Purkinje fibers serve a critical role in ensuring the electrical activation of the ventricles, but spontaneous Ca2+ release in the Purkinje system is considered a possible trigger of arrhythmias. To understand the underlying mechanisms, we explored the rate-dependence of Ca2+ transients in single canine Purkinje cells loaded with fluo3 and imaged with a confocal microscope at room temperature. Ca2+ transients were evoked by electrical field stimuli applied at rates ranging from 0.1 to 5 Hz. At slow rates, stimuli induced Ca2+ transients that originated at the cell periphery then spread into the cell interior as a large-amplitude propagating Ca2+ wave. At faster rates, Ca2+ transients were smaller and remained localized to the subsarcolemmal space near the periphery. The origination of Ca2+ transients directly under the cell membrane, with or without an accompanying Ca2+ wave, is consistent with the lack of transverse-tubules in Purkinje cells. In addition, during steady pacing, the amplitude of local Ca2+ transients showed significant and unusual beat-to-beat variability, as neither constant amplitude Ca2+ transients nor stable beat-to-beat alternans were observed (n = 27 cells). The degree of variability, quantified as the coefficient of variation (s.d./mean) increased as the pacing rate increased (at 1 Hz, COV = 0.25 ± 0.12; at 3.3 Hz, COV = 0.53 ± 0.21, n=6 cells). The results indicate that fast pacing increases the instability of sarcoplasmic reticulum Ca2+ release in Purkinje cells, even though the amplitude of Ca2+ release decreases. We speculate that the beat-to-beat variability results from stochastic recruitment of small populations of Ca2+ release channel clusters in the small volume near the cell periphery. These results provide insight into Ca2+ and electrical instability originating in the Purkinje system, a possible precursor of arrhythmia.