Distinct properties and metabolic mechanisms of postresuscitation myocardial injuries in ventricular fibrillation cardiac arrest versus asphyxiation cardiac arrest in a porcine model

Abstract

Background: The two most prevalent causes of sudden cardiac death are ventricular fibrillation cardiac arrest (VFCA) and asphyxiation cardiac arrest (ACA). Profound postresuscitation myocardial dysfunction has been demonstrated in both VFCA and ACA animal models. Our study aimed to characterize the two porcine models of cardiac arrest and postresuscitation myocardial metabolism dysfunction.

Methods: Thirty-two pigs were randomized into two groups. The VFCA group (n = 16) were subject to programmed electrical stimulation and the ACA group (n = 16) underwent endotracheal tube clamping to induce cardiac arrest (CA). Once induced, CA remained untreated for a period of 8 minutes. Two minutes following initiation of cardiopulmonary resuscitation (CPR), defibrillation was attempted until return of spontaneous circulation (ROSC) was achieved or animals died. To assess myocardial metabolism, (18)F-FluoroDeoxyGlucose Positron Emission Tomography was performed at baseline and 4 hours after ROSC.

Results: ROSC was 100% successful in VFCA and 50% successful in ACA. VFCA had better mean arterial pressure and cardiac output after ROSC than ACA. Arterial blood gas analysis indicated more detrimental metabolic disturbances in ACA compared with VFCA after ROSC (ROSC 0.5 hours, pH: 7.01 ± 0.06 vs. 7.21 ± 0.03, P < 0.01; HCO3(-): (15.83 ± 2.31 vs. 20.11 ± 1.83) mmol/L, P < 0.01; lactate: (16.22 ± 1.76 vs. 5.84 ± 1.44) mmol/L, P < 0.01). Myocardial metabolism imaging using Positron Emission Tomography demonstrated that myocardial injuries after ACA were more severe and widespread than after VFCA at 4 hours after ROSC (the maximum standardized uptake value of the whole left ventricular: 1.00 ± 0.17 vs. 1.93 ± 0.27, P < 0.01). Lower contents of myocardial energy metabolism enzymes (Na(+)-K(+)-ATPase enzyme activity, Ca(2+)- ATPase enzyme activity, superoxide dismutase and phosphodiesterase) were found in ACA relative to VFCA.

Conclusions: Compared with VFCA, ACA causes more severe myocardium injury and metabolism hindrance, therefore they should be treated as different pathological entities.