In order to investigate the influence of the effective refractory period on spontaneous ventricular defibrillation, isolated rat hearts were perfused with Krebs-Henseleit solution containing 0.5, 2.7 and 5.1 mM calcium. After measuring the fibrillation threshold at spontaneous rate (SR), ventricular fibrillation (VF) was induced during basic ventricular pacing of 110% SR, or the highest rate permitting 1:1 electromechanical coupling. The VF threshold was significantly reduced from 13.6 +/- 3.5 to 7.9 +/- 5.3 and 5.1 +/- 3.4 mA at 0.5, 2.7 and 5.1 mM Ca++ concentrations, respectively. The incidence of spontaneous recovery from VF, induced during basic pacing, was 100%, 83% and 50% at calcium concentrations of 0.5, 2.7 and 5.1 mM, respectively, (p less than 0.01 for the incidences at 0.5 mM versus 5.1 mM Ca++). The incidence of spontaneous defibrillation decreased when the hearts were driven rapidly, with spontaneous recovery rates of 92%, 58% and 0% (p less than 0.0001] for corresponding increases in Ca++ concentration. Induced ventricular fibrillation of fine morphology was frequently observed at 5.1 mM Ca++. It appears that progressive impairment of spontaneous defibrillation is caused by an increase in calcium concentration, this effect being more pronounced at high ventricular rates. Variations in the effective refractory period, caused by alterations in extracellular calcium concentration and differences in intracellular Ca++ accumulation, may account for the above results.