Cardiovascular Derangements

Several hemodynamic and neurohormonal responses occur in the setting of hypovolemic shock. Initially, a sympathoexcitatory response to hemorrhagic shock predominates. An acute decrease in circulating blood volume activates arterial baroreceptors within the aortic arch and carotid sinus, inducing reflex tachycardia and peripheral vasoconstriction. Stimulation of the sympathetic nervous system leads to catecholamine release from the adrenal gland; α-adrenergic agonism is responsible for peripheral vasoconstriction, shunting blood away from metabolically active organs to preserve flow to the coronary and cerebral circulations. Vasopressin and the renin-angiotensin-aldosterone system contribute to renal water retention, sodium and chloride resorption, and peripheral vasoconstriction. If hemorrhage progresses, a sympathoinhibitory phase occurs, characterized by activation of cardiac C-fiber afferents, resulting in bradycardia and vasodilation.

Various immunologic mediators, such as tissue necrosis factor-α and nitric oxide, are released in response to tissue injury. These proinflammatory mediators can cause myocardial depression, inappropriate vasodilatation, and end-organ dysfunction. Administration of vasopressors, such as norepinephrine and arginine vasopressin, to decrease systemic venous compliance, increase mean systemic filling pressures, and ultimately improve flow to end-organs, has been associated with mixed outcomes.

Acid-Base Disturbances

Metabolic acidosis is almost always seen in association with a shock state. As a result of tissue hypoperfusion, oxygen delivery to vital organs is reduced, resulting in tissue hypoxia and oxygen debt. At the cellular level, there is a change from aerobic to anaerobic metabolism. This switch leads to the production of anaerobic metabolites, such as lactic acid. Sequelae include hypotension, decreased myocardial contractility, arrhythmias, encephalopathy, and worsening end-organ function.