Neural control mechanisms and vasovagal syncope

Abstract

Patients with recurrent unexplained syncope may have cardioinhibitory and vasodepressor responses provokable with head-up tilt with or without exogenous beta-adrenergic stimulation. Although these responses are believed to be neurally mediated, the neural mechanisms involved are poorly understood. Numerous studies have documented peripheral vasodilation, hypotension, and bradycardia at the time of syncope and several case reports have shown sudden withdrawal of vasoconstrictor sympathetic neural outflow to skeletal muscle in human subjects. In cats and rats, a similar response can be provoked with hemorrhage and is prevented by interruption of cardiac vagal C-fiber afferents. In dogs, however, section of these fibers does not prevent the development of a vasodepressor response. The provocation of vasodepressor syncope during nitroprusside infusion in a heart transplant recipient with presumed ventricular denervation also suggests that cardiac afferent nerves may not be required for the development of vasodepressor responses in humans. Other potential mechanisms include release of endogenous opioids or nitric oxide that may inhibit sympathetic nerve firing, and primary central nervous system activation (as in partial seizures) that triggers cardioinhibitory and vasodepressor responses. This article reviews our current understanding of the mechanisms involved in the development of neurally mediated syncope.