Adenosine has affinity for four receptors (A1, A2A, A2B and A3). Activation of A1 receptors mediates the effects of slowing conduction through the AV node and interrupting conduction through the accessory pathways that are responsible for paroxysmal supraventricular tachycardia (such as atrioventricular re-entry and atrioventricular nodal re-entry tachycardia). Adenosine has a half-life of approximately 10 seconds and – if effective – acts rapidly to convert tachycardia to a sinus rhythm. The initial intravenous dose is 6 mg as a bolus.

Being on the receiving end of intravenous adenosine is no walk in the park. Although the effects are very brief (seconds), the combination of hypotension, flushing, non-specific chest discomfort and dyspnoea can put patients in grave fear of their lives. Because adenosine causes bronchoconstriction in asthmatics, it is also used with extreme caution in this cohort of patients. Drugs with A1 receptor selectivity and better pharmacokinetics have been in development for several years and may come to replace adenosine in the treatment of supraventricular arrhythmia. For example, the synthetic adenosine receptor agonist tecadenoson has a longer duration of action – preventing recurrent symptoms – and appears to be well tolerated.

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