Why the study?
Does baseline arterial pressure affect sympathoexcitatory responses to ventricular premature beats in patients undergoing electrophysiological testing?
Does baseline arterial pressure affect sympathoexcitatory responses to ventricular premature beats in patients undergoing electrophysiological testing?
Sympathoexcitation evoked by ventricular dysrhythmias is importantly determined by prevailing arterial pressure, which may influence hemodynamic and electrophysiological stability.
Arterial pressure may modulate sympathetic responses to premature beats during EP testing; leaves open effects on stability and requires prospective validation.
The seconds to minutes before sudden cardiac death are characterized by fluctuations of arterial pressure, cardiac rhythm, and probably sympathetic nerve activity. We explored the interrelations among these factors in seven patients undergoing clinical electrophysiological testing. We measured muscle sympathetic nerve activity (SNA) and arterial pressure responses to ventricular premature beats induced throughout the cardiac cycle under three conditions: 1) lowered arterial pressure and elevated SNA produced by intravenous nitroprusside, 2) baseline arterial pressure and SNA during saline infusion, and 3) elevated arterial pressure and decreased SNA activity produced by intravenous phenylephrine. Sympathetic responses to premature beats were inversely related to diastolic pressure. The magnitude of the sympathetic response was directly related to the prevailing arterial pressure and inversely related to baseline SNA. These data demonstrate that sympathoexcitation evoked by ventricular dysrhythmias is determined importantly by the prevailing arterial pressure and possibly by the background R-R interval and level of sympathetic activity. This effect may influence hemodynamic and electrophysiological stability during dysrhythmias.
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Smith et al. (1995) studied this question.
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