In this paper, a human ventricular acidotic model with pathophysiological consequences of acidosis, such as reduced pH and highly activated calcium/calmodulin dependent protein kinaseⅡ(CaMKⅡ), was developed to analyze the functional influence of acidosis on cardiac electrical activity and ventricular arrhythmia. Dynamic changes of cellular and tissue electrical activity were simulated and the acidosis-induced changes of electrocardiogram waveform were quantified. Results demonstrated that acidosis led to shortened action potential duration and decreased transmural dispersion of repolarization, resulting in reduced QT interval and shortened amplitude and width of T wave. In addition, acidosis also resulted in high resting membrane potential and reduced maximum upstroke velocity, leading to the generation of slow conduction and conduction block. Most importantly, at the early stage of the post acidosis, sarcoplasmic reticulum calcium load increased calcium leak, leading to delayed afterdepolarizations in the cellular membrane potential and premature ventricular contractions in the cardiac tissue model. Slow conduction, conduction block and delayed afterdepolarizations collectively promote and facilitate the formation and maintenance of ventricular re-entry, which may convert into ventricular tachycardia. Therefore, triggered activities induced during post acidosis period play an important role in the genesis of post acidosis arrhythmias.