Adenosine is an extremely short-acting antiarrhythmic drug that slows cardiac nodal tissue. It accomplishes this mainly via an increase in potassium efflux and a decrease in calcium influx. There is a third mechanism in which vasodilation of coronary arteries also occurs. Clinically, adenosine’s effects last 10-15 seconds, making the drug useful for treating tachycardias called PSVTs, or paroxysmal supraventricular tachycardia. Slowing down of conduction at the AV node can disrupt the timing of reentrant circuits, restoring patients to normal heart (sinus) rhythms. Importantly, adenosine can cause brief adverse effects such as a sense of impending doom, chest pain, and flushing.

Key Points

  • Adenosine
    • Mechanism
      • Very short-acting (~15 seconds)
      • Two mechanisms that primarily slow nodal tissue
        • Increases potassium efflux
          • Agonism of adenosine-1 (A1) receptors on heart activates a Gi-mediated pathway, ultimately leading to opening of potassium channels
          • K+ efflux causes hyperpolarization of nodal tissue (suppressing conduction)
          • Prolongs phase 4 of action potential
          • Effects may be blunted by theophylline and caffeine (adenosine receptor antagonists)
        • Inhibits calcium influx
          • Inhibition of L-type calcium (Ca2+) channels prevents influx of calcium in phase 0 of nodal action potential
          • Prolongs phase 4 of action potential
      • Vasodilator of coronary vessels
        • Component of natural feedback mechanism:
          • ATP is usually degraded to adenosine
          • Adenosine then crosses cell membrane and functions as a vasodilator to increase blood flow to replenish energy stores
        • Can cause coronary steal syndrome (hypoperfusion & worsening of existing myocardial ischemia)
          • Because all coronary vessels dilate, impairing physiologic shunting to the area that really needs it
    • Clinical Use
      • Paroxysmal supraventricular tachycardias (PSVTs)
        • Short duration of action is ideal for terminating PSVTs and other acute SVTs
        • PSVTs usually caused by a re-entrant electrical circuit involving AV node, which is disrupted by adenosine’s action on the AV node
          • Reentrance is highly dependent on perfect timing; cells are constantly altering between on and off states and reentry circuits are set up so APs hit them just as they are ready to depolarize.
          • Thus, if you slow down conduction with adenosine, you can disrupt timing to get them out of the arrhythmia
          • Also the drug is not in the bloodstream for long, which reduces long-term side effects -- particularly good for paroxysms, which happen occasionally and always revert back to NSR.
      • Used for pharmacologic cardiac stress tests
        • Global vasodilation of coronary arteries can worsen ischemia in ischemic sites
    • Adverse effects
      • Burning chest pain 
        • Secondary to bronchospasm
      • Sense of impending doom
        • Important because this is actually very salient in wards, and hence clinical vignettes
      • Flushing
      • High grade AV block
        • Obvious side effect of slowing AV nodal conduction
      • Transient hypotension
        • Due to reduced conduction