NEURAL CIRCULATORY CONTROL IN VASOVAGAL SYNCOPE

The orthostatic volume displacement associated with the upright positi on necessitates effective neural cardiovascular modulation. Neural con trol of cardiac chronotropy and inotropy, and vasomotor tone aims at m aintaining venous return, thus opposing gravitational pooling of blood in the lower part of the body. The present concept of the vasovagal r esponse or ''common faint'' implicates the development of inappropriat e cardiac slowing due to sudden augmentation of efferent vagal activit y, and arteriolar dilatation by sudden reduction or cessation of sympa thetic activity. The venous pooling associated with lasting orthostati c stress results in development of central hypovolemia. At a certain p oint during the ongoing reflex adaptation to the hypovolemia in progre ss, a depressor reflex is set in train. The depressor reflex input alo ng this second ''peripheral'' afferent pathway is postulated to origin ate from various sites in the cardiovascular system but remains uncert ain. The common faint in humans is of both vaso- and vagal origin; the pure vagal response is less common than its vasodepressor variant. Th ere is strong evidence for an early loss of vasomotor tone in the majo rity of fainting subjects. Blocking the vagus nerve or cardiac pacing is not of much help in preventing vasovagal syncope; though atropine o r pacing may prevent bradycardia in vasovagal fainting, they have neve r been proven to prevent hypotension. Baroreflex modulation of autonom ic outflow remains present during the presyncopal stages until it beco mes offset by an opposing depressor reflex with relative bradycardia a nd relaxation of arterial resistance vessels. The nature of the vasodi latation associated with the vasovagal response has still not been set tled.