Background
Cycle length (CL) increases as ventricular fibrillation (VF) progresses.
Objectives
We tested the hypotheses that increased CL is due to increased diastolic interval (DI), not increased action potential duration (APD), and that the DI increase is not solely due to increased post-repolarization refractoriness.
Methods
In 10 swine, VF was recorded for 20 min with a floating microelectrode (FME) through a hole in a 504 electrode epicardial plaque. Mean APD, DI, AP amplitude (APA), maximum change in voltage during the AP upstroke (V.max, and CL were calculated from the FME recordings each minute of VF. The refractory period was estimated from the minimum DI (DImin). In 2 animals, rapid pacing was performed to gauge refractoriness.
Results
As VF progressed, CL, DI and DImin increased (p<0.05), while APD, V.max and APA decreased (p<0.05). At 20 min, DImin was not different from mean DI at VF onset. Pacing captured, but 53% of paced wavefronts blocked within the plaque.
Conclusion
Increasing CL in VF is due to increased DI, not APD, which shortens. The increase in DImin over time is much less than the increase in mean DI, indicating that the myocardium is excitable during much of the DI. This finding, along with the ability to pace at a CL shorter than the native VF CL and the poor paced wavefront propagation, suggests that the increase in DI is not only due to increased post-repolarization refractoriness but also to poor wavefront propagation because of decreased APA and, V.max secondary to global ischemia caused by VF.