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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 2 0min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。
Objective: To investigate the pathogenesis of high altitude pulmonary edema. Methods: Right heart floating catheter detection method, 9 cases of high altitude pulmonary edema patients and 9 cases with the same altitude human health indicators were measured, but also observed the inhalation of pure oxygen in patients with high altitude pulmonary edema hemodynamics The impact of learning. Results: The average pulmonary artery pressure, pulmonary vascular resistance and cardiac index were significantly higher in the patients with high altitude pulmonary edema than those in the same height group. There was no significant difference in pulmonary artery wedge pressure and right atrial pressure between the two groups After oxygen, heart rate, mean pulmonary artery pressure, pulmonary vascular resistance and cardiac index were significantly decreased in patients with pulmonary edema in high altitude, especially pulmonary hypertension and pulmonary vascular resistance decreased significantly, the average pulmonary pressure after 1min oxygen was obvious Decreased, oxygen 5min, down to the lowest value, but still not reached the control group after 20min oxygen levels. Conclusion: High altitude pulmonary edema is non-cardiogenic pulmonary edema, pulmonary hypertension plays an important role in its pathogenesis.