Electrical ablation techniques (ECT) have had limited success in achieving control of arrhythmias originating in the right atrial free wall (RAFW). To ascertain determinants for successful ECT, we studied the clinical and cellular electrophysiologic effects of electrical ablation of the RAFW. After performing electrical ablation of the RAFW in 12 beagle puppies, the following studies were performed: Holter monitoring first 24 hours (eight puppies), and 11 weeks later (four puppies); clinical electrophysiologic study (four puppies); and microelectrode study (ME) (eight puppies). Arrhythmias (AR) and conduction disturbances (CD) frequently occurred immediately following ECT: ventricular tachycardia (VT) (seven puppies), junctional tachycardia (one puppy), and asystole or complete AV block (AVB) (four puppies). Holter monitoring during the first 24 hours after ECT revealed VT (four puppies), frequent ventricular premature depolarizations (one puppy), and type 2 second-degree AVB (four puppies). AR were rarely seen late after ECT. During clinical EP study 11 weeks after ablation, atrial fibrillation was induced in three of four puppies; none had AR prior to ECT. Early ME study revealed a nonhomogeneous atrial infarct--a central zone of "dead" cells surrounded by peripheral islands of depressed cellular activity. Cells with normal action potential characteristics were noted in between. We conclude that Electrical ablation of the RAFW is associated with a high incidence of early AR and CD. Because of the nonhomogeneous nature of tissue injury produced during ECT, careful atrial mapping is critically important. Local regions of conduction delay and block may provide a substrate for the late development of atrial arrhythmias.