Orthostatic hypotension may result from neurogenic and nonneurogenic causes. Brain hypoperfusion, resulting from orthostatic hypotension from any cause, can lead to symptoms of orthostatic intolerance (eg, lightheadedness) and falls, and if the hypotension is severe, to syncope. Drugs can produce orthostatic hypotension by interfering with the autonomic pathways or their target end-organs or by affecting intravascular volume. Injury to any limb of the baroreflex causes neurogenic orthostatic hypo tension, although with afferent lesions alone, the hypotension tends to be modest and accompanied by wide fluctuations in blood pressure, including severe hypertension. Orthostatic hypotension is the result of baroreflex failure (autonomic failure), end-organ dysfunction, or volume depletion. This compensatory mechanism is termed a baroreflex it is mediated by afferent and efferent autonomic peripheral nerves and is integrated in autonomic centers in the brainstem. This gravity-induced drop in blood pressure, detected by arterial baroreceptors in the aortic arch and carotid sinus, triggers a compensatory reflex tachycardia and vasoconstriction that restores normotension in the upright position. This fluid shift produces a decrease in venous return, ventricular filling, cardiac output, and blood pressure. When we stand up, the blood goes down from the chest to the distensible venous capacitance system below the diaphragm.

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