Short-term cardiac memory refers to the effects of pacing history on action potential duration (APD). Although the ionic mechanisms for short-term memory occurring over many heartbeats (also called APD accommodation) are poorly understood, they may have important effects on reentry and fibrillation. To explore this issue, we incorporated a generic memory current into the Phase I Luo and Rudy (LR1) action potential model, which lacks short-term memory. The properties of this current were matched to simulate quantitatively human ventricular monophasic action potential accommodation. We show that, theoretically, short-term memory can resolve the paradox of how Mother Rotor fibrillation is initiated in heterogeneous tissue by physiological pacing. In simulated heterogeneous 2D tissue and 3D ventricles containing an IK1 gradient, short-term memory could spontaneously convert Multiple Wavelet fibrillation to Mother Rotor fibrillation, or to a mixture of both fibrillation types. This was due to progressive acceleration and stabilization of rotors as accumulation of memory shortened APD and flattened APDR slope non-uniformly throughout the tissue.