Chapter 33 Shock and Multisystem Organ Dysfunction Syndrome

1. Chapter 33 Shock and Multisystem Organ Dysfunction Syndrome

2. 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.

3. 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.

4. 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.

5. 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

6. 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.

7. 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)

8. Pathophysiology

9. 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

10. 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

11. 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

12. 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.

13. 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.

14. 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

15. Management • Optimize cardiac output and preload (left ventricular end-diastolic 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

16. 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

17. 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.

18. 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.

19. Anaphylactic Shock • Anaphylaxis is an allergic reaction that evokes a life-threatening 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.

20. 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.

21. Clinical Manifestations of Anaphylaxis • Generalized erythema • Urticaria/pruritus • Anxiety and restlessness • Dyspnea/wheezing • Chest tightness • Stridor • Laryngeal edema • Bronchoconstriction with stridor • Hypotension • Angioedema

22. 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.

23. 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

24. 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

25. Answer • A. Epinephrine • Rationale: Epinephrine is given to reverse the vasodilation and bronchoconstriction.

26. 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, anti-inflammatory cytokines are released causing an “out of control” inflammatory response. • Cardiovascular, pulmonary, and hematologic alterations

27. 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

28. 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

29. Management • Identify and treat the cause. • Volume repletion • Mechanical ventilation • Maintain adequate cardiac output. • Correct coagulopathies • Nutritional support

30. 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.

31. 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.

32. Question • Which of the following classifications best describes septic shock? • A. Hypovolemic shock • B. Cardiogenic shock • C. Vasodilatory shock • D. Anaphylactic shock

33. 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.