Introduction: The reason for the increased defibrillation efficacy of biphasic shocks over monophasic shock is not definitely known. Methods and Results: In six anesthetized pigs, we mapped the epicardium after transvenous defibrillation shocks to compare the activation patterns following successful biphasic shocks with unsuccessful monophasic shocks of the same voltage. The heart was exposed and a 510-electrode sock with approximately 4-mm interelectrode spacing was pulled over the entire ventricular epicardium and sutured to the pericardium. Defibrillation catheters were placed in the right ventricular apex and in the superior vena cava. Paired monophasic 12 msec and biphasic 6/6 msec defibrillation shocks were given using an up-down protocol to keep shock strength between the defibrillation thresholds for the two waveforms so that the biphasic shock was successful while the monophasic shock was not. Activation fronts immediately following 60 paired shocks were recorded and analyzed by animated maps of the first derivative of the electrograms. The ventricles were divided into apical (I), middle (II), and basal (III) thirds, and early sites, i.e., the sites from which activation fronts first appeared on the epicardium following the shock, were grouped according to their location. Postshock intervals, i.e., the time from the shock until earliest epicardial activation occurred, were also determined. No ectopic activation fronts followed the shock in 20 biphasic episodes. In the other 40 paired episodes, the number of early sites was smaller after biphasic shocks than after monophasic shocks [monophasic: 198 (total), 3.3 ± 0.9 (mean ± SD) per shock episode; biphasic: 67, 1.1 ± 1.0, P < 0.05]. For biphasic but not monophasic shocks, early sites were less likely to arise from the middle (II) and basal (III) thirds than from the apical third (I) [monophasic: I: 84 (42%), II: 68 (34%), III: 46 (23%); biphasic: I: 49 (73%), II: 10 (15%), III: 8 (12%), P < 0.05]. Postshock intervals were significantly shorter for monophasic shocks (54 ± 14 msec) than for biphasic shocks (75 ± 23 msec, P < 0.05). Conclusion: The decreased number of activation fronts and the longer delay following the shock for the earliest epicardial appearance of those activation fronts that do occur may be responsible for the increased defibrillation efficacy for biphasic shocks.