Schäfer H, Hasper E, Ewig S, Koehler U, Latzelsberger J, Tasci S, Lüderitz B
Dept of Internal Medicine, University of Bonn, Germany.
Eur Respir J. 1998 Sep;12(3):679-84. doi: 10.1183/09031936.98.12030679.
Changes in pulmonary artery pressure within an obstructive apnoea and elevations of transmural pulmonary artery pressure (Ppa,tm) towards the end of apnoea are well known. The purpose of our study was to examine which factors contribute to the increase of Ppa,tm in an apnoea. In addition, the time course of Ppa,tm and associated factors during a sleep study was investigated. We analysed the association of changes in arterial oxygen saturation (Sa,O2), oesophageal pressure (Poes) to estimate intrathoracic pressure, systolic blood pressure (BPsys) to estimate left ventricular afterload, apnoea duration and the change in Ppa,tm (deltaPpa,tm) during the course of obstructive apnoeas. Consecutive apnoeas in nonrapid eye movement (NREM)-sleep at the beginning, the middle and the end of the sleep study were analysed in six patients with obstructive sleep apnoea. The mean systolic Ppa,tm was 28.0+/-12.1 mmHg at the beginning of apnoea and 38.6+/-15.5 mmHg at the end (deltaPpa,tm 10.5+/-7.4 mmHg; p<0.0001). DeltaSa,O2 (p<0.0001; odds ratio (OR) 1.45; confidence interval (CI) 1.20-1.76) and deltaPoes (p<0.0001; OR 1.22; CI 1.11-1.34) were independently associated with deltaPpa,tm in a multiple regression analysis. Apnoea duration as well as deltaPoes, deltaPpa,tm and deltaSa,O2 were all significantly higher (p<0.05) in apnoeas at the middle of the sleep study than at the beginning or the end. In conclusion, hypoxaemia and mechanical factors as an increase in negative thoracic pressure contribute to elevations of the transmural pulmonary artery pressure during an obstructive apnoea. The time course of pulmonary haemodynamics within a steep study reveals that the highest transmural pulmonary artery pressure occurs in the middle of the night with no progressive increase towards the end of the sleep study.
阻塞性呼吸暂停期间肺动脉压力的变化以及呼吸暂停接近尾声时跨壁肺动脉压力（Ppa,tm）的升高是众所周知的。我们研究的目的是探讨哪些因素导致呼吸暂停时Ppa,tm升高。此外，还研究了睡眠研究期间Ppa,tm的时间进程及相关因素。我们分析了动脉血氧饱和度（Sa,O2）变化、用于估计胸腔内压力的食管压力（Poes）、用于估计左心室后负荷的收缩压（BPsys）、呼吸暂停持续时间与阻塞性呼吸暂停过程中Ppa,tm变化（deltaPpa,tm）之间的关联。对6例阻塞性睡眠呼吸暂停患者睡眠研究开始、中间和结束时非快速眼动（NREM）睡眠期的连续呼吸暂停进行了分析。呼吸暂停开始时平均收缩期Ppa,tm为28.0±12.1 mmHg，结束时为38.6±15.5 mmHg（deltaPpa,tm为10.5±7.4 mmHg；p<0.0001）。在多元回归分析中，DeltaSa,O2（p<0.0001；优势比（OR）1.45；置信区间（CI）1.20 - 1.76）和DeltaPoes（p<0.0001；OR 1.22；CI 1.11 - 1.34）与deltaPpa,tm独立相关。睡眠研究中间阶段呼吸暂停的持续时间以及DeltaPoes、deltaPpa,tm和DeltaSa,O2均显著高于开始或结束时（p<0.05）。总之，低氧血症和机械因素（如胸腔负压增加）导致阻塞性呼吸暂停期间跨壁肺动脉压力升高。睡眠研究期间肺血流动力学的时间进程显示，最高跨壁肺动脉压力出现在午夜，睡眠研究结束时无逐渐升高。
