Abstract 2: Sodium Nitroprusside--Enhanced Cardiopulmonary Resuscitation Facilitates Intra-arrest Cerebral Therapeutic Hypothermia in a Porcine Model of Prolonged Ventricular Fibrillation
Introduction: Intra-arrest cooling has been shown to improve survival and neurologic outcome in animal models. The aim of this study was to assess the effect of Sodium Nitroprusside enhanced Cardiopulmonary Resuscitation (SNPeCPR) on heat exchange during surface cooling. We hypothesized that SNPeCPR would decrease the time to reach brain temperature to <35°C compared to Active Compression Decompression plus Impedance Threshold Device (ACD+ITD) CPR alone, when surface cooling starts during CPR. Further, addition of epinephrine during SNPeCPR would mitigate heat exchange.
Methods: After 10 minutes of untreated ventricular fibrillation, 26 animals were randomized to 3 different protocols: SNPeCPR (n=6), SNPeCPR plus epinephrine (SNP+EPI, n=10) and ACD+ITD alone (Control, n=10). All animals received surface cooling with ice bags at the initiation of CPR. SNPeCPR included ACD+ITD plus abdominal binding, 2mg of SNP every 4min, and no epinephrine during CPR. Control and SNP+EPI groups included 0.5mg of epinephrine every 4min during CPR. Defibrillation occurred after 10 minutes of CPR. After ROSC, an Arctic Sun® at maximum cooling was used on all animals. The primary endpoint was the time to reach brain temperature <35°C. Hemodynamic parameters were recorded continuously. Data are presented as mean ± SEM. ANOVA or Kruskal Wallis test were used to compare continuous variables.
Results: Time to reach brain temperature of 35°C was decreased with SNPeCPR vs. Control or SNP+EPI (18 ± 6 min, 53 ± 8 min and 40 ± 9 min, respectively, p=0.03). All animals survived 2h in the SNPeCPR group and 9/10 in the two other groups. Carotid blood flow was higher during CPR in the SNPeCPR group (96 ± 16 ml/min versus 26 ± 7 and 35 ± 5 in the Control and SNP+EPI group, respectively p=0.04). There were no other differences in hemodynamic parameters.
Conclusion: This study demonstrates that SNPeCPR facilitates intra-CPR hypothermia, with the brain reaching target temperature (35°C) in less than half of the time of controls without impairing hemodynamics. The addition of epinephrine to SNPeCPR during CPR attenuated its effect on heat exchange.
Author Disclosures: G. Debaty: None. T. Matsuura: None. J. Bartos: None. J. Rees: Employment; Significant; Advanced Circulatory Systems, Inc.. S. McKnite: None. K. Lurie: Ownership Interest; Significant; Advanced Circulatory Systems, Inc. D. Yannopoulos: Research Grant; Significant; NIH 1R01HL123227-02; R01 HL108926-04.
- © 2014 by American Heart Association, Inc.