Despite the large body of research over the previous several decades, the mechanisms that underlie the initiation and maintenance of life-threatening cardiac arrhythmias are incompletely understood. For example, investigation into arrhythmogenesis has primarily focused into the electrical sources of excitation, such as ectopic foci and reentrant circuits. However, recent studies have demonstrated the contribution of mechano-electric feedback initiated by the abnormal mechanical loading of the heart. During ventricular fibrillation passive flow of blood from the left side of the heart into the right causes the right ventricular free wall to extend. Increased ventricular loading and the ensuing ventricular volume increase can engage stretch- activated ionic channels in the cardiac membrane. Opening of the stretch activated channels can cause shortening of the action potential and change in the velocity of propagation. Stretch can also be associated with a decrease in the refractory period, thus reducing the wavelength and making arrhythmias more likely to take place and be maintained. Clearly, the electrophysiological changes associated with tissue stretch will affect the dynamics of arrhythmia and fibrillation by modifying molecular transport mechanisms. Thus, the specific aim of this project is to further extend the scope of cardiac arrhythmogenisis and defibrillation by incorporating the contribution of mechano-electrical feedback into cardiac electrical behavior.