Purkinje cells (Pcell) are characterized by different electrophysiological properties and Ca²⁺ cycling processes than ventricular myocytes (Vcell) and are frequently involved in ventricular arrhythmias. Yet, the mechanistic basis for their arrhythmic vulnerability is not completely understood. The objectives were to: (1) characterize Pcell electrophysiology, Ca²⁺ cycling, and their rate dependence; (2) investigate mechanisms underlying Pcell arrhythmogenicity; and compare Pcell and Vcell electrophysiology, Ca²⁺ cycling, and arrhythmic properties. We developed a new mathematical model of Pcell. The Ca²⁺ subsystem includes spatial organization and receptors distribution unique to Pcell. Results were: (1) in Pcell and Vcell, Na⁺ accumulation via its augmentation of repolarizing I_NaK dominates action potential duration adaptation and, in Pcell, I_NaL contributes additional action potential duration shortening at short cycle length; (2) steep Pcell restitution is attributable to slow recovery of I_NaL; (3) biphasic Ca²⁺ transients of Pcell reflect the delay between Ca²⁺ release from junctional sarcoplasmic reticulum and corbular sarcoplasmic reticulum; (4) Pcell Ca²⁺ alternans, unlike Vcell, can develop without inducing action potential alternans; (5) Pcell action potential alternans develops at a shorter cycle length than Vcell, with increased subcellular heterogeneity of Ca²⁺ cycling attributable to refractoriness of Ca²⁺ release from corbular sarcoplasmic reticulum and junctional sarcoplasmic reticulum; (6) greater Pcell vulnerability to delayed afterdepolarizations is attributable to higher sarcoplasmic reticulum Ca²⁺ content and ionic currents that reduce excitation threshold and promote triggered activity; and (7) early after depolarizations generation in Pcell is mostly attributable to reactivation of I_NaL2, whereas I_CaL plays this role in Vcell. Steeper rate dependence of action potential and Ca²⁺ transients, central peripheral heterogeneity of Ca²⁺ cycling, and distinct ion channel profile underlie greater arrhythmic vulnerability of Pcell compared to Vcell.