The Exposure to atmospheric pollutants, such as carbon monoxide (CO), promotes the appearance of cardiovascular diseases. Studies have shown that CO blocks calcium channels, leading to a decrease of the ICaL current and to a shortening of the action potential duration (APD); favoring the generation of cardiac arrhythmias. The aim of this work is to study the CO effects, at different concentrations, on the atrial and ventricular tissues using computational simulations. An equation of the CO effect on ICaL was developed. It was included in two mathematical models of human atrial and ventricular cells, under normal physiological conditions. Atrial and ventricular 2D models were developed to evaluate the CO effect on the generation of reentries as an arrhythmogenic mechanism. The results show that CO blocks the ICaL current in a greater fraction as its concentration increases, causing APD shortening. Such effect is larger in atrial cardiomycytes. Arrhythmic events (rotors) were generated at the high CO concentration in atrial tissue. In ventricular tissue it was not possible to generate rotors. This study provides a first step in investigating the proarrhythmic effects of CO in healthy people.