Chronic obstructive pulmonary disease is heavily examined across both its chronic management and its acute exacerbations, and it carries a memorable trap — the oxygen target. This guide covers COPD as examiners frame them, to the current NICE standard (NG115). Follow current guidance and local protocols in practice; this reflects guidance as of mid-2026.
What COPD is
COPD is a chronic, progressive airflow obstruction that is not fully reversible, caused predominantly by smoking, with airway inflammation, mucus hypersecretion and parenchymal destruction (emphysema). It presents with chronic breathlessness, cough and sputum, and a history of significant smoking or other exposure. Unlike asthma, the obstruction is largely fixed, and the diagnosis is made objectively. Long-standing COPD can lead to recurrent exacerbations, chronic respiratory failure, cor pulmonale (right heart failure from chronic lung disease), polycythaemia and weight loss. Examiners may contrast it with asthma: COPD typically presents later in life in a smoker, with persistent rather than variable symptoms and little diurnal variation, whereas asthma is more variable, often allergic, and more reversible.
Diagnosis
Diagnosis requires post-bronchodilator spirometry showing airflow obstruction — an FEV1/FVC ratio below 0.7 — in a person over 35 with risk factors and symptoms. The severity of obstruction is graded by the FEV1 as a percentage of predicted. As a rough guide, an FEV1 of 50 to 79% predicted is moderate, 30 to 49% severe, and below 30% very severe airflow obstruction. A blood eosinophil count, a history of asthma or atopy, and variability in lung function help identify "asthmatic features" that influence treatment. Spirometry should not be the sole basis for assessing severity or response — symptoms, exacerbation frequency and exercise capacity matter too, and additional tests such as a chest X-ray, a full blood count and body mass index help build the picture.
Chronic management
Treatment is stepwise and built on non-pharmacological foundations:
- Foundations: smoking cessation is the single most important intervention and the one measure that alters the disease course; add pulmonary rehabilitation, annual influenza and pneumococcal vaccination, and self-management support. Vaccination and pulmonary rehabilitation both reduce exacerbations and admissions, and pulmonary rehabilitation also improves exercise capacity and quality of life.
- Initial inhaled therapy: a short-acting bronchodilator — a SABA or SAMA — as needed for breathlessness.
- Dual therapy: for ongoing symptoms or exacerbations, a long-acting bronchodilator combination — LABA plus LAMA — for those without asthmatic features, or LABA plus inhaled corticosteroid (ICS) where there are asthmatic features or features suggesting steroid responsiveness.
- Triple therapy: LABA plus LAMA plus ICS for those who remain symptomatic, have a severe exacerbation needing hospitalisation, or have two or more moderate exacerbations in a year.
- Long-term oxygen therapy is assessed for patients with chronic hypoxaemia, and is of benefit only in those who have stopped smoking. Inhaler technique and adherence should be checked at every step, as poor technique is a common reason for apparent treatment failure, and the device chosen is guided by what the patient can use effectively.
Acute exacerbation
An exacerbation is a sustained, acute worsening of symptoms beyond normal variation — more breathlessness, cough, and increased sputum volume or purulence. Common triggers are respiratory infections, both viral and bacterial. The high-yield management points are:
- Controlled oxygen: this is the classic trap. Aim for oxygen saturations of 88 to 92%, not the usual 94 to 98%, using a Venturi mask (such as 24 or 28%), because some patients with COPD retain carbon dioxide and uncontrolled oxygen can worsen this. Titrate to an arterial blood gas.
- Bronchodilators: increase the dose and frequency, usually nebulised salbutamol and ipratropium.
- Steroids: oral prednisolone 30 mg for 5 days.
- Antibiotics: only if there are clinical features of infection, such as more purulent sputum.
- Non-invasive ventilation: for persistent type 2 respiratory failure with a respiratory acidosis (a raised carbon dioxide with a low pH, typically 7.25 to 7.35) despite initial medical treatment. Where non-invasive ventilation fails or is inappropriate, escalation to invasive ventilation is considered according to the patient's wishes and overall prognosis, and a clear ceiling-of-care decision should be documented early.
High-yield exam points and traps
- The oxygen target in COPD is 88 to 92% — controlled oxygen via a Venturi mask, not high-flow.
- Non-invasive ventilation is for type 2 respiratory failure with respiratory acidosis after initial treatment.
- Smoking cessation is the single intervention that changes the disease course.
- Diagnosis is objective: post-bronchodilator FEV1/FVC below 0.7, and spirometry should be performed when the patient is stable, not during an exacerbation.
- A normal or rising carbon dioxide with a falling pH signals decompensated type 2 respiratory failure.
- An arterial blood gas is essential in an exacerbation to assess for carbon dioxide retention and acidosis.
- Always look for and treat the trigger — most often a viral or bacterial infection, but consider pneumothorax, pulmonary embolism and heart failure. Non-adherence and cold weather are common precipitants too.
A few common questions
What is the oxygen target in a COPD exacerbation? Saturations of 88 to 92% using controlled oxygen via a Venturi mask, titrated to an arterial blood gas — lower than the usual 94 to 98% because of the risk of carbon dioxide retention.
When is non-invasive ventilation used in COPD? For persistent type 2 respiratory failure with a respiratory acidosis (a raised carbon dioxide and a low pH) despite initial medical treatment.
How is COPD diagnosed? With post-bronchodilator spirometry showing an FEV1/FVC ratio below 0.7 in a person over 35 with risk factors and symptoms.
What is the treatment of an acute exacerbation? Controlled oxygen, increased nebulised bronchodilators, oral prednisolone for 5 days, antibiotics if there are signs of infection, and non-invasive ventilation for respiratory acidosis, alongside treating the underlying trigger.
What is the most important long-term intervention? Smoking cessation — the one intervention shown to alter the natural course of COPD; pulmonary rehabilitation and vaccination add further benefit.
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