3. Acute Asthma Flashcards
You are called to the accident and emergency department to see a 31-year-old lady, known to have asthma, who has been admitted with acute shortness of breath.
How would you make a clinical assessment of the severity of this attack?
History
From patient/relative/paramedic
Speed of onset
Previous and current treatment (steroids, home nebulisers)
Previous attacks requiring artificial ventilation
Clinical features
acute severe asthma include:
- Inability to complete sentences in one breath
- Tachycardia > 110 beats/min
- Respiratory rate > 25/min
- PEFR < 50% of predicted or best
Life-threatening asthma include any one of:
Silent chest
Cyanosis (SpO2 <92% or PaO2 <8 kPa)
Bradycardia or arrhythmias
Exhaustion, confusion, coma
A normal PaCO2 (4.6–6.0 kPa)
PEFR < 33% of predicted or best
What investigations might be helpful?
Asthma is primarily a clinical diagnosis,
but further information may be gained
from a few investigations.
- Peak expiratory flow rate – as outlined above
- CXR – performed to exclude a pneumothorax
and may show pulmonary hyperinflation - Arterial blood gases –
initially these may show hypocarbia with some degree of hypoxia.
As the acute attack progresses, worrying results include
a normal/high PaCO2 as ventilation worsens
and PaO2 < 8 kPa.
Some degree of metabolic acidosis is inevitable - ECG – .
this invariably shows a tachycardia,
but may also reveal P pulmonale,
right axis deviation,
arrhythmias and ST elevation.
Apart from an acute exacerbation of asthma, what would you include
in your differential diagnosis?
The two most common differential diagnoses in adults
would probably be left
ventricular failure and chronic obstructive airways disease.
Others include:
Pulmonary embolism
Upper airway obstruction
Inhaled foreign body
Aspiration
Churg–Strauss syndrome (allergic granulomatosis)
Aspergillosis
What would be your immediate management of this lady?
- Sit the patient up
- Oxygen
As high a concentration as possible from a facemask (reservoir) - β2 agonists
- Anticholinergics
- Steroids
- Magnesium
- Aminophylline
- Fluids and electrolytes
β2 agonists
Starting with 2.5–5mg of salbutamol nebulised in oxygen and repeated as required.
If there is no response (or a deterioration),
this may be given intravenously at a dose of 3–20 μg/min.
It should be noted, however,
that some investigators have concluded that intravenous
β2 agonists may be less effective than nebulised.
Side effects include tachycardia, arrhythmias,
tremor, hyperglycaemia, hypokalaemia and lactic acidosis.
Anticholinergics
Ipratropium bromide 0.5mg nebulised in oxygen if initial response to salbutamol is poor.
These agents may be synergistic with the β2 agonists
Steroids
The role of steroids in acute severe asthma is now well established
and they should be given soon after presentation.
Normal practice is to give 200mg of intravenous hydrocortisone.
Peak response is at 6–12 hours.
Magnesium
IV magnesium sulphate (1.2–2 g IV infusion over 20 minutes)
single bolus for those with life-threatening asthma or a
poor response to inhaled bronchodilators.
(Mechanism of action:
Ca2+ antagonist effect in bronchial smooth muscle,
reduces Ach release at the neuromuscular junction,
may increase sensitivity of β receptors to catecholamines.)
Aminophylline
In acute asthma, the use of intravenous aminophylline
does not result in any additional bronchodilatation compared
with standard care with beta-agonists.
No subgroups in which aminophylline might be more effective could be
identified in a recent Cochrane review and the frequency of adverse effects was higher.
Fluids and electrolytes
These patients will have both reduced intake and increased losses and careful fluid replacement is indicated.
Hypokalaemia is relatively common.
What other less well-established treatments do you know about?
- Adrenaline
No benefit from nebulised route, may be of benefit
in refractory bronchospasm. Beware arrhythmias. - Ketamine
No conclusive evidence.
May have a sedative role in
the ITU if a trial bolus helps with bronchospasm. - Inhalational agents
These have bronchodilator effects but there is the
risk of cardiovascular side effects. - Helium This reduces the work of breathing by reducing gas
density and therefore turbulent flow. FiO2 limited. - ECMO
What are the indications for mechanical ventilation?
- Respiratory arrest
- Reducing level of consciousness or coma
- Exhaustion
- Increasing hypoxaemia despite maximal medical treatment
- Increasing acidosis despite maximal medical treatment
Mechanical ventilatory support is required in
1%–3% of acute admissions with asthma.
What are the important points of the ventilator settings in asthmatics?
There are many changes in lung physiology that cause problems for
mechanical ventilation:
- Airflow obstruction means lung overinflation is a hazard –
risk of barotrauma/pneumothorax - Lung units will have variably increased time constants,
so long inspiratory times may be necessary
to provide time for adequate gas exchange.
This is not as commonly appreciated as the need for long expiratory times.
- Lung overinflation reduces venous return, compresses the heart and
increases pulmonary vascular resistance
The principles in ventilation are to limit peak and mean airway pressures,
allow a prolonged expiratory time and maintain adequate oxygenation
in the face of a high PaCO
