Clinical meaning
Hypovolemic shock is the most common type of shock, resulting from a critical reduction in intravascular volume (>15-30% of circulating blood volume). It is classified as hemorrhagic (trauma, GI bleed, ruptured aneurysm, postpartum hemorrhage, surgical bleeding) or non-hemorrhagic (severe dehydration, third-spacing from burns/pancreatitis, excessive diuresis, vomiting/diarrhea). The fundamental defect is decreased preload leading to reduced stroke volume and cardiac output. Compensatory mechanisms activate in stages: Stage I (compensated) involves baroreceptor-mediated sympathetic activation causing tachycardia, peripheral vasoconstriction, and venoconstriction to maintain MAP; the renin-angiotensin-aldosterone system (RAAS) retains sodium and water; and ADH secretion concentrates urine. Stage II (progressive) shows worsening tachycardia, narrowing pulse pressure, cool/clammy skin from vasoconstriction, oliguria (<0.5 mL/kg/hr), anxiety, and rising lactate as tissues shift to anaerobic metabolism. Stage III (irreversible/refractory) involves cellular death, loss of vascular tone, organ failure, and refractory hypotension despite maximal resuscitation. At the cellular level, inadequate oxygen delivery causes mitochondrial dysfunction, ATP depletion, lactic acidosis, and eventual cell membrane rupture releasing intracellular contents (potassium, phosphate, myoglobin) that compound organ injury. The ischemia-reperfusion injury that occurs during resuscitation generates reactive oxygen species (ROS) that cause additional cellular damage.