Physiology and consequences of lung hyperinflation in COPD

O’Donnell, Denis E.; Laveneziana, Pierantonio

doi:10.1183/09059180.00010002

Cited by 168 publications

(164 citation statements)

References 52 publications

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“…The presence of airflow obstruction appears to be crucial here, although loss of elastic recoil in some fit elderly individuals is associated with a tendency to DH at the end of exercise but not during it [26]. This problem is discussed in detail in one of the accompanying articles in this issue of the European Respiratory Review [27]. It is sufficient to say that there is abundant evidence that DH is highly prevalent in COPD, is more likely to occur as the airflow obstruction progresses and can be demonstrated even after self-paced corridor walking [28].…”

Section: Mechanical Determinants Of Exercise Impairment In Copdmentioning

confidence: 99%

Exercise and dyspnoea in COPD

Calverley¹

2006

European Respiratory Review

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Dyspnoea provoked either by exercise or during a disease exacerbation is one of the most feared symptoms of the chronic obstructive pulmonary disease (COPD) patient. It contributes to impaired quality of life and patients who are more limited by exertional dyspnoea are more likely to die. The physiological mechanisms responsible for these two outcomes vary in different settings, but in both situations, changes in the resting lung volume and increased activation of the respiratory muscles relative to their maximum capacity is the final common pathway.Although increased metabolic carbon dioxide production from weak or poorly conditioned muscles is an important cofactor, most patients limited by exertional dyspnoea exhibit dynamic hyperinflation that parallels their symptom intensity. This results from the longer respiratory time constant of the lungs in COPD and coexisting expiratory flow limitation during tidal breathing. The response of the chest wall muscles to this change in lung volume is variable: most patients with more severe COPD allow chest wall volume to increase, while others try to defend chest wall volume. The latter is not a good breathing strategy as the patient's exercise capacity is very limited.Treatment with bronchodilators reduces operating lung volumes and delays the time until tidal volume is mechanically limited by the inspiratory reserve volume. Breathing oxygen and heliox gas mixtures further increases exercise endurance and slows the rate at which end-expiratory lung volume increases.During exacerbations there is a consistent increase in end-expiratory lung volume and this parallels the reduction in forced vital capacity. This suggests that gas trapping due to airway closure is the main mechanism involved here, although changes in lung volume still track the symptomatic improvement in dyspnoea reported by patients both as the episode resolves and after nebulised bronchodilator treatment.

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Section: Mechanical Determinants Of Exercise Impairment In Copdmentioning

confidence: 99%

Exercise and dyspnoea in COPD

Calverley¹

2006

European Respiratory Review

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“…O'DONNELL and LAVENEZIANA [2] discuss how expiratory flow limitation leads to DH, with an emphasis on the mechanisms of air trapping. They have contrasted breathing at rest with breathing during exercise and stress the important role of respiratory rate in the process of DH.…”

Section: Introductionmentioning

confidence: 99%

Untitled

Wanner¹

2006

European Respiratory Review

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P ulmonary hyperinflation is commonly divided into static and dynamic in patients with chronic obstructive pulmonary disease (COPD). The former can be directly attributed to the emphysema-related reduction in lung elasticity, leading to a larger volume at which lung and chest wall recoil pressures are balanced. As a consequence, both total lung capacity and functional residual capacity increase above their normal levels. Conversely, dynamic hyperinflation (DH) is caused by expiratory airflow limitation, air trapping and ''autopositive end-expiratory pressure''. This further increases functional residual capacity.Extensive literature has accumulated on the objective and subjective manifestations and sequelae of pulmonary hyperinflation in COPD, including effects on respiratory muscle function, ventilation, work of breathing, exercise tolerance, cardiovascular function, dyspnoea and health status. The purpose of the articles in this issue of the European Respiratory Review is to summarise some of this information by addressing the physiology, clinical consequences and several established and novel treatment modalities targeting pulmonary hyperinflation in patients with COPD.Inflammation is now recognised as a key element in the pathogenesis of COPD. AUGUSTI and SORIANO [1] therefore seek to point out interactive processes that may exist between hyperinflation and inflammation.Soon after the re-introduction of lung volume reduction surgery to treat COPD, it became clear that a major benefit of the procedure was related to a reduction in static and DH, and an increase in inspiratory capacity. Since then, other surgical and nonsurgical therapies have been tested and found to reduce hyperinflation and its clinical consequences. In some of these studies, hyperinflation as an end-point rather than the intervention itself was novel. Other studies have highlighted new experimental approaches to reversing hyperinflation. Most of these therapeutic modalities are covered in this issue of the Review.O'DONNELL and LAVENEZIANA [2] discuss how expiratory flow limitation leads to DH, with an emphasis on the mechanisms of air trapping. They have contrasted breathing at rest with breathing during exercise and stress the important role of respiratory rate in the process of DH. They also point to the clinical consequences of DH in COPD, especially dyspnoea and exercise intolerance.AGUSTI and SORIANO [1] propose that DH could have a pro-inflammatory action in patients with COPD and that the resulting inflammation could lead to structural and mechanical changes in the lung, which further promote DH. Given these interrelationships, AGUSTI and SORIANO [1] speculate that bronchodilators should have antiinflammatory effects by reducing DH, and that anti-inflammatory agents should have a beneficial effect on DH in patients with COPD.CALVERLEY [3] addresses the relationship between exercise and dyspnoea, and the critical role of DH in the process. By using a new noninvasive method to continuously assess chest wall dimensions, CALVERLEY [3] h...

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“…Another putative mechanism is the effect of increased systemic inflammation, with airflow obstruction as an independent predictor of atherosclerosis [15]; treatment to reduce systemic inflammation in COPD has yet to be successful [16,17]. There are likely to be direct effects on cardiac function as a consequence of vascular remodelling, originally described in the seminal paper by DORNHORST [18], and that of dynamic hyperinflation [19].…”

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confidence: 99%