高原肺水肿患者血流动力学变化及对吸氧反应的测定

目的:探讨高原肺水肿的发病机理。方法:采用右心漂浮导管检测法, 对9例高原肺水肿患者及9例同海拔高原健康人的血流动力学指标进行了检测, 同时也观察了吸入纯氧对高原肺水肿患者血流动力学的影响。结果:高原肺水肿患者发病时, 肺动脉平均压、肺血管阻力、心脏指数均明显高于同海拔高度健康人, 而患者肺动脉楔压, 右心房压力同对照组相比, 未见显著差异;吸氧后, 高原肺水肿患者心率、肺动脉平均压力, 肺血管阻力及心脏指数均较吸氧前明显下降, 特别是肺动脉平均压及肺血管阻力下降尤为明显, 肺动脉平均压力在吸氧1min后即明显下降, 吸氧5min后, 下降至最低值, 但吸氧20min后仍未达对照组水平。结论:高原肺水肿是非心源性肺水肿, 肺动脉高压在其发病中起重要作用。

Haemodynamic changes in high altitude pulmonary edema and effects of oxygen breathing

AIM: To explore the pathogenic mechanism of high altitude pulmonary edema(HAPE). METHODS: Haemodynamic changes and effects of 100 percent oxygen breathing were measured by Swan-Ganz thermistor catheters, high altitude healthy volunteers were served as controls. RESULTS: The important features of haemodynamic changes in HAPE: (1)Pulmonary arterial pressure was raised; (2)Pulmonary arterial resistance and cardiac output were raised; (3)Pulmonary artery wedge pressures and right atrial pressure were normal; (4)Pulmonary arterial pressure and resistance were induced by oxygen breathing. CONCLUSIONS: The normal pulmonary artery wedge pressures with a high cardiac output indicated that HAPE was recognized as a form of noncardiogenic pulmonary edema. The pulmonary hypertension may play an important role in the development of HAPE.