Marrone O, Bonsignore M R, Romano S, Bonsignore G
Istituto di Fisiopatologia Respiratoria del CNR, Palermo, Italy.
Eur Respir J. 1994 Dec;7(12):2192-8. doi: 10.1183/09031936.94.07122192.
Our purpose was to assess how pulmonary artery pressure changes in relation to hypoxia and oesophageal pressure during obstructive sleep apnoeas. Transmural systolic pulmonary artery pressure (Ppa,STM), oxyhaemoglobin saturation (SaO2) and oesophageal pressure were analysed in two samples of consecutive obstructive apnoeas in each of four patients. In the first samples (samples A; probably recorded during non-rapid eye movement (NREM) sleep), SaO2 swings were small and repetitive. In the second samples (samples B; probably recorded during rapid eye movement (REM) sleep), they were large and more variable. Oesophageal pressure oscillated similarly in the two groups of samples. In all cases, transmural systolic pulmonary artery pressure progressively increased throughout apnoeas, and subsequently decreased in the interapnoeic periods. However, both early and end-apnoeic transmural systolic pulmonary artery pressure, remained stable in samples A; whilst they progressively increased in samples B. Transmural systolic pulmonary artery pressure at the beginning of each apnoea was inversely correlated with SaO2 at the end of the preceding apnoea. These results suggest that transmural systolic pulmonary artery pressure is influenced by SaO2, but does not vary at the same speed as SaO2. In all cases, beat-by-beat analysis showed, as expected, that the lower the oesophageal pressure, the higher the transmural systolic pulmonary artery pressure however, at each oesophageal pressure level, transmural systolic pulmonary artery pressure was more variable and higher, in samples B. In conclusion, transmural systolic pulmonary artery pressure in obstructive apnoeas shows rapid changes, which reflect oesophageal pressure variations, and slower changes, which are likely to be caused by SaO2.
我们的目的是评估在阻塞性睡眠呼吸暂停期间肺动脉压如何随缺氧和食管压力而变化。对4例患者连续出现的阻塞性呼吸暂停的两个样本中的跨壁收缩期肺动脉压（Ppa,STM）、氧合血红蛋白饱和度（SaO2）和食管压力进行了分析。在第一个样本（样本A；可能记录于非快速眼动（NREM）睡眠期间）中，SaO2波动较小且重复出现。在第二个样本（样本B；可能记录于快速眼动（REM）睡眠期间）中，SaO2波动较大且更具变异性。两组样本中食管压力的振荡情况相似。在所有情况下，跨壁收缩期肺动脉压在整个呼吸暂停期间逐渐升高，随后在呼吸暂停间期降低。然而，在样本A中，早期和呼吸暂停末期的跨壁收缩期肺动脉压保持稳定；而在样本B中，它们则逐渐升高。每次呼吸暂停开始时的跨壁收缩期肺动脉压与前一次呼吸暂停末期的SaO2呈负相关。这些结果表明，跨壁收缩期肺动脉压受SaO2影响，但变化速度与SaO2不同。在所有情况下，逐搏分析显示，正如预期的那样，食管压力越低，跨壁收缩期肺动脉压越高；然而，在每个食管压力水平上，样本B中的跨壁收缩期肺动脉压变化更大且更高。总之，阻塞性呼吸暂停中的跨壁收缩期肺动脉压显示出快速变化，这反映了食管压力的变化，以及较慢的变化，这可能是由SaO2引起的。
