COPD: Emphysema and Chronic Bronchitis
COPD is an obstructive lung disease with persistent, not fully reversible airflow limitation, predominantly caused by tobacco smoke (90% of cases). Encompasses emphysema and chronic bronchitis.
Emphysema: destruction of alveolar walls → loss of elastic recoil → air trapping. 'Pink puffer' (Type A COPD): thin, tachypneic, pursed-lip breathing, barrel chest, minimal hypoxemia until advanced.
Chronic bronchitis: productive cough ≥3 months/year for ≥2 consecutive years. Mucus hypersecretion, airway inflammation. 'Blue bloater' (Type B COPD): hypoxic, hypercapnic, polycythemic, edematous, frequent exacerbations.
Diagnosis requires a post-bronchodilator FEV1/FVC <0.70. GOLD then grades airflow limitation by post-bronchodilator FEV1 % predicted: GOLD 1 (mild ≥80%), GOLD 2 (moderate 50–79%), GOLD 3 (severe 30–49%), GOLD 4 (very severe <30%).
Since GOLD 2023, treatment is guided by a separate ABE assessment of symptoms and exacerbation history: Group A — 0–1 moderate exacerbations (none leading to hospitalization) and few symptoms (mMRC 0–1, CAT <10); Group B — the same exacerbation history with more symptoms (mMRC ≥2, CAT ≥10); Group E — ≥2 moderate exacerbations or ≥1 leading to hospitalization in the past year, whatever the symptoms. The grade (1–4) and group (A, B, E) are reported together, e.g. GOLD 3, Group E.
- Emphysema: alveolar destruction, reduced elastic recoil, air trapping
- Chronic bronchitis: productive cough 3 mo/yr × 2 years
- GOLD 1–4 (airflow severity) by post-BD FEV1%: ≥80, 50–79, 30–49, <30
- GOLD ABE groups (2023+): A and B by symptoms with 0–1 moderate exacerbations; E = ≥2 moderate or ≥1 hospitalized
- Smoking cessation is the only intervention proven to slow COPD progression
- Long-term O2 therapy (LTOT): indicated when PaO2 ≤55 mmHg or SpO2 ≤88% at rest
Oxygen therapy for COPD: target SpO2 88–92%. Avoid excessive O2 — can worsen hypercapnia by releasing hypoxic vasoconstriction and Haldane effect.