Shock

SHOCK

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.

Major Causes of Shock

·              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.

Stages of Shock

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.