Bender K A, Alexander J A, Enos J M, Skimming J W
Department of Graduate Nursing Education, University of Florida, College of Medicine, Gainesville, USA.
Am J Crit Care. 1997 Mar;6(2):127-31.
Cardiopulmonary bypass can increase pulmonary vascular tone and decrease ventilation-perfusion matching by impairing the pulmonary endothelial production of nitric oxide.
We tested the hypothesis that inhalation of exogenous nitric oxide decreases the ratio of mean pulmonary arterial pressure to mean system arterial pressure and the intrapulmonary shunt fraction and increases the ratio of arterial blood oxygen tension to fraction of inspired oxygen in patients in whom the ratio of mean pulmonary arterial pressure to mean systemic arterial pressure is more than 0.50, and the ratio of arterial blood oxygen tension to fraction of inspired oxygen is less than 300 mm Hg in the first 24 hours after cardiopulmonary bypass surgery.
Only those patients who had estimates of the ratio of mean pulmonary arterial pressure to mean systemic arterial pressure and the ratio of arterial blood oxygen tension to fraction of inspired oxygen determined preoperatively were enrolled. Hemodynamic variables were recorded, and blood samples were obtained for oximetric analysis 5 minutes before and 30 minutes after inhalation of nitric oxide began. The concentration of nitric oxide inhaled was maintained at 20 parts per million. The data were analyzed by using Friedman's repeated measures analysis of variance.
Thirteen patients were enrolled in the study. The mean preoperative ratio of mean pulmonary arterial pressure to mean systemic arterial pressure was 0.63 +/- 0.08 (standard error of the mean), and the mean preoperative ratio of arterial blood oxygen tension to fraction of inspired oxygen was 131 +/- 15 mm Hg. No differences between preoperative and postoperative values were detected. Inhalation of nitric oxide decreased the ratio of mean pulmonary arterial pressure to mean systemic arterial from 0.53 +/- 0.07 to 0.39 +/- 0.5 and increased the ratio of arterial blood oxygen tension to fraction of inspired oxygen from 167 +/- 35 mm Hg to 235 +/- 45 mm Hg. Inhalation of nitric oxide also decreased the intrapulmonary shunt fraction from 0.29 +/- 0.05 to 0.19 +/- 0.04.
Inhalation of nitric oxide selectively decreases pulmonary vascular tone and increases ventilation-perfusion matching in patients with persistent pulmonary hypertension and hypoxemia after surgery requiring cardiopulmonary bypass. Inhalation of nitric oxide may be a valuable adjunctive therapy for these patients.
体外循环可通过损害肺内皮细胞一氧化氮的生成,增加肺血管张力并降低通气-灌注匹配。
我们检验了如下假设,即对于体外循环手术后24小时内平均肺动脉压与平均体动脉压之比大于0.50且动脉血氧分压与吸入氧分数之比小于300 mmHg的患者,吸入外源性一氧化氮可降低平均肺动脉压与平均体动脉压之比以及肺内分流分数,并提高动脉血氧分压与吸入氧分数之比。
仅纳入术前测定了平均肺动脉压与平均体动脉压之比以及动脉血氧分压与吸入氧分数之比的患者。记录血流动力学变量,并在开始吸入一氧化氮前5分钟和吸入后30分钟采集血样进行血氧分析。吸入的一氧化氮浓度维持在百万分之二十。采用弗里德曼重复测量方差分析对数据进行分析。
13例患者纳入本研究。术前平均肺动脉压与平均体动脉压之比为0.63±0.08(均值的标准误),术前动脉血氧分压与吸入氧分数之比为131±15 mmHg。未检测到术前和术后值之间存在差异。吸入一氧化氮使平均肺动脉压与平均体动脉压之比从0.53±0.07降至0.39±0.5,并使动脉血氧分压与吸入氧分数之比从167±35 mmHg升至235±45 mmHg。吸入一氧化氮还使肺内分流分数从0.29±0.05降至0.19±0.04。
对于需要体外循环的手术后持续性肺动脉高压和低氧血症患者,吸入一氧化氮可选择性降低肺血管张力并增加通气-灌注匹配。吸入一氧化氮可能是这些患者的一种有价值的辅助治疗方法。