Neural circulatory control in vasovagal syncope

Abstract

The orthostatic volume displacement associated with the upright position necessitates effective neural cardiovascular modulation. Neural control of cardiac chronotropy and inotropy, and vasomotor tone aims at maintaining venous return, thus opposing gravitational pooling of blood in the lower part of the body. The present concept of the vasovagal response or "common faint" implicates the development of inappropriate cardiac slowing due to sudden augmentation of efferent vagal activity, and arteriolar dilatation by sudden reduction or cessation of sympathetic activity. The venous pooling associated with lasting orthostatic stress results in development of central hypovolemia. At a certain point during the ongoing reflex adaptation to the hypovolemia in progress, a depressor reflex is set in train. The depressor reflex input along this second "peripheral" afferent pathway is postulated to originate from various sites in the cardiovascular system but remains uncertain. The common faint in humans is of both vaso- and vagal origin; the pure vagal response is less common than its vasodepressor variant. There is strong evidence for an early loss of vasomotor tone in the majority of fainting subjects. Blocking the vagus nerve or cardiac pacing is not of much help in preventing vasovagal syncope; though atropine or pacing may prevent bradycardia in vasovagal fainting, they have never been proven to prevent hypotension. Baroreflex modulation of autonomic outflow remains present during the presyncopal stages until it becomes offset by an opposing depressor reflex with relative bradycardia and relaxation of arterial resistance vessels. The nature of the vasodilatation associated with the vasovagal response has still not been settled.