Preparatory Mindset
COPD is now one of the top three causes of death worldwide and is the classic exam topic for "chronic airflow limitation." Two things are always tested: (1) spirometric diagnosis — persistent airflow obstruction defined as post-bronchodilator FEV₁/FVC < 0.70, with GOLD grades 1–4 by FEV₁ % predicted; and (2) management — stable disease by the GOLD ABE group (bronchodilators, LABA+LAMA, ± ICS by eosinophil count) and acute exacerbations (controlled oxygen to SpO₂ 88–92%, SABA ± ipratropium, corticosteroids, antibiotics for purulent sputum, NIV for hypercapnic acidosis — pH ≤7.35 with PaCO₂ >6.0 kPa). The LMCHK must-know is the HKHA AECOPD algorithm — the oxygen target and the NIV/intubation thresholds are frequently examined.
Core Concepts
Definition & epidemiology
- COPD = common, preventable, treatable disease characterised by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities, usually caused by significant exposure to noxious particles or gases.
- Encompasses chronic bronchitis (cough + sputum ≥3 months/year for ≥2 years) and emphysema (alveolar destruction); most patients have both.
- Diagnostic criterion: post-bronchodilator FEV₁/FVC < 0.70 (persistent airflow obstruction).
- Epidemiology: global prevalence ~11.7%; among >40-year-olds in China ~8.2% (M 12.4%, F 5.1%; ~32.8 million); top-3 cause of death, ~90% of COPD deaths in low/middle-income countries; respiratory disease ≈6% of healthcare budget, COPD ≈56% of that.
Risk factors
- Cigarette smoking (the dominant risk factor — recognised for >5 decades).
- Air pollution: particulate matter (PM), ozone, NOₓ/SOₓ, heavy metals.
- α₁-antitrypsin (AAT) deficiency (<1% of COPD; liver-produced, lung-protective; early-onset emphysema).
- Asthma history: ~20% of asthmatics develop irreversible airflow limitation.
- Occupational dusts/chemicals, recurrent infections, impaired lung growth.
Pathophysiology
- Chronic inflammation (neutrophils, macrophages, CD8+ T cells) → small-airway disease (obstructive bronchiolitis) + parenchymal destruction (emphysema) + mucus hypersecretion → progressive airflow limitation, gas trapping, hyperinflation, V/Q mismatch → hypoxaemia, and eventually pulmonary hypertension/cor pulmonale.
Clinical manifestations
- Chronic cough, sputum, progressive exertional dyspnoea; exacerbations (infections, pollution).
- Signs: prolonged expiration, hyperresonance, barrel chest, distant breath sounds, pursed-lip breathing, accessory muscle use; cyanosis/oedema in advanced disease (cor pulmonale).
- History key points: smoking pack-years, occupational exposures, childhood infections, family history (AAT), symptoms over time.
Diagnosis & GOLD staging
- Spirometry: post-bronchodilator FEV₁/FVC <0.70 confirms obstruction; severity by FEV₁ % predicted:
| GOLD grade | Severity | FEV₁ (% predicted) |
|---|---|---|
| 1 | Mild | ≥80 |
| 2 | Moderate | 50–79 |
| 3 | Severe | 30–49 |
| 4 | Very severe | <30 |
- FEV₁ <50% predicted = high risk; lower FEV₁ = higher risk.
- ABE assessment (symptoms + exacerbation history): Group A (0–1 moderate exacerbation, low symptoms), Group B (more symptoms), Group E (≥2 moderate exacerbations OR ≥1 hospitalisation — high exacerbation risk).
- HRCT: emphysema extent (centrilobular/panlobular), bronchiectasis co-existence.
- Differential: asthma (reversibility), bronchiectasis, TB (chronic fibro-cavernous), heart failure.
Management of stable COPD (GOLD 2024)
- Group A: a bronchodilator (SABA/SAMA or LABA/LAMA). - Group B: LABA + LAMA. - Group E: LABA + LAMA; consider LABA+LAMA+ICS if blood eosinophils ≥0.3×10⁹/L.
- Universal: smoking cessation (single most effective), physical activity, vaccination (influenza, pneumococcal), pulmonary rehabilitation (Groups B & E), nutrition, self-management + exacerbation action plan.
- Initial pharmacological treatment by group:
- Escalate stepwise; add ICS for repeated exacerbations with eosinophilia; long-term oxygen therapy (LTOT) if chronic severe hypoxaemia; consider lung volume reduction/surgery/transplant in selected patients; treat comorbidities (osteoporosis, anxiety/depression, anaemia, heart failure).
Management of acute exacerbation (AECOPD)
- Workup for precipitating cause (exclude pneumothorax, respiratory infection, PE).
- Supplemental oxygen — start 1–2 L/min nasal prongs, target SpO₂ 88–92%; check ABG 30–60 min later (avoid O₂-driven CO₂ retention).
- Short-acting bronchodilators: salbutamol (Ventolin) ± ipratropium bromide (Atrovent) with spacer; nebulise if severe.
- Corticosteroids: hydrocortisone 100 mg IV q6–8h OR oral prednisolone 30–40 mg daily, discontinued after the acute episode (5–10 days).
- Antibiotics if requiring NIV/invasive ventilation, and/or ≥2 cardinal symptoms (one being ↑ sputum purulence): ↑dyspnoea, ↑sputum volume, ↑sputum purulence.
- NIV (BIPAP) to relieve dyspnoea (↓ work of breathing), improve respiratory acidosis, avoid intubation — consider when: respiratory acidosis (PaCO₂ >6.0 kPa, pH ≤7.35), severe dyspnoea with respiratory-muscle fatigue/↑WOB (accessory muscles, paradoxical abdominal motion, intercostal retraction), persistent hypoxaemia despite O₂. Check ABG 30–60 min after starting NIV; do not delay intubation if no improvement.
- Invasive mechanical ventilation (ICU): NIV failure/intolerance ± life-threatening hypoxaemia, diminished consciousness/uncontrolled agitation, massive aspiration/persistent vomiting, inability to clear secretions, severe haemodynamic instability/arrhythmia, post-respiratory/cardiac arrest.
- Manage complications: pneumothorax, cor pulmonale, electrolyte/acid-base disturbances.
HKHA Handbook (LMCHK) — Key Points
- AECOPD algorithm (HA standard) — oxygen start 1–2 L/min, target SpO₂ 88–92%, ABG at 30–60 min; salbutamol ± ipratropium with spacer; hydrocortisone 100 mg IV q6–8h or prednisolone 30–40 mg daily (stop after 5–10 days); antibiotics only for NIV/intubation or ≥2 cardinal symptoms with ↑purulence.
- NIV indications: respiratory acidosis PaCO₂ >6.0 kPa AND pH ≤7.35; severe dyspnoea with muscle fatigue/↑WOB; persistent hypoxaemia despite O₂. ABG 30–60 min post-initiation; never delay intubation if no improvement.
- Intubation criteria (ICU): NIV failure/intolerance with life-threatening hypoxaemia, depressed consciousness/agitation, massive aspiration/vomiting, inability to clear secretions, haemodynamic instability/arrhythmia, arrest.
- Stable COPD (GOLD 2024): GOLD 1–4 by FEV₁ (≥80 / 50–79 / 30–49 / <30); initial therapy A: bronchodilator, B: LABA+LAMA, E: LABA+LAMA ± ICS if eosinophils ≥0.3×10⁹/L; all patients — smoking cessation, exercise, vaccination; rehab for B&E.
- Massive haemoptysis (P 1) and oxygen therapy (P 6–7) sections complement COPD care (see respiratory failure chapter).
High-Yield Points
- COPD = post-bronchodilator FEV₁/FVC <0.70 (the single most tested criterion).
- GOLD: 1 ≥80, 2 50–79, 3 30–49, 4 <30 (% predicted FEV₁).
- Smoking = dominant cause; AAT deficiency <1%; ~20% of asthmatics develop irreversible obstruction.
- Stable: A = bronchodilator; B = LABA+LAMA; E = LABA+LAMA ± ICS (eos ≥0.3).
- AECOPD: O₂ target 88–92% (start 1–2 L/min), SABA ± ipratropium, steroids 5–10 days, antibiotics if purulent sputum.
- NIV if pH ≤7.35 + PaCO₂ >6.0 kPa; intubate if NIV fails or consciousness/hemodynamics deteriorate.
- FEV₁ <50% = high risk; long-term O₂ for chronic hypoxaemia.
Topic Summary
COPD is defined by persistent, post-bronchodilator airflow obstruction (FEV₁/FVC <0.70), graded 1–4 by FEV₁ % predicted, and driven overwhelmingly by smoking (with AAT deficiency and asthma as notable causes). Stable management follows GOLD 2024: universal smoking cessation, exercise, vaccination and rehabilitation, with escalating bronchodilator therapy by ABE group (bronchodilator → LABA+LAMA → ±ICS with eosinophilia). Exacerbations are treated with controlled oxygen (SpO₂ 88–92%), SABA ± ipratropium, short-course corticosteroids, and antibiotics for purulent exacerbations; hypercapnic acidosis (pH ≤7.35) is the trigger for NIV and, failing that, intubation — the HKHA AECOPD algorithm being a core LMCHK item.