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Role of the Nitric Oxide (NO) in Pre-oxygenation Before Anesthetic Induction in Patients With a Pulmonary Hypertension in Cardiac Surgery. Pilot Study of Feasibility

University Hospital, Clermont-Ferrand · 2015
ClinicalTrials.gov · Datasets · License: Public Domain · 2015
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cardiac-surgerynitric-oxidepulmonary-hypertension
The pulmonary hypertension (HTP) due to a left heart disease or a hypoxemiant lung disease is frequent in cardiac surgery. The HTP represents an independent risk factor of morbidity and mortality in cardiac surgery, entering to the criteria of Euroscore evaluation (European System for Cardiac Operative Risk Evaluation). An acute perioperative hemodynamic decompensation of these patients is frequent. Perioperative hemodynamic modifications, hypoxemia, hypercapnia, sympathetic stimulation, increase pulmonary vascular resistances (RVP) and might provoke right ventricular failure. The anesthetic induction and the beginning of mechanical ventilation are the most sensible times due to the risk of hemodynamic decompensation. The suppression of the sympathetic tonus which is consequence of the anesthetic induction, decrease the systemic vascular resistances and lead to decrease of blood pressure. In return, the anesthetic induction is associated with an increase of pulmonary vascular resistances, resulting in increase of the postcharge and the work of the right ventricle (VD). These systemic and pulmonary hemodynamic modifications can lead to equalization, or even an inversion of the systemic and pulmonary pressures. As consequence, a hemodynamic collapse or even a heart arrest can arise. The patients suffering from HTP are hypoxemic. They have very limited oxygen reserves due to decrease of the functional residual capacity (CRF). The apnea period, which follows the anesthetic induction, is often associated with a fast desaturation, even if a good pre-oxygenation was performed before. This desaturation causes an increase of the pulmonary vascular resistances with the hemodynamic consequences previously mentioned. A risk of hypoxic heart arrest is also present. Nitric Oxide (NO) is an endogenous mediator produced from the vascular endothelium. The NO is a powerful vasodilator and is used in intensive care in inhaled way as selective pulmonary vasodilator (iNO). NO decrea
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