Prior studies in dogs with normal hearts have demonstrated that lidocaine increases but procainamide does not change the energy required for successful defibrillation. Because many postinfarct patients receiving implantable cardioverter defibrillator devices require adjunctive antiarrhythmic therapy, we have studied the effects of lidocaine and procainamide on the relationship between delivered voltage and defibrillation success in mongrel dogs 21 +/- 3 days following ligation of the left anterior descending and first diagonal coronary arteries. Internal defibrillation testing using a patch-patch electrode configuration was performed before and during the administration of saline controls (n = 10), lidocaine (n = 10) and procainamide (n = 10). The mean infarct size as determined by staining with tetrazolium was 13.4% +/- 8.3% of right and left ventricles, and did not differ significantly between groups. The 50% effective defibrillation (ED50) voltage increased with infusions of saline (16% +/- 15%), lidocaine (40% +/- 22%), and procainamide (13% +/- 15%) and the ED50 energy increased 41% +/- 44%, 104% +/- 62%, and 35% +/- 36%, respectively. However, the increase in ED50 voltages and energies were significantly greater in animals receiving lidocaine compared to those receiving either saline control or procainamide (P < 0.01). There were trends toward change of hemodynamic parameters in all animals following baseline defibrillation testing; stroke volume declined 21% +/- 16%; and mean pulmonary artery and aortic pressure increased by 22% +/- 25% and 11% +/- 15%, respectively. In conclusion, unlike our previous studies in dogs with normal hearts, in this model hemodynamic deterioration occurred with repeated fibrillation and defibrillation, and defibrillation voltage requirements increased in the control series. Taking into consideration the increase in defibrillation voltage requirements over the duration of the experiments, lidocaine increases and procainamide does not change ED50; thus, their effects are similar in normal and infarcted canine hearts.