Chronic Obstructive Pulmonary Disease (COPD)

• Establish progressive exertional breathlessness – when it began, how far they can walk, and whether it is worsening?

• Document smoking status and calculate pack-years (number smoked per day ÷ 20 × years smoked)?

• Confirm a chronic cough with regular sputum – daily pattern, volume and colour?

• Ask about occupational exposure to dusts, fumes, vapours or biomass smoke?

• Ask about wheeze, chest tightness or frequent winter chest infections?

• Explore personal or family history of asthma, atopy or alpha-1 antitrypsin deficiency?

• Quantify functional limitation using the MRC dyspnoea scale (see below)?

• Screen for features suggesting steroid responsiveness – night waking with wheeze, marked day-to-day variability?

• Ask about previous exacerbations, courses of steroids or antibiotics, and hospital admissions?

• Ask about red-flag symptoms – haemoptysis, weight loss, anorexia or chest pain?

• Assess impact on sleep, mood, work and daily activities, screening for anxiety and depression?

• Note any ankle swelling, fatigue or unintentional weight loss suggesting cor pulmonale or alternative pathology?

➤ "Explore the patient's understanding of the link between smoking and their breathing, and any worries or barriers about stopping?"

➤ "Ask how breathlessness affects their independence, work and confidence, and what matters most to them?"

➤ Haemoptysis → exclude lung cancer or bronchiectasis → urgent chest X-ray / 2-week-wait pathway

➤ Significant unexplained weight loss or anorexia → investigate for malignancy

➤ Unexplained chest pain → consider cardiac, pulmonary embolism or malignant cause

➤ Finger clubbing → not a feature of COPD → suspect lung cancer, fibrosis or bronchiectasis

➤ New or worsening central cyanosis, acute confusion or drowsiness → severe exacerbation / respiratory failure → emergency admission

➤ Symptoms disproportionate to lung function, or rapid FEV1 decline → reconsider the diagnosis and refer

• Hyperinflation (barrel chest), pursed-lip breathing and use of accessory muscles of respiration.

• Auscultation – quiet breath sounds, expiratory wheeze and a prolonged expiratory phase; coarse crackles suggest infection or bronchiectasis.

• Signs of cor pulmonale in advanced disease – raised JVP, peripheral oedema, loud P2, parasternal heave.

• Central cyanosis, cachexia / muscle wasting and tar staining of the fingers.

• Measure respiratory rate, SpO2 on air, blood pressure and temperature; remember that finger clubbing is not a feature of COPD and should prompt a search for another cause.

⚠️ Common pitfall

Labelling every breathless smoker as COPD. A normal-looking chest does not confirm it, and a single low FEV1/FVC ratio in an asymptomatic older person may simply reflect ageing. Always confirm with post-bronchodilator spirometry, and actively look for asthmatic features (atopy, eosinophilia, FEV1 variability, diurnal peak-flow change) – that distinction decides whether an inhaled corticosteroid belongs in the regimen, and whether you are missing treatable asthma or heart failure.

COPD is a long-term lung condition, usually caused by smoking, that makes breathing gradually harder over the years.
We can't undo the damage already done, but inhalers, vaccinations and exercise-based rehab can ease your breathlessness and cut down flare-ups.
The single most powerful thing you can do is stop smoking – and we'll give you all the help you need to do it.

🧠 Clinical pearl

The blood eosinophil count is the closest thing to a biomarker for treatment choice. A higher count (commonly ≥ 300 cells/microlitre) predicts benefit from an inhaled corticosteroid and supports adding one; a low count (< 100 cells/microlitre) predicts little benefit and tilts the balance against ICS, given its real pneumonia risk. The same ≥ 300 threshold now also defines eligibility for the biologic dupilumab in uncontrolled disease – so one eosinophil count guides both the steroid inhaler and the newest add-on. Check eosinophils before escalating, and document the reason whenever you prescribe an ICS.

• Confirm the diagnosis with post-bronchodilator spirometry before committing to lifelong treatment.

• Hospital admission for a severe exacerbation – marked breathlessness, acute confusion, new cyanosis, SpO2 below 90%, rapid onset or inability to cope at home.

• Treat tobacco dependence at every contact – the one intervention that slows decline and reduces mortality.

• Onset of cor pulmonale → optimise COPD treatment, treat oedema with a diuretic and assess for long-term oxygen.

• Offer annual influenza, a one-off pneumococcal (PPV23) and seasonal COVID-19 vaccination.

• Assess for long-term oxygen therapy if SpO2 is 92% or less on air, FEV1 below 30%, or there is cyanosis, polycythaemia, oedema or raised JVP – confirm with arterial blood gases on two occasions and only in a non-smoker.

• Refer to pulmonary rehabilitation if functionally limited (MRC grade 3 and above) or after a hospitalised exacerbation.

• Refer for palliative / supportive care in advanced disease for refractory breathlessness (low-dose opioids) and advance care planning.

• Co-produce a written self-management and exacerbation action plan; supply a rescue pack (steroids ± antibiotics) only if they have exacerbated in the last year and can use it appropriately.

• Review at least annually (twice yearly if very severe), checking symptoms, exacerbations, inhaler technique, BMI, smoking status and mood.

🔑 Key principle – only two things change survival

Inhalers, rehabilitation and vaccines improve symptoms, quality of life and exacerbation frequency, but the only interventions proven to prolong life in COPD are smoking cessation (at any stage) and long-term oxygen therapy in those with chronic hypoxaemia. So treat tobacco dependence relentlessly, identify the hypoxaemic for oxygen assessment, and be honest that the rest is about living better, not necessarily longer.

➤ Step 1 – Initial empirical treatment (breathlessness and exercise limitation)

→ A short-acting bronchodilator as required – SABA (salbutamol) or SAMA (ipratropium).

➤ Step 2 – Add long-acting therapy if still breathless or exacerbating despite a short-acting bronchodilator, treatment for tobacco dependence, optimised non-pharmacological care and vaccinations.

➤ The choice turns on one question: are there asthmatic features / features suggesting steroid responsiveness?

→ No asthmatic features → LABA + LAMA (e.g. umeclidinium/vilanterol – Anoro Ellipta; tiotropium/olodaterol – Spiolto Respimat; indacaterol/glycopyrronium – Ultibro Breezhaler).

→ Asthmatic features (previous secure asthma or atopy, higher blood eosinophils, FEV1 variation of at least 400 mL, or diurnal peak-flow variation of at least 20%) → LABA + ICS (e.g. beclometasone/formoterol – Fostair; budesonide/formoterol – Symbicort; fluticasone furoate/vilanterol – Relvar Ellipta).

➤ Step 3 – Escalate to triple therapy (LABA + LAMA + ICS)

→ If on LABA + ICS: offer triple therapy if day-to-day symptoms still impair quality of life, or there is one severe (hospitalised) or two moderate exacerbations in a year.

→ If on LABA + LAMA: consider triple therapy after one severe or two moderate exacerbations in a year; for persistent symptoms impairing quality of life, trial triple therapy for 3 months only and stop if there is no benefit. Examples: fluticasone furoate/umeclidinium/vilanterol – Trelegy Ellipta; beclometasone/formoterol/glycopyrronium – Trimbow.

➤ Inhaled corticosteroids – cautions

→ ICS increase the risk of pneumonia; document the indication, review at least annually, and consider de-escalation if eosinophils are low and there are no exacerbations. Follow MHRA advice on psychological and behavioural side effects of inhaled corticosteroids.

➤ Specialist-only add-ons for frequent exacerbations despite optimised triple therapy

→ Azithromycin prophylaxis (usually 250 mg three times a week) – only in non-smokers with optimised therapy who still have frequent (typically 4 or more per year), prolonged or hospitalised exacerbations; first exclude bronchiectasis (CT thorax), check sputum culture (including TB), and obtain a baseline ECG (QT interval) and LFTs. Off-label; warn about hearing loss and tinnitus.

→ Roflumilast – for severe COPD (FEV1 below 50%) with chronic bronchitis and two or more exacerbations a year despite triple therapy; started by a respiratory specialist.

→ Dupilumab (Dupixent) – the first biologic licensed for COPD (NICE TA1142, 2026) and a specialist-initiated add-on for the eosinophilic phenotype. Recommended for uncontrolled COPD with raised blood eosinophils (≥ 300 cells/microlitre, i.e. 0.3 × 10⁹/L) in adults already on triple therapy (ICS + LABA + LAMA), or on LABA + LAMA if an ICS is not appropriate. ‘Uncontrolled’ means one or more severe or two or more moderate exacerbations in the past year. It blocks the shared IL-4 / IL-13 receptor and is given as 300 mg subcutaneously every 2 weeks; review at 12 months and stop if exacerbations have not improved.

→ Theophylline – only after trials of short- and long-acting bronchodilators, or if inhalers cannot be used; monitor plasma levels and reduce the dose with macrolides or fluoroquinolones.

→ Mucolytic (carbocisteine) – for a chronic productive cough; continue only if symptoms improve.

• Able to cope at home, with good general condition and mobility.

• Unable to cope at home; poor or deteriorating condition; confined to bed.

• Mild breathlessness, no new cyanosis, normal conscious level.

• Severe breathlessness, new cyanosis, acute confusion or impaired consciousness.

• SpO2 maintained; no worsening oedema; not on long-term oxygen.

• SpO2 below 90%; worsening peripheral oedema; already on long-term oxygen.

• Good social support; gradual onset; no major comorbidity.

• Lives alone / poor support; rapid onset; significant comorbidity (especially cardiac disease or insulin-treated diabetes).

➤ Bronchodilator

→ Increase the dose and frequency of the short-acting bronchodilator (SABA ± SAMA) using a spacer – or a nebuliser if severe. If the person is hypercapnic or acidotic, drive the nebuliser with air, not oxygen.

➤ Oral corticosteroid

→ Prednisolone 30 mg once daily for 5 days if increased breathlessness interferes with daily activities; consider osteoporosis prophylaxis with frequent courses.

➤ Antibiotic – only if indicated

→ Add an antibiotic only if sputum becomes purulent AND increases in volume or thickness, or there is consolidation / pneumonia – not for breathlessness alone with clear sputum. First-line: amoxicillin 500 mg three times a day for 5 days, OR doxycycline 200 mg on day 1 then 100 mg once a day (5-day course), OR clarithromycin 500 mg twice a day for 5 days. Sputum culture is not routine in primary care.

➤ Oxygen (only if hypoxaemic)

→ Give controlled oxygen to a target SpO2 of 88–92% in those at risk of hypercapnia, and avoid over-oxygenation. Oxygen treats hypoxaemia, not breathlessness.

➤ When this is not enough

→ Persistent hypercapnic ventilatory failure despite optimal therapy → NIV (in hospital); admit per the criteria above.

• Treatment chosen by symptoms and asthmatic features – not by FEV1 or formal groups.

• Treatment chosen by the ABE group (symptom burden + exacerbation history).

• SABA/SAMA → LABA + LAMA, or LABA + ICS if asthmatic features.

• By group: A = one bronchodilator; B = LABA + LAMA; E = LABA + LAMA (± ICS).

• ICS decided by “asthmatic features” – includes a higher eosinophil count but sets no numeric threshold.

• ICS decided by blood eosinophils: ≥ 300 favours ICS; < 100 little benefit (pneumonia risk).

• Escalate to triple after 1 severe or 2 moderate exacerbations, or QoL-limiting symptoms.

• Escalate to triple in exacerbators on LABA + LAMA, especially if eosinophils are raised.

• LABA + ICS retained as a recognised option.

• LABA + ICS no longer preferred (favours LABA + LAMA or triple).

📌 DVLA – fitness to drive (asthma and COPD)

• Group 1 (car / motorcycle): may continue to drive and need not notify the DVLA unless complications are associated with cough syncope, disabling dizziness, fainting or loss of consciousness – in which case the ‘transient loss of consciousness’ rules apply.

• Group 2 (bus / lorry): the same standard applies – may drive and need not notify the DVLA unless those same complications occur.

• COPD in itself is not a notifiable condition; it is the syncopal / consciousness complications (and, separately, any coexisting obstructive sleep apnoea causing excessive sleepiness) that trigger notification and a driving review.

• Severe exacerbation – marked breathlessness, acute confusion, impaired consciousness, new cyanosis, SpO2 below 90% or unable to cope → emergency admission

• Haemoptysis or a chest X-ray suspicious for malignancy → lung cancer pathway

• Diagnostic uncertainty (asthma, bronchiectasis or cardiac cause) → respiratory referral

• New cor pulmonale or rapidly deteriorating symptoms → urgent assessment

• Suspected alpha-1 antitrypsin deficiency (early onset / family history) → specialist centre

• Frequent exacerbations (2 or more a year) despite optimal therapy, or assessment for LTOT, nebulisers, roflumilast, azithromycin or lung volume reduction

🧭 AKT – high-yield facts

• Diagnosis is a post-bronchodilator FEV1/FVC below 0.7 in someone over 35 with a risk factor and symptoms; mild airflow obstruction only counts as COPD if symptomatic.

• Severity by FEV1 % predicted: stage 1 ≥ 80% · stage 2 50–79% · stage 3 30–49% · stage 4 < 30%.

• The inhaled fork: no asthmatic features → LABA + LAMA; asthmatic features (previous asthma/atopy, eosinophilia, FEV1 variation ≥ 400 mL, diurnal peak-flow variation ≥ 20%) → LABA + ICS.

• Exacerbation: prednisolone 30 mg once daily for 5 days; first-line antibiotics (only if purulent + increased sputum) are amoxicillin, doxycycline or clarithromycin.

• Azithromycin prophylaxis is for non-smokers with frequent exacerbations after excluding bronchiectasis, with baseline ECG and LFTs; roflumilast (specialist) needs FEV1 < 50%, chronic bronchitis and ≥ 2 exacerbations despite triple therapy.

• Dupilumab (NICE TA1142) is the first biologic for COPD – a specialist add-on for uncontrolled disease with eosinophils ≥ 300 cells/microlitre on triple (or LABA + LAMA) therapy; 300 mg subcutaneously every 2 weeks, reviewed at 12 months.

• Only smoking cessation and long-term oxygen therapy (in chronic hypoxaemia) improve survival; finger clubbing is not a feature of COPD.

🎯 SCA

A 74-year-old man with very severe COPD (FEV1 26% predicted) and three hospital admissions this year attends with his daughter. He is breathless dressing, frightened by the sensation of “fighting for air”, and asks directly, “Is this what's going to kill me?” His daughter wants “everything done”; he quietly says he never wants to be on a ventilator again. The challenge is to answer an honest question about a life-limiting illness truthfully without removing hope, while opening advance care planning and reconciling differing wishes within the family.

A strong consultation explores his ideas, concerns and expectations and what matters most to him; gives honest, paced information about prognosis and the limits of treatment without false reassurance; explains symptom relief for refractory breathlessness (low-dose opioids, a handheld fan) so that “nothing more for the lungs” never means “nothing more for you”; agrees a shared plan covering ceilings of care, preferred place of care and a rescue plan; and safety-nets clearly – all with empathy and respect for his autonomy and his daughter's distress.