The concern with using adenosine in patients with WPW is that if the AV node is blocked than impulses from the atria will be able to reach the ventricles at a very rapid rate, since they are not slowed down through the accessory pathway as they are at the AV node. Rapid ventricular rates (ventricular tachycardia or ventricular fibrillation) lead to incomplete ventricular filling, poor output, and cardiac arrest. This is why AV nodal blockers are contraindicated in patients with WPW and atrial fibrillation, which can see atrial rates up to 600bpm.
From a pragmatic standpoint, single syringe adenosine makes sense, and although we now have two small studies that show single syringe adenosine to be non-inferior to two syringe adenosine, we have to be cautious about making robust conclusions based on this level of evidence.
While most drugs are metabolized in the liver, adenosine doesn’t even make it that far, being metabolized in the erythrocytes and vascular endothelial cells. With this extremely short half-life (10 seconds), it is important to help it reach the heart before it’s metabolized and excreted without being effective.
Go low and go slow. Although the diltiazem dose used in the Lim study was 2.5 mg/min to a maximum of 50 mg, 75% of patients had converted by 18mg. I tend to give 15 mg of diltiazem over 10 minutes. It almost always works, but when it doesn’t I just repeat the dose.
Typical doses for terminating SVT are 6mg rapid IV push and flush in a proximal, large bore IV. If this is ineffective, then two subsequent doses of 12mg can be attempted. In children under 50kg, the dose is 0.05-0.1mg/kg. This dose can be increased by 0.05-0.1mg/kg and attempted twice more, with a maximum dose of 0.3mg/kg or 12mg. There are no dosing adjustments needed for patients with renal or liver disease.
If the first dose does not result in elimination of the supraventricular tachycardia within 1-2 minutes, 12 mg should be given as a rapid intravenous bolus. This 12 mg dose may be repeated a second time if required.