حالات حرجة -2022كتاب النظري

‫كلية معتمدة مه الهيئة القىمية‬
‫لضمبن جىدة التعليم واالعتمبد‬
CRITICAL CARE NURSING DEPARTMENT

THERIOTICAL MANIUAL FOR CRITICAL CARE
Prepared by
THEORETICAL MANUAL
FOR
CRITICAL CARE NURSING
Prepared by (PART I)
Prepared by
All staff members of Critical Care and
Emergency Nursing Department
Assiut
All staff members University
of Critical Care Nursing Department
2021-2022
5th Edition
‫رؤية الكلية‬
‫تتطهع كهُخ تًرَض جبيعخ أسُىط نهتًُس وانرَبدح فٍ يجبالد انتًرَض وانجحج انعهًٍ‬
‫وانخذيخ انًجتًعُخ‪.‬‬
‫رسبلة الكلية‬
‫كهُخ انتًرَض جبيعخ أسُىط يؤسسخ حكىيُخ تعهًُُخ ثحثُخ تعًم عهً إعذاد كىادر يؤههخ عهًُب ً‬
‫ويهبرَب ً ويهُُب ً قبدرح عهً االثتكبر وانًُبفسخ فً سىق انعًم وانتصذٌ نًشكالد انًجتًع فً‬
‫يجبالد انتًرَض ورنك يٍ خالل ثرايج تعهًُُخ تستُذ عهً يعبَُر أكبدًَُخ يعتًذح وثحج‬
‫عهًٍ َىاكت يتطهجبد انحبضر وانًستقجم وَراعً يعبَُر انجىدح ‪ .‬وتقىو انكهُخ ثتأدَخ رسبنتهب‬
‫فٍ إطبر يٍ انقُى وانتقبنُذ انجبيعُخ انًتعبرف عهُهب‪.‬‬
‫األهداف االستراتيجية للكلية‬
‫نتطىَر انًستًر نهقذرح انتعهًُُخ نًرحهخ انجكبنىرَىش‪.‬‬ ‫‪‬‬

‫تعسَس انذعى انطالثٍ واألَشطخ انطالثُخ‪.‬‬ ‫‪‬‬
‫تطىَر انعًهُخ انتعهًُُخ فً يرحهخ انذراسبد انعهُب‪.‬‬ ‫‪‬‬
‫تحذَج انخطخ انجحثُخ نهكهُخ‪.‬‬ ‫‪‬‬
‫يتبثعخ ورعبَخ انخرَجٍُ‪.‬‬ ‫‪‬‬
‫تعسَس دور انكهُخ فً انًشبركخ انًجتًعُخ‪.‬‬ ‫‪‬‬
‫تطىَر أداء انعبيهٍُ ثبنجهبز اإلدارٌ و انقُبداد األكبدًَُخ ثبنكهُخ ‪.‬‬ ‫‪‬‬
‫تطىَر يستىي أداء وحذح ضًبٌ انجىدح‪.‬‬ ‫‪‬‬
‫انتقىَى انًستًر نهقطبعبد انثالث ثبنكهُخ ( قطبع شئىٌ انتعهُى و انطالة ‪ -‬قطبع‬ ‫‪‬‬
‫شئىٌ انذراسبد انعهُب و انجحج انعهًٍ‪ -‬قطبع شئىٌ خذيخ انًجتًع و تًُُخ انجُئخ)‪.‬‬
‫‪ii‬‬
Content
No. Subject Pag.
Unit 1: The concept critical care nursing practice
1 Scope of Critical Care and Emergency Nursing Practice 1
2 Ethical Issues I n Critical Care Nursing 6
3 Acid base balance 13
Unit 2: Respiratory system
4 Acute Respiratory Failure 20
5 Mechanical ventilation and weaning 25
6 Acute Respiratory Distress Syndrome 44
7 COVID-19 in ICU 52
8 Pulmonary Edema 59
9 Pulmonary Embolism 62
Unit 3: Cardiovascular system
10 Acute Heart failure (HF) 65
11 Acute Coronary Syndrome 79
12 Cardiac dysrhythmia 87
Unit 4: Gastrointestinal system
13 Acute liver Failure 97
14 Sever Acute Pancreatitis 104
Unit 5: Renal system
15 Acute kidney Injury 109
Unit 6: Nervous system
16 Head injury 117
17 Spinal Cord Injury 123
Unit 7: Multisystem dysfuncation
18 Shock 128
19 MODS 138
Unit 8: Endocrine system
20 Diabetic crisis 140
Unit 9: Special population in critical care
21 Organ transplantation 145
22 Safety in critical care units 153
GLOSSARY
ABBREVIATIONS
iii
Critical Care Nursing
Scope of Critical Care and emergency Nursing

Learning Objectives based on competence:
1. State goals of critical care nursing

2. Describe scope of critical care and emergency nursing
3. Differentiate between physical and non-physical needs of critical
ill patient
4. Summarize nursing process based on patients‘ needs in ICU
5. Recognize role of emergency nurse in emergency nursing
6. Clarify the ways of communication for critically ill patient in
ICU
Critical care nursing: is a nursing specialty that deals specifically
patients whose conditions are life-threatening and who require
comprehensive care and constant monitoring, usually in intensive care
units.
Emergency nursing
Is the delivery of specialized care to variety of ill or injured patient‘s such
patients may be unstable, have complex needs and require intensive
nursing care.
Emergency patient
Patient with serious problems and needs immediately or timely nursing
and medical intervention.
Goal of critical care nursing

 Acute and critical care nurses rely on a body of specialized
knowledge, skills, abilities, and experiences to:
- Restore, support, promote, and maintain the physiologic and
psychosocial stability of patients of all ages across the lifespan.
- Prioritize information in order to take immediate and decisive
evidence-based, patient-focused action.
- Respond with confidence and adapt to rapidly changing patient
conditions.
- Establish and maintain a safe, respectful, healing, and caring
environment.
1
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

Critically ill patients are defined by the AACN as being at high
risk for 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

The needs of the critically ill are considerable. 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.
 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.
 Note: The nature of critical care is such that physical needs
are considered a priority and are almost always met.
However, the critical care environment can actually obstruct
the fulfillment of non-physical needs contributing to the
stressful nature of critical illness.
2
B. A critical care nurse

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.
C. Critical care unit

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:
 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.
The intensive care unit is not merely a room or series of room filled with
patients attached to interventional technology; it is the home of an
organization: the intensive care team.
Common illness and injuries seen in emergency department

 Trauma and orthopedic injury
 Cardiovascular disorder such as heart failure ,ACS-----ect
 Respiratory disorders as ARF, pulmonary embolism---ect
 GIT disorder as acute pancreatitis ,gastric and hepatic bleeding
 Renal disorder as acute renal injury
 Shock due to Hypovolemia shock, cardiac dysrhythmia
 Drug overdose
 Burns
3
Functions of emergency nursing
 Immediately resuscitation
 First aid
 Emergency investigations
 Hospitalization or referral to specific specialty by calling down the
concerned doctor
Facilities to management patient in emergency department
 Examination room
 Treatment room
 Observation area
 Storage space
 Space
 Nursing station
 Dressing room
 Other supportive services as clinical laboratory ,radiology---ect
Staff requirement in emergency department
 Officer man
 Genior and senior physician
 Specialized doctors
 Nursing staff
 Labor staff(workers and auxiliary nurses)
Role of emergency nurse in emergency nursing
1-primary survey begins with an assessment of ABCD
2-secondary survey:-
 Obtain a full set of vitals including :RR,HR,BI.P and temperature
 Initiate cardiac monitoring
 Obtain continuous pulse oximetry reading
 Inserted NGT for stomach decompression if needs
 Obtain laboratory studies as toxicology, blood sugar ,electrolytes -
--ect
Characteristics of emergency nursing practice include:
 Assessment, analysis, nursing diagnosis, planning, implementation
of interventions,
 outcome identification, and evaluation of human responses of
individuals in all age
 Triage and prioritization.
4
 Emergency operations preparedness.

 Stabilization and resuscitation.
 Crisis intervention for unique patient populations, such as sexual
assault survivors.
 Provision of care in uncontrolled or unpredictable environments.
 Consistency as much as possible across the continuum of care.
 Other characteristics of emergency nursing environments include
unanticipated situations requiring intervention, allocation of
limited resources, need for immediate care as perceived by the
patient/others, and contextual factors. Contextual factors are the
variety of geographic settings, unpredictable numbers of patients,
and unknown patient variables which include severity, urgency,
and diagnosis.
5
Ethical Issues in Critical Care Nursing

OBJECTIVES
Learning objectives based on competence:
1-Explain the way ethics assists nurses and other clinicians in resolving
moral problems.
2. Name and describe ethical principles applicable to clinical ethics.
3. Describe steps in the process of ethical decision making.
4. Identify resources available to nurses to help resolve ethical dilemmas.
5-Differentiating Between Ethics and Morals
Definition:
Ethics is the study of morality or standards of conduct1 and a critical
reflection or evaluation of moral choices that are made.
Morals: are commonly shared beliefs by members within a society about
the ―rightness‖or ―wrongness‖ of actions and behaviors that include the
―shoulds,‖ ―should nots,‖ ―oughts,‖ and ―ought nots‖ and are usually
learned through family systems as well as religious and cultural traditions
Ethical Principles
Ethical principles serve as general guidelines in health care decision
making. Principles, such as autonomy, beneficence, non-maleficence,
veracity, fidelity, and justice, can guide conduct and provide a basis for
ethical reasoning.
 Autonomy
Autonomy is the right to self-determination or the right to make
independent decisions about one‘s own body or actions free from
interference or coercion from others.
6
Informed consent respects autonomy by providing patients and families
with the pertinent information they need to make an ethically sound
decision
 Beneficence
Nurses are ethically, legally, and professionally obligated to avoid harm
and promote benefit for their patients.
This includes acts of caring and compassion as well as protection from
harm. The ethical principle of beneficence is guiding all nurses in their
daily interactions and activities with patients. The principle of
beneficence presupposes that any harm patients are exposed to is justified
by the potential benefits.
 Non-maleficence
The ethical principle of non-maleficence obligates us to avoid causing
undue pain and suffering or harm to another. This principle is often
discussed along with the principle of beneficence because the two are
intricately linked. Non-maleficence is a prima facie duty for the nurse,
meaning that it is morally binding unless there are other conflicting moral
obligations that outweigh its primacy. Non-maleficence obligates nurses
to avoid harm of not only a physical or bodily nature but also
psychological or emotional distress; in some cases, harm can be caused by
a breach of professional standards of care.
 Veracity
Veracity or ―Truth-telling and the process of reaching informed choice
underlie the exercise of self-determination, which is basic to respect for
persons…. Clients have the moral right to determine what will be done
with their own person; to be given accurate information, and all the
information necessary for making informed judgment.
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 Fidelity
Fidelity is the duty to be faithful to one‘s patients by keeping promises
and fulfilling contracts and commitments. It is the moral covenant
between individuals in a relationship
Confidentiality is an aspect of fidelity that is an essential component of
trusting relationships.
 Justice
Justice is an important ethical principle in critical care settings and is
usually defined in terms of fairness or that which is due to others. In
health care, it is often discussed in terms of distributive justice or how one
allocates scarce or finite resources.
Nursing Code of Ethics

Is a document that embodies the moral values of the profession.It
represents not only the expectations for ethical conduct in clinical practice
but also the duty of the nurse to protect his or her own integrity within the
health care environment.
1. The nurse, in all professional relationships, practices with compassion
and respect for the inherent dignity, worth, and uniqueness of every
individual, unrestricted by considerations of social or economic status,
personal attributes, or the nature of health problems.
2. The nurse‘s primary commitment is to the patient, whether an
individual, family, group, or community.
3. The nurse promotes, advocates for, and strives to protect the health
safety, and rights of the patient.
4. The nurse is responsible and accountable for individual nursing practice
and determines the appropriate delegation of tasks consistent with the
nurse‘s obligation to provide optimum patient care.
8
5. The nurse owes the same duties to self as to others, including the
responsibility to preserve integrity and safety, to maintain competence,
and to continue personal and professional growth.
6. The nurse participates in establishing, maintaining, and improving
health care environments and conditions of employment conducive to the
provision of quality health care and consistent with the values of the
profession through individual and collective action.
7. The nurse participates in the advancement of the profession through
contributions to practice, education, administration, and knowledge
development.
8. The nurse collaborates with other health professionals and the public in
promoting community, national, and international efforts to meet health
needs.
9. The profession of nursing, as represented by associations and other
members, is responsible for articulating nursing values, for maintaining
the integrity of the profession and its practice, and for shaping social
policy.
Ethical Issues
An ethical issue or problem can occur in any clinical situation where there
are concerns about what might be ―morally right or wrong‖ in the care of
the critically ill patient and his or her family.
There are many ethical issues in critical care. These can include but are
not limited to:
 End-of-life treatment decisions,
 Truth-telling,
 Transplantation,
 Do not resuscitate (DNR),
9
 Informed consent,
 Clinical research with critically ill patients,
 Assisted suicide,
 The use of aggressive measures,
 Conflict among colleagues,
 Resource allocation
Moral Distress
Strategies to minimize moral distress and to create a healthy workplace
have been outlined by the American Association of Critical Care Nurses
(AACN) and include the four As: Ask, Affirm, Assess, and Act.
Ethical Decision Making

Steps in Ethical Decision Making:
1. Assessment of the problem
2. Define the ethical issues
3. Delineate the goals; decision making and implement plan of action
10
4. Evaluation of the process and modify action as needed.
Strategies for Promoting Ethical Decision Making
Two strategies for developing an environment that is supportive of ethical
concerns are: institutional ethics committees and ethics rounds and
conferences.
 Institutional Ethics Committees
Many health care facilities have institutional ethics committees (IEC) to
help resolve ethical conflicts in patient care as well as address ethics-
related questions that might arise in clinical practice. Ethics committees
usually involve a diverse group of individuals, including physicians,
nurses, social workers, pastoral care counselors, legal counsel,
administrators, and community members. IECs provide ethics
consultation and can assist practitioners by providing an external voice on
contentious ethical issues that may seem irresolvable and facilitate
education for all members of the health care team.
Recommendations by the IEC can be either binding or nonbinding,
depending on the individual committee.
However, an IEC can offer support to practitioners, patients, and families
and improve their satisfaction with the delivery of care. Some institutions
provide an ethics consultation service by a subset of the IEC or an
independent consultant.
 Ethics Rounds and Conferences
Ethics rounds may be an important and useful aspect of patient care, as
they provide an opportunity to discuss a particular patient‘s health care
needs in-depth and identify clinical, social, or ethical problems early in
the course of care.
Importantly, ethics rounds allow providers to express their views on
issues of concern as well as clarify the most salient values and preferences
at stake. This can include questions on DNR status, palliative care versus
11
curative care, advance directives, conflicts associated with family
systems, disagreements among health care providers about future goals of
care, organ donation, cultural and religious differences, and many others.
Nurses can make ethics rounds a regular part of their unit‘s activities by
establishing a set time to focus on a specific case that raised ethical
concerns or was particularly distressing for the staff. Interdisciplinary
ethics rounds also provides an opportunity to build trusting work
relationships with multidisciplinary care providers and develop a team
approach to addressing value conflicts that arise in the unit. An individual
patient ethics conference can be useful in resolving complex cases and
opening a dialogue with patients, families, and the nursing staff or a
multidisciplinary group.
12
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-).
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).
Expected ABG Outcomes
- PH: hydrogen ion concentration of blood and is an indicator of Acid-

Base status.
PH 7.35-7.45
13
↓ 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.
HCO3 22- 26 mEq/L
↓ HCO3 metabolic acidosis
↑ HCO3 metabolic alkalosis
- SaO2:-the saturation of hemoglobin by oxygen
SaO2: 95- 99%
- 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
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
14
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 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
 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
15
 Airway obstruction
- Retained secretions -Tumors
- Anaphylaxis -Laryngeal spasm
- Lung diseases that alter alveolar ventilation.
Signs and symptoms:
Tachycardia, dyspnea with rapid, shallow respirations, nausea and

vomiting, decreased deep tendon reflexes (DTRs), warm flushed skin ,
diaphoresis
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
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.
16
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.
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
Signs and symptoms:
 Tachycardia ,syncope
 Dyspnea and increased respiratory rate and depth.
 Diaphoresis, hyperreflexia,Paraesthesias, Tetany, Anxiety
 Confusion,Restlessness
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
o Serum magnesium level below normal
o Serum chloride level below normal
o Other blood test: Toxicology screening with evidence of salicylate
poisoning
17
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 protection of organic acids from; hepatic disease, or
endocrine disease (disorders) as diabetes mellitus, drug
intoxication.
3. In adequate excretion of acids from renal disease.
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(.
18
Metabolic Alkalosis (HCO3 retention, acid loss)
Possible causes:-
1. loss of hydrochloric acid (HCL) from prolonged vomiting or

gastric suctioning
2. excessive alkali ingestion
3. potassium loss from increased renal excretion
Signs and symptoms:
slow, shallow respiration (compensated), hypertonic

muscle, tetany, restlessness, convulsion, confusion, coma
Management: It is aimed at treating the underlying disorder
 Chloride supplementation for the kidney to absorb sodium with

chloride (allowing the excretion of excess bicarbonate(.
 Restore normal fluid volume, Maintain potassium
 Carbonic anhydrase inhibitor if unable to tolerate volume
expansion (as heart failure).
19
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.
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.
20
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.
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.
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
21
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 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 hypoxemia and hypercapnia: Hypoxemia
Respiratory Cerebral
• Dyspnea • Agitation
• Tachypnea • Disorientation
• Prolonged expiration (I:E = 1:3, • Restless, combative behavior
1:4) • Delirium
• Nasal flaring • Confusion
• Intercostal muscle retraction • ↓ Level of consciousness
• Use of accessory muscles in • Coma (late)
respiration
• ↓ SpO2 (<80%) Cardiac
• Paradoxic chest or abdominal • Tachycardia
wall movement with respiratory • Hypertension
cycle (late) • Skin cool, clammy, and
• Cyanosis (late) diaphoretic
• Dysrhythmias (late)
• Hypotension (late)
Other
• Fatigue
• Inability to speak in complete
sentences without pausing to
breathe
22
Hypercapnia
Respiratory Cerebral
• Dyspnea • Morning headache
• Use of tripod position • Disorientation
• Pursed-lip breathing • Progressive somnolence
• ↓ Respiratory rate or • Elevated intracranial pressure
• rapid rate with (if monitored)
• shallow respirations • Coma (late)
• ↓ Tidal volume
• ↓ Minute ventilation Cardiac
• Dysrhythmias
• Hypertension
• Tachycardia
• Bounding pulse
Neuromuscular
• Muscle weakness
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)
23
• Treatment of pulmonary infections (e.g., antibiotics)
• Reduction of severe anxiety, pain, and agitation (e.g., fentanyl,
morphine)
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
 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.
24
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.
Indications for Ventilator support
Global indications
• Clinical conditions requiring ventilator support

 “VOPS” vs “The Look”
 Ventilation
 Oxygenation
 Airway Protection
 Secretions
 No single ―level‖ of any vital sign, physical exam finding, or lab
value is an indication for intubation
A. Global pathophysiologic indications
1. Apnea
2. Acute ventilator failure
a. PaCO2 >50 mm Hg and pH <7.30
3. Impending acute ventilator failure
25
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
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 determining how much work of
breathing the patient has to do. These include
26
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.
- 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
27
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.
 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.
- 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,
28
- 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).
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 hyper inflation 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.
29
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 silence the alarm. If you can not
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 or  Unkink tubing Check for
endotracheal tube (ETT) adequate lung sounds bilaterally
 Patient biting the ETT  Place an oral airway in
High pressure Water in the ventilator patient's mouth so that he bites
tubing. the airway, not the ETT.
 Empty water from tubing
 ETT advanced into right main  Notify the doctor, who will
stem bronchus order a chest X-ray to
evaluate ETT position
 Disconnected tubing  Secure all connections
Low pressure  A Leak in the system from ( Deflate, then reinflate the
cuff leak - A hole in the cuff Recheck cuff pressure
tubing -ETT or (normal pressure is about
ventilator tubing) - A leak in 18mmHg) Change the tube.
the humidifier Tighten the humidifier
Oxygen  The oxygen supply is Notify staff to correct the

Insufficient or is not malfunction and manually
30
properly connected. ventilate the Patient with O2
source
Monitor oxygen saturation
High respiratory rate: caused by Episodes of tachypnea, anxiety, pain, hypoxia,

fever.
Apnea  Assess respirations, V.S

During weaning, indicates
that the patient has a slow
ABGs,SaO2 & report
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.
 Check gas flow
Temperature Alarm Overheating due to too 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
Nursing Interventions;
*To promote patient's comfort
*To provide airway patency
*To relieve anxiety or fear
*To maintain Bowel elimination
31
*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.)
- 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.
32
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)
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,
33
• 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.)
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
- 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
34
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
• 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.
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
35
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:
• 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.
36
 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:
 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.
37
Documentation
The nurse should record all:
• Ventilator settings • Patient's measurements
• Nursing care provided
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 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
38
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.
39
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 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
40
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
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
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
41
- 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)
- 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
 Increase or decrease in blood pressure of > 20 mm Hg
42
 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.
43
Acute Respiratory Distress Syndrome

a1. Define acute respiratory distress syndrome
a2. Mention risk factors associated with ARDS
b1. Relate the etiology and pathophysiology of acute respiratory
distress syndrome
b2. Describe the nursing role for patients with acute respiratory
distress syndrome
B3.Compare between phases of acute respiratory distress syndrome
c1. Write laboratory studies for acute respiratory distress syndrome
c2. Deign collaborative care, and nursing management of the patient
with of acute respiratory distress syndrome
Definition of acute respiratory distress syndrome . Severe form of

acute lung injury resulting in high morbidity and mortality. This
syndrome is characterized by noncardiogenic pulmonary edema, diffuse
pulmonary infiltrates, and hypoxemia refractory to oxygen delivery.
Causes and predisposing factors :
Predisposing Factors Leading to acute Respiratory Distress
Syndrome
Direct Lung Injury Indirect Lung indirect Lung Injury Indirect Lung
Injury Injury
 Aspiration  Acute pancreatitis
 Acute bacterial pneumonia  Blood transfusions
 Lung contusions, Near  Burns, Cardiopulmonary
drowning, Neurogenic bypass, Drug reaction,
pulmonary edema  Drug overdose
 Severe acute respiratory  Fractures (multiple and long
syndrome bone)
 Toxic inhalation (fumes or  Sepsis and septic shock
smoke)  Severe bleeding
 Upper airway obstruction  Transplantation (bone or
lung)
 Trauma
The pathogenesis of ARDS typically is described in 3 phases: (1)
exudative, (2) proliferative, and (3) fibrotic.
44
The exudative phase is the initial response to the lung injury. In this
phase, damage occurs to both the endothelial and epithelial walls of the
alveoli. The resulting increased capillary permeability leads to impaired
fluid drainage from the alveolar space and increased protein-rich fluid
inside the alveoli, leading to further alveolar damage and the release of
pro-inflammatory cytokines. Neutrophils and macrophages then are
recruited by the lungs and toxic mediators are released, resulting in
further cell damage, destroy surfactant inflammation, and pulmonary
edema. Intrapulmonary shunting increases, leading to severe hypoxemia.
During the proliferative phase, the patient‘s lung begins its repair
processes; the epithelial integrity is reestablished, the alveolar fluid is
reabsorbed, and the alveolar structure and function is restored.
The fibrotic phase, which may not occur in all patients, is due to
inadequate or delayed epithelialization and the formation of interstitial
and alveolar fibrosis. This phase can lead to increased ventilator days and
mortality.
Diagnosis; The American-European Consensus on ARDS Diagnostic
Criteria5
 Acute onset
 Bilateral infiltrates on chest radiograph
 Pulmonary capillary wedge pressure ≤18 mm Hg and no
indication of left atrial hypertension
 PaO2/FIO2 ratio (regardless of PEEP level) <200
45
Berlin Criteria for Acute Respiratory Distress Syndrome
Timing Within 1 week of clinical insult or new or worsening
symptoms
Chest Bilateral opacities that are not explained by effusions,
imaging collapse, or nodules
Edema Respiratory failure not explained by cardiac failure of
fluid overload Respiratory failure not explained by
cardiac failure of fluid overload
Oxygenation
Mild PaO2/FIO2 200 mm Hg to ) 300 mm Hg with PEEP/CPAP * 5

cm H2O
Moderate PaO2/FIO2 100 mm Hg to ) 200 mm Hg with PEEP * 5 cm
H2O
Sever PaO2/FIO2 ) 100 mm Hg with PEEP * 5 cm H2O
Management
1-Mechanical Ventilation Strategies
 Positive End-Expiratory Pressure.
 increased PEEP may improve alveolar recruitment and reduce the
effects of atelectrauma. Patients with moderate to severe ARDS
and larger amounts of potentially recruit able lung benefit the
greatest from high PEEP. High PEEP should not be used for all
patients with ARDS because risk of alveolar injury, increased
shunt, and dead space, along with the hemodynamic effects of
increased pulmonary vascular resistance.
 Implement mechanical ventilation using lower tidal volumes (4–8
mL/kg predicted body weight, PBW) and lower inspiratory
pressures (plateau pressure < 30 cmH2O).
 In adult patients with severe ARDS, prone ventilation for 12–16
hours per day is recommended
 Use a conservative fluid management strategy for ARDS patients
without tissue hypoperfusion
 In patients with moderate or severe ARDS, higher PEEP instead
of lower PEEP is suggested.
46
 In patients with moderate-severe ARDS (PaO2/FiO2 < 150),

neuromuscular blockade by continuous infusion should not be
routinely used.
 Avoid disconnecting the patient from the ventilator, which results
in loss of PEEP and atelectasis.
 Use in-line catheters for airway suctioning and clamp
endotracheal tube when disconnection is required (for example,
transfer to a transport ventilator).
 High-flow nasal oxygen (HFNO) should be used only in selected
patients with hypoxemic respiratory failure.
 Non-invasive ventilation (NIV) should be used only in selected patients
with hypoxemic respiratory failure.
 Patients treated with either HFNO or NIV should be closely
monitored for clinical deterioration
 In settings with access to expertise in extracorporeal membrane
oxygenation (ECMO), consider referral of patients who have
refractory hypoxemia despite lung protective ventilation.
 Lung Recruitment Maneuvers. An LRM consists of a brief

application of high (30-40 cm H2O) continuous positive airway
pressure, incremental PEEP increases at a constant driving
pressure, or a high driving pressure. The physiologic benefits of an
LRM include decreased ventilator-induced lung injuries(VILI) and
decreased mortality. The LRM, however, may lead to
hemodynamic instability and barotrauma. Lung recruitment
maneuvers done in conjunction with a higher PEEP strategy
makes it difficult to isolate the direct benefits of the LRM. The
guidelines suggest caution using LRM in patients who have
concurrent hypovolemia or shock.
 Extracorporeal Membrane Oxygenation.(ECMO) Extracorporeal
membrane oxygenation uses a mechanical artificial lung to
provide oxygenation and removal of carbon dioxide. This strategy
may allow recovery from the primary lung injury and minimize
VILI. The patient‘s respiratory system may contribute to
ventilation during ECMO.
 High-Frequency Oscillatory Ventilation. High-frequency
oscillatory ventilation delivers very small tidal volumes at higher
47
mean airway pressures with a rapid oscillatory respiratory rate
of up to 900 breaths per minute. This ventilator strategy has not
been shown to be beneficial in adult patients with ARDS; in
contrast, studies have shown patients are sig nificantly harmed
with routine HFO use.
 Inversed I:E ratio to improve oxygenation
 Permissive hypercabnia
2-Prone Positioning: The positive effects of prone positioning, including
an increase in oxygenation and pulmonary hygiene. Because of the
dramatic positive results in some patients in the study, placement in the
prone position was used as a rescue mode after other ventilator strategies
proved unsuccessful.
3-Pharmacological Management:-commonly used medications for

ventilated patients with ARDS.
 Sedatives/hypnotics as Ativan (lorazepam),Diprivan (propofol),
Precedex (dexmedetomidine) and Versed (midazolam)
 Narcotic analgesics as Sublimaze (fentanyl) , Dilaudid
(hydromorphone, Morphine sulfate
 Neuromuscular-blocking agents as Nimbex (cisatracurium besylate),
Norcuron (vecuronium bromide), Pavulon (pancuronium bromide) and
Tracrium (atracurium besylate)
4-Exogenous surfactant improves lung compliance and oxygenation.
However, studies, to date, have found that the use of surfactant therapy
does not significantly improve mortality rates.
5-Fluid Management the presence of noncardiogenic pulmonary edema
and increasing hydrostatic pressures from fluid replacement.
6- Nutritional Support:Caloric, protein, carbohydrate, and fat intake
should be determined based on the patient‘s daily metabolic needs, with
most requiring 35 to 45 kcal/kg per day.2 A low-carbohydrate, high-fat
enteral regimen, with anti-inflammatory and vasodilating components,
leads to improved oxygenation and decreased mortality rates.
48
Sepsis and Ventilator-Associated Pneumonia „„Bundles‟‟2
Sepsis Ventilator-Associated
Pneumonia
 Appropriate antibiotic  Head of bed elevation 30-45
therapy degrees
 Early goal-directed  Chlorhexidine antiseptic use
fluid
 resuscitation
 Steroid administration  Toothbrushing

 Activated protein C  Subglottic secretion suctioning
 DVT prophylaxis  Daily ventilator weaning
assessment
 Peptic ulcer  Daily sedation withholding
prophylaxis  DVT prophylaxis
 Peptic ulcer prophylaxis
Signs and Symptoms of Hemodynamic deterioration in adult

respiratory distress syndrome
Increasing Decreasing cardiac Decreasing blood
tachycardia output pressure
Arrhythmias, Increasing right atrial Narrowing pulse
Decreasing UOP pressures pressures, Weaker
pulses
Nursing intervention of ARDS requires careful monitoring and
supportive care.
 When your patient isn‘t intubated, watch carefully for signs of

respiratory failure, which can happen quickly and necessitate
intubation and mechanical ventilation.
 Assess the patient‘s respiratory rate, rhythm, and depth at least
every 2 hours or more often, if indicated.
 Report the presence of dyspnea and accessory muscle use. Be
alert for inspiratory retractions.
 Administer oxygen as ordered. Monitor Fio2 levels.
49
 Auscultate lungs bilaterally for adventitious or diminished breath

sounds. Inspect the color and character of sputum; clear, frothy
sputum indicates pulmonary edema. To maintain PEEP, suction
only as needed.
 Check ventilator settings often. Assess oxygen saturation
continuously by pulse oximetry or Svo2 by PA catheter.
 Monitor serial ABG levels; document and report changes in
oxygen saturation as well as metabolic and respiratory acidosis
and Pao2 changes.
 Monitor vital signs. Institute cardiac monitoring and observe for
arrhythmias that may result from hypoxemia, acid–base
disturbances, or electrolyte imbalance.
 Monitor the patient‘s LOC, noting confusion or mental
sluggishness.
 Be alert for signs of treatment induced complications, including
arrhythmias, disseminated intravascular coagulation, GI bleeding,
infection, malnutrition, paralytic ileus, pneumothorax, pulmonary
fibrosis, renal failure, thrombocytopenia, and tracheal stenosis.
 Be alert for the development of multiple organ dysfunction
syndrome.
 Monitor renal, GI, and neurologic system function.
 Give sedatives as ordered to reduce restlessness.
 Administer sedatives and analgesics at regular intervals if the
patient on mechanical ventilation is receiving neuromuscular
blocking agents.
 Provide routine eye care and instill artificial tears to prevent
corneal drying and abrasion from the loss of the blink reflex in
mechanically ventilated patients receiving neuromuscular
blocking agents.
 Administer antiinfective agents as ordered if the underlying cause
is sepsis or an infection.
 Place the patient in a comfortable position that maximizes air
exchange, such as semiFowler‘s or high Fowler‘s position.
 A continuous rotation bed or prone positioning may be needed.
 ECMO, compensating the lungs, ensures highly protective
ventilation, provided its optimal functioning is appropriately
50
ensured by the nurse. Blood flow may be variable and should be
controlled continuously.
 Complication of ARDS; includes Sepsis, multiple organ failure
,ventilator associated pneumonia, hemodynamic deterioration
associated with high PEEP, barotrauma/volutrauma
51
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.
 While most people with COVID-19 develop only mild or

uncomplicated illness, approximately 14% develop severe disease
that requires hospitalization and oxygen support, and 5% require
admission to an intensive care unit. In severe cases,
 COVID-19 can be complicated by the acute respiratory distress

syndrome (ARDS), sepsis and septic shock, multiorgan failure,
including acute kidney injury and cardiac injury. Older age and
co-morbid disease have been reported as risk factors for death.
Definition of SARS : A suspect case is a person presenting with

1. High fever (> 38_C) and cough or difficulty of breathing. The person is
also a suspect case if one or more of the following exposures are present
10 days prior to onset of symptoms such as close contact with a person
who is a suspect or probable case of SARS, history of travel to an area
with recent local transmission of SARS, and/or residing in an area with
recent local transmission of SARS.
52
2. A probable case is a suspect case with a chest radiographic evidence of
infiltrates consistent with pneumonia or RDS, positive for SARS corona
virus by one or more assays,
and autopsy findings consistent with the pathology of RDS without an
identifiable cause.
Clinical manifestations of SARS: observed in patients admitted in

hospitals included fever of more than 38_C ranging from 2 to 16 days
accompanied by chills and rigors, myalgia, headache and dizziness. Some
patients complained of sore throat, , nausea and vomiting, purulent
sputum and diarrhoea. Severe respiratory symptoms manifest on the 3rd–
7th day and in some patients could progress to severe hypoxaemia
mimicking acute respiratory distress syndrome (RDS) requiring intubation
and mechanical ventilation.
Pathophysiology of SARS
SARS is a new infectious disease. In March, preliminary data on two
causative agents of SARS, metapneumovirus and coronavirus, the
incubation period of SARS is typically 2–10 days (average 2–7
days).Pathological studies of patients who died showed alveolar damage
in the pulmonary tree, focal unilateral interstitial infiltrates of the lung,
progressing to more 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. The clinical course of SARS can be divided into
three phases: (1) viral replicative phase,(2) immune replicative phase, and
(3) lung destructive phase. From the clinical picture of patients who died
in Hong Kong hospitals, the 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
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
53
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,
 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
 Initiate IPC at the point of entry of the patient to hospital.
Screening should be done at first point of contact at the emergency
department or outpatient department/clinics. Suspected COVID-19
patients should be given a mask and directed to separate area. Keep at
least 1 m distance between suspected patients.
Standard precautions should always be applied in all areas of health care
facilities. Standard precautions include hand hygiene and the use of
personal protective equipment (PPE) when in indirect and direct contact
with patients‘ blood, body fluids, secretions (including respiratory
secretions) and non-intact skin. Standard precautions also include
prevention of needle-stick or sharps injury; safe
waste management; cleaning and disinfection of equipment; and
cleaning of the environment.
In addition to standard precautions, health care workers should do
a point-of-care risk assessment at every patient contact to determine
whether additional precautions (e.g. droplet, contact, or airborne) are
required.
3-Collection of specimens for laboratory diagnosis

 Collect blood cultures for bacteria that cause pneumonia and
sepsis, ideally before antimicrobial therapy. DO NOT delay
antimicrobial therapy to collect blood cultures.
54
 Collect specimens from the upper respiratory tract (URT and
LRT)for COVID-19 virus testing by RT-PCR and bacterial
stains/cultures.
 In hospitalized patients with confirmed COVID-19, repeated URT
and LRT samples can be collected to demonstrate viral clearance. The
frequency of specimen collection will depend on local epidemic
characteristics and resources. For hospital discharge, in a clinically
recovered patient, two negative tests, at least 24 hours apart, is
recommended.
4-Management of mild COVID-19: symptomatic treatment and

monitoring
 Patients with mild disease do not require hospital interventions,
but isolation is necessary to contain virus transmission and will
depend on national strategy and resources.
Prevention of Interventions
complications
Anticipated outcome
Reduce days of invasive • Use weaning protocols that include daily assessment for
mechanical ventilation readiness to breathe spontaneously
• • Minimize continuous or intermittent sedation,
targeting specific titration endpoints (light sedation unless
contraindicated) or with daily interruption of continuous
sedative infusions
Reduce incidence of
ventilator- associated • Oral intubation is preferable to nasal intubation in adolescents
pneumonia and adults
• Keep patient in semi-recumbent position (head of bed
elevation 30–45º)
• Use a closed suctioning system; periodically drain and
discard condensate in tubing
• Use a new ventilator circuit for each patient; once patient is
ventilated, change circuit if it is soiled or damaged, but not
routinely
• Change heat moisture exchanger when it malfunctions, when
soiled, or every 5–7 days
Reduce incidence of
55
venous thromboembolism • Use pharmacological prophylaxis (low molecular-weight
heparin [preferred if available] or heparin 5000 units
subcutaneously twice daily) in adolescents and adults without
contraindications. For those with contraindications, use
mechanical prophylaxis (intermittent pneumatic compression
devices)
Reduce incidence of
catheter-related • Use a checklist with completion verified by a real-time
bloodstream infection observer as reminder of each step needed for sterile insertion
and as a daily reminder to remove catheter if no longer needed
Reduce incidence of • Turn patient every 2 hours

pressure ulcers
Reduce incidence of stress • Give early enteral nutrition (within 24–48 hours of
ulcers and gastrointestinal admission)
(GI) bleeding • • Administer histamine-2 receptor blockers or proton-
pump inhibitors in patients with risk factors for GI bleeding.
Risk factors for GI bleeding include mechanical ventilation for
≥ 48 hours, coagulopathy, renal replacement therapy, liver
disease, multiple comorbidities, and higher organ failure score
Reduce incidence of ICU- • Actively mobilize the patient early in the course of illness
related weakness when safe to do so
 Provide patients with mild COVID-19 with symptomatic treatment

such as antipyretics for fever.
 Counsel patients with mild COVID-19 about signs and symptoms
of complicated disease. If they develop any of these symptoms,
they should seek urgent care through national referral systems.
5- Management of severe COVID-19: oxygen therapy and monitoring

-Give supplemental oxygen therapy immediately to patients with SARI
and respiratory distress, hypoxaemia or shock and target SpO2 > 94%.
-Closely monitor patients with COVID-19 for signs of clinical
deterioration, such as rapidly progressive respiratory failure and sepsis
and respond immediately with supportive care interventions
-Understand the patient‘s co-morbid condition(s) to tailor the
management of critical illness
56
-Use conservative fluid management in patients with SARI when there is
no evidence of shock.
6-Management of severe COVID-19: treatment of co-infections

• Give empiric antimicrobials to treat all likely pathogens causing
SARI and sepsis as soon as possible, within 1 hour of initial assessment
for patients with sepsis.
• Empiric therapy should be de-escalated on the basis of
microbiology results and clinical judgment.
7. Management of critical COVID-19: acute respiratory distress

syndrome ( see ARDS) .Recognize severe hypoxemic respiratory failure
when a patient with respiratory distress is failing to respond to standard
oxygen therapy and prepare to provide advanced oxygen/ventilatory
support
8- Management of critical illness and COVID-19: prevention of

complications
9- Management of critical illness and COVID-19: septic shock (see

shock)
The following recommendations pertain to resuscitation strategies for
adult and paediatric patients with septic shock.
• In resuscitation for septic shock in adults, give 250–500 mL and
10-20 ml for children crystalloid fluid as rapid bolus in first 15–30
minutes and reassess for signs of fluid overload after each bolus.
Closed monitoring for volume overload, (e.g. jugular venous distension,
crackles on lung auscultation, pulmonary oedema on imaging, or
hepatomegaly in children), then reduce or discontinue fluid
administration. This step is particularly important in patients with
hypoxemic respiratory failure.
• Do not use hypotonic crystalloids, starches, or gelatins for

resuscitation
Starches are associated with an increased risk of death and acute kidney
injury compared with crystalloids. The effects of gelatins are less clear,
57
but they are more expensive than crystalloids. Hypotonic (vs isotonic)
solutions are less effective at increasing intravascular volume. In adults,
administer vasopressors when shock persists during or after fluid
resuscitation. The initial blood pressure target is MAP ≥ 65 mmHg in
adults and improvement of markers of perfusion.
10-Adjunctive therapies for COVID-19: corticosteroids do not

routinely give systemic corticosteroids for treatment of viral pneumonia
outside clinical trials
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.
58
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 permeabil ity
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
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
59
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)
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
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
60
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 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.
61
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
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
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 Massive embolus (above manifestation plus the following)

- Cyanosis - Restlessness - Anxiety
- Confusion - Cool, clammy skin
- Decreased urinary output
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
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:
63
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.
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)
learning objectives of the heart failure (HF) nurse curriculum
1. Recognize patients with suspected HF and have a critical

awareness of triggers for clinical deterioration
2. Assess and monitor common symptoms and signs
3. Apply educational theory to develop, implement and evaluate
effective patient and family HF education
4. Manage the effective use of pharmacological and device therapies
5. Competently and rapidly assess need and deliver care to the
patient with acute HF
6. Recognize the importance of co-morbidity in HF and plan and
deliver individualized patient care
7. Identify the need for and understand novel strategies in the
management of advanced HF, such as mechanical circulatory
support and heart transplantation
8. Provide self-care and lifestyle advice (including diet, exercise and
travel)
9. Leadership in HF nursing
Acute Heart failure, onset refers to the sudden abnormal clinical

syndrome that involves inadequate pumping and/or filling of the heart,
and leads to unable it to provide sufficient blood to meet the oxygen
needs of the tissues., usually over days or hours. Acute symptoms have
progressed to a point at which immediate or emergency intervention is
necessary to save the patient‘s life.
Acute decompensated heart failure (ADHF) is a sudden

worsening of the signs and symptoms of heart failure, The condition is
caused by severe congestion of multiple organs by fluid that is
inadequately circulated by the failing heart. An attack
of decompensationcan be caused by underlying medical illness, such
as myocardial infarction, infection, or thyroid disease.
65
Etiology:
HF may be caused by any interference with the normal
mechanisms regulating cardiac output (CO). CO depends on (1) preload,
(2) afterload, (3) myocardial contractility, and (4) heart rate (HR). Any
changes in these factors can lead to decreased ventricular function and
HF.
The major causes of HF may be divided into two subgroups:

primary causes precipitating causes
 Coronary artery disease, including myocardial  Anemia
infarction  Dysrhythmias
 Hypertension, including hypertensive crisis  Pulmonary
 Rheumatic heart disease embolism
 Congenital heart defects (e.g., ventricular septal  Nutritional
defect) deficiencies
 Pulmonary hypertension  Hypervolemia
 Cardiomyopathy
 Hyperthyroidism
 Valvular disorders (e.g., mitral stenosis)
 Myocarditis
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Classification:
HF is classified as systolic or diastolic failure. Systolic failure
results from an inability of the heart to pump blood effectively. The left
ventricle (LV) in systolic failure loses its ability to generate enough
pressure to eject blood forward through the aorta. Over time, the LV
becomes dilated and hypertrophied. The hallmark of systolic failure is a
decrease in the left ventricular ejection fraction (EF). The EF is defined
as the amount of blood ejected from the LV with each contraction.
Normal EF is 55% to 60%. Patients with systolic HF generally have an
EF less than 45%.
Diastolic failure is the inability of the ventricles to relax and fill
during diastole. Diastolic failure is often referred to as HF with normal
EF. Decreased filling of the ventricles results in decreased stroke volume
and CO. Diastolic failure is characterized by high filling pressures
because of stiff ventricles. This results in venous engorgement in both the
pulmonary and systemic vascular systems. Diastolic failure is usually the
result of left ventricular hypertrophy.
Mixed Systolic and Diastolic Failure. These patients often have
extremely low EFs (less than 35%), high pulmonary pressures, and
biventricular failure (both ventricles are dilated and have poor filling and
emptying capacity).
Pathophysiology:
The Compensatory Mechanisms to try to maintain adequate
CO. include: Sympathetic Nervous System Activation, the first
mechanism triggered in low-CO states. In response to an inadequate
stroke volume and CO, SNS activation increases, resulting in the
increased release of catecholamines (epinephrine and norepinephrine).
This results in increased HR, increased myocardial contractility, and
peripheral vasoconstriction. Initially, this increase in HR and contractility
improves CO. However, over time these factors are harmful, since they
increase the already failing heart‘s workload and need for oxygen. The
vasoconstriction causes an immediate increase in preload, which may
initially increase CO. However, an increase in venous return to the heart,
which is already volume overloaded, actually worsens ventricular
performance.
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Neurohormonal Response. As the CO falls, blood flow to the
kidneys decreases. In response, the kidneys release renin, which converts
angiotensinogen to angiotensin I is subsequently converted to angiotensin
II by a converting enzyme made in the lungs. Angiotensin II causes (1)
the adrenal cortex to release aldosterone, which results in sodium and
water retention; and (2) increased peripheral vasoconstriction, which
increases BP. This response is known as the renin-angiotensinaldosterone
system (RAAS).
Low CO causes a decrease in cerebral perfusion pressure. In
response, the posterior pituitary gland secretes antidiuretic hormone
(ADH), also called vasopressin. ADH increases water reabsorption in the
kidneys, causing water retention. As a result, blood volume is increased in
a person who is already volume overloaded.
Dilation is an enlargement of the chambers of the heart. It occurs
when pressure in the heart chambers (usually the LV) is elevated over
time. Dilation starts as an adaptive mechanism to cope with increasing
blood volume. Eventually this mechanism becomes inadequate because
the elastic elements of the muscle fibers are overstretched and can no
longer contract effectively, thereby decreasing the CO.
Hypertrophy is an increase in the muscle mass and cardiac wall
thickness in response to overwork and strain. It occurs slowly because it
takes time for this increased muscle tissue to develop. Initially, the
increased contractile power of the muscle fibers leads to an increase in
CO and maintenance of tissue perfusion. Over time, hypertrophic heart
muscle has poor contractility, requires more oxygen to perform work, has
poor coronary artery circulation (tissue becomes ischemic more easily),
and is prone to dysrhythmias.
The Counterregulatory Mechanisms. The body‘s attempts to

maintain balance are demonstrated by several counterregulatory
processes. Natriuretic peptides (atrial natriuretic peptide [ANP] and b-
type, natriuretic peptide [BNP]) are hormones produced by the heart
muscle. ANP is released from the atria and BNP is released from the
ventricles in response to increased blood volume in the heart. The
natriuretic peptides have renal, cardiovascular, and hormonal effects.
Renal effects include (1) increased glomerular filtration rate and diuresis
and (2) excretion of sodium.
68
Cardiovascular effects include vasodilation and decreased BP.
Hormonal effects include (1) inhibition of aldosterone and renin secretion
and (2) interference with ADH release. The combined effects of ANP and
BNP help to counter the adverse effects of the SNS and RAAS in patients
with HF. Nitric oxide (NO) is substance released from the vascular
endothelium in response to the compensatory mechanisms activated in
HF. NO works to relax the arterial smooth muscle, resulting in
vasodilation and decreased afterload.
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Types of Heart Failure

Left-Sided Heart Failure. The most common form of HF is left-
sided HF. Left-sided HF results from left ventricular dysfunction. This
prevents normal, forward blood flow and causes blood to back up into the
left atrium and pulmonary veins. The increased pulmonary pressure
causes fluid leakage from the pulmonary capillary bed into the
interstitium and then the alveoli. This manifests as pulmonary congestion
and edema.
Right-Sided Heart Failure. Right-sided HF occurs when the right
ventricle (RV) fails to contract effectively. Right-sided HF causes a
backup of blood into the right atrium and venous circulation. Venous
congestion in the systemic circulation results in jugular venous distention,
hepatomegaly, splenomegaly, vascular congestion of the gastrointestinal
tract, and peripheral edema.
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Clinical Manifestations
Acute Decompensated Heart Failure
71
Complications of Heart Failure

 Pleural Effusion.
 Dysrhythmias.
 Left Ventricular Thrombus.
 Hepatomegaly.
 Renal Failure.
Diagnostic
 History and physical examination
 Determination of underlying cause
 Investigation:
Laboratory studies Diagnostic studies
- Cardiac markers - Hemodynamic monitoring
- BNPor NT-proBNP level - Chest x-ray
- liver function tests - 12-lead ECG
- Thyroid function tests, - 2-dimensional echocardiogram
- CBC - Measurement of LV function
- lipid profile - Nuclear imaging studies
- kidney function tests - Cardiac catheterization
- Endomyocardial biopsy
Collaborative Therapy
 Treatment of underlying cause
 High Fowler‘s position
 O2 by mask or nasal cannula
 BiPAP
 Circulatory assist device: intraaortic balloon pump
 Endotracheal intubation and mechanical ventilation
 Vital signs, urine output at least q1hr
 Continuous ECG and pulse oximetry monitoring
 Hemodynamic monitoring (intraarterial BP, PAWP, CO)
 Drug therapy (Diuretics. Vasodilators. Morphine. Positive
Inotropes
 Possible cardioversion (e.g., atrial fibrillation)
 Ultrafiltration
 Daily weights
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 Sodium- and, possibly, fluid-restricted diet

NURSING DIAGNOSIS:
 Decreased Cardiac Output related to impaired contractility and

increased preload and afterload
 Impaired Gas Exchange related to alveolar edema due to elevated
ventricular pressures
 Excess Fluid Volume related to sodium and water retention
 Activity Intolerance related to oxygen supply and demand
imbalance
 Knowledge Deficit related to lack of previous exposure to
information
Nursing Interventions:
Maintaining Adequate Cardiac Output
1. Place patient at physical and emotional rest to reduce work of heart.
a. Provide rest in semi-recumbent position or in armchair in air-
conditioned environment—reduces work of heart, increases heart
reserve, reduces BP, decreases work of respiratory muscles and
oxygen utilization, improves efficiency of heart contraction;
recumbency promotes diuresis by improving renal perfusion.
b. Provide bedside commode—to reduce work of getting to bathroom
and for defecation.
c. Provide for psychological rest—emotional stress produces
vasoconstriction, elevates arterial pressure, and speeds the heart.
i. Promote physical comfort.
ii. Avoid situations that tend to promote anxiety and agitation.
iii. Offer careful explanations and answers to the patient‘s questions.
2. Evaluate frequently for progression of left-sided heart failure. Take
frequent blood pressure readings.
a. Observe for lowering of systolic pressure.
b. Note narrowing of pulse pressure.
c. Note alternating strong and weak pulsations (pulsus alternans).
3. Auscultate heart sounds frequently and monitor cardiac rhythm.
a. Note presence of S3 or S4 gallop (S3 gallop is a significant indicator
of heart failure).
b. Monitor for premature ventricular beats.
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c. Assess chest pain.
d. Measure CVP.
4. Observe for signs and symptoms of reduced peripheral tissue perfusion:
cool temperature of skin, facial pallor, poor capillary refill of nailbeds.
5. Administer pharmacotherapy as directed.
a. Monitor for adverse effects and effects of drug therapy.
6. Monitor clinical response of patient with respect to relief of symptoms
(lessening dyspnea and orthopnea, decrease in crackles, relief of
peripheral edema)
Improving Oxygenation
1. Raise head of bed 8 to 10 inches (20 to 25 cm)—reduces venous return
to heart and lungs; alleviates pulmonary congestion.
a. Support lower arms with pillows—eliminates pull of patient‘s
weight on shoulder muscles.
b. Sit orthopneic patient on side of bed with feet supported by a chair,
head and arms resting on an over the-bed table, and lumbosacral
area supported with pillows.
2. Auscultate lung fields at least every 4 hours for crackle and wheezes in
dependent lung fields (fluid accumulates in areas affected by gravity).
a. Mark with indelible ink the level on the patient‘s bac where
adventitious breath sounds are heard.
b. Use markings for comparative assessment over time and among
different care providers.
3. Observe for increased rate of respirations (could be indicative of falling
arterial pH).
4. Observe for Cheyne-Stokes respirations (may occur in elderly patients
because of a decrease in cerebral perfusion stimulating a neurogenic
response).
5. Position the patient every 2 hours (or encourage the patient to change
position frequently)—to help prevent atelectasis and pneumonia.
6. Encourage deep-breathing exercises every 1 to 2 hours— to avoid
atelectasis.
7. Offer small, frequent feedings—to avoid excessive gastric filling and
abdominal distention with subsequent elevation of diaphragm that
causes decrease in lung capacity.
8. Administer oxygen as directed
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Restoring Fluid Balance

1. Administer prescribed diuretic as ordered.
2. Give diuretic early in the morning—nighttime diuresis disturbs sleep.
3. Keep input and output record—patient may lose large volume of fluid
after a single dose of diuretic. Watch fluid intake.
4. Weigh patient daily—to determine if edema is being controlled; weight
loss should not exceed 1 to 2 lb (0.5 to 1 kg)/day.
5. Assess for signs of hypovolemia caused by diuretic therapy—thirst,
decreased urine output, orthostatic hypotension, weak, thready pulse,
increased serum osmolality, and increased urine specific gravity.
6. Be alert for signs of hypokalemia, which may cause weakening of
cardiac contractions and may precipitate digoxin toxicity in the form of
dysrhythmias, anorexia, nausea, vomiting, abdominal distention,
paralytic ileus, paresthesias, muscle weakness and cramps, confusion.
Check electrolytes frequently.
7. Give potassium supplements as prescribed.
8. Be aware of disorders that may be worsened by diuretic therapy,
including hyperuricemia, gout, volume depletion, hyponatremia,
magnesium depletion, hyperglycemia, and diabetes mellitus. Also, note
that some patients allergic to sulfa drugs may also be allergic to
thiazide diuretics.
9. Watch for signs of bladder distention in elderly male patients with
prostatic hyperplasia.
10. Administer I.V. fluids carefully through an intermittent access device
to prevent fluid overload.
11. Monitor for pitting edema of lower extremities and sacral area. Use
convoluted foam mattress and sheepskin to prevent pressure ulcers
(poor blood flow and edema increase susceptibility).
12. Observe for the complications of bed rest—pressure ulcers (especially
in edematous patients), phlebothrombosis, pulmonary embolism.
13. Be alert to complaints of right upper quadrant abdominal pain, poor
appetite, nausea, and abdominal distention (may indicate hepatic and
visceral engorgement).
14. Monitor patient‘s diet. Diet may be limited in sodium— to prevent,
control, or eliminate edema; may also be limited in calories.
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15. Caution patients to avoid added salt in food and foods with high
sodium content
Improving Activity Tolerance

1. Increase patient‘s activities gradually. Alter or modify patient‘s
activities to keep within the limits of his cardiac reserve.
a. Assist patient with self-care activities early in the day (fatigue sets in
as day progresses).
b. Be alert to complaints of chest pain or skeletal pain during or after
activities.
2. Observe the pulse, symptoms, and behavioral response to increased
activity.
a. Monitor patient‘s heart rate during self-care activities.
b. Allow heart rate to decrease to preactivity level before initiating a
new activity.
i. Note time lapse between cessation of activity and decrease in heart
rate (decreased stroke volume causes immediate rise in heart rate).
ii. Document time lapse and revise patient care plan as appropriate
(progressive increase in time lapse may be indicative of increased
left-sided heart failure).
3. Relieve nighttime anxiety and provide for rest and sleep—patients with
heart failure have a tendency to be restless at night because of cerebral
hypoxia with superimposed nitrogen retention. Give appropriate
sedation to relieve insomnia and restlessness
Improving Knowledge
1. Explain the disease process: the term ―failure‖ may have terrifying
implications.
2. Explain the pumping action of the heart: to move blood through
the body to provide nutrients and aid in the removal of waste.
3. Explain the difference between heart failure and heart attack.
Teach about the signs and symptoms of recurrence.
4. Watch for weight gain and report a gain or loss of more than 2 to 3
lb (1 to 1.4 kg) in a few days.
5. Weigh patient at same time daily to detect any tendency toward
fluid retention: swelling of ankles, feet, abdomen; persistent
cough; tiredness; loss of appetite; frequent urinaion at night.
76
6. Review medication regimen.
a. Medications recommended for patients with ejection fraction less
than 40% include preload reductors, such as diuretics, and afterload
reductors, such as ACE inhibitors.
b. Medications to control heart rate include digoxin or beta-adrenergic
blockers.
c. Anticoagulation if indicated.
Patient Education and Health Maintenance

1. Advise patient of symptoms that need to be reported to health care
provider.
a. Breathlessness
b. Increased shortness of breath
c. Wheezing
d. Sleeping upright with pillows
2. Help patient label all medications.
a. Give written instructions.
b. Make sure the patient has a check-off system that will show that he
has taken medications.
c. Inform the patient of adverse drug effects.
d. If the patient is taking oral potassium solution, it may be diluted with
juice and taken after a meal.
e. Tell the patient to weigh self-daily and log weight if on diuretic
therapy.
f. Ask whether patient is taking Coenzyme Q10 or other supplements;
should discuss with health care provider.
3. Review activity program. Instruct the patient as follows:
a. Increase walking and other activities gradually, provided they do not
cause fatigue and dyspnea.
b. In general, continue at whatever activity level can be maintained
without the appearance of symptoms.
c. Avoid excesses in eating and drinking.
d. Undertake a weight reduction program until optimal weight is
reached.
e. Avoid extremes in heat and cold, which increase the work of the
heart; air conditioning may be essential in a hot, humid
environment.
77
f. Keep regular appointment with health care provider or clinic.
4. Restrict sodium as directed.
a. Teach restricted sodium diet and the DASH diet.
b. Give patient a written diet plan with lists of permitted and restricted
foods.
c. Advise patient to look at all labels to ascertain sodium content
(antacids, laxatives, cough remedies, and so forth).
d. Teach the patient to rinse the mouth well after using tooth cleansers
and mouthwashes—some of these contain large amounts of sodium.
Water softeners should be checked for salt content.
e. Teach the patient that sodium is present in alkalizers, cough
remedies, laxatives, pain relievers, estrogens, and other drugs
f. Encourage use of flavorings, spices, herbs, and lemon juice.
g. Avoid salt substitutes with renal disease.
5. Make sure patient sets up follow-up appointments.
6. Advise patient on smoking cessation, provide information, if indicated
78
Acute coronary syndrome
Learning Objectives based on competence (ILOs)
a1. Define ACS , UA,NSTEMI and STEMI
a2. Mention risk factors associated with ACS
b1. Relate the etiology and pathophysiology of acute coronary
syndrome (ACS) to the clinical manifestations of each disorder.
b2. Describe the nursing role in the promotion of therapeutic lifestyle
changes in patients with acute coronary syndrome (ACS)
b3. Differentiate the clinical characteristics and ECG patterns of
normal sinus rhythm, common dysrhythmias, and acute coronary
syndrome (ACS).
b4. Compare between UA,NSTEMI and STEMI
c1. Write laboratory studies for ACS
c2. Deign collaborative care, and nursing management of the patient
c3. with of acute coronary syndrome (ACS)
ACS can result from a sudden drop in blood flow through the coronary
arteries supplying the different regions of the myocardium. This can
compromise the myocardium, leading to reversible ischemia or a
complete loss of blood supply, which leads to myocardial infarction and
myocardial cell death (necrosis).
Definition of ACS refers to potentially life-threatening conditions that

affect the coronary artery blood supply to the heart muscle these include
unstable angina, non-ST segment elevation myocardial infarction
(NSTEMI) and ST segment elevation myocardial infarction (STEMI).
Pathophysiology of ACS
 Most ACS cases are caused by atherosclerosis, which takes place
in the coronary arteries. The formation of an atherosclerotic
plaque begins with low-grade inflammation in the inner layer of
blood vessels.
 The endothelial cells lining blood vessels sustain injury, change
shape and become increasingly permeable to fluid, lipids and
white blood cells.
 These lipid-rich plaques contain inflammatory cells, cellular
debris, smooth muscle cells with cholesterol, and a fibrous
capsule. Over time they can progress and cause luminal narrowing
of the blood vessel, thereby limiting blood flow.
79
 ACS is usually triggered by the rupture of an atherosclerotic

plaque in the wall of a coronary artery; this causes activation,
adhesion and aggregation of platelets and the clotting systems,
leading to the formation of a thrombus.
 If the thrombus completely occludes the coronary artery, the
section of the myocardium supplied by that artery is starved of
oxygen, leading to myocardial cell necrosis, and typical ST
elevation changes are seen on an electrocardiogram .In addition,
cardiac enzymes are released from damaged myocardial cells
(troponin I and T,creatinine kinase MB isoenzyme), which can be
measured in the blood.
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 contain fibrinogen
Clinical manifestation of UA and NSTEMI

These symptoms include typical or central chest pain, fatigue, and
shortness of breath, indigestion, and anxiety. Fatigue is the most
prominent symptom. And theses manifestation relieved by vasodilators
and rest.
Clinical manifestation of STEMI
Includes severe chest pain not relieved by rest, position change, or
vasodilator administration (nitrates) .pain as a heaviness, pressure,
tightness, burning, constriction, or crushing. Common locations are
substernal, retrosternal, or epigastric areas. But relieved only by
fibrinolysis (thrombolytic agents)
80
Risk factors
Modifiable Non-modifiable
Elevated blood pressure Age
Hyperlipidemia Gender
Diabetes mellitus Family history
Obesity Race
Physical inactivity
Cigarette smoker
Stress
DIAGNOSTIC STUDIES ACUTE CORONARY SYNDROME

 Patient‘s history of pain clinical manifestation , risk factors, and
health history
 SOCRATES, can be used to assess patients‘ chest pain:
 S – site of pain;
 – onset of pain;
 C – character of the pain;
 R – any radiation;
 A – associated factors;
 T – timing of the pain;
 E – exacerbating/alleviating factors; for example, position or
inspiration;
 S – severity of the pain using a rating scale of 1-10 (10 being
the worst pain).
 12-lead Electrocardiogram changes: during anginal episode or
NSTEMI, show T-wave inversions and ST-segment depressions.
Ectopic beats may also be present during anginal episode. ST-
segment elevation in STEMI
 Laboratory investigations (cardiac enzymes, lipogram, renal and
hepatic function tests, complete blood count, glucose level ).
Cardiac Biomarker Summary
Cardiac Specificity / Rise Peak Duration

Biomarker Sensitivity
Myoglobin Sensitive but Within 2 4to 10 hours < 24 hours
not specific hours
81
CK-MB Highly specific 4 to 6 18 to 24 2 to 3 days
hours hours
Troponin I Highly specific 4 to 6 18 to 24 10 or more
or T and sensitive hours hours days
 Coronary angiography is the definitive tool to diagnosis CAD

 Exercise or pharmacological stress test after relieve of acute
attack.
 Echocardiography to evaluate wall motion abnormalities and
thickness, valvular function, and ejection fraction.
 MRI and coronary computed tomography angiography to view
structure cardiovascular abnormalities.
 In Unstable angina: The patient has clinical manifestations of
coronary ischemia, but ECG and cardiac biomarkers show no
evidence of acute MI.
 In NSTEMI: The patient has mind elevated cardiac biomarkers
but no definite ECG evidence of acute MI. During recovery from
an MI, the ST segment often is the first ECG indicator to return to
normal (1 to 6 weeks). The T wave becomes large and
symmetric for 24 hours, and it then inverts within 1 to 3 days
for 1 to 2 weeks. Q-wave alterations are usually permanent.
 In STEMI: The patient has ECG evidence of acute MI with
characteristic elevated ST segment on a 12-lead ECG that face the
same area of the heart . In this type of MI, there is significant
damage to the myocardium. • Chest pain for longer than 20
minutes, un relieved by nitroglycerin ST-segment elevation in at
least two leads
 ECG changes seen in STEMI, which include ST elevation of ≥1mm
height in two adjacent chest leads, ST elevation of ≥2mm in two
adjacent limb leads, and new left bundle branch block. If STEMI is
suspected.
 An old STEMI is usually indicated by an abnormal Q wave or
decreased height of the R wave without ST-segment and T-wave
changes.
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Pharmacological therapy for unstable angina and NSTEMI is (

MONA)
1-Pain relief
Patients presenting with chest pain may need sublingual or buccal
glycerol triturate (GTN) to relieve pain. GTN promotes venodilation and
dilatation of the coronary arteries. It can be given to patients with
ischaemic chest pain provided their systolic blood pressure is >90mmHg.
Some patients with nitrate-refractory pain receive opioids, such as
intravenous morphine, at small doses every few minutes until they are
pain free
M ----morphine to relieve pain
O----oxygen to increase the amount of oxygen delivered to the
myocardium and to decrease pain.
N----Nitrates to dilate veins and arteries(vasodilator) It is contraindicated
in patients with an inferior MI or suspected right ventricular
involvement, as it can cause hemodynamic deterioration.
A----antiplatelet (dual antiplatelet therapy is crucial in ACS management.
give patients 300mg of non-enteric coated aspirin on presentation and
clopidogrel "Plavix") and anticoagulant (heparin)
- Glycoprotein IIb/IIIa inhibitors (GPIs) GPIIb/IIIa receptor
activation is the last
83
Step in platelet aggregation when a clot is forming, so GPIs can be
effective but, are linked to bleeding.
-Blockers: Used to ↓ myocardial oxygen consumption/demand by
reducing myocardial contractility
-Calcium channel blockers: It increase myocardial oxygen supply by
dilating the smooth muscle wall of the coronary arterioles and decrease
(afterload).
-Anti lipidemic to decrease cholesterol level. Statins, aimed at lowering
cholesterol,
are crucial to secondary prevention
-Angiotensin-converting enzyme inhibitor within 24 hours
Coronary reperfusion strategies\ for STEMI: as previous in

UA&NSTEM plus: Primary Percutaneous Coronary Intervention
(PCI) if available this technique includes remove of thrombus , dilation of
coronary arteries by balloon called percutaneous transluminal coronary
angioplasty (PTCA) ,insert stent and atherectomy
If PCI un available: Fibrinolytic therapy: It‘s used to establish
reperfusion and lyse coronary thrombi by converting plasminogen
(fibrinogen ) to (fibrin) plasmin.
Contraindication for thrombolytic therapy
Absolute Contraindications
• Active internal bleeding
• Known history of cerebral aneurysm or arteriovenous
malformation
• Known intracranial neoplasm (primary or metastatic)
• Recent (within past 3 months)
Relative Contraindications
• Active peptic ulcer disease
• Pregnancy
• surgery (including eye laser surgery)
• Severe uncontrolled hypertension (BP >180/110 mm Hg)
Notes----NSTEMI -patient with hemodynamic deterioration may be
need PCI
Nursing Considerations
 Bed rest for a minimum of 12 to 24 hours
84
 Minimize the number of times the patient‘s skin is punctured
 Avoid intramuscular injections
 Draw blood for laboratory tests when starting the IV line
 Start IV lines before thrombolytic therapy; designate one line to
use for blood draws
 Avoid continual use of noninvasive blood pressure cuff
 Monitor for acute dysrhythmias and hypotension
 Monitor for reperfusion: resolution of angina or acute ST segment
changes
 Check for signs and symptoms of bleeding: decrease in
 hematocrit and hemoglobin values, decrease in blood pressure,
 increase in heart rate, oozing or bulging at invasive
 procedure sites, back pain, muscle weakness, changes in
 level of consciousness, complaints of headache
 Treat major bleeding by discontinuing thrombolytic therapy and
any anticoagulants; apply direct pressure and notify the physician
immediately treat minor bleeding by applying direct pressure if
accessible and appropriate; continue to monitor
 Use rapid transit to the hospital.
 Obtain 12-lead electrocardiogram (ECG) to be read within10
minutes.
 Obtain laboratory blood specimens of cardiac biomarkers,
 Including troponin.
 Obtain other diagnostics to clarify the diagnosis.
 Begin routine medical interventions:
 Evaluate for indications for reperfusion therapy: Percutaneous
coronary intervention, Thrombolytic therapy ,Continue therapy
includes IV heparin, low-molecular-weight heparin, Clopidogrel
(Plavix) and Glycoprotein IIb/IIIa inhibitor
Nursing diagnosis:
 Chest Pain related to reduced coronary blood flow.
 Decreased Cardiac Output related to alternation in preload,
afterload, or left ventricular failure
 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
85
 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.
Complications of MI: Complications of STEMI includes:-
Dysrhythmias Cardiogenic Shock
Complete heart block Papillary Muscle Dysfunction
Heart Failure Ventricular Aneurysm
Pericarditis Dressler Syndrome
Secondary Prevention ACS

Cardiac rehabilitation (CR)
Advise patients about CR and encourage them to attend. CR consists of:
Physical activity Travel and health advice, Psychological and social
support, Advice on sexual activity Support with lifestyle changes.
Cardiac risk factors and lifestyle changes Control blood
pressure,Reduce LDL cholesterol, Maintain glycaemic contro, Stop
smoking,Maintain a healthy diet,Take up appropriate physical
activity,Restrict alcohol use to safe levels, Maintain a healthy weight.
Drug therapy for secondary prevention
Offer all of the following drugs: ACE inhibitor,Dual platelet
therapy,Beta-blocker and Statin.
86
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.
 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).
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 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.
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,
88
suctioning, severe pain, extreme emotions), medications (e.g., calcium
channel blockers, amiodarone, beta-blockers), increased intracranial
pressure, and myocardial infarction (MI), especially of the inferior wall.
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 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.
89
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.
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
3. QRS shape and duration: Usually normal, but may be abnormal.
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
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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.
 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.
(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
91
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.
2-Ventricular Fibrillation.:
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 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.
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3- 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 different leads. There is no heartbeat,
no palpable pulse, and no respiration.
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
 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.
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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
3. QRS shape and duration: Usually normal, but may be abnormal
4. P wave: In front of the QRS complex; shows sinus rhythm, regular
shape
5. PR interval: Greater than 0.20 seconds; PR interval measure-ment is
constant.
2. 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.
3. QRS shape and duration: Usually normal, but may be 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
94
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 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.
3. 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.
Complete block (third-degree AV block) has the following characteristics:
1. Ventricular and atrial rate: Depends on the escape and under-lying
atrial rhythm
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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 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.
96
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.
Classification
Acute liver failure classifies into 3 categories based on the interval
between the development of jaundice and the onset of encephalopathy.
1. Hyperacute liver failure: the onset of encephalopathy less than 7
days after the development of jaundice.
2. Acute liver failure: the onset of encephalopathy 8 to 28 days after
the development of jaundice.
3. Sub-acute liver failure: the onset of encephalopathy from 29 days
to 12 weeks after the development of jaundice.
97
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.
Autoimmune Diseases Autoimmune hepatitis
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
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
98
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 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.
 Nursing measures to protect the patient with mental status
changes from harm are a priority.
99
 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 (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
100
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
 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.
 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.
101
 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.
 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.
 Conduct range-of-motion and strengthening exercises.
 Monitor SIRS criteria: increased WBC, increased
temperature, tachypnea, tachycardia.
102
 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.
 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
 Hepatorenal Syndrome
 Spontaneous Bacterial Peritonitis
103
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.
The pancreas is an organ located behind the stomach and near

the small intestine. It produces and distributes insulin, digestive enzymes,
and other necessary hormones.
Definition:
Acute pancreatitis is sudden inflammation of the pancreas that
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.
Pathophysiology
factors as ( Alcoholism, Biliary tract disease, Trauma, Infection, Drugs
,Postoperative GI surgery)
104
↓
Premature activation of pancreatic enzymes and Injury to pancreatic
cells
↓
Autodigestive effects of pancreatic enzymes of pancreatic tissue
Trypsin
Edema , Necrosis,Hemorrhage
Phospholipase A and lipase
Fat necrosis, Edema , Smooth muscle contraction, Shock
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
 Less common
 Ischemia from bypass surgery
 Heart valve surgery
 Fat necrosis
 Pregnancy
 Hyperparathyroidism
 Cystic fibrosis
Symptoms
 Sharp and sudden abdominal pain can be a sign of
pancreatitis.
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Typically, the patient will experience a sudden onset of pain in
the center of the upper abdomen, below the breastbone (sternum).
pain cannot be relieved even with strong painkillers
 nausea , vomiting
 diarrhea
 loss of appetite
 rapid pulse
 pain with coughing, vigorous movements, and deep breathing
 tenderness when the abdomen is touched
 fever and a temperature of at least 100.4 °F (38 °C)
 jaundice, when the skin and whites of the eyes take on a
yellowish tinge
 Grey-Turner's sign (hemorrhagic discoloration of the flanks)
 Cullen's sign (hemorrhagic discoloration of the umbilicus)
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
 Anther diagnostic study :
 ERCP endoscope is inserted into the digestive system.
 An ultrasound scan
 CECT (contrast-enhanced computed tomography)

scan: take pictures of the same area from many angles;
 Chest X-ray
Treatment:
Treatment of mild acute pancreatitis usually involves short-
term hospitalization where fluids are given (intravenously), analgesics
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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.
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 and nausea are
controlled with drugs given intravenously, antibiotics .
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.
Complications:
Pancreatitis can lead to potentially fatal complications.
These include:
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 obstruction of a bile or pancreatic duct
 leakage from the pancreatic duct
 pseudocysts, with a risk of rupture, hemorrhage, or infection
 damage to the pancreas
 pleural effusion
 splenic vein thrombosis
 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. Pancreatic pseudocyst
Nursing diagnoses :
• Acute pain related to distention of pancreas, peritoneal irritation,
obstruction of biliary tract.
• Deficient fluid volume related to nausea, vomiting, restricted oral
intake.
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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.
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
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 Sepsis
Reno-vascular obstruction
 Arterial embolism
 Arterial or venous thrombosis
 Tumor
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)
 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.
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• -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.
• 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.
• 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.
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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 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 blood transfusion and
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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.
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
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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.
-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.
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.
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-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.
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.
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.
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-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.
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.
116
Head Injury
1-Define head injury.

2- Describe etiology of head injury.
3-Determine the clinical manifestation of head injury.
4-Summarize diagnostic studies needed for patient with head injury.
5-Formulate nursing care plan for patient with 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.
Caused of head injury.

 Motor vehicle accidents
 Firearm-related injuries
 Falls
 Assaults
 Sports-related injuries
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
Types of Brain Injury: Concussion, cerebral contusion, epidural

hematoma, subdural hematoma, and skull fracture.
 Concussion:-closed head injury ,A temporary loss
consciousness that results from a transient interruption of the
brain's normal functioning. Recovery is usually complete within
24-48hours.
 Contusion: Bruising of the brain tissue,. Actual small amounts of
bleeding into the brain tissue.common in frontal and temporal
lobes
 Epidural hematoma: Collection of blood , located between the
Dura matter and the inner surface of the skull
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 Intracranial hemorrhage: Significant bleeding into a space brain

tissue. This is a serious complication of head injury with a high
mortality rate
Pathophysology:
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
B. Secondary Brain Injury leading to further brain damage after the

initiating trauma
Clinical Manifestations:
1) Neurologic deficits result from Location of fracture, ischemia,
hemorrhage, and cerebral edema .
2) Disturbances in consciousness: confusion to coma.
3) Otorrhea ( leak of CSF into ear)
4) Rhinorrhea ( leak of CSF into nose)
5) Battle‘s sign (ecchymosis behind the ear )
6) Extensive sub-conjunctival hemorrhage
7) Periorbital ecchymosis ( eyes)
8) Headache, vertigo.
9) Persistent, localized pain
10) Facial paralysis
11) Agitation, restlessness.
12) Respiratory irregularities.
13) Cognitive deficits.
14) Coma and coma syndromes; persistent vegetative state.
Diagnostic Evaluation
1) CT scan to identify and localize lesions, edema, bleeding.
2) Skull and cervical spine X ray films to identify fracture displacement.
3) Cerebral angiography.
4) MRI
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5) Neuropsyeho logical tests during rehabilitation phase to determine
cognitive deficits.
Medical management
1) Management of increased ICP.
2) Antibiotics to prevent infection with open skull fractures or
penetrating wounds.
3) Surgery : the goal for Surgery evacuation of interracial hematomas,
4) Cleaning and debridement of wounds, remove fragment, necrotic
tissue, elevation of skull fractures, or repair of CSF leaks.
Complications
1) Infection: systemic (respiratory, urinary), neurologic (meningitis, ).
2) Increased 1CP, hydrocephalus.
3) Posttraumatic seizure disorder.
4) Permanent neurologic deficits: cognitive, motor, sensory, speech,
5) Neurobehavioral alterations: aggression, emotional lability.
Emergency Care
Primary Assessment
1) Airway: assess for vomitus, bleeding, and foreign objects.
2) Breathing; assess for abnormally slow or shallow respirations. An
elevated Pco2, worsen cerebral edema.
3) Circulation: assess pulse and bleeding.
Primary Interventions
1) Open the airway using the jaw-thrust technique without head tilt.
Oral suction equipment (handle heavy vomits).
2) Administer high-flow O2: the most common cause of death from
head injury is cerebral anoxia.
3) Assist inadequate respirations with a bag-valve mask. In general,
head-injured patients should be hyperventilated with a respiratory
rate of 20 to 25 breaths per-minute.
4) Control bleeding-do not apply pressure to the injury Sit Apply a
bulky, loose dressing.
5) Do not attempt stop the flow of blood or CSF from the nose ears;
apply a loose dressing if needed.
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6) Initiate an intravenous (IV) line to run at a keep-vein-open rate.
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)
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.
120
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.
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.
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2) Be aware of patient's cognitive alteration, and adjust interaction and
environment.
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 .
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.
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Spinal Cord Injuries

1- Clarify the initial assessment and management of patient with
spinal cord injury.
2- Generate symptoms of autonomic dysryflexia.
3-Explore mechanisms for spinal cord injuries.
4-Illustrate complications of spinal cord injuries.
5-Differentiate between complete and incomplete injury of spinal
cord.
6-Instruct a plan of care for patient with spinal cord injury .
7-Apply 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.
Definition
A spinal cord injury (SCI) is damage to the spinal cord that causes
temporary or permanent changes in its function. Symptoms may include
loss of muscle function, sensation, or autonomic function in the parts of
the body served by the spinal cord below the level of the injury
Types of SCI may be classified as:

1. Complete (total loss of sensory and motor function below the level of
injury. causes permanent damage to the area of the spinal cord that is
affected. Paraplegia or tetraplegia are results of complete spinal cord
injuries:
SCIs are graded according to the American Spinal Injury
Association (ASIA) grading scale, which describes the
severity of the injury. The scale is graded with letters:
 ASIA A: injury is complete spinal cord injury with no sensory or
motor function preserved.
 ASIA B: a sensory incomplete injury with complete motor
function loss.
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 ASIA C: a motor incomplete injury, where there is some
movement
 ASIA D: a motor incomplete injury
 ASIA E: normal.
2. Incomplete (a mixed loss of voluntary motor activity and sensation and
leaves some tracts intact. Patient may be able to move one limb more
than another, able to feel parts of the body that cannot be moved, or more
functioning on one side of the body than the other.
Classification of spinal cord injury according to affected part.
There are four sections of the spinal

cord: (cervical, thoracic, lumbar, and sacral.) Each section of the spine
protects different groups of nerves that control the body.
Cervical Spinal Cord Injuries ( head and neck region above the
shoulders affected)
Lumbar Spinal Cord Injuries ( hips and legs are affected by lumbar).
Thoracic Spinal Cord Injuries ( upper chest, mid-back, and abdominal

muscles)
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Sacral Spinal Cord Injuries ( hips, back of the thighs, buttocks, and
pelvic organs)
Causes of SCI
1-Hyperflexion 2Hyperextension
3-Rotation 4-Compressin
5-Penetrating Injuries 6- lateral stress
Anther Causes of SCI include:

■ Blunt force trauma
■ Penetrating force trauma
■ Rheumatoid arthritis
■ Spinal abscesses and tumors
Pathophysiology:
Spinal cord injuries are the result of a mechanical force that
disrupts neurologic tissue or its vascular supply, or both→↓ blood flow to
gray matter of spinal cord with 8-hour delay of → ↓blood flow to white
matter → thrombi form furthering→ ↓ blood flow to spinal cord.
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 occur within minutes of injury and can last for
days to weeks.
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Emergency situation after injury

I- Spinal Shock.
Spinal shock is a condition that can occur shortly after traumatic injury to
the spinal cord.
II- Neurogenic Shock.
Neurogenic shock is caused by vasoconstriction and venous pooling
(veins dilated and filled with blood), ↓ HR, ↓ CO.
III- Autonomic Dysreflexia.
Autonomic dysreflexia is a life-threatening complication that may
occur with SCI. caused by a massive sympathetic response to a noxious
stimulus (full bladder, line insertions, fecal impaction) which results in
bradycardia, hypertension, facial flushing, and headache.
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.
 Breathing.
Assessment of breathing patterns and gas exchange is made after an
airway has been secured.
 Circulation.
The patient with an SCI is assessed for adequate tissue perfusion by
means of both invasive and noninvasive hemodynamic monitoring
techniques.
 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.
II- Diagnostic Procedures.

X-ray, CT scan, tomograms, myelography, and MRI may be used in the
diagnostic process.
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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.
 Surgical Management.
Surgical intervention performed to achieve decompression and
stabilization for spinal cord.
 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.
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 loss of muscle function
 Impaired Physical Mobility related to immobilization, paralysis
 Risk for Impaired Skin Integrity related to immobility
 Bowel Incontinence or Constipation related to disruption of altered
fluid and food intake
 Impaired Urinary Elimination related to disruption in bladder
innervation, bladder atone
 Disturbed Body Image related to actual change in body structure.
Complications of spinal cord injuries

Acute Phase Complications:
 Autonomic dysreflexia
 Pulmonary embolism
 Neurogenic shock
 Hysterical paralysis
Long-Term phase Complications:
 Pneumonia and other respiratory complications
 Urological complications
 Pressure ulceration
 Deep vein thrombosis (DVT)
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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:
Complex syndrome of decrease blood flow to the body tissue
resulting inadequate delivery o2 and nutrient to meet metabolic
demands of body cells.
Aetiology:
Adequate tissue perfusion depends on 3 factors:
 Blood volume.
 Capacity of the blood vessels.
 Pumping action of the heart.
SO: disturbance of any of these 3 factors cart lead to shock.
Types of shock :
(1) Hypovolemic shock:
Causes :
 Loss of blood  haemorrhage (internal, external).
 Loss plasma  burns.edema ,ascites ,peritonitis
 Loss of fluid  severe vomiting & diarrhea. excessive diuretics
(2) Cardiogenic shock :

a. Insefficient cardiac contraction  as in myocardial infarction,
severe arrythmias, cardiomyopathy. etc.
b.  Cardiac filling  as in cardiac tamponade and pulmonary
embolism.
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(3) Vasogenic shock :

a. Septic shock: due to release of substances which leads to impaired
microcirculation.
b. Neurogenic shock: either in the form of vasovagal attack due to 
parasympathetic stimulation or spinal shock due to loss of vasomotor
tone due to sympathetic paralysis.
c. Anaphylactic shock: severe vasodilation + capillary permeability due
to histamine release from antigen-antibody reaction.
d. Endocrine shock: in patient with adrenal insufficiency.
Hypovolaemic Shock:
Pathophysiological Stages:
a. Heart:  Myocardial contractility by coronary ischaemia   cardiac
output   hypoxia.,myocardial infaction and dysrythmia
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
d. Kidney: Renal hypoperfusion  G.F.R.  Acute tubular necrosis 
acute renal failure.
e. Lungs : Adult respiratory distress syndrome
f. Brain: Cerebral ischaemia  coma.
129
Assessment
Clinical findings are directly related to the severity and acuity of
volume loss.
LABORATORY STUDIES
Useful laboratory studies include determinations of increased
serum lactate, arterial pH, Metabolic laboratory studies and electrolyte
determination assist with adjustment of fluid and electrolytes Serial
hemoglobin and hematocrit determinations and coagulation panels to
assess the need for blood product replacement.
Diagnosis of Shocked Patient:
 Clinically: Pulse, blood pressure, state of filling of veins.

 C.V.P.: decreased < 2cm H2o
 Foley's catheter: For urine output monitoring (the optimum=
30ml/h).
 Pulmonary artery wedge pressure: By the use of Swan Ganz
catheter , C.V.P
 ECG. : to detect any arrhythmias.
 Blood gases :
 decrease, H.B%, hematocrit value, & kidney function tests.
 Serum lactate increased 2.2mEqu due to anaerobic metabolism
Clinical Picture :.
The manifestations correlate with the amount of bleeding
Cool and clammy skin with weak and thread pulses , tachycardia due
to activation of the sympatatic nervous system
 Symptoms :
a. Weakness and fainting when standing.
b. Hypoxemia Pao2 <90 mmHg due to hypoventilation and hypo
perfusion
c. In severe late condition  comatose.
 Signs :
a. CNS : Vary from anxious to drowsy.
b. Pulse : Tachycardia>100b/m (weak, rapid pulse), thready.
Tachycardia
Rapid due to
Adrenaline secretion  stimulates SA node
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Weak: due to  systolic more than diastolic = small pulse volume
Pulse
c. Blood Pressure: Hypotension. ( VR ,  cardiac output )

d. Respiratory rate:
e. Tachypnea and air hunger  from stimulation of respirator center
early increase depth of RR and late decrease RR.
f. Early hpervention with respirator alkalosis lead to compensatory
mechanism.,PH<7.45 ,Pco2 < 35.
g. -late change lead to hypovention and respiratory acidosis due to
exhaustion of compensatory mechanism, PH>7.35,Paco2 >45
h. Temperature: Hypothermia from  metabolism by hypoxia &
hypotension.
i. O2 saturation decreased
j. Skin: Pale , Cold, Clammy sweaty from  catecholamincs with
collapsed veins.
k. Urine output : Oliguria from renal hypoperfusion +  ADH and
Aldosterone.
Approach to the Patient in Shock
o Cardiorespiratory monitor
o Pulse oximetry
o Supplemental oxygen
o IV access
o ABG, labs
o Foley catheter
Treatment of hypovolaemic shock :

1. Fluids and Blood transfusion :
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).
b. Patients with severe blood loss or persistent bleeding will show
transient improvement and well require blood transfusion or blood
substitutes (plasma expanders).
2. Positioning : The patient should lie supine with elevation of lower
limbs  venous return, and it should not be over heated by excessive
blankets to avoid cutaneous V.D.
131
3. Oxygen : Administration by facial mask, nasal catheter or endotracheal
tube.
4. Hydrocortisone I.V : May be givens in patients with adrenal
suppression or insufficiency.
5. Inotropic agents : (Dopamine) improve myocardial contractility +
renal blood flow.
6. I.V Na+ bicarbonate to correct metabolic acidosis .
7. Analgesia pethidine 50-100mg I.V. to anxious patients.
8. Frequent monitoring of the vital signs, Pulse oximetry, urine output.

C.V.P. etc
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Septic Shock
Definition
- Septic shock is the end result of numerous complex interactions
between several endotoxins, endogenous mediators and host
body responses to these exogenous stimuli.
- Endotoxins of Gram-ve bacteria or Candida stimulates
macrophages, which in turn stimulates the production of large
amounts of inflammatory mediators (cytokines)
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
 the body compensates 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).
o Bicarbonate.
Clinical Picture :
1] Hyper dynamic Septic Shock: (Septicemia)
-The patient presents by fever chills, hypotension, tachycardia,
warm dry skin, and tachypnea.
-At the end of this stage, blood start to shunt away from tissue
cells which become damaged by anaerobic metabolism 
oliguria, confusion.
-Proper treatment of the patient at this stage can lead to survive.
2] Hypo dynamic Septic Shock :
-It follows the above stage if not treated properly.
-The clinical picture = is that of hypovolaemic shock +
hypothermia.
-The end result is combined clinical picture of D. I.C. +

multiorgan failure.
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Assessment:
PHYSICAL FIDINGS
Changes in mental status, increased respiratory rate as compensation
for the metabolic acidosis and either fever or hypothermia. Because of the
exaggerated inflammatory response with release of vasoactive
mediators.
LABORATORY STUDIES
 Cultures: blood, sputum urine. Surgical or nonsurgical wounds.
 CBC: WBCs usually will be elevated and may decrease, with
progression of shock.
 Sequential multiple analysis-
 Arterial blood gages .
 CT scan may be needed to identify sites of potential abscesses.
 Chest and abdominal radiographs may reveal infectious processes.
Svo2 pulmonary artery catheter will assist.
 Lactate level: increase levels of lactate.
Increase :
  TLC with increased immature forms.
  Lactate level in blood.
 Repeated blood culture.
Monitoring of septic shock : Look Hypovolemia.
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 if PO2 <60 mmHg.
6. Vitamin C.
7. Vasopressors and Inotropics if persistent hypotension, measures to
support cardiac contractility & cardiac output + renal blood flow.
8. Endomethacin & corticosteroids I.V.: To antagonize inflammatory
mediators.
9. Frequent monitoring by C.V.P., ECG, P.A.W.P., pulse, mean blood
pressure, temperature, urine output, arterial blood gases.
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Neurogenic Shock
Definition
There is paralysis of the vasomotor fibers  lead to massive peripheral
vasodilatation  peripheral pooling of blood  inadequate venous return
 decrease cardiac output  shock.
Causes:
 Vaso-Vagal attack : Due to hearing bad news or trauma , excessive
vagal stimulation  Bradycardia  Hypotension.
 High transaction of spinal cord in spine fracture or following spinal
anesthesia
Treatment:
 The patient should lie flat, elevation of the legs help to increase venous
return.
 Supplement O2 ,monitor Svo2
 intubation ,MV
 Crystalloids like Ringer's lactate.
 Vasopressor drugs.
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Cardiogenic Shock
Definition
Decreased C.O   systolic and diastolic pressure  hypotension 
 tissue hypo perfusion  picture of shock (BUT the Neck Veins arc
congested and C.V.P. is high).
Assessment,
Assessment parameter similar to the signs and symptoms of congestive
heart failure changes that cardiogenic shock.
HISTORY
History provides the information at risk for of cardiogenic..
PHYSICAL FINDINGS
Clinical manifestations associated with cardiogenic shock outlined.
LABORATORY STUDIES
 Elevated myocardial tissue markers accompanied by progressive
hemodynamic compromise, hallmarks myocardial necrosis,
creatine phosphokinase (MB-CPK).
 ECG
Management: Aimed:
 Increasing myocardial oxygen delivery.
 Maximizing cardiac output, and decreasing left ventricular
workload. And improve tissue perfusion.
 Use of narcotic analgesics and sedatives to minimize the
sympathetic nervous system response can increase venous.
Treatment :
 Potent analgesics in myocardial infarction.
 Oxygen administration.
 Inotropeic  to  cardiac contractility.
 Vasodilators   after load of the heart.
 Mechanical support by intra-aortic balloon counter-pulsations.
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Anaphylactic Shock
Assessment
HISTORY
Avoiding known allergens is usually the best way to prevent
anaphylactic shock. Responses to drugs foods, blood products, or
anesthetic agents.
PHYSICAL FINDINGS
 Generalized erythema, urticarial, pruritus, and subsequent
angioedema may occur.
 Later symptoms may include. Anxiety and restlessness, dyspnea,
wheezing, warm feeling, and even pain.
 Respiratory manifestations, laryngeal edema, or severe
bronchoconstriction soon stridor.
 Hypotension from vasodilation soon.
Nursing care:
 Maintaining adequate airway and monitoring patient response to
the antigen.
 The nurse also monitors respirations, heart rate, blood pres sure,
and level of anxiety,
 Comfort measures for dermatological manifestations.
 Patient education regarding prevention and treatment is critical
for any person who experiences a significant anaphylactic.
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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
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
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■ 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.
 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
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.
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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 of treatment.
 Myocardial infarction  Cerebrovascular stroke.
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.
140
 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
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 cardia,PH
and bicarbonates
141
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
Hypoglycaemic 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.
Investigations
1-Urine: Contains glucose. and Blood glucose: Markedly decreased.
142
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.
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.
3- Blood Na: Elevated.
Treatment:
143
1- Insulin replacement: As in ketoacidosis.
2- 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.
 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.
144
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.
Organ Indications Common causes
Kidney End-stage renal disease Hypertension, diabetes
mellitus, glomerular
nephritis, cancer, trauma
nephrotoxins, congenital
anomalies
Liver Adults: irreversible liver Acute or chronic hepatitis,
disease, malignancy, and primary sclerosing
hepatic failure resulting in cholangitis, primary biliary
synthetic liver dysfunction cirrhosis, hepatocellular
carcinoma, alcoholic
cirrhosis
Heart End-stage heart disease Ischemic cardiomyopathy,
idiopathic cardiomyopathy,
valvular heart disease,
congenital anomalies
Pancreas Type 1 diabetes mellitus Diabetes mellitus
with end-stage renal
disease either alone or in
145
combination with a kidney
transplant
Lung Chronic obstructive Emphysema and

pulmonary disease bronchiectasis, idiopathic
pulmonary fibrosis,
primary pulmonary
hypertension
Malignant disorders Leukemia, and selected
solid tumors (eg, renal cell
tumors)
Nonmalignant disorders Asickle cell, and selected
Stem cell
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.
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)
146
 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.
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.
 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.
147
 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 surges
consequent to endogenous catecholamine mobilization
produce hypotension. Short-acting agents, such as
nitroprusside or esmolol, which have a short duration of
action and are used to control blood pressure and heart rate.
 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
148
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) 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.
 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.
149
- 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.
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.
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.
150
- 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 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.
151
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 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).
152
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
 Limited ability to multitask
 Interruptions
 Stress
 Fatigue and other physiological factor
153
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
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.
154
 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
 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
155
‫كلية معتمدة من الهيئة القومية‬ Critical Care & Emergency
‫لضمان جودة التعليم واالعتماد‬ Nursing Department
CRITICAL CARE NURSING DEPARTMENT

THERIOTICAL MANIUAL FOR CRITICAL CARE
Prepared by
THEORETICAL MANUAL
FOR
EMERGENCY NURSING
(PART II)
Prepared by
All staff members of Critical Care and

Emergency
Prepared by Nursing Department
Assiut University
2021-2022
5th Edition
‫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 علمياً‬
‫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)‪.‬‬
Content
No. Subject Page
2 Triage 1
3 Chest trauma 8
4 Heat stroke 13
5 Acute upper gastrointestinal bleeding 15
6 Drug overdose& poisoning 19
7 Hypertensive crisis 23
8 Advanced life support 27

Emergency nursing
Triage

1-Define the triage.
2-Identify Goals of Triage.
3-List advantages of Triage.
4-Recall Component of triage assessment
5-Demonstrate an understanding a triage system e,g. The S.T.A.R.T.
System
6-Perform an accurate triage assessment and allocate a triage category
based on that assessment.
Triage is the process of determining the priority of patients' treatments

based on the severity of their condition. This rations patient treatment
efficiently when resources are insufficient for all to be treated
immediately.
Definition of nurse triage:

'Nurse Triage' refers to the formal process of early assessment of patients
attending an accident and emergency (A&E) department by a trained
nurse, to ensure that they receive appropriate attention, in a suitable
location, with the requisite degree of urgency. The benefits claimed for
nurse triage include better patient outcomes, through clinical management
reaching those in greatest need of it first.
GENERAL TRIAGE GUIDELINES:

The triage nurse should have rapid access or be in view of the registration
and waiting areas at all times.
1. Greets client and family in a warm empathetic manner.
2. Performs brief visual assessments.
3. Documents the assessment.
4. Triages clients into priority groups using appropriate
guidelines.
5. Transports client to treatment area when necessary.
6. Gives report to the treatment nurse or emergency
physician, documents who report was given to and returns
to the triage area.
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Emergency nursing
7. Keeps patients/families aware of delays.
8. Reassesses waiting clients as necessary.
9. Instructs clients to notify triage nurse of any change in
condition.
Accurate assignment of triage levels is based on:

• Practical knowledge gained through experience and
training.
• Correct identification of signs or symptoms.
• Use of guidelines and triage protocols.
Advantages of Triage
1. Streamlines patient flow.
2. Reduces risk of further injury/deterioration.
3. Improves communication and public relations.
4. Enhances teamwork.
5. Identifies resource requirements.
6. Establishes national benchmarks
N.B: Triage is a dynamic process: A patient’s condition may improve OR

deteriorate during the wait for entry to the treatment area.
Component of triage assessment

1. Chief complaint.
2. Brief triage history.
3. Injury or illness (signs & symptoms).
4. General appearance.
5. Vital signs.
6. Brief physical appraisal at triage.
A triage system
(1) The S.T.A.R.T. System
START is a mnemonic for Simple Triage and Rapid Treatment. This
program was developed in southern California by a group of emergency
physicians, firefighters, and an emergency nurse.
2
Emergency nursing
START: Step 1
- Triage officer announces that all patients that can walk should get
up and walk to a designated area for eventual secondary triage.
- All ambulatory patients are initially tagged as Green
START: Step 2
- Triage officer assesses patients in the order in which they are
encountered
- Assess for presence or absence of spontaneous respirations
- If breathing, move to Step 3
- If apneic, open airway
- If patient remains apneic, tag as Black
- If patient starts breathing, tag as Red
START: Step 3
- Assess respiratory rate
- If <30, proceed to Step 4
- If > 30, tag patient as Red
START: Step 4
- Assess capillary refill
- If < 2 seconds, move to Step 5
- If > 2 seconds, tag as Red
START: Step 5
- Assess mental status
- If able to obey commands, tag as Yellow
- If unable to obey commands, tag as Red
Triage Tags and Categories
Red:
Life-threatening but treatable injuries requiring rapid medical attention
Yellow:
3
Emergency nursing
Potentially serious injuries, but are stable enough to wait a short while for
medical treatment
Green:
Minor injuries that can wait for longer periods of time for treatment
Black:
Dead or still with life signs but injuries are incompatible with survival in
austere conditions
(2)Another assessment system

Objectives for time to nursing reassessment are related to triage level:
There should be a nursing reassessment on all patients at the time
intervals recommended for physician assessment. That is:
• Level I patients should have continuous nursing care
• Level II every 15 minutes
• Level III every 30 minutes
• Level IV every 60 minutes
• Level V every 120 minutes.
Example for Triage Priorities

Highest Priority
1. Respiratory arrest, airway obstruction and severe breathing
difficulties.
2. Cardiac arrest.
3. Uncontrolled severe bleeding.
4. Severe head injuries.
5. Open chest wounds
6. Open abdominal wounds.
7. Severe shock.
8. Bums involving respiratory tract.
9. Medical problems like heart attack and poisoning.
10. Unconsciousness.
Second Priority
1. Injuries to the spine.
2. Moderate bleeding.
3. Conscious patients with head injuries.
4. Multiple fractures.
4
Emergency nursing
Lowest Priority
1. Minor bleeding.
2. Fractures.
3. Moderate minor bums.
4. Obvious mortal wounds where survival is not expected.
5. Obvious death.
Emergency assessment and intervention:

Assessment Interventions
Airway
• Assess for respiratory distress. • Open airway.
• Assess airway for patency. • Use jaw-thrust maneuver.
• Check for loose teeth or foreign • Remove or suction any foreign
bodies. bodies.
• Assess for bleeding, vomitus, or • Insert oropharyngeal or
edema. nasopharyngeal airway,
endotracheal tube, crico-
thyroidotomy.
• Immobilize cervical spine using
rigid cervical collar and cervical
immobilization device. Secure
forehead to backboard.
Breathing
• Assess ventilation. • Give supplemental O2 via
• Scan chest for signs of breathing. appropriate delivery system (e.g.,
• Look for paradoxic movement of non-rebreather mask).
the chest wall during inspiration • Ventilate with bag-valve-mask
and expiration. with 100% O2 if respirations are
• Note use of accessory muscles or inadequate or absent.
abdominal muscles. • Prepare to intubate if severe
• Observe and count respiratory respiratory distress (e.g., agonal
rate. breaths) or arrest.
• Note color of nail beds, mucous • Have suction available.
membranes, skin. • If absent breath sounds, prepare
• Auscultate lungs. for needle thoracostomy and chest
• Assess for jugular venous tube insertion.
distention and position of trachea.
Circulation
• Check carotid or femoral pulse. • If absent pulse, initiate
• Palpate pulse for quality and rate. cardiopulmonary resuscitation and
5
Emergency nursing
• Assess skin color, temperature, advanced life-support measures.

and moisture. • If shock symptoms or
• Check capillary refill. hypotensive, start two large-bore
• Assess for external bleeding. (14- to 16-gauge) IVs and initiate
• Measure blood pressure. infusions of normal saline or
lactated Ringer’s solution.
• Control bleeding with direct
pressure and pressure dressings, if
appropriate.
• Administer blood products if
ordered.
• Consider autotransfusion if
isolated chest trauma.
• Consider use of a pneumatic
antishock garment or pelvic splint
in the presence of pelvic fracture
with hypotension.
• Obtain blood samples for type and
crossmatch.
Disability
Brief Neurologic Assessment • Periodically reassess level of
• Assess level of consciousness by consciousness, mental status,
determining response to verbal pupil size and reactivity.
and/or painful stimuli (e.g., AVPU,
Glasgow Coma Scale).
• Assess pupils for size, shape,
equality, and reactivity.
Brief Pain Assessment • Periodically reassess pain using
• Assess pain (e.g., PQRST standardized pain scale.
Exposure and Environmental
Control • Remove clothing for adequate
• Assess full body for additional or examination.
related injuries • Keep patient warm with blankets,
warmed IV fluids, overhead lights
to prevent heat loss, if appropriate.
• Maintain privacy.
Documentation Standards
1. Date and time of triage assessment
2. Nurse’s name, chief complaint or presenting concerns
3. Limited subjective history: onset of injury/symptoms
4. Objective observation,triage level
6
Emergency nursing
5. Location in the department
6. Report to treatment nurse
7. Allergies, medications
8. Diagnostic, first aid measures, therapeutic interventions
9. Reassessment(s)
Triage Nurse Qualifications

1. Communication skills are crucial. Provider must interact with
patient, family, police, EMT and visitors.
2. Must have tact, patience, understanding, and discretion.
3. Organizational skills — patient line-ups, inquiries, etc. (constantly
under patient scrutiny)
4. Able to perform in hectic situations.
5. Can recognize who is sick. (Depends on experience, skill and
expert clinical judgment.)
7
Emergency nursing
Chest trauma
1-Create different types of chest trauma.
2-Found symptoms that may help identify different types of chest trauma.
3- Create management of different types of chest trauma.
4-Compare between pneumothorax and hemothorax.
5- Analyze laboratory and diagnostic finding of different types of chest
trauma.
6-Formulate medical emergency care for each type.
Definition
Traumatic injuries to the chest contribute to 75% of all traumatic.
Thoracic injuries range from simple rib fractures to complex life-
threatening rupture of organs.
Mechanisms of injuries causing chest trauma are :

✓ Blunt trauma occurs when the chest strikes or is struck by
an object.as( Motor vehicle accident ,Pedestrian accident ,Fall, Crush
injury)
✓ Penetrating trauma is an open injury in which a foreign body
Impales or passes through the body tissues, creating an open
wound.as (Knife, Gunshot, Stick, Arrow)
Types of chest truam

I. Rib fracture: Fracture of one or more ribs Possibly resulting in severe
damage to underlying structures( Lungs , Sbclavian artery
(SCA),Subclavian vein (SCV))
Causes
1. Eighty-five percent of patients with blunt chest trauma experience rib
fractures
2. Associated with motor vehicle crashes (MVCs), assaults, and falls
Manifestation
1. Pain, worsening with breathing, coughing, movement, and on
palpation
2. Shallow respirations
3. Splinting of region
4. Crepitus
8
Emergency nursing
5. Decreased breath sounds on the affected side
Laboratory/Diagnostic findings
1. Chest x-ray may reveal fracture, atelectasis
2. Arterial blood gas analysis (ABGs) may reveal respiratory acidosis if
the patient is hypo ventilating
c. Also, hypoxia may be observed (PaO2, less than 90 mmHg) if severe
pulmonary contusion is present
3. CBC if hemothorax is suspected E.
Management
1. Rule out underlying structural damage (e.g., lacerated SCA or SCV,
pneumothoraxjlacerated liver or spleen) by ordering arteriography, x-rays,
CT scan
2. Pain medications
such as aspirin, acetaminophen, and NSAIDs (e.g., Ibuprofen, 400-600
mg 4 times a day)
3. Aggressive pulmonary therapy, such as Turn, Cough, Deep Breathe,
chest physiotherapy should be used on non-affected side, along with
incentive spirometry
4. Monitor oxygen saturation; consider giving O2 at 2 L per nasal cannula,
with oxygen saturation (SaO2) maintained at above 92
II. Flail chest: Fracture of two or more adjacent ribs in two or more
places with loss of chest wall stability
Cause: Most serious chest wall injury, Caused by blunt force/trauma
Manifestation
1. Pain
2. Shortness of breath
3. Paradoxical chest wall movement-inspiration/expiration
5. Tachypnea
6. Decreased level of consciousness (LOC) related to hypoxia
7. Cyanosis
8. Tachycardia
9. Splinting of chest wall
9
Emergency nursing
10. Crepitus
11. Decreased breath sounds on affected side
1. ABGs: hypoxia, possible respiratory acidosis
2. Chest x-ray: reveals rib fractures
Management
1. Administer O2 correct possible respiratory acidosis, and consider
ventilatory support with positive end-expiratory pressure (PEEP) and
pressure support
2. Administer crystalloids, such as lactated Ringer's solution
3. Consider supporting/stabilizing flail segment with sandbags.
4. Pain medications Morphine sulfate
5. If lung contusion occurs, the patient may require long-term ventilation.
III.Collapsed lung:
➢ types
A. Pneumothorax : Air in pleural space causing complete or partial
collapse of the lung
B. Hemothorax : Occurs when blood accumulates in the pleural space
C. Open pneumothdrax :referred to as "sucking chest wound" , Air flows
form atmosphere to pleural space and back again or Can lead to tension
pneumothorax if covered with an occlusive dressing .caused by
penetrating trauma, such as gunshot wounds or knife wounds
D. Tension pneumqthorax : Collapse of the lung caused by one-way air

flow into the pleural space that does not escape. The increased air in the
pleural space shifts organs and increases intra thoracic pressure as heart
Manifestation
1. Respiratory distress
2. Hypoxia
3. Tachypnea
4. Decreased LOC
5. Hypotension
10
Emergency nursing
6. Cyanosis
7. Tachycardia
9. Chest pain
10. Decreased or absent breath sounds on affected side
11. Deviation of the trachea to the non-affected side
12.Tension pneumothorax may cause severe respiratory distress, leading
to circulatory collapse (i.e., decreased cardiac output, decreased blood
pressure)
1. ABGs may reveal respiratory acidosis
2. Chest x-ray reveals collapsed lung and possible mediastina shift
3. ECG may show heart strain
Management
1. Smaller than 15% to 20% pneumothorax requires only observation;
chest tube at fourth to fifth intercostal space (ICS), midaxillary line
(MAL) as needed
2. If tension pneumothorax, rapid insertion of large-bore (14- to 16-
gauge) needle into the second ICS, mid clavicular line of the affected side
3. Chest tube insertion to low wall suction (-20 cm)
4. Consider mechanical ventilation with PEEP
5. Open pneumothorax: Apply a dressing, leading one side untapped to
allow air to escape
6. Massive hemothorax: Fluid resuscitation with lactated Ringer's solution
should be considered prior to thoracotomy owing to loss of tamponed
effect
IV. Cardiac tamponed: Blood rapidly collects in pericardial sac,

compresses myocardium because the pericardium does not stretch, and
prevents ventricles from filling.
Manifestation: Muffled, distant heart sounds, hypotension, neck vein

distention, increased central venous pressure
11
Emergency nursing
Medical emergency: pericardiocentesis with surgical repair as
appropriate
V. Aortic rupture: An interruption of the wall of the aorta caused by

blunt traumatic deceleration
Manifestation
1. Shortness of breath
2. Weakness
3. Blood pressure and pulse amplitude are greater in upper extremities.
4. Chest or back pain
5. Circulatory collapse
Laboratory/diagnostic findings: Chest x-ray may reveal a widened

mediastinum
Management
1. Thoracotomy to repair the rupture with cardio pulmonary bypass
2. Adequate fluid as crystalloids (e.g., normal saline, Ringer's lactate
solution)
3. Packed red blood cells
4. Consider nitroprusside (Nitride), 0.5-8 meg/kg/minute to maintain
systolic blood pressure at below 140 mmHg until patient can be taken to
surgery
5. Mechanical ventilation
12
Emergency nursing
Heat stroke

1-Define head stroke.
2-Memorize risk factor and etiology.
3 -Compere between types of head stroke.
4- Predicte clinical manifestation of head stroke.
5-Prioritize emergency nursing care for management head stroke.
Definition: heat stroke is a life threatening illness characterized by an

altered level of consciousness with an elevated core body temperature ≥
40 °C.
Risk factors:
Those most susceptible (at risk) individuals to heat stroke include:
Infants The elderly (often with associated heart diseases, lung diseases,
kidney diseases, diabetis or who are taking medications that make them
vulnerable to dehydration and heat strokes) AthletesIndividuals who work
outside and physically exert themselves under the sun Infants, children, or
pets left in cars.
Types ;
1-Exertional heat stroke may developed in able bodies individual
performed rigorous physical activity in hot environment .
2-Non Exertional heat stroke may developed may arise in elderly or

infirm person confined indoors during protracted hot weather
Signs &symptoms
Throbbing headache
Dizziness and light-headedness
Lack of sweating despite the heat
Red, hot, and dry skin
Muscle weakness or cramps
Nausea and vomiting
Rapid heartbeat, which may be either strong or weak
Rapid, shallow breathing
Behavioral changes such as confusion, disorientation, or staggering
13
Emergency nursing
Seizures
Unconsciousness
Emergency care of patient with heat stroke

Patient of heat stroke must receive immediate treatment to avoid
permanent organ damage.
Begins by securing ABC and maintaining adequate oxygen therapy
• Get the victim to a shady area, remove clothing, apply cool or
tepid water to the skin (for example, you may spray the person
with cool water), fan the victim to promote sweating and
evaporation, and place ice packs under the armpits and groin.
• If the person is able to drink liquids, have them drink cool water or
other cool beverages that do not contain alcohol or caffeine.
• If blood pressure is low ; establish an IV line give IV of NS
500ml.
• Monitor vital signs regular time
• Monitor body temperature with a thermometer and continue
cooling efforts until the body temperature drops to 101 to 102 F
(38.3 to 38.8 C).
14
Emergency nursing
Acute Upper Gastrointestinal Bleeding

1-Define Upper Gastrointestinal Bleeding.
2-List causes of Upper Gastrointestinal Bleeding.
3-Differentiate types of Upper Gastrointestinal Bleeding.
4-Demonstrate assessment of patients with Upper Gastrointestinal.
Bleeding.
5-Design nursing care plan for patient with GIT bleeding.
Definition:
a sudden onset, vomiting insidious occult bleeding can also be a major
problem. The severity of bleeding depends on whether the origin is
venous, capillary, or arterial.
Type of GIT bleeding:

1. Hematemesis: Bloody vomitus appearing as fresh, bright red
blood or “coffee-ground” appearance (dark, grainy digested
blood).
2. Melena: Black, tarry stools (often foul smelling) caused by
digestion of blood in the GI tract. Black appearance is from the
presence of iron.
EEDING
Causes of upper gastrointestinal bleeding:
Drug Induced Esophagus Stomach and Systemic Diseases
• Corticosteroids • Esophageal Duodenum • leukemia, aplastic
• Nonsteroidal varices • Stomach anemia)
antiinflammatory • Esophagitis cancer • Renal failure
drugs (NSAIDs) • Mallory-Weiss • Hemorrhagic
• Salicylates tear gastritis
• Peptic ulcer
disease
• Polyps
Emergency Assessment Upper Gastrointestinal Bleeding:
1. Past health history: Precipitating events before bleeding episode,
previous bleeding episodes and treatment, peptic ulcer disease,
esophageal varices, esophagitis, acute and chronic gastritis, stress-
15
Emergency nursing
related mucosal disease. Medications: Aspirin, nonsteroidal anti-
inflammatory drugs, Corticosteroids, anticoagulants
2. Family history of bleeding, smoking, alcohol use
3. Nutritional-metabolic: Nausea, vomiting, weight loss, thirst
4. Elimination: Diarrhea; black, tarry stools; decreased urine
output;Sweating
5. Activity-exercise: Weakness, dizziness, fainting
Clinical Manifestations:
General Fever
Integumentary: Respiratory
Clammy, cool, pale skin; pale Rapid, shallow respirations.
mucous membranes.
Cardiovascular Gastrointestinal
Tachycardia, weak pulse,Red or “coffee-ground”vomitus;
orthostatic hypotension, slow tense, rigid abdomen,
capillary refill ascites;hypoactive or hyperactive
bowel sounds; black, tarry stools
Urinary Neurologic
Decreased urine output, Agitation, restlessness; decreasing
concentrated urine level of consciousness
Possible Diagnostic Findings
↓ Hematocrit and hemoglobin; hematuria; ↓ levels of clotting factors; ↑
liver enzymes; abnormal endoscopy results
Diagnostic Studies:
1. Endoscopy is the primary tool for diagnosing the source (e.g.,
esophageal or gastric varices, gastritis).
2. Angiography is used in diagnosing upper GI bleeding when
endoscopy cannot be done or when bleeding persists Angiography
is an invasive procedure. In this procedure, a catheter is placed
into the left gastric or superior mesenteric artery and advanced
until the site of bleeding is discovered.
3. Laboratory studies include CBC, blood urea nitrogen (BUN),
serum electrolytes, prothrombin time, partial thromboplastin time,
liver enzymes, arterial blood gases (ABGs), and a type and
crossmatch for possible blood transfusions. All vomitus and stools
16
Emergency nursing
should be tested for gross and occult blood. The hemoglobin and
hematocrit values are
Medical treatment of upper gastrointestinal bleeding:

1. Endoscopic Therapy: The first-line management of upper GI bleeding
is endoscopy and endotherapy. Endoscopy performed within the first 24
hours of bleeding is important for diagnosis
2. Surgical Therapy:
Surgical therapy may be necessary when the patient continues to bleed
after rapid transfusion of up to 2000 mL of whole blood or remains in
shock after 24 hours. The site of the hemorrhage determines the choice of
operation.
3. Medications:
1. Vasopressin (Pitressin) Causes vasoconstriction. ↓ Pressure in the
portal circulation and stops bleeding.
2. Octreotide (Sandostatin) Somatostatin analog that ↓ blood flow to
GI tract ↓ HCl acid secretion by ↓ release of gastrin.
3. Epinephrine bleeding from ulceration Injection during endoscopy
produces hemostasis.
4. Nursing diagnosis for GIT bleeding:
1. Decreased Cardiac Output related to fluid loss
2. Ineffective tissue perfusion related to bleeding
3. Fluid Volume Deficit related to bleeding
4. Impaired gas exchange related to blood loss
5. Ineffective breathing pattern related to shock
6. Imbalance nutrition: less than body requirements related to bleeding
5. Nursing intervention:
1. Maintain the I.V line for fluid (saline, ringer lactate)or blood
transfusion replacement.
2. Record vital signs every 15 minutes.
3. Monitor intake and output.
4. Measure the urine output hourly. If the patient has a central
venous pressure line or pulmonary artery catheter in place, record
these readings every 1 to 2 hours.
5. Keep the head of the bed elevated to provide comfort and prevent
aspiration.
17
Emergency nursing
6. ECG monitoring is also used to evaluate cardiac function.is
important because dysrhythmias may ooccur.
7. Gastric lavage and observe the aspirate for blood. Or iced gastric
lavage is used.
8. Insert sengstaken baloon in case of esophageal varises.
9. Monitor for blood in the stools.
18
Emergency nursing
Acute poisoning& drug overdose

1-Explain the initial assessment and management of acutely poisoned or
overdosed patients.
2-Describe the groups of symptoms that may help identify the drug(s) or
toxin(s) to which a patient may have been exposed.
3- Mention nursing interventions for stabilization.
4- Compare between methods used to prevent absorption and enhance
elimination of a drug or toxin.
5-Formulate a plan of care for the poisoned patient.
6- Implement gastric decontamination for the poisoned patient.
7-Utilize critical thinking skills in the nursing care of the poisoned
patients
Definition:
Accidental or intentional drug overdoses and poisonings can cause
physical and mental changes that may require admission to a critical care
unit.
-Types of poisoning
- Inhalation, ingestion, and injection. Toxic chemical reactions
-
*assessment
1. History
A history of the patient obtained from the patient`s family members that
include:-
1. Identifying the drugs or toxins
2. Time and duration of the exposure
3. First aid treatment given before arrival at the hospital
4. Allergies (food- drugs)
2. Physical Examination
■ Assess, establish, and maintain the airway.
■Evaluate respiratory rate, depth
■Monitor vital signs
■Monitor electrocardiogram.
19
Emergency nursing
■Maintain or correct acid–base balance and electrolyte
homeostasis. ■Assess mental status
3- laboratory investigations
That includes(electrolytes, hepatic function, renal function test,
urinalysis, electrocardiography, and serum osmolality tests and toxicology
test to identify type of poisoning
Examples of Nursing Diagnoses

and Collaborative Problems for the Poisoned Overdosed Patient
Ineffective Breathing Pattern
■Impaired Gas Exchange
■Ineffective Tissue Perfusion
■Fluid Volume Imbalance, Risk for
■Impaired Thought Processes
■Violence, Risk for (to self or others)
■Self-Esteem Disturbance
■Ineffective Individual/Family Coping
■ Risk for Injury,
■Ineffective Role Performance
■Acidosis/Alkalosis
Example of some poisoning over dose

Drug overdose S&S
Paracetamol, Anorexia, Nausea, Malaise
carbon • Elevated aspartate aminotransferase (AST),
monoxide, alanine aminotransferase (ALT), and total bilirubin
• Prolonged prothrombin time
• Jaundice and Metabolic acidosis
Nursing care:
Prevention of absorption:
-Activated charcoal with gastric lavage
-vital signs
Monitor daily AST, ALT, total bilirubin, BUN, creati-
nine, and prothrombin time
-Antidote:
-Repeat any dose not retained 2 h, may need
-large doses of antiemetics to control vomiting
Opioids (e.g. Lethargy, Confusion, Coma

codeine, heroin, • Decreased respiratory rate
20
Emergency nursing
morphine) • Decreased tidal volume

• Decreased bowel sounds
• Constricted pupils
• Mild hypotension
• Hypothermia
Nursing care:
-warm the patient
-Prevention of absorption gastric lavage
- Monitor vital sings
-Laboratory:
Serum toxicology screen
-dopamine i.v infusion
-Careful administration of naloxone
antidot
organophosphate. Excessive salivation, diarrhea, emesis, diaphoresis,

bradycardia, bronchorrhea, CNS depression,
constricted pupils.
Nursing care:
Prevention of absorption gastric lavage /2 hrs
- Monitor vital sings
-Monitor mental status
-Laboratory:
Serum toxicology screen
-Treatment:
-atropin
-Drugs and Toxins Well Adsorbed by Activated Charcoal
■Acetaminophen ■ Amphetamines ■Antihistamines ■ Aspirin ■
Barbiturates ■ Benzodiazepines ■ Beta blockers ■ Calcium channel
blockers ■ Cocaine ■ Opioids ■ Phenytoin ■ Theophylline ■ Valproic
acid
- Drugs and Toxins Not Well Adsorbed by Activated Charcoal
■ Acids ■ Alkalis ■ Alcohols ■ Iron ■ Lithium ■ Metals
-Some definitions
- Antagonist is a substance that counteracts the action of another
drug .
- Antitoxin is a substance neutralize a toxin .
21
Emergency nursing
- Antivenins are substance that neutralize the venom of the snake
or spider
-General nursing intervention for patients with drug overdose:

1. Assess, establish, and maintain the airway.
2. Evaluate respiratory effort.
3. Maintain adequate hydrations.
4. Monitor ECG.
5. Maintain or correct acid–base balance and electrolyte homeostasis.
6. Assess level of consciousness.
7. Identify injuries and disease processes that increase risk.
8. Measure vital signs and temperature frequently to track changes.
9. Gastric lavage/2hrs
22
Emergency nursing
Hypertensive Crisis
Intended Learning Objectives (ILOs)
A.Knowledge and understanding skills:
a1. Define hypertensive crisis, hypertensive urgency and hypertensive
emergency
a2. List causes of hypertension crisis
B.Intellectual skills:
b1. Differentiate between hypertensive urgency and hypertensive
emergency
b2. Construct a plan nursing care for patient with hypertensive crisis
C.Professional skills:
c1. Assess hypertension crisis patient.
c2. Apply cardiac monitoring
Define hypertensive crisis

Hypertensive crisis OR malignant hypertension refers to the abrupt, acute
and market increase in blood pressure from the patient's baseline. MAP is
greater than 120mmHg.
Types of hypertensive crisis

Hypertensive crisis includes hypertensive urgency and emergency
.Hypertensive emergency are defined as an acute blood pressure
elevation greater than 180/120 mm Hg complicated by impending or
progressive target organ dysfunction. Hypertensive Urgency
characterized by a serious elevation in blood pressure but do not put the
patient at risk for end-organ damage
Causes of Hypertensive crisis

• Essential hypertension: poorly controlled blood pressure
antihypertensive drugs withdrawal
• Other drugs such as amphetamines, phencyclidine (PCP), and
lysergic acid diethylamide (LSD) can also cause hypertensive
crisis
• Autonomic dysreflexia
• Thyrotoxicosis and cushing's syndrome
• Renal parenchymal diseases: acute ,vasculitis, haemolytic
uraemic syndrome, thrombotic thrombocytopenic purpura
Renovascular diseases
23
Emergency nursing
• Central nervous system disorders: head injury,cerebral

infarction/haemorrhage, brain tumors
• Eclampsia
Clinical Manifestations
A hypertensive emergency is often manifested as hypertensive
encephalopathy, a syndrome in which a sudden rise in BP is associated
with severe headache, nausea, vomiting, seizures, confusion, and coma.
The manifestations of encephalopathy are the result of increased cerebral
capillary permeability. This leads to cerebral edema and a disruption in
cerebral function. On retinal examination, exudates, hemorrhages,
and/or papilledema is found. Renal insufficiency ranging from minor
injury to complete renal failure can occur. Rapid cardiac
decompensation ranging from unstable angina to MI and pulmonary
edema is also possible. Patients can have chest pain and dyspnea. Aortic
dissection can develop and will cause sudden chest and back pain and
possibly reduced or absent pulses in the extremities.
Assessment and Diagnosis
Hypertensive emergency can manifest as any of the following symptoms,
depending on the target organ involved:
1. CNS compromise, identified by headache, blurred vision, change in
level of consciousness, or coma
2. Cardiovascular compromise, identified by the chest pain of ACS or
aortic dissection
3. Acute kidney failure, identified by a sudden absence of urine output
4. Catecholamine excess Worsening of symptoms may indicate
hypertensive encephalopathy.
➢ Diagnostic studies include blood pressure measurement in both arms. A

12-lead ECG reading is taken to evaluate for evidence of acute MI or
left ventricular hypertrophy. cardiac monitor, lab investigation according
to each patient condition.
Patient assessment is extremely important through:-

• Assess eight vital signs( pulse, RR, Bl.P, temperature, pain, UOP,
LOC and o2 saturation)
• Monitor for signs of neurologic deficits, retinal damage, heart
failure, pulmonary edema, and renal failure. The neurologic
changes are often similar to those related to a stroke. However, a
24
Emergency nursing
hypertensive crisis does not show focal or lateralizing signs often
seen with a stroke.
Management of hypertensive crisis

➢ Initial goals of therapy in hypertensive emergencies limit
reducing mean arterial blood pressure by no more than 20% to
25% over a period of several minutes to several hours require
hospitalization, IV administration of antihypertensive drugs, and
intensive care monitoring. In treatment of hypertensive
emergencies, the mean arterial pressure (MAP) is often used
instead of BP readings to guide and evaluate drug therapy. MAP
is calculated as follows: MAP= SBP +2DBP/3
• Notes; Lowering the BP too quickly or too much may decrease

cerebral, coronary, or renal perfusion.IV drugs used for
hypertensive emergencies include vasodilators (e.g., sodium
nitroprusside [Nitropress], , the ACE inhibitor enalapril (Vasotec
IV), and the calcium channel blocker. Sodium nitroprusside is the
most effective IV drug to treat hypertensive emergencies. Oral
agents may be given along with IV drugs to help make an earlier
transition to long-term therapy.
• Hypertensive urgencies usually treated with rapid-acting oral

antihypertensive agents. Many medication categories are
available, including ACEIs, ARBs, calcium channel blockers, and
beta-blockers. A loop diuretic (e.g., furosemide) often is
prescribed in addition to the antihypertensive agents when the
patient has fluid retention.
• Nursing diagnosis
➢ Risk for Ineffective Cerebral Tissue Perfusion,
➢ Risk for Ineffective Peripheral Tissue Perfusion,
➢ Anxiety, related to threat to biologic, psychologic, or social
integrity,
➢ Deficient Knowledge, related to lack of previous exposure to
information,
25
Emergency nursing
Nursing instruction:
• Change positions slowly to limit orthostatic hypotension.
• Avoid hazardous activities, since the drug may cause drowsiness.
• Do not discontinue the medication abruptly to prevent rebound
hypertension. Not every patient with an elevated BP and no target
organ disease will require emergent drug therapy or
hospitalization.
• Allowing the patient to sit for 20 or 30 minutes in a quiet
environment may significantly reduce BP.
• Additional nursing interventions include encouraging the patient
to verbalize any concerns or fears, answering questions regarding
hypertension, and eliminating any adverse stimuli (e.g., excess
noise) in the patient’s environment.
26
Emergency nursing
Advanced Life Support (ALS)
Learning Objectives of ACLS Provider Course
1. Apply the BLS, Primary, and Secondary Assessment sequence for

a systematic evaluation of adult patients.
2. Perform prompt, high-quality BLS, including prioritizing early
chest compressions and integrating early AED use.
3. Recognize and perform early management of respiratory & cardiac
arrest.
4. Demonstrate effective and safe use of manual defibrillator.
5. Model effective communication as a member of a high-
performance team.
6. Recognize the impact of team dynamic on overall team
performance.
7. Recognize bradyarrhythmias / tachyarrhythmias that may result in
a cardiac arrest or complicated resuscitative outcome.
8. Perform early management of bradyarrhythmias /
tachyarrhythmias that may result in cardiac arrest or complicate
resuscitation.
Advanced Life Support (ALS) is basic life support with the addition of
invasive techniques e.g. manual defibrillation, advanced airway
management, intravenous access and drug therapy.
ALS interventions aimed at preventing cardiac arrest include airway

management, ventilation support, and treatment of bradyarrhythmias and
tachyarrhythmias. For the treatment of cardiac arrest, ACLS interventions
build on the basic life support (BLS) foundation of immediate recognition
and activation of the emergency response system, early CPR, and rapid
defibrillation to further increase the likelihood of ROSC with drug
therapy, advanced airway management, and physiologic monitoring.
Following ROSC, survival and neurologic outcome can be improved with
integrated post–cardiac arrest care.
➢ Airway Management
Oxygen Administration During CPR
27
Emergency nursing
Empirical use of 100% oxygen during resuscitation from cardiac arrest is
reasonable
Oxygen delivering devices: Advanced Airways:Supraglottic airways and

Endotracheal Tube.
Supraglottic airways are devices designed to maintain an open airway

and facilitate ventilation. Insertion of a supraglottic airway does not
require visualization of vocal cord and so it is possible to insert without
interrupting chest compression during resuscitation. A number of
supraglottic airways are available: Laryngeal mask airway (LMA), (2)
combitube and (3) laryngeal tube. The LMA provides a more secure and
reliable means of ventilation and is widely used in clinical practice.
Ventilation with an Advanced Airway and Chest Compression

When a cardiac arrest patient has an advanced airway in place during
CPR, there is no more cyclical CPR (i.e. 30 compression interrupted by
pauses for 2 ventilations). Chest compressions are delivered at rate of at
least 120 per minute. Ventilations are delivered at 10 per minute (1
ventilation every 6 seconds)
➢ Defibrillation
The passage of an electrical current across the myocardium to depolarise a
critical mass of myocardium and enable restoration of coordinated
electrical activity, Only for VF or pulseless ventricular tachycardia (VT).
28
Emergency nursing
➢ Synchronized Cardioversion
A shock delivery that is timed (synchronized) with the QRS complex
Use of Synchronized Cardioversion

• Indicated in a hemodynamically unstable patient (low blood pressure)
with a perfusing rhythm (pulse present)
• Recommended in supraventricular tachycardia due to re-entry, atrial

fibrillation,atrial flutter, and atrial tachycardia
• Recommended in monomorphic VT with pulses

➢ Transcutaneous Pacing (TCP)
Transcutaneous pacing (TCP) is a highly effective emergency method of
pacing for severe symptomatic bradycardias.
Access for Parenteral Medications During Cardiac Arrest

Peripheral IV Drug Delivery
If a resuscitation drug is administered by a peripheral venous route, it
should be administered by bolus injection and followed with a 20-mL
bolus of IV fluid to facilitate the drug flow from the extremity into the
central circulation.
Intraosseous (IO) Drug Delivery
IO cannulation provides access to a noncollapsible venous plexus,
enabling drug delivery similar to that achieved by peripheral venous
access at comparable doses. It is reasonable for providers to establish IO
access if IV access is not readily available
29
Emergency nursing
➢ Drugs
Adrenaline
Action & Indication: Naturally occurring cathech-olamines with alpha
and beta effect and administration in cardiac arrest will cause intense
vasoconstriction (alpha adrenergic action) and divert cardiac output to
vital organ such as brain and heart. Dose and Administration :IV/IO:
1mg (10ml of 1:10000 solution), administered every 3-5minutes followed
by 20ml flush. Adverse Effects: Hypertension after resuscitation,
Tachyarrhythmias, Tissue necrosis if extravasation occurs.
Amiodarone
Action&Indecation: An antiarrhythmica and administration in cardiac
arrest with Refractory pulseless VT/VF (between the third and fourth
shock when refractory to defibrillatory shock and vasopressor) and Stable
and unstable tachyarrhythmias
Dose and Administration :-For refractory VF/pulseless VT is IV/IO
300mg bolus (dilute in 20mL Dextrose 5% solution) , Can repeat in 3-
5minutes, 150 mg -For unstable tachyarrhythmias where cardioversion
fails 3X, 300mg IV over 10- 20 minutes. -For stable tachyarrhythmias,
300mg IV over 20-60 minutes. -For Maintenance infusion: 900 mg IV
over 24h g. Adverse Effects: Can cause hypotension, bradycardia and
heart block
Atropine
Action & Indication: Antagonises the action of the parasympathetic
neuro-transmitter acetylcholine. Therefore, it blocks the effect of the
vagus nerve on both the sino-atrial (SA) node and the atrio-ventricular
(AV) node, increasing sinus automaticity and facilitating AV node
conduction. It is First line drug for symptomatic Bradycardia. Dose and
Administration: The recommended dose for bradycardia is 0.5mg IV
every 3 to 5 minutes to a max total dose of 3mg
Dopamine
Action &Indication
• A chemical precursor of noradrenaline that stimulates both alpha and
beta adrenergic receptors
• In addition, there are receptors specific for dopamine (DA1, DA2
dopaminergic receptors)
30
Emergency nursing
• Stimulates the heart through both alpa and betareceptors
• Both a potent adrenergic receptor agonist and a strong peripheral
dopamine receptor agonist. These effects are dose dependent.
• Second-line drug for symptomatic bradycardia
Dose and Administration: Usual infusion rate is 2-20μg/kg/minute and

dose titrated according to response. Side Effects: Can cause tachycardia,
hypertension, and precipitate arrhythmias and May cause excessive
systemic and splanchnic vasoconstriction for higher dose (10-
20μg/kg/minute)
p/
31
Emergency nursing
Adult Cardiac Arrest Algorithm - 2018
32
Emergency nursing
33
Emergency nursing
Reference:
1. American Heart Association. Web-based Integrated Guidelines
for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care – Part 7: Adult Advanced Cardiovascular
Life Support. ECCguidelines.heart.org © Copyright 2018
American Heart Association, Inc.
34

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‫كلية معتمدة مه الهيئة القىمية‬

‫لضمبن جىدة التعليم واالعتمبد‬

CRITICAL CARE NURSING DEPARTMENT

‫نتطىَر انًستًر نهقذرح انتعهًُُخ نًرحهخ انجكبنىرَىش‪.‬‬ ‫‪‬‬

Scope of Critical Care and emergency Nursing

1. State goals of critical care nursing

Goal of critical care nursing

Scope of critical care nursing practice

A. The critically ill patients and their significant social relationship.

A. Critically ill patients

 The needs of the critically ill

 Physical needs are equated with basic physiological or biological

 May include social, and psychological needs. Social integrity

B. A critical care nurse

C. Critical care unit

- The critical care environment must contain the following:

 Resources that constantly support the direct interaction

Common illness and injuries seen in emergency department

 Emergency operations preparedness.

Ethical Issues in Critical Care Nursing

Nursing Code of Ethics

Ethical Decision Making

Objectives based on competence:

1- Define acid/base disorders.

Chemically, the pH scale ranges from 0-14, making pH 7

Acid/base balance is controlled through these functions:

Expected ABG Outcomes

- PH: hydrogen ion concentration of blood and is an indicator of Acid-

- 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

HCO3 22- 26 mEq/L

↓ HCO3 metabolic acidosis

↑ HCO3 metabolic alkalosis

- SaO2:-the saturation of hemoglobin by oxygen

SaO2: 95- 99%

- BE: - base excess reflects an increase or decrease in total buffer base.

- PaO2:- the partial pressure of oxygen in the arterial blood

Values less than 60 may result in lactic acid production and

Mechanisms to maintain acid base balance:

Respiratory regulations: Respiratory system controls carbon dioixide

Renal regulations: the kidneys defend blood pH by controlling

In respiratory acidosis, the pulmonary system can't rid the body of

Tachycardia, dyspnea with rapid, shallow respirations, nausea and

 ABG findings indicative of respiratory acidosis

 Maintain a patent airway

It results from alveolar hyperventilation and hypocapnia.

In Respiratory Alkalosis, pH is greater than 7.45, and partial pressure of

o ABG findings indicative of respiratory Alkalosis

 Correct the underlying cause, for example by treating Salicylates

1. HCO3 depletion from renal disease, diarrhea, or small bowel

 Rapid, deep respiration  headache

 Maintain tissue perfusion and oxygenation

1. loss of hydrochloric acid (HCL) from prolonged vomiting or

slow, shallow respiration (compensated), hypertonic

 Chloride supplementation for the kidney to absorb sodium with

Acute Respiratory Failure

Learning objectives based on competence:

Definition: Acute Respiratory failure results when one or both of these

Etiology and Pathophysiology

Nursing diagnoses for the patient with acute respiratory failure

Learning objectives based on competence: