Are Adrenergic Overactivity and Splanchnic Vasoconstriction the Prime Pathophysiological Events in Shock?

Abstract

During the past three decades, an hypothesis has evolved to explain the pathophysiology of lethal human shock states. I shall refer to this hypothesis as the “adrenergic theory of shock”. The adrenergic theory is widely accepted (2,6,7). In essence, the theory holds that the stress that produces shock—whether by blood loss, sepsis, myocardial infarction, or trauma—activates mechanisms in the body which initially restore arterial pressure and cardiac output back to normal. Among these compensatory mechanisms is stimulation of the sympathetic nervous sytem and release of circulating catecholamines. The adrenergic system is overstressed by the severe and prolonged cause of shock. The result is widespread arteriolar constriction, particularly in the splanchnic region. Poor perfusion of critical abdominal viscera ensues, leading to ischemic damage of tissues in the liver, the reticulo-endothelial system, and the gut. Impaired defense processes, deranged metabolic activity, and loss of function of the intestinal barrier are major consequences of splanchnic vasoconstriction. Toxic molecules, such as endotoxins, enter the circulation and cannot be cleared by normal defenses.