Strong electrical shocks can induce arrhythmias, which might explain why shocks fail to defibrillate. In this work, the localization of arrhythmia source and the relationship with local changes of transmembrane potential (V(m)) were determined in geometrically defined cell cultures using optical mapping technique. Uniform-field shocks with strength (E) of 10 to 50 V/cm were applied across cell strands with width of 0.2 and 0.8 mm. The threshold for arrhythmia induction was dependent on the strand width: in the 0.8- and 0.2-mm strands, arrhythmias were induced at E>/=20.6+/-1.8 V/cm (n=8) and E>/=30.3+/-1.8 V/cm (n=8), respectively. At the same shock strength, the arrhythmia rate and duration were larger in the wider strands. During shocks that induced arrhythmias, the V(m) waveforms on the anodal side revealed a positive V(m) shift that followed the initial large hyperpolarization and postshock elevation of the diastolic V(m). These V(m) changes were absent during failed shocks. To determine the localization of the arrhythmia source, arrhythmias were induced in narrow cell strands containing regions of local expansion. Optical mapping of the first extrabeat with a coupling interval of 315+/-60 ms revealed that in the majority of cases (9 out of 13) the source of arrhythmias was localized in the areas of shock-induced hyperpolarization. Thus, (1) induction of postshock arrhythmias, their rate, and their duration strongly depend on the tissue structure; (2) arrhythmia induction coincides with the appearance of a positive V(m) shift in the areas of hyperpolarization; and (3) the source of postshock arrhythmias is located in the areas of shock-induced hyperpolarization.