Since lung volume reduction surgery (LVRS) reduces end-expiratory lung volume, we hypothesized that it may improve diaphragm strength. We evaluated 37 patients for pulmonary rehabilitation and LVRS. Before and 8 wk after pulmonary rehabilitation, 24 patients had spirometry, lung volumes, diffusion capacity, incremental symptom limited maximum exercise test, 6-min walk test, maximal static inspiratory and expiratory mouth pressures, and transdiaphragmatic pressures during maximum static inspiratory efforts and bilateral supramaximal electrophrenic twitch stimulation measured. Twenty patients (including 7 patients who crossed over after completing pulmonary rehabilitation) had baseline measurements postrehabilitation, and 3 mo post-LVRS. Patients were 58 +/- 8 yr of age, with severe COPD and hyperinflation (FEV1, 0.69 +/- 0.21 L; RV, 4.7 +/- 1.4 L). Nineteen patients had bilateral LVRS performed via median sternotomy and stapling, and 1 patient had unilateral LVRS via thorascopy with stapling. After rehabilitation, spirometry and DL(CO)/VA were not different, and lung volumes showed a slight worsening in hyperinflation. Gas exchange, 6-min walk distance, maximum oxygen uptake (VO2max), and breathing pattern during maximum exercise did not change after rehabilitation, but total exercise time was significantly longer. Inspiratory muscle strength (PImax, Pdi(max combined), Pdi(max sniff), Pdi(max), Pdi(twitch)), was unchanged after rehabilitation. In contrast, after LVRS, FVC increased 21%, FEV1 increased 34%, TLC decreased 13%, FRC decreased 23%, and FRC(trapped gas) and RV decreased by 57 and 28%, respectively. PCO2 was lower (44 +/- 6 versus 48 +/- 6 mm Hg, p < 0.003) and 6-min walk distance increased (343 +/- 79 versus 250 +/- 89 m, p < 0.001), as did total exercise time during maximum exercise (9.2 +/- 1.9 versus 6.9 +/- 2.7 min, p < 0.01). Minute ventilation (29 +/- 8 versus 21 +/- 6 L/min, p < 0.001) and tidal volume (1.0 +/- 0.33 versus 0.84 +/- 0.25 L, p < 0.001) during maximum exercise increased whereas respiratory rate was lower (28 +/- 6 versus 32 +/- 7 breaths/min, p < 0.02). Measurements of respiratory muscle strength (PImax, 74 +/- 28 versus 50 +/- 18 cm H2O, p < 0.002; Pdi(max combined), 80 +/- 25 versus 56 +/- 29 cm H2O, p < 0.01; Pdi(max sniff), 71 +/- 7 versus 46 +/- 27 cm H2O, p < 0.01; Pdi(twitch), 15 +/- 5 versus 7 +/- 5 cm H2O, p < 0.01) were all greater post-LVRS. Inspiratory muscle workload as measured by Pdi TTI was lower following LVRS (0.07 +/- 0.02 versus 0.09 +/- 0.03, p < 0.03). On multiple regression analysis, increases in PImax correlated significantly with decreases in RV and FRC(trapped gas) after LVRS (r = 0.67, p < 0.03). We conclude that LVRS significantly improves diaphragm strength that is associated with a reduction in lung volumes and an improvement in exercise performance. Future studies are needed to determine the relationship and stability of these changes over time.

The National Emphysema Treatment Trial used a multidisciplinary team approach to implement the maximum medical care protocol, including adjustment of medications and outpatient pulmonary rehabilitation for all patients and nutritional and psychological counseling as needed. This article discusses the benefits of such an approach in the care of the patient with chronic obstructive pulmonary disease. Team member roles complement each other and contribute to the goal of providing the highest-quality medical care. The primary focus of the team is to reinforce the medical plan and to provide patient education and support. This article reviews the elements of the initial patient assessment and the functional and nutritional assessment. Patient education focuses on medication use, recognition and management of chronic obstructive pulmonary disease exacerbation symptoms, smoking cessation, advance directives, and travel.

Lung volume reduction surgery (LVRS) has been suggested as improving respiratory mechanics in patients with severe chronic obstructive pulmonary disease (COPD). We hypothesized that LVRS might lengthen the diaphragm, increase its area of apposition with the chest wall, and thereby improve its mechanical function. To determine the effect of bilateral LVRS on diaphragm length, we measured diaphragm length at TLC, using plain chest roentgenograms (CXRs), in 25 patients (11 males and 14 females) before LVRS and 3 to 6 mo after LVRS. A subgroup of seven patients (reference data) also had diaphragm length measurements made with CXRs, using films made within a year before their presurgical evaluation. Right hemidiaphragm silhouette length (PADL) and the length of the most vertically oriented portion of the right hemidiaphragm muscle (VDML) were measured. Diaphragm dome height was determined from the: (1) distance between the dome and transverse diameter at the manubrium; and (2) highest point of the dome referenced horizontally to the vertebral column. Patients also underwent spirometry, measurements of lung volumes and diffusion capacity, an incremental symptom-limited maximum exercise test, and measurements of 6 min walk distance (6MWD) and transdiaphragmatic pressures during maximum static inspiratory efforts (Pdimax sniff) and bilateral supramaximal electrophrenic twitch stimulation (Pditwitch) both before and 3 mo after LVRS. Patients were 58 +/- 8 yr of age, with severe COPD and hyperinflation (FEV1 = 0.68 +/- 0.23 L, FVC = 2.56 +/- 7.3 L, and TLC = 143 +/- 22% predicted). Following LVRS, PADL increased by 4% (from 13.9 +/- 1.9 cm to 14.5 +/- 1.7 cm; p = 0.02), VDML increased by 44% (from 2.08 +/- 1.5 cm to 3.00 +/- 1.6 cm, p = 0.01), and diaphragm dome height increased by more than 10%. In contrast, diaphragm lengths were similar in subjects with CXRs made before LVRS and within 1 yr before evaluation. The increase in diaphragm length correlated directly with postoperative reductions in TLC and RV, and also with increases in transdiaphragmatic pressure with maximal sniff (Pdimax sniff), maximal oxygen consumption (V O2max), maximal minute ventilation (V Emax), and maximum voluntary ventilation following LVRS. We conclude that LVRS leads to a significant increase in diaphragm length, especially in the area of apposition of the diaphragm with the rib cage. Diaphragm lengthening after LVRS is most likely the result of a reduction in lung volume. Increases in diaphragm length after LVRS correlate with postoperative improvements in diaphragm strength, exercise capacity, and maximum voluntary ventilation.

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