Hemodynamic recovery, atrial natriuretic peptide, and catecholamines during simulated ventricular tachycardia: effects of ventriculoatrial conduction

Abstract

Ventriculoatrial (VA) sequence and neurohumoral responses may be important modulators of hemodynamic recovery during VT. We studied the effects of VA conduction on blood pressure recovery, and levels of atrial natriuretic peptide (ANP), epinephrine, and norepinephrine during simulated VT. After diagnostic coronary angiography, VT was simulated by rapid right ventricular pacing (150 beats/min, 3 mins) in a consecutive series of patients. Whenever the patients demonstrated VA dissociation during ventricular pacing, they were included in the study. After 10 minutes of recovery, a group of nine patients then underwent an additional VA pacing (150 beats/min, 3 mins, VA delay of 150 msec). Intra-arterial blood pressure was continuously monitored, and plasma ANP and catecholamine levels were measured before, during, and after both pacing protocols. The mean arterial pressures declined rapidly by 26% and 30% after initiation of ventricular and VA pacing, respectively. The blood pressure then gradually recovered, the hemodynamic recovery being better during VA pacing. Plasma ANP and catecholamine levels increased toward the end of both pacing periods. The observed increase in ANP concentration was more prominent during VA pacing than ventricular pacing (P < 0.001), whereas catecholamine levels increased similarly. The results show that during simulated VT hemodynamic recovery is partially dependent on VA sequence. The increases in circulating ANP and catecholamines occur too slowly to account for the rapid changes in blood pressures observed after initiation of simulated VT. Therefore, other mechanisms, such as reflex stimulation of the sympathoadrenergic nervous system, must be involved, too. ANP release increases when atrial contraction frequency increases, but the exact determinants for this release remain unknown.