MECHANISMS OF GAS-EXCHANGE IMPAIRMENT IN IDIOPATHIC PULMONARY FIBROSIS
MECHANISMS OF GAS-EXCHANGE IMPAIRMENT IN IDIOPATHIC PULMONARY FIBROSIS
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DOI：
10.1164/ajrccm/143.2.219
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发表时间：
1991-02-01
期刊：
影响因子：
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通讯作者：
RODRIGUEZROISIN, R
中科院分区：
文献类型：
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作者：
AGUSTI, AGN;ROCA, J;RODRIGUEZROISIN, R
为了研究特发性肺纤维化（IPF）患者肺气体交换功能障碍的机制，并评估其与CO弥散量（DL（CO））的潜在关系，我们研究了15例IPF患者（平均DL（CO），预测值的52%）在休息（呼吸室内空气和纯氧）和运动时的情况。我们测量了肺血流动力学和呼吸气体交换变量，并使用多种惰性气体消除技术分离了动脉低氧血症的通气-灌注（VAQ）不匹配和O2扩散限制成分。静息时VA/Q不匹配为中度（2 - 4%的心输出量灌注不良或不通气的肺单位），19%的AaPo 2是由于O2扩散限制。运动时VA/Q不匹配没有恶化，但动脉低氧血症的弥散成分显著增加（40%AaPo2，p < 0.005）。我们观察到，肺血管张力较高（低氧性肺血管收缩释放较多）的患者运动时肺动脉高压较轻（p < 0.005），VA/Q不匹配较少[静息时（p < 0.005）和运动时（p < 0.0025）]，运动时动脉PO 2较高（p = 0.01）。我们还发现，经肺泡容积（Kco）校正的DL（CO）与运动期间低氧血症的机制[VA/Q不匹配（p < 0.025）和O2扩散限制（p < 0.05）]以及运动引起的肺血管阻力增加（p < 0.005）相关。总之，我们发现肺血管异常是调节IPF气体交换的关键，尤其是在运动期间。我们建议在IPF患者的临床评估中对肺泡容积（Kco）进行DL（co）的常规校正，因为后者似乎是运动期间气体交换受损严重程度和肺血管受累程度的有用功能指标。
To investigate the mechanisms of pulmonary gas-exchange impairment in idiopathic pulmonary fibrosis (IPF) and to evaluate their potential relationship to the CO diffusing capacity (DL(CO)), we studied 15 patients with IPF (mean DL(CO), 52% of predicted) at rest (breathing room air and pure O2) and during exercise. We measured pulmonary hemodynamics and respiratory gas-exchange variables, and we separated the ventilation-perfusion (VAQ) mismatching and O2 diffusion limitation components of arterial hypoxemia using the multiple inert gas elimination technique. At rest VA/Q mismatching was moderate (2 to 4% of cardiac output perfusing poorly or unventilated lung units), and 19% of AaPo2 was due to O2 diffusion limitation. During exercise VA/Q mismatch did not worsen but the diffusion component of arterial hypoxemia increased markedly (40% AaPo2, p < 0.005). We observed that those patients with higher pulmonary vascular tone (more release of hypoxic pulmonary vasoconstriction) showed less pulmonary hypertension during exercise (p < 0.005), less VA/Q mismatching [at rest (p < 0.005) and during exercise (p < 0.0025)], and higher arterial PO2 during exercise (p = 0.01). We also found that DL(CO) corrected for alveolar volume (Kco) correlated with the mechanisms of hypoxemia during exercise [VA/Q mismatching (p < 0.025) and O2 diffusion limitation (p < 0.05)] and with the increase in pulmonary vascular resistance elicited by exercise (p < 0.005). In conclusion, we showed that the abnormalities of the pulmonary vasculature are key to modulate gas exchange in IPF, especially during exercise. We recommend the routine correction of DL(co) for alveolar volume (Kco) in the clinical assessment of patients with IPF because the latter seems to be a useful functional indicator of both the severity of gas-exchange impairment during exercise and the degree of pulmonary vascular involvement.