TY - JOUR
T1 - The influence of myocardial substrate on ventricular fibrillation waveform
T2 - A swine model of acute and postmyocardial infarction
AU - Indik, Julia H.
AU - Donnerstein, Richard L.
AU - Hilwig, Ronald W.
AU - Zuercher, Mathias
AU - Feigelman, Justin
AU - Kern, Karl B.
AU - Berg, Marc D.
AU - Berg, Robert A.
N1 - Funding Information:
Supported by National Institutes of Health grant, NHLBI R01 HL71694-01, and by the Steven M. Gootter Foundation in conjunction with the Sarver Heart Center, University of Arizona. All work was performed at the University of Arizona.
PY - 2008/7
Y1 - 2008/7
N2 - 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.
AB - 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.
KW - Cardiopulmonary resuscitation
KW - Defibrillation
KW - Heart arrest
KW - Myocardial infarction
KW - Sudden cardiac death
KW - Ventricular fibrillation
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UR - http://www.scopus.com/inward/citedby.url?scp=47249158147&partnerID=8YFLogxK
U2 - 10.1097/CCM.0b013e31817d798c
DO - 10.1097/CCM.0b013e31817d798c
M3 - Article
C2 - 18552696
AN - SCOPUS:47249158147
SN - 0090-3493
VL - 36
SP - 2136
EP - 2142
JO - Critical care medicine
JF - Critical care medicine
IS - 7
ER -