[Skip to Navigation]
September 1980

Current Management Concepts in Orthostatic Hypotension

Author Affiliations

From the Department of Medicine, University of Hawaii, John A. Burns School of Medicine, Honolulu.

Arch Intern Med. 1980;140(9):1152-1154. doi:10.1001/archinte.1980.00330200028014

Why does man not faint when upright? Normally, the slight decrease in systolic arterial pressure that occurs when one stands triggers a series of physiologic adjustments designed to maintain adequate cerebral perfusion. Stimulated baroreceptors provoke autonomic nervous system activity, which results in an increase in peripheral arterial and venous constriction, heart rate, and myocardial contractility. Concurrent release of norepinephrine and of an antidiuretic hormone, and activation of the renin-angiotensin-aldosterone mechanism help maintain intravascular volume and pressure. Without these changes, the effect of gravity would cause excessive pooling of blood in the peripheral veins, with consequent substantial reduction in central blood volume, left ventricular filling pressure, cardiac output, and cerebral blood flow.

Clearly, ample opportunities exist for disturbances of any of these delicate mechanisms. The results of such decompensation would run the spectrum from trivial and asymptomatic decreases in systolic pressure through profound hypotension and syncope. Such episodes of low blood