Critical Care Nursing 2023-2024

‫ق سم تمريض العنايه‬
‫الحرجه والطوارئ‬
THERIOTICAL MANIUAL FOR CRITICAL CARE
REPARED BY
ALL STAFF MEMBERS OF CRITICAL CARE AND
EMERGENCY NURSING DEPARTMENT
2023-2024
7th Edition
‫‪Critical Care and Emergency Nursing‬‬
‫رؤية الكلية‬
‫تتطلع كلية تمريض جامعة أسيوط للتميز والريادة في مجاالت التمريض‬
‫والبحث العلمي والخدمة المجتمعية‪.‬‬
‫رسالة الكلية‬
‫كلية التمريض جامعة أسيوط مؤسسة حكومية تعليمية بحثية تعمل على إعداد كوادر‬
‫مؤهلة علميا ً ومهاريا ً ومهنيا ً قادرة على االبتكار والمنافسة فى سوق العمل والتصدي‬
‫لمشكالت المجتمع فى مجاالت التمريض وذلك من خالل برامج تعليمية تستند على‬
‫معايير أكاديمية معتمدة وبحث علمي يواكب متطلبات الحاضر والمستقبل ويراعى‬
‫معايير الجودة ‪ .‬وتقوم الكلية بتأدية رسالتها في إطار من القيم والتقاليد الجامعية‬
‫المتعارف عليها‪.‬‬
‫األهداف االستراتيجية للكلية‬
‫‪ ‬لتطوير المستمر للقدرة التعليمية لمرحلة البكالوريوس‪.‬‬

‫‪ ‬تعزيز الدعم الطالبي واألنشطة الطالبية‪.‬‬
‫‪ ‬تطوير العملية التعليمية فى مرحلة الدراسات العليا‪.‬‬
‫‪ ‬تحديث الخطة البحثية للكلية‪.‬‬
‫‪ ‬متابعة ورعاية الخريجين‪.‬‬
‫‪ ‬تعزيز دور الكلية فى المشاركة المجتمعية‪.‬‬
‫‪ ‬تطوير أداء العاملين بالجهاز اإلداري و القيادات األكاديمية بالكلية ‪.‬‬
‫‪ ‬تطوير مستوى أداء وحدة ضمان الجودة‪.‬‬
‫‪ ‬التقويم المستمر للقطاعات الثالث بالكلية ( قطاع شئون التعليم و الطالب‬
‫‪ -‬قطاع شئون الدراسات العليا و البحث العلمي‪ -‬قطاع شئون خدمة المجتمع‬
‫و تنمية البيئة)‪.‬‬
‫‪ii‬‬
Critical Care and Emergency Nursing
Content
No. Subject Pag.
Unit 1: Introduction
1 Sustainable Development 5
2 Overview of Artificial Intelligence (AI) 11
3 Climate change in critical ill patients 15
4 COVID-19 in ICU 18
Unit 2: The concept critical care nursing practice
5 Scope of Critical Care and Emergency Nursing 22
Practice
6 Ethical Issues I n Critical Care Nursing 31
7 Acid base balance 39
Unit 3: Respiratory system
8 Acute Respiratory Failure 51
9 Mechanical ventilation and weaning 60
10 Non-invasive ventilation 90
10 Pulmonary Edema 95
11 Acute Respiratory Distress Syndrome 100
12 Pulmonary Embolism 109
Unit 4: Cardiovascular system
13 Acute Heart failure (HF) 114
14 Acute Coronary Syndrome 130
15 Cardiac dysrhythmia 153
iii
Unit 5: Gastrointestinal system

16 Acute liver Failure 171
17 Sever Acute Pancreatitis 185
Unit 6: Renal system
18 Acute kidney Injury 194
Unit 7: Nervous system
19 Head injury 208
20 Shock 221
Unit 8: Multisystem dysfunction
21 Spinal Cord Injury 245
Unit 9: Endocrine system
22 Diabetic crisis 261
Unit 10: Special population in critical care
23 Organ transplantation 269
24 Safety in critical care units 282
iv
Sustainable Development
Learning objectives based on competence:

1. Define Sustainable Development
2. List Sustainable Development goal
3. Correlate Sustainable Development goals with critical care
nursing
Introduction:
The Sustainable Development Goals (SDGs) are a call for
action by all countries – poor, rich and middle-income –
to promote prosperity while protecting the planet. They
recognize that ending poverty must go hand-in-hand with
strategies that build economic growth and address a range
of social needs including education, health, social
protection, and job opportunities, while tackling climate
change and environmental protection.
In September 2015, the Unit Nation General Assembly adopted

the new development agenda: transforming our world: the 2030
agenda for sustainable development. Comprising 17 SDGs, the
2030 Agenda integrates all three dimensions of sustainable
development (economic, social and environmental) around the
themes of people, planet, prosperity, peace and partnership. The
5
Sustainable Development Goals were built on the achievements

of the millennium development goals but are broader, deeper
and far more ambitious in scope.
Definition of the Sustainable Development Goals: -

A set of plans that were made by the United Nations in 2000 to
try to reduce hunger and improve the environment and other
conditions in poor countries around the world.
Purpose of Sustainable Development:

1. To compete the political, social, and economical
challenges that face our future

2. Higher the standard of living
3. Improve the quality of life
4. Enhance wellbeing for everyone
5. Satisfy the needs of human without compromising the
ability of future generation to meet their own needs
17 Sustainable Development Goals 2015 to 2030:

Goal 1: End poverty in all its forms everywhere
Goal 2: End hunger, achieve food security and improved
nutrition and promote sustainable agriculture.
6
Goal 3: Ensure healthy lives and promote well-being for all at

all ages.
Goal 4: Ensure inclusive and equitable quality education and
promote lifelong learning opportunities for all.
Goal 5: Achieve gender equality and empower all women and
girls
Goal 6: Ensure availability and sustainable management of
clean water and sanitation for all.
Goal 7: Ensure access to affordable, reliable, sustainable and
modern energy for all.
Goal 8: Promote sustained, inclusive and sustainable economic
growth and productive employment and decent work for all.
Goal 9: Build infrastructure, promote inclusive and sustainable
industrialization and foster innovation.
Goal 10: Reduce inequality within and among countries
Goal 11: Make sustainable cities and human settlements
inclusive, safe and sustainable.
Goal 12: Ensure sustainable consumption and production
patterns
Goal 13: Take urgent action to combat climate change and its
impacts.
Goal 14: Conserve and sustainably use the oceans, seas and
marine resources.
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Goal 15: Protect and promote sustainable use of terrestrial

ecosystems, sustainably manage forests, and halt land
degradation (life on land)
Goal 16: Promote inclusive societies for sustainable
development; provide access to justice for all.
Goal 17: Strengthen the means of implementation and the
global partnership for sustainable development.
Goal 5 Targets: -
 By 2030, ensure that all girls and boys complete free,
equitable and quality primary and secondary education
leading to relevant effective learning outcomes.
 By 2030, eliminate gender disparities in education and

ensure equal access to all levels of education and
vocational training for the vulnerable, including persons
with disabilities, indigenous peoples and children in
vulnerable situations.
 Build and upgrade education facilities that are child,

disability and gender sensitive and provide safe,
nonviolent, inclusive and effective learning environments
for all.
8
Sustainable Development in critical care nursing education

- Education enables upward socioeconomic mobility and is
a key to escaping poverty. Over the past decade, major
progress was made towards increasing access to
education and school enrollment rates at all levels,
particularly for girls. Nevertheless, about 260 million
children were still out of school in 2018-nearly one fifth
of the global population in that age group. And more than
half of all children and adolescents worldwide are not
meeting minimum proficiency standards in reading and
mathematics.
- In 2020, as the COVID-19 pandemic spread across the
globe, a majority of countries announced the temporary
closure of schools, impacting more than 91% of students
worldwide. By April 2020, close to 1.6 billion children
and youth were out of school. And nearly 369 million
children who rely on school meals needed to look to other
sources for daily nutrition.
- Never before have so many children been out of school at
the same time, disrupting learning and upending lives,
especially the most vulnerable and marginalized. The
global pandemic has far-reaching consequences that may
9
jeopardize hard won gains made in improving global

education.
Example for Sustainable Development ins relation to health

1-COVID-19 Response: -
- In an effort to foster international collaboration and
ensure that education never stops, UNESCO is mounting
a response with a set of initiatives that include the global
monitoring of national and localized school closures.
- To protect the well-being of children and ensure they
have access to continued learning, UNESCO in March
2020 launched the COVID-19 Global Education
Coalition, a multi-sector partnership between the UN
family, civil society organizations, media and IT partners
to design and deploy innovative solutions. Together they
help countries tackle content and connectivity gaps, and
facilitate inclusive learning opportunities for children and
youth during this period of sudden and unprecedented
educational disruption.
2- 3D CARTO ablation use for suppression of "Complex
Cardiac Arrhythmia: One of the new innovation that is very
important for satisfaction of patient needs through suppression
of some complex Arrhythmias as Ventricular ectopics,
Tachycardia, Atrial flutter and tachycardia , Atrial fibrillation.
This use reflect Continuing the development of the medical
system within hospitals and giving special attention to the
medical sector in its various medical departments.
10
Overview of Artificial Intelligence (AI)

Learning objectives based on competences:
1. Define of Artificial Intelligence
2. Mention the importance of Artificial Intelligence
3. List of building AI systems:
4. Differentiate the applications of AI
Definition:
Artificial Intelligence (AI) is a branch of Science which deals
with helping machines find solutions to complex problems in a
more human-like fashion. AI is unique, sharing borders with
Mathematics, Computer Science, Philosophy, Psychology,
Biology, Cognitive Science and many others.
A more or less flexible or efficient approach
Importance of AI
Game Playing
Speech Recognition
Understanding Natural Language
Computer Vision
the inputs to the human eye and computers' TV cameras are two
dimensional.
Expert Systems
11
Building AI Systems:
1) Perception Intelligent biological systems are physically

embodied in the world and experience the world through their
sensors (senses ) For a medical diagnosis system, perception is
the set of symptoms and test results that have been obtained and
input to the system manually.
2) Reasoning
Includes areas of knowledge representation, problem solving,
decision theory, planning, game theory, machine learning,
uncertainty reasoning, etc.
3) Action Biological systems interact within their environment
by actuation, speech, etc. All behavior is centered around
actions in the world.
12
The applications of AI :
Consumer Marketing
- Have you ever used any kind of credit/ATM/store card while
shopping?
-All of this information is recorded digitally
-Algorithms (“data mining”) search data for patterns based on
mathematical theories of learning
Identification Technologies
-ID cards e.g., ATM cards can be a nuisance and security risk:
cards can be lost, stolen, passwords forgotten, Biometric
Identification, walk up to a locked door
13
– Camera, Fingerprint device, Microphone, Computer uses

biometric signature for identification, Face, eyes, fingerprints,
voice pattern
– This works by comparing data from person at door with stored
library
Security Detection
– like to learn the “signature” of each authorized user
– can identify non-authorized users, record user’s commands
and time intervals , characterize the patterns for each user
Machine Translation
-Language problems in international business e.g., at a meeting
of Japanese, Korean, Vietnamese and Swedish investors,
Teaching and learning methods
Medical monitoring and diagnosis
Genetic Programming
14
Climate change in critical ill patients

1. Define climate changes and global worming
2. Determine the effect of climate change and global
warming on health
3. Mention Challenges for intensive care and nursing action
to overcome this problem.
Global warming” refers to the rise in global temperatures due

mainly to the increasing concentrations of greenhouse gases in
the atmosphere.
Greenhouse gases: any gas that has the property of

absorbing infrared radiation emitted from Earth’s surface and
reradiating it back to Earth’s surface)
“Climate change” refers to the increasing changes in the

measures of climate over a long period of time – including
precipitation, temperature, and wind patterns
15
Influences of climate change and global warming on health

with potential impact on intensive care
Challenges for intensive care medicine in the context

of global warming and climate changes
Challenges Nursing actions

Increasing number of Increase capacity of ICU
critically ill patients due to beds, especially in coastal
heat waves, natural disasters, regions or megacities
air pollution or forest fire
16
Mass casualties of critically Implement a ‘reserve’ of staff

ill patients due to rapid and ICU beds, which can be
weather changes, foods, heat easily activated
attacks
Increasing incidence of Provide sufficient capacities
‘uncommon’ infectious or of patient isolation Instruct
non-infectious diseases the ICU staff in the diagnosis
and management of
‘uncommon’ diseases
Increasing number of Provide sufficient machines

nephropathy during heat for renal replacement
waves
17
COVID-19 in ICU
1. Mention risk factors associated with SARs
2. Relate the etiology and pathophysiology of SARs
3. Describe the WHO guidelines for patient with SARs
4. Differentiate the clinical characteristics between
SARs and ARDS
5. Write laboratory studies for SARs
6. Deign collaborative nursing care of the patient SARs
Introduction
 Coronavirus disease 2019 (COVID-19) is a respiratory
tract infection caused by a newly emergent coronavirus,
that was first recognized in Wuhan, China, in December
2019. Genetic sequencing of the virus suggests that it is a
beta coronavirus closely linked to the SARS virus.
Definition of SARS : A suspect case is a person presenting with

1. High fever (> 38_C) and cough or difficulty of breathing.
Pathophysiology of SARS
 Pathological studies of patients who died showed
alveolar damage in the pulmonary tree, focal unilateral
interstitial infiltrates of the lung, progressing to more
18
generalized patchy interstitial infiltrates to bilateral

patchy consolidation of the lungs within a week,
lymphopenia, thrombocytopenia, elevated lactase
dehydrogenase and creatinine kinase levels; however,
the significance of these abnormalities in patients with
SARS is still unclear.
 four most important factors related to the fatality were
old age, comorbid chronic illness, delay in
presentation for treatment and severity of
pneumonia
Diagnosis of SARS by clinical presentation
1. Presence of new radiological infiltrates of the lungs
compatible with pneumonia, and
2. fever >38_C, or history of fever any time in the last 2 days,
and
3. chest X-ray shows lobar consolidation, and
4. the pathogen is already identified. and at least two of the
following:
 3.1. chills any time in the last 2 days,
 3.2. new or increased cough,
 3.3. general malaise,
 3.4. typical physical signs of consolidation of the lungs,
19
 3.5. known history of exposure. If there was no history

of exposure, exclusion is then considered if:
WHO guidelines
1- Screening and triage: early recognition of patients with SARI
associated with COVID-19
2-Immediate implementation of appropriate infection
prevention and control ( IPC) measures
3-Collection of specimens for laboratory diagnosis
4-Management of mild COVID-19: symptomatic treatment and
monitoring
5- Management of severe COVID-19: oxygen therapy and
monitoring
6-Management of severe COVID-19: treatment of co-infections
7. Management of critical COVID-19: acute respiratory distress
syndrome ( see ARDS)
8- Management of critical illness and COVID-19: prevention of
complications
9- Management of critical illness and COVID-19: septic shock
(see shock)
10-Adjunctive therapies for COVID-19: corticosteroids do not
routinely give systemic corticosteroids for treatment of viral
pneumonia outside clinical trials
20
Treatment modalities in ICU for covid19

1. Management of respiratory failure
2. Oxygen therapy and invasive MV
3. Awake prone position
4. Noninvasive MV and high flow nasal cannula
5. Extracorporeal membrane oxygenation
6. Fluid therapy
7. Antibiotic
8. Thromboprophylaxis
9. Supportive therapies
corticosteroid,Ivermectin,remdesivir,plasma
pharesis,blood purification devices
10.Infection control measures
11.Nutritional support
12.Family/public support
13.Vaccinate all health care personnel as prevention.
21
Scope of Critical Care and Emergency Nursing
Learning Objectives based on competence:
1- Describe scope of critical care and emergency nursing.

2- State goals of critical care nursing.
3- Differentiate between physical and non-physical needs
of critical ill patient.
4- Differentiate between different roles of critical care and
emergency nursing.
5- Summarize principles of emergency Nursing.
6- Explore qualities of Emergency nurse.
7- Explain function of emergency nurse.
Definitions
 Critical care nursing: is the delivery of specialized care
to critically ill patients who have life-threatening illnesses
or injuries, have complex needs, and require intensive
nursing care.
 The American Association of Critical Care Nurses
(AACN) defines acute and critical care nursing as the
specialty that manages human responses to actual or
potential life-threatening problems.
22
Goal of Critical Care Nursing

Nurses rely on a body of specialized knowledge, skills,
and abilities to:
- Restore, support, promote, and maintain the physiologic
and psychosocial stability of patients of all ages across
the life span.
- Assimilate and prioritize information in order to take
immediate and decisive evidence-based, patient-focused
action.
- Anticipate and respond with confidence and adapt to
rapidly changing patient conditions.
- Respond to the unique needs of patients and families
coping with unanticipated treatment as well as quality-of-
life and end-of-life decisions.
- Establish and maintain safe, respectful, healing, and
caring environments.
- Use health care interventions designed to restore,
rehabilitate, cure, maintain, or palliate for patients of all
ages across the life span.
23
Scope of Critical Care Nursing practice

- The scope of critical care nursing practice is described as a
dynamic process with three components:
A. The critically ill patients and their significant social
relationship.
B. The critical care nurse.
C. The environment where critical care nursing is
practiced.
A. Critically ill patients: are those at high risk of actual or
potential life-threatening health problems. The needs of
these patients require continuous assessment and
intervention to restore health and prevent complications.
 The needs of the critically ill

These needs may be categorized as physical or non-
physical
1- Physical needs:-
 Physical needs are equated with basic physiological or
biological needs for air, nutrition, and elimination.
2- Non-physical needs:-
 May include social, and psychological needs. Social
integrity (self-esteem), information, and communications
are also included.
24
 The comfort and support provided by social relationships

can enhance effective coping. Therefore, the concept of
the critically ill patient includes the interaction and
impact of the patients’ family and / or significant others.
B. A critical care nurse : is a licensed professional nurse who

is responsible for ensuring that acutely and critically ill
patients and their families receive optimal care.
Role of critical care nurse:

Critical care nurses fill many roles in the critical care setting,
such as
 Staff nurses
 Nurse-educators
 Nurse-managers
 Case managers
 Clinical nurse specialists
 Nurse practitioners
 Nurse researchers.
25
C. Critical care unit : is a specially designed and equipped

facility staffed by skilled personnel to provide effective and safe
care for dependent patients with a life threatening problem.
- The safety of both patients and staff in the critical care unit is
a primary consideration in designing of critical care unit in
which critical care nursing is carried out.
- The critical care environment must contain the following:
26
 Resources that constantly support the direct

interaction between the critical care nurse and the
critically ill patient. E.g. emergency equipment and
supplies.
 The presence and application of technology as a
common component of patient management is
another key feature of critical care nursing practice.
Definitions:
 Emergency Nursing: is a specialty of nursing focusing
on the care of patients with medical emergency who
require prompt medical attention to avoid long term
disability or death.
 Emergency patient: Patient with serious problems and
needs immediately or timely nursing and medical
intervention.
Principles of Emergency Nursing:

Principles of Emergency Nursing includes –
1. Guiding principles for emergency care
 Quick assessment of the casualty and situation to institute
life saving measures.
 Keep casualty in dorsal position and cover his/her body
with whatever cloth is available to prevent heat loss.
27
 Avoid unnecessary handling except to remove the victim

from additional danger.
 Give first aid to the injured part.
 Observed and keep a medical record of the casualty’s
initial condition till he reaches the hospital.
 Reassurance should be given to the victim and relatives
that he/she is in safe hands.
 Prevent people crowding near the victim; allow fresh air
to circulate around the victim.
 Do not give water to drink to the victims with abdominal
injuries may requiring immediate surgery.
 Make arrangements for safe transportation to hospital
after first aid.
 In few emergencies like unconsciousness, uncontrollable
bleeding, respiratory difficulties etc., require coordinated
efforts for speedy transportation for medical facilities
with simultaneous lifesaving appropriate care is
important.
28
2. Principles of emergency management

 Maintain patent airway & provide adequate ventilation
employing resuscitation measures when necessary.
 Control hemorrhage & its consequences.
 Evaluate and restore cardiac output.
 Prevent and treat shock, maintain or restore effective
circulation.
 Carry out a rapid initial and ongoing physical
examination.
 Assess the patient consciousness, whether the patient can
follow commands or not, evaluate the size & reactivity of
pupils.
 Start ECG monitoring if appropriate.
 Apply Splint of suspected fractures sites including
cervical spines in patients with head injuries.
 Protect wounds with sterile dressings.
 Start a flow sheet of patient’s vital sign, neurological
state, to guide in decision-making.
29
Qualities of Emergency Nurse

The Nurses working in Emergency or trauma units must have
specialized skills in handling emergencies. Some of these skills
are:
 Observation and assessment skills.
 Quick decision making skills.
 Patient care skills in emergency situations.
 Emotional stability.
 Self-confidence with ability to lead and control the
patients as well as attendants.
 Recording and reporting skills.
30
Ethical issues in Critical Care Nursing

1-Differentiate between ethics and morals
2. Name and describe ethical principles applicable to clinical
ethics
3. Explore nursing obligation and patients' rights according to
ethical principles in critical care
4. Explain code of ethics for critical care nurses
5. Describe Ethics and the Nursing Process
6. Explain SFNO model for deliberation of ethical problems
Introduction
Critical care nurses need a strong understanding of
professional nursing ethics and ethical principles and the ability
to use a decision-making model to guide nursing actions.
Definitions
Morals versus Ethics
 Morals: are traditions of belief about right or wrong
human behavior. Informed by individual and group
values, morality consists of standards of conduct that
include moral principles, rules, virtues, rights, and
responsibilities.
31
 Ethics: is a generic term for the reasoned inquiry and

understanding of a moral life, in other words, a systematic
examination of morality.
 Ethical problems: (also called ethical or moral
dilemmas) occur only when there is some conflict
surrounding an ethical decision.
Ethical Principles:
 Respect for persons\autonomy
Definition: Respect for the inherent and unconditional
dignity of persons and to freely exercise choice about what
happens to them.
 Beneficence
Definition: Promoting and maximizing benefit.
 Non-maleficence
Definition: Avoiding and minimizing harm
 Justice
Definition: Equitable distribution of benefits and burdens
and scarce resources.
32
Ethical Principles in Critical Care
Principles Example Nursing Obligations Patient Rights
-Respect for Truth-telling, provision of Self-determination;

persons\autonomy complete, accurate, and privacy;
understandable information; confidentiality
maintaining privacy and
confidentiality; self-reflection to
minimize bias
-Beneficence Competent practice; advocacy for Appropriate,
patient safety; acting for best evidence-based care;
interest of the patient effective care
-Non-maleficence Careful practice; self-reflection to Safe care and

minimize errors treatment
-Justice Advocacy for equitable public Access to care;

policy in health care; self- equitable care
reflection and advocacy to
minimize disparities in care
33
Nursing code of Ethics

The nursing code of ethics contains statements and directives
for ethical nursing behavior. The American Nurses Association
(ANA) Code of Ethics for Nurses, updated in 2015, provides the
major source of ethical guidance for the nursing profession. The
nine statements of the code are presented in this box.
34
Causes of ethical problems in critical care

 The critical care nurse encounters ethical issues on a daily
basis that occur when there is
(1) Conflict between the right action and the ability to take it,
(2) Uncertainty about the right action, or
(3) Conflict about which of several right actions is most ethical.
 To facilitate the ethical decision-making process, a model
or framework should be used. There are numerous ethical
decision-making models as mapped onto the nursing
process.
Ethics and the Nursing Process

 Initial Steps: Clarify and Define Nature of the Problem
• What is the crisis (or dilemma) requiring a decision?
 Assessment: Identify Key Facts and Values That Are
Applicable
• What are the crucial facts of the case?
• What moral principles are at issue here?
• What decision-making procedure is appropriate?
 Planning: Explore Available and Best Means to Reach
Our Goal
• What is the primary aim or good for which we are acting?
35
• What objectives, benefits, and moral goals are

achievable?
• What previous cases or contingencies should we take
into account?
 Implementation: Take Decisive and Effective Action to
Implement Plan
• How do we begin, continue, and finish the process of
intervention?
• How do we assess costs/benefits of the intervention?
• How do we monitor success/failure in the overall
process?
 Evaluation: Evaluate Progress and Outcomes with
Planned Objectives
• What means have we set up for debriefing and feedback?
• Have we used the “right” means to a “good” end?
• How do we review the pros/cons for the action taken?
 Final Steps: In Retrospect, Apply the Following Tests
• Could I/we provide a reasonable ethical justification for
the course of action taken?
• Can I/we identify what we have learned from applying
this model to decision making?
• How do we integrate this learning into the next decision-
making cycle?
36
SFNO model for deliberation of ethical problems

SFNO is an easily memorized acronym that stands for
S: Stakeholders, F: Facts, N: Norms, O: Options.
To illustrate the use of this model, consider the following
straightforward example. An older-adult woman with chronic
obstructive pulmonary disease (COPD) is on a ventilator,
receiving artificial nutrition through a gastric tube, intravenous
fluids, and antibiotics for pneumonia. The patient does not have
capacity and does not have an advance directive. The patient’s
only child, an adult daughter, approaches the team and says the
patient would not want to remain on the ventilator and requests
that it be withdrawn. The treating physician believes that after
the pneumonia is treated, it may be possible to wean the patient
from the ventilator. The initial question is whether withdrawing
the ventilator is ethically appropriate.
 Stakeholders:
 The patient, the patient’s adult daughter, and extended
family all are stakeholders. The nurses, other health care
team members, and the health system are also
stakeholders.
 Facts:
 The underlying severity of the COPD.
 The patient’s prognosis if the pneumonia is treated.
37
 The degree to which the patient is in pain or is suffering.

 The likelihood of suffering both with continued
ventilation and if the ventilation is withdrawn.
 The time in which evidence of improvement from the
pneumonia is expected.
 The anticipated likelihood of successfully weaning the
patient from the ventilator.
 Norms:
 Respect for persons means that the patient’s autonomous
decisions should be honored.
 Beneficence requires the caregivers to maximize
benefit.
 Nonmaleficence requires the caregivers to minimize
harm.
 Options:
 The team could do nothing (i.e., maintain the ventilation).
 The team could also begin weaning the ventilator but
continue the other treatments. For example, if
improvement from the pneumonia is expected after a few
additional days of intravenous antibiotics,
 The team could work with the daughter to reach
agreement to postpone removal for a few days and
reassess the situation in light of the facts at that time.
38
Acid-Base Balance
Objectives based on competence:
1- Define acid/base disorders.
2- Interpret PH scale.
3- Analyze arterial blood gas.
4- Summarize mechanisms to maintain acid base balance.
5- Comparison between causes of respiratory acidosis and
respiratory alkalosis.
6- Comparison between causes of metabolic acidosis and
metabolic alkalosis.
7- Demonstrate appropriate management of respiratory
acidosis or respiratory alkalosis.
8- Demonstrate appropriate management of metabolic
acidosis or metabolic alkalosis.
Acid/base definitions: Acids can release hydrogen ions; base

(alkali) can accept (buffer) hydrogen ions. Strong acids (e.g.
hydrochloric) release many free hydrogen ions, whereas weak
acids (e.g. carbonic) release few. hydrogen ions (H+), a
positively charged ion (cation), can be buffered by a negatively
charged ion (anion), such as bicarbonate (Hco3-).
39
PH measurement:
Chemically, the pH scale ranges from 0-14, making pH
7 chemically neutral. Arterial blood is normally slightly
alkaline (pH 7.35- 7.45). Blood pH < 7.35 is acidotic, while
pH > 7.45 is alkalotic. Arterial pH below 7.0 usually leads to
coma and death, while levels above 7.8 over stimulate the
nervous system, causing convulsions and respiratory arrest.
Acid/base balance is controlled through these
functions: Respiratory and metabolic (renal function,
chemical buffers).
ABG Outcomes
- PH: hydrogen ion concentration of blood and is an indicator
of Acid-Base status.
PH 7.35-7.45
↓ PH acidosis
↑ PH alkalosis
- PaCO2:- the partial pressure of carbon dioxide in the arterial
blood.
PaCO2 35-45 mmHg
↓ PaCO2 respiratory alkalosis
↑ PaCO2 respiratory acidosis
- HCO3:- the serum bicarbonate, which is the major component
of the renal compensatory mechanism.
40
HCO3 22- 26 mEq/L

↓ HCO3 metabolic acidosis
↑ HCO3 metabolic alkalosis
- BE: - base excess reflects an increase or decrease in total
buffer base.
BE: - -2 to +2 mEq/L
↓ BE metabolic acidosis
↑ BE metabolic alkalosis
- PaO2:- the partial pressure of oxygen in the arterial blood
PaO2:-80-100 mmHg
- SaO2:-the saturation of hemoglobin by oxygen
SaO2: 95- 99%
Values less than 60 may result in lactic acid production
and metabolic acidosis because of anaerobic metabolism
brought on by hypoxemia.
Mechanisms to maintain acid base balance:
1. buffer system
2. respiratory regulations
3. renal regulations
Buffer system: Chemical buffers, are substances are that
minimize changes in pH when either acids or bases are added.
Buffer systems occupy various locations in the body. Proteins
41
and phosphates are buffers in the cells, hemoglobin is a buffer

in red blood cells, and bicarbonate & proteins again, are buffers
in the extracellular fluid. The combination of all the buffer
system is called the total buffer base.
Respiratory regulations: Respiratory system controls

carbon dioixide tension of the blood by regulating alveolar
ventilation, that may very quickly correct an acid-base
disturbance through hypoventilation or hyperventilation.
Renal regulations: the kidneys defend blood pH by

controlling bicarbonate concentration. This is accomplished by
excretion of hydrogen ions in the urine when the blood is too
acidic and excretion of bicarbonate in the urine when the blood
is too alkaline. It may take hours to days for the kidney to affect
pH.
Respiratory acidosis
In respiratory acidosis, the pulmonary system can't rid the

body of enough carbon dioxide (CO2) to maintain a healthy pH
(hydrogen ion H+) balance.
Causes:
 neuromuscular problems
- Guillain-Barre syndrome -Myasthenia gravis
- Poliomyelitis -Spinal cord injury
42
 Respiratory center depression

- CNS trauma -Brain lesions
- Obesity -Primary hypoventilation
- Use of certain drugs
 Lung diseases
- Respiratory infection -COPD
- Acute asthma attacks -Chronic
bronchitis
- ARDS -Pulmonary
edema
- Chest trauma
 Airway obstruction
- Retained secretions -Tumors
- Anaphylaxis -Laryngeal spasm
- Lung diseases that alter alveolar ventilation.
43
Signs and symptoms: -
Diagnostic test:
 ABG findings indicative of respiratory acidosis
 Chest X-ray
o Evidence of COPD
o Evidence of pneumonia, pneumothorax or other
causes
 Electrolyte levels
o Potassium level greater than 5 mEq/L
 Other blood test
44
o Drug screening that may detect overdose

Management;
 Maintain a patent airway
 Give bronchodilator to open constricted airways
 Administer supplemental oxygen as needed. Watch for
worsening hypercapnia in patient with COPD.
 Give an antibiotic to treat infection
 Perform chest physiotherapy to remove secretions from
the lung
 Perform tracheal suctioning, incentive spirometry, and
postural drainage, and assist with coughing and deep
breathing as needed.
 Monitor for changes in the patient's cardiac rhythm and
respiratory pattern.
 Closely observe the patient's neurologic status and report
significant changes.
 Promote fluid intake and carefully track fluid intake and
output.
Respiratory Alkalosis
It results from alveolar hyperventilation and hypocapnia.
In Respiratory Alkalosis, pH is greater than 7.45, and partial
pressure of arterial carbon dioxide Pao2 is less than 35 mmHg.
45
Causes:
 Hyperventilation
o Anxiety, Pain, salicylates intoxication (early onset)
o Use of certain drugs
 Hypermetabolic states
o Fever, Liver failure, Early sepsis
 Conditions that affect respiratory control center
 Other causes
o Acute hypoxia secondary to high altitude
o Pulmonary disease, Severe anemia, Pulmonary
embolus
o Hypotension
46
Signs and symptoms:
 Diagnostic test:
o ABG findings indicative of respiratory Alkalosis
o ECG changes, arrhythmia
o Characteristics indications of hypokalemia,
hypocalcemia, or hypomagnesemia
o Electrolyte levels
o Serum calcium level below normal
o Serum Potassium level below normal
47
o Serum magnesium level below normal

o Serum chloride level below normal
o Other blood test: Toxicology screening with evidence of
salicylate poisoning
Management:
 Correct the underlying cause, for example by treating

Salicylates intoxication or Early sepsis
 Administer supplemental oxygen as needed.
 Give sedative or anxiolytic if anxiety is the cause.
 If the cause is iatrogenic, adjust the ventilator settings
 Monitor vital signs. Report changes in neurologic,
neuromuscular, or cardiovascular functioning.
 Monitor ABG and serum electrolyte levels and
immediately report any changes
 Instituste seizure precautions as needed.
Metabolic acidosis
Causes:
1. HCO3 depletion from renal disease, diarrhea, or small
bowel fistula.
2. Excessive production of organic acids from; hepatic
disease, or endocrine disease (disorders) as diabetes
mellitus and drug intoxication.
3. In adequate excretion of acids from renal disease.
48
Signs and symptoms:

 Rapid, deep respiration  headache
 fruity breath  lethargy  drowsiness
 fatigue  coma if sever  vomiting
Management: it is aimed at correcting the metabolic defect:
 Maintain tissue perfusion and oxygenation
 IV bicarbonate
 Potassium management (Hyperkalemia may also occur
due to shift of potassium out of the cells. Hypokalemia
may occur once the acidosis is corrected.(
Metabolic Alkalosis (HCO3 retention, acid loss)
Possible causes:-
1. loss of hydrochloric acid (HCL) from prolonged vomiting
or gastric suctioning
2. potassium loss from increased renal excretion
3. Metabolic alkalosis may be caused by consuming
excessive amount of certain medications or supplements
such as:
- Antacids, which often contain the chemical sodium
bicarbonate.
- Excessive alkali ingestion (baking soda and
antiacid).
- Diuretics or water pills.
49
- Certain laxatives.
- Steroids.
Signs and symptoms:
 slow, shallow respiration (compensated),
hypertonic muscle, tetany, restlessness,
convulsion, confusion, coma
Management: It is aimed at treating the underlying disorder

 Metabolic alkalosis treatment uses an intravenous (IV)
line to deliver fluid and other substances, such as:
- IV infusion to restore normal fluid volume.
- Chloride supplementation for the kidney to absorb
sodium with chloride (allowing the excretion of
excess bicarbonate(.
- Potassium replacement.
- Magnesium replacement.
- Stopping the medications that caused the
condition, for example high doses of diuretics.
50
Acute Respiratory Failure

1-Define acute respiratory failure.
2-Compare between etiology and pathophysiology of two types
of acute respiratory failure.
3-Differentiate between S&S of two types of acute respiratory
failure.
4-Predicte clinical manifestation of respiratory failure.
5-Summaize a nursing diagnoses for management acute
respiratory failure.
6- Design a collaborative nursing care plan for management
acute respiratory failure.
Definition: Acute Respiratory failure results when one or both

of these gas-exchanging functions are inadequate (e.g.,
insufficient O2 is transferred to the blood or inadequate CO2 is
removed from the lungs)
Types of Acute Respiratory Failure: classified as hypoxemic

or hypercapnic.
1. Hypoxemic respiratory failure is also referred to as
oxygenation failure because the primary problem is inadequate
O2 transfer between the alveoli and the pulmonary capillaries.
51
2. Hypercapnic respiratory failure is also referred to as

ventilator failure because the primary problem is insufficient
CO2 removal.
Etiology and Pathophysiology

A. Hypoxemic Respiratory Failure. Four physiologic
mechanisms may cause hypoxemia and subsequent hypoxemic
respiratory failure: (1) mismatch between ventilation (V) and
perfusion (Q), commonly referred to as V/Q mismatch; (2)
shunt; (3) diffusion limitation; and (4) alveolar hypoventilation.
1. Ventilation-Perfusion Mismatch, In a perfectly matched
system, each portion of the lung would receive 1 mL of air
(ventilation) for each 1 mL of blood flow (perfusion). This
match of ventilation and perfusion would result in a V/Q ratio
of 1:1, which is expressed as V/Q = 1. When the match is not
1:1, a V/Q mismatch occurs.
The most common causes are those in which increased
secretions are present in the airways (e.g., also result from
alveolar collapse (atelectasis) or as a result of pain. Pain
interferes chronic obstructive pulmonary disease [COPD]) or
alveoli (e.g., pneumonia), and in which bronchospasm is present
(e.g., asthma). effect on airflow to the alveoli.
52
2. Shunt. occurs when blood exits the heart without having

participated in gas exchange. A shunt can be viewed as an
extreme V/Q mismatch. There are two types of shunt:
anatomic(e.g., a ventricular septal defect) and
intrapulmonary((e.g., acute respiratory distress syndrome
[ARDS], pneumonia).
3. Diffusion Limitation. Diffusion limitation occurs when gas
exchange across the alveolar-capillary interface is compromised
by a process that thickens, damages, or destroys the alveolar
membrane or affects blood flow through the pulmonary
capillaries(e.g. severe COPD or recurrent pulmonary emboli
and ARDS)
4. Alveolar Hypoventilation. is a generalized decrease in
ventilation that results in an increase in the PaCO2 and a
consequent decrease in PaO2. Alveolar hypoventilation may be
the result of restrictive lung diseases, central nervous system
(CNS) diseases, chest wall dysfunction, acute asthma, or
neuromuscular diseases.
N.B, Interrelationship of Mechanisms. Frequently, hypoxemic
respiratory failure is caused by a combination of two or more of
the following: V/Q mismatch, shunt, diffusion limitation, and
alveolar hypoventilation.
53
B. Hypercapnic respiratory failure results from an imbalance

between ventilatory supply and ventilatory demand. Ventilatory
supply is the maximum ventilation Hypercapnic respiratory
failure is sometimes called ventilator failure because the
primary problem is the respiratory system’s inability to remove
sufficient CO2 to maintain a normal PaCO2.
Many different diseases can cause a limitation in ventilator
supply.
1. Airway and Alveoli Abnormalities. Patients with asthma,
COPD, and cystic fibrosis are at high risk for hypercapnic
respiratory failure because the underlying pathophysiology of
these conditions results in airflow obstruction and air trapping.
2. Central Nervous System Abnormalities. A variety of CNS
problems may suppress the drive to breathe. A common
example is an overdose of a respiratory depressant drug (e.g.,
opioids). A brainstem infarction , severe head injury and high-
level spinal cord injuries may also interfere with normal
function of the respiratory enter in the medulla.
3. Chest Wall Abnormalities. In patients with flail chest,
fractures prevent the rib cage from expanding normally because
of pain, mechanical restriction, and muscle spasm. These
conditions place patients at risk for respiratory failure because
54
they limit lung expansion or diaphragmatic movement and

consequently gas exchange.
4. Neuromuscular Conditions. Various types of neuromuscular
diseases may result in respiratory muscle weakness or paralysis.
For example, patients with Guillain-Barré syndrome,
myasthenia gravis (acute exacerbation), are at risk for
respiratory failure because the respiratory muscles are
weakened or paralyzed. Therefore they are unable to maintain
normal PaCO2 levels. 55
Manifestations of acute respiratory failure
Manifestations of hypoxemia
Respiratory Cerebral
• Dyspnea • Agitation
• Tachypnea • Disorientation
• Prolonged expiration (I:E = • Restless, combative behavior
1:3, 1:4) • Delirium
• Nasal flaring • Confusion
• Intercostal muscle retraction • ↓ Level of consciousness
• Use of accessory muscles in • Coma (late)
respiration Cardiac
• ↓ SpO2 (<80%) • Tachycardia
• Hypertension
55
• Paradoxic chest or • Skin cool, clammy, and

abdominal wall movement diaphoretic
with respiratory cycle (late) • Dysrhythmias (late)
• Cyanosis (late) • Hypotension (late)
Other
• Fatigue
• Inability to speak in complete
sentences without pausing to
breathe
Manifestations of Hypercapnia
Respiratory Cerebral
• Dyspnea • Morning headache
• Use of tripod position • Disorientation
• Pursed-lip breathing • Progressive somnolence
• ↓ Respiratory rate or • Elevated intracranial pressure (if
• rapid rate with monitored)
• shallow respirations • Coma (late)
• ↓ Tidal volume
• ↓ Minute ventilation Cardiac
• Dysrhythmias
• Hypertension
• Tachycardia
• Bounding pulse
Neuromuscular
• Muscle weakness
56
Diagnostic
• Vital signs
• History and physical examination
• Arterial blood gases
• Pulse oximetry
• Chest x-ray
• CBC
• Serum electrolytes and urinalysis
• ECG
• Blood and sputum cultures (if indicated)
• Hemodynamic parameters: CVP, SVV, PAWP
Medical Supportive Therapy
• Management of the underlying cause of respiratory failure
• Maintenance of adequate cardiac output
• Maintenance of adequate hemoglobin concentration
Drug Therapy
• Relief of bronchospasm (e.g., albuterol [Proventil])
• Reduction of airway inflammation (corticosteroids)
• Reduction of pulmonary congestion (e.g., furosemide
[Lasix], morphine)
• Treatment of pulmonary infections (e.g., antibiotics)
• Reduction of severe anxiety, pain, and agitation (e.g.,
fentanyl, morphine)
57
Nursing diagnoses for the patient with acute respiratory

failure
Impaired gas exchange related to alveolar hypoventilation,
intrapulmonary shunting, V/Q mismatch, and diffusion
impairment
Ineffective airway clearance related to excessive
secretions, decreased level of consciousness, presence of an
artificial airway, neuromuscular dysfunction, and pain
Critical and Emergency Nursing Care

• Monitor respiratory status for rate, effort, use of accessory
muscles, sputum production, and breathe sounds.
• Administration of O2 therapy and monitor pulse oximetry to
check oxygen saturation levels.
• Monitor sputum for changes in color and amount.
 Monitor vital signs for changes.
 Place patient in high Fowler’s or semi-Fowler’s position on
bed rest to decrease respiratory effort by allowing optimal
diaphragmatic excursion.
 Monitor ventilator settings if appropriate.
 Change patient position every 2 hours to mobilize secretions.
 Monitor intake and output of fluids to check for balance.
 Nutrition support
58
 Explain to the patient:

• The importance of doing coughing and deep-breathing
exercises to fully expand lungs and enhance the expelling of
mucous.
• How to identify the signs of respiratory distress.
.Provide emotional support to the client and family members'.
.Provide teaching in order to provide sufficient care at home and
to prevent future incidence.
59
Mechanical ventilation
1-Clarify mechanical ventilation and its types.
2- Memorize indication of mechanical ventilation.
3-Recognize common ventilator setting and complications of
MV.
4-Summarize modes of MV.
5-Interpret to ventilator alarms.
6-Develop nursing care plan related to patient on MV.
Mechanical Ventilation is ventilation of the lungs by artificial

means usually by a ventilator. Once a patient's PaO2 cannot be
maintained by the basic methods of oxygen delivery systems,
i.e. masks, cannula; endotracheal intubation and mechanical
ventilation are instituted. A ventilator delivers gas to the lungs
with either negative or positive pressure.
It must be understood that no mode of mechanical ventilation

can or will cure a disease process but merely supports the patient
until resolution of his/ her symptoms is accomplished.
60
Indications for Ventilator support

Global indications
• Clinical conditions requiring ventilator support
A. Global pathophysiologic indications
1. Apnea
2. Acute ventilator failure
a. PaCO2 >50 mm Hg and pH <7.30
3. Impending acute ventilator failure acidosis
a. Gas exchange data trending to failure (i.e., Paco2
increasing, pH decreasing) despite treatment
4. Severe refractory hypoxemia
a. Pao2 ≤60 mm Hg (SaO2 <90%)
b. FlO2 ≥60%
5. Clinical signs of severe respiratory failure
a. Unconsciousness b- Obtundation
c. Agonal breathing
d. Rapid, shallow breathing
e. Severe abdominal paradox
B. Common and important clinical conditions when need for

ventilator support is high
1. ARDS 2. Asthma
3. Acute exacerbation of COPD 4. Chest trauma
asthma , severe pneumonia , acute exacerbation of copd , ards
sepsis ,drug overdose
chest trauma , head trauma 61
post cardiac , thoracic surgery //severe neurologic ,neuromuscular
dysfunction
5. Post-cardiac/thoracic surgery 6. Drug overdose

7. Severe neurologic/neuromuscular dysfunction
8. Head trauma 9. Severe pneumonia
10. Sepsis
Criteria for institution of ventilator support:
Ventilation Normal
Parameters
indicated range
Pulmonary function studies:
 Respiratory rate (breaths / min). >35 10-20
 Tidal volume (ml/kg body wt) <5 5-7
 Vital capacity (ml/kg body wt) <15 65-75
 Maximum inspiratory force (cm H2o) <-20 75-100
Arterial blood gases:

 PH <7.25 7. 35 -7. 45
 PaO2 (mmHg) <60 75- 100
 PaCO2 (mmHg) >50 35 – 45
Modes of mechanical ventilation
The term "ventilator mode" refers to the way the machine

ventilates the patient .i.e. how much the patient will participate
in his own ventilator pattern. Each mode is different in
62
determining how much work of breathing the patient has to do.

These include
Control Mode CM
• Ventilation is completely provided by the mechanical
ventilator with a preset tidal volume, respiratory rate and
oxygen concentration prescribed by the physician.
• Ventilator totally controls the patient's ventilation i.e. the
ventilator initiates and controls both the volume delivered and
the frequency of breath.
• Client does not breathe spontaneously.
• Client cannot initiate breathe
Assist Control Mode A/C

- The ventilator provides the patient with a pre-set tidal
volume at a pre-set rate and the patient may initiate a
breath on his own, but the ventilator assists by delivering
a specified tidal volume to the patient.
- Client can initiate breaths that are delivered at the preset
tidal volume.
- Client can breathe at a higher rate than the minimum
number of breaths/minute that has been set.
63
- The total respiratory rate is determined by the number of

spontaneous inspiration initiated by the patient plus the
number of breaths set on the ventilator.
Intermittent Mandatory Ventilation IMV

- The ventilator provides the patient with a pre-set number
of breaths/minute at a specified tidal volume and fiO2.
In between the ventilator-delivered breaths, the patient is
able to breathe spontaneously. The ventilator does not
assist the spontaneous breaths i.e the patient determines
the respiratory rate and tidal volume
- Between machine breaths, the client can breathe
spontaneously at his own tidal volume and rate with no
assistance from the ventilator.
- The mandatory (ventilator) breaths are not synchronized
with the patient's spontaneous breathing i.e are delivered
at a set rate regardless of the patient is in inspiration or
expiration, (stacking result)
Synchronized Intermittent Mandatory Ventilation SIMV
- Same as Intermittent Mandatory Ventilation except
stacking is avoided i.e. Ventilators breaths are
synchronized with the patient spontaneous breathe.
- Used to wean the patient from the mechanical ventilator.
64
Positive End-Expiratory Pressure PEEP

- Positive pressure applied at the end of expiration during
ventilator breaths
Continuous Positive Airway Pressure CPAP (a variation of

PEEP)
- Positive pressure applied at the end of expiration during
spontaneous breaths i.e. for patients breathing
spontaneously.
- No mandatory breaths (ventilator-initiated are delivered
in this mode)
- All ventilation is spontaneously initiated by the patient.
NB: PEEP & CPAP are used in patients with hypoxemia refractory
to oxygen therapy. They improve oxygenation by opening
collapsed alveoli & preventing them from collapsing at the end
of expiration. CPAP allows the nurse to observe the ability of
the patient to breathe spontaneously while still on the ventilator.
Pressure Support Ventilation PSV

- With pressure support ventilation, the patient breathes
spontaneously while the ventilator applies a pre-
determined amount of positive pressure to the airways
upon inspiration.
65
- Pressure support ventilation augments patient's

spontaneous breaths with positive pressure boost during
inspiration i.e. assisting each spontaneous inspiration.
- Helps to overcome airway resistance and reducing the
work of breathing.
- Patient must initiate all pressure support breaths.
- Pressure support ventilation may be combined with other
modes such as SIMV or used alone for a spontaneously
breathing patient.
- Indicated for patients with small spontaneous tidal
volume and difficult to wean patients,
- It is a mode used primarily for weaning from mechanical
ventilation.
Common ventilator settings/ parameters/ controls

Fraction of inspired oxygen (FlO2): The percent of oxygen
concentration that the patient is receiving from the ventilator.
(Between 21 % & 100%)
Tidal Volume (VT): Is the volume of gas delivered to a patient
during a ventilator breath? i.e. the amount of air inspired and
expired with each breath. (Usual volume selected is between 5
to 15 ml/ kg body weight).
66
Respiratory Rate (f): Is the number of breaths the ventilator

will deliver/minute (10-16 b/m). Total respiratory rate equals
patient rate plus ventilator rate.
I:E Ratio (inspiration to expiration ratio): Is the ratio of
inspiratory time to expiratory time during a breath (Usually 1:2)
Minute Volume: Is the volume of expired air in one minute (Vt
x f)
Sigh Volume: Is a deep breath. A breath that has a greater
volume than the tidal volume. It provides hyperinflation and
prevents atelectasis. (Usual volume is 1.5 -2 times tidal volume,
and usual rate is 4 to 5 times an hour)
Humidification and Airway temperature
• Humidifier temperatures should be kept close to body
temperature 35 °C- 37°C.
• Decreased humidity will cause dried secretions and plugging.
• The humidifier should be checked for adequate water levels.
• Humidifier should not be overfilled as this may increase circuit
resistance and interfere with spontaneous breathing.
Alarm systems
Mechanical ventilators comprise audible and visual alarm
systems, which act as immediate warning -signals to altered
ventilation. If an alarm sounds, respond immediately because
the problem could be serious. Assess the patient first, while you
67
silence the alarm. If you cannot quickly identify the problem,

take the patient off the ventilator and ventilate him with a
resuscitation bag connected to oxygen source until the physician
arrives.
Nurses' guide to ventilator alarms:
 High pressure
 Low pressure
 Oxygen
 High respiratory rate: caused by
 Episodes of tachypnea, anxiety, pain, hypoxia, fever.
 Apnea
 Temperature Alarm
Alarm Causes Nursing Interventions

 Increased secretions  Suction the patient
 Kinked ventilator tubing  Unkink tubing Check for
or endotracheal tube adequate lung sounds
(ETT) bilaterally
High
 Patient biting the ETT  Place an oral airway in
pressure
Water in the ventilator patient's mouth so that he
tubing. bites the airway, not the
 ETT advanced into right ETT.
main stem bronchus  Empty water from tubing
68
 Notify the doctor, who will

order a chest X-ray to
evaluate ETT position
 Disconnected tubing  Secure all connections

 A Leak in the system Deflate, then reinflate the
Low
from ( cuff leak - A hole cuff Recheck cuff
pressure
in the tubing -ETT or pressure (normal pressure is
ventilator tubing) - A about 18mmHg) Change the
leak in the humidifier tube. Tighten the humidifier
Oxygen  The oxygen supply is Notify staff to correct the

Insufficient or is not malfunction and manually
properly connected. ventilate the Patient with O2
source
Monitor oxygen saturation
High respiratory rate: caused by Episodes of tachypnea, anxiety, pain,
hypoxia, fever.
Apnea During weaning,  Assess respirations, V.S
indicates that the ABGs,SaO2 & report
patient has a slow
69
Respiratory rate and a A rapid or slow

period of apnea. respiratory rate denotes
patient's intolerance to
weaning and a need for
ventilator setting changes.
Temperature  Check gas flow
Overheating due to too
Alarm low or no gas flow.  check water levels
Improper water levels
Nursing care of patients on mechanical ventilation

Assessment:
* Assess the patient Assess the ventilator
* Assess the tracheostomy or endotracheal tube
Nursing Diagnosis:
* Comfort, Altered pain
* Ineffective, airway clearance
* Anxiety / Fear
* Bowel Elimination, Altered: constipation
* Fluid volume excess
*Nutrition, Altered: less than body requirements
* Altered oral mucous membrane
* Communication, Impaired verbal *High risk for infection
*High risk for impaired skin integrity
70
Nursing Interventions;
*To promote patient's comfort
*To provide airway patency
*To relieve anxiety or fear
*To maintain Bowel elimination
*To maintain normal fluid volume
*To provide G.I.T. Care and Nutritional support
*To provide mouth care
*To provide eye care
*To provide method of communication
*To prevent infection. *To maintain skin
integrity
Assessment or maintaining the ventilated patient

1. Assess the patient at least hourly for the following;
Vital signs. Regularly monitor the vital signs (according to
policy)
Respiratory status
- Respiratory rate should be counted for a full minute &
compared with the set ventilator rate. (To identify whether they
are machine-controlled breaths or combined machine-
controlled and spontaneous breaths.)
71
- Inspect both sides of chest during the machine breath to

determine: Symmetry of chest movement; Synchronization of
chest movement with ventilator.
- Listen for breath sounds, (lack of breaths sounds may indicate
that the ETT is displaced)
- ABGs & pulse oximetry. (to evaluate oxygenation & acid-
base status)
- Assess the need for suctioning. (As secretions heard during
respiration, a rise in ventilator peak inspiratory pressures, assess
color, amount, consistency & odor of sputum.)
Cardiovascular status
- Continuous cardiac monitoring should be initiated,
(dysrhythmia may occur due to hypoxia, acidosis, alkalosis and
electrolyte Imbalance.)
- Central venous pressure measurement (reflect right heart
function)
Renal status
- Monitor fluid and electrolyte balance
- Daily weight
- Intake and output measurement. Neurological status
- Assess the level of consciousness; changes in arousability or
behavior, or ability to follow commands, may be early
indicators of hypoxia.
72
Castro-intestinal status
- Gastric secretions should be closely monitored for bleeding,
(Because these patients arc at risk of developing stress
ulceration)
- Listen for bowel sound
- Perform a nutritional assessment
Monitor for signs of complications
- Monitor for decreased cardiac output evidenced by decrease
in B,P & pulse.
- Monitor for signs of pneumothorax (barotrauma):
- Asymmetrical chest movements; diminished / absent breath
sounds on affected side; tachycardia with weak pulse; cyanosis;
decreased cardiac output with hypotension.
2. Assess the ventilator parameters/ settings at least hourly
for the fallowing;
• Mode of ventilation FIO2
• Tidal volume Vt
• Minute ventilation VE
• Respiratory rate (number of breaths / minute delivered by the
ventilator)
• PEEP level if in use or CPAP • I:E ratio
• Sigh (frequency and volume)
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Check:
• Alarm settings, that alarms are turned on.
• Level of water in the humidifying unit , Temperature of the
humidifier
• Tubing and connections to ensure circuit leaks do not occur
• Tubing to ensure that it is well drained and free from water
build-up
3- Assess the tracheostomy or endotracheal tube:

• Assess the tissue around the endntracheal tube; as this patient
is at high risk for developing pressure ulcers, (if possible the
tube should be placed in a central position to avoid contact with
the of the mouth and the lips. Or it can be rotated from side to
side,)
• Check the tape regularly to make sure it is not soiled or
loosened,
• Check the endotracheal tube position through marking the
point at which the tube exits the mouth or nose. (By this way
you will know whether it is moved in or out)
• Check cuff inflation pressure, (inadequate cuff pressure can
lead to loss of delivered tidal volume.)
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Nursing Interventions
Discomfort related to uncomfortable body position, infrequent
position changes, physical restraints, arterial blood gas sticks,
EIT sectioning, dry mouth & throat. Nursing interventions
include:
• Performance of arterial punctures by skilled personnel
• Skillful and gentle suctioning technique.
• Frequent and adequate oral hygiene
• Frequent position changes
• Range of motion exercises' to reduce the effect of immobility
• Assisting the patient to a chair as often as possible when he
is stable.
Airway clearance ineffective related to inability to get rid of

the secretion, tube obstruction, immobilization Nursing
Interventions to maintain airway patency consists of:
- Providing adequate humidification and warming
- Performing measures to mobilize secretions through chest
physiotherapy and proper suctioning technique to clear the
airway (guideline for proper suctioning technique to be
revised.)
- Tube care through:
- Anchoring ETT securely to prevent lube movement
75
- Placing an oral bite block to prevent the patient from biting on

the lube
- Anchoring a large loop of the tube to the bed to facilitate
patient rnovemesit without tube movement,
- Checking the tube cuff pressures.
Fear and Anxiety related to alarm noises, dyspnea associated

with suctioning, suction- induced coughing, constant bright
lighting, inability to differentiate between night and day, fear of
not being able to return to normal activities, fear of dying
Nursing Interventions include:
• Provide adequate information and explanation of all
procedures before they are initiated.
• Answer alarms promptly.
• Describe the alarm system and explain that it will alert staff
in the event of an accidental disconnection.
• Oxygenate the patient before and after suctioning and remain
with the patient until his respiratory pattern and vital signs
return to normal.
• Keep noise levels to a minimum especially during rest periods
• Diminish lights during the night to stimulate night and day
cycles
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• Place clocks & calendars within the patient's view & verbally
confirm time & dale with the patient
• Provide a T. V or radio for the patient.
• Communicate a ciiring and unhurried attitude to the patient.
High risk for alteration in nutritional status less than body

requirement related to inability to take oral feeding, catabolic
state, hypermetabolism, and malabsorption. Malnutrition may
pose many problems for the person experiencing respiratory
problems such as:
• Increased potential for infection
• Decreased oxygen delivery to the tissues
• Weakened respiratory muscles
Nursing Interventions should focus on:

o Testing the PH of the patient's gastric secretion
o Administering the prescribed medication (cimetidine ,
ranitidine, and antacid prophylactically)
o Providing the correct proportions of fats, CHO, and proteins
as well as water through parenteral or enteral routes.
o Monitoring urea, creatinine, albumin and total protein
regularly to assess patient's nutritional status.
77
Eye, Mouth and Skin Problems

Nursing interventions to provide eye, mouth and skin care
should focus on: Eye care includes:
o Use of artificial tears
o Application of antibiotic drops or ointments as ordered
o Closing the eyelids with tape to prevent corneal ulceration
Oral care includes:
o Performing regular oral hygiene (every 2 hours) to
prevent infection particularly in the intubated patient
Skin care: Skin care should focus on the frequent relief of
pressure through:
• Turning the patient every 2 hours
• Using special mattresses
• Bathing the patient daily and whenever necessary
• Keeping patient's clothes clean and dry
• Keeping the linen clean, dry and unwrinkled
Massaging & lubricating the back and over the bony
prominences
Elimination Problems
In mechanically ventilated patients, sodium and water
retention may occur. These changes may be manifested by
electrolyte imbalance.
Nursing Interventions should focus on:
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• Monitoring fluid balance

• Monitoring urinary output & should be maintained at 30-60
ml/hour
• Accurate recording of intake and output.
Constipation is a problem that is often overlooked in the
acutely ill patient; It can be avoided with the use of:
• Mild cathartic - Suppositories - Enemas
High Risk for Infection when upper airway defense

mechanisms are bypassed with the use of ETT, patients are more
at risk of developing a pulmonary infection; also may be related
to tissue destruction during intubation or suctioning. Sinusitis is
also a problem to patients with nasal intubation
Nursing interventions to prevent infection:

 Frequent hand washing
 Meticulous sterile technique should be used when:
 Suctioning and suction on "as needed basis"
 Suction the tracheobronchial tree before suctioning the
oropharynx to avoid introducing oral pathogens into
tracheobronchial tree.
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 Changing tracheostomy dressings; skin around tracheostomy

stoma should be kept free of secretions, dry and clear at all
times.
 Perform stoma care at least every 8 hours using aseptic
technique until stoma is completely healed.
 Mouth care should be performed every 2 to 4 hours, to reduce
the potential of the oropharynx as a focus of infection.
 Ventilator equipment and tubing should be changed regularly
and sterilized before being used again.
 Maintain asepsis of ventilator connector when disconnected
by placing them on opened sterile gauze pads and avoid
unnecessary disconnection.
 Change the ventilator circuit every 24 to 72 hours.
 Only sterile water should be used in the humidifier and
nebulizer
 Condensation in the ventilator tubing should be drained &
discarded regularly
 Keep the connectors on manual resuscitator bags clean and
free of secretions between uses. Resuscitator bag should not be
used between patients without sterilization.
 If oral airway is present, remove and clean every 8 to 12 hours
 Monitor the following for early detection of infection:
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 Vital signs; increase temperature above 38°C, heart rate

above 100 b/m
 Erythema of tracheostcfrny
 Change in secretions; color, amount consistency & odor,
should be evaluated with each suctioning
 Blood work
 Chest X-ray
Difficulty in Communication related to inability to vocalize
because of the presence of an endotracheal tube, the intubated
patients experience fear and helplessness and communication is
necessary.
The critical care nurse should use alternative methods of

communication such as:
□ Touch or hand gesturing □ Provide paper and
pencil
□ Use word or letter boards / picture boards
□ Use erasable marker board.
Documentation
The nurse should record all:
• Ventilator settings • Patient's measurements
• Nursing care provided
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N.B It is essential, for the critical care nurse to consider the

family needs of the critically ill patient through:
• Familiarizing the family with the physical surroundings of
the critical care unit.
• Informing the family of the visiting hours.
•Providing the family with progress reports about their patient's
condition
• Encouraging family participation in patient care whenever
the patient's condition allows through guiding and observing the
family while participating in hygienic care, feeding....
Complications of mechanical ventilation

1- Airway problems
a- Endotracheal tube out of position
b- Unplanned extubation
c- Laryngeal and tracheal injury
d- Damage to the oral or nasal mucosa
2- Pulmonary system
a- Trauma: barotrauma, which means “ pressure
trauma” is the injury to the lungs associated with
mechanical ventilation. In barotrauma, alveolar injury
or rupture occurs as a result of excessive pressure,
excessive peak inflating volume (volutrauma), or
both. barotrauma may occur when the alveoli are
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overdistended, such as with positive-pressure

ventilation, PEEP, and high VT. The alveoli rupture or
tear so that air escapes various parts of the thoracic
cavity, causing subcutaneous emphysema (air in the
tissue space), pneumothorax or tension
pneumothorax, pneumomediastinum,
pneumopericardium, or pneumoperitonem.
b- Oxygen toxicity
c- Respiratory Acidosis or Alkalosis
d- Infection: The principal mechanism for the
development of VAP is aspiration of colonized gastric
and oropharyngeal secretions. Factor that contribute to
VAP include poor oral hygiene, aspiration,
contaminated respiratory therapy equipment
e- Dysphagia and aspiration
f- Cardiovascular system: Hypotension and decreased
cardiac output may occur with mechanical ventilation
and PEEP, secondary to increased intrathoracic
pressure, which can result in decreased venous return
g- Gastrointestinal system: stress ulcers and
gastrointestinal bleeding may occur in patient who
undergo mechanical ventilation
h- Psychosocial complications: patients may experience
stress and anxiety because they require a machine for
breathing.
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Weaning
1- Clarify Weaning and weaning criteria.
2-Specify method of weaning.
3-Apply nursing role during weaning and diagnostic procedure
for assessment criteria of weaning (ABG).
4-Describe continuously monitoring the patient for signs of
weaning intolerance
Weaning is the process whereby a patient is transferred

from mechanical ventilation support to spontaneous breathing
i.e. Weaning is the gradual process of removing the patient from
mechanical ventilation therapy.
Methods of weaning
• T-piece trial
• Continuous Positive Airway pressure CPAP
• Synchronized Intermittent. Mantadory Ventilation SIMV
• Pressure Support Ventilation PSV
T-Piece trial consists of removing the patient from the

ventilator and having him / her breathe spontaneously on a T-
tube connected to oxygen source. After a time, the patient is
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placed back on the ventilator The goai is to progressively

increase the time spent off the ventilator. During T-piece
weaning, periods of ventilatory support are alternated with
spontaneous breathing.
Continuous Positive Airway pressure weaning CPAP is very
similar to T-piece trial, except the patient placed or the CPAP
mode instead of a T-tube. When placed on CPAP, the patient
does all the work of breathing without the aid of a backup role
or tidal volume. No mandatory (ventilator-initiated) delivered in
this mode i.e. all ventilation is spontaneously initiated by the
patient.
Synchronized intermittent mandatory ventilation weaning
SIMV is the most common method of weaning it consists of
gradually decreasing the number of breaths delivered by the
ventilator to allow the patient increase the number of to
spontaneous breaths.
Pressure Support Ventilation Weaning PSV consists of
placing the patients on the pressure support mode. The patient
must initiate all pressure support breaths. PSV weaning is
indicated for patients who are difficult to wean from the
mechanical ventilator using conventional means (T-piece,
SIMV, CPAP), and patients with small spontaneous tidal
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volume. During weaning the level of pressure support is

gradually decreased.
CPAP & PSV are modes of mechanical ventilation that are

completely dependent on the spontaneous effort of the
patient for initiation of inspiration. These modes are often
used for weaning purposes.
Weaning Criteria / Parameters

 Awake and alert -PaO2>60mmHg onFiO2<50%
 PaCO2 acceptable with PH of 7.35 - 7.45
 F < 25 / minut -Vt 5 ml / kg
 VC> 10-15ml/kg -VE 5-10 L/m (fxVt)
 NIF > - 20 cm H2O (indicates patient's ability to take a deep
breath &cough)
Nursing Role in Weaning

Before weaning
Assessment parameters indicating readiness to weaning:
Underlying cause for mechanical ventilation resolved
- Improved chest radiograph findings
- Minimal secretions
- Normal breath sounds
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Hemodynamic stability adequate cardiac output

- Absence of hypotension
- Minimal vasopressor therapy
Adequate respiratory muscle strength
- Respiratory rate <25-30 breaths perminute
- Negative inspiratory pressure of force that exceeds – 20
cm H2 O
- Spontaneous tidal volume 5mL/kg IBW
- Minute ventilation 5-10 L/min
- Rapid shallow breathing index <105
Adequate oxygenation without a high fio2 and/ o a high
PEEP
- PaO2> 60 mm Hg with FiO2≤ 0.4
- Pa O2 / FiO2> 150-200 (consider), ideally > 250
- PEEP <5-8 cm H2O
Absence of factors that impair weaning
- Infection
- Anemia
- Fever
- Sleep deprivation
- Pain
- Abdominal distension, bowel abnormalities (diarrhea
constipation)
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- Mental readiness to wean: calm, minimal anxiety,

motivated
- Minimal need for sedative and other medications that
may cause respiratory depression.
During weaning
• Wean only during the day
• Remain with the patient during initiation of weaning
• Instruct the patient to relax and breathe normally
• Frequently monitor the respiratory rate, vital signs, ABGs,
diaphoresis and use of accessory muscles
• Record:
- Date & time of starting weaning
- Method of weaning used
- ABGs & oxygen saturation
- Spontaneous respiratory rate
- Use of accessory muscle
-Time spent in the weaning process
- Patient's response
Continuously monitoring the patients for signs of weaning
intolerance:
 Dysrhythmias
 Increase or decrease in heart rate of > 20 beats /min. or heart
rate > 110
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 Increase or decrease in blood pressure of > 20 mm Hg

 Increase in respiratory rate of > 10 above baseline or > 30
 Tidal volume of < 5) ml/kg
 Diaphoresis
 Dyspnea
 Restlessness
 Decrease in level of consciousness
 SaO2 < 90%
 Pa02 < 60 mmHg
 Increase in PaCO2 with a decrease in PH of < 7.35.
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Noninvasive ventilation

1-Define noninvasive ventilation.
2- Clarify main types of noninvasive ventilation
3-Memorize the terminology in the area of noninvasive
ventilation.
4-Explain the way the noninvasive ventilation can be delivered.
5- Recognize indications and contraindication of noninvasive
ventilation.
6- Recognize complications of noninvasive ventilation.
What is noninvasive ventilation?

Noninvasive ventilation is mechanical ventilation without the
use of an endotracheal tube or tracheotomy.
What are the main types of noninvasive ventilation?
The two main types are positive-pressure and negative-

pressure noninvasive ventilation. With the former, positive
pressure is applied to the airway to inflate the lungs directly.
With negative-pressure ventilation, negative pressure is applied
to the abdomen and thorax to draw air into the lungs through the
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upper airway. This chapter deals mainly with positive-pressure

ventilation, the most commonly used noninvasive ventilator
mode in the intensive care unit (ICU).
The terminology in the area of noninvasive ventilation is
confusing. Some of the more common terms include:
1. NV (nasal ventilation)
2. NIMV (nasal intermittent mandatory ventilation)
3. SNIMV (synchronized nasal intermittent mandatory
ventilation)
4. NPSIMV (nasopharyngeal synchronized intermittent
mandatory ventilation)
5. NPPV (noninvasive positive pressure ventilation)
6. BiPAP (bilevel positive airway pressure) systems used in
older patients have a similar underlying rationale, with a
system allowing spontaneous breathing throughout the
respiratory cycle and patient triggering of the inspiratory
phase.
How noninvasive ventilation can be delivered

Airflow can be delivered via binasal prongs, or a by single prong
placed with the tip in the nose or nasopharynx. Nasal ventilation
can be delivered in either a synchronized or nonsynchronized
mode. Use of a face mask held in place by a device or netting
91
around the head is not recommended because it has been

associated with cerebellar hemorrhage
Indications for Use:
 Obstructive sleep apnea syndrome.

 Chronic obstructive pulmonary disease with
exacerbation.
 Bilateral pneumonia.
 Acute congestive heart failure with pulmonary edema.
 Neuromuscular disorders.
 Acute lung injury
Contraindications of Non Invasive Mechanical Ventilation:
 Undrained pneumothorax
 Frank haemoptysis
 Vomiting blood (haematemesis)
 Facial fractures
 Cardiovascular system instability
 Cardiac Arrest
 Respiratory Failure
 Raised ICP
 Recent upper GI surgery
 Active Tuberculosis
 Lung abscess
 Facial trauma/burns
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 Fixed upper airway obstruction

 Active vomiting
 Respiratory or cardiac arrest
Complications of noninvasive ventilation

For facial and nasal pressure injury and sores, note the
following:
 Result of tight mask seals used to attain adequate
inspiratory volumes.
 Minimize pressure by intermittent application of

noninvasive ventilation.
 Schedule breaks (30-90 min) to minimize effects of mask

pressure.
 Balance strap tension to minimize mask leaks without

excessive mask pressures.
 Cover vulnerable areas (erythematous points of contact)

with protective dressings.
For gastric distension, note the following:

 Rarely a problem
 Avoid by limiting peak inspiratory pressures to less than

25 cm water
 Nasogastric tubes can be placed but can worsen leaks

from the mask
 Nasogastric tube also bypasses the lower esophageal

sphincter and permits reflux
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For dry mucous membranes and thick secretions, note the

following:
 Seen in patients with extended use of noninvasive
ventilation
 Provide humidification for noninvasive ventilation

devices
 Provide daily oral care
For aspiration of gastric contents, note the following:

 Especially if emesis during noninvasive ventilation
 Avoid noninvasive ventilation in patient with ongoing

emesis or hematemesis
Complications of both noninvasive and invasive ventilation

These include the following:
 Barotrauma (significantly less risk with noninvasive
ventilation)
 Hypotension related to positive intrathoracic pressure

(support with fluids)
Complications avoided by noninvasive ventilation

These include the following:
 Ventilator-associated pneumonia
 Sinusitis
 Reduction in need for sedative agents - Sedatives used in
less than 15% of noninvasive ventilation patients in one
survey
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Pulmonary Edema
1-Define pulmonary edema.
2-List causes of pulmonary edema.
3-Identify clinical manifestation of pulmonary edema.
4-Describe medical management of pulmonary edema.
5-Apply nursing care management of Pulmonary edema.
Definition:
Pulmonary edema is the abnormal accumulation of
fluid in the lungs The fluid may accumulate either in the
interstitial spaces or in the alveoli.
Etiology:
I. Altered capillary permeability
a. Infectious pulmonary edema (viral or bacterial)
b. Inhaled toxins
c. Circulating toxins
d. Vasoactive substances (histamine, kinins)
e. Disseminated intravascular coagulation
f. Immunologic reactions
g. Radiation pneumonia
h. Uremia
i. Near-drowning
j. Aspiration pneumonia
95
k. Smoke inhalation
l. Adult respiratory distress syndrome
II. Increased pulmonary capillary pressure
a. Cardiac causes
1. Left ventricular failure from any cause
2. Mitral stenosis
3. Subacute bacterial endocarditis
b. Noncardiac causes
1. Pulmonary venous fibrosis
2. Congenital stenosis of the origin of the pulmonary
veins
3. Pulmonary venoocclusive disease
c. Over infusion of fluids
III. Decreased notice pressure: Hypoalbuminemia from any
cause (renal, hepatic, nutritional, or protein-losing
enteropathy)
IV. Lymphatic insufficiency
V. Mixed or unknown mechanisms
a. High-altitude pulmonary edema
b. Neurogenic pulmonary edema (CNS trauma,
subarachnoid bleeding)
c. Heroin overdose (also other narcotics)
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Clinical manifestation:-
 Shortness of breathe
 Difficulty in breathing
 Wheezing
 Feeling of "air hunger" or "drowning"
 Grunting or gurgling sounds with breathing
 Shortness of breath with lying down, causing the
patient to sleep with head propped up or using extra
pillows
 Cough, Anxiety, Restlessness, Excessive sweating
 Pale skin, Coughing up blood, Inability to speak from
air hunger
 Decrease in level of awareness,
 Rapid breathing and increased heart rate
 Crackles in the lungs and abnormal heart sound
Medical management: -
Clinical management of a patient with acute pulmonary
edema is directed toward improving the pumping ability of
the left ventricle and improving respiratory exchange. These
goals are accomplished through a combination of oxygen and
medication therapies and nursing support
97
Pharmacologic therapy
1- Oxygen therapy. Oxygen is administered to relieve
hypoxia and dyspnea. Usually mask is initially used. If
respiratory failure is sever, endotracheal intubation and
mechanical ventilation are required. The use of positive
end expiratory pressure (PEEP) is effective in reducing
venous return, decreasing fluid movement out of the
pulmonary capillaries, and improving oxygenation.
Oxygenation is monitored with pulse oximetry and by
measurement of arterial blood gases.
2- Morphine. Morphine is administered to reduce peripheral
resistance and venous return so that blood can be
redistributed from the pulmonary circulation to other
parts of the body. This action decreases pressure in the
pulmonary capillaries and decreases seepage of fluid into
the lung tissue. The effect of morphine in decreasing
anxiety is also beneficial.
3- Diuretic therapy. It is used to increase rate of urine
production and removal of excess extracellular fluid from
the body.
4- Other intravenous medications. These include
dobutamine, a catecholamine that increases myocardial
98
contractility; amrinone, which dilates the arteries and

increases CO; and digitalis, which increases contractility.
Nursing Management
1- Positioning the patient to promote circulation
Proper positioning can help reduce venous return to
the heart. The patient is positioned upright, preferably
with the legs dangling over the side of the bed.
2- Providing psychological support
As the ability to breathe decreases, the patient’s sense
of fear and anxiety rises proportionately, which makes the
condition more severe. reassuring the patient. The nurse
should give the patient simple, concise information, in a
reassuring voice, about what is being done to treat the
condition and the expected results.
3- Monitoring medications
The patient receiving morphine is observed for
excessive respiratory depression, hypotension and
vomiting; a morphine antagonist, such as naloxone
hydrochloride (narcan), is kept available.
The patient receiving diuretic therapy will experience
a large volume of urine formation within minutes after a
potent diuretic is given. An indwelling catheter may be
used to decrease the amount of energy required by the
patient and to reduce the resultant increase in cardiac
workload induced by getting on and off a bedpan.
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Acute Respiratory Distress Syndrome

a) Define acute respiratory distress syndrome

b) Mention risk factors associated with ARDS
c) Relate the etiology and pathophysiology of acute
respiratory distress syndrome
d) Compare between phases of acute respiratory distress
syndrome
e) list laboratory studies for acute respiratory distress
syndrome
Introduction:
Acute respiratory distress syndrome (ARDS) is a

systemic process that is considered to be the pulmonary
manifestation of multiple organ dysfunction syndrome. It is
characterized by noncardiac pulmonary edema and disruption of
the alveolar capillary membrane as a result of injury to either
the pulmonary vasculature or the airways.
Definition
ARDS is an acute diffuse, inflammatory lung injury, leading to

increased pulmonary vascular permeability, and loss of
aereated lung tissue with hypoxemia and bilateral
100
radiolographic opacities associated with increased physiologic

dead space and decreased lung compliance
Etiology and predisposing condition :
Direct Pulmonary Injury Indirect Pulmonary Injury
•Aspiration (gastric fluids, • Sepsis

near drowning) • Burns
• Infectious pneumonia • Trauma
• Lung contusions with • Blood transfusion (TRALI)
trauma • Lung or bone marrow
• Toxic inhalation transplantation
• Upper airway obstruction • Drug or alcohol overdose
(relieved) • Drug reaction
• SARS coronavirus • Cardiopulmonary bypass
• Neurogenic pulmonary • Acute pancreatitis
edema • Multiple fractures
• Acute eosinophilic • Venous air embolism
pneumonia* • Amniotic fluid embolism
• Bronchiolitis obliterans • Pancreatitis
with organizing pneumonia*
•Tuberculosis*
101
Pathogenesis of ARDS:
Clinical manifestation of Acute Respiratory Distress

Syndrome
Dyspnea, tachypnea
cyanosis hypoxemia
tachycardia, coarse crackles,
Hyperdynamic hemodynamic parameters, SIRS presentation
102
ARDS is characterized by the following:

• Timing—within 1 week of known clinical insult or new or
worsening respiratory symptoms
• Chest imaging—bilateral opacities not fully explained by
effusions, lobar/lung collapse or nodules
• Origin of edema—respiratory failure not fully explained by
heart failure or fluid overload
• Oxygenation—
-Mild ARDS (than Pao2/Fio2 of 300-201 mm Hg with positive
end respiratory airway pressure [PEEP] or constant positive
airway pressure [CPAP] greater than or equal to 5 cm H2O);
-Moderate ARDS (Pao2/Fio2 200-101 mm Hg with PEEP
greater than or equal to 5 cm H2O)
-Severe ARDS (Pao2/Fio2 of 100 mm Hg or less with PEEP
greater than or equal to 5 cm H2O)
Stages of ARDS:
Exudative stage
Within the first 48-72 hours after the initial insult. Once
released, the mediators cause injury to the pulmonary
capillaries, resulting in increased capillary membrane
permeability leading to the leakage of fluid filled with protein,
blood cells, fibrin, into the pulmonary interstitium. Damage to
the pulmonary capillaries also causes the development of
103
microthrombi and elevation of pulmonary artery pressures. The

hypoxemia is resistant to supplemental oxygen administration,
and mechanical ventilation is required.
Proliferative stage:
Develops from the 2nd to the 10th day after injury. Evidence of
SIRS (SIRS) describes the inflammatory response occurring
throughout the body and these symptoms are often manifested
in patients with ARDS) with hemodynamic instability,
generalized edema, possible onset of nosocomial infections,
increased hypoxemia, and lung involvement.
Fibrotic stage
Develops after 10 days and is typified by few additional
radiographic changes. There is increasing multiorgan
involvement, SIRS, and increases in the arterial carbon dioxide
tension (PaCO2) as progressive lung fibrosis and
emphysematous changes result in increased dead space. Fibrotic
lung changes result in ventilation management difficulties
Diagnostic Studies:
Radiographic Studies
In the early phase of ARDS, the chest radiographic changes are
usually negligible. Within a few days, the chest radiographic
findings show patchy bilateral alveolar infiltrates, usually in the
dependent lung fields. This may be mistaken for cardiogenic
104
pulmonary edema. Over time, these patchy infiltrates progress

to diffuse infiltrates
Arterial blood-gas analysis
Arterial blood-gas analysis reveals a low Pao2,despite
increases in supplemental oxygen administration (refractory
hypoxemia).
Initially the Paco2 is low as a result of hyperventilation, but
eventually the Paco2 increases as the patient fatigues. The pH
is high initially but decreases as respiratory acidosis develops
Intrapulmonary Shunt Measurement
An intrapulmonary shunt is a type of ventilation–perfusion
mismatch defined as the percentage of cardiac output that is not
oxygenated owing to pulmonary blood flowing past collapsed
or fluid-filled and nonventilated alveoli (a physiologic shunt),
absence of blood flow to ventilated alveoli (alveolar dead
space), or a combination of both of these conditions
Lung Compliance, Airway Resistance, and Pressures
Lung compliance, (means distensibility of lung), decreases as
the alveoli fill with fluid or collapse. More effort and greater
pressure are required to move air into the lungs as they become
increasingly “stiff.” In addition, the resistance to airflow into
and out of the lungs increases with the accumulation of
secretions and mediator-induced bronchoconstriction.
105
NURSING DIAGNOSES:
•Impaired Gas Exchange related to ventilation/perfusion
mismatching
• Decreased Cardiac Output related to alterations in preload
• Imbalanced Nutrition: Less Than Body Requirements related
to lack of exogenous nutrients or increased metabolic demand
• Risk for Aspiration
• Risk for Infection
• Anxiety related to threat to biological, psychological, and/or
social integrity,
• Disturbed Body Image related to functional dependence on
life-sustaining technology
• Compromised Family Coping related to critically ill family
member
Collaborative Management
•Administer oxygen therapy:
• Intubate patient.
• Initiate mechanical ventilation:
• Permissive hypercapnia: Permissive Hypercapnia.
Permissive hypercapnia uses low tidal volume ventilation in
conjunction with normal respiratory
rates, in an attempt to limit the effects of atelectrauma and
biotrauma.
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•Low tidal volume ventilation: uses smaller tidal volumes (6

mL/kg) to ventilate the patient, in an attempt to limit the
effects of barotrauma and volutrauma
• Inverse ratio ventilation: IRV prolongs the inspiratory (I)
time and shortens the expiratory (E) time, thus reversing the
normal I : E ratio. The goal of IRV is to maintain a more
constant mean airway pressure throughout the ventilatory cycle,
which helps keep alveoli open and participating in gas
exchange.
• Use PEEP: The purpose of using PEEP in the patient with
ARDS is to improve oxygenation while reducing Fio2 to less
toxic levels. PEEP has several positive effects on the lungs,
including opening collapsed alveoli, stabilizing flooded
alveoli,
• Administer medications:
• Bronchodilators
• Sedatives
• Analgesics
• Neuromuscular blocking agents
• Fluid management :
Diuretics and reduced fluid administration have been studied
to reduce lung edema.
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• Prone position: A number of studies have shown that prone

positioning the patient with ARDS results in an improvement
in oxygenation
• Suction as needed.
• Provide adequate rest and recovery time between various
procedures.
• Initiate nutritional support.
• Maintain surveillance for complications:
• Encephalopathy
• Cardiac dysrhythmias
• Venous thromboembolism
• Gastrointestinal bleeding
• Atelectrauma
• Biotrauma
• Volutrauma
• Barotrauma
• Oxygen toxicity
•Extracorporeal gas exchanges are techniques used in the
treatment of severe ARDS when conventional therapy has
failed. These methods allow the lungs to rest by facilitating the
removal of carbon dioxide and providing oxygen external to the
lungs
• Provide comfort and emotional support.
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Pulmonary Embolism
1-Define pulmonary embolism.
2-Identify risk factor of Pulmonary embolism.
3-Interpret ABG for patient with pulmonary embolism.
4-Analyze diagnostic study of pulmonary embolism
5-Describe signs and symptoms.
6-Apply diagnostic study of pulmonary embolism.
7-Describe medical management of patient with pulmonary
embolism.
Definition: -
Pulmonary embolism is a clot (thrombotic emboli) or fat,
tumors, amniotic fluid, air and foreign bodies (nonthrombotic
emboli) lodges in the pulmonary arterial (PA) system disrupting
the blood flow to a region of the lungs.
Risk factor:
A number of predisposing factors and precipitating
conditions put a patient at risk for developing a PE
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A. Predisposing factors: -
 Venous Stasis: Decreased cardiac output, immobility
 Hypercoagulability: Polycythemia
 Injury to vascular endothelium: Infection,
atherosclerosis
B. Precipitating conditions: Previous pulmonary embolism,
cardiovascular disease, congestive heart failure and right
ventricular infarction
C. Trauma (injury or burn): Lower extremities, pelvis, hips,
cancer, surgery, orthopedic, vascular, abdominal, gynecologic
status, pregnancy, postpartum, and oral contraceptives
Assessment:-
1. History: History for the previous risk factors
2. Clinical manifestation:-
 Sub massive embolus
- Dyspnea - Chest pain - Cough
- Apprehension - Diaphoresis -
Wheezing
 Massive embolus (above manifestation plus the
following)
- Cyanosis - Restlessness - Anxiety
- Confusion - Cool, clammy skin
- Decreased urinary output
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3. Diagnostic study
 ABG; low Pao2, low Paco2, and high pH (respiratory
alkalosis)
 Electrocardiogram (ECG), Chest x-ray, Ventilation-
perfusion lung scan
 Pulmonary angiography
Medical management:-
Prevention strategies include the use of prophylactic
anticoagulation with low-dose or adjusted-dose heparin, LMW
heparin, and oral anticoagulants
Treatment strategies include preventing the recurrence of
a PE administrating thrombolytic therapy, reversing the effects
of pulmonary hypertension, promoting gas exchange
(supplement o2, intubation and mechanical ventilation) and
preventing complications
Collaborative management
1. Administer oxygen therapy, Intubate patient, Initiate
mechanical ventilation
2. Administer medication
 Thrombolytic therapy, anticoagulants, bronchodilators,
intropic agents
 Sedatives, and analgesics
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3. Administer fluids
4. Position patient to optimize ventilation/perfusion matching
5. Maintaining surveillance for complications
6. Bleeding
7. Acute respiratory distress syndrome
8. Provide comfort and emotional support
Nursing management:-
measures for prevention of pulmonary embolism:
Nursing actions are aimed at preventing the development
of DVT, which is a major complication of immobility and a
leading cause of PE. This measures include:-
 Use of antiembolic and pneumatic compression stockings
 Elevation of the legs
 Active/passive range of motion (ROM) exercises
 Adequate hydration
 Progressive ambulation
Patients at risk should be routinely assessed for signs of a DVT,

specifically, deep calf pain (Homans signs), calf tenderness, or
redness.
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Optimizing Oxygenation and Ventilation

Nursing interventions to optimize oxygenation and
ventilation include
 Positioning
 Preventing desaturation
 Promoting secretion clearance
Monitoring for Bleeding
The patient receiving anticoagulant or thrombolitic
therapy should be observed for signs of bleeding. The patient’s
gum, skin, urine, stool, and emesis should be screened for signs
o overt or covert bleeding. In addition monitoring the patient’s
INR or apt is critical to managing the anticoagulation therapy.
Providing Patient Education
Early in the patient’s hospital stay the patient and family
should be taught about PE and its causes and treatment. As the
patient moves toward discharge. Teaching should focus on the
interventions necessary for preventing the recurrence of deep
vein thrombosis and subsequent emboli, signs and symptoms of
deep vein thrombosis and anticoagulant complications and
measures to prevent bleeding.
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Acute Heart failure (HF)

1-Define heart failure
2-list risk factor and etiology.
3 -Compere between types of heart failure
4- Predict clinical manifestation of heart failure
5-Enumerate preventive measures of heart failure
6-Mention emergency nursing care for managing heart failure
Definition of Heart Failure
Heart failure is a clinical syndrome caused by a structural

or functional impairment in the ability of the ventricle to fill or
eject blood effectively. The cardinal symptoms of heart failure
are fatigue and dyspnea on exertions (DOE); other symptoms
include edema, orthopnea, and paroxysmal nocturnal dyspnea
(PND)
Risk factors of heart failure are including:
 High blood pressure.
 Coronary artery disease.
 Heart attack
 Diabetes.
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 Some diabetes medications:
Some diabetes drugs have been found to increase the risk of heart failure.
 Sleep apnea
 Congenital heart defects
 Viral infection
 Alcohol use
 Arrhythmias
Causes of Heart Failure

There are thought to be many causes for the development of
heart failure. Common causes either independent or in
combination are listed below:
Impaired Cardiac Function
Myocardial disease
• Cardiomyopathies
• Myocarditis
• Coronary insufficiency
• Myocardial infarction
Valvular heart disease
• Stenotic valvular disease
• Regurgitant valvular disease
Congenital heart defects
Constrictive pericarditis
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Excess Work Demands

Increased pressure work
• Systemic hypertension
• Pulmonary hypertension
• Coarctation of the aorta
Increased volume work
• Arteriovenous shunt
• Excessive administration of intravenous fluids
Increase perfusion work
• Thyrotoxicosis
• Anemia
Type of heart failure:
 Acute Versus Chronic
The terms acute and chronic are used to describe both the
onset of symptoms of heart failure and the intensity of
symptoms. Heart failure of acute onset refers to the sudden
appearance of symptoms, usually over days or hours. Heart
failure of chronic onset refers to the development of symptoms
over months to years. Chronic symptoms represent the baseline
condition, the limitations the patient lives with on a daily basis.
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 Left sided versus right sided heart failure

Left-sided heart failure: Left-sided heart failure refers to
failure of the left ventricle to fill or empty properly. This
leads to increased pressures inside the ventricle and
congestion in the pulmonary vascular system. Left-sided
heart failure may be further classified into systolic and
diastolic dysfunction.
-Systolic dysfunction: is usually estimated by ejection

fraction, or the percentage of the left ventricular end-
diastolic volume (LVEDV) that is ejected from the
ventricle in one cycle.
-Diastolic dysfunction is caused by impaired relaxation and

filling. Left ventricular filling, a complex process that takes
place during diastole, is a combination of passive filling
and atrial contraction.
 Right-Sided Heart Failure
Right-sided heart failure refers to failure of the right

ventricle to pump adequately. The most common cause of right-
sided heart failure is left-sided heart failure, but right-sided heart
failure can exist in the presence of a perfectly normal left
ventricle, and does not lead to left-sided heart failure. Right-
sided heart failure can also result from pulmonary disease (cor
117
pulmonale) and primary pulmonary artery hypertension.

Pulmonary embolus is a common cause of acute right-sided
heart failure.
Clinical manifestation of right and left sided heart failure

left ventricular heart failure Right ventricular heart failure
Signs Symptoms Signs symptoms
Tachypnea Fatigue Peripheral weakness
Edema
tachycardia Dyspnea Hepatomegaly anorexai
Cough Orthopnea Splenomegaly indigestion
Bibasilar crackles Paroxysmal Hepatojugular Reflux Weight gain
nocturnal
dyspnea
Gallop rhythms Nocturia Ascites Mental changes
Increased Jugular venous Distention
pulmonary
artery pressures
Hemoptysis Increased central venous pressure
Cyanosis Pulmonary Hypertension
Pulmonary edema
Investigations that may be done to diagnose heart failure
may include:
 Blood tests. Beta Natriuretic peptide (BNP) – this
laboratory study can help to identify CHF as the origin for
unclear dyspnea. When serum levels of BNP are less than
100pg/ml the diagnosis of CHF is unlikely. Serum levels
of BNP that range between 100 – 500 pg/ml is probably
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caused by CHF and BNP levels that are > 500 pg/ml are
considered to be definitely consistent with a diagnosis of
CHF.
 Chest X-ray. X-ray images can show the condition of the
lungs and heart.
 Electrocardiogram (ECG or EKG). .
 Echocardiogram
 Exercise tests or stress tests
 CT scan of the heart. Also called a cardiac CT scan, this
test uses X-rays to create cross-sectional images of the
heart.
 Heart MRI scan,
 Coronary angiogram. This test helps spot blockages in
the heart arteries
Treatment for heart failure
 ABC’s (airway, breathing, circulation).

 Oxygen therapy as needed (100% non-rebreather
mask or intubation with mechanical ventilation may
be initially required).
 Continuous cardiac/Pulse oximetry monitoring.
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 Pharmaceutical therapy often begins with nitrates and

diuretics (appropriate medication regimens are the
major focus of treatment).
 Restrict sodium and fluid intake (strict I&O)
 Bed rest is tolerated (patients may not tolerate bed rest
and may wish to sit up with legs dangling off the bed).
 Pain relief (Morphine for chest pain). .
Pharmaceutical Treatment Options

1- Captopril (Capoten), Ramapril (Altace), or Zestril (Lisnopril)
Angiotensin converting enzymes (ACE) inhibitors such as
captopril are recommended for the treatment of congestive
heart failure because they produce vasodilation and blockage
of the RAAS process.
2- Carvedilol (Coreg) – Coreg is a non-selective B-blocker
that improves left ventricular function and increases survival
rates by increasing the force of contraction.
3- Furosemide (Lasix) – Lasix is a loop diuretic and is often
ordered to reduce or eliminate excessive fluid
4- Morphine
5- Nitroglycerin – Nitrates such as Nitroglycerin cause
vasodilation of the vessels and help to decrease cardiac oxygen
demand, cardiac preload and afterload while increasing cardiac
output.
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6- Dopamine – Dopamine has both and b-adrenergic effects

(as well as dopaminergic effects).
7- Dobutamine – Dobutamine stimulates B-receptors of the

heart and provide a direct acting positive inotrope effect.
8- Milrinone (Incor)
9- Digitalis (Digoxin) – Digoxin is a cardiac glycoside that
works by inhibiting the sodium-potassium pump system. The
result of this action is increased cardiac contractility.
Nursing Care Plan
Nursing Assessment
Nursing assessment for patients with heart failure emphasizes
evaluating the efficacy of treatment and the patient’s adherence
to self-management strategies. Monitoring and reporting
worsening signs and symptoms of heart failure are essential for
adjusting therapy.
Health History
 Assess the signs and symptoms such as dyspnea,
shortness of breath, fatigue, and edema.
 Assess for sleep disturbances, especially sleep suddenly
interrupted by shortness of breath.
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 Explore the patient’s understanding of HF, self

management strategies, and the ability and willingness
to adhere to those strategies.
Physical Examination
 Auscultate the lungs for presence of crackles and
wheezes.
 Auscultate the heart for the presence of an S3 heart
sound.
 Assess JVD for presence of distention.
 Evaluate the sensorium and level of consciousness.
 Assess the dependent parts of the patient’s body for
perfusion and edema.
 Measure the urinary output carefully to establish a
baseline against which to assess the effectiveness of
diuretic therapy.
 Weigh the patient daily in the hospital or at home.
Assess for the following subjective and objective data:
 Increased heart rate (tachycardia)
 ECG changes
 Changes in BP (hypotension/hypertension)
 Extra heart sounds (S3, S4)
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 Decreased urine output (oliguria)

 Diminished peripheral pulses
 Orthopnea
 Crackles
 Jugular vein distention
 Edema
 Chest pain
 Weakness
 Fatigue
 Changes in vital signs
 Presence of dysrhythmias
 Dyspnea
 Pallor
 Diaphoresis
 Weight gain
 Respiratory distress
 Abnormal breath sounds
Nursing diagnoses for heart failure :
Impaired Gas Exchange, related to ventilation/perfusion
mismatching or intrapulmonary shunting:
Goal: improving Respiratory Function
Nursing intervention:
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 observe the color of skin, mucous membranes,

and nail beds, noting the presence of peripheral cyanosis
 Monitor potassium levels.
 Instruct patient in effective coughing and deep
breathing.
 Encourage frequent position changes.
 Position the patient in a High Fowler’s position with the
head of the bed elevated up to 90°.
 Suction secretions PRN
 Graph serial ABGs, pulse oximetry.
 Administer supplemental oxygen as indicated.
 Administer medications as indicated.
 Assist patient to use relaxation techniques
Decreased Cardiac Output, related to alterations in

contractility& alterations in heart rate or rhythm,
Goal : the patient will exhibit optimal cardiac output
 Auscultate apical pulse, assess heart rate.
 Obtain a comprehensive health history focusing on HF
symptoms and self-management strategies.
 Note heart sounds.
 Assess rhythm and document dysrhythmias if telemetry
is available.
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 Assess for palpitations or irregular heartbeat.

 Palpate peripheral pulses.
 Monitor blood pressure (BP).
 Inspect the skin for mottling.
 Inspects the skin for pallor or cyanosis.
 Monitor urine output, noting decreasing output and
concentrated urine.
 Evaluate the patient’s level of consciousness for changes
that may indicate decreased cerebral perfusion.
 Examine lower extremities for edema and rate its
severity
 Assess the abdomen for tenderness, hepatomegaly, and
signs of ascites.
 Monitor for signs and symptoms of fluid and electrolyte
imbalances.
 Assess jugular vein distention (JVD).
Activity Intolerance, related to cardiopulmonary

dysfunction:
 Check vital signs before and immediately after activity,
especially if the patient receives vasodilators, diuretics,
or beta-blockers.
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 Document cardiopulmonary response to activity. Note

tachycardia, dysrhythmias, dyspnea, diaphoresis, and
pallor.
 Assess for other causes of fatigue (treatments, pain,
medications).
 Identify factors that could affect the desired level of
activity and motivation.
 Monitor and evaluate the patient’s response to activities.
 Consider the use of the 6-minute walk test (6MWT) to
determine the patient’s physical ability.
 Assist in identifying and overcoming barriers to physical
activity.
 Encourage daily physical activity.
 Collaborate with the primary provider and patient to
develop a personalized exercise schedule.
 Provide guidelines for safe physical activity. Start slow
and low.
Anxiety, related to threat to biologic, psychologic, or social

integrity
Ineffective Coping, related to situational crisis and personal
vulnerability:
Goal: reduce level of anxiety improve coping
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Nursing interventions:
 Encourage the patient to express fears, feelings
regarding the condition.
 Identify present and past measures that the patient uses
to cope with fear.
 Assess for factors contributing to a sense of
powerlessness.
 Assess for feelings of apathy, hopelessness, and
depression.
 Note tachycardia, dysrhythmias, dyspnea, diaphoresis,
and pallor.
 Assess for other causes of fatigue (treatments, pain,
medications).
 Identify factors that could affect the desired level of
activity and motivation
 Administer oxygen during acute events.
 Validate observations by asking the patient, “Are you
feeling anxious now?”
 Recognize awareness of the patient’s anxiety.
 Interact with patients in a calm, peaceful manner.
 Monitor and evaluate the patient’s response to activities.
 Evaluate the patient’s decision-making competence.
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Deficient Knowledge, related to lack of previous exposure

to information
Goal : improve Knowledge
 Discuss normal heart function.
 Reinforce treatment rationale.
 Encourage developing a regular home exercise program,
and provide guidelines for sexual activity.
 Discuss the importance of being as active as possible
without becoming exhausted and rest between activities.
 Discuss the importance of sodium limitation. Provide a
list of the sodium content of common foods that are to
be avoided and limited. Encourage reading of labels on
food and drug packages.
 Refer to a dietitian for counseling specific to individual
dietary customs.
 Review medications, purpose, and side effects. Provide
both oral and written instructions.
 Recommend taking diuretic early in the morning.
 Instruct and receive return demonstration of ability to
take and record daily pulse and blood pressure
Explain and discuss the patient’s role in controlling risk factors
(smoking, unhealthy diet) and precipitating or aggravating
factors (high-salt diet, inactivity, overexertion, exposure to
extremes in temperature).
128
Acute Decompensated Heart Failure

Definition:
Chronic disease is characterized by variable periods of
relative stability or compensation interrupted by periods of
exacerbation or decompensation. Patients with chronic heart
failure may live from day to day with no symptoms of heart
failure or well-controlled symptoms. However, chronic heart
failure may become acutely worse, resulting in an increase in
symptoms and limitations associated with left ventricular
dysfunction.
Causes:
1. myocardial ischemia
2. nonadherence to medial therapy
3. Poorly controlled hypertension
4. arrhythmias
5. pulmonary emboli, alcohol
6. or illicit drug use
7. infections such as pneumonia
8. Endocarditis and valvular abnormalities.
9. Any factor that increases oxygen demand, and therefore
demands for increased CO beyond the ability of ventricle
to function (eg, hypertension, tachycardia, anemia,
exercise)
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Acute coronary syndrome

Learning Objectives based on competence
1- Define ACS , UA,NSTEMI and STEMI
2-Mention risk factors associated with ACS
3-Relate the etiology and pathophysiology of acute coronary
syndrome (ACS) to the clinical manifestations of each disorder.
4-Describe the nursing role in the promotion of therapeutic lifestyle
changes in patients with acute coronary syndrome (ACS)
5-Differentiate the clinical characteristics and ECG patterns of
normal sinus rhythm, common dysrhythmias, and acute coronary
syndrome (ACS).
6-Compare between UA,NSTEMI and STEMI
7- Write laboratory studies for ACS
8-Deign collaborative care, and nursing management of the patient
with of acute coronary syndrome (ACS)
Definition:
Acute coronary syndrome (ACS) refers to a spectrum of
clinical presentations ranging from those for ST-segment elevation
myocardial infarction (STEMI) to presentations found in non–ST-
segment elevation myocardial infarction (NSTEMI) or in unstable
angina. It is almost always associated with rupture of an
atherosclerotic plaque and partial or complete thrombosis of the
infarct-related artery.
130
Pathophysiology:
Angina pectoris is caused by transient, reversible

myocardial ischemia precipitated by an imbalance between
myocardial oxygen demand and myocardial oxygen supply. In
most cases, angina pectoris is the result of a reduced oxygen
supply. The most common cause of a reduced supply of oxygen
is from atherosclerotic narrowing of the coronary arteries. A
non-occlusive thrombus develops on a disrupted atherosclerotic
plaque, resulting in a reduction in myocardial perfusion. As
blood flow to the myocardium decreases, autoregulation of
coronary blood flow occurs as a compensatory mechanism.
131
Degree and duration
 If the patient UA, a thrombus partially occludes a

coronary vessels. This thrombus is full of platelets .the
partially occluded may have distal microthrombi that
cause necrosis in some myocytes.
 If smaller vessels infarct, the patient is at higher risk for
MI, which may progress to NSTEMI. usually only the
innermost layer of the heart is damage.
 STEMI results when reduced blood flow through one of
the coronary arteries causes myocardial ischemia, injury,
and irreversible necrosis. The damage extends through
all myocardial layers. This thrombus contains
fibrinogen.
132
 Risk factors
Modifiable Non-
modifiable
Elevated blood Physical inactivity Age

pressure
Hyperlipidemia Cigarette smoker Gender
Diabetes mellitus Mental illness and Psychosocial stress Family

history
Obesity Low socio-economic status Race
Inflammation and Use of certain medications, including some oral

Alcohol use contraceptives and hormone replacement therapy
Acute coronary syndromes cover a spectrum of conditions. This

group comprises:
1) Unstable angina
Unstable angina: The patient has clinical manifestations of
coronary ischemia, but ECG and cardiac biomarkers show no
evidence of acute MI.
2) non-ST segment elevation myocardial infarction
(NSTEMI)
NSTEMI: The patient has elevated cardiac biomarkers but no
definite ECG evidence of acute MI.
133
3) ST segment elevation myocardial infarction (STEMI)

STEMI: The patient has ECG evidence of acute MI with
characteristic changes in two contiguous leads on a 12-lead
ECG. In this type of MI, there is significant damage to the
myocardium.
134
Unstable angina &NSTEMI

Definition:
Angina is chest pain resulting from myocardial ischemia caused by
inadequate myocardial blood and oxygen supply. Unstable angina
occurs when the blood clot causes a reduced blood flow, but not a
total blockage. This means that the heart muscle supplied by the
affected artery does not infarct (die).
Pathophysiology
Unstable angina deals with blood flow obstacles causing a lack
of perfusion to the myocardium. The left coronary artery will
divide into the circumflex and the left anterior descending
artery. Subsequently, this will divide into much smaller
branches. The right coronary will divide into smaller
branches as well. Unstable angina results when the blood flow
is impeded to the myocardium. Most commonly, this block can
be from intraluminal plaque formation, intraluminal thrombosis,
vasospasm, and elevated blood pressure. Often a combination
of these is the provoking factor.
135
Several factors are associated with typical anginal pain
Physical exertion Eating a heavy meal Thyrotoxicosis
Exposure to cold Fever. Stress or any emotion-

provoking situation
Pericarditis Pulmonary embolism Aortic dissection
Pneumothorax Peptic ulcer disease
Clinical Manifestations:
136
1. Pain 2. Dyspnea. 6. Dizziness

Pain can develop slowly or quickly. and syncope
Pain usually is described as mild or moderate.
3. Pallor. 7.
Substernal, crushing, squeezing pain may occur.
Hypertension
Pain may radiate to the shoulders, arms, jaw, neck, or back.
Pain intensity is unaffected by inspiration and expiration. 4. Sweating. 8. Digestive
Pain usually lasts less than 5 minutes; however, disturbances
pain can last up to 15 to 20 minutes.
5. Palpitations
Pain is relieved by nitroglycerin or rest.
and tachycardia.
Diagnostic studies
- Electrocardiography: Readings are normal during rest with ST
- depression or T-wave inversion during an episode of pain.
- Stress ECG testing: Chest pain or changes in the ECG or vital
signs during testing may indicate ischemia.
137
- Cardiac enzyme and troponin levels: Findings are normal in

angina.
- Cardiac catheterization: Catheterization provides a definitive
diagnosis by providing information about the patency of the
coronary arteries.
Complications
1- Acute myocardial infarction.
2- Cardiogenic shock.
3- Ischemic mitral regurgitation.
4- Supraventricular arrhythmias: rare complication of ischemia but
precipitate ischemic events.
5- Ventricular arrhythmias: simple and complex premature ventricular
contractions and no sustained ventricular tachycardia
6- Atrioventricular nodal blockade: usually transient in setting of
reversible ischemia (treatment is guided by location of block and
homodynamic stability).
Treatment:
The mainstay of treatment focuses on improving perfusion of the
coronary arteries. This is done in several ways.
Remember MONA:
 Morphine – give 5 mg IV
 Oxygen – high flow
 Nitrate – give sublingual GTN
138
 Aspirin – give 300 mg as a stat dose even if already on

aspirin.
- Antiplatelet therapies Patients are often treated with aspirin
orally, or rectally if the patient is unable to swallow. The aspirin
should be administered with 30 minutes.
- Nitroglycerin comes in several forms (intravenous, sublingual,
transdermal, orally) and improves perfusion by vasodilation of
the coronaries allowing improved flow and improved blood
pressure.
- Supplemental oxygen should be given as well via nasal cannula
to maintain appropriate oxygen saturation. These 3 actions are
the quickest and most important functions to be performed in
evaluating and treating for unstable angina. In patients with
continued pain or longer recovery time, the patient's response
should be evaluated because they are at much higher risk
for myocardial infarction.
- Other potential therapies include anticoagulation with either
low or high molecular weight heparin. Beta-blockers also can
decrease the energy demand by decreasing blood pressure and
heart rate.
- ACE inhibitors: are administered to those with evolving
MI with ST segment elevation or left bundle branch block
to reduce afterload and preload and to prevent remodeling.
139
- Early PCI in NSTEMI (within 6 hours) has been shown to have

lower mortality than those who undergo delayed PCI.
Stable Angina Versus Un stable Angina
Characteristics Stable Angina Un stable Angina

Definition The seizures: The seizures:
-Appear in physical -Have started recently
exertion or emotional - occur in lesser
stress. provocation or
-appear for more than one spontaneously
month. -Are longer and stronger
-There are no significant than those instable angina.
changes in the main
features of the pain.
Chest pain -Occur in physical exertion - Occur at rest.
or emotional stress. - Last more than 10
-Last 2-5 minutes. minutes.
Pathology Ischemia due to fixed Ischemia due to dynamic
stenosis of the arteries , obstruction of the of the
supplying blood to the heart arteries , supplying blood to
the heart, resulting from
rupture of the plaque with
superimposed spasm and
thrombosis
140
Predictability Predictable Not predictable

Treatment The pain passes quickly Emergent treatment is
after dis continuation of the necessary due to the risk of
physical effort or taking myocardial infarction and
nitroglycerin under the cardiac arrest
tongue
Diagnosis -The ECG in exercise is an -The ECG in exercise is
important supplementary contraindicated. Coronary
method. Coronary angiography is
angiography is usually not recommendable
done.
ECG The ECG is often normal The ECG frequently shows
changes ST segment
depression and ischemia T-
wave but without changed
in QRS
141
Myocardial infarction
Definition:
A heart attack (also known as a myocardial infarction or MI) results
in irreversible damage to the heart muscle due to lack of oxygen. An
MI may lead to impairment in diastolic and systolic function and
make the patient prone to arrhythmias.
Location of the infarction
Location of the infarction is an important determinant of
ventricular function. MI can be in the anterior, septal, lateral,
posterior or inferior walls of the left ventricular.
1. Obstruction of the LAD artery results in anterior wall or septal
MI, or both.
2. Obstruction of the circumflex artery results in posterior MI or
lateral wall MI.
3. Obstruction of the right coronary artery results in inferior wall
MI.
142
Causes a heart attack.
The etiology of acute myocardial infarction is decreased

coronary blood flow. The available oxygen supply cannot meet
oxygen demand, resulting in cardiac ischemia. Decreased coronary
blood flow is multifactorial. Atherosclerotic plaques classically
rupture and lead to thrombosis, contributing to acute decreased blood
flow in the coronary. Other etiologies of decreased
oxygenation/myocardial ischemia include coronary artery
embolism, cocaine-induced ischemia, and coronary vasospasm.
MI can also occur as a result of:
Trauma, vasculitis, drug use (cocaine), coronary artery

anomalies, coronary artery emboli, aortic dissection and
excess demand on the heart (hyperthyroidism, anemia)
143
Pathophysiology and natural history

Most patients who sustain an MI have coronary atherosclerosis.
The thrombus formation occurs most often at the site of an
atherosclerotic lesion, thus obstructing blood flow to the
myocardial tissues. Plaque rupture is believed to be the
triggering mechanism for the development of the thrombus in
most patients with an MI. As mentioned previously, the role of
inflammatory processes in the development of atherosclerotic
plaque is an area of intense scientific investigation.
Cardiovascular risk factors play a role in endothelial damage
resulting in endothelial dysfunction. The dysfunction
endothelium contributes to the activation of the inflammatory
response and the formation of atherosclerotic plaques. When the
plaques rupture, a thrombus is formed at the site that can
occlude blood flow, thus resulting in an MI. Irreversible damage
to the myocardium can begin as early as 20 to 40 minutes after
interruption of blood flow.
Signs and symptoms
Chest pain described as 2. Associated 3. Syncope or

a pressure sensation, fullness, or dyspnea or shortness near syncope
squeezing in the of breath. without other
-Radiation of chest pain into the jaw or cause
144
teeth, shoulder, arm, and/or back. Impairment of

-Pain may occur without cause, cognitive
primarily early in the morning. function without
-Pain is unrelieved by rest or other cause
nitroglycerin and is relieved only by
4. Associated 5. Associated
opioids.
epigastria discomfort diaphoresis or
-Pain lasts 30 minutes or longer.
with or without sweating
nausea and vomiting.
Diagnosis:
1- Laboratory studies
- Troponin levels: Troponin is a contractile protein that
normally is not found in serum; it is released only when
myocardial necrosis occurs.
- Creatine kinase (CK) levels: CK-MB levels increase within
3-12 hours of the onset of chest pain, reach peak values
within 24 hours, and return to baseline after 48-72 hours.
- Myoglobin levels: Myoglobin is released more rapidly from
infracted myocardium than is troponin; urine myoglobin
levels rise within 1-4 hours from the onset of chest pain.
- Complete blood count (CBC). - Chemistry profile.
- Lipid profile. - C-reactive protein and other
inflammation markers.
145
2- Electrocardiography
St Segment elevation, inverted t- wave and deep Q.
3- Cardiac imaging
Echo cardiograghy show segmental wall motion.
Complications of Myocardial infarction
Hemodynamic Myocardial Mechanical

Complications Complications Complications
• Hypotension • Diastolic dysfunction • Mitral valve
• Pulmonary congestion • Systolic dysfunction regurgitation from
• Cardiogenic shock • Heart failure papillary muscle rupture
• Right ventricular infarction • Left ventricular free
• Recurrent ischemia wall rupture
• Recurrent infarction • Ventricular septal
rupture
• Left ventricular
aneurysm
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Dysrhythmia Complications Pericardial Thromboembolic

• Ventricular tachycardia Complications Complications
• Ventricular fibrillation • Pericarditis • Deep venous
• Supraventricular • Dressler syndrome thrombosis
tachydysrhythmias • Pericardial effusion • Pulmonary embolism
• Brady dysrhythmias
• Atrioventricular block (first,
second, or third degree)
147
Treatment
Therapeutic options for coronary artery disease today are

based on three principles:
1- Medical treatment -
- Thrombolytic therapy: in the first 4-6 hrs As tissue
plasminogen activator or streptokinase. Thrombolytic drugs
lyse coronary thrombi by converting plasminogen
to plasmin.
- Beta-blockers - Morphine for relieving pain -
Nitroglycerin
148
- Calcium antagonists - Anti-coagulants -

Oxygen
- Aspirin - Glucose –insulin-K: recently used - ACE
inhibitor
2. Coronary interventions as angioplasty and coronary stent-
implantation;
3. Coronary artery bypasses grafting (CABG - coronary artery
bypass surgery).
Nursing diagnosis:
 Chest Pain related to reduced coronary blood flow.
 Decreased Cardiac Output related to alternation in
preload, afterload, or left ventricular failure
149
 Ineffective cardiac tissue perfusion related to reduced

coronary blood flow
 Risk for ineffective peripheral tissue perfusion related to
decreased cardiac output from left ventricular
dysfunction
 Death anxiety related to cardiac event
 Deficient knowledge about post-ACS self-care related to
lack of reference
 Noncompliance to therapeutic regimen related to un-
acceptance of necessary lifestyle changes
 Anxiety related to fear of illness, death, and critical care
environment
 Activity Intolerance related to ↓ CO or alterations in
myocardial tissue perfusion
 Risk for Ineffective Tissue Perfusion related to ↓ CO.
Nursing intervention
1. Assess quality, duration, and location of pain.
2. Administer IV morphine sulfate
3. monitor pain and hemodynamic response.
4. Administer analgesics appropriately for chest pain and
assess response.
5. Monitor physiologic response to pain during procedures
or after administration of pain medication.
150
6. Provide a calm, quiet environment.

7. Assess respiratory rate, effort, and breath sounds every 2
to 4 hours.
8. Obtain arterial blood gases per order or signs of
respiratory distress.
9. Monitor arterial saturation by pulse oximeter.
10. Provide supplemental oxygen by nasal cannula or face
mask for oxygen saturation <90%.
11.Provide intubation and mechanical ventilation as
necessary.
12.Encourage non intubated patients to use incentive
spirometer,
13.cough, and deep breath every 4 hours.
14. Ensure bed rest, turn patient side to side every 2 hours.
15.Monitor HR and BP every 1 to 2 hours
16.CVP, or right atrial pressure every 1 hour and cardiac
output
17.. Maintain patent IV access.
18.Administer positive inotropic agents, and reduce
afterload with vasodilating agents guided by
hemodynamic parameters as orders.
19.Evaluate effect of medications on BP, HR, and
hemodynamic parameters.
151
20.Restrict volume administration as indicated by CVP

21. Assess for neck vein distention, pulmonary crackles,
peripheral edema
22. Monitor 12-lead ECG daily.
23.Monitor cardiac markers, magnesium, phosphorus,
calcium, and potassium as ordered.
24.Monitor ECG for changes consistent with angina or MI.
25.Document rhythm strips every shift.
26.After PCI or fibrinolytic therapy, patient will
27.Assess, monitor, and treat pain .
28.Monitor signs of reperfusion, such as dysrhythmias, ST-
segment return to baseline.
29.Monitor PT, PTT.
30.Monitor ECG, heart sounds, hemodynamic parameters,
level of consciousness, and breath sounds for changes.
31.Report and treat deleterious changes as indicated
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Cardiac Arrhythmia
1-Define cardiac dysrhythmia.
2-Memorize conduction system of the heart.
3-Classify types of arrhythmia.
4-Explore complications of arrhythmia.
5-Differentiate between atrial flutter and atrial fibrillation.
6-Compare between ventricular fibrillation and ventricular
tachycardia.
7-Prioritize nursing care for each types of arrhythmia
8-Interpret ECG for patient with first degree, second degree, and
third degree heart block.
 Definition:
Dysrhythmias: are disorders of the formation or conduction (or
both) of the electrical impulse within the heart.
153
 NORMAL ELECTRICAL CONDUCTION:
 Normal Sinus Rhythm:

Normal sinus rhythm occurs when the electrical impulse starts at
a regular rate and rhythm in the sinus node and travels through
the normal conduction pathway.
The following are the ECG criteria: for normal sinus rhythm:
The impulse is initiated at the sinus node in a regular rhythm at
rate of 60 to 100 beats minute. a P wave interval is within normal
limits and equal duration (0.12 to 0.2 second).
154
(Normal Sinus Rhythm)

How to interpret ECG
1. Is there any electrical activity?
2. What is the ventricular (QRS) rate?
3. Is the QRS rhythm regular or irregular?
4. Is the QRS width normal or prolonged?
5. Is atrial activity present?
6. How is it related to ventricular activity?
7. Is their ischemic manifestation?
 Types of Dysrhythmias
Dysrhythmias include: (sinus node, atrial, junctional, and
ventricular dysrhythmias and their various subcategories.
 Arrhythmias originating at the sinus node dysrhythmias
1) Sinus Tachycardia. Sinus tachycardia occurs when the sinus

node creates an impulse at a faster-than-normal rate.
155
(Sinus Tachycardia)
It may be caused by acute blood loss, anemia, shock,

hypervolemia, hypervolemia, congestive heart failure, pain,
hyper metabolic states, fever, exercise, anxiety, or
sympathomimetic medications.
The ECG criteria: the upper limits of sinus tachycardia extend
to 160 to 180 beats \minute, All ECG criteria for sinus
tachycardia are the same as those of normal sinus rhythm, except
for the rate.
Treatment of sinus tachycardia is usually directed at abolishing
its cause. Calcium channel blockers and beta-blockers may be
used to reduce the heart rate quickly, O2 therapy and sedation
2 ) Sinus Bradycardia:
Sinus bradycardia occurs when the sinus node creates an impulse
at a slower-than-normal rate.
Causes include lower metabolic needs (e.g., sleep, athletic
training, hypothermia, hypothyroidism), vagal stimulation (e.g.,
from vomiting, suctioning, severe pain, extreme emotions),
156
medications (e.g., calcium channel blockers, amiodarone, beta-

blockers), increased intracranial pressure, and myocardial
infarction (MI), especially of the inferior wall.
(Sinus Bradycardia)
The following are characteristics of sinus bradycardia:.All
characteristics of sinus bradycardia are the same as those of
normal sinus rhythm, except for the rate.
Treatment:
- Atropine, 0.5 to 1.0 mg given rapidly as an intravenous
(IV) bolus, is the medication of choice in treating sinus
bradycardia.
- Cardiac pacing.
 ATRIAL DYSRHYTHMIAS:
1- Atrial Flutter.
Atrial flutter occurs in the atrium and creates impulses at an atrial
rate between 250 and 400 times per minute. Because the atrial
rate is faster than the AV node can conduct, not all atrial impulses
are conducted into the ventricle, causing a therapeutic block at
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the AV node. This is an important feature of this dysrhythmia. If

all atrial impulses were conducted to the ventricle, the ventricular
rate would also be 250 to 400, which would result in ventricular
fibrillation, a life-threatening dysrhythmia. Causes are similar to
that of atrial fibrillation. Causes with advanced age, valvular
heart disease, coronary artery disease, hypertension,
cardiomyopathy, hyperthyroidism, pulmonary disease, acute
moderate to heavy ingestion of alcohol (“holiday heart”
syndrome), or the aftermath of open heart surgery.
Atrial flutter is characterized by the following:
1. Ventricular and atrial rate: Atrial rate ranges between 250
and 400; ventricular rate usually ranges between 75 and 150.
2. Ventricular and atrial rhythm: The atrial rhythm is regular;
the ventricular rhythm is usually regular but may be irregular
because of a change in the AV conduction.
3. QRS shape and duration: Usually normal, but may be
abnormal or may be absent
4. P wave: Saw-toothed shape. These waves are referred to as F
waves.
5. PR interval: Multiple F waves may make it difficult to deter-
mine the PR interval.
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(Atrial Flutter)
2-Atrial Fibrillation.
Atrial fibrillation causes a rapid, disorganized, and
uncoordinated twitching of atrial musculature. It is the most
common dysrhythmia that causes patients to seek medical
attention. It may start and stop suddenly. Atrial fibrillation may
occur for a very short time (paroxysmal), or it may be chronic.
Atrial fibrillation is usually associated with advanced age,
valvular heart disease, coronary artery disease, hypertension,
cardiomyopathy, hyperthyroidism, pulmonary disease, acute
moderate to heavy ingestion of alcohol (“holiday heart”
syndrome), or the aftermath of open heart surgery.
Atrial fibrillation is characterized by the following :

1. Ventricular and atrial rate: Atrial rate is 300 to 600.
Ventricular rate is usually 120 to 200 in untreated atrial
fibrillation.
2. Ventricular and atrial rhythm :Highly irregular
abnormal.
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4. P wave: No discernible P waves; irregular undulating waves

are seen and are referred to as fibrillatory or f waves
5. PR interval: Cannot be measured
NB: low cardiac output
Treatment of atrial fibrillation and flutter :

- depends on its cause and duration and the patient’s symptoms,
age, and comorbidities. Administered of digitalis and Ca
channel blocker (verapamil. Deltazim), B blocker, amiodarone
as prescribed.
- Prepare patient for cardioversion if the patient
haemodynamically unstable.
- Assess for peripheral and apical pulse.
(Atrial Fibrillation)
 VENTRICULAR DYSRHYTHMIAS
1- Ventricular Tachycardia VT is usually associated with
coronary artery disease and may precede ventricular fibrillation.
VT is an emergency because the patient is usually (although not
always) unresponsive and pulseless.
160
(VT) has the following characteristics:

1. Ventricular and atrial rate: Ventricular rate is 100 to 200
beats per minute; atrial rate depends on the underlying rhythm
(eg, sinus rhythm)
2. Ventricular and atrial rhythm: Usually regular; atrial
rhythm may also be regular.
3. QRS shape and duration: Duration is 0.12 seconds or more;
bizarre, abnormal shape
4. P wave: Very difficult to detect, so atrial rate and rhythm may
be indeterminable
5. PR interval: Very irregular, if P waves seen.
6. P: QRS ratio: Difficult to determine, but if P waves are
apparent, there are usually more QRS complexes than P
waves.
If the patient is stable, continuing the assessment, especially
obtaining a 12-lead ECG, may be the only action necessary. Cardio-
version may be the treatment of choice, especially if the patient is
unstable. Several factors: determine the initial medication used for
treatment, including the following:
VT in a patient who is unconscious and without a pulse is treated
in the same manner as ventricular fibrillation: immediate
defibrillation is the action of choice.
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(Ventricular Tachycardia)
2: Ventricular fibrillation is a rapid but disorganized ventricular
rhythm that causes ineffective quivering of the ventricles. There is
no atrial activity seen on the ECG. Causes of ventricular fibrillation
are the same as for VT; it may also result from untreated or
unsuccessfully treated VT.
Causes include electrical shock and Brugada syndrome, in
which the patient (frequently of Asian descent) has a structurally
normal heart, few or no risk factors for coronary artery disease,
and a family history of sudden cardiac death.
1. Ventricular fibrillation has the following characteristics:

2. Ventricular rate: Greater than 300 per minute
3. Ventricular rhythm: Extremely irregular, without specific
pattern
4. QRS shape and duration :Irregular, undulating waves
without recognizable QRS complexes This dysrhythmia is
162
always characterized by the absence of an audible heartbeat, a

palpable pulse, and respirations. Because there is no coordinated
cardiac activity, cardiac arrest and death are imminent if
ventricular fibrillation is not corrected.
Treatment of choice is immediate defibrillation and activation
of emergency services. After defibrillation, eradicating causes
and administering vasoactive and antiarrhythmic medications
alternating with defibrillation are treatments used to try to
convert the rhythm to normal sinus rhythm.
(Ventricular Fibrillation)
4- Ventricular A systole .Commonly called flat line, ventricular

a systole is characterized by absent QRS complexes, al-
though P waves may be apparent for a short duration in two
163
different leads. There is no heartbeat, no palpable pulse, and

no respiration.
(Ventricular A systole)
Without immediate treatment, ventricular a systole is fatal.

Assessment to identify a possible cause, which may be hypoxia,
acidosis, severe electrolyte imbalance, drug overdose, or
hypothermia. Intubation and establishment of intravenous access
are the first recommended actions.
Treatment:
- Start CPR as soon as possible if patient have no pulse
- Give repeated dose for epinephrine.
- Prepare for transcutaneous pacing
164
 CONDUCTION ABNORMALITIES:
AV blocks occur when the conduction of the impulse through
the AV nodal area is decreased or stopped. These blocks can be
caused by medications (e.g., digitalis, calcium channel blockers,
beta-blockers), myocardial ischemia and infarction, valvular
disorders, or myocarditis. If the AV block is caused by increased
vagal tone (eg, suctioning, pressure above the eyes or on large
vessels, anal stimulation), it is commonly accompanied by sinus
bradycardia.
1. First-Degree Atrioventricular Block :
First-degree heart block occurs when all the atrial impulses are
conducted through the AV node into the ventricles at a rate
slower than normal.
This conduction disorder has the following characteristics :
1. Ventricular and atrial rate :Depends on the underlying
rhythm
2. Ventricular and atrial rhythm: Depends on the underlying
rhythm
abnormal
4. P wave: In front of the QRS complex; shows sinus rhythm,
regular shape
165
5. PR interval: Greater than 0.20 seconds; PR interval measure-

ment is constant.
Second-Degree Atrioventricular Block, Type I. Second-

degree, type I heart block occurs when all but one of the atrial
impulses are conducted through the AV node into the ventricles.
Each atrial impulse takes a longer time for conduction than the
one before, until one impulse is fully blocked. Because the AV
node is not depolarized by the blocked atrial impulse, the AV
node has time to fully repolarize, so that the next atrial impulse
can be conducted within the shortest amount of time.
a-Second-degree AV block, type I has the following
characteristics :
1. Ventricular and atrial rate: Depends on the underlying
rhythm
2. Ventricular and atrial rhythm: The PP interval is regular if
the patient has an underlying normal sinus rhythm; the RR
interval characteristically reflects a pattern of change. Starting
from the RR that is the longest, the RR interval gradually
shortens until there is another long RR interval.
166

abnormal
4. P wave: In front of the QRS complex; shape depends on
underlying rhythm
5. PR interval: PR interval becomes longer with each
succeeding ECG complex until there is a P wave not followed
by a QRS. The changes in the PR interval are repeated between
each “dropped” QRS, creating a pattern in the irregular PR
interval measurements.
b.Second-Degree Atrioventricular Block, Type II. Second-

degree, type II heart block occurs when only some of the atrial
impulses are conducted through the AV node into the ventricles.
Second-degree AV block, type II has the following
characteristics
1. Ventricular and atrial rate: Depends on the underlying
rhythm
2. Ventricular and atrial rhythm: The PP interval is regular if
the patient has an underlying normal sinus rhythm. The RR
167
interval is usually regular but may be irregular, depending on

the PQRS ratio.
3. QRS shape and duration : Usually abnormal, but may be
normal
4. P wave: In front of the QRS complex; shape depends on
underlying rhythm.
5. PR interval: PR interval is constant for those P waves just
before QRS complexes.
2. Third-Degree Atrioventricular Block. Third-degree heart

block occurs when no atrial impulse is conducted through the AV
node into the ventricles. In third-degree heart block, two
impulses stimulate the heart: one stimulates the ventricles (e.g.,
junctional or ventricular escape rhythm), represented by the QRS
complex, and one stimulates the atria (e.g., sinus rhythm, atrial
fibrillation), represented by the P wave. P waves may be seen,
but the atrial electrical activity is not conducted down into the
ventricles to cause the QRS complex, the ventricular electrical
activity. This is called AV dissociation.
168
Complete block (third-degree AV block) has the following

characteristics:
1. Ventricular and atrial rate: Depends on the escape and
under-lying atrial rhythm
2. Ventricular and atrial rhythm: The PP interval is regular
and the RR interval is regular; however, the PP interval is not
equal to the RR interval.
3. QRS shape and duration: Depends on the escape rhythm; in
junctional escape, QRS shape and duration are usually nor-
mal, and in ventricular escape, QRS shape and duration are
usually abnormal.
4. P wave: Depends on underlying rhythm
5. PR interval: Very irregular
Based on the cause of the AV block and the stability of the
patient, treatment is directed toward increasing the heart rate to
maintain a normal cardiac output. If the patient is stable and has
no symptoms, no treatment is indicated other than decreasing or
eradicating the cause (e.g., withholding the medication or treat-
ment). If the patient is short of breath, complains of chest pain or
lightheadedness, or has low blood pressure, an intravenous bolus
of atropine is the initial treatment of choice. If the patient does
not respond to atropine or has an acute MI, transcutaneous pacing
169
should be started. A permanent pacemaker may be necessary if

the block persists.
Complications of arrhythmias:
Certain arrhythmias may increase your risk of developing
conditions such as:
 Stroke. When your heart quivers, it's unable to pump blood
effectively, which can cause blood to pool. This can cause
blood clots to form. If a clot breaks loose, it can travel to and
obstruct a brain artery, causing a stroke.
 Heart failure. This can result if your heart is pumping in
effectively for a prolonged period due to a bradycardia or
tachycardia, such as atrial fibrillation.
170
Acute Liver Failure

Objectives based on competence
1. Evaluate the clinical manifestations of acute liver
failure
2. Summarize the management of hepatic
encephalopathy
3. Diagnose complications of acute liver failure
4. Analyze the causes of acute liver failure
5. Formulate the nursing diagnoses of acute liver
failure
6. Investigate results of laboratory tests for patient
with acute liver failure
Definition:
Acute liver failure (ALF) (also called fulminant hepatic failure)
is life threatening condition characterized by the abrupt onset of
severe liver injury, manifest as a profound liver dysfunction as
well as a confusional state called hepatic encephalopathy in
individuals with no prior history of liver disease.
Hepatic encephalopathy (HE) is an altered level of
consciousness as a result of liver failure. Its onset may be
gradual or sudden. Other symptoms may include movement
problems, changes in mood, or changes in personality. In the
advanced stages it can result in a coma.
171
The cause of the hepatic encephalopathy is related to:

 The accumulation of toxic agents because the liver
has lost the ability to metabolize and detoxify these
substances.
 Elevated serum ammonia, a byproduct of protein
and amino acid metabolism, is one of the suspected
neurotoxins. Normally, ammonia is metabolized
into urea before entering the systemic circulation,
and the urea is then excreted.
 If the liver is unable to perform this detoxification,
the circulating level of ammonia rises. If ammonia
and the other toxic agents can be reduced through
effective therapy, the encephalopathy gradually
clears.
Classification of Acute liver failure

Acute liver failure classifies into 3 categories based on the
interval between the development of jaundice and the onset of
encephalopathy.
 Hyperacute liver failure: the onset of
encephalopathy less than 7 days after the
development of jaundice.
172
 Acute liver failure: the onset of encephalopathy 8

to 28 days after the development of jaundice.
 Sub-acute liver failure: the onset of
encephalopathy from 29 days to 12 weeks after the
development of jaundice.
Four Grades of Encephalopathy
Changes in behaviour with minimal change in
Grade I
level of consciousness.
Gross disorientation, drowsiness, possibly
Grade II
asterixis, inappropriate behaviour.
Marked confusion, incoherent speech, sleeping
Grade III
most of the time but rousable to vocal stimuli
Comatose, unresponsive to pain, decorticate or
Grade IV decerebrate posturing.
Etiology:
Drugs and Toxins Acetaminophen, Isoniazid,
Salicylates, Anticonvulsants
Infectious Diseases: Viral hepatitis (A, B, C, D, E), Herpes
simplex virus
Vascular Budd-Chiari syn., veno-occlusive
disease.
173
Autoimmune Autoimmune hepatitis

Diseases
Metabolic disease Rare metabolic diseases, such as
Wilson's disease (a hereditary
syndrome with deposition of copper in
the liver) and acute fatty liver of
pregnancy
Shock Shock can severely impair blood flow
to the liver, causing liver failure.
Miscellaneous Causes Nonalcoholic fatty liver, Severe right-
sided congestive heart failure,
Clinical manifestations:
Constitutional Fever, chills, Generalized weakness,
malnutrition
Gastrointestinal Right upper quadrant pain, Left upper
quadrant pain, Loss of appetite,
Abdominal distention, Nausea,
vomiting/hematemesis, Clay-colored
feces, Diarrhea, Melena, hematochezia
Pulmonary Shortness of breath, Increased work of
breathing, decreased oxygen saturation,
Decreased partial pressure of oxygen
174
Cardiac Increased heart rate, Decreased blood

pressure, Dysrhythmias, Peripheral
edema
Neurological Headache, Depression/irritability,
Asterixis
Genitourinary Frothy, dark amber urine
Integumentary Jaundice, Dry skin, Bruising, ecchymosis,
Spider nevi, Palmar erythema, Hair loss
Endocrine Hypoglycemia, Increased weight
Immune Infection, spontaneous bacterial
peritonitis
Laboratory and diagnostic tests:
 Elevated levels of liver enzymes: Alanine transaminase
(ALT) - Aspartate transaminase (AST), Alkaline
phosphatase (ALP), Gamma-glutamyltransferase (GGT)
 Decreased level of serum albumin
 Elevated levels of serum bilirubin
 Elevated levels of serum ammonia.
 ABGs reveal respiratory alkalosis or metabolic acidosis
or both. Metabolic acidosis due to decrease lactate acid
clearance. Respiratory Alkalosis is an acid base
disturbance characterized by elevated arterial pH,
hyperventilation resulting in a low pCO2 and a usually
175
compensatory decrease in plasma HCO3- concentration.

 Blood glucose: hypoglycemia
 Electrolytes; hypokalemia, and hyponatremia.
 Platelet count less than 100,000/mm3.
 Prothrombin time (PT) is prolonged.
 Hepatitis markers
 Paracetamol level
 Imaging tests: an ultrasound exam to look at your
liver or abdominal computerized tomography (CT)
scanning or magnetic resonance imaging (MRI) to
look at your liver and blood vessels.
 Liver biopsy for examination of liver tissue
Medical management:
 Paracetamol overdose: give N-acetylcysteine
 Encephalopathy:
 Protein intake is limited to 20 to 40 g/d for the
treatment of acute HE.
 Lactulose is used to facilitate bowel movements and
clearance of nitrogenous products. Lactulose
decreases the colonic pH to prevent the absorption of
ammonia.
 Neomycin or metronidazole may be given to clear the
gut of bacteria that promote nitrogenous production.
176
 Nursing measures to protect the patient with mental

status changes from harm are a priority.
 Coagulopathy:
 Give vitamin K: give at least one dose (10mg IV)

 Fresh Frozen Plasma if there is bleeding or
undergoing surgical procedure
 Platelet support if thrombocytopenic and bleeding.
platelet counts 10,000/mm3 or invasive procedures
 Ascites:
 Low-sodium diet of no more than 2,000 mg/d, fluid
restriction, and diuretic therapy.
 Paracentesis is also used to treat ascites in patients
unresponsive to salt restriction and maximal diuretic
therapy.
 A venous–peritoneal (VP) shunt is used to relieve
ascites that is resistant to other therapies.
 Measuring and recording daily weights, abdominal
girth, and intake and output
 Treatment with albumin has been used in ALF due to
its oncotic properties, in order to expand plasma volume
and to increase effective circulatory volume.
 Metabolic changes: monitor glucose 2hourly and treat
with 10% or 50% glucose.
 Cerebral edema: ICP monitoring, give mannitol
177
(100mL of 20% mannitol).

 Hemodynamic support: correct the hypovolemia with
colloid or blood but avoid fluid overload. Persistent
hypotension may respond to noradrenaline infusion.
 Respiratory support: monitor O2 saturation
continuously and give oxygen by mask if Sao2 less than
90% and intubation and MV if needed.
 Sepsis: prophylactic antibiotics and antifungals.
 Wilson’s disease: consider penicillamine and IV vitamin
E
 Prophylaxis for stress ulceration: gastric acid
suppression and Proton pump inhibitors (IV or PO) are
recommended.
 Renal failure: monitor renal function, treat by
hemofilteration.
Nursing diagnosis:
 Ineffective breathing pattern RT decreased lung
expansion.
 Impaired gases exchange RT V/Q mismatching.
 Decreased cardiac output RT alteration in preload.
 Decreased cardiac output RT alteration in HR.
 Imbalanced nutrition: less than body requirements RT
increased metabolic demand
178
 Risk for infection.

 Decreased intracranial adaptive capacity RT failure of
normal compensatory mechanism.
 Ineffective renal tissue perfusion RT decreased renal
blood flow.
Nursing Management
 Maintaining adequate Oxygenation/Ventilation
 Monitor pulse oximetry and ABG values,
respiratory rate and pattern, and ability to clear
secretions.
 Assist patient to turn, cough, deep breathe, and use
incentive spirometer every 2 h.
 Provide chest percussion with postural drainage if
indicated every 4 h.
 Monitor effect of ascites on respiratory effort and
lung compliance.
 Position patient on side and with head of bed
elevated to improve diaphragmatic movement.
 Assist physician with intubation and initiation of
mechanical ventilation as indicated.
179
 Maintaining adequate Circulation/Perfusion

 Monitor vital signs, including cardiac output.
 Monitor lactate daily until it is within normal limits.
 Administer RBCs, positive inotropic agents, colloid
infusion as ordered to increase oxygen delivery.
 Monitor PT, PTT, complete blood count daily.
 Assess for signs of bleeding (eg, blood in gastric
contents, stools, or urine); observe for petechiae,
bruising.
 Administer blood products as indicated.
 Perform gastric lavage as needed.
 Maintaining adequate body Fluids/Electrolytes

 Daily weights
 Monitor intake and output.
 Monitor electrolyte values.
 Measure abdominal girth daily at the same location
on the abdomen.
 Monitor signs of volume overload: Pulmonary
crackles, Shortness of breath, Jugular vein
distention, Peripheral edema
 Administer diuretics as ordered.
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 Nutrition
 Provide nutrition by oral, enteral, or parenteral
feeding.
 Adhere to sodium, protein, fat, or fluid restrictions
as necessary.
 Consult dietitian or nutritional support service to
evaluate nutritional needs and restrictions.
 Provide small, frequent feedings.
 Monitor albumin, BUN, cholesterol, triglycerides,
bilirubin, aspartate transaminase, alanine
transaminase.
 Administer cleansing enemas and cathartics if
ordered.
 Monitor patient's caloric intake and weight daily to
ensure adequacy of nutritional interventions.
 Provide patient with oral care before eating to
ensure optimal consumption of diet.
 Mobility/Safety
 Assess serum ammonia level.
 Administer lactulose as ordered.
 Monitor level of consciousness, orientation.
 Assess asterixis.
 Take precautions to prevent falls.
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 Conduct range-of-motion and strengthening

exercises.
 Monitor SIRS criteria: increased WBC, increased
temperature, tachypnea, tachycardia.
 Use aseptic technique during procedures and
monitor others.
 Maintain invasive catheter tube sterility.
 Change invasive catheters, culture blood, line tips,
or fluids, provide site care, etc., according to
hospital protocol.
 Skin Integrity
 Assess skin every 8 h and each time patient is
repositioned.
 Turn patient every 2 h. Assist or teach patient to
shift weight or reposition.
 Consider pressure relief/reduction mattress.
 Comfort/Pain Control
 Assess pain and discomfort from ascites, bleeding.
 Administer analgesics cautiously and monitor patient
response.
 Bathe with cool water, blot dry.
 Lubricate skin.
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 Administer antipruritic medication; apply to skin PRN as

ordered.
 Nursing interventions that can help to reduce ICP:
 Place head of bed flat or at 30 degrees elevation per orders
 Maintain head in neutral position
 Avoid hip flexion
 Assess agitation in restrained patients
 Frequent temperature checks because cerebral metabolic rate
increases with elevated body temperature
 Monitor serum glucose because alterations in glucose can
produce neurological changes
 Administer daily stool softeners as ordered
Complications:
 Cirrhosis: Cirrhosis can cause severe alterations in the
structural architecture of the liver and function of the
hepatocytes. Necrosis is followed by regeneration of liver
tissue but not in a normal fashion.
 Hepatorenal Syndrome:
- It is defined as the development of renal failure in patients
with severe liver disease (acute or chronic) in the absence of
any other identifiable cause of renal pathology.
183
- Clinical findings: Ascites, jaundice, hypotension, and

oliguria.
- Laboratory findings typically include azotemia (elevated
blood urea nitrogen), elevated serum creatinine, and
hyponatremia.
- Management goals include therapies to support liver and
kidney functions. It is now being suggested that both a liver
and kidney transplantation would improve patient survival
 Spontaneous Bacterial Peritonitis (SBP):

- Patients with acute liver failure may be more susceptible to
infection because the hepatic Kupffer cells, which are
responsible for uptake and subsequent degradation of foreign
and potentially harmful substances in the body, do not
function as efficiently.
- Causes: SBP occurs when there is a large accumulation
ascitic fluid contains low concentrations of albumin, which
normally provide some protection against bacteria.
Subsequent leakage of bacteria through the abdominal wall
or from invasive procedures.
184
Acute Pancreatitis
1. Illustrate causes of severe acute Pancreatitis.
2. Detect signs and symptoms of severe acute
Pancreatitis
3. Apply nursing care for patient with severe acute
Pancreatitis
Introduction: The pancreas is an organ located behind the

stomach and near the small intestine. that helps with digestion ,
distributes insulin, digestive enzymes, and other necessary
hormones.
Definition:
acute pancreatitis is a condition where the pancreas becomes
inflamed (swollen) over a short period of time may be mild or
life threatening, It occurs suddenly and causes pain in the upper
abdominal (or epigastric) region. The pain often radiates to your
back.
In acute pancreatitis, inflammation develops quickly and
subsides within a few days but can last for to a few weeks.
In chronic pancreatitis, the pancreas is persistently inflamed,
which causes permanent damage.
185
Pathophysiology
Factors as ( Alcoholism, Biliary tract disease, Trauma,
Infection, Drugs ,Postoperative GI surgery)
↓
Premature activation of pancreatic enzymes and Injury to
pancreatic cells
↓
Autodigestive effects of pancreatic enzymes of pancreatic
tissue
Trypsin
Edema , Necrosis, Hemorrhag, Shock
Types or stages:
The latest classification of acute pancreatitis (AP):
(1) Mild AP (MAP) is characterized by the absence of both
pancreatic necrosis and organ failure;
(2) Moderate AP is characterized by the presence of sterile
pancreatic necrosis and/or transient organ failure;
(3) Severe AP (SAP): also called necrotic or hemorrhagic
pancreatitis, there is
extensive fat necrosis in and around the pancreas, pancreatic
cellular necrosis, and
186
hemorrhage in the pancreas. Severe acute pancreatitis is

associated with local and
systemic complications
Causes:
 Most common The most common causes (more than
70% of cases) of acute pancreatitis are
 gallstones (Gallstones cause about 40% of cases of
acute pancreatitis)
 Alcohol in 30% of cases The risk of developing
pancreatitis increases with increasing amounts of alcohol
(4 to 7 drinks per day in men and 3 or more drinks per
day in women)
 Idiopathic in 15-25% of cases
 Metabolic disorders
 Abdominal trauma
 Penetrating ulcers
 Carcinoma of the head of pancreas, and
other cancer
 Infections: viral hepatitis.
 Radiotherapy
 Autoimmune pancreatitis
187
 Less common
 Ischemia from bypass surgery
 Heart valve surgery
 Fat necrosis
 Pregnancy
 Hyperparathyroidism
 Cystic fibrosis
Signs and symptoms

Signs and symptoms of pancreatitis may vary, depending
on which type you experience
 Acute pancreatitis signs and symptoms include:
 Sharp and sudden upper abdominal pain below the
breastbone (sternum) that radiates to your back ,pain
cannot be relieved even with strong painkillers
 Tenderness when touching the abdomen
 Fever
 Rapid pulse
 Nausea
 Vomiting
 jaundice, when the skin and whites of the eyes take on a
yellowish tinge
188
 Grey-Turner's sign (hemorrhagic discoloration of the

flanks)
 Cullen's sign (hemorrhagic discoloration of the umbilicus)
 Chronic pancreatitis signs and symptoms include:

 Upper abdominal pain
 Abdominal pain that feels worse after eating
 Losing weight without trying
 Oily, smelly stools (steatorrhea)
 fever
Diagnosis:
 Blood tests
 Serum amylase and lipase.
 Liver- associated enzymes.
 Blood urea nitrogen and Blood glucose
 Serum cholesterol and triglyceride
 Complete blood count (CBC) and hematocrit.
 C- reactive protein
 Arterial blood gas values(ABG)
 Immunoglobulin
189
 diagnostic study :
 An ultrasound scan
 ERCP endoscope is inserted into the digestive
system.
 CECT (contrast-enhanced computed
tomography) scan: take pictures of the same area
from many angles;
 Chest X-ray
Treatment:
1. Treatment of mild acute pancreatitis usually
involves short-term hospitalization where fluids
are given (intravenously), analgesics are given for
pain relief, and the person fasts to try to rest the
pancreas. A low-fat, soft diet is usually started
soon after admission if there is no nausea,
vomiting, or severe pain.
2. People with moderately severe acute
pancreatitis need to be hospitalized for a longer
period of time and given intravenous fluids. If
people are unable to eat, they are given food
through a tube that is inserted through the nose
and into the stomach or intestine (tube feeding or
enteral tube nutrition). Symptoms such as pain
190
and nausea are controlled with drugs given

intravenously, antibiotics.
3. People with severe acute pancreatitis are
admitted to an intensive care unit, where vital
signs (pulse, blood pressure, and rate of breathing)
and urine production can be monitored
continuously
Treatment for sever acute pancreatitis ,include:
 Painkillers: Mild acute pancreatitis can be moderately or
severely painful.
 Nasogastric tubes: A tube may remove excess liquids and air
as a treatment for nausea and vomiting.
 Bowel rest: The gastrointestinal tract will need to rest for a few
days, so the person will not take any food or drink by mouth
until their condition improves.
 Preventing dehydration: Fluid is often provided
intravenously for the first 24-48 hours.
 Antibiotics to stop any infection e.
 Breathing assistance: Ventilation equipment will help the
patient breathe.
 Surgery: the dead tissue may need to be surgically removed.
191
Complications:
Pancreatitis can cause serious complications, including:
 Kidney failure. Acute pancreatitis may cause kidney
failure, which can be treated with dialysis.
 Breathing problems. Acute pancreatitis can cause
decrease the level of oxygen in blood to dangerously low
levels.
 Infection. Acute pancreatitis can cause Pancreatic
infections in tissue are serious and require intensive
treatment, such as surgery to remove the infected tissue
and Infection in bloodstream (septicemia) is an
emergency.
 Pseudocyst. Acute pancreatitis can cause fluid collect in
cyst like pockets in pancreas. A large pseudocyst that
ruptures can cause complications such as internal
bleeding and infection.
 Malnutrition. Both acute and chronic pancreatitis can
cause your pancreas to produce fewer of the enzymes that
are needed to digestion. lead to diarrhea and weight loss,
 Diabetes. Damage to insulin-producing cells in your

pancreas from chronic pancreatitis can lead to diabetes.
192
 Pancreatic cancer. Long-standing inflammation in

pancreas caused by chronic pancreatitis is a risk factor
for developing pancreatic cancer.
 Organ failure (Heart, lung, and kidney failure may
occur. In severe cases, organ failure can happen
around 48 hours after symptoms appear without
treatment, these can lead to death.
Nursing diagnoses :
• Acute Pain and discomfort related to edema, distention of the
pancreas, and peritoneal irritation
• Deficient fluid volume related to nausea, vomiting, restricted
oral intake.
 Imbalanced nutrition: less than body requirements related
to inadequacy dietary intake, impaired absorption.
 Activity intolerance related to fatigue
 Ineffective breathing pattern related to severe pain,
pulmonary infiltrates, pleural effusion and atelactasis
 Impaired skin integrity resulting from poor nutritional
status, bed rest, surgical wound
 Fear in response to the diagnosis of pancreatitis
 Ineffective coping related to the diagnosis of pancreatitis
193
Acute Kidney injury

1. Explain the causes of acute kidney injury (AKI).
2. Describe urine production during the non-oliguric, oliguric,
and diuretic phases of acute tubular necrosis.
3. Differentiate between the three types of AKI based on
history and physical examination, laboratory values, and
diagnostic tests.
4. Discuss the major causes and the clinical stages of acute
kidney disease.
5. Discuss the clinical manifestations and management of
renal failure.
Definition:
 Acute kidney injury (AKI ) is the sudden interruption of
renal function resulting from:
• Obstruction
• Reduced circulation
• Renal parenchymal disease.
 Acute renal failure (ARF) is a sudden and almost
complete loss of kidney function (decreased GFR) over
a period of hours to days.
194
Causes of Acute kidney injury:

1) Pre-renal Failure (results from conditions that diminish
blood flow to the kidneys)

• Volume depletion resulting from:
 Hemorrhage
 burn
 Renal losses (diuretics, osmotic diuresis)
 Gastrointestinal losses (vomiting, diarrhea,
nasogastric suction)
• Impaired cardiac efficiency resulting from:
 Myocardial infarction
 Heart failure
 Dysrhythmias
 Cardiogenic shock
• Vasodilation resulting from:
 medications that cause vasodilation as Antihypertensive
drugs
 Sepsis
Reno-vascular obstruction
 Arterial embolism
 Arterial or venous thrombosis
 Tumor
195
2) Intra-renal Failure
• Prolonged renal ischemia resulting from:
 Pigment nephropathy (associated with the breakdown of
blood cells containing pigments that in turn occlude
kidney structures)
 Myoglobinuria (trauma, crush injuries, burns)
 Hemoglobinuria (transfusion reaction, hemolytic anemia)
• Nephrotoxic agents such as:
 Aminoglycoside antibiotics (gentamicin, tobramycin)
 Radiopaque contrast agents
 Heavy metals (lead, mercury)
 Solvents and chemicals (ethylene glycol, carbon
tetrachloride, arsenic)
 Non-steroidal anti-inflammatory drugs (NSAIDs)
 Angiotensin-converting enzyme inhibitors (ACE
inhibitors)
• Infectious processes such as:
 Acute pyelonephritis
 Acute glomerulonephritis
1) Post renal Failure
3) post-renal Failure
• Urinary tract obstruction, including:
 Calculi (stones)
196
 Tumors
 Benign prostatic hyperplasia
 Strictures
 Blood clots
PHASES OF ACUTE RENAL FAILURE

• There are four clinical phases of ARF: initiation, oliguria,
diuresis, and recovery.
The initiation period: begins with an initial insult and lasts until cell
injury occurs.
• -The onset phase lasts from hours to days, depending on the cause,
and is heralded by the appearance of signs of renal failure
(decreased urine output, increased serum creatinine).
• -The major goal during this phase is to determine the cause of the
ATN and initiate treatment to prevent irreversible tubular damage.
The oliguria period:
• Oliguria is a decreased urine output (less than 400 mL/24
hours).
• The minimum amount of urine needed to rid the body of
normal metabolic waste products is 400 mL.
• Pre-renal oliguria results from decreased blood flow to the
kidney.
197
• Before damage occurs, the kidney responds to decreased

blood flow by conserving sodium and water.
• Once damage occurs, the kidney’s ability to conserve
sodium is impaired.
• Untreated pre-renal oliguria may lead to acute tubular
necrosis.
• Hypervolemia also occurs, causing edema, weight gain, and
elevated blood pressure.
• This phase is accompanied by a rise in the serum concentration of
substances usually excreted by the kidneys (urea, creatinine, uric
acid, organic acids, and the intracellular cations [potassium and
magnesium]).
• In this phase uremic symptoms first appear and life-threatening
conditions such as hyperkalemia develop.
• The main goal during this period is to support renal function and
keep the patient alive until renal injury heals.
• Major causes of death during this period are from hyperkalemia,
gastrointestinal bleeding, and infection.
• Oliguric ATN lasts approximately 12 days although it may last
only a few days or as long as 30 days.
198
In the diuresis period,

• The diuretic phase is marked by urine output that can range
from normal (1 to 2 L/day) to as great as 4 to 5 L/day. High
urine volume has two causes, including:
• the kidney’s inability to conserve sodium and water
• Osmotic diuresis produced by high BUN levels.
During the diuretic phase, which lasts several days to 1 week,
BUN and creatinine levels slowly increase and hypovolemia and
weight loss result. These conditions can lead to deficits of
potassium, sodium, and water that can be deadly if left untreated.
If the cause of the diuresis is corrected, azotemia gradually
disappears and the patient improves greatly—leading to the
recovery stage.
• -The degree of diuresis which can exceed 4 to 5 L/day, is primarily
determined by the state of hydration at the time the patient enters
this stage. This puts patients at risk for fluid volume deficits and
electrolyte abnormalities like hypo-natremia and hypokalemia.
• -Laboratory values stop rising and eventually decrease. Although
the volume of urinary output may reach normal or elevated levels,
renal function may still be markedly abnormal.
The recovery period signals the improvement of renal
function and may take 3 to 12 months. Laboratory values
return to the patient’s normal level. Although a permanent
199
1% to 3% reduction in the GFR is common, it is not

clinically significant.
Manifestations:
CHANGE IN KIDNEY CONTOUR INCREASED
BUN AND CREATININE LEVELS (AZOTEMIA)
The BUN level rises steadily at a rate dependent on the
degree of catabolism (breakdown of protein), renal
perfusion, and protein intake. Serum creatinine rises in
conjunction with glomerular damage. Serum creatinine
levels are useful in monitoring kidney function and disease
progression.
HYPERKALEMIA
• With a decline in the GFR, the patient cannot excrete
potassium normally.
• Patients with oliguria and anuria are at greater risk
for hyperkalemia than those without oliguria.
• Protein catabolism results in the release of cellular
potassium into the body fluids, causing severe
hyperkalemia (high serum K+ levels). Hyperkalemia
may lead to dysrhythmias and cardiac arrest.
• Sources of potassium include normal tissue
catabolism, dietary intake, blood in the GI tract, or
200
blood transfusion and other sources (intravenous

infusions, potassium penicillin, and extracellular
shift in response to metabolic acidosis).
METABOLIC ACIDOSIS
• Patients with acute oliguria cannot eliminate the
daily metabolic load of acid-type substances
produced by the normal metabolic processes. In
addition, normal renal buffering mechanisms fail.
CALCIUM AND PHOSPHORUS ABNORMALITIES
• There may be an increase in serum phosphate
concentrations; serum calcium levels may be low in
response to decreased absorption of calcium from the
intestine and as a compensatory mechanism for the
elevated serum phosphate levels.
Medical management
-Because hyperkalemia is the most life-threatening fluid and electrolyte
disturbances.
 The patient is monitored for hyperkalemia through serial serum

electrolyte levels (potassium value more than 5.5 mEq/L [5.5
mmol/L]), electrocardiogram changes (tall, tented, or peaked T
waves), and changes in clinical status.
201
Low-dose dopamine (1 to 3 g/kg) is often used to dilate the renal

arteries
-In patients with severe acidosis, the arterial blood gases or
serum bicarbonate levels must be monitored because the patient
may require sodium bicarbonate therapy or dialysis.
Nutritional therapy
-Dietary proteins are limited to about 1 g/kg during the oliguric
phase to minimize protein breakdown and to prevent
accumulation of toxic end products. Caloric requirements are
met with high-carbohydrate meals because carbohydrates have
a protein sparing effect.
-Foods and fluids containing potassium or phosphorus
(bananas, citrus fruits and juices, coffee) are restricted.
Potassium intake is usually restricted to 40 to 60 mEq/day, and
sodium is usually restricted to 2 g/day. The patient may require
parenteral nutrition.
-The oliguric phase of ARF may last 10 to 20 days and is
followed by the diuretic phase, at which time urine output
begins to increase, signaling that kidney function is returning.
Blood chemistry evaluations are made to determine the
amounts of sodium, potassium, and water needed for
replacement, along with assessment for over-hydration or
under-hydration.
202
-After the diuretic phase, the patient is placed on a high-protein,

high-calorie diet and is encouraged to resume activities
gradually.
Nursing diagnosis:
 Fluid Volume Excess related to decreased kidney function
■ Alteration in Cardiac Output: Decreased related to fluid volume
excess, disturbances in renin–angiotensin system
■ Altered Nutrition: Less than Body Requirements related to
anorexia, nausea and vomiting, dietary restrictions, and altered
oral mucous membranes
■ Impairment of Skin Integrity related to poor nutritional status,
immobility, and edema
Anxiety related to unexpected serious illness and uncertain
prognosis, unfamiliar environment, and current symptoms
■ Activity Intolerance related to fatigue, anemia, retention of
waste products, and dialysis procedure
■ Sleep Pattern Disturbance related to fragmented sleep
■ Potential for Infection related to decreased functioning of
immune system
■ Knowledge Deficit: pathophysiology and etiology of acute
episode, dietary restrictions, medications, complications,
prognosis, and need for follow-up care.
203
Nursing management
Monitoring fluid and electrolyte balance
-The nurse monitors the patient’s serum electrolyte levels and
physical indicators of these complications during all phases of
the disorder.
-Parenteral fluids, all oral intake, and all medications are
screened carefully to ensure that hidden sources of potassium
are not inadvertently administered or consumed.
-The nurse monitors fluid status by paying careful attention to
fluid intake, urine output, apparent edema, distention of the
jugular veins, alterations in heart sounds and breath sounds,
and increasing difficulty in breathing.
-Accurate daily weights, as well as intake and output records,
are essential.
-Indicators of deteriorating fluid and electrolyte status are
reported immediately to the physician, and preparation is made
for emergency treatment.
-Hyperkalemia is treated with glucose and insulin, calcium
gluconate, or dialysis.
-Fluid and other electrolyte disturbances are often treated with
hemodialysis, peritoneal dialysis, or other continuous renal
replacement therapies.
204
Reducing metabolic rate

-The nurse also directs attention to reducing the patient’s
metabolic rate during the acute stage of renal failure to reduce
catabolism and the subsequent release of potassium and
accumulation of endogenous waste products (urea and
creatinine).
-Bed rest may be indicated to reduce exertion and the metabolic
rate during the most acute stage of the disorder. Fever and
infection, both of which increase the metabolic rate and
catabolism, are prevented or treated promptly.
Promoting pulmonary function
-Attention is given to pulmonary function, and the patient is
assisted to turn, cough, and take deep breaths frequently to
prevent atelectasis and respiratory tract infection. Drowsiness
and lethargy may prevent the patient from moving and turning
without encouragement and assistance.
Preventing infection
-Asepsis is essential with invasive lines and catheters to
minimize the risk of infection and increased metabolism. An
indwelling urinary catheter is avoided whenever possible
because of the high risk for UTI associated with its use.
205
Providing skin care

-The skin may be dry or susceptible to breakdown as a result
of edema; therefore, meticulous skin care is important.
Additionally, excoriation and itching of the skin may result
from the deposit of irritating toxins in the patient’s tissues.
-Massaging bony prominences, turning the patient
frequently, and bathing the patient with cool water are often
comforting and prevent skin breakdown.
Prevention:
1. Provide adequate hydration to patients at risk for dehydration:
 Surgical patients before, during, and after surgery
 Patients undergoing intensive diagnostic studies
requiring fluid restriction and contrast agents (eg,
barium enema, intravenous pyelograms), especially
elderly patients who may not have adequate renal
reserve.
 Patients with neoplastic disorders or disorders of
metabolism (ie, gout) and those receiving
chemotherapy
2. Prevent and treat shock promptly with blood and fluid
replacement.
206
3. Monitor central venous and arterial pressures and hourly urine

output of critically ill patients to detect the onset of renal failure as
early as possible.
4. Treat hypotension promptly.
5. Continually assess renal function (urine output, laboratory
values) when appropriate.
6. Take precautions to ensure that the appropriate blood is
administered to the correct patient in order to avoid severe
transfusion reactions, which can precipitate renal failure.
7. Prevent and treat infections promptly. Infections can produce
progressive renal damage.
8. Pay special attention to wounds, burns, and other precursors of
sepsis.
9. Give meticulous care to patients with indwelling catheters to
prevent infections from ascending in the urinary tract.
Remove catheters as soon as possible.
10. To prevent toxic drug effects, closely monitor dosage, duration
of use, and blood levels of all medications metabolized or excreted
by the kidneys.
207
Head Injury
1. Enumerate causes of head injury
2. Differentiate types of head injury by mechanism of
injury and clinical manifestations.
3. Describe the collaborative care and nursing
management of the patient with a head injury.
Definition:
Head injury, also known as traumatic brain injury (TB1),
is the disruption of normal brain tissue, and function due
to trauma, injury resulting in compromised neurologic
'function resulting diffuse symptoms
Causes of head injury:
-Fall from high (FFH).
-Road traffic accident (RTA).
-Violence (assaults, bullet , shell, missiles )
-Sport injury.
TBT is classified as mild (GCS 13 to 15 with loss of

consciousness to 15 minutes), moderate (GCS-9 to 12 with loss
of consciousness for up to 6 hours), or severe (GCS 3 to 8 with
loss of consciousness greater than 6 hours
208
Types of Head Injuries:

1. Scalp injury (scalp contusion, laceration, avulsion,
subgaleal)
2. Skull fracture:
209
3. Brain Injury (closed head injury)

a. Concussion (a sudden transient mechanical head injury
with disruption of neural activity and a change in the

level of consciousness LOC).
b. Contusion is bruising of the brain tissue within a focal
area.
c. Epidural Hematoma: results from bleeding between the
dura and the inner surface of the skull.

d. Subdural Hematoma: occurs from bleeding between the
duramater and the arachnoid layer of the meninges.

e. Intra-cerebral hematoma: occurs from bleeding within
the brain tissue
Pathophysiology:
A-Primary brain injury, injury occurs at the time of
trauma, include
 Scalp lacerations: The most minor type of head trauma
 Skull fractures: face Linear or depressed Simple,
comminuted, or compound, displaced
Closed or open and direct & indirect
A. Secondary Brain Injury leading to further
brain damage after the initiating trauma
210
Clinical Manifestations:
 Neurologic deficits result from Location of fracture,
ischemia, hemorrhage, and cerebral edema .
 Disturbances in consciousness: confusion to coma.
 Otorrhea (leak of CSF into ear)
 Rhinorrhea (leak of CSF into nose)
 Battle’s sign (ecchymosis behind the ear)
 Extensive sub-conjunctival hemorrhage
 Periorbital ecchymosis (eyes)
 Headache, vertigo.
 Persistent, localized pain
 Facial paralysis
 Agitation, restlessness.
 Respiratory irregularities.
 Cognitive deficits.
 Coma and coma syndromes; persistent vegetative state.
Diagnostic Evaluation
 CT scan to identify and localize lesions, edema, bleeding.
 Skull and cervical spine X ray films to identify fracture
displacement.
 Cerebral angiography.
 MRI.
 Neuropsyeho logical tests during
rehabilitation phase to determine cognitive deficits.
211
Medical management
 Management of increased ICP.
 Antibiotics to prevent infection with open skull fractures or
penetrating wounds.
 Surgery: the goal for Surgery evacuation of interracial
hematomas,
 Cleaning and debridement of wounds, remove fragment,
necrotic tissue, elevation of skull fractures, or repair of CSF
leaks
212
The complications of head injury:

1. Hematoma.
2. Meningeal and brain tissue damage.
3. Infection: systemic (respiratory, urinary), neurologic
(meningitis).
4. Increased 1CP, hydrocephalus.
5. Posttraumatic seizure disorder.
6. Permanent neurologic deficits: cognitive, motor, sensory,
speech,
7. Neurobehavioral alterations: aggression, emotional lability.
Nursing Diagnosis
1. Risk for ineffective cerebral tissue perfusion related to
interruption of CBF associated with cerebral

hemorrhage, hematoma, and edema
2. Hyperthermia related to increased metabolism,
infection, and hypothalamic injury.
3. Impaired physical mobility related to decreased LOC
4. Anxiety related to abrupt change in health status,
hospital environment, and uncertain future.

5. Potential complication: increased ICP related to
cerebral edema and hemorrhage.

Emergency Nursing Management:
Primary assessment
• Ensure patent airway.
• Stabilize cervical spine.
• Administer O2.
• Establish IV access with two large-bore catheters
to infuse normal saline or lactated Ringer ‘s
solution.
• Intubate if Glasgow coma scale (GCS) score <8.
• Control external bleeding with sterile pressure dressing.
• Remove patient‘s clothing.
Ongoing Monitoring
• Maintain patient warmth using blankets, warm
IV fluids, overhead, warming lights, warm
humidified O2.
• Monitor vital signs, level of consciousness, O2
saturation, cardiac rhythm, GCS score, pupil size and
reactivity.
Critical Care Nursing
.
• Anticipate need for intubation if gag reflex is
impaired or absent.
• Assume neck injury with head injury.
• Assess for rhinorrhea, otorrhea, scalp wounds.
• Administer fluids cautiously to prevent fluid
overload and increasing ICP.
Subsequent Assessment
1) History: Mechanism of injury, duration of loss of
consciousness, memory of the event,
2) level of consciousness
a. Change in the level of consciousness.
b. Glasgow Coma Score
3) Vital signs
a. Hypertension and bradycardia indicate an
increasing intracranial pressure.
b. Changing patterns of respiration or apnea.
c. Elevated temperature, are associated with
head injury.
4) Unequal or unresponsive pupils
5) Confusion or personality changes
6) Impaired vision
7) Seizure.
8) Rhinorrhea or otorrhea (indicative of leakage of CSF)
215
9) Peroirbital ecchymosis (indicates anterior basilar

fracture).
10) Perform cranial nerve, motor, sensory, and reflex
assessment.
Nursing Diagnoses
 Altered Cerebral Tissue Perfusion related to
increased ICP.
 Ineffective Breathing Pattern related to ↑ICP or
brain stem injury.
 Altered Nutrition: Less Than Body Requirements
related to compromised neurologic function and
stress of injury.
 Altered Thought Processes related to physiology of
injury.
 Risk for Injury related to altered thought processes.
 Ineffective Family Coping related to
unpredictability of outcome.
Nursing Interventions
Maintaining Adequate Cerebral Perfusion.
1) Maintain a patent airway. Monitor O2 saturation.
And ABG
2) Monitor ICP.Assess hemodynamic
3) Monitor for changes in neurologic status,
decreased LOC and cranial nerve deficits.
216
4) Identify emerging trends in neurologic function,

and communicate findings to medical staff.
5) Monitor, response to pharmacologic therapy
including drug levels.
6) Monitor laboratory data CSF cultures,
7) Monitor intake and output
8) Monitor results of serial serum, urine, and
electrolyte to maintain the level of dehydration
ordered to reduce cerebral edema.
9) Assess dressing and drainage tubes after surgery
for potency, security, and characteristics of
drainage.
10) Institute measures to minimize ICP, cerebral
edema, seizures, or. Neurovascular compromise
such as provide rest, careful positioning to avoid
flexing head, and reducing hip flexion over 24-
hour period.
Maintaining Respiration
1) Monitor respiratory rate, depth, and pattern of
respirations: every 15 min, report any abnormal
pattern, such as Cheyne- Stokes respiration's or
apnea.
2) Assist with intubations and ventilator assistance, if
needed.
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3) Turn patient every 2 hr, and assist with coughing

and deep breathing.
4) Suction patient as needed; however, hyperventilate
the patient before suctioning to prevent hypoxia.
Meeting Nutrition needs
1) Provide nasogastric. feedings once bowel sounds
have returned if patient is unable to swallow;
elevate the head of the bed after feeding, and
check residuals to prevent aspiration.
2) Administer H2 blocking agents to prevent gastric
ulceration and hemorrhage from gastric acid
hypercorrection.
3) Consult with dietitian to provide the increased
calories and nitrogen requirement resulting from
the metabolic changes of brain injury.
4) Administer IV, TPN as ordered.
5) During rehabilitation, recognize and encourage
oral feeding or soft foods. Refer to speech physical
therapist as indicated for feeding difficulties.
Promoting Cognitive Function
1) Periodically, assess patient's LOC, and compare to
baseline.
2) Be aware of patient's cognitive alteration, and
adjust interaction and environment.
218
3) Provide stimulation using all senses visual, and

tactile.
4) Observe patient for fatigue or restlessness from
over stimulation.
5) Involve family in sensory stimulation program.
6) Decrease environmental stimuli when patient is in
agitated
7) state Reorient to surroundings using repetition,
verbal and visual
8) Break down ADLs into, simple steps that patient
can progressively.
9) Identify and maintain usual patterns of behavior
sleep, medication use, elimination, food intake,
and self- care routine.
Preventing Injury
1) Instruct the family regarding the behavioral
phases of recovery from brain injury, such as
restlessness.
2) Investigate for physical sources of restlessness,
such as uncomfortable position; signs of
urinary tract infection, or pressure ulcer
development.
3) Reassure patient and family during periods of
agitation.
219
4) Use side rails, and wrap hands if patient is

agitated, maintain constant vigilance, and avoid
restraints if possible.
5) Keep environment stimuli to a minimum.
6) Perform passive range- of motion exercises to
release muscle tension
7) Avoid sedatives to avoid medication- induced
confusion and altered states of cognition.
220
SHOCK
1-Define different types of shock.
2-Clarify shock and its underlying pathophysiology.
3-Compare clinical findings of the compensatory and
progressive stages of shock.
4-Differentiate between types of shock in terms of causes,
pathophysiologic effects
5-Determine the collaborative care, drug therapy, and nursing
management of patients experiencing different types of shock.
Definition:- is a life-threatening condition with a variety of

underlying causes. It is characterized by inadequate tissue
perfusion, inadequate to deliver oxygen and nutrients to support
vital organs and cellular function metabolic and hemodynamic
alterations. Shock affects all body systems results in MODS and
death
Aetiology:
Adequate tissue perfusion depends on 3 factors:
 Blood volume.
 Capacity of the blood vessels.
 Pumping action of the heart.
221
Stages of Shock:-
1-Compensatory stage
- In this stage, the patient’s BP remains within normal limits
-Vasoconstriction, increased heart rate, and increased

contractility of the heart maintaining adequate cardiac output
(CO).
-stimulation of the SNS and release of (epinephrine and

norepinephrine).The body shunts blood from organs such as the
skin, kidneys, and GIT to the brain and heart. As a result,
patient’s skin is cold and clammy, bowel sounds are hypoactive,
and urine output decreases in response to the release of
aldosterone and ADH.
During the statue of low perfusion, compensatory mechanism

increase in heart rate, systematic vascular resistance and cardiac
contractility in effort to restore the circulatory volume. 2--
Progressive stage
In this stage, - regulate blood pressure can no longer
compensate and the MAP falls. below normal limits and
hypotensive this is defined as systolic BP of less than 90mmhg
or decrease in systolic BP of 40 mmhg .
Compensatory mechanisms that maintain normal perfusion
begin to fail, metabolic and circulatory
222
At this time signs of failure in one or more organs .As ineffective

tissue perfusion, the cells from aerobic to anaerobic metabolism
to produce energy, and that causing production of lactic acid.
Increased vascular permeability, hypoxia,
Refractory stage
The irreversible stage of shock organ damage is severe,
that the patient does not respond to treatment and , BP remains
low, renal and liver failure, the release of necrotic tissue toxins,
metabolic acidosis. Respiratory system failure prevents adequate
oxygenation and ventilation despite mechanical ventilatory
support, and the cardiovascular system is in effective in
maintaining an adequate MAP for tissue perfusion. Multiple
organ dysfunctions progressing to complete organ failure
Types of shock:
(1) Hypovolemic shock:
(2) Cardiogenic shock:
(3) Vasogenic shock:
a. Septic shock:
b. Neurogenic shock:
c. Anaphylactic shock:
d. Endocrine shock:
223
Hypovolemic Shock
Definition is the most common type of shock, is characterized
by a decreased intravascular volume of body fluid including the
intracellular and extracellular volume. Hypovolemic shock
occurs when there is a reduction in intravascular volume by 15%
to 25%, which represents a loss of 750 to 1300 mL of blood
Causes: - hypovolemic Shock

 Loss of blood as hemorrhage (internal, external).
Ex., liver or splenic rupture from trauma
 Loss plasma as burns. edema, ascites, peritonitis
 Loss of fluid as severe vomiting & diarrhea. excessive
diuretics severe dehydration
Pathophysiological Stages:
a. Heart:  decrease myocardial contractility by coronary
ischemia  decrease cardiac output  hypoxia., myocardial
infarction and dysrhythmia
b. Small intestine: persistent hypoperfusion of the bowel  gut
barrier dysfunction  translocation of bacteria into
circulation.
c. Liver: Hepatic dysfunction and jaundice from liver
hypoperfusion
224
d. Kidney: Renal hypoperfusion  G.F.R.  Acute tubular

necrosis  acute renal failure.
e. Lungs : Adult respiratory distress syndrome
f. Brain: Cerebral ischaemia  coma.
Assessment
Clinical findings are directly related to the severity and acute of
volume loss.
1- History
2- Clinical manifestations
3- Laboratory studies
225
LABORATORY STUDIES
- Serum lactate elevated
- arterial pH,
-Serial hemoglobin and hematocrit
-coagulation to assess the need for blood product replacement.
Clinical manifestations:
 C.V.P : decreased
 Foley's catheter: Decreased urine output
 Blood gases :
 Decreased hemoglobin and hematocrit value, & kidney
function
 Serum lactate increased 2.2mEqu due to anaerobic
metabolism
- Skin, Pale, Cold, Clammy sweaty (due to
vasoconstriction).
- ECG: to detect any arrhythmias.
-Weakness and fainting when standing.
-Hypoxemia Pao2 <90 mmHg due to hypoventilation and
hypo perfusion
Pulse: Tachycardia>100b/m (weak, rapid pulse), thread.
Tachycardia due to activation of the sympathetic nervous

system
CNS: Vary from anxious to drowsy,
226
Tachycardia
Rapid due to
Adrenaline secretion  stimulates
Pulse SAmore
Weak: due to  systolic nodethan diastolic = small
pulse volume
Blood Pressure: Hypotension. with loss of more than 30 % of

total blood volume. ( VR ,  cardiac output )
Respiratory rate: Rapid and deep respiration, which gradually
become and shallower as the patient's condition deteriorates.
a. Tachypnea from stimulation of respirator center early increase
respiratory rate and late decrease respiratory rate
b. Temperature: Hypothermia from  metabolism by hypoxia
& hypotension.
c. O2 saturation decreased
Urine output: Oliguria from renal hypoperfusion
In severe late condition  comatose.
Treatment of hypovolaemic shock:

Fluid resuscitation:-
- Venous access.
At least two large cannula are inserted into appropriate vein.
Fluids and Blood transfusion:
- Crystalloid solutions are used primarily first line therapy.
- Isotonic solutions such as lactated ringer's solution or 0.9% normal
saline
227
a. Start I.V infusion of 1000-2000 cc of lactated Ringer's

solution over the first 45 minutes (at the same time, a blood
sample is obtained for cross-matching & preparation of
blood transfusion).
Colloid solution:-
In absences of whole blood, many substances have been
proposed as human plasma, albumin, dextran and artificial blood
substitute.
1. Positioning : The patient should lie supine with elevation of
lower limbs  venous return, and it should not be over
heated by excessive
2. Oxygen : Administration by facial mask, nasal catheter or
endotracheal tube.
3. Hydrocortisone I.V : May be givens in patients with adrenal
suppression or insufficiency.
4. Inotropic agents : (Dopamine) improve myocardial
contractility + renal blood flow.
5. I.V Na+ bicarbonate to correct metabolic acidosis .
Analgesia pethidine 50-100mg I.V. to anxious patients.
- Pulmonary support:- Oxygen mask for all shocked
patients oxygen at a high concentration is initially administered
through face mask.
ETT and MV is indicated when evidence of respiratory failure.
228
Monitoring:-
1-Clinical parameter as pulse, Bp, state of vein filling.
2-A folly catheter is introduced to check urine output every
hour. Optimum output is 0.5-1 ml/kg/h.
3-Central venous pressure: - where high CVP indicate over
transfusion, while low pressure indicates hypovolemia.
 ECG.
Nursing management of hypovolemic shock:-
1- vital signs, heart rate, respiratory rate and depth,
(hemodynamic monitoring, electrocardiography monitoring,
arterial blood gases, serum electrolyte levels, physical and
mental status changes), oxygen saturation, urine output, as well
as laboratory results
1. Care must be taken to administer fluids as rapidly as
possible without compromising the pulmonary system.
2. Fluid given too rapidly may cause pulmonary congestion
and inhibit adequate oxygenation, further compromising oxygen
delivery to the tissues.
3. Fluids should also be warmed during infusion to limit the
negative effects of hypothermia.
229
Figure (1):- Proper positioning (modified Trendelenburg) for

the patient who shows signs of shock. The lower extremities
are elevated to an angle of about 20 degrees; the knees are
straight, the trunk is horizontal, and the head is slightly
elevated.
230
Septic Shock
Definition
Septic shock is a complex and generalized process that
involves all organ systems. Sepsis, severe sepsis, and septic
shock represent progressive stages of the same illness.
Causes of septic shock

The most common causative microorganisms of septic
shock are gram negative bacteria. Gram positive bacterial
infections. Currently, gram-positive bacteria are responsible for
50% of bacteremic events. Other infectious agents, such as
viruses and fungi,
Predisposing Factors:
- Suppress the immune system predispose to septic shock
- Old age, DM.
- Corticosteroids, chemotherapy, and malignancy
Pathophysiology
- Acid-base imbalance: Excess of lactic acid  metabolic
acidosis by hyperventilation to wash CO2  later on renal
ischemia  renal failure  frank acidosis.
- Blood gas analysis   Low PH (acidosis).
o PO2 (respiratory distress)
o  PCO2 (Hyperventilation).
231
Clinical Picture:
1] Hyper dynamic Septic Shock: (Septicemia)
- Fever
- Hypotension,
-Tachycardia,
-warm dry skin,
- Tachypnea.
-At the end of this stage, anaerobic metabolism
-Oliguria, confusion. Changes in mental status
-Proper treatment of the patient at this stage can lead to
survive.
2] Hypo dynamic Septic Shock:
- If not treated properly.
-The clinical picture = is that of hypovolaemic shock,
hypothermia.
-The end result is clinical picture of D. I.C. + multiorgan

failure.
LABORATORY STUDIES
 Cultures: blood, sputum urine. Surgical or nonsurgical
wounds.
 CBC: WBCs usually will be elevated
 Arterial blood gages.
 CT scan may be needed to identify sites of potential
abscesses.
232
 Chest and abdominal radiographs may reveal infectious

processes.
 Lactate level: increase levels of lactate.
Increase:
  TLC with increased immature forms.
  Lactate level in blood.
 Repeated blood culture.
Monitoring of septic shock:

Treatment:
1. Admission into I.C.U. for proper monitoring and care.
2. Eradicate the source of infection: e.g. Gangrenous parts,
drainage of intra-abdominal abscess.... etc.
3. Antibiotics: Start with a combination of 3rd generation
(according to culture and sensitivity).
4. Correction of fluid imbalance: by Ringer's lactate + plasma or
blood transfusion.
5. Oxygen mask or mechanical ventilation.
6. Vitamin C.
7. Vasopressors
8. Inotropics if persistent hypotension, measures to support
cardiac contractility & cardiac output + renal blood flow.
9. Endomethacin & corticosteroids I.V.: To antagonize
inflammatory mediators.
233
10-Monitoring pulse, mean blood pressure, temperature, C.V.

P., arterial blood gases, ECG, urine output,
Neurogenic Shock
Definition:
It is type of distributive shock.
Neurogenic shock occurs as the result of vasodilatation loss of
balance between parasympathetic and sympathetic stimulation.
Lack of sympathetic tone leads to decreased tissue perfusion
Pathophysiology
Loss of sympathetic tone, paralysis of the vasomotor fibers lead
to massive peripheral vasodilatation  drop in BP ,peripheral
pooling of blood  inadequate venous return  decrease
cardiac output  impaired tissue perfusion .shock.
Causes:
 Due to hearing bad news - trauma ,
 fracture spinal cord
following spinal anesthesia
Clinical manifestations
1. Hypotension
2. Bradycardia
3. Warm, dry extremities
4. Peripheral vasodilatation
5. venous pooling
234
6. Decreased cardiac output (with cervical or high thoracic

injury).
Treatment:
 The patient should lie flat, elevation of the legs help to
increase venous return. Warming measures to regulate
temperature
 Supplement O2 ,
 intubation ,MV
 Crystalloids like Ringer's lactate.
 Vasopressor drugs.
Cardiogenic Shock
Definition
A drop in blood pressure and blood flow caused by the heart’s
inability to pump blood as a result of a cardiac emergency, such
as cardiac tamponade, myocardia ischemia, myocarditis, or
cardiomyopathy (a disease of the heart that deteriorates the heart
muscle).
Risk Factors of Cardiogenic Shock
- Old age
■ myocardial infarction.
■ History of diabetes mellitus.
Causes of cardiogenic shock:-
Coronary cardiogenic shock
235
1- Acute myocardial infarction (commonest cause).

2- Sever arrhythmia.
Non coronary causes of cardiogenic shock
1- Massive pulmonary embolism.
2-severe hypoxemia, acidosis, hypoglycemia, hypocalcaemia,
and tension pneumothorax.
4- Cardiac tamponade ,cardiomyopathies, valvular damage,
5- High spinal anesthesia.
6- Myocarditis.
7- Sepsis
8- Aortic or mitral stenosis
Pathophysiology:-
Stroke volume and heart rate decrease, and tissue perfusion,
BP is reduced. insufficient cardiac contraction
Decreased cardiac output (C.O)   systolic and diastolic
pressure  hypotension  tissue hypo perfusion  shock (the
Neck Veins congested and C.V.P. is high).
Assessment,
.HISTORY
History provides the information at risk for of cardiogenic.
236
1- Hemodynamic findings
Systolic blood pressure <90mm hg.
Mean arterial pressure <70 mm hg.
Narrow pulse pressure.
- Distended neck vein Arrhythmias.
-Chest pain. -Cool, pale,
moist skin.
-Oliguria - Decreased level of conscious.
3- Pulmonary findings
-Dyspnea. Increased respiratory rate.
-Inspiratory crackles, - Arterial blood gases show
decreased in PaO2.
-Respiratory alkalosis.
LABORATORY STUDIES
 Elevated cardiac enzyme markers by progressive
myocardial necrosis, as creatine phosphokinase (MB-
CPK).
 serial 12-lead ECG are obtained to assess the degree of
Myocardial damage
 Continuous ECG and ST-segment monitoring is also used
to closely monitor the patient for ischemic changes
237
Management:-
1- Correction of Underlying Causes.
2- Initiation of First-Line treatment:
-Increasing myocardial oxygen.
In the early stages of shock, supplemental oxygen is
administered by nasal cannula at a rate of 2 to 6 L/min
-Oxygen saturation more than 90%.
-Monitoring of arterial oxygen saturation
-Hemodynamic Monitoring
Fluid Therapy
- Pulse oximetry
- ECG monitoring
-+Pharmacologic Therapy
 Pain Control:- ( chest pain ) analgesics, IV morphine
morphine dilates the blood vessels.
 Inotropeic (Dobutamine:)  to  cardiac
contractility, stroke volume ejection cardiac output.
 Vasodilators as IV nitroglycerin   after load of the
heart.
Mechanical support by intra-aortic balloon counter-pulsations.
Nursing Management
1- Monitoring Homodynamic Status and cardiac status.
Arterial lines
breathe sound changes
238
monitoring respiratory and renal function.

cardiac rhythm , abnormal physical assessment .
-prevent pulmonary edema from fluid over load
3- Enhancing Safety and Comfort
preventing infection
protecting the skin,
Anaphylactic Shock
Definition
Anaphylactic shock occurs rapidly and is life threatening. An
antigen–antibody reaction causes antibody of mast cells
basophiles and to release substances, such as histamine causing
vasodilation and capillary permeability broncho-constriction,
coronary vasoconstriction, and urticaria.. Characteristics of
severe, rapid hypotension, neurologic compromise, respiratory
distress, and cardiac arrest.
Assessment
HISTORY
Avoiding known allergens is usually the best way to pre-
vent anaphylactic shock. Responses to drugs, foods, blood
products, or anesthetic agents.
239
 Initially generalized erythema,
 urticarial, pruritus,
 Later symptoms. anxiety and restlessness, dyspnea,
 Wheezing , warm feeling, Chest tightness and pain.
 Respiratory manifestations, laryngeal edema, or severe
bronchoconstriction soon stridor.
 Hypotension from vasodilation soon.
 angioedema (swelling of the lips, face, neck and throat):
life threatening
Medical Management:-
1- Intravenous crystalloid.
2- Intravenous hydrocortisone.
3- Antihistaminic.
4- ETT may be needed if laryngeal oedema and steroid are
developed.
Nursing care:
 Maintaining adequate airway and monitoring patient
response to the antigen.
 Monitors respirations, heart rate, blood pressure, and
level of anxiety,
 Comfort measures for dermatological manifestations.
240
 Patient education regarding prevention and treatment is

critical for any person who experiences a significant
anaphylactic.
Multiple organ dysfunction syndromes
Multiple organ dysfunction syndromes (MODS) is the

failure of two or more organ systems in an acutely ill patient such
that homeostasis cannot be maintained without intervention.
MODS results from systemic inflammatory response syndrome
(SIRS).
SIRS: The systemic response to infection. It is manifested by

two or more of the following conditions:
■ Temperature >38°C or <36°C
■ Heart rate >90 beats/minute
■ Respiratory rate >20 breaths/minute or PaCO2 <32 mm Hg
■ WBC count >12,000 cells/mm3, <4,000 cells/mm3, or>10%
immature forms
Clinical manifestation of MODS:

Pulmonary dysfunction: lungs are the first failure organ
- Acute lung injury - ARDS
Cardiovascular dysfunction:
- Decrease cardiac output - arrhythmia
- Hypotension - vasodilatation
241
Renal dysfunction: - acute kidney injury

Liver dysfunction: - liver failure (manifested by elevations
in liver enzymes and bilirubin, coagulation defects, and failure
to excrete toxins such as ammonia, which lead to worsening
encephalopathy.)
Hematological dysfunction: - thrombocytopenia -
DIC
Neurological dysfunction: - altered level of consciousness -

confusion - delirium
Nursing diagnosis:
■ Ineffective Tissue Perfusion
■ Altered Cardiac Output
■ Deficient Fluid Volume and Electrolytes
■ Ineffective Breathing Pattern
■ Impaired Gas Exchange
■ Prolonged Immobility
■ Altered Pain Management
■ Fear and Anxiety
Collaborative Nursing Management :

Prevention and treatment of infection
 Aggressive infection control strategies are essential to
decrease the risk for hospital acquired infection.
242
 Early, aggressive surgery is recommended to remove

necrotic tissue (e.g., early debridement of burn tissue) that
can provide a culture medium for microorganisms.
 Strict asepsis technique can decrease infections related to
intra-arterial lines, endotracheal tubes, indwelling bladder
catheters, IV lines, and other invasive devices or
procedures.
 Daily assessment of the ongoing need for invasive lines
and other devices is an important strategy.
 Send cultures and initiate broad-spectrum antibiotic
therapy, as ordered
Maintenance of tissue oxygenation

 Sedation, mechanical ventilation, analgesia, and rest may
decrease oxygen demand and should be considered.
 Oxygen delivery may be optimized by maintaining
normal levels of hemoglobin and PaO2 (80 to 100 mm
Hg),
Nutritional and metabolic needs
 The enteral route is preferred, but if it cannot be used or
cannot meet caloric needs, parenteral nutrition should be
initiated or added.
 glycemic control with a goal of 140 to 180 mg/dL using
insulin infusions
243
Support of failing organs

 Support of any failing organ is a primary goal of therapy.
For example, the patient with ARDS requires aggressive
oxygen therapy and mechanical ventilation; renal failure
may require continuous renal replacement therapy.
244
Spinal Cord Injuries

Learning Objectives based on competence:
1. Explain the initial assessment and management of patient
with spinal cord injury.
2. Describe symptoms of autonomic dysryflexia.
3. Mention mechanisms for spinal cord injuries
4. List complications of spinal cord injuries
5. Differentiate between complete and incomplete injury of
spinal cord.
6. Formulate a plan of care for patient with spinal cord
injury.
7. Implement airway management for patient with spinal
cord injury.
Introduction:
Spinal cord consists of 31 pairs of spinal nerves, cervical
(8), thoracic (12), lumber (5), sacral (5), and coccyx. The nerves
are grouped together in different bundles called Ascending and
Descending tracts. Ascending tracts carry sensory information
from the body, upwards to the brain, such as touch, skin
temperature, pain and joint position. Descending tracts carry
information from the brain downwards to initiate movement and
control body functions.
245
Mechanism of Injury:
Hyperflexion is seen in the cervical area, especially at the level
of C5 to C6, because this is the most mobile portion of the
cervical spine. It is caused by sudden deceleration motion, as in
head-on collisions. Injury occurs from compression of the cord
as a result of fracture fragments or dislocation of the vertebral
bodies. Instability of the spinal column occurs because of the
rupture or tearing of the posterior muscles and ligaments.
Hyperextension involve backward and downward motion of the
head, often seen in rear-end collisions or MVCs, the spinal cord
is stretched and distorted. Neurologic deficits associated with
this injury are often caused by contusion and ischemia of the
cord without significant bony involvement.
Rotation. occur in conjunction with a flexion or extension
injury. Severe rotation of the neck or body results in tearing of
the posterior ligaments and displacement (rotation) of the spinal
column.
Axial Loading. or vertical compression, injuries occur from
vertical force along the spinal cord. It is seen in a fall from a
height in which the person lands on the feet or buttocks.
Compression injuries cause burst fractures of the vertebral body
that often send bony fragments into the spinal canal or directly
into the spinal cord
246
Penetrating Injuries. can be caused by a bullet, knife, or any

other object that penetrates the cord. These types of injury cause
permanent damage by anatomically transecting the spinal cord.
1- 2-Hyperextension
Hyperflexion
3- 4-Compression
Rotation
5-Penetrating Injuries 6- lateral stress
Pathophysiology:
Spinal cord injuries are the result of a mechanical force
that disrupts neurologic tissue or its vascular supply, or both. The
injury process includes both primary and secondary injury
mechanisms.
Primary injury is the neurologic damage that occurs at the
moment of impact. Secondary injury refers to the complex
biochemical processes affecting cellular function and can lead to
247
spinal cord ischemia and loss of neurologic function. Secondary

injury can occur within minutes of injury and can last for days
to weeks. A cascade of events is initiated that includes systemic
and local vascular changes, electrolyte and biochemical changes,
neurotransmitter accumulation, and local edema.
Functional Injury of the Spinal Cord.
It refers to the degree of disruption of normal spinal cord
function. This depends on what specific sensory and motor
structures within the cord are damaged.
Classification of SCI:
I- Complete Injury.
Complete SCI results in a total loss of sensory and motor
function below the level of injury and complete dissection of the
spinal cord and its neurochemical pathways, resulting in one of
two conditions: quadriplegia or paraplegia.
 Quadriplegia: The injury occurs from the C1 to T1 level.
 Paraplegia: The injury occurs in the thoraco-lumbar
region (T2 to L1). Patients may have full use of the arms
and may need a wheelchair.
II- Incomplete Injury.
Incomplete cord involvement results in a mixed loss of voluntary
motor activity and sensation and leaves some tracts intact. The
degree of sensory and motor loss varies depending on the level
of injury and reflects the specific nerve tracts damaged.
248
Incomplete injuries can result in a variety of syndromes, which

are classified according to the degree of motor and sensory loss
below the level of injury. Some of the more common syndromes
are described here.
Brown-Séquard Syndrome: The Brown-Séquard syndrome is
associated with damage to only one side of the cord. This
produces loss of voluntary motor movement on the same side as
the injury, with loss of pain, temperature, and sensation on the
opposite side. Functionally, the side of the body with the best
motor control has little or no sensation, whereas the side of the
body with sensation has little or no motor control.
Central Cord Syndrome: Central cord syndrome is associated
with cervical hyperextension–hyperflexion injury and
hematoma formation in the center of the cervical cord. This
injury produces a motor and sensory deficit more pronounced in
249
the upper extremities than in the lower extremities. Various

degrees of bowel and bladder dysfunction may be present.
Anterior Cord Syndrome: The anterior cord syndrome is
associated with injury to the anterior gray horn cells (motor), the
spinothalamic tracts (pain), anterior spinothalamic tract (light
touch), and the corticospinal tracts (temperature). The result is a
loss of motor function and loss of the sensations of pain and
temperature below the level of injury. However, below the level
of injury, position sense and sensations of pressure and
vibrations remain intact. Anterior cord syndrome is commonly
caused by flexion injuries or acute herniation of an intervertebral
disk.
Posterior Cord Syndrome: Posterior cord syndrome is
associated with cervical hyperextension injury with damage to
the posterior column. This results in the loss of position sense,
pressure, and vibration below the level of injury. Motor function
and sensation of pain and temperature remain intact. These
patients may not be able to ambulate because the loss of position
sense impairs spontaneous movement.
III- Spinal Shock.
Spinal shock is a condition that can occur shortly after traumatic
injury to the spinal cord. Spinal shock is a temporary complete
loss of all muscle tone and normal reflex activity below the level
of injury.
250
IV- Neurogenic Shock.

Neurogenic shock results from injury to the descending
sympathetic pathways in the spinal cord. This results from loss
of vasomotor tone and sympathetic innervation to the heart. A
relative hypovolemia and hypovolemic shock ensues, causing
hypotension and decreased systemic vascular resistance.
Patients with SCI at T6 or above may have profound neurogenic
shock as a result of interruption of the sympathetic nervous
system and loss of vasoconstrictor response below the level of
the injury. Blood vessels cannot constrict, and the heart rate is
slow, which results in hypotension, venous pooling, and
decreased cardiac output. Cellular oxygenation is threatened as
cardiac output declines because of a decrease in stroke volume
(hypovolemia) and heart rate (bradycardia).
Because hypotension is a problem, the nurse must be cautious
when adjusting backrest position or when repositioning a
patient in bed because orthostatic blood pressure changes can
occur
V- Autonomic Dysreflexia.
Autonomic dysreflexia is a life-threatening complication that
may occur with SCI. This condition is caused by a massive
sympathetic response to a noxious stimulus (full bladder, line
insertions, fecal impaction). A stimulus causes sympathetic
nervous system response below the level of SCI and systemic
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vasoconstriction which results in bradycardia, hypertension,

facial flushing, and headache. Immediate intervention is needed
to prevent cerebral hemorrhage, seizures, and acute pulmonary
edema. Treatment is aimed at alleviating the noxious stimulus.
If symptoms persist, antihypertensive agents can be
administered to reduce blood pressure. Prevention of autonomic
dysreflexia is imperative and can be accomplished through the
use of a good bowel and bladder program.
Collaborative Management of Autonomic Dysreflexia
 If patient is supine, immediately sit the patient up.
 Begin frequent vital sign monitoring: perform every 5
minutes.
 Survey for instigating causes: begin with urinary system.
 Loosen clothing, constrictive devices.
 If indwelling catheter is not present, catheterize the
patient:
 If indwelling catheter is present:
- Check system for kinks, obstructions to flow.
- Irrigate bladder with small amount of fluid.
- If not draining, remove catheter and replace.
 If systolic blood pressure is greater than 150 mm Hg,
consider rapid-onset, short duration antihypertensive
agent.
 If acute symptoms persist, suspect fecal impaction:
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- Instill lidocaine jelly into rectum; wait at least 5

minutes.
- Perform digital examination to check for presence of
stool; if present, gently remove. If signs of autonomic
dysreflexia persist, stop exam; instill additional
lidocaine jelly, and wait 20 minutes to reexamine.
- If no stool found and abdominal distention noted,
consider administration of laxative
Management of spinal cord injuries
I- Assessment:
 Airway.
The primary assessment begins with an evaluation of airway
clearance. In an unresponsive person, an oral airway is inserted
while the patient's neck is maintained in a neutral position. The
patient must undergo intubation before severe hypoxia can
occur, which could further damage the spinal cord.
 Breathing.
Assessment of breathing patterns and gas exchange is made after
an airway has been secured. Because complete injuries above the
C3 level result in paralysis of the diaphragm, patients with these
injuries require ventilatory assistance.
 Circulation.
The patient with an SCI is assessed for adequate tissue perfusion
by means of both invasive and noninvasive hemodynamic
253
monitoring techniques. Cardiac monitoring is required to detect

bradycardia and other dysrhythmias.
 Neurologic.
The initial neurologic assessment focuses on the rapid and
accurate identification of present, absent, or impaired
functioning of the motor, sensory, and reflex systems that
coordinate and regulate vital functions. A detailed motor and
sensory examination includes the assessment of all 32 spinal
nerves for evidence of dysfunction.
II- Diagnostic Procedures.

X-ray, CT scan, tomograms, myelography, and MRI may be
used in the diagnostic process.
III- Medical Management: Medical interventions are divided

into pharmacologic, surgical, and nonsurgical interventions.
 Pharmacologic Management.
Methylprednisolone has been shown to improve neurologic
outcome after spinal cord injury. Methylprednisolone directly
affects the changes that occur within the spinal cord after injury,
primarily by preventing posttraumatic spinal cord ischemia,
improving energy metabolism, restoring extracellular calcium,
and improving nerve impulse conduction.
 Surgical Management.
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Surgical intervention performed to achieve decompression and

stabilization for spinal cord.
Laminectomy: The laminectomy procedure is the removal of
the lamina of the vertebral ring to allow decompression and
removal of bony fragments or disk material from the spinal
canal.
Spinal Fusion: Spinal fusion entails the surgical fusion of two
to six vertebral elements to provide stability and to prevent
motion. Fusion is accomplished through the use of bone parts or
bone chips taken from the iliac crest or by use of wire or acrylic
glue.
Rodding: The rodding procedure stabilizes and realigns larger
segments of the spinal column by means of a variety of rodding
procedures, such as the use of Harrington rods. The rods are
attached by screws and glue to the posterior elements
of the spinal column
 Nonsurgical Management.
If the injury to the spinal cord is stable, the immobilization of the
fracture site and realignment of any dislocation will
accomplished through skeletal traction.
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Nursing Management:-
Nursing Diagnoses
 Decreased Cardiac Output related to lack of sympathetic
innervation
 Risk for Autonomic Dysreflexia related to spinal cord injury
above T8
 Impaired Gas Exchange related to alveolar hypoventilation
 Ineffective Breathing Pattern related to impairment of
innervation of diaphragm, complete or mixed loss of intercostal
muscle function
 Impaired Physical Mobility related to neuromuscular
impairment, immobilization, paralysis
 Risk for Impaired Skin Integrity related to immobility,
traction, tissue pressure, altered peripheral circulation, and
sensation
 Bowel Incontinence related to disruption of innervation to
bowel and rectum, perceptual impairment, altered fluid and
food intake
 Constipation related to disruption of innervation to bowel and
rectum, perceptual impairment, altered fluid and food intake
 Impaired Urinary Elimination related to disruption in bladder
innervation, bladder atony
 Disturbed Body Image related to actual change in body
structure, function, or appearance
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 Ineffective Coping related to situational crisis and personal

vulnerability
Nursing interventions:
Cardiovascular.
 Assess fluid volume
 Monitor for hypotension and bradycardia
 Continuous cardiac monitoring for dysrrythmia
 Avoid changes in body temperture, hypothermia can
produce brady-dysrrhythmias and sinus arrest.
 Apply strategy to prevent orthostatic hypotension as
reposition slowly, wear pressure stockings.
 Apply strategy to prevent occurrence of deep vein
thrombosis (DVT) as maintain a strict repositioning
schedule, administer low molecular weight heparin as
ordered, and use compression stockings
Pulmonary
 Observe respiratory rate and rhythm
 Assess symmetry of chest expansion and use of accessory
muscles.
 Use suctioning cautiously and inspect quantity and
character of secretions.
 Auscultation of breath sounds.
 Assess arterial blood gas values.
 Promote adequate breathing and airway clearance.
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 Monitor pulse oximetry.

 Chest Physiotherapy.
 Humidification.
 Adequate hydration.
 Assess for signs of respiratory infection.
 Intubate and ventilate.
Musculoskeletal.
 Maintain proper alignment at all times.
 Reposition frequently.
 Irreversible contractures may result in skin breakdown,
inability to perform activities of daily living, poor
wheelchair posture, and inability to use adaptive devices.
 Physical therapy and occupational therapy personnel
should be consulted early in the patient's ICU course.
 Range of motion exercises are initiated as soon as the
spine has been stabilized.
 Foot and hand drop splints should be applied and
reapplied every 2 hours.
 Inspection of pins and traction for security with correct
positioning and turning.
Maintain skin integrity
 Use logroll to reposition patient until cleared from c-spine
precautions
 Prevent pressure ulcer
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 Relieve pressure by repositioning and turning at least

every 2 hours while maintaining spinal precautions
 Administer preventive measures, perform baseline skin
assessment on backboard
 Keep the area under the patient clean and dry
 Prevent temperature elevation
Maintain Urinary and Bowel Function
 Intermittent or indwelling catheter to avoid overdistention
of bladder.
 A bowel program to prevent fecal impaction and
encourage normal, regular bowel function must be
instituted.
 Aspects of a successful bowel program include consistent
timing of evacuation, proper positioning, physical
activity, appropriate fluid intake, and high-fiber diet.
 Laxatives and stool softeners may be needed.
Maximizing Psychosocial Adaptation.

In the critical care unit, the patient and family experience
anxiety, grief, denial, anger, frustration, and hopelessness,
because long-term neurologic deficits remain unknown.
 Nursing interventions include the promotion of coping
mechanisms, support systems, and adaptive skills.
259
 Simple, accurate, and consistent information can alleviate

fear and anxiety.
 Feelings of powerlessness may be reduced by including
the patient and family in care and decision making.
Complications of spinal cord injuries
Acute Phase Complications
 Deep vein thrombosis (DVT)
 Pulmonary embolism
 Neurogenic shock
 Hysterical paralysis
Long-Term Complications
 Pneumonia and other respiratory complications
 Autonomic dysreflexia
 Urological complications
 Pressure ulceration
260
Diabetic Ketoacidosis
1-Define diabetic ketoacidosis.
2-Clarify precipitating factors.
3-Memorize clinical features.
4- Explore pathophysiology and complications of therapy.
5-Analyze investigations required for the diagnosis
6-Explain medical treatment.
7-Apply nursing management .
Definition:
A potentially life threatening complication in patients
with diabetes mellitus. Lead to disorder metabolism of protein,
carbohydrates and fats from sever insulin deficiency with type 2
diabetes and type I
Etiology:
1. Severe diabetes , usually type 1.
2. Precipitating factor: stress, which needs high energy as:
 Infection.  Severe exertion.
 Trauma & operations  Pregnancy & labour.
 Severe vomiting  Starvation.
 Excess intake of fats.  Negligence
 Myocardial infarction oftreatment.
 Cerebrovascular stroke.
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Pathogenesis:
  Insulin → hyperglycemia → osmotic diuresis→
dehydration.
  Utilization of fat to produce energy → ketone bodies →
ketone acidosis metabolic acidosis.
Clinical features:
S & S of acidosis & dehydration.
 The onset is usually gradual.
 Marked polyuria & polysepsia.
 Kussmaul's respiration and fruits breath
 Rapid and shallow respiration.
 Acetone odour in breath.
 Anorexia, nausea & vomiting.
 Abdominal pain.
 Dry tongue, dry cold skin & sunken eyes.
 Weak, rapid pulse.
 Confusion, stupor & then coma, cerebral edema.
Investigations:
1- Urine analysis: Contains glucose & acetone.
2- Blood glucose: Markedly elevated.
3- Blood electrolytes: K:  due to extra-cellular shift.
HCO3:: due to acidosis. ,PH <7.4 andlactic acid
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Management of diabetic ketoacidosis:

1-Hospitalisation: Is a must in every case.
2-Measures to care for the comatose patient.
3- Insulin replacement:
-Low doses of soluble insulin are given regularly either IV or
IM.
 IM: 20 units initially, then 6 units / hour.
 IV: 6 units initially, then 6 units / hour by infusion.
Monitoring of blood glucose every hour.
4. Fluid replacement:
- Starting by normal saline infusion as follows:
- One. litre in 1/2 hour. Followed by
- One liter in 1 hour. Followed by
- One liter in 2 hours followed by
- One liter: in 4 hours.
The subsequent rate will depend on:
-The clinical State: judged by the BP, neck veins & lung
crepitation’s.
- CVP. -The urine output.
- 5% glucose is given instead of saline:
- When blood glucose reaches 200 mg / ml, to avoid
hypoglycemia.
- KCL: 20 mmol is added to each litre of infused fuid.
-monitor vital signs every 1hour and assess dehydration, tachy
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cardia,PH and bicarbonates

5. Monitoring & correction of potassium levels:
- Hyperkalaemia is present at first due to extracellular shift of k
- Hypokalaemia occurs with insulin due to intracellular shift of
K.
- K level is monitored /4 hours & corrected if needed. Monitor
ABG
6-Correction of acidosis: By sodium bicarbonate infusion.
7-Treatment of cause: Ex. treatment of myocardial infarction.
8-Broad spectrum antibiotics: If there is infection.
N.B: Complications of therapy are: Hypoglycemia,
Hypokalemia, shock, seizure, Pulmonary edema, pulmonary
crackles, and renal failure
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Hypoglycemic Coma
Etiology
1- Over dose of insulin or sulphonylurea.
2- Missing a meal or excercising while using
hypoglycaemic drugs.
3- Excess intake of alcohol while using hypoglycaemic
drugs.
Pathogenesis
- Hypoglycaemia causes lack of energy to the brain,
confusion & coma.
- Adrenaline is secreted to convert liver glycogen to
glucose.
- Hyperadrenalism causes stimulation of the sympathetic
system.
Clinical features
S & S of sympathetic over activity:
 The onset is usually sudden.
 The patient is irritable, confused & then comatosed.
 Palpitation & sense of fear. - Sweating & tremors.
 Wet skin. - Dilated pupil.
 Rapid & strong pulse. - Increased systolic BP.
 Exaggerated deep reflexes. - Rapid response to oral or IV
glucose.
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Investigations
1-Urine: Contains glucose. and Blood glucose: Markedly
decreased.
Treatment
1. Oral glucose: In early hypoglycaemia.
2. IV glucose: In severe hypoglycaernia.
Hyperosmolar hyperglycemic Non-Ketotic Coma

Definition:
hyperosmolar hyperglycemic nonketotic syndrome HHNS is an
acute hyperglycemic crisis accompanied by hyperosmolality and
severe dehydration without ketoacidosis.
Etiology: Usually interaction of 2 factors:

1-Uncontrolled type 2 diabetes.
2-Precipitating factor as:
- Ingestion of high glucose diets.
- The use of corticosteroids or thiazide diuretics.
Pathogenesis:
 Low insulin hyperglycaemia  osmotic diuresis 
dehydration.
  fluid with no  sodium  hyperosmolarity  brain
affection.
 No need for excess fat utilization  no acidosis.
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Clinical features:
S & S of dehydration with no features of acidosis:
1- The onset is usually gradual.
2- Marked polurea & polydepsia.
3- Dry tongue, dry skin & sunken eyes.
4- Weak & rapid pulse.
5- Disturbed consciousness & coma.
6- Hyperosmolarity predisposes to cerebral stroke &
myocardial infarction.
Investigation:
1- Urine: Contains glucose & no acetone.
2-Blood glucose:Markedly increased.
4- Blood Na: Elevated.
Treatment:
1- Insulin replacement: As in ketoacidosis.
1- Fluid replacement: By normal saline.
Prevention diabetic complication.
Control blood sugar level as close to normal as possible.
 Eat of healthy foods. Avoid saturated fat, cholesterol, salt
 Maintain a healthy weight. If you're overweight, you doctor
can give you advice on how to lose weight safely.
 Control your blood pressure and cholesterol levels.
 Be physically active on a regular basis, Stop smoking.
267
 See your doctor regularly, even when you feel fine. You
doctor will check for early signs of complications.
 Call your doctor right away if you have any of the warning
sings listed in this handout
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Organ transplantation
Objectives based on competence

1. Summarize causes of organ transplantation
2. Clarify contraindications of organ transplantation
3. Differentiate between living donor and cadaveric donor
4. Investigate laboratory investigations required for patient
undergoing organ transplantation.
5. Recognize the common complications of organ
transplantation.
6. Conduct appropriate preoperative and postoperative care
for patient undergoing organ transplantation.
Organ transplantation
Solid organ transplantation is a treatment option to
improve the quality of life of people at any age suffering from
irreversible and end-stage chronic conditions.
Indications for organ transplantation

Many factors influence the indications and patient
eligibility for transplantation. Currently, end-stage disease is the
primary reason for most organ transplantations.
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Organ Indications Common causes

Kidney End-stage renal Hypertension, diabetes
disease mellitus, glomerular
nephritis, cancer,
trauma nephrotoxins,
congenital anomalies
Liver Adults: irreversible Acute or chronic
liver disease, hepatitis, primary
malignancy, and sclerosing cholangitis,
hepatic failure primary biliary
resulting in synthetic cirrhosis,
liver dysfunction hepatocellular
carcinoma, alcoholic
cirrhosis
Heart End-stage heart Ischemic
disease cardiomyopathy,
idiopathic
cardiomyopathy,
valvular heart disease,
congenital anomalies
Pancreas Type 1 diabetes Diabetes mellitus
mellitus with end-
stage renal disease
either alone or in
combination with a
kidney transplant
Lung Chronic obstructive Emphysema and

pulmonary disease bronchiectasis,
idiopathic pulmonary
270
fibrosis, primary
pulmonary
hypertension
Malignant disorders Leukemia, and
selected solid tumors
(eg, renal cell tumors)
Nonmalignant Asickle cell, and
Stem cell
disorders selected metabolic
disorders; thalassemia;
and immunodeficiency
syndromes
Contraindications for organ transplantation

Contraindications are based on conditions and behaviors that
decrease the chance of survival. For solid organ transplantation,
these include:
 Serious active infection or sepsis,
 Recent cancer (unless that is the reason for
transplantation),
 Current substance abuse
 HIV infection
 Severe cachexia
 Active peptic ulcer disease
 Psychiatric disorders that impair the ability to give
informed consent or adhere to the treatment regimen.
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Laborartory investigations to all transplantation procedures

include the following:
 ABO typing
 Transfusion history
 Infectious disease screening (tuberculin skin test, human
immunodeficiency virus [HIV], hepatitis B surface
antigen, hepatitis C virus)
 Liver function studies
 Renal function studies
 Complete blood count (CBC)
 Coagulation studies
 Gastrointestinal evaluation (depending on age and
history)
 Gynecological examination
 Electrocardiogram (ECG)
 Chest radiograph
 Dental examination to rule out infection
 Social history, review of patient motivation, ability to
follow postoperative regimen, and psychiatric evaluation.
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Donor selection
After a person is determined to be a candidate for
transplantation, a donor source must be selected.
 Determining Compatibility
- Determination of compatibility in transplantation involves
the evaluation of two major antigen systems. The primary
determinant for solid organ transplantation is ABO
grouping. A mismatch in compatibility may cause an
immediate reaction leading to organ loss.
- Organ Transplantation: The rules of compatibility that
apply to the administration of blood products also apply
to solid organ transplantation: type A blood has the A
antigen, type B blood has the B antigen, type AB blood
has both A and B antigens, and type O blood has neither
antigen. Histocompatibility testing (tissue typing) is the
identification of donor and recipient antigens and the
evaluation of donor antigens against recipient antibodies.
This evaluation determines the compatibility between
donor and recipient, which predicts the chances of graft
acceptance.
- Stem Cell Transplantation: Selection of a donor for
SCT is based on the type and stage of the underlying
disease, age, comorbidities, and availability of an
appropriate matched donor.
-
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Types of donors
 Living donors
- Living donors are increasingly being used in kidney, liver,
pancreas, and lung transplantation. Living donors are used
exclusively in SCT. Once identified, a potential donor has
a thorough medical evaluation to determine that the organ
functions normally, and there is no underlying disease.
 Cadaveric donor
- Cadaveric donors are people who have been declared
brain-dead and whose organs are kept viable by
ventilators or other mechanical mechanisms until they can
be excised for transplantation.
Role of the Nurse for donor

- Critical care nurses are an integral part of the organ
donation team.
- A nurse who is specially trained to maintain
hemodynamic stability of the donor so that the vital
organs are perfused adequately.
- Hemodynamic management occurs in two phases.
 In the first phase: hemodynamic disturbance occures
consequent to endogenous catecholamine
mobilization. Short-acting agents, such as esmolol,
which have a short duration of action and are used to
control blood pressure and heart rate.
274
 Phase 2 begins after depletion of catecholamine

stores, at which time the donor experiences a
dramatic fall in blood pressure. Initial intervention in
phase 2 involves rapid replacement of circulating
blood volume with crystalloid or colloid intravenous
(IV) fluids.
 The administration of vasopressors and inotropes, in
addition to providing cardiovascular support for the
organ donor, promotes a lower incidence of kidney
rejection and better long-term graft survival.
- Optimal pulmonary management, including:
 Suctioning for airway clearance and aspiration
precautions, is necessary.
 Ventilator management should include close titration
of fluids to minimize the risk for pulmonary edema.
Positive end-expiratory pressure should be less than
5 cm H2O, and 30 mm Hg if possible.
- It is also essential to assess urine output hourly to detect
diabetes insipidus. This is common in organ donors and is
caused by failure of the posterior pituitary to produce or
release antidiuretic hormones. This can lead to electrolyte
imbalances.
- Laboratory results, such as electrolytes, CBC, liver and
renal function tests, and arterial blood gases (ABGs)
275
values, are necessary to assess organ function and

determine appropriate intervention. An ECG and
echocardiogram are required for heart donation. Serial
chest radiographs, bronchoscopy, sputum for Gram stain
and visual inspection at the time of organ procurement are
required for lung donation.
Preoperative phase
- The immediate preoperative phase, which is usually only
a matter of hours, includes comprehensive laboratory
studies, chest radiograph, ECG, and, for kidney transplant
recipients, dialysis within 24 hours of transplantation.
Laboratory studies usually include CBC, prothrombin
time (PT), partial thromboplastin time (PTT), electrolytes,
blood glucose, blood urea nitrogen (BUN), creatinine,
liver function tests, type and cross-match, and urinalysis.
- Intraoperative phase
 The nurse ensures the donor is connected to a transport
monitor; oxygen and emergency medications must be
available.
 In the operating room, hemodynamic support and
continued medical management is coordinated between
the organ transplantation staff, anesthesiologist, and the
recovery surgeons.
276
 Organs are flushed with preservative solution

containing electrolytes and nutrients.
 The organs are then removed from the donor, examined
individually in a sterile basin, and packed in sterile
containers for transport.
 Preservation Time
- There is a broad range of acceptable preservation
times for organs. However, the goal is to transplant
organs as soon as possible.
- Kidneys can be stored for up to 48 hours using
pulsatile perfusion preservation and for 24 to 36
hours using cold storage.
- Livers can be stored for up to 20 hours, pancreas up
to 12 hours
- Hearts and lungs for 4 to 6 hours.
- To decrease cellular injury, organs are stored in a
solution and kept in ice. The preservative solutions
used are different for each organ and are based on the
metabolic needs of the organ, with center-specific
variability. The focus of preservation is to protect the
organ from ischemic injury.
277
Postoperative phase
- Immediately after surgery, transplant recipients require
care in a closely monitored area until their condition
stabilizes.
- When a patient arrives in intensive care area, the nurse
makes the following assessments:
 Blood pressure, heart rate, Respirations, temperature,
central venous pressure, oxygenation and ventilator
settings,
 Patient’s level of consciousness and degree of pain.
 Closely monitor urine out put on range 0.5 ml/kg (50-
60ml/hour)
 Number of IV and arterial lines, noting the site, type
of solution, and flow rate
 Abdominal or chest dressing for drainage, noting the
presence
of drains and amount and type of drainage
 Attachment of nasogastric tube to appropriate
drainage system and amount and character of
drainage.
 Most recent hemodynamic and intraoperative
laboratory results.
278
Immunosuppressive therapy:
- In solid organ transplantation, the transplanted organ is
foreign to the recipient, whose immune system eventually
will recognize this and mobilize to reject the transplanted
organ. Therefore, immunosuppressive therapy is
necessary to suppress the immune response so the
transplanted organ will be accepted.
- To suppress the immune response in solid organ and stem
cell transplant recipients, several drugs may be necessary.
- A single medication usually cannot do this effectively.
Therefore, immunosuppressive regimens include
medications that complement each other and increase the
effectiveness of the immunosuppression.
- Triple therapy is a combination of low-dose prednisone,
azathioprine, and cyclosporine A or tacrolimus. By
combining these three agents, the dose of each drug is
lower so that patients experience fewer adverse effects
than they would from one drug alone. For example, the
risk for aseptic necrosis, diabetes mellitus, cataracts, and
gastrointestinal complications attributed to chronic steroid
therapy is greatly reduced with the combination therapy.
- Quadruple, or sequential, therapy is a combination of the
same three drugs that are used in triple therapy
(prednisone, azathioprine, and either cyclosporine A or
tacrolimus) plus antithymocyte antibody preparations or
279
monoclonal antibody. Quadruple therapy permits both

broad and specific immunosuppression while limiting
toxicity until renal function has improved.
Complications of organ transplantation

1. Organ Rejection
- Because the transplanted organ is not immunologically
identical to the recipient, it acts as an antigen or foreign
substance and triggers the immune system to reject it.
- Rejection can vary in degree from mild to severe and may
be irreversible.
- Rejection may occur at any time, but the risk is highest in
the first 3 months after transplantation.
- It is important to maintain therapeutic levels of
immunosuppression and to provide patient and family
education about the importance of taking all medications
as instructed and the rationale for routine laboratory
monitoring of the levels of immunosuppressive drugs.
2. Infection
- Infection is the most common post-transplantation
complication.
- The causative agents are often from the patient’s own
flora, particularly from the gastrointestinal tract and
280
integumentary system. Pathogens may be bacteria, fungi,

and viruses.
- All transplant recipients are at risk for bacterial infections
from intravascular lines and urinary drainage catheters,
but organ transplant recipients can also acquire
postoperative wound and lung infections.
- Usually broad-spectrum antibiotics are given
prophylactically for 48 hours after organ transplantation
or until invasive lines and drains are removed.
3. Bleeding
- Bleeding, oozing from the surface of the transplanted
organ or the presence of hematoma or lymphocele may
occur after surgery.
- After liver transplantation, bleeding may occur as a result
of coagulopathy because of liver dysfunction or from
small vessels that continue to bleed after surgery.
4. Gastrointestinal Complications Related to Steroid
Therapy
- Chronic steroid therapy increases the risk for peptic
ulceration and erosive gastritis because it increases the
secretion of hydrochloric acid.
- Massive gastrointestinal bleeding may occur not only from steroid
therapy but also from stress and decreased tissue viability caused
by long-term protein restriction.
- For these reasons, patients usually are given histamine-2 (H2) receptor
antagonists (eg, ranitidine) or proton pump inhibitors (eg, omeprazole).
281
Safety in critical care unites

Learning objectives based on competences:
1. Define safety in ICU
2. List causes of patients’ harm
3. Mention factors that increase human error
4. Discuss International Patient Safety Goals (IPSG):
5. Compare hospital regulations for patient safety
Definition:
Patient safety: is the prevention of errors and adverse effects
to patients associated with providing nursing care
Causes of patient harm
1- Medication errors
2- Health care-associated infections
3- Unsafe surgical care procedures
4- Unsafe injections practices
5- Diagnostic errors
6- Unsafe transfusion practices
7- Sepsis
8- Radiation errors
9-Venous thromboembolism (blood clots)
Factors that increase human error:-
 Limited short-term memory
 Being late or a hurry
282
 Limited ability to multitask

 Interruptions
 Stress
 Fatigue and other physiological factor
International Patient Safety Goals (IPSG):

Goal 1: Identify patients correctly
Goal 2: Improve effective communication
Goal 3: Improve the safety of high-alert medications
Goal 4: Ensure safe surgery
283
Goal 5: Reduce the risk of health care-associated infections

Goal 6: Reduce the risk of patient harm resulting from fall
Hospital regulations for patient safety
Despite sanitation protocol, patients cannot be entirely isolated

from infectious agents. Furthermore, patients are often
prescribed antibiotics and other antimicrobial drugs to help
treat illness.
 Sterilization
Sterilization goes further than just sanitizing. It kills all
microorganisms on equipment and surfaces through
exposure to chemicals, ionizing radiation, dry heat, or
steam under pressure
 Isolation
Isolation is the implementation of isolating precautions
designed to prevent transmission of microorganisms by
common routes in hospitals
 Hand washing
Hand washing frequently is called the single most important
measure to reduce the risks of transmitting skin
microorganisms from one person to another or from one site to
another on the same patient
284
 Gloves
In addition to hand washing, gloves play an important role in
reducing the risks of transmission of microorganisms
 Surface sanitation
Sanitizing surfaces is part of Nosocomial infection in health
care environments. Modern sanitizing methods such as Non-
flammable Alcohol Vapor in Carbon Dioxide systems have
been effective against gastroenteritis, MRSA, and influenza
agents.
 Antimicrobial surfaces
Micro-organisms are known to survive on inanimate ‘touch’
surfaces for extended periods of time
285

Critical Care Nursing 2023-2024

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Critical Care Nursing 2023-2024

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‫ق سم تمريض العنايه‬

THERIOTICAL MANIUAL FOR CRITICAL CARE

‫‪ ‬لتطوير المستمر للقدرة التعليمية لمرحلة البكالوريوس‪.‬‬

Unit 5: Gastrointestinal system

Learning objectives based on competence:

In September 2015, the Unit Nation General Assembly adopted

Sustainable Development Goals were built on the achievements

Definition of the Sustainable Development Goals: -

Purpose of Sustainable Development:

challenges that face our future

3. Improve the quality of life

4. Enhance wellbeing for everyone

5. Satisfy the needs of human without compromising the

ability of future generation to meet their own needs

17 Sustainable Development Goals 2015 to 2030:

Goal 3: Ensure healthy lives and promote well-being for all at

Goal 15: Protect and promote sustainable use of terrestrial

 By 2030, eliminate gender disparities in education and

 Build and upgrade education facilities that are child,

Sustainable Development in critical care nursing education

jeopardize hard won gains made in improving global

Example for Sustainable Development ins relation to health

Overview of Artificial Intelligence (AI)

1) Perception Intelligent biological systems are physically

– Camera, Fingerprint device, Microphone, Computer uses

Climate change in critical ill patients

Learning objectives based on competence:

Global warming” refers to the rise in global temperatures due

Greenhouse gases: any gas that has the property of

“Climate change” refers to the increasing changes in the

Influences of climate change and global warming on health

Challenges for intensive care medicine in the context

Challenges Nursing actions

Mass casualties of critically Implement a ‘reserve’ of staff

Increasing number of Provide sufficient machines

Definition of SARS : A suspect case is a person presenting with

generalized patchy interstitial infiltrates to bilateral

 3.5. known history of exposure. If there was no history

Treatment modalities in ICU for covid19

Scope of Critical Care and Emergency Nursing

Learning Objectives based on competence:

1- Describe scope of critical care and emergency nursing.

Goal of Critical Care Nursing

Scope of Critical Care Nursing practice

 The needs of the critically ill

 The comfort and support provided by social relationships

B. A critical care nurse : is a licensed professional nurse who

Role of critical care nurse:

C. Critical care unit : is a specially designed and equipped

 Resources that constantly support the direct

Principles of Emergency Nursing:

 Avoid unnecessary handling except to remove the victim

2. Principles of emergency management

Qualities of Emergency Nurse

Ethical issues in Critical Care Nursing

 Ethics: is a generic term for the reasoned inquiry and

Ethical Principles in Critical Care

Principles Example Nursing Obligations Patient Rights

-Respect for Truth-telling, provision of Self-determination;

-Non-maleficence Careful practice; self-reflection to Safe care and

-Justice Advocacy for equitable public Access to care;

Nursing code of Ethics

Causes of ethical problems in critical care