The influence of myocardial substrate on ventricular fibrillation waveform: A swine model of acute and postmyocardial infarction

Julia H. Indik, Richard L. Donnerstein, Ronald W. Hilwig, Mathias Zuercher, Justin Feigelman, Karl B. Kern, Marc D. Berg, Robert A. Berg

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


OBJECTIVE: In cardiac arrest resulting from ventricular fibrillation, the ventricular fibrillation waveform may be a clue to its duration and predict the likelihood of shock success. However, ventricular fibrillation occurs in different myocardial substrates such as ischemia, heart failure, and structurally normal hearts. We hypothesized that ventricular fibrillation is altered by myocardial infarction and varies from the acute to postmyocardial infarction periods. DESIGN: An animal intervention study was conducted with comparison to a control group. SETTING: This study took place in a university animal laboratory. SUBJECTS: Study subjects included 37 swine. INTERVENTIONS: Myocardial infarction was induced by occlusion of the midleft anterior descending artery. Ventricular fibrillation was induced in control swine, acute myocardial infarction swine, and in postmyocardial infarction swine after a 2-wk recovery period. MEASUREMENTS AND MAIN RESULTS: Ventricular fibrillation was recorded in 11 swine with acute myocardial infarction, ten postmyocardial infarction, and 16 controls. Frequency (mean, median, dominant, and bandwidth) and amplitude-related content (slope, slope-amp [slope divided by amplitude], and amplitude-spectrum area) were analyzed. Frequencies at 5 mins of ventricular fibrillation were altered in both acute myocardial infarction (p < .001 for all frequency characteristics) and postmyocardial infarction swine (p = .015 for mean, .002 for median, .002 for dominant frequency, and <.001 for bandwidth). At 5 mins, median frequency was highest in controls, 10.9 ± .4 Hz; lowest in acute myocardial infarction, 8.4 ± .5 Hz; and intermediate in postmyocardial infarction, 9.7 ± .5 Hz (p < .001 for acute myocardial infarction and p = .002 for postmyocardial infarction compared with control). Slope and amplitude-spectrum area were similar among the three groups with a shallow decline after minute 2, whereas slope-amp remained significantly altered for acute myocardial infarction swine at 5 mins (p = .003). CONCLUSIONS: Ventricular fibrillation frequencies depend on myocardial substrate and evolve from the acute through healing phases of myocardial infarction. Amplitude related measures, however, are similar among these groups. It is unknown how defibrillation may be affected by relying on the ventricular fibrillation waveform without considering myocardial substrate.

Original languageEnglish (US)
Pages (from-to)2136-2142
Number of pages7
JournalCritical care medicine
Issue number7
StatePublished - Jul 2008


  • Cardiopulmonary resuscitation
  • Defibrillation
  • Heart arrest
  • Myocardial infarction
  • Sudden cardiac death
  • Ventricular fibrillation

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine


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