During tachyarrhythmias, central venous pressures increases while arterial blood pressure (BP) decreases. The result is mixed messages to the central nervous system. On one hand, the unloading of the arterial baroreceptors results in reflex tachycardia and an increase in sympathetic nerve activity (SNA). On the other hand, the increase in filling pressure and thus the activation of the cardiopulmonary baroreceptors result in reflex bradycardia and sympathoinhibition. The investigators have previously shown that during supraventricular and ventricular tachycardia, arterial baroreflex gain (BRG) predominates with minimal contribution from the cardiopulmonary BRG. In addition, the investigators found that arterial BRG directly correlates with BP recovery following tachycardia termination. The roles of the arterial and cardiopulmonary BRGs during ventricular fibrillation (VF) however, remain unknown. Furthermore, the role of the arterial BRG in determining 1) BP recovery following VF induction and 2) the frequency of ventricular tachycardia (VT)/VF events in patients undergoing implantation of an implantable cardioverter/defibrillator (ICD) remain unknown. Analysis of the changes in sinus node cycle length during VF inductions in patients undergoing the implantation of a dual chamber or triple chamber ICD, provide a unique opportunity at looking at the autonomic changes that accompany VF.