Mechanisms of hyperinflation in asthma

ABSTRACT: We studied 11 mUd asthmatics to verify whether the mecha-nJsms of hyperinflation In asthma could be inhibited or overcome by pas..<;lve ly changing lung volumes. On day 1, we Induced a fall In forced expirator y volume In one second (FEV1) of 30-60 % by methacholine inhalation and measured the resulting Increase In FRC (t.FRC). The liFRC was 729±.378 ml (mean±sn). On day 2, with the subject supine in an iron lung, we measured oesophageal (Poes), gastric (Pgas) and transdlaphrag-matic (Pdl) pressures, and changes ln functional residual capacity (FRC) (t.V) Induced by extratboracic pressures from-20 to +20 cmHzO before and after bronchoprovocatJon. With positive pressures, the FRC decreased and reached a plateau at 10 cmHp pressure or higher. This plateau was at a mean FRC of 839 ml higher after the bronchoprovocatlon than before. Pdl at FRC varied In the same direction as the extrathoraclc pressure and was not modified by the bronchospasm. Peak Inspiratory Pdl, without pressure applied In the iron lung, Increased from 13.6±5.4 to 28.1±13.5 cmHlO arter methacholine; extrathoracic pressure of-20 cmH10 decreased this Jatler value to 15.4±7.3 cmH10 (p<O.Ol). The Increased lung volume and the displaced chest wall recoil curve after provocation were not Inhib-Ited by positive or negative extrathoraclc pressures. Our data show that the mechanisms of hyperinflation are not eliminated or overcome by pas-sively 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