论文部分内容阅读
目的 :对风湿性心脏病 (风心病 )二尖瓣狭窄合并肺动脉高压患者 ,观察术前和术后吸入 40 ppm一氧化氮 (NO)其血液动力学效应 ,以及体外循环对其效应的影响。 方法 :选择 15例风心病合并肺动脉高压行择期瓣膜置换术的患者 ,在体外循环前、后吸入 40 ppm NO气体。 结果 :术前肺血管阻力 (PVR)为 2 0～ 135 k Pa·s/ L,肺动脉压为 2 8/ 17～ 87/ 45 mm Hg(1mm Hg=0 .133k Pa)。吸入 40 ppm NO后肺动脉收缩压、肺动脉舒张压、肺动脉平均压及 PVR在体外循环前、后均明显降低 (P均 <0 .0 0 1)。在体外循环前、后肺血管阻力差值 (△ PVR) / PVR分别为 (5 3.2± 18.5 ) % (P<0 .0 0 1)和 (2 2 .7± 2 2 .2 ) % (P<0 .0 1) ,体外循环前、后两者差异极显著 (P<0 .0 0 1)。吸入 NO治疗前、后肺毛细血管楔压均无明显改变 (P>0 .0 5 ) ,而心排血量均明显增加 (P<0 .0 1)。 结论 :风心病合并肺动脉高压患者吸入 40 ppm NO,可选择性地扩张肺动脉 ,体外循环可明显减弱其效应。
Objective: To observe the hemodynamic effects of preoperative and postoperative inhalation of 40 ppm nitric oxide (NO) in patients with rheumatic heart disease (rheumatic heart disease) complicated with pulmonary hypertension and mitral stenosis, and the effects of cardiopulmonary bypass on their effects. Methods: Fifteen patients with rheumatic heart disease undergoing elective valve replacement under pulmonary hypertension were enrolled, and 40 ppm of NO gas was inhaled before and after cardiopulmonary bypass. Results: Preoperative pulmonary vascular resistance (PVR) ranged from 20 to 135 kPa · s / L and pulmonary arterial pressure ranged from 28/17 to 87/45 mm Hg (1 mm Hg = 0.133 kPa). Pulmonary artery systolic pressure, pulmonary artery diastolic pressure, pulmonary artery mean pressure and PVR decreased significantly (P <0.01) before and after cardiopulmonary bypass. The difference of PVR / PVR before and after cardiopulmonary bypass was (52.2 ± 18.5)% (P <0.01) and (22.7 ± 2.2.2)% (P <0. 01). There was significant difference between before and after cardiopulmonary bypass (P <0. 001). There was no significant change in pulmonary capillary wedge pressure before and after inhalation of NO (P> 0.05), while cardiac output was significantly increased (P <0.01). Conclusion: In patients with rheumatic heart disease and pulmonary hypertension, inhalation of 40 ppm of NO selectively expands the pulmonary artery, and its effect can be obviously attenuated by cardiopulmonary bypass.