Troyer A D, Yernault J C, Englert M
Am Rev Respir Dis. 1977 Mar;115(3):413-21. doi: 10.1164/arrd.1977.115.3.413.
Mechanics of breathing and pulmonary diffusing properties were investigated in 24 adult patients with atrial septal defect. The patients were divided into 3 groups according to mean pulmonary artery pressure: less than 19 mm Hg (group I), 20 to 24 mm Hg (group II), and greater than 25 mm Hg (group III). The only change observed in group I was a marked increase in diffusing capacity. Patients of group II showed not only an increase in diffusing capacity, but also an overt decrease in maximal expiratory flow at all lung volumes and at any given driving pressure. For these two groups, a highly significant inverse correlation was found between changes in diffusing and elastic lung properties (r = -0.71; P less than 0.001). In patients of group III, the expiratory flow remained clearly decreased; furthermore, lung compliance and lung volumes were sharply reduced, airway resistance was elevated, and diffusing capacity was normal. Finally, from group I to group III, the lung elastic recoil became progressively diminished at small lung volumes. These results suggest that an increased pulmonary blood volume induces an increase in diffusing capacity and a slight decrease in lung compliance. Simultaneous existance of high intravascular pressure strengthens the effects of increased pulmonary blood volume on lung mechanics and results in significant abnormalities in the lung mechanical behavior. It is postulated that these effects are due to a competition for space between vessels and airways within the bronchovascular sheaths, with a subsequent compression of small airways.
对24例成人房间隔缺损患者的呼吸力学和肺弥散特性进行了研究。根据平均肺动脉压将患者分为3组:低于19 mmHg(I组)、20至24 mmHg(II组)和高于25 mmHg(III组)。I组观察到的唯一变化是弥散能力显著增加。II组患者不仅弥散能力增加,而且在所有肺容积和任何给定驱动压力下最大呼气流量明显降低。对于这两组患者,发现弥散和肺弹性特性的变化之间存在高度显著的负相关(r = -0.71;P < 0.001)。III组患者的呼气流量仍明显降低;此外,肺顺应性和肺容积急剧降低,气道阻力升高,弥散能力正常。最后,从I组到III组,小肺容积时肺弹性回缩逐渐减弱。这些结果表明,肺血容量增加会导致弥散能力增加和肺顺应性略有降低。高血管压力的同时存在会增强肺血容量增加对肺力学的影响,并导致肺机械行为出现显著异常。据推测,这些影响是由于支气管血管鞘内血管和气道之间的空间竞争,随后小气道受压所致。