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SALBUTAMOL

CLASS

Beta agonist

PRESENTATION

White powder aerosolised by a blue Metered Dose Inhaler (MDI).
Clear, colourless solution, clear vial.

Formulations

  • MDI; 200 doses, 100mcg/dose
  • 2.5ml nebule solution; 2.5mg, 1mg/ml
  • 2.5ml nebule solution; 5mg, 2mg/ml
  • 1ml vial; 500mcg, 500mcg/ml
  • 5ml vial; 5mg, 1mg/ml

INDICATIONS & DOSING

Bronchospasm (of any cause), prevention & management

  • Adult MDI; 12 puffs
  • Adult nebuliser; 5mg or continuous max 10-20mg/hr
  • Adult IV; 250-500mcg IV
  • Paediatric MDI; <6 years 6 puffs, >6 years 12 puffs
  • Paediatric nebuliser; <25kg 2.5mg, >25kg 5mg, or continuous max 10-15mg/hr
  • Paediatric IV; 3-10mcg/kg IV
  • Adult/paediatric infusion; 5-10mcg/kg/min IV for the first hour, followed by 0.5-2mcg/kg/min IV 

Hyperkalaemia

  • Adult/paediatric nebuliser; 2.5-5mg or continuous at 10-15mg/hr
  • Adult/paediatric infusion; 5-10mcg/kg/min IV for the first hour, followed by 0.5-2mcg/kg/min IV 

Tocolysis (second-line therapy)

  • Infusion; 10mcg/min IV, increase by 5mcg IV every 30 minutes, maximum 30mcg/min

PRACTICALITIES

Administration

  • Shake MDI prior to use
  • MDI doses should be delivered via a spacer if possible
  • MDI dose can be delivered in-circuit to the ventilated patient via a purpose-made MDI connector, time with inspiration
  • Infusion; 5mg ampoule mixed with N/Saline or 5% dextrose to 100mL (50mcg/ml)

Practice tips

  • The preferred route of administration in treating bronchospasm is dependent on availability of route, clinical urgency, and response
  • Inhaled therapy preferred for initial management
  • Reserve intravenous therapy for cases of severe bronchospasm due to higher incidence of severe side-effects and less-well established efficacy
  • Always co-administer salbutamol with oxygen due to possible precipitation of hypoxaemia due to worsening of pulmonary VQ matching

PHARMACOKINETICS

Onset

  • Bronchodilation; 1-3 minutes IV, 2-5 minutes neb
  • Potassium shift; ~30 minutes
  • Tocolysis; 15 minutes

Duration of action

  • Bronchodilation; 10-20 minutes IV, 15-60 minutes neb
  • Potassium shift; up to 2 hours
  • Tocolysis; may delay delivery for up to 48hrs

Metabolism
Majority hepatic metabolism, to salbutamol 4-O-sulfate

Elimination
Mixed renal and biliary elimination

MECHANISM

Direct agonism of beta sympathetic adrenoreceptors. Higher affinity for beta-2 than beta-1 receptors, with minimal beta-1 activity in the lower dose range.

DESIRED CLINICAL EFFECTS

Respiratory

  • Bronchodilation due to bronchial smooth muscle relaxation, increasing expiratory gas flow 

Renal & electrolytes

  • Reduction in potassium level of ~1mmol/L due to beta-2 mediated increased Na/K/ATPase pump activity causing an intracellular shift of potassium 

Obstetric

  • Tocolysis secondary to uterine smooth muscle relaxation

OTHER CLINICAL EFFECTS, ADVERSE EFFECTS & TOXICITIES

Respiratory

  • Hypoxaemia due to an impairment of hypoxic pulmonary vasoconstriction, increasing pulmonary VQ mismatch and shunt

Cardiovascular

  • Hypotension, a fall in diastolic blood pressure of 10-20mmHg due to beta-2 mediated peripheral vasodilatation (lower dose range)
  • Tachycardia and raised cardiac output, precipitation of myocardial ischaemia, due to beta-1 mediated chronotropy and inotropy (higher dose range)
  • Arrhythmogenicity, particularly in the presence of hypokalaemia 

Neurological

  • Anxiety, tremor, diaphoresis 

Renal & electrolytes

  • Hypokalaemia (mechanism as above)
  • Lactic acidosis (higher dose range) 

Endocrine

  • Hyperglycaemia, ketosis, raised plasma fatty acid concentration and stimulation of insulin secretion due to stimulation of glycolysis/gluconeogenesis, ketosis, lipolysis 

Obstetric

  • Foetal tachycardia following placental drug transfer

CONSIDERATIONS

Precautions

  • Hypertension/tachycardia
  • Hypokalaemia
  • Hyperglycaemia
  • Lactic acidosis

Obstetric 
ADEC category A

Drug interactions
Adrenaline; additive clinical effects, may precipitate adverse cardiovascular effects, hypokalaemia

  • Non-depolarising neuromuscular blockers; potentiates neuromuscular blockade
  • MAO inhibitors, tricyclic antidepressants; may result in exaggerated hypertensive response
  • Digoxin; salbutamol reduces digoxin serum concentration
  • Non-selective beta-blockers; antagonise effects of salbutamol

REFERENCES

Drug information has been compiled from multiple sources including

  • Drugs in Anaesthesia and Intensive Care (Scarth & Smith)
  • Micromedex (IBM)
  • BJA Education (Oxford Academic)
  • Pharmacology for Anaesthesia and Intensive Care (Cambridge)
  • Australian Prescriber (NPS MedicineWise)

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