ASTHMA Flashcards

1
Q

treatment for mild to moderate asthma

A

Follow the patient’s asthma action plan if they have one.

  1. Administer bronchodilators using one of the following:
    a) Administer one puff of a short acting beta agonist (for example, salbutamol) via a metered dose inhaler (MDI) and spacer, followed by six breaths. Repeat this six times.

b) Administer 5 mg of nebulised salbutamol in combination with 0.5 mg of nebulised ipratropium using oxygen as the driving gas.

  1. Administer an oral steroid:
    40 mg of prednisone PO for an adult.
  2. Administer further doses of salbutamol as required.
  3. Consider the likelihood that transport may not be required if the patient rapidly improves with bronchodilators via an MDI or following one dose of nebulised bronchodilators.
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2
Q

severe asthma treatment

A
  1. Administer 5 mg of nebulised salbutamol in combination with 0.5 mg of nebulised ipratropium using oxygen as the driving gas.
    Administer continuous nebulised salbutamol until improvement occurs.
  2. Administer adrenaline IM if the patient is not improving:
    Administer 0.5 mg IM for an adult. (Repeat adrenaline IM every ten minutes if the patient is deteriorating and adrenaline IV is not being administered)
  3. Begin transport without delay, providing most treatments en route.
  4. Gain IV access.
  5. ICP for magnesium IV: 10 mmol

6.Consider application of CPAP if the patient is not improving. See the ‘CPAP’ section.

The administration of an oral steroid is not a priority but should occur if the patient is able to swallow, using the doses described above

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3
Q

life threatening asthma treatment

A

ICP for IV adrenaline PLUS

  1. Administer 5 mg of nebulised salbutamol in combination with 0.5 mg of nebulised ipratropium using oxygen as the driving gas.
    Administer continuous nebulised salbutamol until improvement occurs.
  2. Administer adrenaline IM if the patient is not improving:
    Administer 0.5 mg IM for an adult. (Repeat adrenaline IM every ten minutes if the patient is deteriorating and adrenaline IV is not being administered)
  3. Begin transport without delay, providing most treatments en route.
  4. Gain IV access.
  5. ICP for magnesium IV: 10 mmol

6.Consider application of CPAP if the patient is not improving. See the ‘CPAP’ section.

The administration of an oral steroid is not a priority but should occur if the patient is able to swallow, using the doses described above

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4
Q

Non transport criteria for asthma

A
  1. Age greater than or equal to 12 years, and

2.Known asthma, and

3.Talking in full sentences, and

4.An SpO2 greater than or equal to 92% when breathing air, and
Observed by ambulance personnel for a minimum of 20 minutes following completion of the last bronchodilator administration, and

5.Observed to mobilise normally, and

6.Able to see an appropriate healthcare professional within two days, and

  1. Provided with a prednisone pack (if indicated and available), and an information sheet with the contents clearly explained to the patient and to any carers.
  2. If the patient has signs of a chest infection (for example fever or purulent sputum), the patient should be seen by an appropriate healthcare professional within 12 hours. This should usually be in a primary care facility if all of the other non-transport criteria are met.
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5
Q

characteristics of mild to moderate asthma

A

Patients with mild to moderate asthma are short of breath but are able to speak in sentences, are usually moving enough air to generate a loud wheeze, do not have significant chest or neck indrawing, have a normal SpO2 and a normal level of consciousness.

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6
Q

characteristics of severe asthma

A

Patients with severe asthma are very short of breath, are only able to speak a few words with each breath, may only be moving enough air to generate a quiet wheeze, usually have significant chest or neck indrawing, may be in the tripod position, usually have an SpO2 of greater than 90% (SpO2 falls very late in the progression of asthma) and may be agitated.

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7
Q

characteristics of life-threatening asthma

A

Patients with immediately life-threatening asthma are extremely short of breath, are usually unable to speak, are moving very little air and may not be moving enough air to create wheeze, usually have marked indrawing but this may not be present if they are exhausted, may have a rapidly falling SpO2 and usually have severe agitation or a falling level of consciousness.

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8
Q

why do bronchodilators provide very little benefit to under 5 y/o

A

Children aged less than one year have poorly developed bronchial smooth muscle and fewer beta-2 receptors than adults

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9
Q

Children aged less than one year who are short of breath and wheezy usually have

A

bronchiolitis as asthma does not occur at this age. Treating hypoxia is the most important aspect of treating bronchiolitis and bronchodilators do not usually have a role.

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10
Q

Steroid administration does not usually have a role in children aged less than five years because

A

it does not generally alter the course of their asthma exacerbation. However, an oral steroid is indicated if the child has a clear history of asthma and has previously received oral steroids.

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11
Q

Prednisone pack requirements

A
  1. If the patient is aged greater than or equal to 12 years and is not transported, a prednisone pack should be provided unless the patient already has an asthma action plan for administering their own steroid.

2.Provide an information sheet, ensuring the information is explained to the patient and any carers.

  1. The pack contains a supply of prednisone, and this is usually sufficient for a complete course of prednisone. However, it is important to advise the patient to be seen in primary care for a review of their treatment within two days.
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12
Q

when would you consider reducing the dose of IM adrenaline

A

particularly if the patient is small, frail or has ischaemic heart disease.

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13
Q

in what context is ketamine used for asthma

A

Clinical judgement is required and ketamine administration should occur if the patient’s agitation is severe enough to impair the ability to safely provide treatment and/or transport. Although ketamine may have some bronchodilator activity, in this setting the focus is on treating severe agitation. Personnel should seek clinical advice if uncertain.

Patients with severe agitation are likely to require RSI and backup must be requested early.

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14
Q

Dynamic hyperinflation (gas trapping) occurs when

A

the amount of gas within the lungs increases in the presence of severe bronchoconstriction.

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15
Q

why dose dynamic hyperinflation occur

A

This occurs because the resistance to gas leaving the lungs during expiration is higher than the resistance to gas entering the lungs during inspiration.

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16
Q

dynamic hyperinflation causes

A

commonly causes reduced venous return to the heart by increasing intrathoracic pressure.

17
Q

who is at the highest risk of dynamic hyperinflation

A

Dynamic hyperinflation occurs in spontaneously breathing patients when their asthma is severe, but those most at risk of life-threatening dynamic hyperinflation are those receiving positive pressure ventilation or CPAP. For this reason, the ventilation rate must be kept at six breaths/minute in patients receiving positive pressure ventilation for immediately life-threatening asthma.

18
Q

Diagnosing tension pneumothorax can be very difficult in the presence of immediately life-threatening asthma because:

A

Breath sounds are already reduced because the patient is moving very little air.

The jugular veins are already distended because of raised intrathoracic pressure.

Cardiac output is already reduced because of dynamic hyperinflation.

The percussion note is already hyperresonant because of dynamic hyperinflation.

19
Q

In the setting of immediately life-threatening asthma, the convincing signs of tension pneumothorax are most likely to be:

A

A very clear difference in breath sounds and percussion note between the two sides, and

Signs of a progressively falling cardiac output in the absence of signs of dynamic hyperinflation.

20
Q

Bronchodilators do not have a significant role in the treatment of

A

bronchospasm resulting from smoke inhalation, toxic gas inhalation or chest infection. However, bronchodilators (but not adrenaline or oral steroids) may be administered if bronchospasm is prominent.

21
Q

asthma is characterized by

A

-bronchial hypersensitivity
- bronchoconstriction
-bronchial inflammation
-reversible airway constriction

22
Q

what causes asthmatics to go into cardiac arrest?

A
  • mucus plugging contributing to asphyxiation
  • prolonged hypoxia leading to arrythmia
    gas trapping leading to inadiquate venous return
23
Q

what can lead to airway remodeling in poorly managed asthma

A

layer of the epithelium cells peels off and smooth muscle of the lungs enlarge.

24
Q

why is magnesium used in asthma

A

induces smooth muscle relaxation, inhibits histamine and enhances affinity of B2

25
Q

Ipratropium mechanism

A

Ipratropium is an anticholinergic agent with predominantly antimuscarinic activity. It antagonises (blocks) acetylcholine receptors, causing vagal inhibition resulting in bronchodilation.

26
Q

salbutamol mechanism

A

Salbutamol is a bronchodilator. It is an agonist (stimulator) of beta-2 receptors.

27
Q

prednisone mechanism

A

Prednisone is a prodrug that is metabolised to prednisolone in the liver.
Prednisolone is a corticosteroid with anti-inflammatory and immunosuppressant actions. It inhibits the production of inflammatory mediators, including prostaglandins and leukotrienes, resulting in a reduction in the inflammatory and immune response