Background After
cardiopulmonary resuscitation, the protective effects of
therapeutic hypothermia induced by conventional cooling are limited. Recently, esophageal cooling ( EC ) has been shown to be an effective, easily performed approach to induce
therapeutic hypothermia. In this study we investigated the efficacy of EC and its effects on early markers of postresuscitation cardiac and neurological injury in a porcine model of
cardiac arrest. Methods and Results Thirty-two male domestic swine were randomized into 4 groups:
sham control, normothermia, surface cooling, and EC .
Sham animals underwent the surgical preparation only.
Ventricular fibrillation was induced and untreated for 8 minutes while defibrillation was attempted after 5 minutes of
cardiopulmonary resuscitation. At 5 minutes after
resuscitation,
therapeutic hypothermia was induced by either EC or surface cooling to reach a target temperature of 33°C until 24 hours postresuscitation, followed by a
rewarming rate of 1°C/h for 5 hours. The temperature was normally maintained in the control and normothermia groups. After
resuscitation, a significantly faster decrease in blood temperature was observed in the EC group than in the surface cooling group (2.8±0.7°C/h versus 1.5±0.4°C/h; P<0.05). During the maintenance and
rewarming phases the temperature was maintained at an even level between the 2 groups. Postresuscitation cardiac and neurological damage was significantly improved in the 2 hypothermic groups compared with the normothermia group; however, the protective effects were significantly greater in the EC group. Conclusions In a porcine model of
cardiac arrest, faster
hypothermia successfully induced by EC was significantly better than conventional cooling in improving early markers of postresuscitation cardiac and neurological injury.