Definition

Persistent respiratory symptoms with airflow obstruction that is not fully reversible, confirmed by a post-bronchodilator FEV1/FVC ratio below 0.7 in a person over 35 with a relevant exposure history.

Epidemiology

COPD is common in later adult life, mostly smoking-related, and often undiagnosed until activity is limited. Occupational dust, fumes and biomass smoke also cause it. Alpha-1 antitrypsin deficiency is a rare inherited cause of early-onset disease.

Pathophysiology

Inhaled irritants drive mucus hypersecretion, airway inflammation and small-airway fibrosis, while protease activity destroys alveolar walls. Losing elastic recoil lets airways collapse in expiration, so gas is trapped and the lungs hyperinflate. Lost alveolar-capillary surface and hypoxic pulmonary vasoconstriction produce hypoxaemia, pulmonary hypertension and cor pulmonale.

First principles

The obstruction is fixed, so treatment targets emptying, exacerbations and exposure

Bronchodilators shorten the time needed to breathe out, which relieves symptoms, but they do not rebuild destroyed alveoli. Only removing the exposure changes the rate of decline. So every review returns to smoking, inhaler technique, exercise, vaccination and the exacerbation plan.^1,2

Breathlessness tracks hyperinflation, not FEV1

Faster breathing on exertion leaves less time to breathe out. Trapped gas accumulates, the diaphragm flattens and the respiratory muscles work at a mechanical disadvantage. So NICE grades disability with the Medical Research Council (MRC) dyspnoea scale, and forbids judging bronchodilator response on lung function alone.¹

Exacerbation count, not baseline spirometry, drives escalation

NICE escalates inhaled therapy on symptoms and exacerbations, not FEV1. A severe exacerbation needing admission, or two moderate ones in a year, triggers adding an inhaled corticosteroid. Typically four or more a year opens the door to prophylactic azithromycin.¹

Uncontrolled oxygen causes carbon dioxide retention by worsening gas exchange

Most of the carbon dioxide rise on high-flow oxygen comes from deteriorating matching of blood flow to gas flow. Loss of hypoxic drive is a minor and largely outdated explanation. Hence a target of 88% to 92%, and hence hypoxaemia is still corrected rather than tolerated.^3,4

Presentation

Someone over 35 with a smoking or occupational exposure history, progressive exertional breathlessness, chronic cough or sputum, wheeze and recurrent winter chest infections. Symptoms persist between flare-ups rather than coming and going.^1,2

Cardinal features

Progressive exertional breathlessness, graded 1 to 5 on the Medical Research Council (MRC) dyspnoea scale
Chronic cough, with or without regular sputum production
Recurrent winter chest infections, wheeze, prolonged expiration and quiet breath sounds
Smoking, passive smoke, occupational dust or fumes, or biomass smoke exposure
Low BMI, muscle wasting, ankle swelling and a raised JVP in advanced disease

Red flags

Exhaustion, drowsiness, confusion or inability to complete a sentence
Respiratory acidosis: pH below 7.35 with PaCO2 above 6.5 kPa
Saturations falling despite treatment, or PaCO2 rising on a repeat gas
Peripheral oedema, raised JVP or a parasternal heave suggesting cor pulmonale
Haemoptysis, weight loss or focal signs suggesting lung cancer
Pleuritic pain or unilateral signs suggesting PE or pneumothorax

Investigations

Post-bronchodilator spirometry

Obstruction must be measured, not inferred. A pre-bronchodilator test overstates obstruction and cannot separate COPD from asthma.

Expected finding: FEV1/FVC (forced expiratory volume in 1 second divided by forced vital capacity) below 0.7 after a bronchodilator confirms obstruction. Grade on FEV1 percent predicted: stage 1 mild 80% or above with symptoms, stage 2 moderate 50% to 79%, stage 3 severe 30% to 49%, stage 4 very severe below 30%.

¹

Chest X-ray, FBC and BMI at diagnosis

NICE requires all three at diagnosis: chest X-ray to exclude other pathology, FBC for anaemia or polycythaemia, BMI for nutritional risk.

Expected finding: Hyperinflated lungs, flat diaphragms and a narrow heart shadow support the phenotype, but a normal film does not exclude COPD. A mass, consolidation or effusion changes the pathway.

¹

Symptom, exposure and exacerbation assessment

Inhaled treatment escalates on symptoms and exacerbations, not spirometry. Record pack-years, MRC grade, exacerbations and admissions this year, inhaler technique and comorbidity.

Expected finding: MRC grade 3 (walks slower than contemporaries on the flat, or stops for breath at own pace) or above triggers pulmonary rehabilitation referral.

^1,4

Pulse oximetry, and arterial blood gas when indicated

Oximetry screens, gases decide. A low stable resting saturation prompts arterial gases for long-term oxygen assessment; in an exacerbation, gases identify carbon dioxide retention.

Expected finding: pH below 7.35 with PaCO2 above 6.5 kPa is acidotic hypercapnic (type 2) failure. Persisting after optimal medical treatment, it needs non-invasive ventilation.

^4,5,1

Alpha-1 antitrypsin and specialist testing

Measure serum alpha-1 antitrypsin when onset is early, the smoking history minimal, or there is a family history. Refer anyone whose symptoms began under 40.

Expected finding: Deficiency changes counselling, family screening and specialist follow-up. Add sputum culture, CT or transfer factor for frequent infection, diagnostic doubt or surgical assessment.

^1,6

Management

Step	Detail	Source
Treat tobacco dependence at every contact	Treat every current smoker: combination nicotine replacement therapy (a long-acting patch plus a short-acting form), varenicline, cytisinicline or bupropion, each with behavioural support. Remove occupational dust and fumes too. Inhalers relieve symptoms, but only stopping the exposure changes the rate of decline.^1,7,2	NICE NG115; NICE NG209 rec 1.12.2
Vaccinate, rehabilitate and hand over a written plan	Offer annual influenza vaccination and a single dose of pneumococcal vaccine (PPV23 or PCV20), with no booster for this risk group. Refer for pulmonary rehabilitation at MRC dyspnoea grade 3 or above, and after any admission for an exacerbation. Give a personalised self-management and exacerbation action plan.^1,4,8	NICE NG115 recs 1.2.80, 1.2.81, 1.2.85, 1.2.124; Green Book ch 25
Start with a short-acting bronchodilator, then check the device	Initial treatment is a short-acting beta-2 agonist (SABA), for example salbutamol 100 to 200 micrograms inhaled as needed, or a short-acting muscarinic antagonist (SAMA) such as ipratropium. Before calling it a failure, watch them use the inhaler: poor technique looks exactly like poor response.^1,9,10	NICE NG115 recs 1.2.6, 1.2.9; Ventolin Evohaler SmPC 4.2
Choose long-acting therapy at the asthmatic-features branch point	The branch point is asthmatic features or steroid responsiveness. These are: previous secure asthma diagnosis or atopy, a higher blood eosinophil count, FEV1 variation of at least 400 mL, or diurnal peak flow variation of at least 20%. Absent, offer a long-acting muscarinic antagonist (LAMA) plus a long-acting beta-2 agonist (LABA). Present, consider LABA plus an inhaled corticosteroid (ICS).^1,11,12,13	NICE NG115 recs 1.2.10, 1.2.11
Add triple therapy on defined criteria, then keep reviewing the steroid	On LABA plus ICS with symptoms still limiting quality of life: offer LAMA plus LABA plus ICS. On LAMA plus LABA: consider adding ICS after a severe exacerbation needing admission, two moderate exacerbations in a year, or as a 3-month trial. Stop the trial if symptoms do not improve, and record why any ICS continues.^1,13	NICE NG115 recs 1.2.8, 1.2.14 to 1.2.17
Consider prophylactic azithromycin only after full optimisation	Azithromycin 250 mg three times a week, on specialist advice, for a non-smoker on optimised treatment with typically four or more exacerbations a year. Check sputum culture including mycobacteria, ECG for QT prolongation, liver function and a CT thorax before starting.^1,14	NICE NG115 recs 1.2.45 to 1.2.47
Assess for long-term oxygen therapy on two stable blood gases	A stable resting saturation of 92% or less triggers arterial blood gases on two occasions at least 3 weeks apart. Offer long-term oxygen therapy (LTOT) if PaO2 is below 7.3 kPa, or 7.3 to 8 kPa with secondary polycythaemia, peripheral oedema or pulmonary hypertension. It must be worn at least 15 hours a day.^1,4	NICE NG115 recs 1.2.56, 1.2.57, 1.2.61; QS10 statement 3
Exacerbation: bronchodilator, corticosteroid, then the antibiotic decision	Increase the short-acting bronchodilator; nebulise salbutamol 2.5 to 5 mg with ipratropium 500 micrograms if they are too breathless for a hand-held device. Give prednisolone 30 mg orally once daily for 5 days, and to everyone admitted. Add an antibiotic only after weighing severity, admission need, cultures and resistance.^1,15,16,17	NICE NG115 recs 1.3.13, 1.3.14, 1.3.16; nebuliser doses from UK SmPCs
When an antibiotic is indicated, use the NG114 first-line options	Amoxicillin 500 mg three times a day for 5 days; doxycycline 200 mg on day 1 then 100 mg once daily to complete 5 days; or clarithromycin 500 mg twice a day for 5 days. If there is no improvement in 2 to 3 days, switch to a different first-line class.^6,18,19,20	NICE NG114 antibiotic table, adults 18 and over
Control the oxygen, then re-target it on the blood gas	Before the gas is back, target 88% to 92% using a 24% Venturi mask at 2 to 4 litres/minute in hospital. Drive the nebuliser with compressed air if they are hypercapnic or acidotic, with oxygen by nasal cannulae alongside. Recheck at 30 to 60 minutes: a normal PaCO2 moves the target to 94% to 98%.^3,4,1	BTS oxygen guideline 2017; QS10 statement 6; NICE NG115 rec 1.3.11
Start non-invasive ventilation for persistent respiratory acidosis	Start non-invasive ventilation (NIV) when pH is below 7.35 with PaCO2 above 6.5 kPa despite optimal medical treatment. BTS standards ask for it within 60 minutes of that gas and within 120 minutes of arrival, in a designated NIV area. Keep saturations 88% to 92% and agree a ceiling of care.^5,4,1,21	BTS/ICS 2016 recs 4, 23, 25; QS10 statement 7; BTS acute NIV standards
Discharge on a care bundle, then review at least annually	Discharge on a care bundle: inhaler technique, tobacco treatment, vaccination, rehabilitation referral, oxygen need, self-management plan and follow-up. Hospital-at-home and assisted discharge are safe alternatives to admission. Review at least yearly, and twice yearly in very severe COPD.^4,1,2	NICE QS10 statement 8; NG115 recs 1.3.4, 1.2.138, 1.2.140
Safety, allergy and monitoring for this chapter	Penicillin allergy: use doxycycline or clarithromycin. Doxycycline is avoided in pregnancy; clarithromycin prolongs the QT interval and interacts widely. Cytisinicline, varenicline and bupropion are not for under-18s, and cytisinicline not for those aged 66 and over. Follow the local antimicrobial policy.^6,7,1,20,19	NICE NG114; NG209 recs 1.12.4, 1.12.5; NG115 rec 1.2.58

Illustrations

Small-airway disease and emphysemaNormal airways and alveoli contrasted with mucus-filled small airways, thickened airway walls and emphysematous destruction of alveolar walls.PassFinals · original

Chest X-ray of hyperinflationChest radiograph showing hyperinflated lung fields, flattened diaphragms and a narrow cardiac silhouette.James Heilman, MD, Wikimedia Commons · CC-BY-SA-3.0

Spirometry and air trappingFlow-volume loop showing the concave expiratory curve of fixed airflow obstruction, with dynamic hyperinflation on exertion.PassFinals · original

Differentials

Asthma

Variable symptoms, atopy and reversible obstruction; the two can coexist.

Bronchiectasis

Daily copious purulent sputum, recurrent infection or haemoptysis, with dilated airways on CT.

Heart failure

Orthopnoea, paroxysmal nocturnal dyspnoea, oedema, raised JVP and a raised natriuretic peptide.

Lung cancer

Haemoptysis, weight loss, or a focal or non-resolving abnormality on imaging.

Pulmonary embolism or pneumothorax

Sudden or disproportionate deterioration, pleuritic pain or unilateral findings.

Complications

Recurrent exacerbations and hospitalisation
Type 1 or type 2 respiratory failure
Pulmonary hypertension and cor pulmonale
Pneumothorax from bullous disease
Secondary polycythaemia, low BMI, muscle wasting and functional disability
Anxiety and depression
Lung cancer and other smoking-related disease

Prognosis

Stopping smoking slows the rate of decline. Frequent exacerbations, admissions, hypercapnia, low BMI, frailty and comorbidity all worsen outcomes. NICE advises against using a multidimensional index such as BODE to estimate prognosis in stable COPD.

Guidelines

Chronic obstructive pulmonary disease in over 16s: diagnosis and management (NG115) (NICE, 2018)
COPD acute exacerbation: antimicrobial prescribing (NG114) (NICE, 2018)
COPD in adults, quality standard (QS10) (NICE, 2023)
Oxygen use in adults in healthcare and emergency settings (British Thoracic Society, 2017)
Ventilatory management of acute hypercapnic respiratory failure in adults (British Thoracic Society and Intensive Care Society, 2016)

Chronic Obstructive Pulmonary Disease