Chronic Obstructive Pulmonary Disease
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Direct answer
COPD is persistent airflow limitation defined spirometrically by a post-bronchodilator FEV1/FVC ratio below 0.7, assessed for therapy by symptoms (mMRC, CAT) and exacerbation history. Smoking cessation is the only intervention shown to change its natural history; maintenance treatment rests on long-acting bronchodilators, with an inhaled corticosteroid added mainly when blood eosinophils are high or exacerbations are frequent. An exacerbation is treated with short-acting bronchodilators, a short course of oral corticosteroids, antibiotics when sputum is purulent, controlled oxygen targeting SpO2 88 to 92 per cent, and non-invasive ventilation for respiratory acidosis.
What you must remember
- Diagnosis: post-bronchodilator FEV1/FVC below 0.7; severity by FEV1 per cent predicted — mild 80 and above, moderate 50 to 79, severe 30 to 49, very severe below 30.
- Current GOLD assessment groups: group A (few symptoms, no more than one moderate exacerbation, none hospitalised) and group E (two or more moderate exacerbations or one hospitalisation).
- Initial therapy: group A a bronchodilator; group E a LABA-LAMA; add an ICS when blood eosinophils are 300 per microlitre or more or exacerbations recur despite dual therapy — ICS alone is never used and raises pneumonia risk.
- Non-pharmacological: smoking cessation, influenza and pneumococcal vaccination, pulmonary rehabilitation, and long-term oxygen therapy for chronic respiratory failure (PaO2 about 55 mmHg or less), which improves survival.
- Exacerbation: nebulised salbutamol with ipratropium, prednisolone 40 mg for five days, antibiotics (amoxicillin-clavulanate, doxycycline or azithromycin) when sputum turns purulent; controlled oxygen for SpO2 88 to 92 per cent.
- Non-invasive ventilation is first-line for exacerbation with respiratory acidosis (pH below 7.35 with PaCO2 above 45 mmHg), reducing intubation and mortality.
- Suspect alpha-1 antitrypsin deficiency in a young or non-smoking patient with basal emphysema; lung volume reduction surgery or transplantation for selected advanced disease.
Managing an exacerbation, from triage to ward
A 70-year-old smoker arrives with three days of increasing breathlessness, purulent sputum and confusion; SpO2 is 84 per cent and the gas shows pH 7.29 with PaCO2 62. Start with controlled oxygen through a Venturi mask targeting 88 to 92 per cent — the single most testable act in the whole encounter, because uncontrolled high-flow oxygen in a chronic hypercapnic patient invites carbon dioxide narcosis. Nebulise salbutamol with ipratropium, driven by air rather than oxygen if hypercapnia is significant. Give prednisolone 40 mg orally for five days, and add amoxicillin-clavulanate, doxycycline or azithromycin because the sputum is purulent. Recheck the gas within the hour: pH still below 7.35 with PaCO2 above 45 means non-invasive ventilation, which in this setting reduces both intubation and mortality — and the confused, drowsy patient can still try it, with readiness to intubate if he deteriorates or cannot protect his airway. Before discharge, arrange the pieces that change the disease's course over years: smoking cessation support, influenza and pneumococcal vaccination, pulmonary rehabilitation, review of inhaler technique, and assessment for long-term oxygen therapy if chronic hypoxaemia (PaO2 about 55 mmHg or less) persists — one of the few interventions, with cessation, that improves survival.
Where students slip
Asthma versus COPD is still the confusion examiners reach for first: significant reversibility, atopy and early onset favour asthma; fixed obstruction in a smoker favours COPD — and overlap exists. On therapy, three details decide questions: the post-bronchodilator 0.7 ratio (not pre), the eosinophil threshold of around 300 per microlitre that justifies adding an ICS to LABA-LAMA (ICS alone is never the answer and raises pneumonia risk), and the current GOLD grouping that pairs symptoms with exacerbation history rather than FEV1 alone. The old "pink puffer, blue bloater" phenotypes still appear as distractors — they describe emphysema-predominant and bronchitis-predominant pictures but are teaching simplifications, not distinct diseases. And a young patient with basal emphysema, especially non-smoking or with liver disease, should trigger alpha-1 antitrypsin deficiency rather than a shrug.
Frequently asked questions
How is COPD diagnosed?
By a post-bronchodilator FEV1/FVC ratio below 0.7 in a patient with risk factors; severity is graded by FEV1 per cent predicted.
What is the only intervention proven to alter the natural history of COPD?
Smoking cessation, which slows the decline in lung function; no drug has an equivalent effect.
When is an inhaled corticosteroid indicated?
When blood eosinophils are high (around 300 per microlitre or more), when exacerbations recur despite LABA-LAMA, or with asthma overlap; never as ICS alone.
Why is the oxygen target 88 to 92 per cent?
Uncontrolled high-concentration oxygen removes hypoxic drive and worsens hypercapnia; controlled oxygen prevents carbon dioxide narcosis.
When is non-invasive ventilation indicated?
For an exacerbation with respiratory acidosis (pH below 7.35, PaCO2 above 45 mmHg); it reduces intubation and mortality.
What suggests alpha-1 antitrypsin deficiency?
Early-onset, predominantly basal emphysema in a young patient, sometimes with liver disease or a family history.