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

Children with asthma, even those with severe persistent disease, can have forced expiratory volume in 1 second (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 00.9 L/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.