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Dr. Baydur is Professor of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California.
Correspondence to: Ahmet Baydur, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Southern California, 2025 Zonal Avenue, GNH 11-900, Los Angeles, CA 90033
Since lung volume reduction surgery (LVRS) was introduced in 1992, considerable controversy has revolved around this procedure that improves dyspnea and quality of life in patients with COPD. Measurements of physiologic variables of airway obstruction, elastic recoil pressure, gas exchange, and exercise capacity all improve within the first year after LVRS. These findings occur more dramatically with bilateral rather than with unilateral resection. In addition to these changes in conventional lung volumes and mechanics, there are at least short-term improvements in respiratory muscle function or control of ventilation in patients with severe emphysema who have undergone LVRS. In this issue of CHEST (see page 1593), Lahrmann and colleagues describe an elegant study in which they assessed the relationship between dyspnea and respiratory mechanics, muscle function, and central drive at 1, 6, and 12 months after LVRS. As expected, they found significant increases from preoperative values in FEV1 and decreases in residual volume (RV) and total lung capacity (TLC) 1 month after LVRS. More intriguing were their findings that maximum exercise capacity, maximum oxygen uptake, respiratory muscle strength, endurance capacity, central diaphragmatic drive, and dyspnea during loaded breathing all reached statistical significance not less than 6 months after LVRS. Of some clinical importance is their additional finding that even as FEV1, TLC, and RV began to return to preoperative values 12 months after LVRS, respiratory muscle function continued to improve, while intrinsic positive end-expiratory pressure decreased further during this period. Since it has been shown that diaphragmatic activity decreases when muscle length decreases for a given neural drive,1 factors other than changes in lung volume and a resumption of a more advantageous operational length of the respiratory muscles must account for the improvement in respiratory muscle function and dyspnea.
The hyperinflation of COPD takes many years to develop and may be accompanied by adaptive changes in the chest wall and respiratory muscles. Acute reductions in muscle fiber length, as occur in the diaphragm during acute hyperinflation, decrease the length of all the sarcomeres, leading to a reduction in muscle contraction force (length-tension relationship). Several animal experiments have shown that limb muscles can be remodeled2 : when muscles are immobilized for a few weeks in stretched position, they lose sarcomeres. Studies by others have demonstrated similar adaptive changes that occur in the diaphragm in experimental emphysema.3 Prolonged hyperinflation results in loss of sarcomeres with a shift of the active length-tension relationship toward shorter lengths. In addition, loss of diaphragm weight, thickness, and surface area in many COPD patients also contribute to decreased force generation.4 5 It is therefore reasonable to assume that such structural and functional changes revert towards a more normal state over a period of several weeks following LVRS. Adaptive responses would also explain the continued improvement in respiratory muscle function even as lung volumes began to deteriorate after 1 year.
In addition to respiratory muscle weakness, peripheral (limb) muscle weakness is commonly observed in patients with COPD and may contribute to exercise intolerance.6 In a recent study, Bernard and colleagues7 demonstrated that the quadriceps strength/muscle cross-sectional ratio in patients with COPD was similar to that of normal subjects, suggesting that weakness in COPD is due to muscle atrophy related to deconditioning, disuse atrophy, and possibly malnutrition. Thus, improved exercise performance and activities of daily living observed following LVRS8 may also account for the phase lag between the observed changes in lung and respiratory muscle function.
The data of Lahrmann and colleagues also show that while the intensity of dyspnea decreased by 37% 1 year after LVRS, the FEV1 actually lost more than half of the amount it had gained immediately after surgery. Indeed, several authors have found, at best, a weak correlation between FEV1 and chronic dyspnea.9 10 By contrast, in COPD patients, there is a close association between chronic dyspnea (MRC scale) and expiratory flow limitation during tidal breathing at rest,9 a common finding in patients with severe airway obstruction. Murciano and colleagues11 showed that following single lung transplantation for end-stage COPD, expiratory flow limitation at rest became uncommon, contributing to a reduction in chronic dyspnea. Furthermore, a decrease in functional residual capacity following single lung transplantation, and likely LVRS, leads to a substantial improvement in inspiratory capacity, in turn leading to a marked improvement in tidal volume during muscular exercise, and hence to enhancement of exercise performance.
The important issue is how long these adaptive changes in remodeling last after LVRS and allow the patient to continue a reasonable degree of quality of life. It is hoped that this question will be answered by the outcomes arising from the nationwide, multicenter, 7-year randomized controlled trial initiated by the National Institutes of Health. The study by Lahrmann provides an early idea by showing that, at least during the first year after LVRS, a reduced ventilatory drive contributes to a reduction in dyspnea, even as certain measurements of lung and respiratory muscle function begin to return to preoperative values. Gelb and colleagues10 showed that while several variables of lung mechanics showed significant improvement 6 to 12 months following LVRS, there was also a variable tendency for many of these indices to drift back towards presurgical values after 2 years. Such changes are akin to the loss in
elasticity of a stocking or fishnet after repeated sewing of holes in its torn fabric: the supporting fibers continue to deteriorate and stretch even as the rents are repaired. Over time the lung loses its elasticity, resulting in increased volume, dynamic airway collapse with increased intrinsic positive end-expiratory pressure, worsening dyspnea and disability, and ultimately, respiratory failure.
It remains to be seen whether surgical approaches (in conjunction with or without a rehabilitation program) offer a long-term advantage over a carefully planned and directed rehabilitation program alone.
References
This article has been cited by other articles:
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  T. Takayama, C. Shindoh, Y. Kurokawa, W. Hida, H. Kurosawa, H. Ogawa, and S. Satomi Effects of Lung Volume Reduction Surgery for Emphysema on Oxygen Cost of Breathing Chest, June 1, 2003; 123(6): 1847 - 1852. [Abstract] [Full Text] [PDF]
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