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ADENOSINE

CLASS

Anti-arrhythmic

PRESENTATION

Clear, colourless solution.

Formulations

  • 2ml vial, 6mg, 3mg/ml

INDICATIONS & DOSING

Termination of AV nodal re-entrant supraventricular arrhythmias
Termination of orthodromic AV re-entrant arrhythmias in Wolff-Parkinson-White syndrome
Differentiation of SVT/VT/atrial fibrillation/atrial flutter
Intraoperative cardiac standstill

  • Adult; 6mg IV/IO bolus, subsequent doses 12mg IV/IO 1-2 minutely, max 3 doses
  • Paediatric; 0.05-1mg/kg IV/IO max 6mg, subsequent doses 1-2 minutely, increasing by 0.05-0.1mg/kg until maximum single dose 0.3mg/kg is used

PRACTICALITIES

Administration

  • Administer in a proximal vein followed by a rapid fluid flush

Practice tips

  • Administered only where cardiac monitoring and resuscitation equipment are immediately available

PHARMACOKINETICS

Onset

  • 10-20 seconds

Duration of action

  • <10 seconds

Metabolism
Rapidly taken up and metabolised by vascular endothelial cells and erythrocytes. Phosphorylated to adenosine monophosphate or deaminated.

Elimination
Products taken up endogenously

MECHANISM

Negatively chronotropic by agonism of nodal adenosine A1 receptors, leading to suppression of SA and AV node electrical activity. Negative inotropic via antagonism of cAMP-mediated catechol stimulation of ventricular cardiac muscle.

DESIRED CLINICAL EFFECTS

Cardiovascular

  • Depression of SA and AV node activity leading to termination of nodal re-entrant or orthodromic atrioventricular rhythms
  • Transient slowing of ventricular response facilitating diagnosis of underlying rhythm disturbance (VT vs. SVT with aberrant conduction, or revealing an underlying atrial flutter/fibrillation)

Respiratory

  • Decreases pulmonary vascular resistance in patients with pulmonary hypertension

OTHER CLINICAL EFFECTS, ADVERSE EFFECTS & TOXICITIES

Respiratory

  • Dyspnoea, chest discomfort
  • Hyperventilation
  • Bronchospasm

Cardiovascular

  • Transiently reduced cardiac output, hypotension (uncommon with usual bolus dosing)
  • Prolonged bradycardia, sinus arrest, cardiac arrest
  • Tachyarrhythmias; atrial flutter, atrial fibrillation, ventricular fibrillation
  • Transient facial flushing

Neurological

  • Feeling of dread, dizziness
  • Head and neck discomfort

Endocrine

  • Inhibition of lipolysis
  • Stimulation of glycolysis

Antidote

  • Aminophylline has been used (competitive antagonism)

CONSIDERATIONS

Precautions

  • Bronchospastic pulmonary disease (asthma, COPD); adenosine-mediated bronchospasm
  • Conduction block (2nd/3rd degree conduction block, sick sinus syndrome); risk of sustained bradycardia
  • Wolff-Parkinson-White with atrial fibrillation, atrial flutter, antidromic AVRT; may facilitate conduction via accessory tract, leading to rapid ventricular response and degeneration to ventricular tachycardia/fibrillation
  • Risk of significant haemodynamic compromise (decompensated heart failure, hypovolaemia, fixed cardiac output states, myocardial ischaemia); precipitation of significant hypotension/cardiac arrest
  • Cardiac transplant; increased sensitivity due to cardiac denervation
  • Long QT syndrome, structural heart disease; increased risk of generation of ventricular arrhythmias
  • No dose adjustment required for renal or hepatic impairment

Obstetric 

ADEC category B2

Drug interactions

  • Xanthines (aminophylline, theophylline); competitive antagonism reduces the effect of adenosine, combination may result in seizure activity
  • Dipyridamole; augments the effect and duration of adenosine
  • Digoxin, verapamil; rare risk of ventricular fibrillation
  • Carbamazepine: may result in prolonged conduction blockade

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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