BACKGROUND AND OBJECTIVES: Tachycardias have various clinical features according to the heart rate, the left ventricular systolic function, the site of origin and the mechanisms of the tachycardias. The primary purpose of this study was to evaluate the role of the origin site and cycle length on the ventricular tachycardia (VT) hemodynamics. Our secondary purpose was to explore the possible hemodynamic differences between the two common supraventricular tachycardias (SVT). MATERIALS AND METHODS: VT was simulated in 18 dogs that had there chests opened by using ventricular pacing (VP) at 3 different sites: the left ventricular apex (LVA), the right ventricular outflow tract (RVOT), and the right ventricular apex (RVA). The mean arterial pressure (MAP), the mean left atrial pressure (MLAP) and the mean pulmonary artery pressure (MPAP) were monitored during VP. To simulate SVT, the right atrial appendage and the right ventricular basal septum were stimulated at different cycle lengths with different ventriculo-atrial (VA) time intervals in another 11 dogs that had their chests opened. The arterial pressure, the pulmonary capillary wedge pressure and the cardiac output was observed during simulated atrial tachycardia (Group I), AVRT (Group II) and AVNRT (Group III). RESULTS: In the VT study, at the same pacing site as of the VP, the MAP was significantly decreased with the VP, and the deltaMAP was significantly increased as the length of the VP cycle shortened. At the same pacing cycle length of the VP, the deltaMAP was significantly greater at the RVA or RVOT than at the LVA. At the same pacing site of the VP, the MLAP and the deltaMLAP were significantly increased as the VP cycle length shortened. In the SVT study, MAP was highest in Group I and it decreased with the decreasing VA interval, but this was not significant. The systolic arterial pressure was significantly higher in Group II than in Group III. The CO was higher in Group I than in the other two groups, with a significant difference, and the CO decreased with shortening of the VA interval, but this was not significant. CONCLUSION: The above results suggest that in addition to the tachycardia rate, the origin site could be an independent factor of the VT hemodynamics. Episodes of AVRT and AVNRT may have a different hemodynamic impact that probably originates from the different timing of the ventricular and atrial contraction.