Effect of mild hypothermia on lung injury after cardiac arrest in swine based on lung ultrasound

Abstract

Abstract Background Lung injury is common in post-cardiac arrest syndrome, and is associated with increased morbidity and mortality. The aim of this study was to evaluate the effect of mild hypothermia on lung injury after cardiac arrest in swine based on lung ultrasound. Methods Twenty-three male domestic swine weighing 36 ± 2 kg were randomly assigned to three groups: therapeutic hypothermia (TH, n = 9), normothermia (NT, n = 9), and sham control (control, n = 5) groups. Sham animals only underwent surgical preparation. The animal model was established with 8 min of ventricular fibrillation followed by 5 min of cardiopulmonary resuscitation. Therapeutic hypothermia was induced and maintained until 24 h post-resuscitation in the TH group by surface blanket cooling, followed by rewarming at a rate of 1 °C/h for 5 h. The extravascular lung water index (ELWI), pulmonary vascular permeability index (PVPI), PO2/FiO2, and lung ultrasound score (LUS) were measured at baseline and at 1, 3, 6, 12, 24, and 30 h after resuscitation. After euthanizing the swine, their lung tissues were quickly obtained to evaluate inflammation. Results After resuscitation, ELWI and PVPI in the NT group were higher, and PO2/FiO2 was lower, than in the sham group. However, those measures were significantly better in the TH group than the NT group. The LUS was higher in the NT group than in the sham group at 1, 3, 6, 12, 24, and 30 h after resuscitation. The LUS was significantly better in the TH group compared to the NT group. The lung tissue biopsy revealed that lung injury was more severe in the NT group than in the TH group. Increases in LUS were highly correlated with increases in ELWI (r = 0.613; p < 0.001) and PVPI (r = 0.683; p < 0.001), and decreases in PO2/FiO2 (r = − 0.468; p < 0.001). Conclusions Mild hypothermia protected against post-resuscitation lung injury in a swine model of cardiac arrest. Lung ultrasound was useful to dynamically evaluate the role of TH in lung protection.