Fifteen patients without sinoatrial (SA) or atrioventricular (AV) node dysfunction underwent electrophysiologic study (EPS) before and after intravenous diltiazem: 0.20 mg/kg bolus followed by 0.0007 mg/kg/min infusion (seven patients) or 0.25 mg/kg bolus followed by 0.0012 mg/kg/min infusion (eight patients). In six patients intravenous digoxin (0.018 mg/kg) was given and 45 minutes later EPS was repeated while the diltiazem infusion continued. Diltiazem prolonged sinus cycle length (+7%, p less than 0.01), lengthened AH conduction time (+22% in constant rate atrial paced rhythm, p less than 0.001), prolonged AV node functional and effective refractory periods (+6%, p less than 0.01 and +16%, p less than 0.05, respectively), lengthened AV node Wenckebach cycle length (+13%, p less than 0.001), shortened atrial functional refractory period (-3%, p less than 0.05), and reduced mean arterial pressure (-8%, p less than 0.005 in constant rate atrial paced rhythm). Subsequently, intravenous digoxin further prolonged sinus cycle length (+12%, p less than 0.05), AH conduction time (+17%, p less than 0.05), AV node Wenckebach cycle length (+9%, p less than 0.05), and AV node functional refractory period (+7%, p less than 0.05), shortened atrial effective refractory period (-7%, p less than 0.05) and ventricular effective refractory period (-6%, p less than 0.05), and increased systolic arterial pressure (+6%, p less than 0.05). Diltiazem and digoxin have additive depressant effects on SA and AV node function without significant adverse effects.