21.1 — Asthma and COPD

Two conditions cause most of the world's breathlessness, and they are opposites in almost every way that matters.

Asthma is reversible narrowing of the airways from inflammation. It comes and goes, it usually starts young, and treated properly it should not limit anyone.

COPD is largely fixed narrowing plus destroyed lung tissue. It comes on slowly, it usually starts after decades of smoking, and it does not reverse.

Getting them the right way round matters, because the treatment that helps one can harm the other.

Asthma

Around 260 million people, and the great majority could be symptom-free on correct treatment.

Which makes the mortality figure — around 450,000 deaths a year — the striking one, because most asthma deaths are preventable. Reviews of asthma deaths repeatedly find the same pattern: over-reliance on the reliever inhaler, under-use of the preventer, and not seeking help early enough in an attack.

What is happening

Three things at once in the airway wall:

Inflammation — the airway lining is swollen and infiltrated with immune cells, particularly eosinophils (Chapter 13.1).

Bronchoconstriction — the smooth muscle wrapped around the airways tightens (Chapter 8.1).

Mucus — excess production, plugging small airways.

And the crucial point about the order: the inflammation is the disease, and the muscle spasm is the symptom.

Which is why the blue reliever inhaler makes you feel better within minutes and does nothing about the underlying problem, and why the brown preventer, which does nothing you can feel, is the one that keeps you alive.

That mismatch between what feels useful and what is useful is the central practical problem in asthma.

Symptoms

Wheeze, cough, chest tightness and breathlessness.

And the pattern is more diagnostic than any single symptom: variable, worse at night and in the early morning, worse with triggers, and better with a reliever.

Triggers: allergens — house dust mite, pets, pollen, mould; viral infections, which are the commonest cause of attacks; exercise; cold air; smoke; NSAIDs and aspirin in a subset; and beta blockers.

Cough-variant asthma — cough as the only symptom, frequently diagnosed as recurrent chest infection for years.

Occupational asthma — around 10 to 15 percent of adult-onset asthma. The clue is improvement on holiday and away from work, and it is worth asking about because removing the exposure early can resolve it entirely.

Diagnosis

Spirometry showing obstruction that improves with a bronchodilator.

Peak flow variability over two weeks — the diurnal swing is characteristic.

FeNO — nitric oxide in exhaled breath, raised in eosinophilic airway inflammation.

And a normal test between attacks does not exclude asthma, which is why the history carries so much weight.

Treatment

And this has genuinely changed, so the older advice is now wrong.

The reliever-alone approach is obsolete. Using a short-acting bronchodilator on its own, without an inhaled steroid, is associated with worse outcomes and increased deaths.

Current practice is that everyone with asthma should be on an inhaled corticosteroid, either regularly or as part of a combined reliever.

The steps:

Inhaled corticosteroid — the foundation. Reduces inflammation, prevents attacks, reduces deaths.

Combined inhaled steroid plus formoterol as both preventer and reliever — the "MART" approach — which means every rescue puff also delivers an anti-inflammatory. It reduces severe attacks compared with using a separate reliever, and it directly addresses the problem of people over-using the blue inhaler.

Add-on options — long-acting muscarinic antagonists, leukotriene receptor antagonists.

Biologic therapy for severe asthma — antibodies against IgE, IL-5 or IL-4/13 pathways, which have transformed severe eosinophilic and allergic asthma. People who spent years on repeated steroid courses can become nearly attack-free.

And inhaler technique, which is unglamorous and enormous. A large proportion of people use their inhaler incorrectly enough to get little drug into the lungs, and correcting technique frequently achieves more than adding a drug. A spacer improves delivery substantially with a metered-dose inhaler.

Rinse your mouth after an inhaled steroid, which prevents oral thrush and hoarseness.

An asthma attack

And this is worth knowing precisely.

Signs it is severe: too breathless to complete a sentence; peak flow well below usual; heart rate and breathing rate high; the reliever not lasting.

Signs it is life-threatening, and these are the frightening ones because they look quieter: a silent chest — no wheeze, because too little air is moving to make a sound; exhaustion; confusion; blue lips; a slowing heart rate.

A silent chest is not improvement. It is the opposite.

What to do:

Sit upright. Do not lie down.

Take the reliever inhaler — one puff every 30 to 60 seconds, up to 10 puffs, ideally through a spacer.

Call an ambulance if it is not improving after 10 puffs, if the person is too breathless to speak, or if you are worried.

While waiting, repeat the reliever every few minutes.

And steroids are given early in any attack needing more than a routine response, because they take hours to work and starting them late wastes those hours.

Living well with it

With correct treatment, the goal is no symptoms, no reliever use, no attacks, and no limitation on activity. That is achievable for the large majority, and anything less should prompt a review rather than acceptance.

A written asthma action plan reduces admissions, and it works because it tells a person exactly what to do at each stage rather than leaving them to judge.

Annual flu vaccination.

And how many reliever inhalers you get through in a year is the single best measure of control — more than about three suggests the underlying inflammation is not being treated.

COPD

Chronic obstructive pulmonary disease — around 3 million deaths a year, the third leading cause of death worldwide.

What is happening

Two overlapping processes:

Chronic bronchitis — inflamed, narrowed, mucus-filled airways.

Emphysema — destruction of the alveolar walls (Chapter 8.2). Small air sacs merge into large floppy ones, so the surface area for gas exchange falls, and the elastic recoil that normally holds small airways open is lost.

And that lost recoil is why people with COPD have trouble breathing out rather than in. Airways collapse during exhalation, air is trapped, and the lungs progressively over-inflate.

Which explains pursed-lip breathing — breathing out against partial resistance raises the pressure inside the airway and holds it open. People work this out for themselves without being taught, and it is genuinely effective.

Causes

Smoking accounts for the majority in high-income countries.

And indoor air pollution from cooking and heating with solid fuels is a major cause worldwide, particularly in women who have never smoked — which is why COPD is not only a smoker's disease.

Occupational dusts.

Alpha-1 antitrypsin deficiency — an inherited condition where the protein that protects lung tissue from its own enzymes is missing. Suspect it in COPD under 45, in a non-smoker, or with a strong family history, because it changes management and has implications for relatives.

Symptoms

Progressive breathlessness on exertion, chronic cough with sputum, and recurrent chest infections.

And the onset is so gradual that people adapt without noticing — walking slower, taking the lift, avoiding hills — so by the time they mention it, substantial lung function is already lost.

Later: weight loss and muscle wasting, ankle swelling from strain on the right side of the heart, and reduced ability to leave the house.

Diagnosis

Spirometry showing obstruction that does not fully reverse. This is required for the diagnosis, and COPD is both over- and under-diagnosed without it.

Treatment

Stopping smoking, and this is the only intervention that alters the rate of decline.

It is worth stating precisely, because it motivates: lung function does not return, and the accelerated rate of loss returns toward normal. Stopping at any stage is worth doing.

Inhalers: long-acting bronchodilators, singly or combined. Inhaled steroids are used more selectively than in asthma, mainly where there are frequent exacerbations or a raised eosinophil count, because they increase pneumonia risk in COPD.

Pulmonary rehabilitation, and it is the most under-used effective treatment in respiratory medicine.

A structured programme of exercise and education over 6 to 12 weeks. It improves breathlessness, exercise capacity and quality of life more than any inhaler, and it reduces admissions.

The mechanism is partly deconditioning: breathlessness leads to less activity, which leads to weaker muscles, which need more oxygen for the same work, which causes more breathlessness. Rehabilitation breaks that spiral.

Vaccination — influenza, pneumococcal, COVID and RSV.

Long-term oxygen therapy — for people with persistently low oxygen levels, where it improves survival. It is not for breathlessness relief in people with normal oxygen, where it does not help — a distinction that surprises people.

Lung volume reduction — surgical or by valves placed at bronchoscopy, removing the worst-affected areas so the better lung can expand. For carefully selected patients.

Nutrition, because weight loss and muscle wasting worsen outcomes.

Exacerbations

A sustained worsening — more breathless, more sputum, or the sputum changing colour.

Treatment: increased bronchodilators, steroids for a short course, and antibiotics if the sputum suggests infection.

A rescue pack at home for those who have frequent exacerbations, with a clear plan for when to use it.

And a safety point that matters in an emergency: in some people with COPD, high-flow oxygen can worsen carbon dioxide retention. Which means oxygen is given to a target range rather than as much as possible. This is never a reason to withhold oxygen from someone who is severely hypoxic — treating the low oxygen comes first — but it is why ambulance crews use a specific target and why an oxygen alert card exists for people known to retain carbon dioxide.

Exacerbations matter beyond the episode: each one accelerates decline, so preventing them is a treatment goal in itself.

Telling them apart

	Asthma	COPD
Onset	Often childhood	After 40
Course	Variable, comes and goes	Slowly progressive
Trigger	Allergens, exercise, cold	Exertion, infection
Night waking	Common	Less common
Reversibility	Good	Limited
Smoking	Not required	Usual cause

And a substantial number of people have features of both, particularly long-standing asthmatics who have also smoked — treated by addressing whichever features dominate.

What the next page fixes

Chapter 21.2 covers the gut and the liver — reflux, ulcers, inflammatory bowel disease, gallstones, and the liver conditions that stay silent until late.