Hemodynamic Responses to Different Ventricular Pacing Sites and Pacing Rates in Dog

Kim, Hee Yeol; Kim, Jae Hyung; Rho, Tai Ho; Kim, Chong Jin; Jin, Seung Won; Yoo, Ki Dong; Lee, Man Young; Chae, Jang Seong; Hong, Soon Jo; Choi, Kyu Bo

Abstract

BACKGROUND
The hemodynamic effects of an episode of ventricular tachycardia (VT) may vary from mild decrease in blood pressure to sustained hypotension, collapse, and death. Little is known about the factors responsible for these diverse effects. Ventricular function, vasomotor tone, and tachycardia cycle length could be major determinants of variable hemodynamic responses to VT. The site of origin was found to be a factor affecting pulse pressure even in an isolated ventricular premature contraction. However, the role of origin site in hemodynamics of VT is not yet elucidated. The purposes of this study were to evaluate the effects of VT origin site and VT cycle length to their hemodynamic changes. And we also have assessed the role of cardiac autonomic receptor activation in hemodynamic recovery during and immediate after VT.
METHODS
In 18 open chest dogs anesthetized with chloralose, bipolar ventricular pacing (VP) was performed using sutured epicardial electrodes at 3 different sites ; left ventricular apex (LVA), right ventricular outflow tract (RVOT), and right ventricular apex (RVA). At each site, VP was repeated for 60 seconds at 3 different rates; 1.75X, 2X, and 2.25X of baseline heart rate (BHR). Mean arterial pressure (MAP), mean left atrial pressure (MLAP) and mean pulmonary artery pressure (MPAP) were monitored during VP. deltaMAP was defined as the difference between the baseline MAP and lowest MAP during VP. deltaMLAP was defined as the difference between highest MLAP during VP and baseline MLAP. Cardiac vagal and beta-adrenoreceptor blockades were achieved by intravenous bolus administration of propranolol (1 mg/kg and then 1 mg/kg/hr) and atropine (0.5 mg/kg and then 0.5 mg/kg/hr). After cardiac autonomic blockade, VP was repeated at 2X of baseline heart rate for 60 seconds at each site.
RESULTS
Baseline MAP, MLAP, and MPAP were 101+/-8.1 mmHg, 0.3+/-0.41 mmHg, and 10+/-2.4 mmHg, respectively. At the same pacing site of VP, MAP was decreased significantly with VP and deltaMAP was increased significantly as VP cycle length shortened (all P<0.001). At the same pacing cycle length of VP, deltaMAP was significantly greater at RVA or RVOT than LVA: LVA vs RVOT ; all P<0.001 at 3 different rates, LVA vs RVA ; P<0.05 (1.75X & 2X of BHR), P<0.001 (2.25X of BHR). But there was no significant difference in deltaMAP between RVA and RVOT. At the same pacing site of VP, MLAP and deltaMLAP were increased significantly as VP cycle length shortened (all P<0.01), but at the same cycle length of VP, there was no significant differences in deltaMLAP at 3 different VP sites. Ventricular pacing after autonomic blockade induced a greater increase in deltaMAP and deltaMLAP compared to controls (all P<0.01 at 3 pacing sites). And cardiac autonomic blockade also resulted in significant blunting of recovery of MAP during VP compared to controls.
CONCLUSION
Above results showed that pacing cycle length plays a major role in determining the hemodynamic outcomes during ventricular pacing, and that the site of origin could be an independent factor of ventricular tachycardia hemodynamics. And also modulation of tone of the adrenergic nervous system is essentially required for the hemodynamic recovery during ventricular tachycardia.