Lung mechanical properties distinguish children with asthma with normal and diminished lung function

Abstract

Children with asthma, even those with severe persistent disease, can have forced expiratory volume in 1second (FEV1 ) values ≥100% of predicted, while others have diminished FEV1 . We sought to characterize the lung mechanical properties underlying these two asthma phenotypes and the mechanisms explaining the paradox of severe asthmatic children, whom when clinically stable can have an FEV1 >100% of predicted, but during an acute bronchospastic episode can experience a life-threatening asthma event. Lung mechanics were evaluated in three groups of children: asthmatics with FEV1 ≥100% (HFEV1 ; n=13), asthmatics with FEV1 ≤80% (LFEV1 ; n=14) and non-asthmatic controls (n=10). A linear mixed model was used to examine the relationship between volume and static transpulmonary pressures obtained at total lung capacity (TLC); actual TLC %of predicted and flow; and static transpulmonary pressure and flow. HFEV1 asthmatics had larger airways (FEV1 z-scores 1.12 vs -2.37; P<.05), greater lung volumes (mean % of predicted TLC 134.8% vs 109.6%; P<.05) and lower airway resistance (mean %of predicted Raw 101.9% vs 199.9%; P<.05) compared to the LFEV1 group. Moreover, HFEV1 asthmatics had significantly reduced elastic recoil pressure (pressure-volume curve shifted upward and to the left) and higher lung compliance (0.21 vs 00.9L/cm H2 O; P<.05) compared to the LFEV1 group. The pressure-flow curves revealed the LFEV1 group to have significantly increased resistance to flow in the upstream segment of the airways at all lung volumes studied compared to HFEV1 . HFEV1 asthmatic children display distinct lung mechanical proprieties compared to their LFEV1 asthmatic peers. With loss of elastic recoil pressure, the HFEV1 group could generate normal FEV1 due to proportionally enlarged airways and reduced airway resistance, while airflow limitation in the LFEV1 is due to increased airway resistance. Loss of elastic recoil and interdependence during acute bronchoconstriction episodes may predispose the HFEV1 group to catastrophic reductions in airflow.