Author(s): Sunil K Jain, MD, Maedot Haymete, BA, Igbagboleke Mobolaji, MD
Originally published: September 20, 2013 Last updated: December 5, 2025
Jump to:

Disease/Disorder

Definition

Chronic obstructive pulmonary disease (COPD) is a disorder characterized by persistent airflow limitation and inflammation, including emphysema and chronic bronchitis.1 COPD may be defined in terms of a fixed postbronchodilator ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity of <0.7.2

Etiology

COPD is recognized as a worldwide health issue. It is most commonly a pathologic consequence of smoking cigarettes, but many environmental toxins, noxious gases, fumes, and dust can also be important causative agents. A genetic factor that enhances risk for developing COPD is deficiency of alpha-1 antitrypsin (AAT). Patients with AAT deficiency often present with concomitant hepatic disease.

Epidemiology including risk factors and primary prevention

COPD is the third leading cause of death globally and affects 384 million people worldwide.3 In the United States, it affects 6.4% of the population, approximately 15.7 million, and is the cause of approximately 120,000 deaths each year.3 While tobacco smoking is the most common cause, chronic exposure to environmental fumes, and dust are causative elements in COPD. The prevalence of COPD in areas of high environmental pollution of individuals who never smoked is 30%.

Patho-anatomy/physiology

Histological changes associated with COPD include fibrosis of the airways,  increased goblets cells contributing to mucus gland hyperplasia as well as narrowing and reduction in the number of small airways leading to reduced airflow.4,5 Most increased inflammatory cells seen in chronic bronchitis are CD8+ T-lymphocytes, neutrophils, and CD68+ monocytes/macrophages, contrasted with asthma, where CD4+ T-lymphocytes and eosinophils predominate with increased interleukin (IL)-4 and IL-5. Recently, sputum eosinophils have been demonstrated as a biomarker of severity, frequent exacerbations, and high degree of emphysematous changes on chest computed tomography in patients with COPD.4 In emphysema, fiber destruction due to imbalance of proteases and their inhibitors results in destruction of alveolar walls. This leads to reduced gas exchange and permanent airspace enlargement. Finally, smooth muscle and intimal hyperplasia within the pulmonary vasculature is thought to occur as a consequence of chronic hypoxia.5 Reduced airflow and alveolar destruction culminate to hyperinflation and diaphragmatic dysfunction.5,6

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Initially, the hallmark of COPD is dyspnea. Patients in the early stage of COPD may present with chronic cough, dyspnea with exertion, or both. As the disease progresses, dyspnea often worsens with associated decline in FEV1. However, patients with sedentary lifestyles may present with a later stage of the disease that was subclinical because of low levels of physical demand. Exercise tolerance decreases progressively in COPD, such that the onset of breathlessness occurs with less exertion. Some patients have a chronic cough with sputum production. Episodic exacerbations vary in severity and are often characterized by a marked acute increase in cough, sputum production, and dyspnea. The frequency of COPD exacerbations is associated with accelerated lung function decline and mortality. Patients with end stage COPD are typically dependent on oxygen supplementation, with oxygen saturation desired at 90-92%.2,7

Specific secondary or associated conditions and complications

The course of chronic, stable COPD is often punctuated with exacerbations of increased cough, sputum production, and dyspnea. Respiratory tract infections are a common complication and cause of exacerbations.8 Influenza, pneumococcal, and COVID infections in these patients can be fatal; vaccination for these common respiratory infections is strongly recommended. Rupture of emphysematous bullae can cause a pneumothorax. Additionally, there is evidence that patients with COPD have at least one comorbid condition including metabolic syndrome, sleep apnea, and cardiovascular disease.9,10

Essentials of Assessment

History

Tobacco smoking is an essential element of the history, described in terms of pack-years which consists of the number of cigarette packs smoked per day multiplied by total duration of smoking history in years. Greater than 15 packs-years significantly contributes to the development of moderate to severe COPD.6 Other contributory factors in the history include duration since symptom onset, dyspnea, frequency of acute exacerbations, sedentary vs active lifestyle, exercise capacity, use of medications, oxygen supplementation, employed self-care methods, cognition, emotional/affective state, and available support system.7

Physical examination

While initial observation of the patient’s general appearance may help to estimate the severity of COPD, the increased anterior-posterior diameter of the chest is often not a reliable indicator of disease progression. Physical exam may reveal the Hoover sign where there may be paradoxical indrawing of the inferior intercostal spaces during inspiration. The patient may also be leaning forward and using accessory muscles of respiration with pursed-lip breathing. Due to hyperinflation, auscultation of lung      and heart sounds may be distant, and the lungs may also have increased resonance to percussion. An accentuated second heart sound in the second intercostal space may suggest pulmonary arterial hypertension. Rhonchi may represent mucus in the airways and wheezing may suggest bronchospasm. Clubbing of the digits is not a typical finding for COPD and may suggest underlying malignancy.

Functional assessment

Commonly used supplemental assessment tools for COPD include the Chronic Respiratory Disease Questionnaire evaluating quality of life,8 the spirometric lung function test with and without a bronchodilator and diffusion capacity for carbon monoxide, as well as exercise capacity using the six-minute walk test. Cardiopulmonary exercise testing employing incremental-exercise testing to symptom-limited maximum, either on cycle ergometer or treadmill, allows assessment of peak oxygen consumption, work, heart rate, and the degree of oxygen desaturation with exercise.9

Laboratory studies

Complete blood count studies test for anemia or acute infection. Elevated bicarbonate may indicate a compensatory metabolic alkalosis in chronic hypercapnia and may be confirmed with arterial blood gas examination. Nutritional assessment includes serum albumin, pre-albumin, and transferrin. The serum natriuretic peptide level helps to rule out symptomatic congestive heart failure. Additionally, in genetically predisposed patients, very low serum AAT level combined with an AAT deficient genotype is diagnostic for alpha-1 antitrypsin deficiency. Patients may also have elevated liver function tests.

Imaging

An upright chest radiograph, in a posterior-anterior view, is helpful to exclude other diagnostic possibilities, such as congestive heart failure, lung cancer, pleural effusion, bronchiectasis, and secondary complications of COPD, such as pneumonia or pneumothorax. Computed tomography is not generally used in the routine diagnosis of COPD. However, it is helpful to exclude alternative diagnoses, determine if emphysema is centriacinar or panacinar for lung cancer screening or staging, or in consideration of lung reduction surgery in patients with emphysema. Any patients with COPD are high risk for lung cancer due to tobacco use. Thus, annual low dose CT (LDCT) scans can be used to reduce lung cancer mortality in specific high-risk groups defined as patients 55 to74 years old who have at least a 30-pack-year smoking history and who currently smoke or have quit within the past 15 years.10

Supplemental assessment tools

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) suggests a combined assessment based on symptoms from modified Medical Research Council dyspnea scale or COPD Assessment Test and exacerbation history to guide therapy.16 The multidimensional BODE index summates body mass index (0-1, score 1 if >21), airflow obstruction by spirometry after bronchodilator (0-3, score 3 if < 35% predicted FEV1), dyspnea (0-3, Modified Medical Research Council Dyspnea, score 3 if housebound because of breathlessness), and exercise capacity in the six-minute walk test (0-3, score 3 if walk <149 m). This index can be used to assess therapeutic response to medications, pulmonary rehabilitation therapy, and other interventions. The COPD foundation system uses five spirometry grades to stage COPD and additionally assesses symptoms, number of exacerbations in the past year, oxygenation, emphysema on computed tomography scan, presence of chronic bronchitis, and comorbidities.17  

Environmental

Smoking, active asthma, and airborne environmental irritants are important risk factors and stimulants for disease progression.12,13 Smoking cessation is of primary importance in the rehabilitation of COPD as the rate decline of FEV1 approaches that of a nonsmoker over time. Reduction of dust, mites, and mold from the home are also recommended.

Social role and social support system

Patients with COPD may suffer from depression, anxiety, fear, guilt, and isolation. Patients with clinical depression do not do as well as patients who have a positive commitment to a healthy lifestyle, and also have adequate family and social support.11 Group instruction on relaxation, stress reduction, and panic control may enhance coping with chronic illness by reducing dyspnea related to anxiety.

Professional issues

Health care professionals caring for patients with COPD should advocate for interdisciplinary smoking cessation given the demonstrated effectiveness of the programs. Barriers to COPD management may include challenge related to addiction treatment. Furthermore, the promotion of programs that support clean air initiatives both locally and globally is needed to address the worldwide problem of COPD.1

Rehabilitation Management and Treatments

Available or current treatment guidelines

Pulmonary rehabilitation is a comprehensive intervention based on a thorough patient assessment followed by patient-tailored therapies. It includes medical management, exercise, education, as well as behavioral modification to improve the physical and emotional condition of patients with COPD and also promote long-term adherence to health-enhancing behaviors.7 Optimum programs last 6-8 weeks and include direct supervision as well as ongoing feedback.16 It has been shown to be the most effective therapeutic strategy to improve shortness of breath, health status, and exercise tolerance.15 Generally, treatment guidelines aim to improve life quality and participation, optimize functional status, reduce symptoms, reduce health care costs, and promote a healthy lifestyle.9 Given the worldwide scope of COPD, guidelines for a standardized evidence-based approach to treatment was published in 2001, with subsequent revisions in 2013 and 2017, and 2021.1,2 There has been some evidence that telerehabilitation is safe and has similar benefits as center based pulmonary rehabilitation.22 However, the evidence base is still evolving, and there are currently no best practices established.

At different disease stages

Pulmonary rehabilitation is appropriate at all stages of COPD. In the early stage, education is most important to emphasize smoking cessation, which can alter disease progression. Although pulmonary rehabilitation does not improve lung function or gas exchange directly, it aims to optimize the function of other body systems so that the effect of lung dysfunction is minimized. Exercise training lowers ventilatory demand, slowing the respiratory rate at a given level of performance. In patients with COPD, a slow respiratory rate prolongs expiratory time and decreases dynamic hyperinflation, resulting in less dyspnea. Exercise training usually combines endurance and strength for both upper and lower limb muscles. Strengthening exercises are particularly important for patients with evident muscular atrophy. Interval training promotes the best compliance, especially for symptomatic patients, but high-intensity training is encouraged. Pulmonary precautions should be included with the exercise prescription for all COPD patients because exercise can trigger dyspnea. Training specific to breathing would be the purse-lip breathing technique to maintain airway pressure, keeping airways open through exhalation. The use of medications should be appropriate to the stage of the disease and the symptoms. In the early stage, short-acting bronchodilators, such as albuterol, can be given as inhaled medication. In later stages, inhaled long-acting anticholinergic or beta-2 agonists are recommended. In the later stages, inhaled corticosteroids can also be added. In patients with severe resting chronic hypoxemia, long-term oxygen therapy improves survival. Pulmonary rehabilitation should be given to all COPD patients with COVID-19. With its core components, including exercise training combined with disease-specific education, pulmonary rehabilitation improves exercise capacity, symptoms, and quality of life across all stages of COPD severity.16,23,24,25

Efficacy

Pulmonary rehabilitation can occur in a variety of settings and individualized intervention at any stage and has been shown to improve dyspnea, reduce hospitalizations among patients with a recent exacerbation, and also reduce symptoms of depression and anxiety.16 Unlike stable COPD, hospitalized patients with acute exacerbation of COPD (AECOPD) are unwell, anxious and breathless. Although difficult, early pulmonary rehabilitation can reduce deconditioning, should be time limited, and commenced at the bedside.20 Systematic reviews have shown that among patients who have had a recent exacerbation (within 4 weeks from prior hospitalization), pulmonary rehabilitation can reduce readmissions and mortality.21  Pulmonary rehabilitation ranks as one of the most cost-effective treatment strategies with an estimated cost per quality adjusted life year (QALY) of $2,500 – $10,500.22  In the United States the estimated direct and indirect costs of COPD are $32 billion and  $20.4 billion respectively.23

Coordination of care

A coordinated pulmonary rehabilitation program should be individualized to the patient’s illness, severity and health literacy. It includes smoking cessation, irritant avoidance, dietary counseling and exercise as mentioned above. Psychological services also enhance coping skills and anxiety control. Medical support for treatment of respiratory exacerbations and assessment to determine the need for supplemental oxygen or noninvasive positive pressure ventilation is required.

Patient & family education

Education is the foundation of any effective rehabilitation treatment plan, specifically regarding the benefits of smoking cessation, exercise, therapy to practice exercises and breathing techniques, use of energy conservation, and efficiency strategies for work. Inhaler techniques need to be assessed regularly.

Emerging/unique interventions

The St George’s Respiratory Questionnaire, the Clinical COPD Questionnaire, and the Medical Outcomes Study 36-Item Short-Form Health Survey are three widely used tools to report positive outcomes of pulmonary rehabilitation programs for COPD patients. The Hospital Anxiety and Depression Scale has been used to evaluate pulmonary treatment outcomes on these domains. Links to these measurement instruments are appended after the references below.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Promotion of long-term adherence to the treatment plan and principles of the program is the greatest challenge in managing the COPD patient. Optimizing medical treatments that are individualized generally promotes better health outcomes in patients with COPD.

Cutting Edge/Emerging and Unique Concepts and Practice

The use of serum procalcitonin has been shown to be elevated in patients with an acute bacterial lung infection, and the level decreasing with effective antibiotic treatment. These observations are promising to allow practitioners to use antibiotic therapy strategically, avoiding ineffective treatment when the infection is viral.24 Additionally, procalcitonin could also be used as a potential biomarker as levels have been found to be elevated in patients with acute exacerbation of COPD.31 Tiotropium/olodaterol provides a useful option for the maintenance treatment of COPD, with the convenience of once-daily administration via a single inhaler.32 Specific targeting of reactive oxygen species using antioxidants in the treatment of COPD is a continued topic of conversation.33

Gaps in the Evidence-Based Knowledge

Long-term antibiotic use in stable COPD patients is controversial. Telerehabilitation is an area of ongoing research. The use of e-cigarettes as a smoking cessation aid is uncertain at present. There are currently no long-term studies on follow up of COPD patients who developed COVID-19 nor recommendations on monitoring these patients.

References

  1. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management and prevention of COPD. 2017. Available at: http://www.goldcopd.org/. Accessed October 30, 2017.
  2. Marçôa R, Rodrigues DM, Dias M, Ladeira I, Vaz AP, Lima R, Guimarães M. Classification of Chronic Obstructive Pulmonary Disease (COPD) according to the new Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017: Comparison with GOLD 2011. COPD 2017; 21:1-6..
  3. Bhome A. COPD in India: iceburg or volcano? J Thorac Dis. 2012;4:298-309.
  4. Hastie AT, Martinez FJ, Curtis JL, et al. Association of sputum and blood eosinophil concentrations with clinical measures of COPD severity: an analysis of the SPIROMICS cohort. Lancet Respir Med. 2017; 5:956-967.
  5. Nici L, Donner C, Wouters E, et al. American Thoracic Society/European Respiratory Society statement on pulmonary rehabilitation. Am J Respir Crit Care Med. 2006;173:1390-1413.
  6. Løkke A, Lange P, Scharling H et al. Developing COPD: a 25 year follow up study of the general population. Thorax 2006;61(11):935-9.
  7. Wagg K. Unraveling self-management for COPD: what next? Chronic Resp Dis. 2012;9:5-7.
  8. Guyatt GH, Berman LB, Townsend M, et al. A measure of quality of life for clinical trials in chronic lung disease. Thorax. 1987 Oct;42(10):773-8.
  9. Goldstein RS, Hill K, Brooks D, Dolmage TE. Pulmonary rehabilitation: a review of the recent literature. Chest. 2012;142:738-749.
  10. Jaklitsch MT, Jacobson FL, Austin JH, et al. The American Association for Thoracic Surgery guidelines for lung cancer screening using low-dose computed tomography scans for lung cancer survivors and other high-risk groups. J Thoracic Cardiovascular Surg. 2012;144:33–38.
  11. Garrod R, Marshall J, Barley E, Jones PW. Predictors of success and failure in pulmonary rehabilitation. Eur Respir J. 2006;27:788-794.
  12. Vonk JM, Jongepier H, Panhuysen CIM et al. Risk factors associated with the presence of irreversible airflow limitation and reduced transfer coefficient in patients with asthma after 26 years of follow up or active asthma. Thorax 2003; 58:322-327.
  13. Silva GE, Sherrill DL, Guerra S et al. Asthma as a Risk Factor for COPD in a Longitudinal Study. Chest 2004; 126:59-65.
  14. Brand PLP, Kerstjens HAM, Jansen HM et al. Interpretation of skin tests to house dust mite and relationship to other allergy parameters in patients with asthma and chronic obstructive pulmonary disease. Allergy Clin Immunol 1993; 91:560-570.
  15. McCarthy B, Casey D, Devane D, Murphy K, Murphy E, Lacasse Y. Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2015; 2(2): CD003793.
  16. Global Initiative for Chronic Obstructive Lung Disease. Documents and resources. Available at: http://www.goldcopd.org/Guidelines/guidelines-resources.html. Accessed July 8, 2013.
  17. Garcia-Aymerich J, Lange P, Benet M, Schnohr P, Ant JM. Regular physical activity reduces hospital admission and mortality in chronic obstructive pulmonary disease: a population based cohort. Thorax. 2006;61:772-778.
  18. Reid DJ, Pham NT. Emerging therapeutic options for the management of COPD. Clin Med Insights Circ Respir Pulm Med. 2013;7:7-15.
  19. Wheaton AG, Cunningham, TJ, Ford ES, Croft JB. Employment and activity limitations among adults with chronic obstructive pulmonary disease – United States, 2013. MMWR. 2015:64 (11):290-295.
  20. Greening NJ, Williams JE, Hussain SF, et al. An early rehabilitation intervention to enhance recovery during hospital admission for an exacerbation of chronic respiratory disease: randomized controlled trial. BMJ 2014; 349: g4315.
  21. Puhan MA, Gimeno-Santos E, Scharplatz M, Troosters T, Walters eh, Steurer J. Pulmonary rehabilitation following exacerbation of chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2011; (10): CD005305
  22. Vogiatzis I, Rochester CL, Spruit MA, Troosters T, Clini EM, American Thoracic Society/European Respiratory Society Task Force on Policy in Pulmonary Rehabilitation. Increasing implementation and delivery of pulmonary rehabilitation: key messages from the new ATS/ERS policy statement. Eur Respir J 2016; 47(5): 1336-41.
  23. Guarascio AJ, Ray SM, Finch CK, Self TH. The clinical and economic burden of chronic obstructive pulmonary disease in the USA. ClinicoEconomics and outcomes research : CEOR 2013; 5: 235-45.
  24. Schuetz P, Miller B, Christ-Crain M, et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev. 2012;9:CD007498.
  25. WHO meeting participants. Alpha 1-antitrypsin deficiency: memorandum from a WHO meeting. Bull World Health Organ 1997; 75(5):397-415.

Links to Measurement Instruments

St. George’s Respiratory Questionnaire: www.healthstatus.sgul.ac.uk/SGRQ…/SGRQ%20Manual%20June%202009.pdf

Clinical COPD Questionnaire

van der Molen T, Willemse BW, Schokker S, et al. Development, validity and responsiveness of the Clinical COPD Questionnaire. Health Qual Life Outcomes. 2003;Apr 28;1:13.

Medical Outcomes Study 36-Item Short-Form Health Survey

https://www.brandeis.edu/roybal/docs/SF-36_website_PDF.pdf

Hospital Anxiety and Depression Scale

www.svri.org/sites/default/files/attachments/2016-01-13/HADS.pdf

Original Version of the Topic

Patricia W. Nance, MD and Catherine Sassoon, MD. Pulmonary rehabilitation in chronic obstructive pulmonary diseases (COPD). Original Publication Date: 9/20/2013.

Previous Revision(s) of the Topic

Patricia W. Nance, MD, Tyler Doornink, MD, Catherine Sassoon, MD. Pulmonary rehabilitation in chronic obstructive pulmonary diseases (COPD). Original Publication Date: 5/29/2018.

Sunil K Jain, MD, Carney Flinn, BS. Pulmonary Rehabilitation in Chronic Obstructive Pulmonary Diseases (COPD). 12/14/2022

Author Disclosures

Sunil K Jain, MD
Nothing to Disclose

Maedot Haymete, BA
Nothing to Disclose

Igbagboleke Mobolaji, MD
Nothing to Disclose