Lung hyperinflation in chronic obstructive pulmonary disease: mechanisms, clinical implications and treatment

Abstract

Lung hyperinflation is highly prevalent in patients with chronic obstructive pulmonary disease and occurs across the continuum of the disease. A growing body of evidence suggests that lung hyperinflation contributes to dyspnea and activity limitation in chronic obstructive pulmonary disease and is an important independent risk factor for mortality. In this review, we will summarize the recent literature on pathogenesis and clinical implications of lung hyperinflation. We will outline the contribution of lung hyperinflation to exercise limitation and discuss its impact on symptoms and physical activity. Finally, we will examine the physiological rationale and efficacy of selected pharmacological and non-pharmacological ‘lung deflating’ interventions aimed at improving symptoms and physical functioning.

Keywords::

• COPD
• dyspnea
• lung hyperinflation
• respiratory mechanics
• respiratory muscles

Financial & competing interests disclosure

D Langer is a postdoctoral fellow of the Research Foundation Flanders, Belgium. DE O’Donnell has received research funding via Queen’s University from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Merck, Novartis, Nycomed and Pfizer; and has served on speakers bureaus, consultation panels and advisory boards for AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Nycomed and Pfizer. JA Neder has received research funding from Novartis and Nycomed and has served on speakers bureaus, consultation panels and advisory boards for Boehringer Ingelheim, Novartis and Chiesi Pharmaceutici. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Key issues

• Lung hyperinflation is closely associated with expiratory flow limitation and has major clinical consequences for breathlessness and exercise intolerance.

• Measurements of inspiratory capacity provide a clinically useful strategy to quantify resting hyperinflation and track dynamic hyperinflation during exercise.

• Acute-on-chronic hyperinflation (e.g., exercise, exacerbations) negatively impacts the demand/capacity imbalance of the already compromised respiratory muscles and influences clinical outcomes.

• A growing disparity between increased central neural drive and the reduced respiratory muscular/mechanical response due to hyperinflation contributes importantly to the perception of respiratory discomfort during exertion.

• Dynamic hyperinflation-related increases in intrinsic positive end-expiratory pressure may have important negative hemodynamic effects.

• Decreases in resting lung hyperinflation with bronchodilators result in a downward shift in operating lung volumes and a delay in the attainment of critical volume constraints during exercise.

• In addition to variable effects on resting lung hyperinflation, heliox, lung volume reduction surgery and slow and deep breathing can decrease the rate of dynamic hyperinflation for a given level of ventilation in selected patients.

• Pressure-generating capacity of the overburdened inspiratory muscles can be passively (assisted ventilation) or actively (inspiratory muscle training) improved with beneficial effects on dyspnea.

• Decreases in the ventilatory demands with exercise training and oxygen supplementation in some patients result in less dynamic hyperinflation for a given work rate and better tolerance to physical exertion.

Notes