Acute Severe Asthma Flashcards

1
Q

what is the definition of asthma

A

a chronic inflammatory disorder characterized by increased airway responsiveness to multiple stimuli leading to lower airway obstruction

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2
Q

categorization of multiple stimuli

A

acute
sub-acute
chronic

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3
Q

symptoms of asthma

A

wheezing
breathlessness
chest pain
chest tightness
coughing

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4
Q

asthma severity

A

can be mild chronic (managed as outpatient) or
acute severe form (presents to the emergency center)

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5
Q

asthma exacerbations/ acute asthma. asthma attacks

A

progressive (usually) or abrupt worsening in asthma symptoms, with increased use of bronchodilators (rescue medication) with progressively decreasing response and/or decrease in pulmonary function as measured by PEF or spirometry

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6
Q

status asthmaticus

A

asthma exacerbation that is severe and continuous and life threatening. they can present with life threatening or near fatal asthma

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7
Q

features of acute asthma

A

narrowing of the airways

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8
Q

the pathophysiology of asthma

A
  • airway narrowing
  • smooth muscle constriction
    *hypersecretion of mucus
    *mucus plugging of small airways
    *oedema of the airway wall with infiltration with inflammatory cells (e.g. neutrophils and eosinophils)
    *disruption of the airway epithelium
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9
Q

cardinal presenting symptoms and signs of severe asthma

A

wheezing
breathlessness/ SOB- even at rest
difficulty in talking
coughing
chest tightness or pain
fast breathing
use of accessory muscles to breath and might show suprasternal retraction
patient doesn’t want to lie down and appears agitated. he/she might want to sit forward in a hunched forward position

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10
Q

signs of asthma

A

fast heart rate
low O2 saturation
pulses paradoxes

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11
Q

silent chest

A

if the attack is very severe, wheezing might be absent. it is immediately life threatening asthma. it occurs either through muscle fatigue setting in and producing very poor respiratory effort or through bronchoconstriction being so severe that no air is entering the chest

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12
Q

if muscle fatigue is so
severe in asthma

A

no pulses paradox might be appreciated, as the negative intrathoracic pressure that is the cause of the pulses paradoxes cannot be generated

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13
Q

differential diagnosis

A

*foreign body obstruction
*heart failure
*anaphylaxis
*COPD
*pulmonary embolism
*inhalation injuries
*pneumothorax
*allergic bronchopulmonary aspergillosis
*bronchiectasis

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14
Q

non- drug treatment of asthma

A

A- airway: protect airway
B- breathing: ensure adequate breathing and ventilation
C- circulation: check adequacy of circulation and perfusion
D- disability: check mental state and glucose

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15
Q

which measurement should be made before treatment

A

A baseline PEF measurement

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16
Q

first line treatment of asthma

A

oxygen
inhaled B2 agonists
systemic corticosteroids

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17
Q

second line treatment of asthma

A

inhaled iprotropium bromide

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18
Q

third line treatment of asthma

A

intravenous magnesium sulphate (MgSO4)

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19
Q

fourth line treatment of asthma

A

intramuscular adrenaline
intravenous salbutamol
intravenous aminophylline
adjunctive therapy

20
Q

What percentage of oxygen are you going to deliver to a patient with asthma

A

not more that 40% O2

21
Q

when you deliver more that 40% of oxygen to patient with asthma what should this tell you

A

there is an underlying lung pathology

22
Q

when you titrate 02 what percentage of 02 saturation ae you aiming for

A

92%

23
Q

how to you measure oxygen saturation

A

pulse oximetry

24
Q

how are nebulizers bronchodilators delivered

A

by oxygen driven nebulizers

25
Q

flow rate of oxygen driven nebulizers

A

6L/ min (due to high respiratory rate)

26
Q

short acting inhaled B2 agonists examples

A

salbutamaol
fenoterol

27
Q

mechanism of inhaled Bb2 agonists

A

They are potent bronchodilators after binding to the β2-adrenoceptors on bronchial smooth muscle.
They may be repeated as frequently as necessary depending on the patient’s response: clinical improvement and improvement in peak flow to >60% predicted or >60% of previous best.

28
Q

how do administer inhaled B2 agonists

A

oxygen driver neublizer (preferred)
or via MDI if a nebulizer is not available

29
Q

goal of using the SABA

A

PEF returns to >60%

30
Q

dosages of SABA

A

Salbutamol 5mg or Fenoterol 1mg nebulized every 20 minutes until satisfactory response achieved

or Salbutamol 10 – 20 puffs (100mcg/puff) MDI via spacer every 20 minutes (take several deep breaths after every 2 puffs.

31
Q

use of corticosteroids

A

recommended for the routine treatment of acute asthma

32
Q

mechanism of Glucocorticosteroids

A

They are used for their anti-inflammatory properties (causing a decrease in the inflammatory component of airway obstruction) and have been shown to prevent relapse

33
Q

when do you administer glucocorticosteroids

A

As the onset of action of this medication is only hours after administration it is imperative that the first dose should be given orally or intravenously immediately as treatment is started and continued for 7 – 14 days

34
Q

which form of corticosteroids if preferred

A

Oral forms are as effective as IV administration and is preferred if feasible.

35
Q

examples of corticosteroids given

A

oral prednisone
IV hydrocortisone

36
Q

inhaled ipotropium bromide

A

anticholinergic agent that acts as bronchodilator via the vagal pathway (inhibition of muscarinic receptors).

Its bronchodilator effect in asthma is inferior to inhaled β2-agonists, and it provides no benefit in mild to moderate acute asthma.

The combination of this drug with an inhaled β2-agonists, however, has better bronchodilator capacity compared to either drug alone and has been shown to decrease hospital admissions in severe acute asthma attacks.

Ipratropium bromide may be administered every 20 minutes via a nebuliser at a dose of 0.5 mg or via an MDI (20 μg/puff, up to 20 puffs).

It is usually reserved for those cases where there is incomplete or refractory response to inhaled β2-agonists.

37
Q

intravenous magnesium sulphate

A

It’s mechanism of action is not fully elucidated, but thought to work by inhibiting smooth-muscle contraction, decreasing histamine release from mast cells, and inhibiting acetylcholine release

It has been shown to decrease hospital admission rates in severe acute asthma in patients with FEV1 <25% and those in which other bronchodilators failed.

38
Q

intramuscular adrenaline

A

Adrenaline has been replaced by the β2-agonists and is rarely indicated for acute asthma attacks.

It may, however, be used if patients condition is dire and up to 3rd line options have been exhausted.

Dose is 0.3 – 0.5mg adrenaline given IMI, up to 3 times.

Caution is advised in the elderly and in underlying cardiac disease.

39
Q

intravenous salbutamol

A

Very low evidence for its use.

Loading dose of 15 mcg/kg (max 0.25 mg) in 200ml 0.9% Saline IVI over 10 min, maintained at 3-20 mcg/min

Serum potassium and lactate should be monitored, and administration best done in ICU setting due to high risk of arrhythmias.

40
Q

intravenous aminophyline

A

Intravenous aminophylline (water soluble form of theophylline) is thought to act by phosphodiesterase inhibition and non-selective adenosine receptor antagonism.

It has a very narrow therapeutic range, and toxicity is common (cardiac arrhythmias, nausea and vomiting, convulsions, hypotension and coma)

Because of its high-risk side effect profile, compared to the low level of evidence with regards to its benefits, its use is only justifiable in the most severe forms of asthma and it should only be used in an ICU setting.

41
Q

adjunctive therapy

A

Antibiotics: Only to be given if definite evidence of infection such as fever, purulent sputum and clinical and/or radiological signs of pneumonia.

Intravenous fluids: Given based on the clinical setting, considering maintenance and replacement requirements.

42
Q

treatment with no evidence and/or should be avoided

A

*Leukotriene modifiers: No role in acute asthma.
*Antihistamines: No role in acute asthma.
*Mucolytics: Contraindicated, may worsen cough and bronchospasm
*Sedatives: Should be avoided because of their respiratory depressant effect.
*Physiotherapy: May provoke bronchospasm and worsen the attack.

43
Q

ongoing monitoring

A

Measurements of pulse rate, respiratory rate and blood pressure must be made at regular intervals.

Monitor pulse oximetry continuously and deliver O2 therapy if saturation below 92%

Peak expiratory flow rate (PEF) at 15-30 minute intervals. This is the best way to monitor response to therapy.

44
Q

bedside investigation

A

Perform an ABG if any life-threatening measure are present. Repeat measurement within one hour of starting treatment if
-Initial PaO2<8kPa
-Initial PaCO2 is normal or raised (more than or equal to 6kPa
-Deteriorating or not improving within 4-6 hours

Monitor blood glucose concentration.

45
Q

laboratory

A

Monitor serum potassium concentrations – salbutamol causes hypokalaemia.

Monitor serum aminophylline levels if on aminophylline infusion.

46
Q

radiography

A

A chest radiograph is not routine but should be done if a complication or other disease (e.g. tuberculosis, lung cancer) is suspected or if there is poor response to treatment, but its acquisition must not compromise ongoing monitoring and treatment.

47
Q

discharge plan

A

Provide a 7 - 14-day course of oral corticosteroid (20 - 40 mg daily of prednisone or equivalent). No tapering required if used for this duration.