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慢性阻塞性肺疾病(COPD)常见并发肺脉高压(PAH),而肺动脉压(PAP)的持续升高是导致肺心病的重要环节。故PAH的产生和严重程度明显地影响着COPD的病程和预后,有效地控制和逆转PAH是防止肺心病发生和发展的关键。近年来,一氧化氮(NO)吸入疗法的开展,对长期氧疗(LTOT)认识的深入及基因治疗等方面的研究,使肺动脉高压治疗进入了一个新阶段。 1 肺动脉高压治疗的必要性 一般认为,尽管COPD病人PAP仅为轻中度升高(2.67～4.0kPa),但在COPD急性发作时、运动及睡眠时可显著上升,进而导致右心衰竭。COPD急性发作时PAP从4.0kPa升到8.0kPa,心输出量增加一倍,肺血管阻力(PVR)也升高。可以推想,PAP的反复性的显著升高可致右心功能衰竭。PVR升高及心输出量增加,说明肺血管已不能适应血流量增加的
Chronic obstructive pulmonary disease (COPD) common pulmonary hypertension (PAH), and pulmonary hypertension (PAP) continued to rise is an important part of pulmonary heart disease. Therefore, the occurrence and severity of PAH significantly affect the course and prognosis of COPD. Effective control and reversal of PAH is the key to prevent the occurrence and development of pulmonary heart disease. In recent years, advances in nitric oxide (NO) inhalation therapy, in-depth understanding of long-term oxygen therapy (LTOT) and gene therapy have led to a new phase of pulmonary hypertension therapy. Necessity of Pulmonary Hypertension It is generally believed that although PAP is only mild to moderate (2.67-4.0 kPa) in patients with COPD, acute exacerbations of COPD may lead to a significant increase in exercise and sleep, leading to right heart failure. In acute exacerbation of COPD, PAP increased from 4.0 kPa to 8.0 kPa, cardiac output doubled and pulmonary vascular resistance (PVR) increased. It can be assumed that a significant increase in the repetitiveness of PAP can cause right heart failure. PVR increased cardiac output and increased, indicating that pulmonary vascular can not adapt to increased blood flow