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© 2007 The American Thoracic Society
doi: 10.1513/pats.200611-159CC
Pathophysiology of Dyspnea in Chronic Obstructive Pulmonary Disease
A Roundtable
1 Queen's University, Kingston, Ontario, Canada; 2 Harvard Medical School, Boston, Massachusetts; 3 University of California at San Francisco School of Nursing, San Francisco, California; 4 Los Angeles Biomedical Research Institute at Harbor–University of California at Los Angeles Medical Center, Torrance, California; 5 University of Florida, Gainesville, Florida; 6 Prince of Wales Medical Research Institute, Randwick, New South Wales, Australia; 7 University of California at Los Angeles School of Medicine, Los Angeles, California; and 8 Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire
Correspondence and requests for reprints should be addressed to Denis E. O'Donnell, M.D., F.R.C.P.I., F.R.C.P.C., Professor of Medicine & Physiology, Head, Division of Respiratory & Critical Care Medicine, Department of Medicine, Queen's University, 102 Stuart Street, Kingston, ON, K7L 2V6 Canada. E-mail: odonnell{at}post.queensu.ca
Effective management of dyspnea in chronic obstructive pulmonary disease (COPD) requires a clearer understanding of its underlying mechanisms. This roundtable reviews what is currently known about the neurophysiology of dyspnea with the aim of applying this knowledge to the clinical setting. Dyspnea is not a single sensation, having multiple qualitative descriptors. Primary sources of dyspnea include: (1) inputs from multiple somatic proprioceptive and bronchopulmonary afferents, and (2) centrally generated signals related to inspiratory motor command output or effort. Respiratory disruption that causes a mismatch between medullary respiratory motor discharge and peripheral mechanosensor afferent feedback gives rise to a distressing urge to breathe which is independent of muscular effort. Recent brain imaging studies have shown increased limbic system activation in response to various dyspneogenic stimuli and emphasize the affective dimension of this symptom. All of these mechanisms are likely instrumental in exertional dyspnea causation in COPD. Increased central motor drive (and effort) is required to increase ventilation during activity because the inspiratory muscles become acutely overloaded and functionally weakened. Abnormal dynamic ventilatory mechanics and excessive chemostimulation during exercise also result in a widening disparity between escalating central neural drive and restricted thoracic volume displacement. This neuromechanical uncoupling may form the basis for the distressing sensation of unsatisfied inspiration. Interventions that alleviate dyspnea in COPD do so by improving ventilatory mechanics, reducing central neural drive, or both—thereby partially restoring neuromechanical coupling of the respiratory system. Self-management strategies address the affective aspect of dyspnea and are essential to successful treatment.
Key Words: dyspnea • mechanisms • respiratory mechanics • exercise • dynamic lung hyperinflation
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