Pathophysiologic basis for vasodepressor syncope

Abstract

The current knowledge regarding the pathophysiologic basis of the vasodepressor response was reviewed. The balance of evidence indicates that the mechanoreceptor hypothesis seems unlikely to be the sole afferent alteration that leads to the vasodepressor response. Alternative afferent mechanisms should include neurohumoral mediated sympathoinhibition triggered by opioid mechanisms as well as impaired endothelial and NO responses to orthostatic stress in susceptible individuals. It is possible that impaired cardiovagal and sympathetic outflow control of arterial baroreceptors is enhanced by the aforementioned mechanisms. The role of central sympathoinhibition and vagal excitation triggered directly from pathways within the temporal lobe or triggered by alterations in regional cerebral blood flow should be considered as potential alternative mechanisms. Efferent autonomic outflow during vasodepressor syncope include sympathetic neural outflow withdrawal in addition to activation of parasympathetic outflow to the heart and abdominal viscera. Further human research is needed to understand the underlying mechanisms that result in the described neural and vascular responses.