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Mechanism of action of adenosine in AVNRT

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"adenosine"[MeSH Terms] AND "tachycardia, atrioventricular nodal reentry"[MeSH Terms]

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Adenosine terminates AVNRT by briefly blocking conduction through the AV node. The AV node is part of the reentry circuit, so blocking it breaks the loop.

Why the AV node is the target

AVNRT depends on a reentrant circuit within or next to the AV node, made of a slow pathway and a fast pathway (dual AV nodal physiology). Adenosine blocks the AV node transiently, which terminates the tachycardia (Fuster and Hurst's The Heart, 15th Edition, p. 1129).

Cellular mechanism

  1. Receptor binding. Adenosine binds the A1 receptor, a G-protein coupled receptor on the surface of nodal and atrial cells. The receptor is coupled to inhibitory G proteins (Gi) (Braunwald's Heart Disease, "Electrophysiologic Actions").
  2. K+ channel activation. The G-protein βγ subunits open the acetylcholine-sensitive inward rectifier K+ channel (IK,ACh, made of Kir3.1/Kir3.4). This works like vagal stimulation by acetylcholine.
  3. Hyperpolarization. Increased K+ efflux hyperpolarizes the nodal cells and shortens the action potential duration. Hyperpolarized AV nodal cells are less excitable and slower to depolarize.
  4. Anti-adrenergic effect. Adenosine also inhibits catecholamine-stimulated adenylyl cyclase. Lower cAMP reduces the L-type Ca2+ current (ICaL) and the pacemaker current (If) and slows phase 0 upstroke (decreased Vmax) (Braunwald's Heart Disease).
  5. Result at the AV node. The AH interval lengthens, with transient first-, second-, or third-degree AV block lasting a few seconds. Conduction delay is rate dependent, so the fast-firing tachycardia circuit is affected strongly. His-Purkinje conduction is generally not directly affected.

Why this terminates AVNRT

AV nodal cells depend on the slow calcium current for conduction, which makes them especially sensitive to adenosine. Block in either limb of the circuit (usually the slow, anterograde limb) interrupts the reentry loop. If the next impulse finds no path to circulate, the tachycardia stops and sinus rhythm resumes. Adenosine is nearly 100% effective in AVNRT.

Pharmacology points

  • Onset takes seconds and half-life is under 10 seconds. It is cleared quickly by red cells and endothelium (adenosine deaminase and cellular uptake).
  • It must be given as a rapid IV bolus followed by a saline flush. The usual dose is 6 mg, then 12 mg if needed.
  • It does not impair contractility.
  • Methylxanthines such as theophylline and caffeine block the A1 receptor, so higher doses may be needed.
  • Dipyridamole blocks adenosine uptake and potentiates its effect.
  • Heart transplant recipients are supersensitive, so start at about 1 mg.
  • Common side effects are transient dyspnea, chest pain, flushing, and brief sinus arrest or bradycardia.
  • Adenosine shortens the atrial refractory period, so atrial ectopy can trigger atrial fibrillation. This is dangerous if an accessory pathway can conduct rapidly.
  • It can cause bronchospasm in asthma.
  • AVNRT can recur after termination because of the short half-life. Repeat the dose or switch to a calcium channel blocker.

Recent evidence check

A quick PubMed search for recent systematic reviews and meta-analyses found nothing that changes this mechanism. One 2025 meta-analysis covers adenosine efficacy and safety in supraventricular tachycardia (PMID 40055614). Its efficacy and safety findings are consistent with the textbook account.
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