Strong electrical shocks can cause focal arrhythmias, the mechanism of which is not well known. Strong shocks have been shown to produce diastolic Ca i2+ increase, which may initiate focal arrhythmias via spontaneous Ca i2+ rise (SCR), activation of inward Na +/Ca 2+ exchange current (I NCX), and rise in membrane potential (V m). It can be hypothesized that this mechanism is responsible for generation of shock-induced arrhythmias. The purpose of this study was to examine the roles of SCRs and I NCX in shock-induced arrhythmias. The occurrence of SCRs during shock-induced arrhythmias was assessed in neonatal rat myocyte cultures. Simultaneous V m-Ca i2+ optical mapping at arrhythmia source demonstrated that V m upstrokes always preceded Ca i2+ transients, and V m-Ca i2+ delays were not different between arrhythmic and paced beats (5.5 ± 0.9 and 5.7 ± 0.4 ms, respectively, P =.5). Shocks caused gradual rise of diastolic Ca i2+ consistent with membrane electroporation but no significant Ca i2+ rises immediately before V m upstrokes. Application of the Ca i2+ chelator BAPTA-AM (10 μmol/L) decreased the duration of shock-induced arrhythmias whereas application of the I NCX inhibitor KB-R7943 (2 μmol/L) increased it, indicating that, despite the absence of SCRs, changes in Ca i2+ affected arrhythmias. It is hypothesized that this effect is mediated by Ca i2+ inhibition of outward I K1 current and destabilization of resting V m. The possible role of I K1 was supported by application of the I K1 inhibitor BaCl 2 (0.2 mmol/L), which increased the arrhythmia duration. Shock-induced arrhythmias in neonatal rat myocyte monolayers are not caused by SCRs and inward I NCX. However, these arrhythmias depend on Ca i2+ changes, possibly via Ca i2+-dependent modulation of outward I K1 current.