Asthma and COPD: mechanisms, inhalers and step-wise treatment

Why airways narrow in asthma and COPD, how inhaled medicines reach the lungs, and how treatment is stepped up or down.

Updated Nov 12, 2026

Asthma and chronic obstructive pulmonary disease (COPD) both narrow the airways, but for different reasons: asthma is variable inflammation and spasm, COPD is mostly fixed damage from smoke. Inhaled drugs deliver medicine straight to the airways, and treatment follows steps based on symptoms and exacerbations. This page also covers drugs for breathlessness and respiratory stimulants.

Key points

Asthma: often allergic (type 2) inflammation with eosinophils, mast cells and IgE, airway hyperresponsiveness and largely reversible obstruction; inhaled corticosteroids are the core.
COPD: neutrophil-driven inflammation, small-airway damage and emphysema from tobacco or biomass smoke; obstruction is persistent and bronchodilators are the core.
Inhaler technique and particle size decide how much drug reaches the airways; most of a badly used dose ends up swallowed.
In asthma, reliever use of a short-acting beta2 agonist alone is no longer favoured; an inhaled corticosteroid–formoterol combination as reliever is preferred in current guidance.
In COPD, long-acting bronchodilators (LAMA, LABA) come first; inhaled corticosteroids are added mainly for frequent exacerbations with high blood eosinophils.
Opioids can ease refractory breathlessness; respiratory stimulants such as doxapram have a small and shrinking role.

Mechanisms: asthma versus COPD

In asthma, allergens, viruses, smoke, cold air or exercise trigger airway inflammation, muscle spasm and mucus. In most patients the inflammation is type 2: Th2 cells and innate lymphoid cells release IL-4, IL-5 and IL-13, which drive IgE production, eosinophils and mucus; mast cells release histamine and leukotrienes. Symptoms vary from day to day, obstruction reverses with bronchodilators, and it often starts in childhood. COPD develops over years from tobacco smoke or, in low- and middle-income countries, smoke from cooking and heating with wood, dung or coal, which WHO highlights as a major cause. Neutrophils, macrophages and CD8 cells release proteases that destroy alveoli (emphysema) and scar small airways; obstruction is only partly reversible and corticosteroids help less. Alpha-1 antitrypsin deficiency is a rare inherited cause. Some patients have features of both.

Getting the drug into the lung

Inhalation puts drug where it acts, with a fast onset and much less systemic exposure than tablets. Particle size matters: large particles hit the mouth and throat and are swallowed, while particles of a few micrometres reach the bronchi and small airways; very fine particles may be breathed out.

Pressurised metered-dose inhalers need a slow, deep breath coordinated with the puff and a breath-hold; a spacer removes the need for coordination and cuts throat deposition. WHO notes that a home-made bottle spacer can work.
Dry-powder inhalers are breath-actuated but need a quick, strong inhalation, which young children and people with severe obstruction may not manage.
Soft-mist inhalers produce a slow aerosol that is easier to inhale.
Nebulisers need no technique and suit infants and severe attacks, but are slower and not more effective than a spacer for most acute asthma.
Rinsing the mouth after inhaled corticosteroids reduces thrush and hoarseness. Poor technique is a common cause of 'treatment failure'.

Asthma step-care

Treatment is stepped up when asthma is not controlled and stepped down when it has been stable for some months. Technique, adherence, triggers and other diagnoses are checked before each step up. A written action plan tells the patient what to do when symptoms worsen.

Mild asthma: a low-dose inhaled corticosteroid–formoterol combination used as needed, which reduces severe attacks compared with a short-acting beta2 agonist alone. Formoterol works fast and lasts long, so it can serve as reliever.
Moderate: the same combination taken daily as maintenance and also as reliever (MART), or a daily ICS–LABA with a separate reliever.
Additional options: a long-acting muscarinic antagonist (tiotropium), leukotriene receptor antagonists (montelukast) or higher ICS doses.
Severe asthma: specialist assessment and biologics chosen by phenotype: omalizumab (anti-IgE), mepolizumab and benralizumab (IL-5 pathway), dupilumab (IL-4/IL-13), tezepelumab (TSLP).
LABAs are never used alone in asthma: without an inhaled corticosteroid they were linked to severe and fatal attacks.

COPD treatment

Stopping smoking and avoiding smoke exposure are the most effective steps; vaccines against influenza, pneumococcus and COVID-19 are recommended.
Short-acting bronchodilators (salbutamol, ipratropium) for symptoms as needed.
Long-acting bronchodilators for persistent symptoms: a LAMA (tiotropium) or a LABA, combined as LAMA–LABA when one is not enough.
Inhaled corticosteroids are added for repeated exacerbations, especially with high blood eosinophils; they raise the risk of pneumonia, so they are not used routinely.
Roflumilast (PDE4 inhibitor) or long-term azithromycin for some patients with frequent exacerbations; theophylline is a weaker, narrow-margin option.
Pulmonary rehabilitation, oxygen for severe resting hypoxaemia, and short courses of oral corticosteroids and antibiotics for flare-ups.

Drugs for breathlessness and ventilatory stimulants

Bronchodilators ease breathlessness when airways are obstructed, but some patients with advanced COPD, heart failure or cancer stay breathless at rest. In palliative care, low doses of opioids such as morphine can reduce the sensation of breathlessness; because they can also depress breathing, they are titrated carefully, especially in severe COPD. Benzodiazepines are used with similar caution, and nebulised furosemide has weak evidence. Respiratory stimulants are seldom needed. Doxapram stimulates carotid chemoreceptors and, at higher levels, the brainstem respiratory centres; its effect is brief, it causes agitation, sweating and raised blood pressure, and non-invasive ventilation has largely replaced it in COPD respiratory failure, where drive is usually already maximal. Almitrine acts on peripheral chemoreceptors but causes neuropathy and is rarely available. Naloxone reverses breathing depression only when it is caused by opioids.

Test yourself

Think of the answer, then tap the question to see it.

Which inflammatory cells dominate in typical asthma and in COPD?

Type 2 inflammation with eosinophils, mast cells and Th2 cytokines in asthma; neutrophils, macrophages and CD8 cells in COPD.

Why does a spacer help with a metered-dose inhaler?

It removes the need to coordinate puff and breath and traps large particles, so more drug reaches the airways and less lands in the throat.

Why can formoterol, but not salmeterol, be used as an asthma reliever with an inhaled corticosteroid?

Formoterol has a fast onset as well as a long action, so it relieves symptoms quickly while each reliever dose also delivers the steroid.

When are inhaled corticosteroids added in COPD?

Mainly for repeated exacerbations, especially with raised blood eosinophils, weighing the higher risk of pneumonia.

Why is doxapram rarely used in COPD respiratory failure?

Its effect is brief, it causes agitation and higher blood pressure, respiratory drive is usually already maximal, and non-invasive ventilation works better.

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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: Asthma (World Health Organization, 2026); Chronic obstructive pulmonary disease (COPD) (World Health Organization, 2026); Asthma - Treatment and Action Plan | NHLBI, NIH (National Heart, Lung, and Blood Institute, 2026).

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