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 .
- Chronic obstructive pulmonary disease: a lung condition characterized by persistent respiratory symptoms (cough, dyspnea) and airflow limitation (postbronchodilator FEV1:FVC ratio < 0.70), which is caused by a combination of small airway obstruction and parenchymal destruction
- Chronic bronchitis: productive cough for at least 3 months per year for 2 consecutive years that cannot be explained by an alternative diagnosis
- Emphysema: permanent dilatation of pulmonary air spaces distal to the terminal bronchioles that is caused by the destruction of the alveolar walls and pulmonary capillaries required for gas exchange
Tobacco use ; 
- Smoking is the major risk factor for COPD, but those who have quit ≥ 10 years ago are not at increased risk. 
- Passive smoking
- Exposure to air pollution or fine dusts 
|GOLD spirometric grades (2023) |
|Grade||Postbronchodilator FEV1% of the predicted value|
|GOLD 1: mild|| |
|GOLD 2: moderate|| |
|GOLD 3: severe|| |
|GOLD 4: very severe|| |
GOLD groups 
COPD is characterized by chronic airway inflammation and tissue destruction. 
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.
- Increased number of neutrophils, macrophages, and CD8+ T lymphocytes → release of cytokines → amplification of inflammation and induction of structural changes of lung parenchyma (e.g., via stimulation of growth factor release)
- Overproduction of growth factor → peribronchiolar fibrosis → narrowing of airway → obliteration → emphysema (airflow limitation)
- Promotion of goblet cell proliferation and hypertrophy, mucus hypersecretion, and impaired ciliary function → chronic productive cough
- Smooth muscle hyperplasia of the small airways and pulmonary vasculature (mainly due to hypoxic vasoconstriction) → pulmonary hypertension → cor pulmonale
Tissue destruction 
- Bronchopulmonary inflammation → ↑ proteases
Nicotine use (or other noxious stimuli) inactivates protease inhibitors (especially α1-antitrypsin) → imbalance of protease and antiprotease → ↑ elastase activity → loss of elastic tissue and lung parenchyma (via destruction of the alveolar walls), which causes:
- Enlargement of airspaces → ↓ elastic recoil and ↑ compliance of the lung → ↓ tethering of small airways → expiratory airway collapse and obstruction → air trapping and hyperinflation → ↓ ventilation (due to air-trapping) and ↑ dead space → ↓ DLCOand ↑ ventilation-perfusion mismatch (V/Q) → hypoxemia and hypercapnia
- Pulmonary shunt and ↓ blood volume in pulmonary capillaries → ↑ number of alveoli that are ventilated but not perfused (↑ dead space) → ↓ DLCO and ↑ V/Q → hypoxemia and hypercapnia
- Imbalance of oxidants and anti-oxidants and an overabundance of free radicals → chronic inflammation and inactivation of anti-elastase → breakdown of elastic tissue.
Symptoms are minimal or nonspecific until the disease reaches an advanced stage.
Presenting findings 
- Chronic cough with expectoration (expectoration typically occurs in the morning)
Dyspnea and tachypnea
- Initial stages: only on exertion
- Advanced stages: continuously
- Pursed lip breathing
- Prolonged expiratory phase, end-expiratory wheezing, crackles, muffled breath sounds, and/or coarse rhonchi on auscultation
- Cyanosis due to hypoxemia
Features of advanced COPD 
- Congested neck veins
- Barrel chest: This deformity is most commonly seen in individuals with emphysema.
- Asynchronous movement of the chest and abdomen during respiration
- Use of accessory respiratory muscles due to diaphragmatic dysfunction
- Hyperresonant lungs, reduced diaphragmatic excursion, and relative cardiac dullness on percussion
- Decreased breath sounds on auscultation: “silent lung”
- Peripheral edema (most often ankle edema)
- Right ventricular hypertrophy with signs of right heart failure and cor pulmonale
- Often weight loss and cachexia
- Secondary polycythemia
- Confusion: due to hypoxemia and hypercapnia
- Nail clubbing in the case of certain comorbidities (e.g., bronchiectasis, pulmonary fibrosis, lung cancer) 
Pink puffer and blue bloater 
|Pink puffer vs. blue bloater|
|Pink Puffer||Blue Bloater|
|Clinical features|| |
|PaO2|| || |
|PaCO2|| || |
Features of COPD due to AATD
Subtypes and variants
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: 
- Centrilobular emphysema (centriacinar emphysema)
- Panlobular emphysema (panacinar emphysema)
- Cicatricial emphysema
- Giant bullous emphysema
- Age-related emphysema
- Suspect COPD in patients with either:
- Obtain spirometry to confirm significant airflow limitation (FEV1:FVC < 70%).
- Screen for AATD.
- Consider additional diagnostic testing as indicated, e.g.:
- Advanced PFTs
- Chest imaging
The USPSTF recommends against screening asymptomatic adults for COPD. 
Initial tests 
- Serum AAT level: Screen all patients with confirmed COPD for AATD upon initial diagnosis.
- Body plethysmography
- Single-breath diffusing capacity: ↓ DLCO
- FEV1 < 12%) is more common in patients with COPD than asthma (see “ ”).: A negative response (change in 
Reversibility of bronchoconstriction is not a reliable factor for differentiating between COPD and asthma. 
Assessment for respiratory failure
- Pulse oximetry
Chest imaging 
Chest imaging is not needed for diagnosis; consider based on clinical context to assess for alternative diagnoses, comorbidities, or complications.
Chest x-ray findings in COPD
- Signs of pulmonary hyperinflation
- Signs of bullous emphysema: parenchymal bullae or pulmonary blebs
- CT chest findings
is discussed in .
- Assess for both:
- Provide for all patients.
- Initiate based on .
- At follow-up:
- In patients with advanced disease, consider:
Nonpharmacological management of COPD 
- and options for pharmacotherapy, e.g., varenicline.
- Encourage physical activity to reduce the risk of acute exacerbations.
- Recommend maintenance of a healthy .
- Educate patients on:
Cessation of tobacco use is the single most effective step to slow the decline in lung function in patients with COPD.
- Recommended immunizations in COPD
- Pulmonary rehabilitation: especially helpful for patients with moderate to severe disease
Management of comorbidities
Screen for common comorbidities at the first visit and at regular intervals, then treat as indicated.
See “” for treatment of acute exacerbations.
General principles 
- 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 .
Initial pharmacological treatment of stable COPD 
|GOLD group|| |
|GOLD group A|
|GOLD group B|
|GOLD group E|
If treatment response is inadequate, consider poor inhaler technique and/or poor adherence as causes.
Follow-up treatment 
- Maintain inhaler therapy if dyspnea and exacerbations are well controlled with the current regimen.
- If not, assess for:
- Inhaler technique
- Comorbid conditions that could explain symptoms
- Reinforce .
- Adjust treatment based on the predominant trait (i.e., dyspnea or exacerbations), not on the at diagnosis.
|Follow-up treatment in COPD |
|Predominant trait||Current treatment||Follow-up treatment|
Follow-up treatment adjustments are based on treatable traits (dyspnea and frequency of exacerbations) and are made irrespective of the patient's (A, B, or, E) at diagnosis. 
Other drugs 
- opiates): may be considered for all patients (e.g.,
- Methylxanthines (e.g., )
Mucolytics (e.g., N-acetylcysteine, erdosteine)
- Liquefy mucus by reducing the disulfide bonds of mucoproteins
- Can be useful in reducing exacerbations in certain patients
Management of advanced disease
- Long-term oxygen therapy (LTOT)
- Ventilatory support
- Surgical bullectomy: indicated in severe emphysema with hyperinflation and large bullae
- Lung volume reduction
- Lung transplantation: may be indicated for very severe COPD, patients not eligible for bullectomy or lung volume reduction, and those with surgical contraindications
- Chronic respiratory failure 
- Cor pulmonale (right heart failure)
- Secondary spontaneous pneumothorax due to rupture of bullae (especially in bullous emphysema)
We list the most important complications. The selection is not exhaustive.
- 40–70% of all COPD patients survive the first 5 years after diagnosis. 
- Survival rates vary significantly depending on the severity of the disease. 
- Measures that improve survival
- COPD is the third most common cause of death worldwide.