Diaphragmatic Mobility Loss in Subjects With Moderate to Very Severe COPD May Improve After In-Patient Pulmonary Rehabilitation.

Abstract

The diaphragm changes in COPD lead to functional inefficiency correlated to lung function loss. Muscle-fiber shortening follows lung hyperinflation, which results in a chronic mechanical disadvantage that impairs diaphragmatic mobility that worsens in COPD exacerbations. To correlate the diaphragmatic mobility loss to COPD severity by using M-mode ultrasonography and to verify if the diaphragmatic mobility can improve after in-patient pulmonary rehabilitation. We used M-mode ultrasonography to access diaphragmatic mobility during normal breathing or breathing at rest and deep inspiration in 52 subjects with moderate to very severe COPD who underwent pulmonary rehabilitation and 16 healthy subjects. Lung function test, arterial blood gas analysis, and a 6-min walk test were also performed. The measurements were performed at rehabilitation admission and discharge. We screened 30 subjects with severe to very severe COPD who had completed pulmonary rehabilitation. At discharge, inspiratory capacity improved, from 1.58 ± 0.5L to 1.7 ± 0.6 L (P = .04). Diaphragmatic mobility during deep inspirations increased from (mean ± SD) 4.58 ± 1.83 cm to 5.45 ± 1.56 cm (P = .05) after pulmonary rehabilitation. The diaphragmatic mobility during rest breathing was higher in the subjects with COPD (2.25 ± 0.83 cm) than in the healthy subjects (1.27 ± 0.3 cm) (P = .01). The diaphragmatic mobility for the rest breathing and deep inspirations were correlated to an FEV1 decrease (r = -0.74, P < .001; and r = 0.8, P < .001, respectively). Our findings demonstrated diaphragmatic mobility loss in the subjects with moderate to very severe COPD. These changes were correlated with COPD severity, and diaphragmatic mobility loss improved after in-patient pulmonary rehabilitation. (ClinicalTrial.gov registration NCT02838953.).