EDITORIAL

Syncope: what is the trigger?

R Hainsworth

Correspondence to:
Correspondence to:
Professor Roger Hainsworth, Institute for Cardiovascular Research, University of Leeds, Leeds, LS2 9JT, UK;
medrh@leeds.ac.uk

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Although a syncopal attack is frequently preceded by prodromal symptoms, sometimes the onset can be so abrupt that there is no warning at all. The switch in autonomic responses responsible for such an attack is quite rapid and dramatic, but the trigger for this remains one of the unresolved mysteries in cardiovascular physiology

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Keywords: vasovagal reaction; vasodilatation; cerebral blood flow

The first 150 words of the full text of this article appear below.

Neurally mediated, or vasovagal, syncope is characterised by an abrupt fall in blood pressure resulting from widespread vasodilatation caused by a sudden cessation of sympathetic vasoconstrictor activity. There is no evidence in humans for an active neurally mediated vasodilatation, although there may be an element of reactive hyperaemia as an intense vasoconstriction suddenly stops.¹ In addition to vasodilatation there is usually some cardiac slowing and this may be a small reduction in peak heart rate or, occasionally, prolonged asystole. The bradycardia is of less significance than the vasodilation² and preventing it by pacing does not usually prevent or even delay the onset of syncope. Vasovagal syncope usually occurs during orthostatic stress when not only is there pooling of something like 500–700 ml of blood in dependent vessels, but there is a progressive loss of a similar volume of plasma through dependent capillaries caused by the increased hydrostatic pressure. The overall . . . [Full text of this article]

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