Recent studies of cholesterol-rich membrane microdomains, called caveolae, reveal that caveolae are reservoirs of recruitable sodium ion channels. Caveolar channels constitute a substantial and previously unrecognized source of sodium current in cardiac cells. In this talk, I will present a family of DE and PDE models to investigate caveolar sodium currents and their contributions to cardiac action potential morphology. We show that the b-agonist-induced opening of caveolae may have substantial impacts on peak overshoot, maximum upstroke velocity, and conduction velocity. Additionally, we show that prolonged action potentials and the formation of potentially arrhythmogenic afterdepolarizations, can arise if caveolae open intermittently throughout the action potential.