In general, pulse pressure of a VPC depends on its prematurity and the site of origin. The pulse pressure of a VPC with a short coupling interval or originating from the left ventricle tends to be smaller. However, the hemodynamic change of a VPC originating from the right ventricular outflow tract (RVOT) is not well elucidated. In addition to their prematurity and the site of the origin of VPCs, the left ventricular filling profile (Ei/Ai ratio) during preceding control beats may affect the occurrence of a subsequent pulse deficit. The purpose of this study is to evaluate the hemodynamic change of different coupling intervals of VPCs originating from the RVOT. Furthermore, this study evaluates whether the left ventricular filling profile during preceding control beats significantly affects the occurrence of pulse deficits by VPCs.

In 12 open-chest dogs anesthetized with a -chloralose, sinus node crushing was done, and then a single bipolar ventricular pacing using sutured epicardial electrodes was done at 3 different sites: left ventricular apex (LVA), right ventricular apex (RVA), RVOT. At each site, a single bipolar pacing was done with a different coupling interval: 500 msec, 450 msec, 400 msec, 350 msec, 300 msec. During the production of VPCs, the mitral filling flow velocity and aortic TVI (time-velocity integral) using pulsed wave Doppler echocardiography, the femoral arterial pressure, the pulmonary arterial pressure, the electrocardiogram, and the intracardiac electrocardiogram were simultaneously recorded.

The arterial pressure during VPC with a short coupling interval was significantly smaller regardless of the site of origin (p<0.05). The arterial pressure with VPCs originating from the RVOT was significantly more reduced than those from the RVA at a same coupling interval (p<0.05). However, the arterial pressure with originating from the LVA was insignificantly reduced than those from the RVOT. The pulmonary arterial pressure with originating from the RVOT was significantly reduced more than those from the LVA at a same coupling interval, except at the coupling interval of 500 msec (p<0.05). However, the pulmonary arterial pressure with VPCs originating from the RVA was insignificantly reduced than those from the RVOT. The aortic TVI during VPCs originating from the LVA was significantly reduced than those from the RVA or the RVOT at a same coupling interval (p<0.05). However, when the aortic TVI during VPCs originating from the RVOT was compared to that during VPCs from RVA, the former was significantly reduced at certain coupling interval (450 msec, p<0.05). A significant positive correlation was observed between the Ei/Ai ratio of preceding control beats and the pulse deficit coupling intervals during VPCs (p<0.05).

The above results show that the origin of the site and the coupling interval of VPCs play a major role in determining hemodynamic outcomes during the occurrence of VPCs. The hemodynamic changes during VPCs originating from the RVOT seem to be similar with those during VPCs originating from the RVA. Furthermore, there is a positive correlation between the left ventricular filling pattern (Ei/Ai ratio) of preceding sinus beats and the pulse deficit coupling intervals of VPCs.