Mechanisms of hyperinflation in asthma.

We studied 11 mild asthmatics to verify whether the mechanisms of hyperinflation in asthma could be inhibited or overcome by passively changing lung volumes. On day 1, we induced a fall in forced expiratory volume in one second (FEV1) of 30-60% by methacholine inhalation and measured the resulting increase in FRC (delta FRC). The delta FRC was 729 +/- 378 ml (mean +/- SD). On day 2, with the subject supine in an iron lung, we measured oesophageal (Poes), gastric (Pgas) and transdiaphragmatic (Pdi) pressures, and changes in functional residual capacity (FRC) (delta V) induced by extrathoracic pressures from -20 to +20 cmH2O before and after bronchoprovocation. With positive pressures, the FRC decreased and reached a plateau at 10 cmH2O pressure or higher. This plateau was at a mean FRC of 839 ml higher after the bronchoprovocation than before. Pdi at FRC varied in the same direction as the extrathoracic pressure and was not modified by the bronchospasm. Peak inspiratory Pdi, without pressure applied in the iron lung, increased from 13.6 +/- 5.4 to 28.1 +/- 13.5 cmH2O after methacholine; extrathoracic pressure of -20 cmH2O decreased this latter value to 15.4 +/- 7.3 cmH2O (p less than 0.01). The increased lung volume and the displaced chest wall recoil curve after provocation were not inhibited by positive or negative extrathoracic pressures. Our data show that the mechanisms of hyperinflation are not eliminated or overcome by passively changing lung volumes and support the hypothesis that persisting activity of inspiratory muscles other than the diaphragm during expiration and perhaps a prolonged expiratory time constant are responsible for hyperinflation in asthma.