Spontaneous premature atrial systolic beats provoked by test stimulation of the atria were examined in groups of dogs anesthetized with 1.0, 1.5 and 2.0 MAC halothane or enflurane. Data for halothane effects on the atrial and AV nodal refractory periods and the AV nodal conduction time of premature atrial test beats are provided and compared with corresponding data previously obtained by the authors for enflurane. The results indicate that the probability of spontaneous premature atrial beats occurring in response to test atrial stimulation was: significantly increased in the dogs anesthetized with halothane as opposed to enflurane; significantly decreased by increasing MAC level of either halothane or enflurane; significantly altered by the basic paced atrial rate with halothane but not with enflurane. Increasing the depth of anesthesia with enflurane, but not with halothane, prolonged the atrial effective refractory period. Increases of both agents prolonged the AV nodal functional refractory period. AV nodal fatigue was similarly affected by both agents. Increasing the concentration of enflurane, but not halothane, prolonged AV nodal minimum conduction time. Increased anesthetic depth with both agents, but significantly more so with halothane, prolonged AV nodal interval-related conductivity. Changes in basic atrial paced rate with halothane, but not with enflurane, altered AV nodal interval-related conductivity. Critical alterations in atrial and AV nodal conduction are believed necessary for supraventricular arrhythmias due to atrial or AV nodal re-entry. The different effects of halothane and enflurane on supraventricular conduction may in part explain the authors' observation that an experimental atrial arrhythmia occurred more frequently with halothane than with enflurane.