Increased cycle length during long-duration ventricular fibrillation is caused by decreased upstroke velocity as well as prolonged refractoriness

• Published in: Heart rhythm Vol. 6; no. 3; pp. 378 - 384
• Main Authors: Robertson, Peter G., MD, Huang, Jian, MD, PhD, Chen, Kang A., MD, Chen, Xiaozhong, PhD, Dosdall, Derek J., PhD, Tabereaux, Paul B., MD, MPH, Smith, William M., PhD, Ideker, Raymond E., MD, PhD
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-03-2009
• Subjects: Action Potentials; Animals; Cardiac Pacing, Artificial; Cardiovascular; Diastole; Electrocardiography; Electrophysiologic Techniques, Cardiac; Heart Conduction System - physiopathology; Microelectrode; Microelectrodes; Myocardial Contraction; Refractoriness; Sus scrofa; Ventricular fibrillation; Ventricular Fibrillation - physiopathology; Microelectrode; Refractoriness; Ventricular fibrillation
• ISSN: 1547-5271; 1556-3871
• DOI: 10.1016/j.hrthm.2008.12.016

Background Cycle length (CL) increases as ventricular fibrillation (VF) progresses. Objective The purpose of this study was to test 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 postrepolarization refractoriness. Methods In 10 swine, VF was recorded for 20 minutes using a floating microelectrode through a hole in a 504-electrode epicardial plaque. Mean APD, DI, action potential amplitude (APA), maximum change in voltage during the AP upstroke (V̇max ), and CL were calculated from the floating microelectrode recordings each minute of VF. The refractory period was estimated from the minimum DI (DImin ). In two animals, rapid pacing was performed to gauge refractoriness. Results As VF progressed, CL, DI, and DImin increased ( P <.05), whereas APD, V̇max , and APA decreased ( P <.05). At 20 minutes, 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 and 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 due not only to increased postrepolarization refractoriness but also to poor wavefront propagation because of decreased APA and V̇max secondary to global ischemia caused by VF.