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(Circulation. 2000;102:2886.)
© 2000 American Heart Association, Inc.

Basic Science Reports

Electrophysiological Deterioration During Long-Duration Ventricular Fibrillation

Presented in part at the 47th Meeting of the American College of Cardiology, March 29–April 1, 1998, and the 72nd Scientific Sessions of the American Heart Association, Atlanta, Ga, November 7–10, 1999, and published in abstract form (JACC. 1998;31:97A) (Circulation. 1999;100:I-90).

Oscar H. Tovar, MD; Janice L. Jones, PhD

From the Department of Physiology and Biophysics, Georgetown University, and the Department of Veterans Affairs Medical Center, Washington, DC.

Correspondence to Oscar H. Tovar, MD, VA Medical Center 151P, 50 Irving St NW, Washington, DC 20422. E-mail otovar01{at}georgetown.edu

Background—Probability of survival from sudden cardiac arrest caused by ventricular fibrillation (VF) decreases rapidly with fibrillation duration. We hypothesized that cellular ischemia/fibrillation-induced electrophysiological deterioration underlies decreased survival.

Methods and Results—We determined fibrillation monophasic action potential (MAP) morphology including action potential frequency content, duration, cycle length, developing diastolic intervals, and amplitude as a function of ischemic fibrillation duration in 10 isolated rabbit hearts. We also correlated ECG frequency (used clinically) and MAP amplitude and frequency. Fibrillation cycle length and diastole duration increased, whereas APD₁₀₀ shortened significantly with time (P<0.001). Between 1 and 3 minutes, diastole appeared primarily as the result of APD₁₀₀ shortening, with only small changes in cycle length. Between 2 and 5 minutes, diastole increased primarily as the result of increased cycle length. Diastole developed progressively from 5% of VF cycles at 5 seconds to 100% of VF cycles by 120 seconds (P<0.001). Diastole increased from 1% of cycle length at 5 seconds to 62% at 5 minutes. Its duration increased from 4.7 ms at 5 seconds to 90 ms at 5 minutes (P<0.001). Both MAP and ECG 1/frequency closely correlated with fibrillation cycle length.

Conclusions—These results show a rapid and progressive electrophysiological deterioration during fibrillation, leading to electrical diastole between fibrillation action potentials. This rapid deterioration may explain the decreased probability of successful resuscitation after prolonged fibrillation. Therefore, a greater understanding of cellular deterioration during fibrillation may lead to improved resuscitation methods, including development of specific defibrillator waveforms for out-of-hospital cardiac arrest.

Key Words: death, sudden • defibrillation • electrophysiology • resuscitation • fibrillation

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