Abstract 12202: Inhaled Nitric Oxide Improves Artificial Circulation and Clinical Outcomes After Prolonged Cardiac Arrest
Introduction: Primary survival after cardiac arrest can be improved by optimizing circulation during CPR when using a minimal invasive left ventricular assist device (iCPR).
Hypothesis: Inhaled nitric oxide may facilitate transpulmonary bloodflow during iCPR and thereby improve the functional outcome following cardiac arrest.
Methods: Ventricular fibrillation (VF) was electrically induced in 20 anesthetized male pigs. Animals were left untreated for 10 minutes before iCPR was attempted. Subjects received either 20ppm of inhaled nitric oxide (iNO, n = 10) or 0ppm iNO (Control, n = 10), simultaneously started with iCPR until 5 hours following return of spontaneous circulation (ROSC). Animals were weaned from the respirator and followed up for five days using overall performance categories (OPC) and a spatial memory task. On day six, all animals were anesthetized again, and brains harvested for neurohistopathologic evaluation.
Results: All animals in both groups achieved ROSC. iNO treated animals reached significantly higher iCPR flow during CPR (1.81 ± 0.30 L/min compared to 1.64 ± 0.51, p<0.001), leading to significantly higher coronary perfusion pressure (CPP) values during the 6 minutes of CPR (25 ± 13 vs. 16 ± 6 mmHg, p = 0.002). iNO animals showed significantly lower S-100 serum levels thirty minutes post ROSC (0.26 ± 0.09 vs. 0.38 ± 0.15 ng/mL, p = 0.048), as well as lower blood glucose values 120-360 minutes following ROSC.
Lower S-100 serum levels were reflected by superior clinical outcome of iNO treated animals as estimated with OPC (3 ± 2 vs. 5 ± 1, p = 0.036 on days 3 to 5). While n = 3 iNO treated animals were able to successfully participate in the spatial memory task, none of the controls were able to do so. Neurohistopathological examination of cerebral structures prone to ischemia-reperfusion injury revealed a trend towards less cerebral lesions in Neocortex, Archicortex, and Striatum when animals had been treated with iNO.
Conclusions: In a model of prolonged cardiac arrest, the administration of 20ppm iNO during and following iCPR improved transpulmonary bloodflow and mitigated post-aggression metabolism, indicated by lower serum glucose levels. These effects translated into improved clinical outcomes in iNO treated animals.
- inhaled nitric oxide
- pulmonary vasodilation
- heart arrest
- cardiopulmonary resuscitation
- heart-assist device
Author Disclosures: M. Derwall: Other Research Support; Modest; Abiomed Europe Inc.. Research Grant; Significant; German Research Foundation, Else Kröner Fresenius Foundation. A. Ebeling: None. A. Brücken: None. C. Nix: Employment; Significant; Abiomed Europe. K.W. Nolte: None. M. Fries: Research Grant; Significant; Else Kröner Foundation, German Research Foundation.
- © 2015 by American Heart Association, Inc.