Reflex Control of Sympathetic Activity During Simulated Ventricular Tachycardia in Humans

Abstract

Background-Ventricular tachyarrhythmias present a unique set of stimuli to arterial and cardiopulmonary baroreceptors by increasing cardiac filling pressures and decreasing arterial pressure. The net effect on the control of sympathetic nerve activity (SNA) in humans is unknown. The purpose of this study was to determine the relative roles of cardiopulmonary and arterial baroreceptors in controlling SNA and arterial pressure during ventricular pacing in humans. Methods and Results-Two experiments were performed in which SNA and hemodynamic responses to ventricular pacing were compared with nitroprusside infusion (NTP) in 12 patients and studied with and without head-up tilt or phenylephrine to normalize the stimuli to either the arterial or cardiopulmonary baroreceptors in 9 patients. In experiment 1, the slope of the relation between SNA and mean arterial pressure was greater during NTP (Ϫ4.7Ϯ1.4 U/mm Hg) than during ventricular pacing (Ϫ3.4Ϯ1.1 U/mm Hg). Comparison of NTP doses and ventricular pacing rates that produced comparable hypotension showed that SNA increased more during NTP (Pϭ0.03). In experiment 2, normalization of arterial pressure during pacing resulted in SNA decreasing below baseline (PϽ0.05), whereas normalization of cardiac filling pressure resulted in a greater increase in SNA than pacing alone (212Ϯ35% versus 189Ϯ37%, Pϭ0.04). Conclusions-These data demonstrate that in humans arterial baroreflex control predominates in mediating sympathoexcitation during ventricular tachyarrhythmias and that cardiopulmonary baroreceptors contribute significant inhibitory modulation. (Circulation. 1999;100:628-634.)

Baroreflex Gain Predicts Blood Pressure Recovery During Simulated Ventricular Tachycardia in Humans

“…We recently showed that SNA response during VP was mediated primarily by the arterial baroreflex and that it was modulated by input from cardiopulmonary baroreceptors. 3 Our findings are consistent with those of Landolina et al 14 : baroreflex gain was markedly reduced in patients with poorly tolerated VP, suggesting that baroreflex gain is an important determinant of BP recovery during VP. In our study, baroreflex-SNA gain was a better predictor than baroreflex-HR gain.…”

“…4,17 Nevertheless, studies in both dogs and humans have shown that in patients with the substrate for VT, arterial baroreflexes tend to predominate in the control of SNA. 3,4 The present study extends these findings to show that arterial baroreflex gain is a predictor of hemodynamic outcome during ventricular tachyarrhythmias.…”

“…Also, the pattern of sympathetic bursts became more irregular, although it tended to fluctuate with variations in arterial pressure as previously observed. 3,5 …”

“…3 Moreover, previous studies in dogs also suggest that relative impairment of cardiopulmonary and/or arterial baroreceptors may affect the net hemodynamic response to ventricular tachyarrhythmias. 4,17 Nevertheless, studies in both dogs and humans have shown that in patients with the substrate for VT, arterial baroreflexes tend to predominate in the control of SNA.…”

“…This response is mediated by the net effects of arterial and cardiopulmonary baroreceptors. 3,4 Usually, sympathetic nerve activity (SNA) increases during sustained VT and is mediated primarily by the arterial baroreflex response to hypotension. The magnitude of this sympathoexcitatory response appears to contribute to the net hemodynamic outcome.…”