The slow (IKs) and rapid (IKr) delayed rectifier K+ currents are responsible for action potential repolarization in ventricular myocytes. Although substantial differences in the voltage-dependent gating kinetics of the two currents have been carefully documented, differences in the physiological roles of IKr and IKs are less established. A recent study comparing simulations with experimental recordings in guinea pig myocytes proposed the hypothesis that IKs might be superior to IKr at stabilizing the ventricular action potential (AP) and protecting cells against arrhythmias. We sought to determine whether IKs is uniformly protective across species and to uncover mechanisms underlying this protective effect. To address this, we performed simulations using 10 ventricular myocyte models describing electrophysiology of human, rabbit, canine, and guinea pig cells. We assessed models using several methods including simulations of heterogeneous populations, susceptibility to action potential prolongation, and simulations of action potential clamps. We found that: (1) models with higher baseline IKs exhibited less cell-to-cell variability in action potential duration; (2) models with higher baseline IKs were less susceptible to early afterdepolarizations (EADs) induced by depolarizing perturbations; (3) as action potential duration (APD) is extended, IKs increases more profoundly than IKr, thereby providing negative feedback that resists excessive APD prolongation; and (4) the increase in IKs that occurs during beta-adrenergic stimulation is critical for protecting cardiac myocytes from EADs under these conditions. Overall, the results confirm a uniformly protective role of IKs across a variety of cell types and support the idea that augmentation of IKs could potentially be an effective antiarrhythmic strategy.