Abstract
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.
