TY - JOUR
T1 - Ventricular fibrillation hampers the restoration of creatine-phosphate levels during simulated cardiopulmonary resuscitations
AU - Hoogendijk, Mark G.
AU - Schumacher, Cees A.
AU - Belterman, Charly N.W.
AU - Boukens, Bas J.
AU - Berdowski, Jocelyn
AU - De Bakker, Jacques M.T.
AU - Koster, Rudolph W.
AU - Coronel, Ruben
PY - 2012/10
Y1 - 2012/10
N2 - 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 resultsTwelve 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).ConclusionsThese 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.
AB - 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 resultsTwelve 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).ConclusionsThese 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.
UR - http://www.scopus.com/inward/record.url?scp=84866918011&partnerID=8YFLogxK
U2 - 10.1093/europace/eus078
DO - 10.1093/europace/eus078
M3 - Article
C2 - 22490373
AN - SCOPUS:84866918011
SN - 1099-5129
VL - 14
SP - 1518
EP - 1523
JO - Europace
JF - Europace
IS - 10
ER -