Compensatory mechanisms during acute hemorrhage include

Acute hemorrhage triggers the potent vasopressor activity of both angiotensin and vasopressin to increase blood flow to the heart and brain via selective vasoconstriction of the skin, kidneys, and splanchnic organs. Adrenergic discharge also results in selective vasoconstriction of skin, renal, and splanchnic vessels. Myocardial contractility and heart rate are increased, with a resultant increased cardiac output. Hyperventilation is the typical response to the metabolic (lactic) acidosis associated with hemorrhagic shock and hypoperfusion. Aldosterone release, with subsequent increased renal sodium resorption, is mediated by angiotensin II and ACTH, which prevents further intravascular depletion.