This study aimed to focus on the ability of Bartolucci-Passini-Severi (BPS) model to represent the pathophysiological effects of acute ischemia, specifically hyperkalemia. The performed simulation lasts for 35 minutes. The first 5-minutes represent the normoxia and the following 30-minutes replicate progressive acute ischemia. All the simulations are done on the single isolated cell level at 1Hz with the BPS model. BPS model is an action potential model of ventricular cardiomyocyte, which could overcome the problem of the previous action potential models in terms of inverse APD-[Ca2+]e dependence. To adopt the model to our desired aim, some ischemic parameters were implemented into BPS model based on the work done by Ferrero et al., in 2023. The results of simulated progressive acute ischemia revealed a different time course of extracellular potassium with respect to the gold standard, O'Hara-Rudy model. BPS model did not demonstrate the expected triphasic trend. During the first 5 minutes from onset of ischemia the models behave in the same way. However, after this time point BPS continues to extrude K+ ions intensively and reaches 27mmol/L in the 10th minute. while at this moment ORd model plateaus at 12 mmol/L. The extrusion of K+ ions by BPS continues with a slight increase and peaks at 35 mmol/L at around 25th minutes of simulated acute ischemia then followed by a decrease. In-depth analysis, revealed a complete interruption of calcium induced calcium released procedure at 4.4th minute, which can be associated to the appearance of the first delayed after depolarization at 4.4th minutes of simulated acute ischemia. To conclude, one of the stunning points of BPS model, representing the DAD, could count as a limitation of the model while studying the acute ischemia since it provokes an APD prolongation and a non-physiological behavior of extracellular potassium concentration.