Key result
In a swine model of ventricular fibrillation, simulated CPR using extracorporeal circulation increased the amplitude spectral area from 7.0 to 12.8 mV-Hz after 6 minutes, without further increases.
Why the study?
Does extracorporeal circulation modeling average CPR alter the amplitude spectral area of the ventricular fibrillation waveform in a swine model?
Does extracorporeal circulation modeling average CPR alter the amplitude spectral area of the ventricular fibrillation waveform in a swine model?
Absolute Event Rate: 12.8% vs 7%
p-value: p=<0.05
In a swine model of ventricular fibrillation, simulated CPR via extracorporeal circulation increased the amplitude spectral area of the VF waveform, which peaked after 6 minutes despite persistent myocardial ischemia.
Does not support changing resuscitation practices; extends preclinical evidence on extracorporeal effects in VF.
BACKGROUND: Several characteristics of the ventricular fibrillation (VF) waveform have been found predictive of successful defibrillation and hypothesized to reflect the myocardial energy state. In an open-chest swine model of VF, we modeled "average CPR" using extracorporeal circulation (ECC) and assessed the time course of coronary blood flow, myocardial metabolism, and myocardial structure in relation to the amplitude spectral area (AMSA) of the VF waveform without artifacts related to chest compression. METHODS: VF was induced and left untreated for 8 minutes in 16 swine. ECC was then started adjusting its flow to maintain a coronary perfusion pressure of 10 mmHg for 10 minutes. AMSA was calculated in the frequency domain and analyzed continuously with a 2.1 s timeframe and a Tukey window that moved ahead every 0.5 s. RESULTS: AMSA progressively declined during untreated VF. With ECC, AMSA increased from 7.0 ± 1.9 mV·Hz (at minute 8) to 12.8 ± 3.3 mV·Hz (at minute 14) (p < 0.05) without subsequent increase and showing a modest correlation with coronary blood flow of borderline statistical significance (r = 0.489, p = 0.0547). Myocardial energy measurements showed marked reduction in phosphocreatine and moderate reduction in ATP with increases in ADP, AMP, and adenosine along with myocardial lactate, all indicative of ischemia. Yet, ischemia did not resolve during ECC despite a coronary blood flow of ~ 30% of baseline. CONCLUSION: AMSA increased upon return of coronary blood flow during ECC. However, the maximal level was reached after ~ 6 minutes without further change. The significance of the findings for determining the optimal timing for delivering an electrical shock during resuscitation from VF remains to be further explored.
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Gazmuri et al. (2016) studied Ventricular Fibrillation (n=16). Extracorporeal circulation (ECC) simulating CPR vs. Untreated ventricular fibrillation was evaluated on Amplitude spectral area (AMSA) of the VF waveform (p=<0.05). In a swine model of ventricular fibrillation, simulated CPR using extracorporeal circulation increased the amplitude spectral area from 7.0 to 12.8 mV-Hz after 6 minutes, without further increases.
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