Shock is characterized by vascular collapse and widespread hypoperfusion of cells and tissue due to reduced blood volume, cardiac output, or vascular tone. The cel-lular injury is initially reversible; if the hypoxia persists, the cellular injury becomes irreversible, leading to the death of cells and the patient.
· Cardiogenic shock (pump failure) can be due to myocardial infarction, car-diac arrhythmias, pulmonary embolism, and cardiac tamponade.
· Hypovolemic shock (reduced blood volume) can be due to hemorrhage, fluidloss secondary to severe burns, and severe dehydration.
· Septic shock (viral or bacterial infection) causes cytokines to trigger vasodilatation and hypotension, acute respiratory distress syndrome (ARDS), DIC, and multiple organ dysfunction syndrome. Mortality rate is 20%.
· Neurogenic shock (generalized vasodilatation) can be seen with anesthesiaand brain or spinal cord injury.
· Anaphylactic shock (generalized vasodilatation) is a type I hypersensitivityreaction.
The stages of shock are arbitrarily defined as follows.
· Stage I: compensation
Perfusion to vital organs is maintained by reflex mechanisms. Compensation is characterized by increased sympathetic tone, release of catecholamines, and activation of the renin-angiotensin system.
· Stage II: decompensation
There is a progressive decrease in tissue perfusion, leading to potentially reversible tissue injury with development of a metabolic (lactic) acidosis, elec-trolyte imbalances, and renal insufficiency.
· Stage III: irreversible tissue injury and organ failure This ultimately results in death.
The organs show various manifestations of shock:
· Kidneys show fibrin thrombi in glomeruli and ultimately, acute tubular failure ensues, which causes oliguria and electrolyte imbalances.
· Lungs undergo diffuse alveolar damage (“shock lung”).
· Intestines show superficial mucosal ischemic necrosis and hemorrhages, and with prolonged injury, bacteremia may ensue.
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