HEMODYNAMIC RECOVERY, ATRIAL NATRIURETIC PEP TIDE, AND CATECHOLAMINESDURING SIMULATED VENTRICULAR-TACHYCARDIA - EFFECTS OF VENTRICULOATRIAL CONDUCTION

Ventriculoatrial (VA) sequence and neurohumoral responses may be impor tant modulators of hemodynamic recovery during VT. We studied the effe cts of VA conduction on blood pressure recovery, and levels of atrial natriuretic peptide (ANP), epinephrine, and norepinephrine during simu lated VT. After diagnostic coronary angiography, VT was simulated by r apid right ventricular pacing (150 beats/min, 3 mins) in a consecutive series of patients. Whenever the patients demonstrated VA dissociatio n during ventricular pacing they were included in the study. After 10 minutes of recovery, a group of nine patients then underwent an additi onal VA pacing (150 beats/min, 3 mins, VA delay of 150 msec). Intra-ar terial blood pressure was continuously monitored and plasma ANP and ca techolamine 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 blo od pressure then gradually recovered, the hemodynamic recovery being b etter during VA pacing. Plasma ANP and catecholamine levels increased toward the end of both pacing periods. The observed increase in ANP co ncentration was more prominent during VA pacing than ventricular pacin g (P < 0.001), whereas catecholamine levels increased similarly. The r esults show that during simulated VT hemodynamic recovery is partially dependent on VA sequence. The increases in circulating ANP and catech olamines occur too slowly to account for the rapid changes in blood pr essures observed after initiation of simulated VT. Therefore, other me chanisms, such as reflex stimulation of the sympathoadrenergic nervous system, must be involved, too. ANP release increases when atrial cont raction frequency increases, but the exact determinants for this relea se remain unknown.