Pulmonary vasodilation during cardiopulmonary resuscitation – A randomized, controlled porcine study

• Published in: Resuscitation Vol. 202; p. 110329
• Main Authors: 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
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 01.09.2024
• Subjects: Advanced Life Support; Cardiac arrest; Cardiopulmonary Resuscitation; Cardiovascular research; Emergency medicine; Inhaled nitric oxide; Intensive Care; Myocardial ischemia; Pulmonary vasodilation therapy; Resuscitation outcomes; Return of spontaneous circulation; Ventricular fibrillation; Cardiopulmonary Resuscitation; Inhaled nitric oxide; Resuscitation outcomes; Emergency medicine; Cardiac arrest; Myocardial ischemia; Pulmonary vasodilation therapy; Cardiovascular research; Intensive Care; Return of spontaneous circulation; Ventricular fibrillation; Advanced Life Support
• ISSN: 0300-9572; 1873-1570; 1873-1570
• DOI: 10.1016/j.resuscitation.2024.110329

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.