Introduction: Numerous studies have confirmed that therapeutic hypothermia is beneficial to improve cardiac outcomes in post-cardiac arrest syndrome. A recent investigation demonstrated that the cooling via esophagus is an effective, easily-performed approach to induce rapid hypothermia. Here we investigated the effects of esophageal cooling on post-resuscitation cardiac outcomes in a porcine cardiac arrest model.
Hypothesis: Therapeutic hypothermia induced by esophageal cooling would be superior to conventional surface cooling in alleviating cardiac dysfunction, tissue injury and inflammation after CPR.
Methods: Ventricular fibrillation (VF) was induced in 27 male domestic pigs weighing between 35-41 kg. CPR was initiated after 7 mins of untreated VF. Defibrillation was attempted after 5 mins of CPR. The animals were randomized into 3 groups: 1) normothermia, 2) surface cooling, and 3) esophageal cooling. At 5 mins after resuscitation, blood temperature was reduced to target temperature of 33°C and then maintained until 24 hrs post-resuscitation in the hypothermic two groups.
Results: Rapid hypothermia was observed in the esophageal cooling group, in which the cooling rate was significantly faster than the surface cooling group (2.8±0.7°C/h vs. 1.5±0.4°C/h, p<0.01). Significant improvement in cardiac dysfunction and tissue injury after resuscitation were observed in the esophageal cooling and surface cooling groups when compared with the normothermia group. The contents of cardiac inflammatory cytokines were also significantly lower in the hypothermic two groups than the normothermia group. However, the cardioprotective effects of hypothermia were further significantly enhanced in animals treated with esophageal cooling compared to the surface cooling group (Table).
Conclusion: Rapid esophageal cooling was significantly better than surface cooling in improving post-resuscitation cardiac dysfunction, tissue injury and inflammation.