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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
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 effect of this stress is to reduce the rate of blood flow returning to the heart and consequently to reduce cardiac output. Blood pressure is normally well controlled mainly by arterial baroreceptors, which because of their exquisite sensitivity to changes in pulsatility,3 are able to induce vasoconstriction and tachycardia without a fall in mean …