Arrhythmic phenomena affect the electrical activity of the heart and are provoked by diverse illnesses. The study of these phenomena is of crucial interest because the mechanisms that produce them are not known accurately until the moment. In the present Doctoral Thesis two phenomena produced by pathological situations are studied by means of mathematical modeling and computer simulation: reflection in ventricular fibers and reentries in the Purkinje-ventricle subsystem that take place during the ischemia-induced phase 1B ventricular arrhythmias. The phenomenon of reflection occurs in cardiac ventricular tissue when an impulse that arrives in a damaged area of tissue, provokes another impulse that propagates in the opposite direction to the original impulse. The arrhythmias induced by ischemia take place in two phases, phase 1A and phase 1B. While the phase 1A of cardiac arrhythmias have been widely studied, the studies on the arrhythmias of the phase 1B are scarce, and it is of interest to explore the mechanisms that provoke this phase of arrhythmias. In the study of both arrhythmic phenomena were implemented one-dimensional (1D) and two-dimensional (2D) models. The 1D model of reflection was composed of two segments of ventricular fiber, one under normal physiological conditions and the other under conditions that facilitate the induction of early afterdepolarizations (EADs) of phase 2. The fiber segments of the model of reflection were coupled through a resistor, whose value was varied in a range from 5 to 30 Ω·cm2. The reentries generated in the subsystem Purkinje-1B ischemic ventricle were studied with three models: Purkinje-1B ischemic ventricle 1D model, Purkinje-1B ischemic ventricle 1D model with a ring structure and Purkinje-1B ischemic ventricle 2D model. The results obtained show that the coupling between the cells of the ventricular tissue has an important influence on both arrhythmic phenomena. For conditions of moderate coupling, the emergence of arrhythmic phenomena is more likely that when the coupling in cells of the ventricular fibers is low or high. The reflection phenomenon observed in cardiac ventricular fibers could occur by a different mechanism than the currently proposed, by early afterdepolarizations (EADS) of phase 2 generated in a damaged zone of ventricular tissue. The simulations realized with the 1D model of ischemia 1B with a ring structure, show that the probability of unidirectional block exists due to the alteration of the resistance of the Purkinje-ventricle junctions and the cellular uncoupling of the endocardials cells induced by phase 1B of ischemia. The unidirectional blocks (UDBs) may have influence on the generation of sustained reentries in a circuit Purkinje-1B ischemic ventricle-Purkinje. The results obtained with the two-dimensional model of ischemia 1B indicate that the increase of the resistance of the Purkinje-ventricle junctions when these connect Purkinje fibers with 1B ischemic ventricular tissue, increases the probability of conduction block from Purkinje to ventricle, which may facilitate the reentries appearance in the phase 1B of arrhythmias induced by ischemia in the Purkinje-ventricle subsystem.