Current Concepts of Pathophysiology of Vasovagal Syncope and its Evaluation and Management: A Review

Abstract

Vasovagal syncope (VVS) with a sudden, temporary loss of consciousness (LoC) is a common phenomenon in the young and the elderly. Though generally described as innocuous, it may lead to serious consequences in special category of people (pilots), or in the elderly in whom LoC may lead to a fall and serious injury. The topic has been copiously researched upon and discussed in medical literature over the last few decades, but the exact mechanisms which lead to the disability have yet to be fully agreed upon. Changes in cardiovascular baroreceptor sensitivity, aberrations in the complex interaction amongst the nucleus of the tractus solitarius and the nuclei around it, inability of the peripheral circulation to respond to autonomic vasoconstrictors, or excess production of vasodilators such as nitric oxide produced locally have been considered in its pathophysiology. Various extraneous situations like dehydration, exposure to heat stress, medications, psychological factors may adversely stress regulatory physiological responses and promote occasional episodes of VVS. More complex dysautonomia could be a reason for the recurrent VVS. Differences between brain structure of VVS sufferers and normal subjects have been proposed. Head-up tilt table (HUT) test is the most widely applied investigation for evaluating VVS episodes. Lower body negative pressure (LBNP) has also been used. Enhancement of the orthostatic stress may be done by simultaneous use of both, or with peripheral vasodilators. As to whether such an enhancement is necessary is debatable. Management with increased salt and fluid intake, corticosteroids, beta adrenergic receptor blockers, alpha adrenergic receptor stimulants, selective serotonin reuptake inhibitors, and nitric oxide synthase inhibitors have been tried with variable success.