Pellegrino R, Brusasco V
Servizio di Fisiopatologia Respiratoria, Azienda Ospedaliera S. Croce e Carle, Cuneo, Italy.
Eur Respir J. 1997 Mar;10(3):543-9.
We reasoned that if flow limitation plays an important role in lung hyperinflation, then bronchodilatation should be associated with a decrease of functional residual capacity (FRC) only in subjects breathing under conditions of flow limitation. This hypothesis was tested in 33 subjects with chronic airway narrowing due to asthma or chronic obstructive pulmonary disease (COPD). Flow limitation during tidal breathing was inferred from the impingement of the tidal flow-volume loop on the flow recorded during submaximally forced expiratory manoeuvres initiated from end-tidal inspiration. At baseline, flow limitation during tidal breathing was present in seven asthmatic (Group 1) and eight COPD subjects (Group 2), but absent in 11 asthmatic (Group 3) and seven COPD subjects (Group 4). FRC (mean+/-SEM) was similar in the four groups (range 117+/-7 to 134+/-6% of predicted). Inhalation of salbutamol (200 microg) caused significant increments of the forced expiratory volume in one second (FEVI) (range 6+/-1 to 21+/-8% of baseline) and forced expiratory flows at 30% of baseline forced vital capacity (V'30) (range 58+/-13 to 235+/-93% of baseline) in all groups. In groups with flow limitation during tidal breathing at baseline the FRC measured by plethysmography decreased significantly (12+/-2% in Group 1, and 9+/-2% in Group 2), and the inspiratory capacity (IC) measured by spirometry increased significantly (17+/-3% in Group 1 and 7+/-3% in Group 2). This was associated with flow limitation disappearing at the volume of baseline end-tidal expiration. In Groups 3 and 4 neither FRC nor IC changed significantly. The breathing pattern was not modified in any group after salbutamol. These findings suggest that flow limitation may contribute to generation of lung hyperinflation both in asthma and chronic obstructive pulmonary disease. We speculate that the increment of functional residual capacity could be triggered by dynamic airway compression downstream from the flow-limiting segment.
我们推断，如果气流受限在肺过度充气中起重要作用，那么支气管扩张仅应在气流受限条件下呼吸的受试者中与功能残气量（FRC）的降低相关。该假设在33名因哮喘或慢性阻塞性肺疾病（COPD）导致慢性气道狭窄的受试者中进行了测试。潮气呼吸时的气流受限是根据潮气流量-容积环对从潮气末吸气开始的次最大用力呼气动作中记录的气流的撞击来推断的。基线时，7名哮喘患者（第1组）和8名COPD患者（第2组）存在潮气呼吸时的气流受限，而11名哮喘患者（第3组）和7名COPD患者（第4组）不存在。四组的FRC（平均值±标准误）相似（范围为预测值的117±7%至134±6%）。吸入沙丁胺醇（200微克）导致所有组的一秒用力呼气量（FEV1）显著增加（范围为基线的6±1%至21±8%）和基线用力肺活量（V'30）的30%时的用力呼气流量显著增加（范围为基线的58±13%至235±93%）。在基线时存在潮气呼吸气流受限的组中，通过体积描记法测量的FRC显著降低（第1组为12±2%，第2组为9±2%），通过肺活量测定法测量的吸气容量（IC）显著增加（第1组为17±3%，第2组为7±3%）。这与在基线潮气末呼气量时气流受限消失有关。在第3组和第4组中，FRC和IC均无显著变化。沙丁胺醇后任何组的呼吸模式均未改变。这些发现表明，气流受限可能在哮喘和慢性阻塞性肺疾病中均导致肺过度充气的产生。我们推测功能残气量的增加可能由气流受限段下游的动态气道压缩引发。
