Nørholt Casper, Johannsen Cecilie M, Baltsen Cecilie D, Lund Margrete H, Kjærsgaard Lykke, Solberg Sara M A, Hørsdal Oskar K, Vammen Lauge, Dam Lyhne Mads, Andersen Lars W, Granfeldt Asger
Department of Anaesthesiology and Intensive Care, Aarhus University Hospital, Denmark; Department of Clinical Medicine, Aarhus University, Denmark.
Department of Anaesthesiology and Intensive Care, Aarhus University Hospital, Denmark.
Resuscitation. 2024 Sep;202:110329. doi: 10.1016/j.resuscitation.2024.110329. Epub 2024 Jul 24.
During resuscitation pulmonary artery pressure (PAP) increases. This reduces left ventricular filling, leading to decreased blood flow. Inhaled nitric oxide (iNO) produces selective pulmonary vasodilation. We hypothesized that iNO would lower PAP during resuscitation resulting in increased survival.
30 pigs (40 kg) were subjected to cardiac arrest for 9.5 min after myocardial ischemia induced by coronary artery occlusion of the left anterior descending artery and ventricular fibrillation. During resuscitation, the pigs were randomized to 40 ppm iNO or placebo. The primary outcome was return of spontaneous circulation (ROSC). Pigs achieving ROSC underwent 4-hours intensive care.
The ROSC rate was 9/14 (64%) in the control group and 11/16 (69%) in the iNO group (OR 1.2 95%CI [0.3;5.6], p > 0.99). There was no difference in diastolic aorta pressure/PAP ratio (mean difference -0.99 [95% CI: -2.33-0.36], p = 0.14). Mean pulmonary artery pressure was lower in the iNO group 60 and 120 min after ROSC (mean difference: -12.18 mmHg [95%CI: -16.94; -7.43] p < 0.01 and -5.43 [95%CI: -10.39; -0.46] p = 0.03). Troponin I levels in the iNO group were significantly higher 60 and 120 min after ROSC (mean difference: 266105 ng/l [95%CI: 6356; 525855] p = 0.045 and 420049 ng/l [95%CI: 136779; 703320], p = 0.004). The area at risk of the heart was 33% (SD 1) in controls and 34% (SD 1) in the iNO group. The infarct size divided by the area at risk was 55% (SD 3) in controls and 86% (SD 1) in the iNO group, p = 0.01.
Application of iNO did not improve the rate of ROSC or hemodynamic function but increased myocardial injury.
在复苏过程中，肺动脉压（PAP）会升高。这会减少左心室充盈，导致血流减少。吸入一氧化氮（iNO）可产生选择性肺血管舒张。我们假设iNO会在复苏过程中降低PAP，从而提高生存率。
30头猪（40千克）在左前降支冠状动脉闭塞和心室颤动诱导的心肌缺血后心脏骤停9.5分钟。在复苏过程中，将猪随机分为40ppm的iNO组或安慰剂组。主要结局是自主循环恢复（ROSC）。实现ROSC的猪接受4小时的重症监护。
对照组的ROSC率为9/14（64%），iNO组为11/16（69%）（比值比1.2，95%置信区间[0.3；5.6]，p>0.99）。舒张期主动脉压/PAP比值无差异（平均差值-0.99[95%置信区间：-².³³-0.36]，p=0.14）。ROSC后60分钟和120分钟时，iNO组的平均肺动脉压较低（平均差值：-12.18mmHg[95%置信区间：-16.94；-7.43]，p<0.01；-5.43[95%置信区间：-10.39；-0.46]，p=0.03）。ROSC后60分钟和120分钟时，iNO组的肌钙蛋白I水平显著更高（平均差值：266105ng/l[95%置信区间：6356；525855]，p=0.045；420049ng/l[95%置信区间：136779；703320]，p=0.004）。对照组心脏的危险区域为33%（标准差1），iNO组为34%（标准差1）。梗死面积除以危险区域，对照组为55%（标准差3），iNO组为86%（标准差1），p=0.01。
应用iNO并未提高ROSC率或血流动力学功能，但增加了心肌损伤。
