The two mechanisms of cardiac arrhythmia that are currently known involve transition of some of the cells into a self-oscillating mode and the emergence of circulating waves. A mechanism for the emergence of circulating waves due to a unidirectional blockage is considered in the present study. A narrow gap between two non-conductive areas may provide the conditions for such a mechanism. However, this mechanism cannot occur in the human heart, since the minimal path length for circulation at the action potential duration of 0.3 s and the wave propagation velocity of 33 cm/s is approximately 10 cm, whereas the average distance from the top of the ventricles to the atrioventricular septum is 8 cm. Therefore, the inhomogeneity that is described above cannot exist on the scale of the human heart. Low-conductivity areas that lead to slow propagation of a wave have been introduced in order to adapt this mechanism to the size of the heart. The conductivity values were calculated using the dependence between the conductivity and the velocity of the wave front that is determined using computational methods. Analysis of wave propagation through the boundary between two areas with different conductivities revealed the dependence of the refractory period on the ratio of the conductivities. A transition zone in which the conductivity value changes linearly from the normal value to a lower value has been introduced to attenuate this dependence. As a result, an inhomogeneity that is 12 mm in size that triggers the formation of a circulating wave was modeled.