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Chapter 33
Shock and Multisystem Organ
Dysfunction Syndrome
Copyright © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins
Shock
• Hypoperfusion, hypercoagulability, and activation of the
inflammatory response
• In hypoperfused states, the lack of sufficient oxygen
causes the cells to convert to anaerobic metabolism.
• If oxygen continues to be insufficient to meet cellular
demands for energy, cell death ensues.
• As more cells die, tissues and organs become
progressively dysfunctional and eventually end-organ
failure ensues.
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Three Stages of Shock
• Stage 1. The body activates compensatory mechanisms
in an effort to maintain circulatory volume, blood
pressure, and cardiac output.
– Normal vital signs and cerebral perfusion, and the
shock state often goes unrecognized.
• Stage 2. Compensatory mechanisms begin to fail,
metabolic and circulatory derangements become more
pronounced, and the inflammatory and immune
responses may become fully activated.
– Signs of dysfunction in one or more organs may
become apparent.
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Three Stages of Shock (cont.)
• Stage 3. In the final, irreversible stage, cellular and
tissue injury are so severe that the patient’s life is not
sustainable even if metabolic, circulatory, and
inflammatory derangements are corrected.
– Full-blown multisystem organ dysfunction syndrome
(MODS) may become evident.
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Question
• Compensatory mechanisms in response to shock states
result in which of the following?
– A. Decreased urine output
– B. Vasodilation of blood vessels
– C. Decreased heart rate
– D. Decreased cardiac output
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Answer
• A. Decreased urine output
• Rationale: In response to decreased venous return or
decreased renal blood flow, compensatory mechanisms
are initiated to maintain cardiovascular function and
maintain blood volume. To maintain blood volume, the
renin-angiotensin-aldosterone system is initiated for the
kidneys to retain sodium and water. The net result is
decreased urine output.
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Hypovolemic Shock
• Result of inadequate circulating blood volume, caused by
sudden blood loss, severe dehydration, or injuries that
cause significant fluid shifts from the intravascular space
to the interstitial space (e.g., burns)
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Pathophysiology
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Assessment
• History
• Monitor vital signs.
– Tachycardia, hypotension
• Monitor respiratory status.
• Use of nonsteroidal anti-inflammatory agents (NSAIDs),
which can cause upper gastrointestinal bleeding
• Clinical findings are related to the severity and acuity of
volume loss.
• Serum lactate, arterial pH, serial hemoglobin, and
hematocrit and coagulation
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Management
• Volume administration
• Large-bore 16-gauge or larger for rapid infusion
• Fluids are warmed during infusion to limit the negative
effects of hypothermia.
• Isotonic crystalloid solutions
• Blood products and other colloid solutions if blood loss is
the primary cause
Copyright © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins
Question
• Which of the following is not a common
pathophysiological manifestation seen in patients with
hypovolemic shock?
– A. Altered mentation
– B. Rapid and deep respirations
– C. Cool and clammy skin
– D. Bradycardia
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Answer
• D. Bradycardia
• Rationale: Patients with hypovolemic shock have signs
and symptoms caused by poor organ perfusion. This
includes tachycardia due to activation of the sympathetic
nervous system; altered mentation, ranging from
lethargy to unresponsiveness; rapid and deep
respirations, which gradually become labored and shallow
as the patient’s condition deteriorates; and cool, clammy
skin.
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Cardiogenic Shock
• Loss of ventricular contractility decreases stroke volume
and cardiac output.
• Neuroendocrine compensatory mechanisms are
activated.
• Increasing preload through retention of sodium and
water
• Increasing afterload (systemic vascular resistance)
through vasoconstriction
• These compensatory mechanisms further impair cardiac
output, exacerbating the problem.
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Assessment
• Develops within a few hours after the onset of myocardial
infarction symptoms
• Close monitoring for progressive hemodynamic
compromise and clinical deterioration
• Systolic blood pressure <90 mm Hg
• Mean arterial pressure (MAP) <70 mm Hg
• Cardiac index <2.2 L/minute/m2
• Pulmonary artery occlusion pressure (PAOP) >18 mm Hg
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Management
• Optimize cardiac output and preload (left ventricular enddiastolic pressure [LVEDP]) of 14 to 18 mm Hg.
• Pharmacological agents to increase contractility
• Antidysrhythmic agents, cardioversion, or pacing can
help to restore a stable heart rhythm and enhance
cardiac output.
• Potassium, calcium, and magnesium replacement
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Management (cont.)
• Decreasing left ventricular workload
• Pharmacotherapy: vasodilators may be administered to
reduce SVR and LVEDP.
• Intra-aortic balloon pump (IABP) or left ventricular assist
device
• Mechanical ventilation may be necessary to improve
oxygen delivery to the tissues.
• Scheduling physical care to ensure periods of rest
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Distributive Shock
• The mechanism underlying all distributive shock states is
vasodilation that causes decreased venous return.
• Distributive shock states include
– Neurogenic shock
– Anaphylactic shock
– Septic shock
• In neurogenic shock, vasodilation results from a loss of
sympathetic innervation to the blood vessels.
• In anaphylactic shock and septic shock, vasodilation
results from the presence of vasodilating substances in
the blood.
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Neurogenic Shock
• Neurogenic shock results from loss or disruption of
sympathetic tone most often due to severe cervical or
upper thoracic spinal cord injury.
– Signs and symptoms include hypotension, severe
bradycardia, and warm, dry skin.
– Volume resuscitation
– Vasoconstrictors may be used.
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Anaphylactic Shock
• Anaphylaxis is an allergic reaction that evokes a lifethreatening hypersensitivity response.
• IgE-mediated anaphylaxis occurs as a result of the
immune response to a specific antigen after being
exposed and forming antibodies.
• Non-IgE responses (anaphylactoid reactions) occur
without the presence of IgE antibodies and can occur the
first time the person is exposed to the antigen.
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Anaphylactic Shock (cont.)
• WBCs secrete chemical mediators causing systemic
vasodilation.
• Increased capillary permeability
• Bronchoconstriction, coronary vasoconstriction, and
urticaria
• Arterial vasodilation causes maldistribution of blood
volume to tissues, and venous dilation decreases
preload, thus decreasing cardiac output.
• Increased capillary permeability
• Death due to circulatory collapse or extreme
bronchoconstriction can occur within minutes or hours.
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Clinical Manifestations of Anaphylaxis
• Generalized erythema
• Stridor
• Urticaria/pruritus
• Laryngeal edema
• Anxiety and restlessness
• Bronchoconstriction with
stridor
• Dyspnea/wheezing
• Chest tightness
• Hypotension
• Angioedema
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Assessment
• History of allergies is used to avoid known allergens and
is the best way to prevent anaphylactic shock.
• Anaphylactic shock may occur without any known
predisposing factors.
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Management
• Remove the offending antigen.
• Reverse effects of chemical mediators.
• Restore adequate tissue perfusion.
• Oxygen
• Subcutaneous or IV antihistamine
• Epinephrine
• Corticosteroids, bronchodilators
• Mechanical ventilation is required.
• Vasoconstrictors and positive inotropic agents
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Question
• What is the initial therapy of choice for the treatment of
anaphylactic shock?
– A. Epinephrine
– B. Rapid infusion of normal saline
– C. Dobutamine
– D. Norepinephrine
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Answer
•
A. Epinephrine
•
Rationale: Epinephrine is given to reverse the
vasodilation and bronchoconstriction.
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Septic Shock
• Complex interactions among invading microorganisms
and the immune system, the inflammatory system, and
the coagulation system
• Proinflammatory cytokines are released.
• Activation of the immune response, complement system,
and coagulation system
• Increased vascular permeability
• To balance the proinflammatory response, antiinflammatory cytokines are released causing an “out of
control” inflammatory response.
• Cardiovascular, pulmonary, and hematologic alterations
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Sepsis
• The systemic response to known infection, manifested by
two or more of the following conditions as a result of
infection:
– Temperature greater than 100.4°F (38°C) or less
than 96.8°F (36°C)
– Heart rate greater than 90 beats/minute
– Respiratory rate greater than 20 breaths/minute or
arterial carbon dioxide tension PaCO2 less than 32
mm Hg
– White blood cell (WBC) count greater than 12,000
cells/mm3 or less than 4,000 cells/mm3 OR more
than 10% immature (band) forms
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Assessment
• Early signs of changes in mental status, an increased
respiratory rate, and either hyper- or hypothermia
• Lab studies
• Cultures, (CBC), SMA-7, ABGs, lactate level, end-tidal
carbon dioxide monitoring
• Pulmonary artery catheterization with mixed venous
oxygen (SvO2) monitoring
• CT, chest and abdominal x-rays
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Management
• Identify and treat the cause.
• Volume repletion
• Mechanical ventilation
• Maintain adequate cardiac output.
• Correct coagulopathies
• Nutritional support
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Multiorgan System Failure (MODS)
• The pathophysiology of similar to sepsis and SIRS
• Endothelial injury, inflammatory mediators, disturbed
hemostasis, and microcirculatory failure
• Tissue hypoxia caused by microvascular thromboses
contributes to MODS.
• Typically, the first organs to manifest signs of
dysfunction are the lungs and kidneys.
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Assessment and Management
• Identifying SIRS and signs and symptoms of organ
failure
• Multiple scoring systems exist to determine the extent of
MODS, including the Sepsis-Related Organ Failure
Assessment (SOFA)
• Treatment is supportive and directed at specific organ
systems.
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Question
• Which of the following classifications best describes
septic shock?
– A. Hypovolemic shock
– B. Cardiogenic shock
– C. Vasodilatory shock
– D. Anaphylactic shock
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Answer
• C. Vasodilatory shock
• Rationale: Widespread vasodilation and maldistribution of
blood flow associated with septic shock result in
decreased venous return to the heart, resulting in a
shock state. Hypovolemic shock is caused by dehydration
or hemorrhage. Cardiogenic shock occurs when the heart
fails to function as a pump as a result of myocardial
infarction, abnormal heart rate or rhythm, or impaired
diastolic filling. Anaphylactic shock occurs as a result of
an antibody-antigen reaction.
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