Jordanoglou J, Latsi P, Chroneou A, Koulouris N G
Respiratory Function Laboratory, Department of Respiratory Medicine, University of Athens Medical School, 'Sotiria' Hospital for Diseases of the Chest, Athens, Greece.
Acta Physiol (Oxf). 2007 Oct;191(2):161-8. doi: 10.1111/j.1748-1716.2007.01742.x.
The classical equations for measuring the mean and the ideal alveolar O(2) tension are based on assumptions, which are shown to be invalid. So we thought to develop a new, non-invasive method for measuring the mean alveolar P,O(2) within the volume domain (PA,O(2(Bohr))). This method is based on the oxygen uptake vs. tidal volume curve (VO(2) vs. VT) obtained during tidal breathing of room air and/or air enriched with oxygen.
PA,O(2(Bohr)) and the ideal alveolar PO(2) (PA,O(2(ideal))) were simultaneously measured in 10 healthy subjects and 34 patients suffering from chronic obstructive pulmonary disease (COPD) breathing tidally room air at rest. Additionally, 10 subjects (three healthy subjects and seven COPD patients) were studied while breathing initially room air and subsequently air enriched with oxygen.
According to the results, PA,O(2(Bohr)) considerably differed from PA,O(2(ideal)) (P = 0.004). The cause of the difference, at the individual's R, is: (1) the difference between the arterial and Bohr's alveolar CO(2) tension, mainly in COPD patients, and (2) the inequality between Bohr's alveolar part of the tidal volume for CO(2) and O(2). Furthermore, end-tidal gas tension (PET,CO(2) and PET,O(2)) differed from Pa,CO(2) and PA,O(2(Bohr)) respectively.
The deviation of PA,O(2(Bohr)) from PA,O(2(ideal)) has a definite impact on Bohr's dead space ratio for O(2) and CO(2), and on the alveolar-arterial O(2) difference. The difference (PA,O(2(Bohr)) - PA,O(2(ideal))) is not related to the pathology of the disease. So, gas exchange within the lungs should be assessed at the subject's R from PA,O(2(Bohr)) and PA,CO(2(Bohr)) but not from PA,O(2(ideal)) nor Pa,CO(2).
用于测量平均及理想肺泡氧分压的经典公式基于一些假设，而这些假设已被证明是无效的。因此，我们试图开发一种新的非侵入性方法来测量容积域内的平均肺泡氧分压（PA,O(2(Bohr))）。该方法基于在室内空气和/或富氧空气潮气呼吸过程中获得的氧摄取量与潮气量曲线（VO(2) 与VT）。
对10名健康受试者和34名患有慢性阻塞性肺疾病（COPD）的患者在静息状态下进行室内空气潮气呼吸时，同时测量PA,O(2(Bohr))和理想肺泡氧分压（PA,O(2(ideal))）。此外，对10名受试者（3名健康受试者和7名COPD患者）在最初呼吸室内空气随后呼吸富氧空气时进行了研究。
根据结果，PA,O(2(Bohr))与PA,O(2(ideal))有显著差异（P = 0.004）。在个体呼吸商（R）时差异的原因是：（1）动脉血与Bohr肺泡二氧化碳分压之间的差异，主要见于COPD患者，以及（2）潮气量中用于二氧化碳和氧气的Bohr肺泡部分不相等。此外，呼气末气体分压（PET,CO(2)和PET,O(2)）分别与动脉血二氧化碳分压（Pa,CO(2)）和PA,O(2(Bohr))不同。
PA,O(2(Bohr))与PA,O(2(ideal))的偏差对氧气和二氧化碳的Bohr死腔率以及肺泡-动脉氧分压差有明确影响。差异（PA,O(2(Bohr)) - PA,O(2(ideal))）与疾病的病理无关。因此，应根据受试者的呼吸商，从PA,O(2(Bohr))和PA,CO(2(Bohr))评估肺内气体交换，而不是从PA,O(2(ideal))或Pa,CO(2)进行评估。
