Lung-volume reduction surgery (LVRS) improves static lung elastic recoil in selected patients with severe chronic obstructive pulmonary disease (COPD). This explains the increase in FEV1 in many COPD patients who undergo LVRS, but fails to explain clinical improvement in those without changes in FEV1. We prospectively evaluated 17 patients after pulmonary rehabilitation but prior to and again at least 3 mo after bilateral LVRS done via median sternotomy. In addition to pulmonary function, lung elastic recoil, walking distance, and exercise capacity, we evaluated static and dynamic respiratory muscle (RM) function, and dyspnea. In 12 patients we also quantified dynamic hyperinflation (end-expiratory and end-inspiratory lung volume [EELV and EILV, respectively]). After LVRS, FEV1 rose from 26.7 +/- 1.8 to 39.0 +/- 3.7% predicted (p < 0.004), whereas TLC dropped from 134.7 +/- 4.8 to 118.3 +/- 4.4% predicted (p < 0.0002), and RV from 239.6 +/- 14.8 to 180.3 +/- 8.7% predicted (p < 0.0002). Isowork dyspnea decreased as assessed with a visual analogue scale (VAS) (79.6 +/- 5.2 versus 49.3 +/- 7.5 mm, p < 0.005) and the Borg scale (7.1 +/- 0.6 versus 3.5 +/- 0.6, p = 0.002). Walking distance improved significantly and, in the 12 patients in whom they were measured, EELV and EILV decreased at rest and at isowork. Maximal transdiaphragmatic pressure rose from 67.1 +/- 8.3 to 92.0 +/- 7.5 cm H2O (p < 0.03). Resting RM function changed little, but at isowork improved significantly after LVRS. Excluding one outlier, there was a strong linear correlation between the change in Borg-scale score at equivalent work loads before and after LVRS and the change in EELV (% predicted TLC, r = 0.75, p < 0.001), as well as between the change in Borg-scale score and the absolute decrease in end-expiratory pleural pressure (Ppl(e)) (r = 0.78, p = 0.004). Successful LVRS improves not only lung recoil, but also respiratory muscle function, and reduces dynamic hyperinflation. These changes help explain the decreased dyspnea and improved exercise capacity seen after LVRS, and add to current understanding of the mechanisms by which this procedure may help selected patients with severe emphysema.

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Respiratory muscle dysfunction limits exercise endurance in severe chronic airflow obstruction (CAO). To investigate whether inspiring O2 alters ventilatory muscle recruitment and improves exercise endurance, we recorded pleural (Ppl) and gastric (Pga) pressures while breathing air or 30% O2 during leg cycling in six patients with severe CAO, mild hypoxemia, and minimal arterial O2 desaturation with exercise. At rest, mean (+/- SD) transdiaphragmatic pressure (Pdi) was lower inspiring 30% O2 compared with air (23 +/- 4 vs. 26 +/- 7 cmH2O, P less than 0.05), but the pattern of Ppl and Pga contraction was identical while breathing either gas mixture. Maximal transdiaphragmatic pressure was similar breathing air or 30% O2 (84 +/- 30 vs. 77 +/- 30 cmH2O). During exercise, Pdi increased similarly while breathing air or 30% O2, but the latter was associated with a significant increase in peak inspiratory Pga and decreases in peak inspiratory Ppl and expiratory Pga. In five out of six patients, exercise endurance increased with O2 (671 +/- 365 vs. 362 +/- 227 s, P less than 0.05). We conclude that exercise with O2 alters ventilatory muscle recruitment and increases exercise endurance. During exercise inspiring O2, the diaphragm performs more ventilatory work which may prevent overloading the accessory muscles of respiration.

Background: Patients with chronic obstructive pulmonary disease (COPD) can experience 'exacerbations' of their conditions. An exacerbation is an event defined in terms of subjective descriptors or symptoms, namely dyspnoea, cough and sputum that worsen sufficiently to warrant a change in medical management. There is a need for reliable markers that reflect the pathological mechanisms that underlie exacerbation severity and that can be used as a surrogate to assess treatment effects in clinical studies. Little is known as to how existing study variables and suggested markers change in both the stable and exacerbation phases of COPD. In an attempt to find the best surrogates for exacerbations, we have reviewed the literature to identify which of these markers change in a consistent manner with the severity of the exacerbation event.