Usage of Inhaled Nitric Oxides in Cases of Eisenmenger Syndrome

Nenny Triastuti, M. P. Airlangga, Muhammad Anas
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引用次数: 4

Abstract

Eisenmenger Syndrome is congenital heart disease with pulmonary hypertension and shunting turning from right to left. The resistance of pulmonary vascular more than 7.5 mmHg/L/min. The right ventricle and pulmonary artery always enlarge. Physiological effects of inhaled nitric oxide therapy cause selective pulmonary vasodilation: Hypoxia alveoli causes reversible vasoconstriction, thereby increasing pulmonary wedge pressure. Inhaled nitric oxide can lower it. Moderate cardiac output and systematic arterial pressure are not affected; Selective in pulmonary because it is activated by hemoglobin; Selective vasodilation in the ventilated area, local hypoxia alveoli constricts the surrounding vascular tissue and redistributes blood flow to the ventilated lungs better and higher intraalveolar oxygen pressure. Inhaled nitric oxide enhances this mechanism by increasing blood flow through a well-ventilated lung; Bronchodilators; Pulmonary surfactant, The combination of high concentrations of inspired oxygen and high concentrations of Inhaled nitric oxide reduces the minimum surfactant surface tension.
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吸入一氧化氮在艾森曼格综合征中的应用
艾森曼格综合征是一种先天性心脏病,伴有肺动脉高压和从右向左的分流。肺血管阻力大于7.5 mmHg/L/min。右心室和肺动脉总是扩张。吸入一氧化氮治疗的生理效应引起选择性肺血管舒张:肺泡缺氧引起可逆性血管收缩,从而增加肺楔压。吸入一氧化氮可以降低血压。中度心输出量和全身动脉压不受影响;在肺中有选择性,因为它被血红蛋白激活;通气区选择性血管舒张,局部缺氧肺泡收缩周围血管组织,使血流重新分配到通气肺更好,肺泡内氧压更高。吸入一氧化氮通过增加通过通风良好的肺的血流量来增强这一机制;支气管扩张剂;肺部表面活性剂,高浓度吸入氧和高浓度吸入一氧化氮的结合降低了表面活性剂的最小表面张力。
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