Medicine chapters
Chronic obstructive pulmonary disease (stepwise management)
COPD is persistent, poorly reversible airflow limitation from smoke or biomass exposure; this chapter covers diagnosis, GOLD grading, stepwise inhaler treatment, oxygen, NIV and exacerbations.
- COPD is persistent airflow limitation (post-bronchodilator FEV1/FVC <0.7) caused mainly by smoking and, in Pakistan, biomass smoke; severity is graded by FEV1 % predicted (GOLD 1–4).
- Stepwise care: stop smoking, vaccines, rehab, then SABA/SAMA, then LAMA or LABA, then LAMA + LABA, adding ICS only for frequent exacerbations (especially with eosinophilia).
- Only smoking cessation and long-term oxygen (PaO2 <7.3 kPa, ≥15 h/day) improve survival; treat exacerbations with controlled O2 (88–92%), nebulisers, prednisolone, antibiotics and NIV if pH <7.35 with high PaCO2.
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Overview
Chronic obstructive pulmonary disease (COPD) is a common, preventable disease with persistent airflow limitation that is not fully reversible and usually gets worse over time. It brings together emphysema, chronic bronchitis and small airways disease.
It is a leading cause of admissions with breathlessness and of type 2 respiratory failure. In Pakistan, women who cook over wood, dung-cake or crop fires in poorly ventilated kitchens develop COPD without ever smoking.
The TOS asks for stepwise management, so learn the steps, the drugs that improve survival and the emergency treatment of an exacerbation.
Definitions
- Chronic bronchitis: productive cough on most days for at least 3 months in each of 2 consecutive years.
- Emphysema: permanent enlargement of air spaces beyond the terminal bronchiole with destruction of their walls.
- Centriacinar (centrilobular): around respiratory bronchioles, upper lobes; typical of smokers.
- Panacinar (panlobular): whole acinus, lower lobes; typical of alpha-1 antitrypsin deficiency.
Causes and risk factors
- Cigarette smoking (the main cause; only a minority of smokers develop COPD, so susceptibility matters).
- Biomass fuel smoke and outdoor pollution (winter smog).
- Occupational dusts (coal, cadmium, silica).
- Alpha-1 antitrypsin deficiency (ZZ genotype): emphysema in a young person or non-smoker, often with liver disease.
Pathophysiology in brief
- Smoke recruits neutrophils, macrophages and CD8 T cells. Their elastase and proteases outweigh antiproteases (alpha-1 antitrypsin) and destroy alveolar walls.
- Goblet cell and mucous gland hyperplasia → sputum.
- Loss of elastic recoil → airways collapse on expiration → air trapping, hyperinflation, raised TLC and residual volume.
- Loss of alveolar surface → low gas transfer (TLCO).
- Chronic hypoxia → pulmonary vasoconstriction → pulmonary hypertension → cor pulmonale, and secondary polycythaemia.
Clinical features
- Smoker over about 40 with cough, sputum, wheeze and progressive breathlessness; frequent winter "chest infections".
- Signs: tachypnoea, pursed-lip breathing, use of accessory muscles, barrel chest, reduced cricosternal distance, hyper-resonance, loss of cardiac and liver dullness, quiet breath sounds, prolonged expiration, wheeze.
- CO2 retention: warm peripheries, bounding pulse, flapping tremor, drowsiness, headache, papilloedema.
- Cor pulmonale: raised JVP, ankle oedema, hepatomegaly, loud P2, tricuspid regurgitation.
| Old label | Picture |
|---|---|
| "Pink puffer" | Emphysema-dominant; breathless, thin, near-normal gases, still responds to CO2 |
| "Blue bloater" | Bronchitis-dominant; cyanosed, oedematous, less breathless, hypercapnic (CO2-insensitive) |
Clubbing is not a feature of COPD. If a COPD patient develops clubbing, look for lung cancer, bronchiectasis or fibrosis.
Investigations
- Spirometry (diagnostic): post-bronchodilator FEV1/FVC below 0.70; little reversibility (usually under 15%).
- Lung volumes: raised TLC and RV; TLCO low in emphysema.
- Chest X-ray: hyperinflated lungs, flat low diaphragms, narrow heart, bullae, pruned peripheral vessels; excludes cancer and pneumothorax.
- HRCT: shows the type and extent of emphysema; used before surgery.
- Full blood count: polycythaemia (raised haematocrit).
- ABG: chronic type 2 failure shows high PaCO2 with raised bicarbonate (renal compensation) and near-normal pH.
- ECG: P pulmonale, right axis deviation, RBBB, RV hypertrophy in cor pulmonale. Echo for pulmonary hypertension.
- Alpha-1 antitrypsin level in young or non-smoking patients, or with a family history.
- Sputum culture in exacerbations: H. influenzae, Strep. pneumoniae, Moraxella catarrhalis; many attacks are viral.
GOLD grades of airflow limitation (FEV1/FVC <0.70)
| Grade | Post-bronchodilator FEV1 (% predicted) |
|---|---|
| GOLD 1 mild | ≥80% |
| GOLD 2 moderate | 50–79% |
| GOLD 3 severe | 30–49% |
| GOLD 4 very severe | <30% |
Smoker: 20 cigarettes a day for 30 years = 20 ÷ 20 × 30 = 30 pack-years
Post-bronchodilator FEV1 1.4 L, FVC 2.8 L, predicted FEV1 3.0 L
FEV1/FVC = 1.4 ÷ 2.8 = 0.50 → below 0.70, so obstructive (COPD)
FEV1 % predicted = 1.4 ÷ 3.0 × 100 = 47% → GOLD 3 (severe)
Symptom burden is scored with the mMRC dyspnoea scale or the COPD Assessment Test (CAT). The BODE index (BMI, Obstruction, Dyspnoea, Exercise capacity) predicts mortality.
Asthma or COPD?
| Feature | Asthma | COPD |
|---|---|---|
| Onset | Often childhood | Over 40, smoker |
| Symptoms | Variable, night and early morning | Persistent, progressive |
| Reversibility | Large (>15%) | Small |
| TLCO | Normal | Low (emphysema) |
| Inflammation | Eosinophils, CD4 (Th2) | Neutrophils, CD8, macrophages |
| Steroid response | Good | Limited |
Stepwise management of stable COPD
Step 0: for every patient
- Stop smoking (counselling plus nicotine replacement, varenicline or bupropion). It is the single most useful measure and slows FEV1 decline.
- Reduce biomass smoke exposure (better ventilation, cleaner stoves).
- Vaccines: annual influenza and pneumococcal vaccine.
- Pulmonary rehabilitation for those limited by breathlessness (improves exercise tolerance and quality of life).
- Check inhaler technique; treat anxiety, depression and weight loss.
Drug steps
| Step | Treatment |
|---|---|
| 1 | Short-acting bronchodilator as needed: SABA (salbutamol) or SAMA (ipratropium) |
| 2 | Regular long-acting bronchodilator: LAMA (tiotropium) or LABA (salmeterol, formoterol) |
| 3 | LAMA + LABA if still breathless or exacerbating |
| 4 | LAMA + LABA + ICS (triple therapy) if exacerbations continue, especially with blood eosinophils ≥300 cells/µL or asthmatic features |
| Add-ons | Roflumilast (PDE-4 inhibitor) if FEV1 <50% with chronic bronchitis and frequent exacerbations; azithromycin long-term in frequent exacerbators; mucolytics (carbocisteine) for sticky sputum; theophylline (limited benefit, many interactions) |
- GOLD groups (2023): group A (few symptoms, few exacerbations) → a bronchodilator; group B (more symptoms) → LABA + LAMA; group E (2 or more moderate exacerbations or 1 hospital admission a year) → LABA + LAMA, consider adding ICS if eosinophils ≥300.
Inhaled steroids alone are not used in COPD, and high doses increase the risk of pneumonia. They are added for frequent exacerbations, not to slow lung function decline.
Tiotropium (LAMA) improves symptoms and reduces exacerbations, but no inhaler has been shown to stop the yearly fall in FEV1.
Long-term oxygen therapy (LTOT)
Assess when stable, on two ABGs at least 3 weeks apart. Offer LTOT if:
- PaO2 <7.3 kPa (55 mmHg) on air, or
- PaO2 7.3–8.0 kPa plus secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension.
- The patient must have stopped smoking (fire risk; carboxyhaemoglobin <3%).
- Give via a concentrator, usually about 2 L/min, for at least 15 hours a day (survival benefit rises with longer use).
Only smoking cessation and LTOT in hypoxaemic patients are proven to prolong life in COPD.
Other measures
- Venesection if packed cell volume is above 55%.
- Diuretics for oedema in cor pulmonale.
- Surgery and procedures: bullectomy for giant bullae; lung volume reduction surgery or endobronchial valves in selected upper-lobe emphysema; lung transplant in end-stage disease.
- Alpha-1 antitrypsin replacement in selected deficient patients.
- Palliative care: opioids for intractable breathlessness, fan therapy.
- Air travel: patients may desaturate at cabin altitude; arrange in-flight oxygen if needed.
Acute exacerbation of COPD
A sustained worsening of breathlessness, cough or sputum volume and purulence beyond day-to-day variation, usually triggered by viral or bacterial infection or pollution.
Rule out pneumonia, pneumothorax, pulmonary embolism and heart failure (chest X-ray, ECG, ABG).
Treatment
- Controlled oxygen by Venturi mask (24–28%) to a target SpO2 of 88–92%; repeat ABG in 30–60 minutes.
- Nebulised salbutamol and ipratropium.
- Prednisolone 30–40 mg daily for 5 days (or IV hydrocortisone if unable to swallow).
- Antibiotics if sputum is purulent or there are signs of infection: amoxicillin, doxycycline or clarithromycin orally; IV if severe.
- Physiotherapy for retained secretions; thromboprophylaxis; manage fluids.
- Non-invasive ventilation (BiPAP) if, despite the above, pH <7.35 and PaCO2 >6.5 kPa (respiratory acidosis), usually with RR >23.
- Intubation if NIV fails or is contraindicated, when there is a reversible cause and an acceptable baseline; agree the ceiling of care early.
In type 2 failure, high-flow oxygen raises PaCO2 (worse V/Q matching, Haldane effect and some loss of hypoxic drive), causing CO2 narcosis. Use controlled oxygen, but never withhold oxygen from a hypoxic patient; severe hypoxaemia kills faster than hypercapnia.
COPD oxygen target "88 to 92, that will do"; everyone else 94–98%.
NIV reduces intubation and death in hypercapnic acidosis. It is not indicated just because PaCO2 is high with a normal pH (compensated chronic retention).
Complications
- Type 2 respiratory failure, CO2 narcosis.
- Pulmonary hypertension and cor pulmonale.
- Secondary polycythaemia.
- Pneumothorax from ruptured bullae.
- Recurrent infections, pneumonia (especially with ICS).
- Lung cancer (shared smoking risk), osteoporosis, depression, muscle wasting.
Prognosis
Worse with older age, lower FEV1, low BMI, hypoxaemia, hypercapnia, cor pulmonale and frequent admissions. The BODE index combines these to estimate survival.
Expect: post-bronchodilator FEV1/FVC <0.7, GOLD 1–4 cut-offs (80, 50, 30), stopping smoking as the most useful measure, LTOT criteria (PaO2 <7.3 kPa, or 7.3–8 with polycythaemia, oedema or pulmonary hypertension, at least 15 hours a day), oxygen target 88–92% by Venturi mask, NIV for acidosis (pH below 7.35) with PaCO2 above 6.5 kPa, prednisolone 30–40 mg for 5 days, tiotropium as a LAMA, roflumilast as a PDE-4 inhibitor, ICS raising pneumonia risk, alpha-1 antitrypsin deficiency with lower-lobe panacinar emphysema, centriacinar emphysema in smokers, and no clubbing in COPD.
Quick revision
- FEV1/FVC <0.7 after bronchodilator; GOLD grades ≥80, 50–79, 30–49, <30%.
- Smokers: centriacinar, upper lobes; AAT deficiency: panacinar, lower lobes.
- Everyone: stop smoking, vaccines, rehab.
- Steps: SABA/SAMA → LAMA or LABA → LAMA + LABA → add ICS if exacerbating with eosinophils ≥300.
- LTOT: PaO2 <7.3 kPa (or 7.3–8 with complications), ≥15 h/day, non-smoker.
- Exacerbation: Venturi O2 to 88–92%, nebs, prednisolone 30–40 mg × 5 days, antibiotics.
- NIV: pH <7.35 and PaCO2 >6.5 kPa despite treatment.
- Survival benefit: stopping smoking and LTOT only.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
What is the single most effective treatment in COPD?
Stopping smoking; it slows the decline in lung function at any stage, and with long-term oxygen in hypoxaemic patients it is one of only two measures shown to prolong life.
Why is oxygen given carefully in COPD?
Some patients with chronic CO2 retention develop a rising PaCO2 and acidosis with high-flow oxygen, so oxygen is titrated through a Venturi mask to a saturation of 88–92%.
When should a COPD patient be offered home oxygen?
When stable, if PaO2 is below 7.3 kPa on air, or 7.3–8 kPa with polycythaemia, nocturnal hypoxaemia, oedema or pulmonary hypertension, and the patient has stopped smoking.
When are inhaled steroids used in COPD?
As an add-on to dual long-acting bronchodilators in patients with frequent exacerbations, particularly when blood eosinophils are high; they are not used alone.