Acute Severe Asthma Flashcards
what is the definition of asthma
a chronic inflammatory disorder characterized by increased airway responsiveness to multiple stimuli leading to lower airway obstruction
categorization of multiple stimuli
acute
sub-acute
chronic
symptoms of asthma
wheezing
breathlessness
chest pain
chest tightness
coughing
asthma severity
can be mild chronic (managed as outpatient) or
acute severe form (presents to the emergency center)
asthma exacerbations/ acute asthma. asthma attacks
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
status asthmaticus
asthma exacerbation that is severe and continuous and life threatening. they can present with life threatening or near fatal asthma
features of acute asthma
narrowing of the airways
the pathophysiology of asthma
- 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
cardinal presenting symptoms and signs of severe asthma
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
signs of asthma
fast heart rate
low O2 saturation
pulses paradoxes
silent chest
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
if muscle fatigue is so
severe in asthma
no pulses paradox might be appreciated, as the negative intrathoracic pressure that is the cause of the pulses paradoxes cannot be generated
differential diagnosis
*foreign body obstruction
*heart failure
*anaphylaxis
*COPD
*pulmonary embolism
*inhalation injuries
*pneumothorax
*allergic bronchopulmonary aspergillosis
*bronchiectasis
non- drug treatment of asthma
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
which measurement should be made before treatment
A baseline PEF measurement
first line treatment of asthma
oxygen
inhaled B2 agonists
systemic corticosteroids
second line treatment of asthma
inhaled iprotropium bromide
third line treatment of asthma
intravenous magnesium sulphate (MgSO4)
fourth line treatment of asthma
intramuscular adrenaline
intravenous salbutamol
intravenous aminophylline
adjunctive therapy
What percentage of oxygen are you going to deliver to a patient with asthma
not more that 40% O2
when you deliver more that 40% of oxygen to patient with asthma what should this tell you
there is an underlying lung pathology
when you titrate 02 what percentage of 02 saturation ae you aiming for
92%
how to you measure oxygen saturation
pulse oximetry
how are nebulizers bronchodilators delivered
by oxygen driven nebulizers
flow rate of oxygen driven nebulizers
6L/ min (due to high respiratory rate)
short acting inhaled B2 agonists examples
salbutamaol
fenoterol
mechanism of inhaled Bb2 agonists
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.
how do administer inhaled B2 agonists
oxygen driver neublizer (preferred)
or via MDI if a nebulizer is not available
goal of using the SABA
PEF returns to >60%
dosages of SABA
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.
use of corticosteroids
recommended for the routine treatment of acute asthma
mechanism of Glucocorticosteroids
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
when do you administer glucocorticosteroids
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
which form of corticosteroids if preferred
Oral forms are as effective as IV administration and is preferred if feasible.
examples of corticosteroids given
oral prednisone
IV hydrocortisone
inhaled ipotropium bromide
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.
intravenous magnesium sulphate
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.
intramuscular adrenaline
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.
intravenous salbutamol
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.
intravenous aminophyline
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.
adjunctive therapy
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.
treatment with no evidence and/or should be avoided
*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.
ongoing monitoring
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.
bedside investigation
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.
laboratory
Monitor serum potassium concentrations – salbutamol causes hypokalaemia.
Monitor serum aminophylline levels if on aminophylline infusion.
radiography
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.
discharge plan
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.
