High-intensity electric shocks are commonly used in clinical practice to terminate atrial and ventricular fibrillation. Such shocks may induce pores in cellular membranes via electroporation, resulting in transient or permanent electrical and mechanical dysfunction of the heart. While high intensity shocks are used routinely, the tissue and cellular responses to large currents are not fully understood. An improved understanding of electroporation may not only reduce the side effects associated with defibrillation therapy but also may help in designing more effective ways to deliver genes and drugs to target cells. In this paper, we review the available literature on electroporation in the heart and relate the findings to several recent experimental studies performed in our laboratory.