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Treatment of patients with chronic obstructive pulmonary disease (COPD) traditionally has been the task of the internal medicine physician. Current American Thoracic Society and World Health Organization 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 The National Emphysema Treatment Trial, a large multicenter randomized clinical trial to evaluate the effectiveness of lung volume-reduction surgery (LVRS) for the treatment of emphysema, has mandated a change in this traditional thinking. The findings of this trial, while applicable only to a defined subset of COPD patients with advanced upper lobe predominant disease and reduced exercise capacity, clearly indicate that LVRS can affect lung physiology, symptoms, and even mortality for this disease.2


Although the results of this trial have provided a new treatment option for many patients with advanced emphysema, LVRS nevertheless is associated with substantial morbidity and mortality. Even when performed by experienced physicians at tertiary referral centers, LVRS is associated with a 5% 90-day mortality rate and a 30–40% incidence of complications, including respiratory failure, prolonged air leak, pneumonia, cardiac arrhythmia, and gastrointestinal complications.3 Furthermore, when expressed in terms of quality-adjusted life-years, LVRS is more expensive than other currently accepted surgical interventions that improve quality of life for individuals with end-stage disease, such as coronary artery bypass grafting, cardiac transplantation, and lung transplantation4 (Table 89-1).

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Table 89-1. Cost Effectiveness of LVRS 

LVRS alters respiratory physiology in several ways, and improvements after treatment result from a combination of these distinct effects.5–9 As originally proposed by Brantigan and Mueller in the 1950s10 and convincingly demonstrated by Fessler and colleagues,13 LVRS partially normalizes the mechanical relationship between the hyperinflated emphysematous lung and surrounding chest wall by increasing the vital capacity and isovolume transpulmonary recoil pressures. This “resizing” process appears to be the primary mechanism responsible for physiologic 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.11 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. 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.12



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