Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by airway obstruction due to inflammation of the small airways. It is caused predominantly by inhaled toxins, especially via smoking, but air pollution and recurrent respiratory infections can also cause COPD. Some individuals are genetically predisposed to COPD, particularly those with α1-antitrypsin deficiency (AATD). COPD begins with chronic airway inflammation that 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 and CO2 release, resulting in hypoxemia and hypercapnia. Most affected individuals present with a combination of dyspnea and chronic cough with expectoration. In later stages, COPD may manifest with more severe symptoms such as tachypnea, tachycardia, and cyanosis. Diagnosis is primarily based on clinical presentation and lung function tests, which typically show a decreased ratio of forced expiratory volume (FEV) to forced vital capacity (FVC). Imaging studies, such as chest x-ray, are helpful in assessing disease severity and the extent of possible complications, but they are not required to confirm the diagnosis. ABG and pulse oximetry are useful for quickly assessing the patient's O2 status. All COPD patients should be staged according to the staging system of the Global Initiative for Chronic Obstructive Lung Disease (GOLD), which considers a variety of factors (e.g., exacerbations, symptom severity, FEV1). Treatment options depend on the GOLD group and mainly consist of short- and long-acting bronchodilators (beta-agonists and parasympatholytics) and glucocorticoids. Individuals with advanced disease may benefit from nonpharmacological treatment with 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 (See ).
- COPD is a chronic pulmonary disease characterized by persistent respiratory symptoms and airflow limitation (postbronchodilator FEV1/FVC < 0.70), which is caused by a mixture of small airway obstruction and parenchymal destruction 
- COPD was formerly subdivided into chronic bronchitis and emphysema. These terms are still widely used to describe patient findings and found as subclasses of COPD in outdated literature. 
- Chronic bronchitis: productive cough (cough with expectoration) for at least 3 months each year for 2 consecutive years
- Emphysema: permanent dilatation of pulmonary air spaces distal to the terminal bronchioles, caused by the destruction of the alveolar walls and the pulmonary capillaries required for gas exchange
Tobacco use (90% of cases) ; 
- 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 
Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification
- A system that combines spirometric classification, symptom assessment, and history of exacerbations to determine the impact of COPD on a patient's health status.
- Grade and groups are calculated separately
- GOLD spirometric grades 1–4
GOLD Groups A–D
- Calculated based on the history of exacerbations and severity of symptoms
- Used to guide management
GOLD spirometric grades 
|GOLD classification of severity of airflow limitation (GOLD report 2022) |
|Grade||Postbronchodilator FEV1% of the predicted value|
|GOLD 1: mild|| |
|GOLD 2: moderate|| |
|GOLD 3: severe|| |
|GOLD 4: very severe|| |
GOLD spirometric grades 1–4 inform the prognosis but correlate weakly with symptoms and functional impairment. 
GOLD groups A–D 
|ABCD group assessment (GOLD report 2022) |
|Exacerbations in the past year|| |
Severity of symptoms
|mMRC dyspnea scale||CAT score|
|COPD group A|| || || |
|COPD group B|| || |
|COPD group C|| || || |
|COPD group D|| || |
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
- Senile emphysema
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
- Obtain spirometry in patients with typical and/or a history of COPD risk factors (e.g., exposure to air pollution) in order to:
- Determine GOLD group (A–D) based on the history of exacerbations and severity of current symptoms.
- Test all patients at diagnosis for AATD.
- Consider imaging to exclude alternative diagnoses and identify significant comorbidities.
- Assess oxygenation in patients with signs of respiratory or right heart failure using pulse oximetry.
Spirometry and body plethysmography 
- Indication: all patients with typical symptoms of COPD and/or exposure to COPD risk factors
- Procedure: Spirometry is performed after inhalation with a short-acting beta-agonist (SABA) or short-acting muscarinic antagonist (SAMA).
- Key finding: : FEV1/FVC < 70% after bronchodilator inhalation
- Typical supportive findings
Postbronchodilator test 
- Used to assess the reversibility of bronchoconstriction
- The degree of reversibility alone cannot reliably distinguish between the diagnosis of . 
- Pulse oximetry
- Indication: O2 saturation < 92% or acute illness (e.g., altered mental status, acute exacerbation)
- Findings: Hypoxemia and hypercapnia are common.
- Serum α1-antitrypsin level: Screen all patients with COPD for AATD at diagnosis. 
Additional studies 
The following tests are not required for a diagnosis. If performed, they may show typical findings.
- ECG/TTE: may show signs of 
X-ray chest: not indicated for confirming the diagnosis (low sensitivity, especially during the early stages)
- To assess for alternative diagnoses and/or identify significant comorbidities (e.g., , , )
- Hyperinflated lungs (barrel chest)
- Hyperlucency of lung tissue (decreased lung markings)
- Increased anteroposterior diameter
- Pushed down and flattened diaphragm
- Horizontal ribs and widened intercostal spaces
- Long narrow heart shadow
- Parenchymal bullae or subpleural blebs (pathognomonic of emphysema)
- Increased retrosternal space on lateral view as a result of emphysematous changes in the lung tissue
- Findings: similar to x-ray findings
is discussed in .
- Communicate treatment goals, including:
- Symptom control
- Reduction of frequency and severity of exacerbations
- Improvement in quality of life
- Counsel all patients on supportive measures, including lifestyle modifications and recommended vaccinations.
- Choose initial medication based on the patient's A–D). (
- Follow-up treatment: Assess the adequacy of symptom control.
- Continue initial treatment if the response is adequate.
- If not, adjust medications based on the severity of dyspnea and history of exacerbations.
- De-escalate treatment if there are adverse effects and/or a lack of clinical benefit.
- In patients with chronic respiratory failure, consider:
Patient education and training on inhaler techniques are central to improving self-management skills, the ability to cope with illness, and health status. Make sure that instructions are provided and proper technique is demonstrated when prescribing an inhaler, and that inhaler technique is observed at each visit. 
|Supportive measures for COPD |
|Lifestyle modifications|| |
|Recommended immunizations in COPD|| |
|Management of comorbidities|| |
|Pulmonary rehabilitation|| |
Cessation of tobacco use is the single most effective step to slow the decline in lung function in patients with COPD.
|Initial pharmacological treatment of stable COPD |
(DPI: dry powdered inhaler; MDI: metered dose inhaler)
|COPD group A|| |
|COPD group B|
|COPD group C|
|COPD group D|
If treatment response is inadequate, consider poor inhaler technique and/or adherence as causes. Common errors include inadequate exhalation prior to inhalation, inadequate inhalation duration, and problems with inspiratory flow.
Bronchodilators are the mainstay of pharmacological treatment of COPD.
Follow-up treatment 
- Check for persistent symptoms and adjust the regimen based on the predominant trait (dyspnea or exacerbations).
- Review the response to treatment escalation; adjust if there is:
- Insufficient improvement
- Adverse drug reactions
- If dyspnea persists after adjustments:
- Consider changing the inhaler or medication within the same class.
- Evaluate for other causes of dyspnea.
|Follow-up treatment in COPD|
|Predominant trait||Initial treatment||Follow-up treatment|
Switching inhalers within a class (e.g., using a different long-acting beta-agonist) in patients with inadequate treatment response may improve management.
- General principles
- Factors that strongly support initiation of ICS
- Factors against initiation ICS
- Indications for stopping ICS 
- 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
- Vitamin D3: may reduce the risk of exacerbations in patients with low baseline levels 
- α1-antitrypsin augmentation therapy
Management of advanced disease
Respiratory support 
- Long-term oxygen therapy (LTOT)
- Ventilatory support
LTOT Increases survival in patients with COPD.
- 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
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. 
- 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
- Cessation of tobacco use
- Long-term oxygen therapy is the only treatment that improves mortality.
- COPD is the third most common cause of death worldwide.