Abstract
IntroductionNeurally-mediated syncope (NMS) is defined as a transient loss of consciousness due to an abrupt and intermittent drop in blood pressure (BP). ObjectivesThis study describes the putative pathophysiological mechanisms giving rise to NMS, the role of baroreflex (BR), and the interaction of its main haemodynamic variables: heart rate (HR) and BP. DevelopmentEpisodic dysregulation affects control over the haemodynamic variables (HR and BP) mediated by baroreflex mechanisms. During active standing, individuals experience a profound transient drop in systolic BP due to the effect of gravity on the column of blood and probably also because of reflex vasodilation. Abnormalities in the BR in NMS could be due to a more profound drop in BP upon standing, or to delayed or incomplete vasoconstriction resulting from inhibited or delayed sympathetic activity. ConclusionsSympathetic hyperactivity is present in patients with NMS at rest and before syncope. During active standing or passive tilting, excessive tachycardia may be followed by bradycardia and profound hypotension. Recovery of systolic BP is delayed or incomplete.
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