Therapeutics in Practice

PATHOPHYSIOLOGY OF HEMORRHAGIC SHOCK Acute hemorrhage results in hypovolemia and a reduction in oxygen-carrying capacity (hemoglobin). A blood volume loss of 15% to 20% is clinically detectable, while life-threatening circulatory failure occurs with a blood volume loss of 30% to 40%.1 Compensatory physiologic mechanisms include vasoconstriction, increased cardiac contractility, and tachycardia (activation of the sympathetic nervous system). In addition, the drop in hydrostatic pressure due to hypovolemia causes filtration fraction to diminish and lymphatic flow to increase as a result of sympathetic activation and a reduction in central venous pressure (CVP). These changes result in a net movement of interstitial fluid into the vascular space. Simultaneously, the renin–angiotensin– aldosterone system is activated, resulting in a decreased glomerular filtration rate, decreased urine production and enhanced renal sodium resorption, increased thirst, and vasoconstriction. Vasopressin contributes to vasoconstriction and thirst. These compensatory mechanisms can maintain circulation in cases of mild blood loss (up to a volume loss of 15%). Losses exceeding this amount require volume replacement and are beyond physiologic compensation. If the patient’s condition is left unchecked, shock results from persistent hypoperfusion, leading to cell dysfunction and, ultimately, apoptosis and necrosis.