A tight coupling between cell structure, ionic fluxes and intracellular Ca2+ transients underlies the regulation of cardiac cell function. To investigate how a distribution of Ca2+ handling proteins may affect these coupled processes we developed a 3-D model of Ca2+-signaling, buffering and diffusion in rat ventricular myocytes. The model geometry was derived from the experiment. A diffusion modeling software using finite element tool kit (FEtK) libraries was implemented to solve the 4 coupled PDE systems. We concluded that the cardiac cell function is tightly regulated by the localization of Ca2+-handling proteins and strongly relays on the presence of mobile and stationary Ca2+ buffers and cell geometry.