In normal cardiac function, orderly activation of the heart is facilitated by the Purkinje system (PS), a specialized network of fast-conducting fibers that lines the ventricles. Its role during ventricular defibrillation remains unelucidated. Physical characteristics of the PS make it a poor candidate for direct electrical observation using contemporary experimental techniques. This study uses a computer modeling approach to assess contributions by the PS to the response to electrical stimulation. Normal sinus rhythm was simulated and epicardial breakthrough sites were distributed in a manner consistent with experimental results. Defibrillation shocks of several strengths and orientations were applied to quiescent ventricles, with and without PS, and electrical activation was analyzed. All shocks induced local polarizations in PS branches parallel to the field, which led to the rapid spread of excitation through the network. This produced early activations at myocardial sites where tissue was unexcited by the shock and coupled to the PS. Shocks along the apico-basal axis of the heart resulted in a significant abbreviation of activation time when the PS was present; these shocks are of particular interest because the fields generated by internal cardioverter defibrillators tend to have a strong component in the same direction. The extent of PS-induced changes, both temporal and spatial, was constrained by the amount of shock-activated myocardium. Increasing field strength decreased the transmission delay between PS and ventricular tissue at Purkinje-myocardial junctions (PMJs), but this did not have a major effect on the organ-level response. Weaker shocks directly affect a smaller volume of myocardial tissue but easily excite the PS, which makes the PS contribution to far field excitation more substantial than for stronger shocks.