Catecholaminergic polymorphic ventricular tachycardia is a heritable arrhythmia unmasked by exertion or stress and is characterized by triggered activity and sudden cardiac death. In this study, we simulated mutations in 2 genes linked to catecholaminergic polymorphic ventricular tachycardia, the first located in calsequestrin (CSQN2) and the second in the ryanodine receptor 2 (RyR2). The aim of the study was to investigate the mechanistic basis for spontaneous Ca²⁺ release events that lead to delayed afterdepolarizations in affected patients. Sarcoplasmic reticulum (SR) luminal Ca²⁺ sensing was incorporated into a model of the human ventricular myocyte, and CSQN2 mutants were modeled by simulating disrupted RyR2 luminal Ca²⁺ sensing. In current-clamp mode, the mutant CSQN2 model recapitulated the smaller calcium transients, smaller time to peak calcium transient, and accelerated recovery from inactivation seen in experiments. In the presence of stimulation, we observed delayed afterdepolarizations, suggesting that accelerated recovery of RyR2 induced by impaired luminal Ca²⁺ sensing underlies the triggered activity observed in mutant CSQN2-expressing myocytes. In a model of mutant RyR2 that is characterized by reduced FKBP12.6 binding to the RyR2 on stimulation, the impaired coupled gating characteristic of these mutations was modeled by reducing cooperativity of RyR2 activation. In current-clamp mode, the mutant RyR2 model exhibited increased diastolic RyR2 open probability that resulted in delayed afterdepolarization formation. In conclusion, these minimal order models of mutant CSQN2 and RyR2 provide plausible mechanisms by which defects in RyR2 gating may lead to the cellular triggers for arrhythmia, with implications for the development of targeted therapy.