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Vasovagal syncope: an enigma.

Syncope is a common clinical problem affecting 3.5% of the general population. About 40% of cases remain undiagnosed and 30% experience recurrent episodes. The article presents an update on the etiopathogenesis and theories of syncope. The pathophysiology of syncope remains elusive. Lewis introduced the term "vasovagal" implying therein that both vasodilatation and bradycardia were involved in the response. Individuals susceptible are unable to maintain adaptive neurocardiovascular responses to upright posture for prolonged periods of time. A complex hemodynamic response develops, with marked hypotension, bradycardia and a loss of consciousness. The "empty ventricle theory", first proposed by Sharpey - Schafer, widely accepted for several years, has been challenged and various other aspects of the vasovagal response have now been studied and implicated in contributing to the episode of unconsciousness. These include baroreflex dysfunction, neuro - endocrine responses, role of respiration and cerebrovascular dysfunction. An episode of syncope represents an episode of unconsciousness. Even a single episode of unconsciousness in the present day lifestyle is a source of distress to a patient, warranting a workup and diagnosis. The etiopathogenesis of the simple faint is complex and we may well be dealing with a constellation of responses and a more detailed classification than hitherto imagined.