COPD (chronic obstructive pulmonary disease)

Definition

Chronic obstructive pulmonary disease (COPD) is a chronic, usually progressive disease of the airways and lungs. It is characterized by airflow obstruction that is not fully reversible after bronchodilation. It is associated with chronic obstructive bronchitis and/or pulmonary emphysema; the extent of obstruction, hyperinflation and impaired gas exchange can vary independently.

• Chronic bronchitis: persistent cough, usually with sputum, for at least one year.
• Pulmonary emphysema: loss of gas exchange surface of the lung through destruction of alveolar walls.

Classification

Severity of airflow obstruction according to GOLD (post-bronchodilator FEV1 in % predicted):

Symptom burden: assessed with the mMRC dyspnea scale and the COPD Assessment Test (CAT); according to GOLD, CAT ≥ 10 or mMRC ≥ 2 indicates a higher symptom burden.

Occurrence & epidemiology

In Germany the GEDA 2014/2015 survey found a 12-month prevalence of known COPD of 5.8 % in adults, at a similar level in women and men. Frequency rises markedly with age: in people over 65 it was 11.0 % (women) and 12.5 % (men). According to claims data, the diagnosed prevalence in people over 40 rose from 5.1 % to 6.4 % between 2009 and 2016. Worldwide, COPD accounted for 3.23 million deaths in 2019 and is the third most common cause of death.

Aetiopathogenesis

• Tobacco smoke: the most important risk factor; the risk rises with the duration of smoking and the cumulative exposure (pack-years).
• Biomass fuels: wood, grasses and other organic materials contribute to frequency in some regions.
• Alpha-1 antitrypsin deficiency: a hereditary cause with panlobular emphysema.
• Bronchial hyperresponsiveness: smokers with increased sensitivity to methacholine are at higher risk.

Pathophysiology: Inhaled noxious agents trigger chronic inflammation involving mainly activated neutrophils and macrophages. An imbalance between proteases and antiproteases as well as oxidative stress destroy the lung parenchyma. Mucus hypersecretion, wall thickening and loss of elastic recoil narrow the airways; the results are air trapping, hyperinflation, hypoxemia and, in late stages, hypercapnia, pulmonary hypertension and cor pulmonale.

Clinical features

• Cardinal symptoms: cough, sputum and breathlessness, initially on exertion; the course is usually progressive.
• Findings: prolonged expiration, wheeze, diminished breath sounds, increased anteroposterior chest diameter (barrel chest); in advanced disease pursed-lip breathing, use of accessory muscles, paradoxical inward movement of the lower ribs on inspiration, cyanosis and signs of right heart failure.
• Severe disease: loss of weight, pneumothorax, frequent acute deteriorations, right heart failure, acute respiratory failure.
• Exacerbation: an acute worsening lasting at least two days, with increased breathlessness, cough, sputum volume and/or purulence; triggered by viral infections, bacteria (Hemophilus influenzae, Streptococcus pneumoniae, occasionally Moraxella catarrhalis) and air pollutants.

Comorbidities

Common comorbidities are cardiovascular disease (mainly arterial hypertension and coronary heart disease), diabetes, obesity, sleep-related breathing disorders, osteoporosis, lung cancer, pulmonary hypertension, cachexia, muscle weakness, anxiety disorders and depression. In a meta-analysis, the prevalence of depression in COPD was 27.1 % (control group 10.0 %).

Diagnosis

Lung function

• Post-bronchodilator spirometry: demonstration of persistent obstruction with a reduced FEV1/FVC ratio. The German NVL COPD prefers the lower limit of normal (LLN) based on Global Lung Initiative (GLI) reference values; the fixed cut-off FEV1/FVC < 0.7 can cause underdiagnosis in younger and overdiagnosis in older people. FEV1 determines the GOLD grade.
• Body plethysmography: hyperinflation and air trapping.
• Diffusing capacity (DLCO): reduced in emphysema, normal or raised in asthma.
• Distinction from asthma: COPD is usually not diagnosed before the sixth decade of life, the obstruction is always demonstrable and never fully reversible, and FeNO is normal to low.

Imaging, laboratory tests and heart

• Chest X-ray: in emphysema, hyperinflation with flattened diaphragm, increased radiolucency and bullae; in chronic bronchitis often normal or with increased bronchovascular markings from bronchial wall thickening. Also used to detect pneumonia or pneumothorax.
• Chest CT: shows changes not visible on the X-ray and comorbidities such as pneumonia, pneumoconioses or lung cancer.
• Laboratory tests: blood count (erythrocytosis with hematocrit above 48 % in chronic hypoxemia), alpha-1 antitrypsin; blood gas analysis in respiratory failure.
• ECG and echocardiography: evidence of right heart strain and cardiac comorbidities.

Keep learning in the app

Further reading (open access)

1. Nationale VersorgungsLeitlinie COPD: Kapitel 1 Definition und Epidemiologie
2. Nationale VersorgungsLeitlinie COPD: Kapitel 2 Diagnostik
3. MSD Manual Profi-Ausgabe: Chronische obstruktive Lungenerkrankung
4. StatPearls: Chronic Obstructive Pulmonary Disease (COPD)
5. MSD Manual Professional Edition: Chronic Obstructive Pulmonary Disease (COPD)
6. Fregonese L, Stolk J: Hereditary alpha-1-antitrypsin deficiency and its clinical consequences (Orphanet J Rare Dis 2008)

Cross-references