title: Physiological and functional failure in chronic obstructive pulmonary disease, congestive heart failure and cancer: a debilitating intersection of sarcopenia, cachexia and breathlessness.
abstract: Loss of skeletal muscle mass and cachexia are important manifestations of chronic obstructive pulmonary disease and have been associated with breathlessness, functional limitation and poor prognosis. A number of other life-limiting illnesses, including cancer and chronic heart failure as well as acute conditions seen in ICU such as sepsis, are characteristically associated with cachexia and sarcopenia. These conditions may have respiratory muscle atrophy of sufficient magnitude to contribute to the development of breathlessness and associated functional limitation. The purpose of this review is to summarize findings related to a direct role for severe respiratory muscle wasting in the etiology of breathlessness in advanced, life limiting illness.
  
  
  
  Localized wasting of respiratory muscles appears to be part of systemic wasting of skeletal muscles, driven by deconditioning, nutritional insufficiencies and inflammation, and because of disease-specific factors (tumor factors and exacerbations), anabolic insufficiency, autonomic dysfunction, drugs (such as corticosteroids and chemotherapy agents), mechanical ventilation and comorbidities. Marked morphological and biochemical abnormalities have been noted in diaphragm muscle biopsies.
  
  
  
  Older patients with multiple comorbidities associated with muscle loss and cachexia are likely to be at elevated risk of respiratory muscle atrophy and functional loss, because of the presence of multiple, interacting etiologic factors.
authors.affiliation: aQueen's University, Kingston, Ontario bDepartment of Oncology, University of Alberta Cross Cancer Institute, Edmonton, Alberta, Canada.
authors.forename: Deborah
authors.initials: D
authors.lastname: Dudgeon
authors.forename: Vickie E
authors.initials: VE
authors.lastname: Baracos
mesh_terms: D000375:Aging / Q000502:physiology; D002100:Cachexia / Q000453:epidemiology* / Q000503:physiopathology; D002908:Chronic Disease; D015897:Comorbidity; D004417:Dyspnea / Q000453:epidemiology* / Q000503:physiopathology; D006333:Heart Failure / Q000453:epidemiology / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D018482:Muscle, Skeletal / Q000503:physiopathology; D009369:Neoplasms / Q000453:epidemiology / Q000503:physiopathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000453:epidemiology / Q000503:physiopathology; D012121:Respiration, Artificial / Q000009:adverse effects; D012132:Respiratory Muscles / Q000503:physiopathology*; D055948:Sarcopenia / Q000453:epidemiology* / Q000503:physiopathology