Sudden cardiac death is mainly provoked by arrhythmogenic processes. During myocardial ischemia many malignant arrhythmias, such as reentry, take place and can degenerate into ventricular fibrillation. It is thus of great interest to unravel the intricate mechanisms underlying the initiation and maintenance of a reentry. In this computational study, we analyze the probability of reentry during different stages of the acute phase of ischemia. We also aimed at the understanding of the role of its main components: hypoxia, hyperkalemia, and acidosis analyzing the intricate ionic mechanisms responsible for reentry generation. We simulated the electrical activity of a ventricular tissue affected by regional ischemia based on a modified version of the Luo-Rudy model (LRd00). The ischemic conditions were varied to simulate different stages of this pathology. After premature stimulation, we evaluated the vulnerability to reentry. We obtained an unimodal behavior for the vulnerable window as ischemia progressed, peaking at the eighth minute after the onset of ischemia where the vulnerable window yielded 58 ms. Under more severe conditions the vulnerable window decreased and became zero for minute 8.75. The present work provides insight into the mechanisms of reentry generation during ischemia, highlighting the role of acidosis and hypoxia when hyperkalemia is present.