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Cited by 94Chronic Obstructive Pulmonary Disease (COPD) ResearchRespiratory Support and MechanismsCardiovascular and exercise physiology

The DOI matches its Crossref record; 98 of the 98 references it cites were found in a registry or an index; none of the 174 sources its claims cite is checked for support yet.

Lung hyperinflation in COPD: applying physiology to clinical practice

Open access
O’Donnell, Denis E., Webb, Katherine A., Neder, J. Alberto·2015·COPD Research and Practice
DOI 10.1186/s40749-015-0008-8
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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 (V R ) 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.

Overview

CoChat Summary

TL;DR

Lung hyperinflation in COPD arises from expiratory flow limitation and altered lung elastic properties, and it contributes to dyspnea, exercise limitation, and cardio-circulatory impairment. This narrative review argues that measuring and targeting lung hyperinflation—especially via bronchodilator-induced deflation—has important clinical value.

Key findings

  • Resting inspiratory capacity (IC) declines as COPD worsens; a 4-year trial reported a mean pre-bronchodilator IC decline of 34–50 mL/year in moderate to very severe COPD, and patients with the lowest baseline IC had the greatest rates of exacerbation and death.
  • Dynamic hyperinflation during exercise is common: increases in end-expiratory lung volume above resting values by 0.3–0.6 L occurred in as many as 85% of patients with moderate to severe COPD during cycle exercise.
  • Severe hyperinflation, defined as an IC/TLC ratio <25%, is associated with increased cardiovascular mortality, impaired left ventricular filling, and reduced exercise tolerance; intrinsic PEEP may be as high as 6–9 cm H₂O during quiet breathing in stable severe COPD.
  • Inhaled bronchodilators increase resting IC by approximately 0.2–0.4 L or 10–15%, and bronchodilator therapy increases cycle exercise endurance time by about 20% on average, often within the clinically important range of about 100 s.

Methods

  • Narrative review of the physiology, clinical consequences, and treatment of lung hyperinflation in COPD.
  • No primary sample or new data collection; the paper synthesizes prior studies, including longitudinal, cross-sectional, exercise, imaging, and randomized bronchodilator trials.
  • Main analysis is conceptual and mechanistic synthesis, covering definitions, determinants, natural history, respiratory muscle and hemodynamic effects, dynamic hyperinflation during exacerbations and exercise, dyspnea mechanisms, and bronchodilator effects.

Limitations

  • The paper states that insufficient longitudinal data are available to precisely chart the natural history of lung hyperinflation in COPD.
  • The paper notes that the impact of dynamic hyperinflation on cardiac output and ventilatory/locomotor muscle competition during exercise merits further study, and that information on exercise responses with dual bronchodilator therapy is currently limited.
  • Evident from the text: this is a narrative review without a stated systematic search strategy or meta-analysis, so its conclusions depend on selected cited studies, some of which are small or have variable outcome measurements.

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Integrity signals

Registry

Crossref · 10.1186/s40749-015-0008-8

Cites

98 of 98 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Figures

Fig. 1 Quasistatic V -P curves of lung (PL), chest wall (P cw), and total respiratory system (P rs ) during relaxation in a sitting position. The static forces of lung and chest wall are indicated by the arrows in the drawings. PL increases its curvature with increasing lung volume, whereas the opposite is true for the Pcw. The fall in the compliance of the respiratory system at high lung volumes is therefore mainly due to the decrease in compliance of the lung, whereas at low lung volume it reflects the decreased compliance of the chest wall. The volume corresponding to each drawing is indicated by the horizontal broken lines. (From: [95])
Fig. 1 Quasistatic V -P curves of lung (PL), chest wall (P cw), and total respiratory system (P rs ) during relaxation in a sitting position. The static forces of lung and chest wall are indicated by the arrows in the drawings. PL increases its curvature with increasing lung volume, whereas the opposite is true for the Pcw. The fall in the compliance of the respiratory system at high lung volumes is therefore mainly due to the decrease in compliance of the lung, whereas at low lung volume it reflects the decreased compliance of the chest wall. The volume corresponding to each drawing is indicated by the horizontal broken lines. (From: [95])CC-BY · From the PDF
Image 2
CC-BY · From the PDF
Image 3
CC-BY · From the PDF
Image 4
CC-BY · From the PDF
Fig. 5 Tidal volume (VT), breathing frequency ( F b), dynamic inspiratory capacity (IC) and inspiratory reserve volume (IRV) are shown plotted against minute ventilation (/ _ VE) during constant work rate exercise for each forced expiratory volume in 1 s (FEV1, expressed as % predicted) quartile (Q). The upper through to lower quartiles (Q1-Q4) represent the mildest to most severe groups, respectively. Note the clear inflection (plateau) in the V T // _ VE relationship which coincides with a simultaneous inflection in the IRV. After this point, further increases in _ VE are accomplished by accelerating F b. Data plotted are mean values at steady-state rest, isotime (i.e., 2 min, 4 min), the V T // _ VE inflection point and peak exercise. (Modified from: [29])
Fig. 5 Tidal volume (VT), breathing frequency ( F b), dynamic inspiratory capacity (IC) and inspiratory reserve volume (IRV) are shown plotted against minute ventilation (/ _ VE) during constant work rate exercise for each forced expiratory volume in 1 s (FEV1, expressed as % predicted) quartile (Q). The upper through to lower quartiles (Q1-Q4) represent the mildest to most severe groups, respectively. Note the clear inflection (plateau) in the V T // _ VE relationship which coincides with a simultaneous inflection in the IRV. After this point, further increases in _ VE are accomplished by accelerating F b. Data plotted are mean values at steady-state rest, isotime (i.e., 2 min, 4 min), the V T // _ VE inflection point and peak exercise. (Modified from: [29])CC-BY · From the PDF
Fig. 6 Relationships between exertional dyspnea intensity and ventilation and the ratio of tidal volume to inspiratory capacity (VT/IC) are shown during symptom-limited cycle exercise in COPD. There is a progressive increase in the dyspnea/ventilation curve with worsening disease. After the VT/IC ratio plateaus (corresponding to the VT inflection point), dyspnea rises steeply to intolerable levels. Quartiles (Q) of COPD severity are based on forced expiratory volume in 1 s (FEV1) expressed as percent predicted (ranges: Q1 = 54.5 -85.1; Q2 = 43.8 -54.1; Q3 = 34.9 -43.6; Q4 = 16.5 -34.9). Data plotted are mean values at steady-state rest, isotime (i.e., 2 min, 4 min), the V T / _ VE inflection point and peak exercise. (From: [29])
Fig. 6 Relationships between exertional dyspnea intensity and ventilation and the ratio of tidal volume to inspiratory capacity (VT/IC) are shown during symptom-limited cycle exercise in COPD. There is a progressive increase in the dyspnea/ventilation curve with worsening disease. After the VT/IC ratio plateaus (corresponding to the VT inflection point), dyspnea rises steeply to intolerable levels. Quartiles (Q) of COPD severity are based on forced expiratory volume in 1 s (FEV1) expressed as percent predicted (ranges: Q1 = 54.5 -85.1; Q2 = 43.8 -54.1; Q3 = 34.9 -43.6; Q4 = 16.5 -34.9). Data plotted are mean values at steady-state rest, isotime (i.e., 2 min, 4 min), the V T / _ VE inflection point and peak exercise. (From: [29])CC-BY · From the PDF
Image 7
CC-BY · From the PDF

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Citations

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Metadata

Authors
O’Donnell, D. E., Webb, K. A., & Neder, J. A.
Affiliations
Queen's University (CA)
Corresponding author
O’Donnell, Denis E.
ORCID
Venue
COPD Research and Practice
Publisher
Springer Science and Business Media LLC
Published
2015-09-07
Volume
1
Issue
1
ISSN
2054-9040 (ISSN-L)
DOI
10.1186/s40749-015-0008-8
OpenAlex
W2117521616
Semantic Scholar
89da9539193c4986802a40915b77e5a618a9951d
Cited by
93
References
98
Citations by year
2026: 8 · 2025: 7 · 2024: 12 · 2023: 6 · 2022: 9 · 2021: 6 · 2020: 12 · 2019: 10 · 2018: 11 · 2017: 10 · 2016: 2
FWCI
5.10
Type
journal article
Language
en
Open access
Licence
Locations
COPD Research and Practice (publishedVersion, cc-by)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
  • Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
Keywords
chronic obstructive pulmonary disease, lung hyperinflation, dynamic hyperinflation, end-expiratory lung volume, expiratory flow limitation, inspiratory capacity, exercise limitation, dyspnea, inspiratory muscle weakness, lung volume reduction, bronchodilator therapy, acute exacerbation, bronchoconstriction

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CoChat. (2026). Citation check: Lung hyperinflation in COPD: applying physiology to clinical practice. https://app.cochat.ai/papers/10.1186/s40749-015-0008-8
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O’Donnell, D. E., Webb, K. A., & Neder, J. A. (2015). Lung hyperinflation in COPD: applying physiology to clinical practice. COPD Research and Practice. https://doi.org/10.1186/s40749-015-0008-8

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