Chronic bronchitis, pulmonary emphysema, chronic obstructive pulmonary disease

Chronic bronchitis, pulmonary emphysema, chronic obstructive pulmonary disease

Airflow limitation that does not fully reverse, from damaged small airways and lung tissue, usually caused by smoking; how it is staged, treated and followed.

COPD, from smoke to an over-inflated chest

6 scenes, 0:55

A film in six scenes on a white page. The lungs, seen from the front, are pale pink and see-through, with the branching airways inside them; with each breath, grey smoke is drawn down the windpipe and out along the airways, and settles in the small ones at the ends of the tree. A bronchus is cut open along its length: its wall shows in layers, its lining is a carpet of amber cilia beating in waves under a thin violet layer of mucus that carries specks of smoke along; then violet goblet cells multiply, the mucus thickens into lumps, the cilia beat more weakly and many are lost, and the smoke stays caught. A cluster of alveoli, cut open like a sponge, holds pale blue white blood cells: neutrophils, their nuclei in lobes, and macrophages with dark soot inside; green specks of elastase drift from the neutrophils and settle on the alveolar walls, while a few larger pale green specks of α1-antitrypsin catch some of them. In the same cluster, a respiratory bronchiole comes in from the upper left, alveoli budding from its wall; the walls round it open, holes widening until several small alveoli become one large space with torn edges, while the alveoli further out stay whole. Two cores of lung, cut open down the small airway through each, breathe in and out: in the healthy one on the left, alveolar walls attached all round the airway hold it open as the breath goes out and the lung shrinks; in the one with COPD on the right, the walls round the airway are gone and its wall is thick, and as the breath goes out it closes in the middle and the lung barely shrinks. Last, the lungs from the front again, with the heart between them and the diaphragm below: the lungs grow larger and longer, and the diaphragm's domes sink and flatten.

0:00 / 0:55

Smoke in the airways

Scenes

About this film

Smoke inflames the airways and the lungs. In the airways, goblet cells multiply and the cilia fail, so mucus builds up. In the alveoli, neutrophils release elastase faster than α1-antitrypsin can block it, and the alveolar walls break down. With fewer walls holding the small airways open, they close early as the patient breathes out, air is trapped, and the lungs over-inflate.

Simplified: Not to scale: cells, enzymes, cilia and alveoli are drawn at sizes that read, and years of disease pass in seconds. The bronchial tree has far fewer divisions than the twenty-odd of a real one, and the lungs have no lobes or fissures. Smoke is drawn as dark particles only; its gases are not shown. The bronchus wall is simplified to a few layers, its glands left out; goblet cells are drawn as beads on the surface, and the squamous cells smoke can turn the lining into are not shown. Lymphocytes, which are also part of the inflammation, are left out. Elastase stands for all the proteases white cells release; each speck stands for many molecules. The elastin fibres in the alveolar walls, which elastase digests, are not drawn. α1-antitrypsin reaches the alveoli from the blood; the capillaries that bring it are not drawn. Air trapping is shown in one airway each, though in a real lung it is patchy; the loss of attachments is exaggerated, and the lost elastic recoil, which drives air out, is not drawn. The chest wall and ribs are left out, and the heart is a simple shape.

3 sources
  1. Kumar and Clark's Clinical Medicine, 10th edition. Elsevier, 2021. Chapter 28, Respiratory disease: the airways (p. 930), and chronic obstructive pulmonary disease (pp. 955–957).
  2. Leopold PL et al. Smoking is associated with shortened airway cilia. PLoS One. 2009;4(12):e8157.
  3. Saetta M et al. Loss of alveolar attachments in smokers: a morphometric correlate of lung function impairment. Am Rev Respir Dis. 1985;132(4):894-900.
Contents6 sections

At a glance

  1. COPD is persistent, usually progressive airflow limitation from damage to the small airways (chronic bronchitis and bronchiolitis) and to the alveoli (emphysema). Smoking causes most of it.
  2. Spirometry makes the diagnosis: a post-bronchodilator FEV1/FVC below 0.70 in a patient with symptoms and a risk factor. The FEV1 grades its severity, as GOLD grades 1 to 4.
  3. Stopping smoking has by far the largest effect on the loss of lung function, and drugs add at most a little; rehabilitation, vaccines and inhalers improve how patients feel, and vaccines and inhalers cut exacerbations.
  4. Treatment follows symptoms and exacerbations: one long-acting bronchodilator, then LABA with LAMA, with an inhaled corticosteroid added when exacerbations continue and blood eosinophils are 100 cells/µL or more.
  5. In an exacerbation, give controlled oxygen to a saturation of 88 to 92 per cent and consider non-invasive ventilation if the pH falls below 7.35 with a raised PaCO2.
  6. The disease is the third leading cause of death worldwide and, once severe, runs a course of recurrent exacerbations, respiratory failure and cor pulmonale.

Definition and overview

Chronic obstructive pulmonary disease (COPD) is a heterogeneous lung condition with chronic respiratory symptoms (breathlessness, cough, sputum, exacerbations) caused by abnormalities of the airways (bronchitis, bronchiolitis) and the alveoli (emphysema) that cause persistent, often progressive airflow obstruction. It is an umbrella for three conditions that overlap:

ComponentWhat it isDefined by
Chronic bronchitisinflamed airways with excess mucusa clinical definition: a productive cough on most days for three months in two successive years
Small airways diseasenarrowing and scarring of airways under 2 mm acrossthe main site of obstruction, seen on CT and physiology
Emphysemapermanent enlargement of the air spaces beyond the terminal bronchioles, with destruction of their wallsan anatomical definition: seen at autopsy or on CT

Asthma that never fully clears and COPD can overlap, and the diagnosis depends on the history: age at onset, smoking, variability of symptoms and the response to treatment.

Etiology and pathophysiology

Causes and risk factors

  • Cigarette smoking accounts for over 70 per cent of cases in high-income countries and 30 to 40 per cent in low- and middle-income countries, but only a minority of smokers, perhaps one in five, develop COPD, so there is a susceptibility that differs between people.
  • Indoor and outdoor air pollution, above all smoke from biomass fuels burnt for cooking and heating in poorly ventilated homes, which matters most in developing countries.
  • Occupational dusts and fumes, such as coal, silica and cadmium.
  • α1-antitrypsin deficiency, a hereditary cause: the ZZ genotype gives early emphysema in the lower lobes, often in a non-smoker or a young smoker, and may also cause liver disease. It explains only about 1 to 2 per cent of cases, but is worth testing for in anyone with COPD, once.
  • Early life: preterm birth, childhood infections and asthma leave smaller or poorly grown lungs that start adult life with less reserve.

From smoke to airflow limitation

Smoke inflames the airways and alveoli with neutrophils, macrophages and CD8+ T lymphocytes, and adds oxidative stress. Three changes follow:

A small airway, healthy and in COPD
Two round fields of lung seen through a magnifier, side by side. In each, a small airway, a bronchiole, is cut across in the middle, surrounded by alveoli, the white air spaces between thin pink alveolar walls that carry small red capillaries. On the left, the healthy airway: a round open lumen, lined by a ring of columnar peach-coloured cells with amber cilia that beat, two violet goblet cells among them, a thin pale wall, a thin ring of rose smooth muscle, and alveolar walls attached to it all round. On the right, the airway in COPD: its lumen narrowed and folded and partly filled by a violet plug of mucus, many goblet cells in its lining and fewer cilia, a thicker wall with pale blue white blood cells and green scar fibres in it, and the alveoli round it broken into larger spaces with stubs of torn walls, so fewer walls tether the airway. Two soot-laden macrophages lie in the enlarged spaces.

Point at a name or a part to light it.

Small airways, under 2 mm across, are a major site of the obstruction in COPD. Smoke inflames them: goblet cells multiply and mucus plugs the lumen, white cells and scar thicken the wall, and the alveolar walls round them break down, so fewer remain to hold the airway open when the patient breathes out.

Simplified: not to scale: the airway's wall, the healthy one especially, drawn thicker than life so its layers read; far fewer alveoli, cells and capillaries than a real field holds, and every capillary drawn cut across; the lining drawn as one ring of columnar ciliated cells; the club cells and basal cells left out, and the alveolar walls drawn without their type I and type II cells; a few cilia on each cell instead of about 200; COPD's changes, which are patchy, all drawn in one field and in one airway; the three kinds of white cell drawn as small, simple cells, and lymphoid follicles left out; the branch of the pulmonary artery that runs beside every bronchiole, the thin mucus layer of the healthy airway, and the squamous cells smoke can turn the lining into, left out; the cilia's beat played far slower than life.

5 sources
  1. Kumar and Clark's Clinical Medicine, 10th edition. Elsevier, 2021. Chapter 28, Respiratory disease: the airways and alveoli (pp. 930–931), and chronic obstructive pulmonary disease (pp. 955–956).
  2. Hogg JC et al. The nature of small-airway obstruction in chronic obstructive pulmonary disease. N Engl J Med. 2004;350(26):2645-53.
  3. Leopold PL et al. Smoking is associated with shortened airway cilia. PLoS One. 2009;4(12):e8157.
  4. Ochs M et al. The number of alveoli in the human lung. Am J Respir Crit Care Med. 2004;169(1):120-4.
  5. Saetta M et al. Loss of alveolar attachments in smokers: a morphometric correlate of lung function impairment. Am Rev Respir Dis. 1985;132(4):894-900.
  1. 1

    Airways narrow

    Mucous glands and goblet cells grow, giving the cough and sputum of chronic bronchitis. The small airways are scarred and their lumens plugged with mucus, which is where most of the resistance to flow arises.
  2. 2

    Alveoli are destroyed

    Neutrophils release proteases such as elastase faster than antiproteases, chiefly α1-antitrypsin, can hold them in check. The alveolar walls break down: centriacinar emphysema around the respiratory bronchioles, which is the common form, or panacinar emphysema throughout the acinus, as in α1-antitrypsin deficiency.
  3. 3

    Recoil is lost

    The lost alveolar walls no longer pull the small airways open, so they collapse early on breathing out. Air is trapped, and the lungs and chest become hyperinflated.
Where emphysema destroys the acinus
Three acini side by side, each drawn as a small pink tree seen from outside: a terminal bronchiole at the top divides into two respiratory bronchioles with a few alveoli budding from their walls, each of those into two alveolar ducts lined with alveoli, and each duct ends in an alveolar sac, a cluster of round alveoli like grapes. On the left a normal acinus. In the middle centriacinar emphysema: the respiratory bronchioles at the centre are replaced by two large pale hollow spaces with stubs of torn wall at their edges, while the ducts and sacs below look normal. On the right panacinar emphysema: the whole acinus is a little larger and every level of it is enlarged evenly, each respiratory bronchiole, each duct and each sac now one pale hollow space of about the same size with stubs of torn wall, so ducts and alveoli can no longer be told apart.

Point at a name or a part to light it.

Emphysema is a permanent enlargement of the air spaces beyond the terminal bronchiole, with destruction of their walls. In centriacinar emphysema, the common kind in smokers and worst in the upper lobes, the damage centres on the respiratory bronchioles and spares the sacs beyond. In panacinar emphysema, the type associated with α1-antitrypsin deficiency and worst in the lower lobes, the whole acinus is enlarged evenly.

Simplified: not to scale, and the airways drawn as plain pink tubes; two of each branch and a handful of alveoli, where a respiratory bronchiole supplies about 200; the acinus drawn from outside, as if it stood alone, though acini lie packed together; the spaces drawn as smooth bubbles, though a centriacinar lesion is a cluster of small dilated spaces; paraseptal emphysema, under the pleura, and irregular emphysema, round scars, left out.

2 sources
  1. Kumar and Clark's Clinical Medicine, 10th edition. Elsevier, 2021. Chapter 28, Respiratory disease: the airways (p. 930) and emphysema (pp. 955–956).
  2. Takahashi M et al. Imaging of pulmonary emphysema: a pictorial review. Int J Chron Obstruct Pulmon Dis. 2008;3(2):193-204.

Hyperinflation flattens the diaphragm so that it works at a disadvantage, and on exertion the breathing rate rises before the lungs have emptied, so the trapping gets worse (dynamic hyperinflation). That is the source of the breathlessness. Poor ventilation of damaged regions mismatches ventilation and perfusion and lowers the PaO2, and as the disease advances, the CO2 is retained too. Chronic hypoxia constricts and remodels the pulmonary arteries, causing pulmonary hypertension and, eventually, right heart failure (cor pulmonale).

Fletcher and Peto's classic study of working men showed that the FEV1 falls faster in susceptible smokers, by about 50 mL a year against about 20 mL a year in healthy people, and that a smoker who stops follows the slower curve again, even if the lost function does not return.

COPD is also a systemic disease: weight and muscle loss, osteoporosis, depression, anaemia, and a high rate of ischaemic heart disease, heart failure and lung cancer share its causes and its inflammation.

Clinical features

The usual story is a smoker over 40 with a long cough and sputum, who is breathless on exertion and has frequent winter "chest infections". The breathlessness is graded with the mMRC dyspnoea scale, and the impact of the disease with the Chronic Airways Assessment Test (CAAT), formerly the COPD Assessment Test (CAT).

Signs are few until late. In moderate and severe disease the patient is breathless, breathes out slowly through pursed lips, uses the accessory muscles and may draw in the intercostal spaces. The chest is hyperinflated: the distance from the cricoid to the sternal notch is shortened, expansion is poor, the cardiac and liver dullness are lost, and breath sounds are quiet, with a prolonged expiratory wheeze.

Later signs are those of its complications:

  • Hypercapnia shows as a flapping tremor, a bounding pulse, warm hands and drowsiness.
  • Cor pulmonale shows as ankle oedema, a raised jugular venous pressure, and a loud pulmonary second heart sound.
  • Secondary polycythaemia and central cyanosis, from chronic hypoxaemia.
  • Weight loss and muscle wasting mark advanced disease.

An exacerbation is a worsening of breathlessness, cough, sputum volume or sputum purulence beyond the day-to-day variation, over days, that needs a change in treatment. It is moderate if it is treated with a short-acting bronchodilator plus antibiotics, oral corticosteroids or both, and severe if it needs a hospital visit or admission. A viral or bacterial infection of the airways (rhinoviruses, influenza, H. influenzae, S. pneumoniae, Moraxella catarrhalis) triggers most of them; air pollution is another. Pneumonia, pneumothorax, a pulmonary embolus, heart failure and arrhythmia can imitate or trigger one. Exacerbations are associated with faster loss of lung function, most clearly in milder disease (the cohort data are observational), and raise the risk of the next.

Diagnosis and management

Diagnosis

Think of COPD in anyone over 35 with a risk factor and a chronic cough, sputum, breathlessness or frequent winter bronchitis, and confirm it by spirometry after a bronchodilator: an FEV1/FVC ratio below 0.70. A fixed ratio over-diagnoses in the elderly and under-diagnoses in the young, so the test is repeated on another occasion when the ratio is between 0.6 and 0.8, the diagnosis is rethought in an older person with a ratio below 0.7 but no typical symptoms, and COPD is still considered in a younger person with symptoms even when the ratio is above 0.7.

The FEV1 as a share of the predicted value grades the airflow limitation:

GOLD gradeSeverityPost-bronchodilator FEV1
1mild80 per cent or more of predicted
2moderate50 to 79 per cent
3severe30 to 49 per cent
4very severebelow 30 per cent

The FEV1 alone does not predict the symptoms or the risk of exacerbation, so the GOLD groups sort patients by their symptoms (mMRC or CAAT) and their exacerbations in the past year (the 2026 version, in which group E was widened):

GOLD groupSymptoms and exacerbationsFirst treatment
Afew symptoms (mMRC 0 to 1, CAAT below 10), no moderate or severe exacerbationone bronchodilator, short- or long-acting
Bmore symptoms (mMRC 2 or more, or CAAT 10 or more), no moderate or severe exacerbationa long-acting β2 agonist with a long-acting muscarinic antagonist (LABA and LAMA)
Eone or more moderate or severe exacerbations in the past year (in 2025, two moderate or one needing admission)LABA and LAMA; add an inhaled corticosteroid if blood eosinophils are 300 cells/µL or more

Other tests have a supporting role:

  • Chest X-ray is often normal but shows hyperinflation (flat diaphragms), large bullae and pruned peripheral vessels, and excludes other disease.
  • CT is used when the picture is unclear, and for emphysema before lung volume reduction.
  • Gas transfer (DLCO) is low in emphysema.
  • Full blood count shows polycythaemia, and the eosinophil count guides inhaled steroids.
  • Blood gases check for respiratory failure.
  • ECG and echocardiogram look for pulmonary hypertension.
  • α1-antitrypsin level is measured once in every patient, and the genotype in anyone with a low level.

Management of stable COPD

  1. 1

    Stop smoking

    The one measure that slows decline. Counselling, nicotine replacement, varenicline or bupropion together double or triple the success rate. Cut the exposure to biomass smoke too.
  2. 2

    Vaccinate

    Influenza yearly, pneumococcus, COVID-19, RSV for older adults and those at risk, and pertussis.
  3. 3

    Rehabilitate

    An exercise and education programme improves breathlessness, exercise capacity and quality of life, and cuts readmissions after an exacerbation.
  4. 4

    Open the airways

    Inhalers, stepped by the GOLD group (below). Check the technique at every visit: a good drug through a poor inhaler does nothing.
  5. 5

    Treat what comes with it

    Heart failure, ischaemic heart disease, osteoporosis, depression and malnutrition, and offer palliative care to those with advanced disease.

A short-acting β2 agonist or antimuscarinic is used on demand. Long-acting drugs, a LABA or a LAMA (tiotropium is the usual example), improve lung function, symptoms and exacerbations, and are given together to patients in groups B and E. In the main trial a LAMA did not slow the decline in FEV1, though pooled trials suggest a small effect of about 5 mL a year. An inhaled corticosteroid is added for continuing exacerbations on LABA with LAMA when blood eosinophils are 100 cells/µL or more, with a larger benefit at higher counts (it is part of the first treatment in group E at 300 or more), and brings a higher risk of pneumonia. UK guidance differs: it gives a steroid for asthmatic features or steroid responsiveness, or as triple therapy after an admission or two moderate exacerbations in a year, without using the eosinophil count. Long-acting theophyllines have little benefit in COPD.

When exacerbations continue despite this treatment, there are four further options:

  • Roflumilast, a phosphodiesterase-4 inhibitor, for patients with an FEV1 under 50 per cent, chronic bronchitis and a previous exacerbation that needed admission.
  • Long-term azithromycin, which cuts exacerbations but needs a check of the hearing, the QT interval and sputum for non-tuberculous mycobacteria first, and is for people who no longer smoke.
  • A mucolytic such as carbocysteine.
  • An anti-type-2 biologic, for selected patients with eosinophils of 300 cells/µL or more despite triple therapy: dupilumab (with chronic bronchitis) or mepolizumab.

Long-term oxygen for at least 15 hours a day extends survival in patients with chronic respiratory failure: a PaO2 on air below 7.3 kPa (55 mmHg) on two occasions when stable, or 7.3 to 8 kPa together with polycythaemia, oedema or pulmonary hypertension, in a patient who no longer smokes (carboxyhaemoglobin under 3 per cent), since smoking near oxygen can start a fire. Patients with severe disease should be assessed before they fly, since the cabin pressure of an aircraft is that of a mountain 2000 to 2400 m high.

Selected patients have an operation: a bullectomy, lung volume reduction for severe emphysema with hyperinflation, or lung transplantation for end-stage disease. Surgical reduction improved survival only in upper-lobe emphysema with low exercise capacity after rehabilitation, and raised mortality in emphysema outside the upper lobes with high exercise capacity. Endobronchial valves need an intact fissure (no collateral ventilation) and cause a pneumothorax in about a quarter of patients, mostly within 3 days.

Management of an exacerbation

  • Bronchodilators: nebulised short-acting β2 agonist, with an antimuscarinic such as ipratropium. If the patient is hypercapnic or acidotic, drive the nebuliser with compressed air, and give oxygen by nasal cannulae.
  • Corticosteroid: prednisolone 30 to 40 mg daily for five days.
  • Antibiotic for five to seven days when sputum is more purulent and breathlessness or sputum volume has also increased, or when the patient needs ventilation. Amoxicillin, doxycycline or a macrolide are typical, with sputum sent where the response is poor.
  • Controlled oxygen: a Venturi mask, starting at 24 to 28 per cent, to keep the saturation at 88 to 92 per cent in anyone at risk of hypercapnia. Too much oxygen can raise the PaCO2 and the acidosis, mainly by worsening ventilation–perfusion matching and through the Haldane effect, with some loss of hypoxic drive. Check blood gases within an hour of starting oxygen.
  • Non-invasive ventilation when the pH is below 7.35 with a PaCO2 above 6.5 kPa despite an hour of optimal medical treatment; some guidelines also start it for severe dyspnoea with signs of respiratory muscle fatigue, or for hypoxaemia that persists despite oxygen. It lowers the need for intubation and the death rate. Intubation is considered when it fails, and depends on a reversible cause and on the patient's overall prognosis and wishes.
  • Look for pneumonia and pneumothorax on the chest X-ray, and for heart failure.

Epidemiology

COPD is among the world's leading causes of death: the third leading cause, with 3.4 million deaths in 2023, about 6 per cent of all deaths. Around 10 per cent of adults aged 30 to 79 had it in 2019, on one global estimate using the fixed ratio of 0.70, about 390 million people, and nearly 90 per cent of the deaths under 70 years are in low- and middle-income countries, where biomass smoke adds to tobacco.

Smoking causes over 70 per cent of the disease in high-income countries, so it follows smoking with a lag: in the UK, the proportion of adults who smoke fell from about half in 1974 to 17 per cent in 2015 and 10.6 per cent in 2024, yet hospital admissions for COPD and asthma together in England and Wales rose by more than 80 per cent between 1999 and 2020. Rates are rising in women and in countries where smoking has risen recently. COPD takes years to develop, so it is mostly diagnosed after 40 and is often found late, when lung function is already much reduced.

Prognosis

COPD is progressive, but the speed varies a great deal from patient to patient, and stopping smoking slows it. Age and a falling FEV1 are the strongest predictors of death. The BODE index, which adds body mass index, the degree of airflow obstruction, dyspnoea and exercise capacity (the 6-minute walk), predicted survival better than the FEV1 in the original study: about 80 per cent of patients with a score of 0 to 2 were alive at four years, against about 18 per cent of those scoring 7 to 10. UK guidance does not recommend the index for prognosis in stable COPD, since later validation found it no better than the FEV1; it is mainly used to time referral for transplant assessment.

Exacerbations are the other main driver. Each one is associated with faster loss of function, and patients admitted to hospital with one have a high risk of readmission and of death in the next year or two. Long-term oxygen for at least 15 hours a day improved survival in two trials (about 30 per cent of the patients not given oxygen survived five years); when 24 hours a day was tested against 15 hours in a later trial, it made no difference to hospitalisation or death.

Death comes from respiratory failure, cor pulmonale, pneumonia, lung cancer or cardiovascular disease, which often kills a patient with mild COPD before the lung disease does. Advance care planning belongs early in the course of severe disease, because the last year or two are marked by breathlessness, repeated admissions, and uncertain outcomes of ventilation.

Check yourselfAnswer, then say how sure you were: a lucky guess still counts as a weak point.

1Which spirometry result confirms airflow obstruction in COPD?

2Which single measure most slows the decline in lung function in a smoker with COPD?

3A patient with COPD arrives drowsy and breathless. Oxygen has been started and the blood gas shows pH 7.28 and PaCO2 9 kPa. What is the right oxygen target and next step?

4Which pattern of emphysema goes with α1-antitrypsin deficiency?

5Which patient with COPD qualifies for long-term home oxygen?

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