Neural Control Mechanisms and Vasovagal Syncope

Vasovagal Syncope, Patients with recurrent unexplained syncope may have cardioinhibitory and vasodepressor responses provokable with head-up tilt with or without exogenousbeta-adrenergic stimulation. Although these responses are believed to be neurally mediated, the neural mechanisms involved are pourly understood. Numerous studies have documentedperipheral vasodilation, hypotension, and bradycardia at the time of syncope and several casereports 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. Theprovocation of vasodepressor syncope during nitroprusside infusion in a heart transplantrecipient with presumed ventricular denervation also suggests that cardiac afferent nerves maynot be required for the development of vasodepressor responses in humans. Other potentialmechanisms include release of endogenous opioids or nitric oxide that may inhibit sympatheticnerve firing, and primary central nervous system activation (as in partial seizures) that triggerscardioinhibitory and vasodepressor responses. This article reviews our current understandingof the mechanisms involved in the development of neurally mediated syncope.