The mechanism of the ULV dose-response curve: A model study

A stimulus given in the T-wave (a ULV stimulus) of a paced cardiac cycle can induce ventricular fibrillation (VF). However, if the ULV stimulus strength is increased, the probability of inducing VF drops in a dose-response fashion. This paper presents a hypothesis which explains this dose-response relationship. We hypothesize that the dose-response relationship arises from the variation in the location of the induction of rotating wavefronts. If the wavefronts are initiated near an anatomical obstacle, such as the A-V groove, they have a high probability of wandering into the obstacle and reducing to quiescence. If the wavefronts are initiated far from such an obstacle, they have a high probability of surviving long enough to disintegrate into VF. Since increasing the stimulus strength can reduce the distance between the A-V groove and the location of the wavefronts, the probability of inducing VF drops with increasing stimulus strength. Modeling results are presented to support a key aspect of this hypothesis. From the hypothesis, several theoretical predictions are made. It is shown that the experimental evidence supports several of these predictions.

Duke Scholars

Author Robert A. Malkin Biomedical Engineering