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 hypoxia 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 stage and mainly consist of short- and long-acting bronchodilators (beta-agonists and parasympatholytics) and glucocorticoids. Individuals with advanced disease typically require oxygen supplementation, which is the only treatment that decreases mortality. COPD may 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 These terms are still widely used to describe patient findings and found as subclasses of COPD in outdated literature.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
Epidemiological data refers to the US, unless otherwise specified.
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) classifications 
- GOLD classifies COPD according to the severity of airflow limitation (GOLD 1–4) and the ABCD assessment tool, which takes into account the modified British Medical Research Council (mMRC) dyspnea scale, COPD assessment test (CAT), and risk of exacerbation.
- Previously, COPD was classified into chronic bronchitis and emphysema based on clinical findings. The use of these terms to classify types of COPD is now considered outdated because most individuals with COPD have a combination of both. However, these terms are still widely used to describe patient findings and found as subclasses of COPD in outdated literature.
Classification based on airflow limitation in patients with FEV1/FVC < 70% 
|FEV1% of the predicted value|
|GOLD 1 (Class I)|| || |
|GOLD 2 (Class II)|| || |
|GOLD 3 (Class III)|| || |
|GOLD 4 (Class IV)|| || |
Classification using combined assessment tools
|Patient group||Degree of severity||Exacerbations per year||Symptoms||mMRC Dyspnea Scale||CAT score|
|A|| || || || || |
|B|| || || |
|C|| || || || || |
|D|| || || |
- CAT score = COPD assessment test score
- mMRC Dyspnea Scale = Modified Medical Research Council Dyspnea Scale
- Low risk = FEV1/FVC ratio ≤ 0.7, FEV1 ≥ 50% predicted, and 0–1 exacerbation in the last year
- High risk = FEV1/FVC ratio ≤ 0.7, FEV1 ≤ 50% predicted, and ≥ 2 exacerbations in the last year
Classification based on underlying morphological changes
Emphysema is 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||Blue Bloater|
|Clinical features|| |
|PaO2|| || |
|PaCO2|| || |
Features of COPD due to AATD
Pulmonary function test (PFT) 
Spirometry and/or body plethysmography
- FEV1/FVC < 70%
- Decreased FEV1
- Normal or decreased FVC
- Increased FRC and RV
- Increased intrathoracic gas volume
- Objective: assesses reversibility of bronchoconstriction
- Results: FEV1/FVC < 0.7 is diagnostic of COPD (in patients with typical clinical features and exposure to noxious stimuli).
Blood gas analysis and pulse oximetry
- Pulse oximetry: assesses O2 saturation
ABG: only indicated when O2 is < 92% or if the patient is severely ill (e.g., altered mental status, acute exacerbation)
- Hypoxemia and hypercapnia are expected findings in patients with acute or chronic respiratory acidosis.
- Indications: not required for routine diagnosis but often used as an initial modality, mainly to rule out alternative conditions (e.g., pulmonary fibrosis, bronchiectasis)
- Not sensitive, especially during the early stages of COPD
- Can be used to determine the etiology for an acute COPD exacerbation (e.g., pneumonia, congestive heart failure)
Signs of hyperinflated lungs (barrel chest)
- Hyperlucency of lung tissue (decreased lung markings)
- Increased anteroposterior diameter
- Diaphragm pushed down and flattened
- Horizontal ribs and widened intercostal spaces
- Long narrow heart shadow
- Parenchymal bullae or subpleural blebs (pathognomonic of emphysema)
- The retrosternal space is increased on lateral view due to emphysematous changes in the lung tissue.
- Evaluates possible complications (e.g., pneumothorax, ARDS)
- Indicated in planning surgery (e.g., lung volume reduction, lung transplantation)
- Rules out differential diagnoses (e.g., bronchiectasis, lung cancer)
- CBC: Increased serum hematocrit
- Testing for AATD: recommended for all patients with COPD regardless of age or ethnicity (see “ ”) 
- Gram stain and sputum culture: in the case of suspected pulmonary bacterial infection (e.g., fever, productive cough, new infiltrate on chest x-ray)
- ECG: may show signs of right ventricular hypertrophy (e.g., P pulmonale, low amplitude of QRS complexes, and poor R wave progression) 
- See “.”
- See “.”
The differential diagnoses listed here are not exhaustive.
General treatment 
- Cessation of tobacco use: single most effective step to slow the decline in lung function
Pneumococcal vaccination: reduces the incidence of community-acquired pneumonia and invasive pneumococcal diseases
- Age 19-64 years: Administer .
Age ≥ 65 years
- Vaccinated: Administer PPSV23 (should be at least 5 years after the previous PPSV23 dose and at least 1 year after PCV13).
- Not vaccinated or unknown vaccination history: Administer followed by PPSV23.
- Influenza vaccination (annual): reduces the incidence of lower respiratory tract infections and death in COPD patients
- Pulmonary rehabilitation
- Physical activity helps maintain endurance and alleviate dyspnea.
- Supportive treatment (e.g., postural drainage)
- Vitamin D3 and calcium in cases of deficiency 
Medical treatment according to GOLD 
Medical treatment in COPD reduces the severity of symptoms, improves overall health status, and lowers the frequency and severity of exacerbation. The first-line treatment of COPD consists of bronchodilators, inhaled corticosteroids, and phosphodiesterase (PDE) type 4 inhibitors.
- Inhaled corticosteroids (ICS): e.g., budesonide, fluticasone, beclomethasone
- PDE type 4 inhibitors: e.g., roflumilast
|Patient group||Exacerbations per year||Symptoms||Initial treatment||Subsequent escalation|
|A|| || || |
|C|| || |
Other treatment options 
Long-term oxygen therapy (LTOT) indicated in the case of:
- PaO2 ≤ 55 mm Hg or SaO2 ≤ 88% at rest
- PaO2 between 55 and 60 mm Hg or SaO2 of 88%, if there is evidence of pulmonary hypertension, congestive cardiac failure, or polycythemia
- Mucolytics (e.g., N-acetylcysteine) liquefy mucus by reducing the disulfide bonds of mucoproteins.
- Ventilatory support: CPAP is useful in patients with COPD and obstructive sleep apnea.
- Surgery may be beneficial in severe cases
- Bronchoscopic interventions may be used to reduce end-expiratory lung volume and improve exercise tolerance.
Chronic respiratory failure 
- Description: occurs in the advanced stages of COPD due to progressive emphysematous changes and loss of diffusion surface area
Management: depends on the severity and etiology 
Long-term oxygen therapy (LTOT): 16 hours oxygen administration per day (minimum dosage) is associated with lower mortality rates.
- Indication: patients with COPD GOLD D and severe respiratory insufficiency failure that exhibit long-standing pO2 < 55 mm Hg, despite administration of optimal medication
- Oxygen administration is regulated in a way that the pO2 value rises and pCO2 drops to a level of 60–70 mm Hg. Hypercapnia would lead to respiratory acidosis and disorientation and should be prevented. 
- Portable respiration
- Principle: a type of non-invasive respiration done overnight when the patient is asleep
- Goal: This allows recovery of the respiratory muscles and in turn permits better respiratory function during the day.
- Lung volume reduction surgery
- Lung transplantation: considered the last resort in patients with emphysema associated with advanced COPD and severe diffusion dysfunction
- Long-term oxygen therapy (LTOT): 16 hours oxygen administration per day (minimum dosage) is associated with lower mortality rates.
Other complications 
- Acute exacerbation: See AECOPD.
- 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.