Mavroudis, Constantine D;
Morgan, Ryan W;
Ko, Tiffany S;
Hefti, Marco M;
Landis, William P;
Boorady, Tiffany W;
Marquez, Alexandra M;
Karlsson, Michael;
Licht, Daniel J;
Berg, Robert A;
Nadkarni, Vinay M;
Sutton, Robert M;
Kilbaugh, Todd J
Abstract 102: Inhaled Nitric Oxide Mitigates Pulmonary Hypertension and Improves Cerebral Hemodynamics During Prolonged Cardiopulmonary Pesuscitation in a Swine Model of Pediatric Cardiac Arrest
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Medientyp:
E-Artikel
Titel:
Abstract 102: Inhaled Nitric Oxide Mitigates Pulmonary Hypertension and Improves Cerebral Hemodynamics During Prolonged Cardiopulmonary Pesuscitation in a Swine Model of Pediatric Cardiac Arrest
Beteiligte:
Mavroudis, Constantine D;
Morgan, Ryan W;
Ko, Tiffany S;
Hefti, Marco M;
Landis, William P;
Boorady, Tiffany W;
Marquez, Alexandra M;
Karlsson, Michael;
Licht, Daniel J;
Berg, Robert A;
Nadkarni, Vinay M;
Sutton, Robert M;
Kilbaugh, Todd J
Beschreibung:
<jats:p>
<jats:bold>Introduction:</jats:bold>
Pulmonary hypertension may play a role in preventing ROSC during prolonged CPR. Targeted pulmonary vasodilation with inhaled nitric oxide (iNO) during CPR may improve pulmonary blood flow and improve outcomes. The purpose of this study was to study the effects of iNO in a randomized, blinded, placebo controlled, pediatric swine model of asphyxial cardiac arrest.
</jats:p>
<jats:p>
<jats:bold>Hypothesis:</jats:bold>
Animals treated with iNO will have lower pulmonary artery pressure, improved systemic hemodynamics, and increased cerebral blood flow during prolonged CPR compared to control.
</jats:p>
<jats:p>
<jats:bold>Methods:</jats:bold>
Four-week-old piglets (n=10) that underwent seven minutes of asphyxia, induction of VF, and 10 minutes of CPR were randomized to either iNO (20 ppm) or placebo in a blinded fashion starting one min into CPR and needed more than 1 defibrillation attempt. Defibrillation was attempted after 10 minutes of CPR. Animals that did not achieve ROSC by 20 minutes were euthanized. Invasive pulmonary and systemic hemodynamics, and both invasive and noninvasive cerebral hemodynamics were continuously measured. Data described as mean ± SD and compared using a generalized estimating equation regression model.
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<jats:p>
<jats:bold>Results:</jats:bold>
All 5 iNO-treated animals and 2/5 placebo-treated animals achieved ROSC. Those treated with iNO had lower mean pulmonary artery pressures (29.5 ± 9.1 vs. 48.3 ± 5.6 mmHg, p=0.04); higher mean aortic pressures (51.9 ± 6.4 vs. 35.5 ± 4.4 mmHg, p=0.01); higher cerebral blood flow (invasive: 230.4 ± 57.4 vs. 28.7 ± 42.1 % baseline, p<0.001; noninvasive: 58.4 ± 10.9 vs. 32.4 ± 8.1 % baseline, p=0.02); and higher cerebral tissue oxygenation (invasive: 33.1 ± 13.0 vs. 1.2 ± 9.8 mmHg, p=0.01; noninvasive: 38.0 ± 4.2 vs. 26.2 ± 3.1%, p=0.005) compared with placebo.
</jats:p>
<jats:p>
<jats:bold>Conclusions:</jats:bold>
Treatment with iNO during prolonged CPR results in lower pulmonary artery pressure, improved systemic hemodynamics, and increased cerebral blood flow and oxygenation. Pulmonary vasodilation may have an important role during prolonged CPR for asphyxial cardiac arrests.
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