BACHELORE OF SCIENCE IN NURSING

NCMB 418 - CARE OF THE CLIENT WITH LIFE-

THREATENING CONDITIONS, ACUTELY ILL / MULTI-
ORGAN PROBLEMS, HIGH ACUITY AND
EMERGENCY SITUATION
COURSE MODULE COURSE UNIT WEEK
3 13 15
Assessment of Critically Ill Clients with Shock and MODS

✓ Comprehend the course unit objectives.

✓ Peruse through the study guide prior to class attendance.
✓ Analyze the required learning resources; refer to course unit
terminologies for jargons.
✓ Proactively participate in classroom discussions.
✓ Participate in weekly discussion board (Canvas).
✓ Answer and submit course unit tasks on time.

At the end of the end of this unit, the students are expected to:

1. Recognize and examine the client with life-threatening conditions, acutely ill/ multi-organ
problems, high acuity and emergency situation.
2. Determine a client’s the health status/ competence and or expected outcomes of nurse –
client working relationship.
3. Record client’s responses/ nursing care services rendered and processes/ outcomes of the
nurse client working relationship.
 4. Ensure completeness, integrity, safety, accessibility, and security of information.
5. Adhere to protocols of confidentiality in safekeeping and releasing of records and other
information.
6. Evaluate the client’s health status / competence and/or expected outcomes of nurse-client
working relationship.

Burns, S. and Delgado, S. (2019). Essentials of Critical Care Nursing, 4th ed. USA: McGraw-Hill.

A. Cardiogenic Shock
➢ A special kind of shock during which the heart does not adequately pump enough blood to
the body’s tissues (blood flow to tissues decreases and oxygen delivery falls)
➢ Due to decreased functioning of the heart leading to decreased forward flow of oxygenated
blood to the tissues
➢ Most common cause – heart attack (myocardial infarction) that can damage 40% or more of
the ventricle

Recall:
1. Stroke volume – the amount of blood pumped out of the heart during each contraction or
heartbeat.
2. CO – the amount of blood pumped out of the heart every minute

IMPORTANT! As stroke volume and CO decrease, blood builds up in the heart and the
left ventricular end diastolic volume (LVEDV) increases. This increases the oxygen
demand. An increased LVEDV also decreases the amount of blood that flows through
the coronary arteries because the blood in the ventricle increases the pressure in the heart
muscle (decreased oxygen delivery to the heart can lead to cardiac hypoxia)

Risk Factors:
• Acute myocardial infarction (ST segment elevation MIs- STEMIs)
• Atrial thrombus
• Cardiac tamponade
• Cardiac tumor
• Cardiomyopathic conditions
• Cardiopulmonary arrest
• Dysrhythmias
• Endocarditis
• Myocarditis
• Open heart surgery
• Pheochromocytoma
• Pneumothorax
• Pulmonary embolus
• Septic shock
• Valvular dysfunction (mitral or aortic regurgitation, mitral stenosis)
• Ventricular aneurysm

Clinical Manifestations:
➢ depend on the severity of the shock, other underlying conditions, and the cause of the pump
failure.
• Some clinical manifestations are a result of the pump’s failure, whereas others are the result of
the body’s response to the shock.
• Cardiovascular signs – low systolic BP (< 90 mmHg), tachycardia (in response to the low BP and
decreased CO of < 2.2 L/min), pulses “weak and thready”
• Capillary refill – sluggish
• Ischemic changes on an ECG – ST segment changes or PVCs
• Chest pain or tightness
• If with severe hypoxia – dark-colored nail beds and mucous membranes
• Anxiety, confusion, lethargy, and coma (the first sign is often a change in mental status)
• Nausea
• Decreased bowel sounds and decreased urine output

B. Hypovolemic shock
➢ The most common form of shock
➢ Cause – inadequate circulating blood volume in the intravascular bed (circulating oxygenated
blood flow to the body organs decreases) leading to inadequate tissue perfusion, causing
cellular hypoxia, organ failure, and death.
➢ Causes
1. Absolute hypovolemia – occurs as a result of fluid loss from the intravascular space
(external fluid loss, internal fluid shifting a.k.a. third spacing)
2. Relative hypovolemia – occurs as a result of vasodilation and an increase in vascular
capacitance in comparison to the amount of circulating volume

IMPORTANT! As the circulating blood volume decreases, the venous return to the right
side of the heart decreases leading to a decrease in cardiac filling pressure and volume
(preload or the end-diastolic volume). The fibers of the sympathetic nervous system
(SNS), as well as the medullary portion of the adrenal glands, release two
neurotransmitter substances— epinephrine and norepinephrine.
Clinical Manifestations
➢ depend on the severity and rate of volume loss, the patient’s ability to compensate, the
patient’s age, and the presence of preexisting illnesses
1. The reversible, compensatory stage occurs with a fluid loss of 15% to 30% or up to 1500mL.
✓ Goal: to restore oxygenation and perfusion to the cells
✓ May exhibit normal BP readings and narrowed pulse pressure
✓ Tachycardia, tachypnea (creating a respiratory alkalosis)
✓ Hypoxia
✓ Decreased urinary output
✓ Thirst
✓ Pale and cool skin, delayed capillary refill (less than 2 seconds)
✓ Changes in the LOC (e.g., confusion, restless, anxiousness)
2. The progressive stage of shock – begins with a fluid loss of 30% to 40% or up to 2000 mL
✓ Compensatory mechanisms begin to fail and tissue perfusion becomes ineffective for the
body organs to function, organs become dysfunctional and all body systems are affected (as
one organ system fails, the others eventually become dysfunctional, leading to multiorgan
dysfunction syndrome or MODS).
✓ Increased heart rate
✓ Cardiac dysrhythmias develop
✓ CO, cardiac index, right atrial pressure, and pulmonary artery wedge pressures decrease
✓ Increased SVR – as a result of the continued vasoconstriction of the arterial system
✓ Hypotension with a narrowed pulse pressure
✓ LOC changes: lethargic, confused, and eventually comatose

C. Anaphylactic Shock
➢ Hemodynamic compromise of cardiac function, decreased SVR, decreased stroke volume,
decreased afterload, decreased end-diastolic volume, and decreased mixed venous
oxygenation saturation leading to decrease CO with ineffective tissue perfusion

D. Septic Shock
➢ an inflammatory response
➢ a distributive shock characterized by tachycardia, hyperthermia or hypothermia, and
hypotension caused by decreased SVR
➢ initiated by the launch of immune mediators that are part of the inflammatory reaction.
➢ Systemic inflammatory response syndrome (SIRS) – a host’s response to a variety of clinical
insults, both infectious and noninfectious, and is part of the acute sepsis process.

Risk Factors:
• Very young children
• Older adults
• Immunocompromised individuals
• Chronically ill patients
• Patients with malignancies

Clinical Manifestations:
1. Early sepsis – manifestations are subtle; therefore, careful monitoring is essential (identifying
the patients who are at the greatest risk is important
• A decline in SVR is one of the first indications of shock
• Along with a documented or suspected infection, at least two or more of the following
signs and symptoms characterize sepsis:
• Temperature > 38.3° or < 36° C; > 100.9 or < 96.8° F
• Tachypnea
• Tachycardia
• Altered mental status
• Positive fluid balance (>20 mL/kg over 24 hours)
• Hyperglycemia (>120 mg/dl) in the absence of diabetes)
• Hypotension (SBP < 90 mm Hg, MAP < 70 mm Hg)
• SvO2 > 70%
• Cardiac index > 3.5 L/min/m2
• White blood cell count (WBC) > 12,000 cells/mm
• WBC < 4000 cells/mm, or differential > 10% bands
• Elevated C-reactive protein
• Elevated procalcitonin
2. Compensatory mechanisms include baroreceptor reflex, which causes an increased heart
rate and vasomotor tone.

IMPORTANT! Once sepsis is present, the stage is set for progression to septic shock.
Therefore, diligence must be taken to identify sepsis early and begin early goal-directed
treatment and monitoring.

Complications:
• May exhibit skin lesions that are most often located on the lower extremities (can be
associated with the development of DIC
• Toxic shock syndrome (TSS) can produce a profound septic shock and has a very distinctive
cutaneous component (staphylococcus aureus or a severe streptococcal infection causes
TSS)

Systemic Inflammatory Response Syndrome (SIRS)

✓ The body’s response to an infectious or noninfectious insult affecting the whole body
✓ Although the definition refers to it as an “inflammatory” response, it actually has pro- and anti-
inflammatory components.
Criteria of SIRS: at least two of the following:
▪ Temperature : hyperthermia > 38°C or hypothermia < 36.0°C
▪ Heart Rate : tachycardia > 90 beats/minute
▪ Respiratory Rate : tachypnea > 20 breaths/min
▪ White Blood Cells : leukocytosis > 12X109/l or leucopenia < 4x 109/l

Multiorgan Dysfunction Syndrome

➢ A progressive dysfunction of more than one organ in patients who are critically ill or injured
➢ The leading cause of death in ICUs

Risk Factors:
• Patients with systemic infection (particularly, a gram-negative sepsis)
• Extensive burns
• End-organ failure
• Pancreatitis
• Hypovolemia
• Cardiogenic shock
• Human immunodeficiency virus (HIV)
• Aspiration
• Multiple blood transfusions
• Trauma

Causes:
The initial insult that stimulates MODS can result from:
1. extensive burns
2. trauma
3. cardiorespiratory failure
4. multiple blood transfusions
5. systemic infection (most common)

Prognosis:
➢ Although the mortality is high, patients can recover
➢ Potential for recovery depends on the severity of illness or injury, underlying organ reserve,
the speed of instituting effective treatment, the adequacy of treatment, and the number and
severity of subsequent injuries and complications. If treatment is unsuccessful, death usually
occurs between 21 and 28 days after the initial insult.
Distributive shock – this is also called circulatory shock, the primary cause of decreasing BP is
massive vasodilation and pooing of blood into the peripheral vessels. Anaphylactic, Septic and
Neurogenic shock are distributive shock

Shock – inadequate tissue perfusion

Systemic Inflammatory Response Syndrome (SIRS) – the body’s response to an infectious or

noninfectious insult affecting the whole body

Burns, S. (2018) AACN Essentials of Critical Care Nursing. Mc Graw Hill Education.

Hinckle, J (2018) Brunner and Suddarth’s Textbook of Medical and Surgical Nursing, Lippincott,
Williams and Wilkins

Tabulate the stages of shock and their clinical manifestations.

Follow the pattern below:

Manifestations Compensatory Progressive Irreversible

BP
HR
RR
Urine output
Skin
Mentation
Burns, S. and Delgado, S. (2019). Essentials of Critical Care Nursing, 4th
ed. USA: McGraw-Hill.

Hinkle, J. and Cheever, K. (2017). Brunner & Suddharth’s Textbook of

Medical-Surgical Nursing, 14th ed. USA: Wolters Kluwer

Norris, T. (2019). Porth's Pathophysiology: Concepts of Altered Health

States, 9th ed. USA: Wolters-Kluwer