We developed a two-dimensional ventricular tissue model in order to probe the determinants of electrocardiographic (ECG) morphology during acute and chronic ischemia. Hyperkalemia was simulated by step changes in [K+]out, while acidosis was induced by reducing Na+ and Ca2+ conductances. Hypoxia was introduced by its effect on potassium activity. During the initial moments of ischemia, ECG changes were characterized by increases in QRS amplitude and ST segment shortening, followed in the advanced phase by ST baseline elevation, T conformation changes, widening of the QRS and significant decreases in QRS amplitude in spite of an enlarged Q. During each phase, potential proarrhythmic mechanisms were investigated. The presence of unexcitable regions of simulated myocardial infarction led to polymorphic ECG. We also observed a nonuniform deflection of the ST segment from beat to beat. We used similar protocols to explore the responses of infarcted myocardium after impairment resolving. We found that despite irreversible uncoupling of the necrotic region, the restored normal ionic concentrations produced an isopotential ST segment and monomorphic ECG complexes, while an enlarged Q wave was still visible. In summary, these numerical experiments indicate the possibility to track in the ECG pathologic changes following the altered electrophysiology of the ischemic heart.