Chronic obstructive pulmonary disease

Last updated: October 18, 2023

Summarytoggle arrow icon

Chronic obstructive pulmonary disease (COPD) is characterized by chronic respiratory symptoms resulting from airflow obstruction and alveolar gas exchange abnormalities. It is predominantly caused by inhaled toxins (e.g., tobacco smoke or air pollution). Some individuals are genetically predisposed to COPD, particularly those with α1-antitrypsin deficiency (AATD). COPD begins with chronic airway inflammation, which usually progresses to emphysema, a condition that is characterized by irreversible bronchial narrowing and alveolar hyperinflation. These changes cause a loss of diffusion area, which can lead to inadequate oxygen absorption (hypoxemia) and CO2 release (hypercapnia). Clinical features include dyspnea and productive cough and, in later stages, tachypnea, tachycardia, and cyanosis. Diagnosis is primarily based on clinical presentation and pulmonary function tests (PFTs), which typically show a decreased ratio of forced expiratory volume (FEV) to forced vital capacity (FVC). Imaging studies are helpful in assessing disease severity and the extent of possible complications. Treatment options mainly consist of short-acting and long-acting bronchodilators and inhaled corticosteroids. Individuals with advanced disease may benefit from oxygen supplementation and/or noninvasive ventilation. COPD can cause complications such as pulmonary hypertension or respiratory failure. The most significant complication is acute exacerbation of COPD.

Definitiontoggle arrow icon

Chronic bronchitis (a clinically defined condition) and emphysema (an anatomically defined condition) often occur simultaneously in patients with COPD. [2]

Epidemiologytoggle arrow icon

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

Exogenous factors

  • Tobacco use ; [6]
    • Smoking is the major risk factor for COPD, but those who have quit ≥ 10 years ago are not at increased risk. [7]
    • Passive smoking
  • Exposure to air pollution or fine dusts [8]
    • Nonorganic dust: such as industrial bronchitis in coal miners [9]
    • Organic dust: incidence of COPD in areas where biomass fuel (e.g., wood, animal dung) is regularly burned indoors

Endogenous factors

Classificationtoggle arrow icon

GOLD classification [1]

GOLD spirometric grades inform the prognosis of a patient; GOLD groups guide pharmacological management.

GOLD grades

GOLD spirometric grades (2023) [1]
Grade Postbronchodilator FEV1% of the predicted value
GOLD 1: mild

≥ 80%

GOLD 2: moderate


GOLD 3: severe


GOLD 4: very severe

< 30%

Cutoff points between GOLD spirometric grades according to the FEV1%: 30 + 50 = 80

GOLD groups [1]

GOLD group assessment (2023) [1]
Group Exacerbations in the past year

Severity of symptoms

mMRC dyspnea scale CAT score
GOLD group A
  • 0
  • Or 1 not leading to hospital admission
  • 0–1
  • 0–9
GOLD group B
  • ≥ 2
  • ≥ 10
GOLD group E
  • ≥ 2
  • Or ≥ 1 leading to hospital admission
  • Any severity

Pathophysiologytoggle arrow icon

COPD is characterized by chronic airway inflammation and tissue destruction. [6][12]

Chronic inflammation

It results from significant exposure to noxious stimuli, increased oxidative stress (most commonly due to cigarette smoke) as well as by increased release of reactive oxygen species by inflammatory cells.

Tissue destruction [14]

Clinical featurestoggle arrow icon

Symptoms are minimal or nonspecific until the disease reaches an advanced stage.

Presenting findings [6]

  • Chronic cough with expectoration (expectoration typically occurs in the morning)
  • Dyspnea and tachypnea
    • Initial stages: only on exertion
    • Advanced stages: continuously
  • Pursed lip breathing
    • The patient breathes in through the nose and breathes out slowly through pursed lips.
    • This style of breathing increases airway pressure and prevents bronchial collapse during the last phase of expiration.
    • More commonly seen in patients with emphysema
  • Prolonged expiratory phase, end-expiratory wheezing, crackles, muffled breath sounds, and/or coarse rhonchi on auscultation
  • Cyanosis due to hypoxemia
  • Tachycardia

Features of advanced COPD [15]

Nail clubbing is not a finding specific to COPD; its presence usually suggests comorbidities such as bronchiectasis, pulmonary fibrosis, or lung cancer.

Pink puffer and blue bloater [15]

According to their clinical appearance, patients with COPD are often categorized as either “Pink Puffer” or “Blue Bloater”.

Pink puffer vs. blue bloater
Pink Puffer Blue Bloater
Main pathomechanism
Clinical features
  • Noncyanotic
  • Cachectic
  • Pursed-lip breathing
  • Mild cough
  • Slightly reduced
  • Markedly reduced

Features of COPD due to AATD

  • Age of onset is generally younger (< 60 years)
  • Also, often have hepatic signs and symptoms (jaundice) related to hepatitis or cirrhosis

Subtypes and variantstoggle arrow icon

Emphysema subtypes

Emphysema is characterized by the destruction of lung parenchyma and is often seen in patients with advanced pulmonary disease. The presence of emphysema does not necessarily correlate with spirometric findings. Emphysema can be divided into the following subtypes: [1][17]

Smoke rises up:” Centriacinar emphysema is associated with smoking and primarily involves the upper lobes of the lungs.

Diagnosticstoggle arrow icon

Approach [1]

The USPSTF recommends against screening asymptomatic adults for COPD. [18]

Initial tests [1][2]

  • Spirometry
    • FEV1:FVC < 70% after bronchodilator inhalation confirms the diagnosis.
    • FEV1 (FEV1% of the predicted value determines the GOLD spirometric grade.)
    • Normal or FVC
  • Serum AAT level: Screen all patients with confirmed COPD for AATD upon initial diagnosis.

“A COP with low FEVer”: FEV1 for COPD patients.

Additional testing

Advanced pulmonary function testing

Characteristic changes are observed in patients with significant emphysema and small airway abnormalities.

Reversibility of bronchoconstriction is not a reliable factor for differentiating between COPD and asthma. [1]

Assessment for respiratory failure

Chest imaging [1][2]

Chest imaging is not needed for diagnosis; consider based on clinical context to assess for alternative diagnoses, comorbidities, or complications.


Differential diagnosestoggle arrow icon

The differential diagnoses listed here are not exhaustive.

Managementtoggle arrow icon

Management of acute COPD exacerbation is discussed in AECOPD.

Approach [1]

Nonpharmacological management of COPD [1]

Lifestyle modifications

Cessation of tobacco use is the single most effective step to slow the decline in lung function in patients with COPD.

Supportive care

Vaccinations against pneumococcus and influenza reduce the risk of respiratory infections and complications in patients with COPD. [1]

Management of comorbidities

Screen for common comorbidities at the first visit and at regular intervals, then treat as indicated.

Pharmacological treatmenttoggle arrow icon

See “Pharmacotherapy for AECOPD” for treatment of acute exacerbations.

General principles [1]

  • Bronchodilators are the mainstay of pharmacological treatment.
  • Inhaled corticosteroids (ICS), e.g., budesonide, fluticasone, or beclomethasone, should only be used in combination with long-acting bronchodilators.
  • A single inhaler may be more effective than multiple inhalers when available and affordable.
  • Patient education on proper inhaler technique is essential for adequate symptom control.
    • Describe and demonstrate when prescribing a new inhaler.
    • Observe the patient's technique for each inhaler at follow-up visits.
    • Identify common errors, e.g., inadequate exhalation prior to inhalation.
  • For patients with both COPD and asthma, choose medications based on stepwise treatment of chronic asthma.

Initial treatment

Initial pharmacological treatment of stable COPD [1]

GOLD group

Daily regimen

Rescue medication
GOLD group A
GOLD group B
GOLD group E
  • DPI: dry powdered inhaler
  • MDI: metered dose inhaler

If treatment response is inadequate, consider poor inhaler technique and/or poor adherence as causes.

Follow-up treatment [1]

  • Maintain inhaler therapy if dyspnea and exacerbations are well controlled with the current regimen.
  • If not, assess for:
    • Adherence
    • Inhaler technique
    • Comorbid conditions that could explain symptoms
  • Reinforce nonpharmacological management of COPD.
  • Adjust treatment based on the predominant trait (i.e., dyspnea or exacerbations), not on the GOLD group at diagnosis.
Follow-up treatment in COPD [1]
Predominant trait Current treatment Follow-up treatment
Persistent dyspnea
  • Consider changing the inhaler or medication within the same class.
  • Evaluate for other causes of dyspnea.
Persistent exacerbations

Follow-up treatment adjustments are based on treatable traits (dyspnea and frequency of exacerbations) and are made irrespective of the patient's GOLD group (A, B, or, E) at diagnosis. [1]

Other drugs [1]

There is insufficient evidence to support treating stable COPD with antitussives, vasodilators, or leukotriene antagonists. [1]

Management of advanced diseasetoggle arrow icon

Respiratory support [1]

For patients started on LTOT, check blood gasses frequently (with ABG or VBG) to ensure adequate oxygenation without unintended acidosis and CO2 retention. [1]

LTOT increases survival in patients with severe resting hypoxemia.

Invasive treatment

Palliative measures (e.g., low-dose opiates, fans blowing onto the patient's face, or acupuncture) can be used if distressing breathlessness persists despite optimal medical therapy. [23][24]

Complicationstoggle arrow icon

We list the most important complications. The selection is not exhaustive.

Prognosistoggle arrow icon

  • 40–70% of all COPD patients survive the first 5 years after diagnosis. [25]
  • Survival rates vary significantly depending on the severity of the disease. [25]
  • Measures that improve survival
  • COPD is the third most common cause of death worldwide. [26]

Referencestoggle arrow icon

  1. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  2. Barnes PJ, Drazen JM, Rennard SI. Asthma and COPD. Academic Press ; 2009
  3. Sarkar M, Mahesh D, Madabhavi I. Digital clubbing. Lung India. 2012; 29 (4): p.354.doi: 10.4103/0970-2113.102824 . | Open in Read by QxMD
  4. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease - 2023 Report. Updated: November 1, 2022. Accessed: November 30, 2022.
  5. Mangione CM, Barry MJ, et al. Screening for Chronic Obstructive Pulmonary Disease. JAMA. 2022; 327 (18): p.1806.doi: 10.1001/jama.2022.5692 . | Open in Read by QxMD
  6. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical ; 2018
  7. Stanojevic S, Kaminsky DA, Miller MR, et al. ERS/ATS technical standard on interpretive strategies for routine lung function tests. Eur Respir J. 2021; 60 (1): p.2101499.doi: 10.1183/13993003.01499-2021 . | Open in Read by QxMD
  8. Global Strategy for Asthma Management and Prevention (2022 update). Updated: January 1, 2022. Accessed: August 29, 2022.
  9. Harrigan RA. ABC of clinical electrocardiography: Conditions affecting the right side of the heart. BMJ. 2002; 324 (7347): p.1201-1204.doi: 10.1136/bmj.324.7347.1201 . | Open in Read by QxMD
  10. Nishimura K, Tsukino M. Clinical course and prognosis of patients with chronic obstructive pulmonary disease. Curr Opin Pulm Med. 2000; 6 (2): p.127-132.doi: 10.1097/00063198-200003000-00008 . | Open in Read by QxMD
  11. The top 10 causes of death. Updated: January 1, 2017. Accessed: March 27, 2018.
  12. Walters JA, Tang JN, Poole P, Wood-Baker R. Pneumococcal vaccines for preventing pneumonia in chronic obstructive pulmonary disease.. Cochrane Database Syst Rev.. 2017; 1 (1): p.CD001390.doi: 10.1002/14651858.CD001390.pub4 . | Open in Read by QxMD
  13. Anderson AE, Foraker AG. Centrilobular emphysema and panlobular emphysema: two different diseases. Thorax. 1973; 28 (5): p.547-550.doi: 10.1136/thx.28.5.547 . | Open in Read by QxMD
  14. Nici L, Mammen MJ, Charbek E, et al. Pharmacologic Management of Chronic Obstructive Pulmonary Disease. An Official American Thoracic Society Clinical Practice Guideline. Am J Respir Crit Care Med. 2020; 201 (9): p.e56-e69.doi: 10.1164/rccm.202003-0625st . | Open in Read by QxMD
  15. Bausewein C, Booth S, Gysels M, Higginson I. Non-pharmacological interventions for breathlessness in advanced stages of malignant and non-malignant diseases.. Cochrane Database Syst Rev.. 2008: p.CD005623.doi: 10.1002/14651858.CD005623.pub2 . | Open in Read by QxMD
  16. Peter J. Barnes. Sex Differences in Chronic Obstructive Pulmonary Disease Mechanisms. American Journal of Respiratory and Critical Care Medicine. 2016.
  17. Georgios Ntritsos, Jacob Franek, Evangelos Evangelou, et al.. Gender-specific estimates of COPD prevalence: a systematic review and meta-analysis. International Journal of Chronic Obstructive Pulmonary Disease. 2018.
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  19. Liu Y, Pleasants R, Croft J, et al. Smoking duration, respiratory symptoms, and COPD in adults aged ≥45 years with a smoking history. International Journal of Chronic Obstructive Pulmonary Disease. 2015: p.1409.doi: 10.2147/copd.s82259 . | Open in Read by QxMD
  20. Household air pollution and health. Updated: February 1, 2016. Accessed: February 27, 2017.
  21. Occupational and work-related diseases. Updated: February 27, 2017. Accessed: February 27, 2017.
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