title: Electrophysiological deterioration during long-duration ventricular fibrillation.
abstract: 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.
  
  
  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 APD(100) shortened significantly with time (P:<0.001). Between 1 and 3 minutes, diastole appeared primarily as the result of APD(100) 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 approximately 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.
authors: Department of Physiology and Biophysics, Georgetown University, Department of Veterans Affairs Medical Center, Washington, DC 20422, USA. otovar01@georgetown.edu
authors: O H
authors: OH
authors: Tovar
authors: J L
authors: JL
authors: Jones
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D004195:Disease Models, Animal; D004562:Electrocardiography / Q000706:statistics & numerical data*; D006321:Heart / Q000503:physiopathology*; D006323:Heart Arrest / Q000401:mortality / Q000503:physiopathology / Q000628:therapy; D011817:Rabbits; D012151:Resuscitation; D016019:Survival Analysis; D014693:Ventricular Fibrillation / Q000175:diagnosis* / Q000503:physiopathology* / Q000628:therapy