Abstract 278: Sodium Nitroprusside Combined With Epinephrine for Prolonged Ventricular Fibrillation Cardiac Arrest

Abstract

Background: A new approach to resuscitation using the potent vasodilator sodium nitroprusside (SNP) combined with mechanical efforts to maintain both coronary and cerebral perfusion pressures (active compression/decompression CPR combined with an impedance threshold device and abdominal binding) has reported improved survival with good neurological function. We hypothesized that a potent vasoconstricting agent like epinephrine (E) might replace the multiple mechanical components of this approach without compromising outcomes. Methods: We studied a total of 24 swine (25±5 kg) utilizing a 10-min period of untreated ventricular fibrillation. This was followed by 2-min of chest compressions and then an attempted defibrillation. The 2-min compression and subsequent defibrillation effort was repeated. Next another 2-min of chest compressions, during which both medications were administered, followed by attempted defibrillation. This first drug administration period occurred at 14 min 20 seconds after the onset of cardiac arrest. A total of five such 2-min of chest compressions followed by drug administration were performed if needed for ROSC. Animals were randomized to receive either SNP/E or placebo. Doses included 0.5 mg of SNP every 2 min for a maximum dose of 2.5 mg over 15 min and 1.3 mg of E every 2 min for a maximum dose of 6.75 mg. The primary endpoint was normal neurological function (CPC =1) at 24 hours. Statistical analysis utilized Fisher’s Exact testing. Results: Three subjects were successfully resuscitated prior to receiving any medications and were eliminated from this comparison. A total of 7/9 SNP/E animals were resuscitated in contrast to 6/13 animal receiving placebo (p=0.2). At 24 hours a CPC score of 1 was seen in 1/7 SNP/E animals compared to 5/6 placebo animals (p=0.03). Conclusion: Sodium nitroprusside combined with epinephrine failed to improve 24-hour neurological function in this protocol designed to mimic the late administration of medications during ACLS resuscitation. Epinephrine was unable to successfully replace the previously reported mechanical components of sodium nitroprusside-enhanced CPR (SNPeCPR). The propensity for epinephrine to increase ROSC, but not longer-term endpoints, remains a concern.