clinical anaesthesia guidance

DRUGS

ADRENALINE

CLASS

Sympathomimetic

PRESENTATION

Clear, colourless solution in a brown vial.

Formulations

  • 1ml vial; 1mg, 1mg/ml (1:1000)
  • 10ml vial; 1mg, 100mcg/ml (1:10,000)

INDICATIONS & DOSING

Cardiac arrest

  • Adult; 1mg IV/IO
  • Paediatric; 10mcg/kg IV/IO
  • Neonate <34/40 or <2kg; 50mcg IV/IO
  • Neonate >34/40; 100mcg IV/IO

Shock

  • Adult; 25mcg-1mg IV bolus
  • Paediatric; 0.5-10mcg/kg IV bolus
  • Adult/paediatric infusion; 0-1mcg/kg/min IV

Anaphylaxis (ANZAAG guideline)

  • Adult IM; 500mcg IM
  • Adult IV; class II anaphylaxis 20mcg IV, class III anaphylaxis 100-200mcg IV
  • Paediatric IM; <6 years 150mcg IM, 6-12 years 300mcg IM (or 10mcg/kg IM)
  • Paediatric IV; class II anaphylaxis 2mcg/kg IV, class III anaphylaxis 4-10mcg IV 

Bronchospasm, airway oedema

  • Adult neb; 5mg/5ml, nebulised
  • Paediatric neb; 0.5ml/kg of 1:1000, maximum 5ml, diluted to 5ml with N/saline, nebulised
  • Adult/paediatric infusion; 0-1mcg/kg/min IV 

Regional anaesthesia additive

  • 5mcg/ml (1:200,000); dilute 100mcg (1ml of 1:10 000) up to 20ml of local anaesthetic solution
  • Maximum dose 2-4mcg/kg

PRACTICALITIES

Administration

  • Boluses; avoid unless clinically peri-arrest/cardiac arrest, start low (~25mcg) and double dose until clinical effect
  • Infusion; mixed with N/saline or 5% dextrose, using a dilution of 3mg in 50ml (60mcg/ml) allows the simplicity of 1ml/hr = 1mcg/min

Incompatibilities

  • Incompatible with alkaline solutions including sodium bicarbonate

Practice tips

  • Consider intramuscular injection as a first-line route in anaphylaxis if not familiar with intravenous use
  • Administration through a large peripheral vein is acceptable in the short-term if warranted; use a dilute concentration, watch for extravasation

PHARMACOKINETICS

Onset

  • IV/IO/neb; rapid onset <1 minute
  • IM (lateral thigh); 3-5 minutes
  • ETT; de-emphasised due to unreliable and prolonged absorption 

Duration of action

  • IV/IO/neb; duration 5-10 minutes
  • IM; depot store prolongs action 

Metabolism

Half-life 2-3 minutes due to rapid metabolism. Majority metabolised in the liver by catechol-O-methyl transferase to met adrenaline and vanillylmandelic acid. Metabolism by a lesser extent by monoamine oxidase after uptake in adrenergic neurones. Metabolised to inactive products 

Elimination

Predominantly renal excretion

MECHANISM

Direct agonism of alpha and beta sympathetic adrenoreceptors

DESIRED CLINICAL EFFECTS

Airway

  • Reduces airway mucosal oedema in nebulised form 

Respiratory

  • Potent bronchodilation

Cardiovascular

  • Beta-adrenergic agonism (lower dose range); increased cardiac output via increased chronotropy, inotropy, lusitropy, dromotropy, increased coronary blood flow
  • Alpha-adrenergic agonism (higher dose range); systemic vasoconstriction, increased systemic vascular resistance and systolic > diastolic blood pressure 

Neurological

  • Cerebral blood flow preserved

OTHER CLINICAL EFFECTS, ADVERSE EFFECTS & TOXICITIES

Respiratory

  • Increases bronchial secretions
  • Increases respiratory rate and tidal volume marginally 

Cardiovascular

  • Increased myocardial work and oxygen consumption; myocardial ischaemia
  • Arrhythmogenicity; cardiac arrhythmias
  • Beta-adrenergic agonism (lower dose range); diastolic pressure may fall due to skeletal muscle vasodilatation
  • Increases pulmonary vascular resistance, acute pulmonary oedema 

Neurological

  • Hypertensive cerebral haemorrhage
  • Tremors, anxiety 

Renal & electrolytes

  • Decreases renal blood flow, GFR largely unaltered
  • Increases sodium reabsorption directly and via stimulation of renin secretion
  • Hypokalaemia due to cellular potassium influx 

Gastrointestinal

  • Decreases gastrointestinal tone and secretions
  • Decreases splanchnic blood flow 

Endocrine

  • Decreases insulin secretion
  • Increases glucagon secretion, glycogenolysis, gluconeogenesis, hyperglycaemia
  • Increases lipolysis
  • Increases plasma renin activation, aldosterone secretion and sodium retention
  • Increases basal metabolic rate
  • Increases plasma lactate, metabolic acidaemia 

Haematological

  • Increases platelet adhesiveness and factor V activity 

Other

  • Extravasation, tissue ischaemia and necrosis 

Antidote

  • Use direct-acting vasodilators or alpha-1 antagonists, non-cardioselective beta-blockers may worsen hypertension due to beta-2 blockade 

CONSIDERATIONS

Precautions

  • Ischaemic heart disease
  • Hypertension, tachycardia
  • Tachyarrhythmia 

Obstetric 

ADEC category C 

Drug interactions

  • Beta-blockade; resistance to beta-1 cardiac effects, resistance to beta-2 effects may potentiate hypertensive response
  • MAO-inhibitors, tricyclic antidepressants; potentiates vasopressor action, adrenergic crisis

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)
  • Clinical experience of authors
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