Abstract 2642: Intravenous Ascorbic Acid Administration During Cardiopulmonary Resuscitation Facilitates Defibrillation and Improves Outcomes in a Rat Model of Ventricular Fibrillation
Background: Our previous study demonstrated that electrical shock generates free radicals inside the cardiomyocyte, and causes contractile impairment and Ca2+ disequilibrium. Administering ascorbic acid improve such damage by eliminating free radicals. Whether ascorbic acid can improve the outcome of VF cardiac arrest remains unclear.
Hypothesis: Intravenous administration of ascorbic acid during cardiopulmonary resuscitation (CPR) facilitates defibrillation, and thus improves rate of return of spontaneous circulation (ROSC) and survival.
Methods: Ventricular fibrillation was induced in 12 rats and untreated for 5 minutes, followed by 1 minutes of CPR, and then a sequence of one electrical defibrillation shock followed by 30 seconds of CPR until ROSC or total 5 minutes of resuscitation. Twelve animals were equally randomized to ascorbic acid group and control group. The ascorbic acid group received intravenous administration of ascorbic acid (100 mg/kg) simultaneously at the start of CPR, and the control group received normal saline of the same volume and PH as placebo.
Results: ROSC was achieved in five out of six rats in the ascorbic acid group, but only one in the control group (83% vs. 17%, P=.04). All the successfully resuscitated animals in the ascorbic acid group survived up to 72 hours, whereas none in the control group survived up to 72 hours (83% vs. 0%, P=.008). The successfully resuscitated animals in the ascorbic acid group had less electrical shock (1.4±0.5 vs. 3, P=.056) and shorter CPR duration (77.2±17.8 seconds vs. 129 seconds, P=.057) than the control group.
Conclusion: Intravenous administration of ascorbic acid during CPR facilitates defibrillation and resuscitation, and thus improves outcomes in a rat model of ventricular fibrillation.