Monophasic ascending and descending ramp (AR and DR) waveforms are known to have significantly different defibrillation thresholds. We hypothesized that this difference arises due to differences in mechanisms of arrhythmia induction for the two waveforms. Methods and Results: Rabbit hearts (n=10) were Langendorff-perfused, AR and DR waveforms (7, 20, 40 ms) were randomly delivered from two line electrodes placed 10 mm apart on the anterior ventricular epicardium. We optically mapped cellular responses to shocks of various strengths (5, 10 and 20 V/cm) and coupling intervals (CI = 120, 180, and 300 ms). Optical mapping revealed that maximum virtual electrode polarization (VEP) was reached at significantly different times for AR and DR of the same duration (p<0.05) for all tested CIs. As a result, VEP for AR were stronger than that for DR at the end of the shock. Post-shock break excitation resulting from AR generated faster propagation and typically could not form reentry. In contrast, partially dissipated VEP resulting from DR generated slower propagation; the wavefront was able to propagate into de-excited tissue and thus formed a shock-induced reentry circuit. Therefore, for the same delivered energy, AR was less proarrhythmic as compared to DR. An active bidomain model was used to confirm the electrophysiological results. Conclusion: VEP hypothesis explains differences in vulnerability associated with monophasic AR and DR waveforms, and by extension, superior defibrillation efficacy of AR waveform compared to DR waveform.