Optical mapping studies have suggested that intracellular Ca²⁺ and T-wave alternans are linked through underlying alternations in Ca²⁺ cycling-inducing oscillations in action potential duration through Ca²⁺-sensitive conductances. However, these studies cannot measure single-cell behavior; therefore, the Ca²⁺ cycling heterogeneities within microscopic ventricular regions are unknown. The goal of this study was to measure cellular activity in intact myocardium during rapid pacing and arrhythmias. We used single-photon laser-scanning confocal microscopy to measure Ca²⁺ signaling in individual myocytes of intact rat myocardium during rapid pacing and during pacing-induced ventricular arrhythmias. At low rates, all myocytes demonstrate Ca²⁺ alternans that is synchronized but whose magnitude varies depending on recovery kinetics of Ca²⁺ cycling for each individual myocyte. As rate increases, some cells reverse alternans phase, giving a dyssynchronous activation pattern, even in adjoining myocytes. Increased pacing rate also induces subcellular alternans where Ca²⁺ alternates out of phase with different regions within the same cell. These forms of heterogeneous Ca²⁺ signaling also occurred during pacing-induced ventricular tachycardia. Our results demonstrate highly nonuniform Ca²⁺ signaling among and within individual myocytes in intact heart during rapid pacing and arrhythmias. Thus, certain pathophysiological conditions that alter Ca²⁺ cycling kinetics, such as heart failure, might promote ventricular arrhythmias by exaggerating these cellular heterogeneities in Ca²⁺ signaling.