Abstract 103: Rewarming Speed Affects Cardiopulmonary and Neurological Functions After Deep Hypothermic Cardiac Arrest

Abstract

Introduction: The optimal rewarming rate from accidental or induced deep hypothermia is still unknown. Fast extracorporeal rewarming by extracorporeal circulation has been associated with cardiac dysfunction, pulmonary edema and poor neurologic outcome. Hypothesis: This study investigates whether the speed of rewarming after deep hypothermic cardiac arrest has neurological and cardiopulmonary effects. Methods: Thirty male Sprague-Dawley adult rats (450-550g) were rapidly cooled (ice packs) until 15°C core body temperature. Deep hypothermic cardiac arrest was maintained for 60 min. Thereafter rats were randomised to receive slow (90 minutes) or fast (30 minutes) rewarming by cardiopulmonary bypass to a target temperature of 35°C. After 90 minutes of reperfusion all animals underwent hemodynamic assessment by biventricular pressure-volume analysis, brain MRI and heart, lungs and brain were collected. Results: Slow rewarming preserved cardiac systolic and diastolic functions, ventricular arterial coupling and endothelium dependent relaxation. Lung edema was attenuated after slow rewarming. Cardimyocytes pro-survival kinases ERK and Akt activation were significantly higher in the slow rewarming group. MRI demonstrated enhancement of cerebral blood flow and reduction of cerebral edema after slow rewarming. Neurologic inflammatory response measured by IL-6, ICAM-1, CCL5 and TNF-α expression was significantly decreased in the slow rewarming group. Oxidative stress assessed by malondialdehyde was significantly reduced after slow rewarming. Conclusion: Slow rewarming by extracorporeal circulation after deep hypothermic cardiac arrest might improve systolic and diastolic function, preserve ventricular-arterial coupling, attenuate cerebral perfusion impairment and reduce neuronal damage.