Key result
In a human heart ventricle myocyte simulation model, a depolarizing defibrillation pulse at certain energy levels extended refractoriness in 90% of cardiomyocytes across different fibrillation phases.
Why the study?
What are the mechanisms of defibrillation by depolarizing pulses in a human heart ventricle myocyte model?
What are the mechanisms of defibrillation by depolarizing pulses in a human heart ventricle myocyte model?
Simulation on a human cardiomyocyte model suggests that defibrillation mechanisms involve long-term extension of refractoriness at low energies and one-time extension at high energies.
In the BeatBox simulation environment on the human heart ventricle myocyte model ten Tusscher-Panfilov 2006 the efficiency areas of the depolarizing defibrillation pulse in the energy/phase diagram for the fibrillation cycle are investigated. At any energy levels, the depolarizing pulse does not provide a long-term extension of refractoriness of all heart cardiomyocytes in different phases of the excitation wave cycle, but at a certain energy level, refractoriness is long-term extended in 90% of the cardiomyocytes in different phases of the fibrillation wave cycle. At high energy levels, the action of the depolarizing pulse leads to a one-time extension of the refractory period of cardiomyocytes to values exceeding the duration of the fibrillation wave period. Presumably long-term extension of refractoriness of cardiomiocites at low energy of depolarising pulse and one-time extension of refractoriness of all cardiomiocites at high energy of depolarising pulse are the mechanisms of defibrillation.
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Gorbunov et al. (2018) studied Fibrillation. Depolarizing defibrillation pulse was evaluated on Extension of refractoriness of cardiomyocytes. In a human heart ventricle myocyte simulation model, a depolarizing defibrillation pulse at certain energy levels extended refractoriness in 90% of cardiomyocytes across different fibrillation phases.
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