Abstract P26: Intra-CPR Hypothermia with and Without Volume Loading in an Ischemic Model of Cardiac Arrest

Abstract

Background: Coronary occlusive ischemic events are responsible for 50 –70% of cardiac arrests in adults. We investigated the effects of intra-CPR mild hypothermia (HTM) (target 32–33°C) with and without volume loading on return to spontaneous circulation (ROSC) and infarction size in a severe, mid-LAD occlusion model of cardiac arrest. Methods: 46 (27±2.3kg) pigs had their mid LAD balloon occluded and were divided in 5 groups. After 15 minutes, ventricular fibrillation (VF) was electrically induced and 5 minutes of untreated VF were followed by 5 minutes of pneumatic vest CPR with a set compression pressure (250mmHg). If ROSC was obtained, animals were followed for another 95 minutes for a total LAD occlusion time of 120 min. Subsequently the balloon was deflated and 90 min of reperfusion were followed by myocardial staining to define area at risk (AAR) and myocardial infarct size. Group A had no additional intervention. Group B received immediately post ROSC surface cooling with cooling blankets and ice. Group C received intra-CPR 680±23ml of 28°C 0.9% NS via a central femoral venous catheter. Group D received during CPR 673±26 of 4°C NS followed by post ROSC surface cooling as in group B. Group E received intra-CPR and post ROSC volume-sparing HTM with an Endovascular Therapeutic Hypothermia System (ETHS) placed into the right atrium and set at a target of 32°C. Results: During CPR, coronary perfusion pressure was significantly decreased in groups C and D compared to groups A, B and E but groups D and E had significantly reduced infarct size. Group E had significantly improved EF compared to all other groups. Table . Conclusions: Intra-CPR HTM significantly reduces myocardial infarction size. Volume loading during CPR is detrimental for ROSC due to reduction of coronary perfusion pressure. ETHS intra-CPR application improves ROSC and post-resuscitation LV function and minimizes infarction in this ischemia-reperfusion cardiac arrest model. Results