Kronik obstrüktif akciğer hastalığı olan olgularda efor kısıtlılığı

Kronik obstrüktif akciğer hastalığı olan olguların fonksiyonel kapasiteleri, submaksimal egzersizlerdeki dayanıklılık süreleri ve maksimal egzersiz performansları, aynı yaş ve cinsteki kişilerle karşılaştırıldığında genellikle azalmıştır. Bu hastalıkla ilgili temel fizyopatolojik değişiklikler, ekspiratuvar hava akımında obstrüksiyon ve/veya akciğer parenkimindeki patolojik değişikliklerdir. Hava yolu direncinin artması, verimsiz ventilasyon, solunumun elastik yükünün artması, hiperenflasyon, gaz değişim anomalileri ve mekanik olarak solunum kaslarının güçsüzlüğü, merkezi ve periferik sinir sisteminde hipoksik yanıtla ilgili değişik derecelerdeki bozukluklar, egzersize toleransın azalmasına yol açmaktadır. İskelet kaslarında da solunum kaslarına benzer şekilde patolojik değişiklikler gözlenmiştir. Zamanla fonksiyonel kapasite ve egzersiz toleransı azalır, bunlara bağlı olarak hafif düzeyde bir aktivite sırasında, hatta istirahat sırasında dahi dispne gelişir. Bu kısır döngünün kırılması için t›bbi tedavinin yanında mutlaka destekleyici rehabilitasyon programları uygulanmalıdır.

Effort restriction in cases with chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease usually manifest decreases in functional capacity, endurance time at submaximal exercise, and maximal exercise performance compared to age- and sex-matched healthy individuals. The main pathophysiologic changes in this disease are obstruction of expiratory airways and/or pathologic alterations in the lung parenchyma. Many factors are associated with decreased exercise tolerance, including increased airway resistance, inadequate ventilation, increased elastic loading of ventilation, hyperinflation, gas exchange abnormalities, mechanical weakness of respiratory muscles, and varying degrees of disturbances in the central and peripheral nervous systems due to hypoxic response. Skeletal muscles also undergo pathological changes similar to those in ventilation muscles. All these result in decreases in functional capacity and exercise tolerance, giving rise to dyspnea during minimal activity and even at rest. In order to break this vicious circle, supporting rehabilitation programs have to be combined with medical treatment.

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  • 1. Çö¤lü L, Selçuk ZT. Kronik obstrüktif akci¤er hastal›¤› tan› ve tedavi rehberi. Toraks Dergisi 2000;1:1-4.
  • 2. Mannino DM. COPD: epidemiology, prevalence, morbidity and mortality, and disease heterogeneity. Chest 2002;121(5 Suppl):121S-126S. ,
  • 3. Foy CG, Rejeski WJ, Berry MJ, Zaccaro D, Woodard CM. Gender moderates the effects of exercise therapy on health-related quality of life among COPD patients. Chest 2001;119:70-6.
  • 4. Tiep BL. Disease management of COPD with pulmonary rehabilitation. Chest 1997;112:1630-56.
  • 5. Bourjeily G, Rochester CL. Exercise training in chronic obstructive pulmonary disease. Clin Chest Med 2000;21:763-81.
  • 6. Nici L. Mechanisms and measures of exercise intolerance in chronic obstructive pulmonary disease. Clin Chest Med 2000;21:693-704.
  • 7. Pathogenesis, pathology and pathophysiology of COPD. Global strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Workshop Report: National Heart, Lung, and Blood Institute; 1998 April; p. 26-43.
  • 8. Karab›y›ko¤lu G. Ventilasyon-perfüzyon iliflkilerinin arter kan gazlar›na etkileri. Solunum 2000;4:193-200.
  • 9. Casaburi R. Skeletal muscle function in COPD. Chest 2000;117:267S-71S.
  • 10. Marchand E, Decramer M. Respiratory muscle function and drive in chronic obstructive pulmonary disease. Clin Chest Med 2000;21:679-92.
  • 11. Whittom F, Jobin J, Simard PM, Leblanc P, Simard C, Bernard S, et al. Histochemical and morphological characteristics of the vastus lateralis muscle in patients with chronic obstructive pulmonary disease. Med Sci Sports Exerc 1998;30:1467-74.
  • 12. Payen JF, Wuyam B, Levy P, Reutenauer H, Stieglitz P, Paramelle B, et al. Muscular metabolism during oxygen supplementation in patients with chronic hypoxemia. Am Rev Respir Dis 1993;147:592-8.
  • 13. Ramirez-Sarmiento A, Orozco-Levi M, Barreiro E, Mendez R, Ferrer A, Broquetas J, et al. Expiratory muscle endurance in chronic obstructive pulmonary disease. Thorax 2002;57:132-6.
  • 14. Mador MJ, Bozkanat E, Kufel TJ. Quadriceps fatigue after cycle exercise in patients with COPD compared with healthy control subjects. Chest 2003; 123:1104-11.
  • 15. Bloomfield SA. Changes in musculoskeletal structure and function with prolonged bed rest. Med Sci Sports Exerc 1997;29:197-206.
  • 16. Polkey MI. Muscle metabolism and exercise tolerance in COPD. Chest 2002;121(5 Suppl):131S-135S.
  • 17. Schols AM, Wouters EF. Nutritional abnormalities and supplementation in chronic obstructive pulmonary disease. Clin Chest Med 2000;21:753-62.
  • 18. Decramer M, de Bock V, Dom R. Functional and histologic picture of steroid-induced myopathy in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1996;153(6 Pt 1):1958-64.
  • 19. Maltais F, LeBlanc P, Simard C, Jobin J, Berube C, Bruneau J, et al. Skeletal muscle adaptation to endurance training in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1996;154(2 Pt 1):442-7.
  • 20. Casaburi R, Patessio A, Ioli F, Zanaboni S, Donner CF, Wasserman K. Reductions in exercise lactic acidosis and ventilation as a result of exercise training in patients with obstructive lung disease. Am Rev Respir Dis 1991;143:9-18.
  • ,21. Öner C. Pulmoner rehabilitasyon. In: Beyazova M, Kutsal YG, editörler. Fiziksel t›p ve rehabilitasyon. Ankara: Günefl Kitapevi; 2000. s. 1191-215.