Chapter 42
Shock, Sepsis, and Multiple Organ Dysfunction Syndrome
KEY POINTS
SHOCK
• Shock is a syndrome characterized by decreased tissue perfusion and impaired cellular
metabolism resulting in an imbalance between the supply of and demand for O2 and
nutrients.
• The 4 main categories of shock are cardiogenic, hypovolemic, distributive (includes
septic, anaphylactic, and neurogenic shock), and obstructive.
Cardiogenic Shock
• Cardiogenic shock occurs when either systolic or diastolic dysfunction of the pumping
action of the heart results in reduced cardiac output (CO).
• Causes of cardiogenic shock include acute myocardial infarction (MI), cardiomyopathy,
blunt cardiac injury, severe systemic or pulmonary hypertension, and myocardial
depression from metabolic problems.
• Manifestations of cardiogenic shock include tachycardia, hypotension, a narrowed pulse
pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy skin,
diaphoresis, decreased capillary refill time, anxiety, confusion, and agitation.
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Hypovolemic Shock
• Hypovolemic shock occurs from inadequate fluid volume in the intravascular space to
support adequate perfusion.
• Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal
(GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis.
• Relative hypovolemia results when fluid volume moves out of the vascular space into
extravascular space, such as with sepsis and burns.
• Manifestations depend on the extent of injury, age, and general state of health. They may
include anxiety; an increase in heart rate, CO, and respiratory rate and depth; and a
decrease in stroke volume, pulmonary artery wedge pressure (PAWP), and urine output.
Neurogenic Shock
• Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a
spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks, or in
response to spinal anesthesia.
• The classic manifestations are hypotension (from the massive vasodilation) and
bradycardia (from unopposed parasympathetic stimulation). The patient may not be able
to regulate body temperature.
Anaphylactic Shock
• Anaphylactic shock is an acute and life-threatening hypersensitivity (allergic) reaction. •
The reaction is caused by a sensitizing substance (e.g., drug, chemical, vaccine, food,
insect venom).
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• Immediate reaction causes massive vasodilation, release of vasoactive mediators, and an
increase in capillary permeability resulting in fluid leaks from the vascular space into the
interstitial space.
• Manifestations include anxiety, confusion, dizziness, chest pain, incontinence, swelling
of the lips and tongue, wheezing, stridor, flushing, pruritus, urticaria, and angioedema.
Septic Shock
• Sepsis is a life-threatening syndrome in response to an infection.
• It is characterized by a dysregulated patient response along with new organ dysfunction
related to the infection.
• Septic shock is the presence of sepsis with hypotension despite adequate fluid
resuscitation along with the presence of inadequate tissue perfusion.
• In severe sepsis and septic shock, the body’s response to infection is exaggerated,
resulting in an increase in inflammation and coagulation, and a decrease in fibrinolysis.
• Septic shock has 3 major pathophysiologic effects: vasodilation, maldistribution of blood
flow, and myocardial depression.
• Patients often have hypotension, respiratory failure, altered neurologic status, acute
kidney injury with decreased urine output, and GI dysfunction.
Obstructive Shock
• Obstructive shock develops when a physical obstruction to blood flow occurs with a
decreased CO.
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• Common causes include restricted diastolic filling of the right ventricle from compression
and abdominal compartment syndrome.
• Patients may have a decreased CO, increased afterload, and variable left ventricular
filling pressures depending on the obstruction. Other signs include jugular venous
distention and pulsus paradoxus.
Stages of Shock
• The initial stage of shock that occurs at a cellular level is usually not clinically apparent.
• The compensatory stage is clinically apparent and involves neural, hormonal, and
biochemical compensatory mechanisms to try to overcome the increasing consequences
of anaerobic metabolism and to maintain homeostasis.
• The progressive stage of shock begins as compensatory mechanisms fail and aggressive
interventions are needed to prevent the development of multiple organ dysfunction
system (MODS).
• In the refractory stage, decreased perfusion from peripheral vasoconstriction and
decreased CO worsen anaerobic metabolism. The patient will have profound hypotension
and hypoxemia, as well as organ failure. At this stage, recovery is unlikely.
Diagnostic Studies
• There is no single diagnostic study to determine shock. The diagnosis is established from
a detailed history and physical examination findings.
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• Studies that aid in the diagnosis include a serum lactate, base deficit, 12-lead ECG,
continuous cardiac monitoring, chest x-ray, continuous pulse oximetry, and
hemodynamic monitoring.
Interprofessional Care
• Successful management of the patient in shock includes: (1) identifying patients at risk
for the development of shock; (2) integrating the patient’s history, physical assessment,
and clinical findings to establish a diagnosis; (3) interventions to control or eliminate the
cause of the decreased perfusion; (4) protecting target and distal organs from dysfunction;
and (5) providing multisystem supportive care.
• General management strategies for a patient in shock begin with ensuring that the patient
has a patent airway and O2 delivery is optimized. The cornerstone of therapy for septic,
hypovolemic, and anaphylactic shock is volume expansion with the appropriate fluid.
• The goal of drug therapy for shock is to correct the decreased tissue perfusion resulting in
tissue hypoxia. Vasopressor or vasodilator therapy is used according to patient needs to
maintain the mean arterial pressure at the appropriate level after adequate volume
resuscitation.
• Protein-calorie malnutrition is one of the main manifestations of hypermetabolism in
shock. Early enteral nutrition is vital to decreasing morbidity from shock.
Measures Specific to Type of Shock
Cardiogenic Shock
• The overall goal is to restore heart function and the balance between O2 supply and
demand in the myocardium.
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• Definitive measures include angioplasty with stenting, emergency revascularization, and
valve replacement.
• Care involves hemodynamic monitoring, drug therapy (e.g., diuretics to reduce preload),
and use of circulatory assist devices (e.g., intraaortic balloon pump, ventricular assist
device).
Hypovolemic Shock
• The underlying principles of managing patients with hypovolemic shock focus on
stopping the loss of fluid and restoring the circulating volume.
Septic Shock
• Patients in septic shock need large amounts of fluid replacement. The goal is to achieve a
targeted response based on CVP, ScvO2, cardiac ultrasound, a focused physical
assessment, fluid responsiveness, or other measures.
• A fluid challenge technique (e.g., a minimum of 30 mL/kg of crystalloids) may be used
and repeated until hemodynamic improvement (e.g., increase in MAP and/or CVP) is
noted.
• Vasopressor drug therapy may be added for a MAP that does not respond to initial fluid
resuscitation. Vasopressin may be given to those refractory to vasopressor therapy.
• IV corticosteroids are only recommended for patients who cannot maintain an adequate
blood pressure (BP) with vasopressor therapy, despite fluid resuscitation.
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• Antibiotics are a critical component of therapy for patients with septic shock. They
should be started after cultures (e.g., blood, urine) are obtained and within the first hour
of severe sepsis or septic shock.
Neurogenic Shock
• The treatment of neurogenic shock is dependent on the cause. In spinal cord injury,
general measures to promote spinal stability are initially used.
• Treatment of hypotension and bradycardia involves the use of vasopressors and atropine,
respectively. Fluids are given cautiously. The patient is monitored for hypothermia.
Anaphylactic Shock
• Epinephrine is the drug of choice to treat anaphylactic shock.
• Maintaining the airway is critical. Endotracheal intubation or tracheostomy may be
needed.
• Aggressive fluid replacement, most often with crystalloids, is needed.
Obstructive Shock
• The main strategy in treating obstructive shock is early recognition and treatment to
relieve or manage the obstruction.
Nursing Management: Shock
Nursing Assessment
• The initial assessment focuses on assessing responsiveness and ABCs: airway, breathing,
and circulation.
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• Further assessment focuses on the assessment of tissue perfusion and includes evaluation
of trends in vital signs, peripheral pulses, level of consciousness, capillary refill, skin
(e.g., temperature, color, moisture), and urine output.
Planning
• The overall goals for a patient in shock include (1) evidence of adequate tissue perfusion,
(2) restoration of normal or baseline BP, (3) recovery of organ function, and (4) avoiding
complications from prolonged states of hypoperfusion, and (5) preventing health care–
associated complications of disease management and care.
Nursing Implementation
• Your role in shock involves (1) monitoring the patient’s ongoing physical and emotional
status, (2) identifying trends to detect changes in the patient’s condition, (3) planning and
implementing nursing interventions and therapy, (4) evaluating the patient’s response to
therapy, (5) providing emotional support to the patient and caregiver, and (6)
collaborating with other members of the health team to coordinate care.
• The patient in shock requires frequent assessment of heart rate/rhythm, BP, CVP, SvO2,
and pulmonary artery (PA) pressures or arterial pressure wave-form analysis for cardiac
output (APCO); neurologic status; respiratory status, urine output, and temperature;
capillary refill; skin for temperature, pallor, flushing, cyanosis, diaphoresis, or
piloerection; and bowel sounds and abdominal distention, as well as prevention of health
care-associated infections.
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• Rehabilitation of the patient who is recovering from shock includes correcting the
precipitating cause, preventing or early treatment of complications, and teaching focused
on disease management and/or prevention of recurrence based on initial cause of shock.
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME AND
MULTIPLE ORGAN DYSFUNCTION SYNDROME
• Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory response to
a variety of insults, including infection (referred to as sepsis), ischemia, infarction, and
injury.
• SIRS is characterized by generalized inflammation in organs remote from the first insult.
• SIRS can be triggered by mechanical tissue trauma (e.g., burns, crush injuries), abscess
formation, ischemic or necrotic tissue (e.g., pancreatitis, myocardial infarction), microbial
invasion, and global and regional perfusion deficits.
• Multiple organ dysfunction syndrome (MODS) is the failure of 2 or more organ systems
in an acutely ill patient such that homeostasis cannot be maintained without intervention.
It often results from SIRS. • The respiratory system is often the first system to show signs
of dysfunction in SIRS and MODS, often ending in acute respiratory distress syndrome
(ARDS). • Cardiovascular changes, neurologic dysfunction, acute kidney injury, DIC, GI
dysfunction, and liver dysfunction are common.
Nursing and Interprofessional Management: SIRS and MODS
• The prognosis for the patient with MODS is poor. The most important goal is to prevent
SIRS from progressing to MODS.
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• A critical part of your role is vigilant assessment and ongoing monitoring to detect early
signs of deterioration or organ dysfunction.
• Interprofessional care for patients with SIRS and MODS focuses on (1) prevention and
treatment of infection, (2) maintaining tissue oxygenation, (3) nutritional and metabolic
support, and (4) appropriate support of individual failing organs.
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