Abstract

In chronic obstructive pulmonary disease (COPD), worsening expiratory flow limitation together with alteration in the elastic properties of the lung are associated with progressive lung hyperinflation and gradual decline in the resting inspiratory capacity over time. Dynamic hyperinflation (DH) refers to the variable increase in end-expiratory lung volume (EELV) above the relaxation volume (VR) of the respiratory system that occurs when expiratory flow limitation is amplified (e.g., during bronchoconstriction and acute exacerbations) or when ventilation is increased in the setting of expiratory flow limitation. During exercise, the combined factors of worsening expiratory flow limitation, increasing respiratory neural drive and breathing pattern alterations dictate the pattern and extent of DH. Acute-on-chronic hyperinflation increases the intrinsic loads on the inspiratory muscles which become functionally weakened. The combined effects of compromised respiratory and integrated cardio-circulatory function due to lung hyperinflation contribute to exercise limitation. In COPD, the resting inspiratory capacity, which indirectly reflects the extent of lung hyperinflation, dictates the limits of tidal volume expansion and thus, peak ventilatory capacity during activity. Moreover, the growing disparity between increased respiratory neural drive and the blunted respiratory muscular/mechanical response due to lung hyperinflation is mechanistically linked to dyspnea during exercise in COPD. From a clinical standpoint, measurement of lung hyperinflation is integral to the assessment of physiological impairment in individuals with COPD and can effectively be targeted for treatment. Moreover, it is now well established that lung volume reduction (deflation) provides a solid mechanistic rationale for observed improvements in dyspnea and exercise tolerance in patients with COPD following bronchodilator therapy.

Highlights

  • Expiratory flow limitation (EFL) is generally regarded as the pathophysiological hallmark of chronic obstructive pulmonary disease (COPD) [1]

  • Similowski et al [41] demonstrated that the reduction in the pressure-generating capacity of the inspiratory muscles of stable COPD patients was related to lung hyperinflation, but that diaphragmatic function in such patients was similar to normal subjects when measurements were compared at the same lung volume

  • Guenette et al found that non-hyperinflators (15 % of the large multicenter group) had similar baseline characteristics compared with FEV1-matched hyperinflators. These results suggest that dyspnea intensity was related to the constraints on Tidal volume (VT) expansion and not the magnitude of acute Dynamic hyperinflation (DH) during exercise [64]

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Summary

Introduction

Expiratory flow limitation (EFL) is generally regarded as the pathophysiological hallmark of COPD [1]. Similowski et al [41] demonstrated that the reduction in the pressure-generating capacity of the inspiratory muscles of stable COPD patients was related to lung hyperinflation, but that diaphragmatic function in such patients was similar to normal subjects when measurements were compared at the same lung volume Despite these impressive temporal adaptations, the presence of severe lung hyperinflation means that IC and ventilatory reserve in COPD is diminished and the ability to increase VT and V_ E is greatly limited when the demand suddenly rises (e.g., with exercise or exacerbation)

Consequences of lung hyperinflation at rest
Bronchodilator therapy
Conclusions
Findings
NS NS

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