Effects of heart rate on vulnerability to fibrillation in a computer model.

Effects of heart rate on refractory period (RP) duration and disparity have opposing actions on vulnerability to fibrillation. Both bradycardia and tachycardia have been reported to increase vulnerability to fibrillation, and the role of their effects on RP duration and disparity in producing that effect is uncertain. That role has been investigated with a computer model of propagated excitation having nonuniform, cycle length-dependent refractoriness and slow propagation during incomplete recovery of excitability. Vulnerability was assessed as fibrillation threshold (FT), defined as the duration of train stimulation required to initiate simulated fibrillation. When measured as a function of train onset time during a cycle, FT initially decreased to a minimum and then increased to the original level. Slower rates shifted that curve upward and to the right, so that the FT was higher during early portions of the cycle but lower in later portions. Longer mean duration of RPs increased FT during all portions of the cycle, increased the difference of FT at various rates during early portions of the cycle, and decreased differences later in the cycle. Greater RP range reduced the FT and decreased the difference of FT with varied rate in early portions of the cycle, while increasing the difference in later portions. Accelerating rate had additional effects on FT-related to nonuniform propagation of responses prior to train stimulation. The findings defined mechanisms based on established effects of rate on RP, by which either tachycardia or bradycardia could increase vulnerability to fibrillation, and demonstrated the effects of RP range and duration on the mechanisms.