Medicine – Acute Asthma

Acute asthma is a sudden or progressive worsening of asthma symptoms caused by increased bronchial smooth-muscle constriction, airway inflammation, mucosal oedema, and mucus production. Patients develop worsening breathlessness, wheeze, cough, and chest tightness, together with a measurable reduction in expiratory airflow.

A severe asthma attack can progress rapidly to life-threatening respiratory failure, so recognising markers of severity and starting treatment promptly are essential.

1. Mortality

Asthma continues to cause preventable deaths in the UK, although the older figure of approximately 1,500 deaths per year varies between years and should not be regarded as a fixed contemporary number.

Many fatal attacks are associated with delayed recognition of severity, inadequate use of anti-inflammatory treatment, or delayed escalation of emergency care.

Assessment of Acute Asthma

The severity of an acute attack should be assessed using the patient’s clinical appearance, ability to speak, respiratory rate, heart rate, oxygen saturation, peak expiratory flow (PEF), and—when indicated—arterial blood gases.

An important correction to the older notes is that some listed findings, particularly PEF <33%, silent chest, hypoxaemia, and normal or raised PaCO₂, are markers of life-threatening asthma, rather than merely severe asthma.

2. Severe Acute Asthma

In adults, acute severe asthma is suggested by the presence of any of the following major features.

Difficulty Speaking

The patient may be unable to complete sentences in one breath because of severe breathlessness.

Speech becoming increasingly fragmented is an important bedside indication of worsening respiratory distress.

Tachycardia

A heart rate ≥110 beats/minute is a marker of acute severe asthma.

Tachycardia can result from respiratory distress, hypoxaemia, sympathetic activation, and β₂-agonist treatment.

Tachypnoea

A respiratory rate ≥25 breaths/minute is commonly used in modern UK adult criteria for acute severe asthma.

The older threshold of >30/min still indicates substantial respiratory distress but is not the usual current threshold for defining acute severe asthma.

Peak Expiratory Flow

A PEF of 33–50% of the patient’s best or predicted value indicates acute severe asthma.

Peak flow provides an objective measurement of the degree of airflow obstruction and should be recorded whenever the patient is capable of performing the manoeuvre safely.

3. Life-Threatening Asthma

Life-threatening asthma is suggested by particularly severe clinical or physiological abnormalities.

These patients require immediate treatment, senior medical involvement, and consideration of intensive care.

Peak Flow Below 33%

A PEF <33% of the patient’s best or predicted value is a major marker of life-threatening asthma.

This represents very severe expiratory airflow limitation.

Silent Chest

A silent chest is an ominous finding.

Although wheezing is characteristic of asthma, extremely severe airflow obstruction can reduce airflow so dramatically that little or no wheeze is audible.

Therefore, disappearance of wheeze in a deteriorating patient does not necessarily indicate improvement.

Hypoxaemia

Significant hypoxaemia indicates severe impairment of ventilation and gas exchange.

Oxygen saturation should therefore be monitored continuously in a severe attack.

Normal or Raised PaCO₂

A normal or elevated arterial PaCO₂ is a particularly concerning finding in acute asthma.

Early in an asthma attack, patients usually hyperventilate and therefore have a low PaCO₂.

As obstruction becomes extreme and respiratory muscles fatigue, the patient can no longer maintain adequate ventilation. PaCO₂ then returns toward normal and subsequently rises.

Therefore:

Low PaCO₂ → expected during significant acute asthma.

Normal PaCO₂ → concerning for deterioration.

Raised PaCO₂ → severe ventilatory failure and potentially impending respiratory arrest.

Other Life-Threatening Features

Additional warning signs include cyanosis, poor respiratory effort, exhaustion, hypotension, arrhythmia, altered consciousness, and confusion.

These features indicate that the patient may be approaching respiratory failure.

4. Pulsus Paradoxus

Pulsus paradoxus refers to an exaggerated fall in systolic blood pressure during inspiration.

It may occur in severe asthma because large changes in intrathoracic pressure influence ventricular filling.

Although historically included in severity assessment, it is not routinely relied upon in modern acute asthma assessment, because simpler clinical and physiological measurements are more useful.

Management of Acute Severe Asthma

Treatment should begin immediately while severity is being assessed.

The major aims are to correct hypoxaemia, reverse bronchoconstriction, suppress airway inflammation, and recognise patients requiring intensive respiratory support.

5. Oxygen

Patients who are hypoxaemic should receive supplemental oxygen, titrated to an appropriate oxygen saturation.

The older instruction to automatically administer unrestricted high-flow oxygen to every patient has been replaced by controlled oxygen therapy guided by oxygen saturation.

In adults with acute asthma, a target oxygen saturation of approximately 94–98% is commonly used.

6. Nebulised β₂-Agonists

A rapidly acting inhaled β₂-agonist, most commonly salbutamol, is a cornerstone of treatment.

In severe attacks, repeated or continuous nebulised therapy may be required.

Nebulisers can be driven by oxygen when appropriate in significantly hypoxaemic patients.

7. Ipratropium Bromide

Nebulised ipratropium bromide should be added to β₂-agonist treatment in severe or life-threatening asthma.

The combination produces greater bronchodilation than either treatment alone in severe attacks.

8. Systemic Corticosteroids

Systemic corticosteroids should be administered early because acute asthma involves significant airway inflammation as well as bronchoconstriction.

Oral prednisolone is often appropriate when the patient can swallow and absorb medication.

Intravenous hydrocortisone can be used when oral treatment is unsuitable.

Steroids do not produce immediate bronchodilation, but they reduce airway inflammation and decrease the likelihood of ongoing deterioration and relapse.

Additional Treatment

9. Intravenous Magnesium Sulfate

Intravenous magnesium sulfate may be considered in severe or life-threatening asthma that responds inadequately to initial inhaled bronchodilator treatment.

Magnesium has a bronchodilator effect and can be useful in selected severe attacks.

It is not routinely required for every asthma exacerbation.

10. Intravenous Aminophylline

Intravenous aminophylline was historically used more frequently in severe asthma.

It is no longer routinely recommended because the additional bronchodilator benefit is limited and adverse effects, including nausea, vomiting, arrhythmias, and seizures, can occur.

It may occasionally be considered in specialist-managed refractory cases.

11. Intravenous Salbutamol

Intravenous β₂-agonists such as salbutamol are also not routinely used when effective inhaled or nebulised therapy can be delivered.

They may occasionally be considered in highly selected refractory cases under specialist supervision.

12. Antibiotics

Antibiotics are not routinely indicated in acute asthma.

Most asthma exacerbations are not caused by bacterial infection, and purulent-looking sputum alone does not necessarily indicate bacterial disease.

Antibiotics should be given when there is convincing evidence of a bacterial infection, such as bacterial pneumonia.

Respiratory Failure

13. When to Consider Intensive Care

Urgent intensive care assessment should be considered when the patient is deteriorating despite appropriate treatment or develops features such as exhaustion, altered consciousness, worsening hypoxaemia, rising PaCO₂, poor respiratory effort, or haemodynamic instability.

A patient with severe asthma can deteriorate very rapidly.

14. Mechanical Ventilation

Mechanical ventilation may become necessary when respiratory failure develops despite maximal medical treatment.

Important indications include worsening hypercapnia, severe hypoxaemia, exhaustion, reduced consciousness, respiratory arrest, or inability to maintain adequate ventilation.

Intubation and ventilation of a patient with severe asthma are challenging because severe airflow obstruction and air trapping can produce dynamic hyperinflation and dangerously high intrathoracic pressures, so experienced critical-care management is essential.

15. Severe vs Life-Threatening Asthma – Note Form

Acute Severe Asthma

Speech: unable to complete sentences in one breath.

Respiratory rate: ≥25/min.

Heart rate: ≥110/min.

PEF: 33–50% of best or predicted.

Life-Threatening Asthma

PEF: <33% of best or predicted.

Chest examination: silent chest.

Oxygenation: significant hypoxaemia.

PaCO₂: normal or raised.

Cyanosis: may be present.

Respiratory effort: poor or decreasing.

Neurological state: exhaustion, confusion, or reduced consciousness.

Cardiovascular features: hypotension or arrhythmia may develop.

16. Immediate Management – Note Form

Oxygen: controlled supplemental oxygen, generally targeting SpO₂ around 94–98%.

Bronchodilator: repeated or nebulised salbutamol.

Antimuscarinic: add nebulised ipratropium in severe or life-threatening attacks.

Steroids: give systemic corticosteroids early.

Magnesium: consider IV magnesium sulfate if the response to initial treatment is inadequate.

Antibiotics: only when bacterial infection is suspected or confirmed.

Aminophylline/IV salbutamol: not routine; reserve for selected refractory cases with specialist input.

Ventilation: consider urgently if respiratory failure, exhaustion, deteriorating consciousness, worsening hypoxaemia, or rising PaCO₂ develops.

Key Clinical Pattern

In acute asthma, a patient initially tends to hyperventilate and lower their PaCO₂. Therefore, a normal PaCO₂ is not reassuring in a severely breathless asthmatic—it may indicate that respiratory muscles are beginning to fail.

Remember the distinction:

Acute severe asthma → PEF 33–50%, RR ≥25/min, HR ≥110/min, inability to complete sentences.

Life-threatening asthma → PEF <33%, silent chest, hypoxaemia, normal/raised PaCO₂, cyanosis, exhaustion, hypotension, arrhythmia, or altered consciousness.

Initial treatment centres on oxygen when hypoxaemic + repeated inhaled/nebulised β₂-agonist + ipratropium + early systemic corticosteroids, with IV magnesium and critical-care support when the response is inadequate.