Lung Hyperinflation in Chronic Obstructive Pulmonary Disease: Clinical and Therapeutic Relevance

Abstract

Patients with chronic obstructive pulmonary disease (COPD) develop lung hyperinflation due to limited expiratory flow, loss of elastic recoil of the lungs or the combination of both, a circumstance that can become intensified during exercise. The increased operating lung volumes, both at rest and during exercise, overload the inspiratory muscles and limit the capacity for lung expansion, resulting in a neuro-mechanical uncoupling that generates or intensifies dyspnoea and limits exercise tolerance. In addition, lung hyperinflation can contribute to cardiovascular dysfunction during exercise and be a risk factor for the development of lung cancer. Bronchodilators are effective for reducing lung hyperinflation, both in static and dynamic situations, and other therapeutic alternatives are also available. In short, lung hyperinflation is a treatable trait of COPD with an important clinical and prognostic impact that requires specific attention.

Implications of Cardiopulmonary Risk for the Management of COPD: A Narrative Review

“…Optimising COPD treatment may confer cardiopulmonary protection [ 82 ]. ICS could reduce inflammation in the lung [ 83 ], and bronchodilators decrease airway resistance and reduce hyperinflation, improving inspiratory capacity, reducing residual volume and potentially improving cardiac function [ 67 , 84 , 85 ]. Both ICS and bronchodilators may improve ventilation-perfusion matching [ 86 – 88 ], resulting in less hypoxaemia [ 86 , 87 ].…”

Dual bronchodilation for the treatment of COPD: From bench to bedside

“…Indeed, the increase in lung volume at the end of expiration can cause a decrease in preload, an increase in afterload of both ventricles and an increase in ventricular interdependence secondary to lung stretching. 81 The improved regional ventilation due to bronchodilation is a second mechanism closely related to the first. In addition, the increase in regional ventilation may improve the ventilation-perfusion mismatch, which improves venous blood flow to the left heart.…”

“…The reduction in air trapping with less compression of the pulmonary microcirculation mediates the effects of bronchodilation on cardiac filling due to increased perfusion 80 (Figure 6). Indeed, the increase in lung volume at the end of expiration can cause a decrease in preload, an increase in afterload of both ventricles and an increase in ventricular interdependence secondary to lung stretching 81 . The improved regional ventilation due to bronchodilation is a second mechanism closely related to the first.…”