Abstract 267: Inhaled Nitric Oxide Lowers Pulmonary Artery Pressure During Cardiopulmonary Resuscitation but Does Not Increase Survival in a Model of Prolonged Cardiac Arrest in Pigs
Introduction: We have previously shown that thoracic chest compressions during cardiac arrest (CA) result in elevated pulmonary vascular resistance (PVR), potentially impeding a return of spontaneous circulation (ROSC) by limiting circulation.
Hypothesis: Applying inhaled nitric oxide (iNO) will lower PVR during cardiopulmonary resuscitation (CPR).
Methods: 8 pigs were instrumented with an arterial line and a pulmonary artery catheter. CA was electrically induced and left untreated for 10 minutes before CPR was performed employing mechanical chest compressions and mechanical ventilation. Animals were randomized to either receive 20ppm of iNO (n = 3, iNO) or 100% Oxygen (n = 5, Control) during CPR. After 6 minutes of CPR, defibrillation was attempted. When no ROSC was achieved, chest compressions were restarted and continued for up to 30 minutes.
Results: Mean pulmonary artery pressure (MPAP) rose significantly from 9 ± 4 following 10 minutes of VF to 21 ± 7 mmHg following 1 minute of CPR in Control animals (p=0.01). Animals receiving iNO showed a significantly lesser increase in MPAP from 5 ± 1 following 10 minutes of VF to 8 ± 3 mmHg following 1 minute of CPR (p=0.18). While MPAP did not differ on baseline or during 10 minutes of VF, iNO treatment resulted in significantly lower MPAP values averaged over the first 6 minutes of CPR (10 ± 1 vs. 22 ± 1 mmHg, p<0.01 ; see Figure ; * indicates p<0.01 for MPAP iNO vs. Control). This was reflected by similar changes in PVR, which remained significantly lower in iNO treated animals during CPR (80 ± 9 vs. 188 ± 17 dyn x sec x cm-5, p<0.01). While no animal achieved ROSC in the iNO group, two of the five control animals could be successfully resuscitated.
Conclusion: Ventilation with 20ppm nitric oxide during CPR reduces MPAP and PVR following prolonged CA, but does not improve survival in these preliminary experiments. Expanding the sample size will be necessary to determine potential impact of this intervention on survival or neurocognitive outcome.
Author Disclosures: M. Derwall: None. A. Ebeling: None. A. Brücken: None. M. Fries: None.
- © 2014 by American Heart Association, Inc.