Paediatric Asthma

Question 1

Nebuliser masks in paed asthma

Answer 1

Nebuliser masks require a minimum volume of fluid to operate correctly. For doses of nebulised
Salbutamol less than a single nebule, draw up appropriate volume of drug and dilute with normal
saline to a minimum of 5 mL.

Question 2

Why should nebulised Salbutamol should be reserved for severely ill children?

Answer 2

Caution should be used when administering nebulised Salbutamol to children as it can cause
profound lactic acidosis.

Question 3

Presentation of paed with mild/moderate asthma

Answer 3

Normal conscious state, some increased work of breathing, tachycardia, speaking in
phrases/ sentences.

Question 4

Presentation of paed with severe asthma

Answer 4

Agitated/distressed, markedly increased work of breathing, including accessory muscle
use/retraction, tachycardia, speaking in words.

Question 5

Presentation of paed with critical asthma

Answer 5

Altered conscious state, maximal work of breathing, marked tachycardia, unable to talk.

Question 6

Mgx of Mild/Moderate Asthma Paed

Answer 6

Salbutamol pMDI w/ spacer
≥6 yrs: 4 - 12 doses
2 - 5 yrs: 2 - 6 doses

Pts to take 4 breaths with each dose
can repeat after 20/60 if required

Question 7

Mgx of Severe Asthma

Answer 7

Small child ( 2 - 4 yrs)
- salbutamol 2.5mg (1.25mL) nebulised
Medium Child (5 - 11 yrs)
- salbutamol 2.5-5mg (1.25 to 2.5mL) nebulised
Repeat at 20/60 intervals if required

Ipratropium bromide 250mcg (1mL) nebulised

Question 8

Mgx of Critical Asthma

Answer 8

All children (2 - 11 yrs) 10mg (5mL) salbutamol nebulised
- repeat 5/60 intervals if required
Ipratropium Bromide 250mcg (1mL) nebulised once only
Adrenaline 10mcg/kg IM
- repeat 5-10/60 intervals if required - MAX 30mcg/kg IM
Dexamethasone 600mcg/kg Oral (max 12mg)

Question 9

Asthma Patho

Answer 9

Smooth muscle in bronchial system are exposed to antigens
↓
Mast cells degranulate and release inflammatory mediators (bronchioles only)
↓
Bronchial smooth muscle constricts due to mast cells located in the bronchial smooth muscle
↓
Vascular engorgement occurs causing increased capillary permeability
↓
Oedema occurs
↓
Thick mucus is formed
↓
Airways become obstructed
↓
Decreased flow rates and decreased exp flow = hyperinflation
↓
Hyperinflation causes the lung stretch receptors to induce hyperventilation
↓
Air becomes trapped
↓
Intrapleural and alveoli pressures increase – perfusion is disrupted
↓
VQ mismatch develops
↓
CO2 is retained causing respiratory acidosis
↓
Gas trapping causes increased intrathoracic pressures
↓
Venous return is impaired
↓
C.O is impaired
Myocardial and cerebral perfusion impaired
Blood pressure falls as venous return continues to be obstructed
↓
RESP Arrest if gas trapping continues

Question 10

Risk Factors associated with Ventilation of Asthmatic Patient

Answer 10

• May cause ↑gas trapping due to higher ventilatory pressure
• May cause further ↑ in intrathoracic pressure and subsequent loss of C.O
• Tension pneumothorax
• Aspiration due to high ventilatory pressures

Question 11

Asthma Definition

Answer 11

A reversible inflammatory disease characterised by hyperresponsiveness of the smooth airways and episodes of bronchospasm. Characterised by bronchospasm, mucous oedema, mucous plugging

Question 12

Triggers for Asthma

Answer 12

Pollen
Dust
Exercise
Allergens
Cold Weather
Thunderstorm
Pets
Smoke

Question 13

Why might asthmatic patients lose cardiac output? If this occurs what is the rationale for the period of apnoea?

Answer 13

Due to high intrathoracic pressure as a result of gas trapping, venous return is
compromised and the patient may lose cardiac output

Apnoea allows the gas trapping to decrease

Question 14

In relation to receptors sites, why is adrenaline an important part of the critical asthmatic treatment regime?

Answer 14

 Adrenaline is a naturally occurring alpha and beta adrenergic stimulant
 Alpha receptor sites cause peripheral vasoconstriction resulting in increased venous return helping to overcome increased intra-thoracic pressures
 Beta 2 receptor sites cause bronchodilation helping to reverse the smooth muscle bronchial constriction

Question 15

What is the preferred route of administration of Ventolin in the mild to moderate asthmatic patient? Why is this method preferred?

Answer 15

A pMDI is the preferred route of administration for Salbutamol in patients with mild or moderate respiratory distress
 Particle sizes created by spacers are smaller than particle spaces created by nebulisers. This leads to better lung deposition as more medication is delivered further down the bronchial tree

Question 16

Describe how AV’s medication regime helps reverse the signs and symptoms of asthma?

Answer 16

Salbutamol – Synthetic beta adrenergic stimulant with primarily beta 2 effects causes bronchodilation
 Ipratropium Bromide – Anticholinergic bronchodilator which allows bronchodilation by inhibiting cholinergic bronchomotor tone (i.e. blocks vagal reflexes which mediate bronchoconstriction)
 Dexamethasone – Is a corticosteroid secreted by the adrenal cortex which relieves inflammatory reactions and provides immunosuppression

Question 17

Explain why the asthmatic patient may arrest?

Answer 17

Hyperinflation of lungs means lung volume reaches maximal capacity
o Leading to inadequate alveolar ventilation

Increase in intra-thoracic pressure leads to impaired cardiac output
o Eventual loss of cardiac output