3. Acute Asthma Flashcards

1
Q

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?

A

History
From patient/relative/paramedic
Speed of onset
Previous and current treatment (steroids, home nebulisers)
Previous attacks requiring artificial ventilation

Clinical features

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2
Q

acute severe asthma include:

A
  1. Inability to complete sentences in one breath
  2. Tachycardia > 110 beats/min
  3. Respiratory rate > 25/min
  4. PEFR < 50% of predicted or best
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3
Q

Life-threatening asthma include any one of:

A

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

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4
Q

What investigations might be helpful?

A

Asthma is primarily a clinical diagnosis,
but further information may be gained
from a few investigations.

  1. Peak expiratory flow rate – as outlined above
  2. CXR – performed to exclude a pneumothorax
    and may show pulmonary hyperinflation
  3. 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
  4. ECG – .
    this invariably shows a tachycardia,
    but may also reveal P pulmonale,
    right axis deviation,
    arrhythmias and ST elevation.
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5
Q

Apart from an acute exacerbation of asthma, what would you include
in your differential diagnosis?

A

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

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6
Q

What would be your immediate management of this lady?

A
  1. Sit the patient up
  2. Oxygen
    As high a concentration as possible from a facemask (reservoir)
  3. β2 agonists
  4. Anticholinergics
  5. Steroids
  6. Magnesium
  7. Aminophylline
  8. Fluids and electrolytes
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7
Q

β2 agonists

A

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.

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8
Q

Anticholinergics

A

Ipratropium bromide 0.5mg nebulised in oxygen if initial response to salbutamol is poor.

These agents may be synergistic with the β2 agonists

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9
Q

Steroids

A

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.

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10
Q

Magnesium

A

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.)

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11
Q

Aminophylline

A

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.

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12
Q

Fluids and electrolytes

A

These patients will have both reduced intake and increased losses and careful fluid replacement is indicated.

Hypokalaemia is relatively common.

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13
Q

What other less well-established treatments do you know about?

A
  1. Adrenaline
    No benefit from nebulised route, may be of benefit
    in refractory bronchospasm. Beware arrhythmias.
  2. Ketamine
    No conclusive evidence.
    May have a sedative role in
    the ITU if a trial bolus helps with bronchospasm.
  3. Inhalational agents
    These have bronchodilator effects but there is the
    risk of cardiovascular side effects.
  4. Helium This reduces the work of breathing by reducing gas
    density and therefore turbulent flow. FiO2 limited.
  5. ECMO
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14
Q

What are the indications for mechanical ventilation?

A
  1. Respiratory arrest
  2. Reducing level of consciousness or coma
  3. Exhaustion
  4. Increasing hypoxaemia despite maximal medical treatment
  5. Increasing acidosis despite maximal medical treatment

Mechanical ventilatory support is required in
1%–3% of acute admissions with asthma.

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15
Q

What are the important points of the ventilator settings in asthmatics?

A

There are many changes in lung physiology that cause problems for
mechanical ventilation:

  1. Airflow obstruction means lung overinflation is a hazard –
    risk of barotrauma/pneumothorax
  2. 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.

  1. 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

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16
Q

Strategies for MV include

A

Low respiratory rate

Low tidal volumes may be necessary to avoid barotrauma.

Prolonged expiratory time (I:E ratio)

Low inspiratory flow rate (with volume-controlled ventilators)

The use of extrinsic PEEP remains controversial.

Permissive hypercapnia. Very high PaCO2 levels may have to be tolerated.

If it becomes impossible to ventilate the patient or there is a precipitous drop
in cardiac output, the ventilator should be disconnected from the endotracheal
tube and the lungs manually deflated by compression on the chest.