. Br J Clin Pharmacol.
2011;4:647–657.

13
14 ICU Quick Drug Guide

Thrombolytics (Table 1.3)

Table 1.3 Thrombolytic Therapy for STEMI
STANDARD
DRUG DOSING (IV) PD/PK COMMENT

Alteplase 15 mg bolus over Hepatic metabo- Original and

1–2 min, then 0.75 lism slow-acting
mg/kg (NTE 50 .50% cleared thrombolytic
mg) over 30 min, within 5 min but clinical
then 0.5 mg/kg after infusion outcomes
(NTE 35 mg) over completed, are no dif-
60 min 80% cleared ferent
Maximum: 100 mg within 10 min
over 90 min
Tenecteplase ,60 kg: 30 mg Hepatic metabo- Fast-acting
60–69 kg: 35 mg lism thrombolytic
70–79 kg: 40 mg Half-life elimina- but clinical
80–89 kg: 45 mg tion: outcomes
90 kg: 50 mg Initial: 20–24 are no dif-
All doses given as min ferent
bolus over 5–10 s Terminal:
90–130 min
Notes:
• Thrombolytic should be administered within 30 min of hospital arrival
• Administer concurrent aspirin, clopidogrel, and anticoagulant (UFH,
enoxaparin, or fondaparinux)
• UFH: 60 units/kg IV bolus, then 12 units/kg/h titrated to target aPTT
1.5–2 times control for 48 h or until revascularization
• Enoxaparin
• STEMI and ,75 yr: 30 mg IV 31 then in 15 min 1 mg/kg subq q12h
(max 100 mg for first two doses)
• STEMI and 75 yr: 0.75 mg/kg subq q12h (max 75 mg for first two
doses)
• Up to 8 days or until revascularization
• CrCl ,30: same bolus as above then maintenance dose q24h
• Fondaparinux: 2.5 mg IV 31 then 2.5 mg subq daily starting the
following day; contraindicated in CrCl ,30
aPTT, Activated partial thromboplastin time; CrCl, Creatinine clearance; IV, Intravenously;
NTE, Not to exceed; PD/PK, Pharmacodynamics/pharmacokinetics; STEMI, ST-elevation
myocardial infarction; subq, subcutaneously; UFH, Unfractionated heparin
 CHAPTER 1 Acute Coronary Syndromes 15

Contraindications (Table 1.4)

Table 1.4 Contraindications to Thrombolytic Therapy

ABSOLUTE CONTRAINDICATIONS RELATIVE CONTRAINDICATIONS

Active bleeding excluding Systolic BP .180 mm Hg or

menses diastolic BP .110 mm Hg
Intracranial neoplasm Active bleeding in past
Arteriovenous malformation or 4 weeks
aneurysm Non-compressible vascular
Suspected aortic dissection punctures
Ischemic stroke within Major surgery in past 3 weeks
3 months Traumatic or prolonged
Prior intracranial hemorrhage (.10 min) cardiopulmonary
Significant closed head or resuscitation
facial trauma within Ischemic stroke .3 months
3 months ago
Intracranial/intraspinal Dementia
surgery/trauma within Active peptic ulcer disease
2 months Pregnancy
Bleeding diathesis Ongoing therapy with warfarin
Data from O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the
management of ST-elevation myocardial infarction: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.
Circulation. 2013;127:e362–e425.
Medical Therapies for Stabilized ACS (Table 1.5)

16 ICU Quick Drug Guide

Table 1.5 Routine Medical Therapies for Stabilized ACS
CLASS INDICATIONS ORAL DRUG REGIMEN (TARGET DOSE) AVOID/CAUTION

b-Blockers All patients without CI Metoprolol tartrate 25–50 mg q6–12h, transi- Signs of HF, low output state
tioned to BID of metoprolol tartrate or daily Increased risk of cardiogenic shock
of metoprolol succinatea (200 mg/day) Prolonged first-degree or high-grade
Carvedilol 6.25 mg BID (25 mg BID) AV block
Bisoprolol 1.25 mg daily (10 mg daily) Reactive airway disease
ACEI All patients with anterior Lisinopril 2.5–5 mg daily (10 mg daily) Hypotension
infarction, post-MI LV Captopril 6.25–12.5 mg TID (25–50 mg TID) Renal failure
systolic dysfunction (EF Ramipril 2.5 mg BID (5 mg BID) Hyperkalemia
#40%), or HF Trandolapril 0.5 mg daily (4 mg daily)
All patients without CI
ARB For patients intolerant of Valsartan 20 mg BID (160 mg BID) Hypotension
ACEI Renal failure
Hyperkalemia
Statins All patients without CI Atorvastatin 80 mg daily DDI: CYP3A4, fibrates
Monitor for myopathy, hepatic toxicity
ACS, Acute coronary syndrome; ACEI, Angiotensin converting enzyme inhibitor; ARB, Angiotensin receptor blocker; AV, Atrioventricular; BID, Twice daily: CI, contraindication;
CYP, cytochrome P450 enzymes; DDI, Drug-drug interaction; EF, Ejection fraction; HF, Heart failure; LV, Left ventricle; MI, Myocardial infarction; TID, Three times daily.
a
Succinate form rather than tartrate recommended if concomitant non-ST-elevation myocardial infarction, stable HF, or reduced systolic function
Data from O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362–e425.
 CHAPTER 1 Acute Coronary Syndromes 17

References
1. O’Gara PT, Kushner FG, Ascheim DD, et al. ACCF/AHA guideline for the
management of ST-elevation myocardial infarction: a report of the Ameri-
can College of Cardiology Foundation/American Heart Association Task
Force on Practice Guidelines. Circulation. 2013;127:e362–e425.
2. Amsterdam EA, Wenger NK, Brindis RG, et al. AHA/ACC guideline for
the management of patients with non–ST-elevation acute coronary
syndromes: executive summary: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation. 2014;130:2354–2394.
3. Levine GN, Bates ER, Blankenship JC, et al. ACCF/AHA/SCAI guideline for
percutaneous coronary intervention: a report of the American College
of Cardiology Foundation/American Heart Association Task Force on
Practice Guidelines and the Society for Cardiovascular Angiography and
Interventions. J Am Coll Cardiol. 2011;58:e44–e122.
4. Wijeyeratne YD, Heptinstall S. Anti-platelet therapy: ADP receptor antagonists.
Br J Clin Pharmacol. 2011;4:647–657.
2
Acutely Decompensated Heart
Failure (ADHF)

This chapter will review the pharmacologic management

of heart failure (HF) according to the American College of
Cardiology Foundation/American Heart Association/Heart
Failure Society of America Practice Guidelines.

DEFINITIONS
• ADHF: new or worsening signs and symptoms of HF,
characterized by acute dyspnea associated with elevated intra-
cardiac filling pressures with or without pulmonary edema.
• HF with reduced ejection fraction (HFrEF): ejection
fraction (EF) #40%.
• HF with preserved EF (HFpEF): EF 50%.
• HFpEF, borderline: EF 41–49%.
• Stages of HF
• Stage A: normal cardiac function/morphology with
increased risk of HF
• Stage B: abnormal cardiac function/morphology
without symptoms of HF
• Stage C: symptomatic HF
• Stage D: end-stage HF
• New York Heart Association (NYHA) functional classification:
• NYHA I: no limitation of physical activity
• NYHA II: slight limitation of physical activity
• NYHA III: marked limitation of physical activity
• NYHA IV: symptoms at rest
18
 CHAPTER 2 Acutely Decompensated Heart Failure (ADHF) 19

PRECIPITATING FACTORS
• Nonadherence with diet
• Worsening renal failure
• Uncontrolled hypertension
• Infection
• Pulmonary embolism
• Myocardial ischemia, arrhythmias
• Hyperthyroidism/hypothyroidism
• Drugs (Table 2.1)

Table 2.1 Critical Care Drugs That Can Promote Heart Failure
THERAPEUTIC CLASS AND DRUG POSSIBLE MECHANISM

Analgesics
NSAIDs (i.e., Ketorolac) Prostaglandin inhibition resulting
COX-2 inhibitors (i.e., Celocoxib) in sodium/water retention and
blunted diuretic response
Anesthesia Medications
Desflurane, isoflurane, Myocardial depression and
sevoflurane peripheral vasodilation
Dexmedetomidine a-Receptor agonist
Etomidate Adrenal suppression
Ketamine Negative inotrope
Propofol Negative inotrope and
vasodilation
Calcium Channel Blockers
Diltiazem, verapamil, nifedipine Negative inotrope
Anti-Infective Medications
Itraconazole Negative inotrope
Amphotericin Unknown
Ampicillin/sulbactam High sodium content
Azithromycin (injection) “
Metronidazole (injection) “
Nafcillin “
Oxacillin “
Piperacillin/tazobactam “
Ticarcillin/clavulanate potassium “
Continued
20 ICU Quick Drug Guide

Table 2.1 C
 ritical Care Drugs That Can Promote Heart
Failure—cont’d
THERAPEUTIC CLASS AND DRUG POSSIBLE MECHANISM

Pulmonary Medications
Albuterol Decreased b-receptor
responsiveness with chronic use
Epoprostenol Unknown
Bosentan “
Miscellaneous
Polyethylene glycol High sodium content in
Sodium phosphates enema formulation
Sodium polystyrene sulfonate “
COX-2, Cyclooxygenase-2; NSAIDs, Nonsteroidal antiinflammatory drugs
Data from Page RL II, O’Bryant CL, Chen D, et al. Drugs that may cause or exacerbate heart failure:
a scientific statement from the American Heart Association. Circulation. 2016;134:e32–e69.

PHARMACOLOGIC MANAGEMENT
Vasodilator
For treatment of normotensive or hypertensive HF; lacks
unwanted cardiac stimulation (Table 2.2)

Inodilator
For systolic dysfunction when vasodilator therapy is not
tolerated due to hypotension (Table 2.3)

Diuretic Therapy
Only if hypervolemia or elevated pulmonary artery wedge
pressure (.20 mm Hg) despite vasodilator or inodilator ther-
apy (Tables 2.4 and 2.5). Must be combined with vasodilator
or inodilator.

Vasopressin Receptor Antagonist

• Tolvaptan: most studied
• Adjunct to diuretics and other standard therapies for
ADHF
• Short-term use (tolvaptan should not be used .30 days)
for volume overload with persistent severe hyponatremia
 CHAPTER 2 Acutely Decompensated Heart Failure (ADHF) 21

Table 2.2 Continuous-Infusion Vasodilator Therapy

STANDARD
DRUG DOSING (IV) COMMENT

Nitroglycerin Start at 5 mcg/min Preferred vasodilator,

(NTG) Titrate by 5 mcg/min especially in patients
q5min to achieve with CAD
desired hemody- Greater venous than arterial
namic effect vasodilation
Max 200 mcg/min Tachyphylaxis can occur
after 16–24 h of
continuous NTG
administration
ADR: methemoglobinemia
(rare)
CI: Phosphodiesterase-5
enzyme inhibitors such as
sildenafil
Nitroprusside Start at 5 mcg/min Preferred in severe hy-
Titrate by 5 mcg/min pertension, acute mitral
q5min to achieve regurgitation, or acute
desired hemody- aortic regurgitation
namic effect Balanced arterial and
Max dose: 400 venous dilation
mcg/min Monitor for cyanide
Max duration: 72 h toxicity
Not recommended in renal/
hepatic insufficiency
CI: myocardial ischemia
Nesiritide Start with a bolus Recombinant human B-type
(no longer 2 mcg/kg, then natriuretic peptide with
available in 0.01 mcg/kg/min same natriuretic and
U.S.) Titrate by 0.005 vasodilator effects as
mcg/kg/min q3h endogenous BNP
Max 0.03 mcg/kg/ Balanced arterial and
min venous dilation
ADR, Adverse drug reaction; BNP, Brain natriuretic peptide; CAD, Coronary artery disease;
CI, Contraindication; IV, Intravenously
Data from Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the manage-
ment of heart failure: executive summary: a report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines. Circulation.
2013;128:1810–1852.
Table 2.3 Continuous-Infusion Inodilator Therapy
DRUG STANDARD DOSING (IV) COMMENT

Dobutamine Start at 2.5 mcg/kg/min Potent b1-receptor agonist: positive inotropic effects
Titrate by 2.5 mcg/kg/min if Weak b2  a1 receptor agonist: vasodilation in addition to inotropic and chronotropic effects
needed ADR: tachycardia, increase in myocardial O2 consumption, increase/decrease in blood pressure
Range: 5–20 mcg/kg/min Least preferred due to deleterious effects of adrenergic stimulation
Dopamine 5–10 mcg/kg/min Consider in addition to loop diuretic therapy to improve diuresis
Dose-related receptor activity:
2–5 mcg/kg/min: dopamine receptor
5–10 mcg/kg/min: b1-receptor
.10 mcg/kg/min: a1-receptor
Levosimendan Bolus 12 mcg/kg over 10 min, Increases cardiac contractility by sensitizing cardiac myofilaments to calcium
(not available in then 0.1 mcg/kg/min Promotes vasodilation by facilitating potassium influx into vascular smooth muscle
U.S.) Max dose: 0.2 mcg/kg/min Preferred agent especially in myocardial ischemia or infarction
Max duration: 24 h
Milrinone Bolus 50 mcg/kg over 10 min, Phosphodiesterase inhibitor: enhances myocardial contractility and relaxation
then 0.375–0.75 mcg/kg/min Less tachycardia than dobutamine but similar risk of ventricular arrhythmias
CrCl 50: 0.43 mcg/kg/min Preferred over dobutamine if recent administration of b-blocker or concomitant pulmo-
CrCl 40: 0.38 mcg/kg/min nary hypertension
CrCl 30: 0.33 mcg/kg/min Slower onset and longer half-life than dobutamine
CrCl 20: 0.28 mcg/kg/min
CrCl 10: 0.23 mcg/kg/min
CrCl 5: 0.2 mcg/kg/min
ADR, Adverse drug reaction; CrCl, Creatinine clearance
Data 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;128:1810–1852.
 CHAPTER 2 Acutely Decompensated Heart Failure (ADHF) 23

Table 2.4 D
 iuretic Therapy in Diuretic Naïve and Normal Renal
Function
USUAL ORAL ORAL DOSE
INITIAL MAXIMUM BIOAVAIL- EQUIVA-
DRUG DOSE (IV) DOSE (IV) ABILITY LENCY

Furosemide 20–40 mg 200 mg 50% 40 mg

Bumetanide 1 mg 8 mg 80% 1 mg
Torsemide 10–20 mg 100 mg 80% 20 mg
Notes:
• If minimal response to the initial dose, double the dose q2h as
needed up to the maximum recommended dose.
• Onset of diuresis 30 min and peak of diuresis 1–2 h after IV diuretic
administration
IV, Intravenous
Data 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;128:1810–1852.

Table 2.5 D
 iuretic Therapy in Diuretic Resistance or Renal
Insufficiency
FUROSEMIDE METOLAZONE
PRIOR DAILY CONTINUOUS
ORAL DOSE IV BOLUS INFUSION ORAL DOSE

#80 mg 40 mg 5 mg/h —
81–160 mg 80 mg 10 mg/h 5 mg daily
161–240 mg 80 mg 20 mg/h 5 mg BID
.240 mg 80 mg 30 mg/h 5 mg BID
Notes:
• Goal diuresis is 3–5 liters of urine per day until clinical euvolemia is
reached
• Hydrochlorothiazide 50 mg BID or chlorthalidone 50 mg daily may
be substituted for metolazone
BID, Two times daily; IV, Intravenously.
From Ellison DH, Felker GM. Diuretic treatment in heart failure. N Engl J Med.
2017;377:1964–1975.
24 ICU Quick Drug Guide

(Na #120 mEq/L; correct for hyperglycemia if appropri-

ate) despite water restriction and maximal medical therapy
• Caution: hepatotoxicity
• Use controversial due to unknown long-term safety

Guideline-Directed Medical Therapy for Stage C HFr EF

• Treatment algorithm (Fig. 2.1)
• Pharmacological management (Table 2.6)

Venous Thromboembolism Prophylaxis Unless

Contraindicated (see Table 24.2)

HFrEF treatment

ACEI/ARB/ARNI
+
β-Blocker

Presistently
NYHA II–IV with Symptomatic NYHA II–IV with
volume overload African Americans CrCl>30 + K<5
NYHA III–IV

Add Add Add

Loop diuretics Hydral-nitrates MRA

Figure 2.1 ​Guideline-Directed Medical Therapy for HfrEF. Data from Yan-
cy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the man-
agement of heart failure: executive summary: a report of the American
College of Cardiology Foundation/American Heart Association Task Force
on Practice Guidelines. Circulation. 2013;128:1810–1852. ACEI, Angiotensin-
converting enzyme inhibitor; ARB, Angiotensin-receptor blocker;
ARNI, Angiotensin receptor-neprilysin inhibitor; CrCl, Creatinine clearance;
HFrEF, Heart failure with reduced ejection fraction; Hydral-Nitrates, Hydrala-
zine and isosorbide dinitrate; K, Potassium; MRA, Mineralocorticoid recep-
tor antagonists; NYHA, New York Heart Association.
Table 2.6 Long-Term Therapy for Systolic Dysfunction
DRUG INITIAL DOSE (PO) TARGET DOSE (PO) COMMENTS

CHAPTER 2 Acutely Decompensated Heart Failure (ADHF)

Angiotensin-Converting Enzyme Inhibitors (ACEIs)
Captopril 6.25 mg TID 50 mg TID Titrate dose q1–2 weeks
Caution: hypotension, hyponatre-
Enalapril (Vasotec) 2.5 mg BID 10–20 mg BID
mia, diabetes, volume depletion,
Fosinopril 5–10 mg daily 40 mg daily renal disease, potassium .5 mEq
Lisinopril (Prinivil, Zestril) 2.5–5 mg daily 20–40 mg daily (mmol)/L, advanced age

Perindopril (Aceon) 2 mg daily 8–16 mg daily

Quinapril (Accupril) 5 mg BID 20 mg BID
Ramipril (Altace) 1.25–2.5 mg daily 10 mg daily
Trandolapril (Mavik) 1 mg daily 4 mg daily
Angiotensin II Receptor Blockers (ARBs)
Candesartan (Atacand) 4–8 mg daily 32 mg daily For patients intolerant to ACEI
Titration and caution as per ACEIs
Losartan (Cozaar) 25–50 mg daily 50–150 mg daily
above
Valsartan (Diovan) 20–40 mg daily 160 mg BID Sacubitril in Entresto is a neprilysin
Sacubitril/valsartan (Entresto) 24/26–49/51 mg BID 97/103 mg BID inhibitor

Continued

25
 26 ICU Quick Drug Guide
Table 2.6 Long-Term Therapy for Systolic Dysfunction.—cont’d
DRUG INITIAL DOSE (PO) TARGET DOSE (PO) COMMENTS

b-Blockers
Bisoprolol 1.25 mg daily 10 mg daily Bisoprolol and metoprolol: b1
selective
Carvedilol (Coreg) 3.125 mg BID 50 mg BID
Carvedilol: blocks b1, b2, and
Carvedilol extended-release 10 mg daily 80 mg daily a1 receptors
(Coreg CR) Do not up-titrate dose until ADR
Metoprolol succinate extended- 12.5–25 mg daily 200 mg daily resolved
release (Toprol-XL) Metoprolol tartrate immediate-release
has no indication for heart failure
Mineralocorticoid Receptor Antagonists (MRAs)
Eplerenone (Inspra) 25 mg daily 50 mg daily Do not start if SCr 2.5 mg/dL in men
CrCl 30–49: 25 mg every CrCl 30–49 or with or 2 mg/dL in women, CrCl #30,
other day moderate CYP3A4 or potassium 5 mEq/L
inhibitors: 25 mg daily Discontinue if potassium .5.5 mEq/L
Increase to target dose after 4 weeks
Spironolactone (Aldactone) 12.5–25 mg daily 25 mg daily or BID
if potassium #5 mEq/L
CrCl 30–49: 12.5 mg daily or CrCl 30–49: 12.5–25 mg
every other day daily
Vasodilators
Hydralazine 25–50 mg TID–QID 100 mg TID Isosorbide dinitrate 20 mg 1

CHAPTER 2 Acutely Decompensated Heart Failure (ADHF)

hydralazine 37.5 mg (BiDil)
Initial dose: one tablet TID
Isosorbide dinitrate (Isordil) 20–30 mg TID–QID 40 mg TID Target dose: two tablets TID
Notes:
• ACEI/ARB can usually be started 24–48 h after presentation, once patient is hemodynamically stable
• Recommend starting a b-blocker after optimization of volume status and discontinuation of intravenous diuretics, vasodilators,
and inotropic agents
• Recommend angiotensin receptor-neprilysin inhibitor (ARNI) for patients who have tolerated high doses of ACEI/ARB (Enalapril
10 mg BID equivalent)
• Criteria for initiating the ARNI Sacubitril/valsartan: elevated natriuretic peptide level, SBP 100, GFR 30, and no history of angioedema
• ACEI, ARB, or ARNI, b-blocker, and MRA reduce morbidity and mortality
• Isosorbide mononitrate extended-release (30–120 mg daily) may substitute isosorbide dinitrate for better adherence
• Ivabradin (Corlanor)
• A new agent that selectively inhibits the If current in the sinoatrial node leading to decrease in heart rate
• Reduces HF hospitalization for patients with stable, symptomatic (NYHA II–III) chronic HF with EF #35% who are on a maximally
tolerated b-blocker (or contraindication to b-blocker) and in sinus rhythm with resting heart rate 70
• Dose: 2.5–7.5 mg twice daily
ADR, Adverse drug reaction; BID, Two times daily; CrCl, Creatinine clearance; CYP, Cytochrome P450 enzymes; EF, Ejection fraction; GFR, Glomerular filtration rate; HF, Heart failure;
NYHA, New York Heart Association; PO, Orally; QID, Four times daily; SBP, Systolic blood pressure; TID, Three times daily
Drugs without brand names are denoted by generic name only
Data 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

27
Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;128:1810–1852.
28 ICU Quick Drug Guide

References
1. Page RL II, O’Bryant CL, Chen D, et al. Drugs that may cause or exacerbate
heart failure: a scientific statement from the American Heart Association.
Circulation. 2016;134:e32–e69.
2. 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;128:1810–1852.
3. Ellison DH, Felker GM. Diuretic treatment in heart failure. N Engl J Med.
2017;377:1964–1975.
3
Adult Advanced Cardiovascular
Life Support

This chapter will review the current recommendations from

the American Heart Association Guidelines for Cardiopulmo-
nary Resuscitation and Emergency Cardiovascular Care.

ASYSTOLE/PULSELESS ELECTRICAL ACTIVITY

• Algorithm (Fig. 3.1)
• Pharmacologic management (Table 3.1)

VENTRICULAR FIBRILLATION/PULSELESS
VENTRICULAR TACHYCARDIA
• Algorithm (Fig. 3.2)
• Pharmacologic management (see Table 3.1)

BRADYCARDIA WITH PULSE

• Algorithm (Fig. 3.3)
• Pharmacologic management (see Table 3.1)

TACHYCARDIA WITH PULSE

• Algorithm (Fig. 3.4)
• Pharmacologic management (see Table 3.1)

POST-CARDIAC ARREST CARE

• Algorithm (Fig. 3.5)
• Pharmacologic management (Table 3.2)
29
Another random document with
no related content on Scribd:
intended to be so,) toward the men who
were disabled in the late war, but a large
majority of the prison survivors are excluded
from a pension under these laws. This
comes partly from the unfriendly spirit in
which the pension department has been
administered for the last six years, and partly
from the peculiar circumstances surrounding
their several cases.
Many paroled prisoners, on reaching the
Union lines were at once sent home on
furlough, without receiving any medical
treatment. The most of these were
afterwards discharged under General Order
No. 77, dated War Department, Washington,
D. C., April 28th, 1865, because physically
unfit for service, and hence there is no
official record whatever as to their disease.
If one of those men applies for a pension,
he is called upon to furnish the affidavit of
some army surgeon who treated him after
his release and prior to discharge, showing
that he then had the disease on which he
now claims a pension. For reasons stated,
this is impossible. The next thing is a call to
furnish an affidavit from some doctor who
treated the man while at home on furlough,
or certainly immediately following his final
discharge, showing that he was then afflicted
with identical disease on which pension is
now claimed. This is generally impossible,
for many reasons.
In most cases the released prisoner felt it
was not medicine he wanted, but the kindly
nursing of mother or wife, and nourishing
food. So no doctor was called, at least for
some months after reaching home. In the
instances where the doctor was called, not
infrequently he cannot now be found, cannot
swear that the soldier had any particular
disease for the first six months after
reaching home, as he was a mere skeleton
from starvation, and it required months of
careful nursing before he had vitality enough
for a disease to manifest itself.
Then again in many cases the poor victim
has never suffered from any particular
disease, but rather from a combination of
numerous ills, the sequence of a wrecked
constitution commonly termed by physicians,
“General Debility.” But the commissioner
refuses to grant a pension on disease save
where the proof is clear and positive of the
contracting of a particular disease while in
the service, of its existence at date of final
discharge, and of its continuous existence
from year to year for each and every year, to
present date.
In most cases it is impossible for a prison
survivor to furnish any such proof, and
hence his application is promptly rejected.
Besides these, there are hundreds of other
obstacles in the way of the surviving prisoner
of war who applies for a pension. One thing
is, he is called upon to prove by comrades
who were in prison with him, the origin and
nature of his disease, and his condition prior
to and at the time of his release. This is
generally impossible, as he was likely to
have but few comrades in prison with whom
he was on intimate terms, and these, if not
now dead, cannot be found, they are men
without sufficient knowledge of anatomy and
physiology, and not one out of a hundred
could conscientiously swear to the origin and
diagnosis of the applicant’s disease. Is it not
ridiculous for the government to insist upon
such preposterous evidence? Which, if
produced in due form, is a rule drawn up by
the applicant’s physican, and sworn to by the
witness—“cum grano salis,”—and in most
cases amounts to perjury for charity’s sake.
Hence, it will be seen the difficulties
surrounding the prison survivor who is
disabled and compelled to apply for a
pension are so numerous and
insurmountable as to shut out a very large
majority of the most needy and deserving
cases from the benefits of the general
pension laws entirely.
We claim, therefore, that as an act of
equal justice to these men, as compared
with other soldiers, there ought to be a law
passed admitting them to pensions on record
or other proof of confinement in a
confederate prison for a prescribed length of
time—such as Bill 4495—introduced by the
Hon. J. Warren Keifer, M. C., of Ohio
provides for. And if this bill is to benefit these
poor sufferers any, it must be passed
speedily, as those who yet remain will, at
best, survive but a few years longer.
This measure is not asked as a pencuniary
compensation for the personal losses these
men sustained, as silver and gold cannot be
weighed as the price for untold sufferings,
but it is asked that they may be partly
relieved from abject want, and their
sufferings alleviated to some extent by
providing them with the necessaries of life,
for nearly all of them are extremely poor,
consequent on the wreck of their physical
and mental powers.
 LIST OF THE DEAD

The following are those who died and were buried

at Andersonville, with full name, Co., Regt., date of
death and No. of grave in the Cemetery at that place,
alphabetically arranged by States. The No. before
each name is the same as marked at the head of the
graves. The list will be found to be very accurate.
ALABAMA.
Sept
7524 Barton Wm Cav 1L 64
1
Berry J M, S’t 1 May
2111 “
A 17
1 Aug
4622 Belle Robert “
A 3
1 Aug
5505 Boobur Wm “
E 13
Sept
8425 Brice J C “ 1L
11
Sept
8147 Guthrie J “ 1 I
8
1 June
2514 Henry P “
F 26
 996 Jones Jno F “ 1 Mar
K 15
1
4715 Mitchell Jno D Aug 4
A
1 Aug
5077 Ponders J Cav
H 8
Aug
5763 Panter R 1L
15
1 Aug
6886 Patterson W D
K 25
1 June
2504 Prett J R
F 3
1
10900 Redman W R Cav Oct 14
G
Aug
4731 Stubbs W 1 I
4
Total 15.

CONNECTICUT.
14 June
2380 Anderson A 64
K 23
16 July
3461 Batchelder Benj
C 17
16 July
3664 Baty John
C 19
14 Aug
7306 Brunkissell H
D 30
14 July
2833 Brennon M
B 3
7 July
3224 Burns Jno
I 12
10414 Blumly E 8 Oct
D 6
Apr
545 Bigelow Wm 7B
14
Nov
11965 Ball H A 3B
11
8 Nov
12089 Brookmeyer T W
H 18
16 Nov
12152 Burke H
D 24
Dec
12209 Bone A 1E
1
14 Oct
10682 Burnham F, Cor
I 11
16 Oct
10690 Barlow O L
E 11
18 Oct
10876 Bennett N
H 13
1 Aug
5806 Brown C H
H 15
Aug
5919 Boyce Wm 7B
17
Aug
6083 Bishop B H Cav 1 I
18
14 Aug
6184 Bushnell Wm
D 19
16 Sept
1763 Bailey F
E 4
21 June
2054 Brewer G E
A 16
6 Aug
5596 Burns B
G 14
5632 Balcomb 11 Aug 64
 B 14
16 Aug
5754 Beers James C
A 15
16 Oct
11636 Birdsell D
D 28
July
4296 Blakeslee H Cav 1L
30
18 July
3900 Bishop A
A 24
14 June
1493 Besannon Peter
B 2
30 July
2720 Babcock R
A 1
July
2818 Baldwin Thos Cav 1L
3
16 June
2256 Bosworth A M
D 21
11 Aug
5132 Bougin John
C 8
Brooks Wm D, 16 Aug
5152
Cor F 9
16 Aug
5308 Bower John
E 11
6 Aug
5452 Bently F
H 12
Aug
5464 Bently James Cav 1 I
12
2 Aug
4830 Blackman A, Cor Art
C 6
16 Sept
7742 Banning J F
E 3
Ballentine 16 Sept
8018
Robert A 6
12408 Bassett J B 11 Jan 65
B 6
Jan
12540 Bohine C 2E
27
Feb
12620 Bennis Charles 7K
8
16 July
3707 Chapin J L 64
A 21
7 July
3949 Cottrell P
C 25
11 July
3941 Clarkson
H 25
July
4367 Culler M 7E
31
18 Aug
4449 Connor D
F 1
16 Aug
4848 Carrier D B
D 6
1 Aug
6060 Cook W H Cav
G 18
16 Aug
6153 Clark H H
F 15
Aug
6846 Clark W 6A
25
10 Aug
5799 Champlain H
F 15
9 Apr
336 Cane John
H 2
Apr
620 Christian A M 1A
19
14 Apr
775 Crawford James
A 28
7316 Chapman M 16 Aug
 E 30
Aug
7348 Cleary P Cav 1B
31
Aug
7395 Campbell Robert 7E
31
16 Aug
7418 Culler M
K 31
16 Sept
7685 Carver John G
B 3
14 Sept
7780 Cain Thomas
G 4
8 Sept
9984 Crossley B
G 29
16 Oct
10272 Coltier W
B 3
11 Oct
11175 Callahan J
I 19
Oct
11361 Candee D M Art 2A 64
23
Mar
25 Dowd F 7 I
8
Aug
7325 Davis W Cav 1L
30
10 July
2813 Davis W
E 3
July
3614 Damery John 6A
20
11 Sept
7597 Diebenthal H
C 2
Sept
8568 Donoway J Cav 1A
12
16 Sept
8769 Dutton W H
K 14
5446 Dugan Charles 16 Aug
K 12
16 Oct
11339 Dean R
H 23
16 Oct
11481 Demmings G A
I 24
18 Nov
11889 Downer S
C 7
16 Nov
11991 Demming B J
G 13
16 July
3482 Emmonds A
K 17
14 July
4437 Easterly Thomas
G 31
Aug
4558 Earnest H C 6 I
2
16 Aug
7346 Ensworth John
C 31
Edwards O J, 8 Sept
7603
Cor G 2
16 Sept
8368 Evans N L
I 10
16 Oct
11608 Emmett W
K 28
Jan
12442 Eaton W 6F 65
12
14 Mar
186 Fluit C W 64
G 27
6 May
1277 Francell Otto
C 22
7 June
2612 Fry S
D 28
4444 Fibbles H 16 Aug
 G 1
Aug
4465 Fisher H 1E
1
Florence J J, 16 Aug
5123
Cor C 8
24 Aug
5382 Fuller H S
H 11
1 Aug
5913 Frisbie Levi Cav
G 17
Aug
5556 Fogg C S’t 7K
13
Sept
8028 Feely M 7 I
6
14 Sept
9089 Filby A
C 18
Oct
10255 Frederick John 7A
3
11 Nov
12188 Fagan P D
A 28
14 July
3028 Gordon John
G 7
9 July
4096 Gray Pat
H 27
July
4974 Grammon Jas Cav 1K
7
Gulterman J, July
4005 1E
Mus 26
16 Aug
5173 Gilmore J
C 9
16 Aug
7057 Gallagher P
D 28
18 Aug
7337 Gott G, Mus
- 30
7592 Goodrich J W 16 Sept
C 2
16 Sept
7646 Graigg W
B 3
11 Sept
9423 Guina H M
G 21
11 Oct
10300 Grady M
B 4
Oct
10397 Gladstone Wm 6K
6
Mar
49 Holt Thomas Cav 1A
15
14 June
2336 Hughes Ed
D 22
16 July
3195 Hitchcock Wm A
C 12
July
3448 Hall Wm G 1K
17
14 July
3559 Holcomb D
D 18
14 May
1350 Hilenthal Jas
C 25
16 July
3033 Haskins Jas
D 8
Aug
5029 Hollister A Cav 1L
8
16 Aug
5162 Hally Thomas
F 9
15 Aug
5352 Hanson F A
I 11
1 Aug
6695 Hodges Geo Cav
H 24
4937 Harwood G 15 Aug
 A 7
17 Aug
6964 Hoyt E S
B 27
16 Aug
7012 Hull M
E 27
16 Aug
7380 Holcomb A A
E 31
16 Sept
7642 Haley W
D 3
16 Sept
7757 Hubbard H D
D 4
18 Sept
8043 Haywood
E 11
16 Sept
8613 Heath I, S’t
K 13
16 Sept
9129 Hall B
G 18
11 Sept
9369 Heart W
F 20
16 Sept
9981 Hurley R A 64
I 29
18 Nov
12086 Hibbard A
D 18
14 Nov
12117 Hancock W
G 22
11 Nov
12163 Hudson Chas
C 26
16 Nov
8148 Hubbard B
A 8
11 Sept
9340 Islay H
- 4
Jamieson 7 April
737
Charles D 26
5221 Johnson John 16 Aug
E 10
11 Aug
7083 Johnson G W
G 28
Jamison J S, Q 1 Aug
7365 Cav
MS - 31
16 Sept
7570 Jones Jno J
B 2
6 Sept
7961 Jones James R
G 6
1 Sept
8502 Johnson F
D 12
16 Nov
11970 Johnson C S
E 12
16 Dec
12340 Johnson W
E 26
14 June
1590 Kingsbury C
K 3
11 Aug
5186 Klineland L
C 9
8 Aug
6374 Kempton B F
G 21
6 Aug
6705 Kershoff B
H 25
14 Aug
6748 Kelley F
I 25
Sept
7749 Kaltry J Cav 1L
3
7 Sept
8065 Kimball H H
H 7
7 Sept
8866 Kohlenburg C
D 15
10233 Kearn T 16 Oct
 A 2
16 July
3401 Lenden H
D 16
10 Aug
5893 Lastry J
I 16
Aug
5499 Lewis J 8E
12
14 Aug
6124 Leonard W
H 19
Lavanaugh W O, 16 Sept
7912
S’t C 5
8 Sept
7956 Linker C
G 6
7 Sept
9219 Lewis G H
G 19
Oct
10228 Lee, farrier Cav 1F
2
6 Mar
74 Mills W J
D 20
14 Mar
119 McCaulley Jas
D 20
14 June
2295 Miller Charles
I 21
16 July
3516 McCord P
G 18
14 July
3644 Miller A
D 19
11 July
3410 Mould James
E 16
15 Aug
3933 McGinnis J W
E 17
July
4079 Miller D Cav 1E
27
4417 Messenger A 16 July
G 31
11 Aug
4492 McLean Wm
F 1
8 Aug
4595 Marshalls B
H 3
16 Aug
5238 Mickallis F
F 10
16 Sept
7852 Miller F D
B
10 Sept
8150 Modger A
I 8
11 Aug
6902 Mape George
B 25
8 July
6240 Marshal L
H 20
1 Sept
7547 Moore A P, S’t Cav
H 2
16 Sept
8446 Mathews S J
K 11
1 Sept
8501 Myers L Cav
- 12
11 Sept
9170 Mertis C
C 18
14 Sept
9321 Milor W, S’t
F 20
16 Aug
5328 Miller H
A 11
16 Aug
6342 Malone John
B 22
Aug
6426 Messey M 7E
22
6451 McGee Thomas 11 Aug
 D 22
Aug
6570 McDavid James 1K
23
11 Aug
6800 Meal John
D 25
14 Oct
10595 McCreieth A
H 10
7 Oct
10914 McKeon J
H 14
16 Oct
11487 Murphy W
C 26
11 Oct
11538 McDowell J
D 27
5 Nov
12134 Montjoy T
C 23
16 Aug
5044 Nichols C
G 8
7 Aug
6222 Northrop John
D 20
1 Aug
7331 North S S, S’t Cav
D 30
Oct
10895 Nichols M 7 I 64
14
Aug
4565 Orton H C 6 I
9
Sept
7511 Olena R Cav 1E
1
14 Sept
8276 Orr A
H 14
14 July
2960 Pendalton W
C 6
14 July
3808 Pompey C
B 24
4356 Parker S B 10 July
B 31
1 July
3803 Phelps S G
H 22
16 Aug
4934 Pimble A
I 7
11 Aug
5002 Plum James
G 8
Aug
5386 Patchey J Cav 1 I
12
16 Sept
7487 Post C, S’t
K 1
7 Sept
7688 Potache A
G 3
Sept
9248 Phillips J I 8B
19
Padfrey 8 Sept
9444
Sylvanus H 21
7 Sept
9533 Painter N P
C 22
Oct
10676 Puritan O Cav 1L
11
7 Oct
11616 Peir A
D 28
July
2804 Ruther J, S’t Cav 1E
3
2 July
2871 Reed H H Art
H 4
10 July
3674 Risley E, S’t
B 20
11 Aug
4636 Reins Wm
I 3
5902 Ross D 10 Aug