Sodium overload of cardiac cells can accompany various pathologies and induce fatal cardiac arrhythmias. We investigate effects of elevated intracellular sodium on the cardiac action potential (AP) and on intracellular calcium using the Luo–Rudy model of a mammalian ventricular myocyte. The results are: 1) During rapid pacing, AP duration (APD) shortens in two phases, a rapid phase without Na⁺ accumulation and a slower phase that depends on [Na⁺]_i. 2) The rapid APD shortening is due to incomplete deactivation (accumulation) of I_Ks. 3) The slow phase is due to increased repolarizing currents I_NaK and reverse-mode I_NaCa, secondary to elevated [Na⁺]_i. 4) Na⁺-overload slows the rate of AP depolarization, allowing time for greater I_Ca(L) activation; it also enhances reverse-mode I_NaCa. The resulting increased Ca²⁺ influx triggers a greater [Ca²⁺]_i transient. 5) Reverse-mode I_NaCa alone can trigger Ca²⁺ release in a voltage and [Na⁺]_i-dependent manner. 6) During I_NaK block, Na⁺ and Ca²⁺ accumulate and APD shortens due to enhanced reverse-mode I_NaCa; contribution of I_K(Na) to APD shortening is negligible. By slowing AP depolarization (hence velocity) and shortening APD, Na⁺-overload acts to enhance inducibility of reentrant arrhythmias. Shortened APD with elevated [Ca²⁺]_i (secondary to Na⁺-overload) also predisposes the myocardium to arrhythmogenic delayed afterdepolarizations.