Treatment of patients with chronic obstructive pulmonary disease (COPD) traditionally has been the task of the internal medicine physician. Global Initiative for Chronic Obstructive Lung Disease recommendations for treatment of COPD include the use of bronchodilators, anti-inflammatory agents, oxygen therapy, aids to assist with smoking cessation, and pulmonary rehabilitation.1 While pharmacotherapy improves lung function, symptoms, quality of life, and exacerbation rates in COPD, no medical therapies have been shown to improve emphysema, where the primary abnormality is destruction of alveoli with loss of elastic recoil, and subsequent lung hyperinflation. The National Emphysema Treatment Trial (NETT), a large multicenter randomized clinical trial to evaluate the effectiveness of lung volume reduction surgery (LVRS) for the treatment of emphysema, suggested that surgical lung volume reduction, which directly addresses the problem of lung hyperinflation through resection of the most damaged tissue, should be considered for selected patients with emphysema. The findings of this trial, while applicable to a defined subset of COPD patients with advanced upper lobe predominant (ULP) emphysema and reduced exercise capacity, clearly indicate that LVRS can affect lung physiology, symptoms, and even mortality for this disease.2
LVRS alters respiratory physiology in several ways—accordingly, posttreatment improvement is multifactorial.3–10 As originally proposed by Brantigan and Mueller in the 1950s11 and convincingly demonstrated by Fessler and Permutt,4 LVRS partially normalizes the mechanical relationship between the hyperinflated emphysematous lung and the surrounding chest wall by increasing the vital capacity and isovolume transpulmonary recoil pressures. Moreover, by reducing the overall size of the hyperinflated lung, LVRS produces space within the less compliant chest cavity for the remaining lung to expand and function.
While this “resizing” process appears to be the primary mechanism responsible for improvements after lung reduction, other factors play a role. Increased recoil pressures cause an increase in airway conductance in a subset of patients, presumably by raising airway isovolume transmural pressures and increasing airway dimensions.12,13 The reduction in lung size after LVRS normalizes diaphragmatic and chest wall dimensions and improves ventilatory capacity by shortening the operating length over which the respiratory muscles contract.8–10 In a smaller number of patients, temporary improvements in oxygenation have been observed as a result of local changes in lung impedance that act to normalize ventilation/perfusion matching. LVRS also may improve dynamic lung mechanics by eliminating lung zones with the longest expiratory time constants, not only reducing the tendency for gas trapping and dynamic hyperinflation during exercise but also increasing the inspiratory capacity.14 Emerging evidence further indicates that the benefits of LVRS go beyond primary respiratory effects; LVRS may in fact improve the compromised cardiac function that is a common comorbidity in this population.15–17
Although LVRS provides a treatment option for many patients with advanced emphysema, it is a major procedure performed in a sick population and is associated with substantial morbidity and mortality. Procedural (90-day) mortality was 5.5% in NETT. ...