Lung de-recruitment in the allergic asthma of obesity: evidence from an anatomically based inverse model

Abstract

The increase in asthma associated with the obesity epidemic cannot simply be due to airway hyperresponsiveness from chronic lung compression because chronic lung compression is a feature of obesity in general. We therefore sought to investigate what other factors might be at play in the impaired lung function seen in obese individuals with asthma. We measured respiratory system impedance in four groups - Lean Control, Lean Allergic Asthma, Obese Control, and Obese Allergic Asthma - before and after administration of albuterol. Impedance measurements were fit with an anatomically based computational model of lung mechanics that represents the airway tree as a branching structure with a uniform degree of asymmetry and a fixed radius scaling ratio, , between branches of sequential order. The two model parameters that define the airway tree, and tracheal radius, varied only modestly between the four study groups, indicating relatively minor differences in airway caliber. In contrast, respiratory system elastance was 57, 34, 143, and 271 cmH2O.L-1, respectively, for the four groups, suggesting that obesity induced significant lung de-recruitment that was exacerbated by allergic asthma. In addition, when the radii of the individual branches of the airway tree were varied randomly, we found that roughly half the terminal airways had to be closed in order to have the model fit the data well. We conclude that de-recruitment of small airways is a particular feature of Obese Allergic Asthma, and this can be inferred from respiratory system impedance fit with an anatomically based computational model.

The role of oscillometry in asthma

“…The presence of airway dysanapsis and peripheral airways dysfunction measured by oscillometry in obese children has been associated with uncontrolled asthma, though this association is not significant when obesity is adjusted for abnormal lung mechanics [54]. Using a computational model, investigators determined respiratory system elastance is more dramatically increased in obesity with allergic asthma than obesity alone, which is partially mitigated by bronchodilators [55 ▪ ]. These findings suggest that changes in reactance in obese people with asthma are more likely due to peripheral airway closure with air trapping than with alveolar collapse and atelectasis.…”