Genetic defects in membrane ion channels can disrupt the delicate balance of dynamic interactions between the ion channels and the cellular environment leading to altered cell function. As ion-channel defects are typically studied in expression systems, away from the cellular environment where they function physiologically, a connection between molecular findings and the physiology and pathophysiology of the cell is rarely established. We use a single-channel-based Markovian modeling approach to bridge this gap. We achieve this by determining the cellular arrhythmogenic consequences of mutations in Markovian current models that modularly replace Hodgkin-Huxley currents in the Luo-Rudy ventricular model.