Abstract 282: Poloxamer 188 Improves Intra-CPR Hemodynamics and Post-Resuscitation LV Function in a Pig Model of Prolonged Cardiac Arrest

Abstract

Introduction: Poloxamer 188 (P188) is a copolymer surfactant that has been shown to protect against ischemia/reperfusion injury. We hypothesized that P188 administration at the initiation of cardiopulmonary resuscitation (CPR) would improve post-resuscitation LV function. Methods: Following 15 min of untreated ventricular fibrillation (VF), 12 pigs received 4 minutes of CPR with automated active compression/decompression and an impedance threshold device. Six animals received an IV bolus (250 mg/kg) at the initiation of CPR and infusion of 120 ml of 150 mg/ml of P188 for 4 hours after return of spontaneous circulation (ROSC). Six other animals received no P188 (CTL). Aortic systolic (AoS), diastolic (AoD), and right atrial diastolic (RAD) pressures were recorded continuously. Coronary perfusion pressure (CPP) was calculated as the difference between AoD and RAD. All animals received 0.5 mg of epinephrine 1 min prior to defibrillation. Left ventricular ejection fraction (LVEF) was obtained with echocardiography 1 and 4 hours after return of spontaneous circulation (ROSC). Unpaired t-tests were used for statistical analysis; significance assumed at p<0.05 (two-tailed). Results: 5/6 animals treated with P188 and 6/6 CTL animals had ROSC. P188 significantly increased intra-CPR hemodynamics (table) and eliminated post resuscitation LV ventricular dysfunction. LVEF at 1 and 4 hours post ROSC with P188 vs. CTL was 58±7 and 62±11% versus 36±12 and 38±9 %, respectively (p<0.05). Conclusion: Poloxamer 188, when administered at the initiation of CPR as a bolus and as an infusion post ROSC, improved intra-CPR hemodynamics and post-ROSC LVEF after 15 minutes of untreated VF in an animal model. The mechanism of action is thought to be membrane stabilization and this will be the aim of future studies.