Chronic Obstructive Pulmonary Disease
A progressive, largely irreversible airflow limitation from smoking-driven small-airway inflammation and alveolar destruction; because the damage is structural, treatment focuses on slowing decline, relieving symptoms and preventing exacerbations.
In a nutshell
Fixed airflow obstruction from smoking-driven small-airway inflammation and alveolar destruction. Because the damage is structural rather than bronchospasm, no drug reverses it: smoking cessation is the only intervention that slows the decline, and long-term oxygen the only other that improves survival.
Classic presentation
A smoker over 35 with years of progressive exertional breathlessness, chronic productive cough and recurrent chest infections, a hyperinflated chest, and a post-bronchodilator FEV1/FVC below 0.7.
Key points
- The obstruction is structural (scarred small airways plus loss of elastic recoil from emphysema), which is why it does not fully reverse with a bronchodilator. That irreversibility is the line between COPD and asthma.
- Loss of recoil collapses airways on expiration and traps air. On exertion there is no time to empty, so dynamic hyperinflation worsens: the mechanical reason breathlessness is exertional, and why pursed-lip breathing helps.
- Diagnosis requires post-bronchodilator spirometry showing an FEV1/FVC ratio below 0.7.
- Chronic hypoxia causes pulmonary vasoconstriction, then pulmonary hypertension and right heart strain: cor pulmonale, with peripheral oedema and a raised JVP.
- Smoking cessation outranks every drug: it alone slows the accelerated decline in lung function.
- Long-term oxygen improves survival in stable chronic hypoxaemia, but is not offered to those who continue to smoke, for fire risk and lack of benefit.
First-line investigation
Post-bronchodilator spirometry, which confirms airflow obstruction that does not fully reverse and separates COPD from asthma.
First-line management
Smoking cessation with behavioural support and pharmacotherapy, plus inhaled long-acting bronchodilators for symptoms and referral for pulmonary rehabilitation.
Exam traps
- Spirometry must be post-bronchodilator. A pre-bronchodilator ratio cannot distinguish COPD from asthma.
- Inhaled corticosteroids are added for frequent exacerbations or eosinophilic features, not given to everyone: they carry a pneumonia risk.
- Do not offer long-term oxygen therapy to a current smoker.
- Lung cancer shares the risk factor. Haemoptysis or weight loss in a smoker is not just COPD.
Educational content pending clinical review. Not medical advice.