Neurocardiogenic syncope.

Most physiologic reflex mechanisms subserve obvious and logical purposes. For example, the arterial baroreflex responds to hypotension by eliciting tachycardia and vasoconstriction, thus increasing cardiac output and raising blood pressure. The raison d'etre for a reflex such as the Bezold-Jarisch is not immediately apparent. Consider, however, the predominant stimulus for the Bezold-Jarisch reflex in the clinical context, namely, rapid forceful ventricular contraction around a relatively empty chamber. Allowing such a situation to continue would be counterproductive. Decreased diastolic filling time, regardless of ventricular contractility, would not permit any improvement in forward cardiac output and hence lead to even further hypotension and thus increasing tachycardia and adrenergic drive to the heart. The cardiac inhibitory reflex acts as a "safety valve," so to speak, slowing the heart rate, increasing diastolic filling, and decreasing afterload. This would be beneficial in myocardial infarction and aortic stenosis. In some persons, however, the reflex may be potentiated, thus predisposing to neurally mediated syncope with relatively minor provocation. We have attempted to explore the role of the cardiac inhibitory reflex in syncope associated with several clinical situations. The advent of direct measurements of sympathetic activity by microneurography, together with the availability of provocative testing such as upright tilt and programmed electrical cardiac stimulation, has provided much new insight but has also given rise to a host of additional questions. Mechanisms other than the Bezold-Jarisch reflex may be implicated. Induction of vasodepressor syncope in heart transplant recipients, as well as the association of bradycardia and syncope with partial seizures, provides some evidence that left ventricular mechanoreceptors may not be the exclusive afferent trigger for syncope and that central mechanisms may be implicated. The study of biochemical mediators such as nitric oxide and serotonin, acting perhaps at a central level, holds promise for an increased understanding of basic cardiovascular physiology, as well as for effective therapy for neurally mediated syncope. These biochemical mediators may in and of themselves give rise to neurogenic syncope or may act to increase the gain of the cardiac inhibitory reflex at a central level.