Transient modification of baroreceptor response during tilt-induced vasovagal syncope

Normally, arterial baroreceptors attempt to minimize systemic hypotension by initiating reflex vasoconstriction and tachycardia. However, in the setting of vasovagal syncope (VVS), these usual compensatory mechanisms either fail to be triggered or the response is inadequate. We hypothesized that in VVS prone individuals, arterial baroreceptor response (BRR) is normal under most conditions, but that a transient functional BRR disturbance occurs during an evolving vasovagal faint and may in part account for failure of the usual compensatory response.

This study assessed BRR in the baseline state and again in association with either VVS induced head-up tilt (HUT) or after a prolonged period of upright posture without VVS. To minimize impact on HUT outcome, BRR was estimated non-pharmacologically by measuring blood pressure and heart rate changes, induced when subjects were returned to the supine position after undergoing diagnostic 70 degrees HUT evaluation. Beat to beat heart rate and arterial blood pressure changes were recorded in 13 patients with syncope and another 16 individuals with negative HUT (control group). Baseline BRR was initially evaluated at the end of a 3 min symptom free HUT (HUT#1), and the measurement was repeated after a 45 min duration HUT in the control group or in conjunction with syncope in VVS prone individuals (HUT#2). Baseline BRR did not differ significantly in controls and VVS prone individuals (controls: 3.37+/-1.56, VVS prone: 6.0+/-2.02 ms/mmHg, p=0.27). Further, at the end of 45 min HUT#2, BRR was unaltered from baseline in control subjects (4.92+/-1.36 ms/mmHg, p=0.48), but was markedly reduced from baseline value in individuals who experienced a faint, -3.30+/-0.81 ms/mmHg (p<0.0003 vs baseline).

Compared with individuals who do not manifest VVS during HUT, VVS prone individuals appear to demonstrate functional diminution of baroreceptor responsiveness. This altered response may undermine the normal expected compensatory response to evolving systemic hypotension. The basis for this transient disturbance in baroreceptor responsiveness is currently unknown.