101. Pathophysiology of Shock – Quiz

📌 Professor’s Notes: Quick Revision

High-yield revision notes for rapid review before university examinations.

• Shock is a life-threatening condition caused by inadequate tissue perfusion, resulting in reduced oxygen and nutrient delivery to cells, cellular hypoxia, and progressive organ dysfunction if untreated.
• Types of shock:
  • Hypovolemic: Due to loss of blood or body fluids (hemorrhage, burns, vomiting, diarrhea, trauma).
  • Distributive: Due to widespread vasodilation (septic, anaphylactic, neurogenic, endotoxic).
  • Cardiogenic: Due to failure of the heart as a pump (myocardial infarction, heart failure, arrhythmias).
  • Obstructive: Due to mechanical obstruction to cardiac filling or outflow (cardiac tamponade, pulmonary embolism, tension pneumothorax).
• Hypovolemic shock is the commonest type. Hemorrhagic shock is its most frequent form and occurs after acute blood loss (>15 mL/kg). Typical features include hypotension, tachycardia, weak thready pulse, cold clammy skin, tachypnea, thirst, restlessness, and later impaired consciousness.
• Shock progresses through two stages:
  • Reversible (compensated) stage: Homeostatic mechanisms maintain blood pressure and organ perfusion.
  • Irreversible (refractory) stage: Compensatory mechanisms fail, causing severe hypotension, multiorgan failure, and death despite treatment.
• Rapid compensatory mechanisms in hemorrhagic shock:
  • Increased sympathetic activity causes tachycardia, peripheral vasoconstriction, venoconstriction, and preservation of cerebral and coronary blood flow.
  • Hyperventilation improves oxygenation and venous return.
  • Autotransfusion (capillary fluid shift) restores intravascular volume.
  • Activation of catecholamines, vasopressin, renin-angiotensin-aldosterone system, and cortisol maintains blood pressure and conserves water and sodium.
• Long-term compensation includes increased erythropoietin production, enhanced erythropoiesis, and increased plasma protein synthesis to restore blood volume and oxygen-carrying capacity.
• In irreversible shock, prolonged hypoxia causes endothelial damage, capillary leakage, severe hypotension, bacterial translocation, disseminated intravascular coagulation, acute respiratory distress syndrome (shock lung), myocardial depression, and multiorgan failure.
• Traumatic shock results from severe tissue injury with internal hemorrhage, rhabdomyolysis, and reperfusion injury. Reperfusion injury occurs due to reactive oxygen species generated after restoration of blood flow.
• Burn shock results from plasma leakage through damaged capillaries, causing hemoconcentration. Burn patients are also prone to infection and septic shock.
• Distributive shock is characterized by widespread vasodilation (warm shock):
  • Anaphylactic shock: Histamine-mediated vasodilation and increased capillary permeability.
  • Septic shock: Infection-induced vasodilation, myocardial depression, and increased permeability.
  • Endotoxic shock: Gram-negative bacterial endotoxins trigger cytokine release.
  • Neurogenic shock: Loss of sympathetic tone causes generalized vasodilation.
• Treatment principles:
  • Correct the underlying cause and restore tissue perfusion.
  • Hemorrhagic shock: Blood transfusion and fluid replacement.
  • Burn shock: Intravenous fluids, plasma, or albumin.
  • Anaphylactic shock: Epinephrine is the drug of choice.
  • Cardiogenic shock: Dopamine improves cardiac contractility and renal perfusion.