AKT · Respiratory/Airways disease

Chronic obstructive pulmonary disease (COPD)

Progressive, largely irreversible airflow obstruction from smoking (chronic bronchitis + emphysema)

Overview

A progressive disease of largely irreversible airflow obstruction, almost always from smoking (consider alpha-1 antitrypsin deficiency in the young/non-smoker). Diagnosis needs post-bronchodilator spirometry showing obstruction (FEV1/FVC <0.7). Management is smoking cessation (the only intervention that alters the course) + inhalers stepped by phenotype, pulmonary rehab, vaccines, and recognising/treating exacerbations and chronic type 2 respiratory failure.

Recognise

Chronic productive cough, progressive exertional breathlessness, wheeze and recurrent infections in a smoker; barrel chest, hyperinflation, prolonged expiration
Post-bronchodilator spirometry: obstructive (FEV1/FVC <0.7) with little reversibility; consider alpha-1 antitrypsin deficiency if young/non-smoker/family history
Cor pulmonale (right heart failure), chronic type 2 respiratory failure (CO2 retention), polycythaemia in advanced disease

Red flags

Exacerbation with type 2 respiratory failure (CO2 retention, acidosis) → controlled oxygen (88–92%) + consider NIV (BiPAP) for persistent respiratory acidosis
Sudden breathlessness/pleuritic pain → exclude pneumothorax (bullae rupture) or PE

Differentials & how to tell them apart

Asthmayounger, atopic, reversible/variable obstruction, diurnal variation, eosinophilic

Bronchiectasislarge-volume purulent sputum, recurrent infections, HRCT tramlines

Heart failureorthopnoea, raised JVP, oedema, raised BNP

Lung cancerhaemoptysis, weight loss, focal mass — a smoker needs a low threshold for a CXR

Investigations

Post-bronchodilator spirometry (obstructive, FEV1/FVC <0.7 — diagnostic); CXR (hyperinflation, bullae, exclude cancer); FBC (polycythaemia/anaemia), BMI; alpha-1 antitrypsin if young/non-smoker; ABG and eosinophils to guide therapy; exacerbation — CXR, ABG, cultures.

Management

Stop smoking + pulmonary rehab + vaccines; SABA/SAMA → LABA+LAMA → +ICS if eos≥300/asthmatic features

1Confirm with post-bronchodilator spirometry (FEV1/FVC <0.7). Smoking cessation is the only step that changes the course — plus pulmonary rehab and vaccines. Step inhalers: SABA/SAMA, then LABA + LAMA.Gate: Add an ICS only for asthmatic/steroid-responsive features or eosinophils ≥300 (it raises pneumonia risk); in an exacerbation give CONTROLLED oxygen (88–92%) and consider NIV for persistent respiratory acidosis — uncontrolled O2 can worsen CO2 retention.
2Exacerbation: controlled O2, nebulised bronchodilators, prednisolone, antibiotics if infective; NIV (BiPAP) for persistent type 2 respiratory failure; long-term oxygen therapy for chronic hypoxia in ex-smokers.

Smoking cessation (the ONLY disease-modifying step) + pulmonary rehab + vaccines (flu/pneumococcal) — foundation; treat all; SABA/SAMA for symptom relief

Inhaled escalation: SABA/SAMA → LABA + LAMA — dual long-acting bronchodilators for persistent breathlessness/exacerbations

Add ICS if asthmatic/steroid-responsive features or blood eosinophils ≥300 (→ LABA+LAMA+ICS) — ICS chosen by phenotype/eosinophils; raises pneumonia risk

Exacerbation: controlled O2 (88–92%), nebulised bronchodilators, prednisolone, antibiotics if infective; NIV for persistent type 2 respiratory failure — long-term oxygen therapy if chronic hypoxia (and stopped smoking)

Key points

Smoker + progressive breathlessness + productive cough + obstructive spirometry (FEV1/FVC <0.7, irreversible) = COPD → STOP SMOKING (only disease-modifier) + rehab + vaccines; SABA/SAMA→LABA+LAMA→+ICS if eos≥300/asthmatic. Exacerbation: CONTROLLED O2 88–92%, steroids, NIV for persistent acidosis. Young/non-smoker → alpha-1 antitrypsin.

Monitor & prognosis

Spirometry/symptoms/exacerbations, MRC dyspnoea, oxygen/ABG, BMI, ICS-pneumonia risk.

Progressive; smoking cessation slows decline; advanced disease → cor pulmonale and respiratory failure.

Source: NICE NG115 (COPD)