VULNERABILITY TO FIBRILLATION IN A MATHEMATICAL MODEL

Abstract

Factors affecting vulnerability to fibrillation and their electrocardiographic expression were investigated using a computer simulation of propagated excitation. The simulation included nonuniform recovery of excitability, cycle length dependent refractoriness, slow propagation during incomplete recovery and nonuniform conduction defects. Vulnerability was assessed as the duration of train stimulation required to initiate self sustained reentrant excitation. Results showed the expected inverse relation of recovery property range to fibrillation threshold and the new findings of a direct relation to mean recovery property duration, gaps in the relation of stimulus train duration to the initiation of fibrillation and an inverse relation of conduction disorder range and mean to fibrillation threshold. Mechanisms of all findings in the model were identified. The effect of recovery property range was due to varied nonuniformity of propagation per premature response while that of mean was varied number of premature responses per unit time. The mechanism of gaps was block of reentrant circuits required for fibrillation by stimuli later than those which initiated fibrillation. The range of conduction defect severity influenced fibrillation threshold by affecting the degree of nonuniformity of propagation per premature response while the mean magnitude of conduction defects altered the degree of nonuniformity required for reentry. Results provide hypotheses suitable for test by experiment and furnish tentative explanations of several features of ventricular fibrillation. These include the greater incidence of fibrillation in acute ischemia with disparate but short refractory periods than in chronic ischemia with equally disparate but long refractoriness. They also provide a possible explanation for the lack of a clear relation between severity of heart disease and occurrence of fibrillation and demonstrate intrinsic effects of conduction disorders on fibrillation threshold. Electrocardiographic expressions of disparate repolarization and conduction in the distributions of QRST and QRS areas were also demonstrated.