• DOI:10.1093/EUROPACE/EUS078
• Corpus ID: 8700007

Ventricular fibrillation hampers the restoration of creatine-phosphate levels during simulated cardiopulmonary resuscitations.

@article{Hoogendijk2012VentricularFH,
  title={Ventricular fibrillation hampers the restoration of creatine-phosphate levels during simulated cardiopulmonary resuscitations.},
  author={Mark G. Hoogendijk and Cees A. Schumacher and Charly N. W. Belterman and Bastiaan J D Boukens and Jocelyn Berdowski and Jacques Mt de Bakker and Rudolph W. Koster and Ruben Coronel},
  journal={Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology},
  year={2012},
  volume={14 10},
  pages={
          1518-23
        }
}

• M. Hoogendijk, C. Schumacher, +5 authors R. Coronel
• Published 1 October 2012
• Medicine, Biology
• Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology

AIMS
Recurrences of ventricular fibrillation (VF) during cardiopulmonary resuscitation (CPR) are associated with a reduced chance of survival. The effect of VF during CPR on the myocardium is unknown. We tested the hypothesis that VF during simulated CPR reduces the restoration of the myocardial energy state and contractile function.

METHODS AND RESULTS
Twelve porcine hearts were isolated and perfused with the pig's own blood. First, cardiac oxygen consumption was measured by blood gas analysis. Secondly, we simulated sudden cardiac arrest by VF (7 min VF, zero flow) followed by simulated CPR (7 min, 0.3 mL/g/min perfusion rate) in the absence and presence of VF [six hearts were maintained in VF (VF-group), six were defibrillated (defib-group)]. The VF increased the cardiac oxygen consumption by 71% (0.87 ± 0.12 vs. 1.49 ± 0.14 μmol O₂/g/min; mean ± SEM, P< 0.001) compared with a ventricular rhythm of 62 beats/min. The presence of VF during simulated CPR after 7 min of cardiac arrest hampered restoration of myocardial creatine-phosphate levels compared with defibrillated hearts (61 ± 9 vs. 87 ± 7% of baseline values, respectively; P< 0.05). The cardiac contractile function was significantly higher in the defib- than in the VF-group (area under the pressure curve 2.29 ± 0.22 vs. 1.72 ± 0.14 s×mm Hg respectively; P< 0.05).

CONCLUSIONS
These data demonstrate that the cardiac oxygen consumption is increased by VF and that the presence of VF during CPR hampers the restoration of the myocardial energy state and contractility. Strategies that reduce VF duration without disrupting chest compressions will benefit the restoration of the cardiac energy state during resuscitations.