From cellular automata model of vagal control of the human right atrium to heart beats patterns

Abstract

It is widely accepted that multilevel relations between heart cells, within a specific heart architecture, constitute the basis which enables efficient propagation of electrochemical excitation waves that lead to heart contractions. The autonomic nervous system, with vagal branch as its subsystem, controls the rhythm of heart contractions, slowing or accelerating its rate to adjust the rhythm to current needs of the organism.A stochastic network of excitable cellular automata, mimicking internal cellular processes affecting initiation of self-organized wave of excitation of the sinoatrial node—the human heart natural pacemaker, and then propagation of waves of excitation in the right atrium to the node transmitting the signal to ventricles, is introduced in our previous model. At present, the model is extended to include the vagal control over the sinoatrial node. The conducted simulations show that our extended model imitates effectively tonic impact of the vagal control in case of the healthy heart, i.e. slowing down heart beats according to level of the vagal activity. Also, the simulations provide arguments explaining respiratory sinus arrhythmia—the healthy heart arrhythmia, i.e. fast adjusting the heart rate to changing vagal activity.The extended model provides conditions when the healthy stabilization could be lost. The transition from the normal rhythm to arrhythmia is observed, when the connection between sinoatrial node and atrium is dense. Also, when time intervals between successive beats become longer, due to the high level of vagal activity, an increase of extrasystoles is observed in the simulations. The presented results support the hypothesis that rapidly changing vagal activity maintains the stable heart rhythm. This effect results from the transition in the self-organized excitation of sinoatrial node automata, i.e. from synchronization in the form of the excitation wave to the common rhythm of excitations. The presented results are of clinical significance in identification of mechanisms of sinus arrhythmia in humans.