In this study, we present an innovative mathematical modeling approach that allows detailed characterization of Ca²⁺ movement within the three-dimensional volume of an atrial myocyte. Essential aspects of the model are the geometrically realistic representation of Ca²⁺ release sites and physiological Ca²⁺ flux parameters, coupled with a computationally inexpensive framework. By translating nonlinear Ca²⁺ excitability into threshold dynamics, we avoid the computationally demanding time stepping of the partial differential equations that are often used to model Ca²⁺ transport. Our approach successfully reproduces key features of atrial myocyte Ca²⁺ signaling observed using confocal imaging. In particular, the model displays the centripetal Ca²⁺ waves that occur within atrial myocytes during excitation–contraction coupling, and the effect of positive inotropic stimulation on the spatial profile of the Ca²⁺ signals. Beyond this validation of the model, our simulation reveals unexpected observations about the spread of Ca²⁺ within an atrial myocyte. In particular, the model describes the movement of Ca²⁺ between ryanodine receptor clusters within a specific z disk of an atrial myocyte. Furthermore, we demonstrate that altering the strength of Ca²⁺ release, ryanodine receptor refractoriness, the magnitude of initiating stimulus, or the introduction of stochastic Ca²⁺ channel activity can cause the nucleation of proarrhythmic traveling Ca²⁺ waves. The model provides clinically relevant insights into the initiation and propagation of subcellular Ca²⁺ signals that are currently beyond the scope of imaging technology.