Get your patient on Adenosine - Adenosine injection, Solution (Adenosine)

The dose recommendation is based on clinical studies with peripheral venous bolus dosing.  Central venous (CVP or other) administration of Adenosine Injection, USP has not been systematically studied.

The recommended intravenous doses for adults are as follows:

Initial dose: 6 mg given as a rapid intravenous bolus (administered over a 1 to 2 second period).

Repeat administration: If the first dose does not result in elimination of the supraventricular tachycardia within 1 to 2 minutes, 12 mg should be given as a rapid intravenous bolus.

This 12 mg dose may be repeated a second time if required.

The dosages used in neonates, infants, children and adolescents were equivalent to those administered to adults on a weight basis.

Pediatric Patients with a Body Weight < 50 kg:

Initial dose: give 0.05 to 0.1 mg/kg as a rapid IV bolus either centrally or peripherally.  A saline flush should follow.

Repeat administration: If conversion of PSVT does not occur within 1 to 2 minutes, additional bolus injections of adenosine can be administered at incrementally higher doses, increasing the amount given by 0.05 to 0.1 mg/kg.  Follow each bolus with a saline flush.  This process should continue until sinus rhythm is established or a maximum single dose of 0.3 mg/kg is used.

Pediatric Patients with a Body Weight > 50 kg:

Administer the adult dose.

Doses greater than 12 mg are not recommended for adult and pediatric patients.

NOTE: Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration.

(see WARNINGS )

The following adverse events have been reported from marketing experience with adenosine injection.  Because these events are reported voluntarily from a population of uncertain size, are associated with concomitant diseases and multiple drug therapies and surgical procedures, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.  Decisions to include these events in labeling are typically based on one or more of the following factors: (1) seriousness of the event, (2) frequency of the reporting, (3) strength of causal connection to the drug, or a combination of these factors.

Prolonged asystole, ventricular tachycardia, ventricular fibrillation, transient increase in blood pressure, bradycardia, atrial fibrillation, and Torsades de Pointes.

Bronchospasm.

Seizure activity, including tonic clonic (grand mal) seizures, and loss of consciousness.

Adenosine slows conduction time through the A-V node, can interrupt the re-entry pathways through the A-V node, and can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT), including PSVT associated with Wolff-Parkinson-White Syndrome.

Adenosine is antagonized competitively by methylxanthines such as caffeine and theophylline, and potentiated by blockers of nucleoside transport such as dipyridamole.  Adenosine is not blocked by atropine.

The intravenous bolus dose of 6 or 12 mg adenosine injection usually has no systemic hemodynamic effects.  When larger doses are given by infusion, adenosine decreases blood pressure by decreasing peripheral resistance.

Intravenously administered adenosine is rapidly cleared from the circulation via cellular uptake, primarily by erythrocytes and vascular endothelial cells.  This process involves a specific transmembrane nucleoside carrier system that is reversible, nonconcentrative, and bidirectionally symmetrical.  Intracellular adenosine is rapidly metabolized either via phosphorylation to adenosine monophosphate by adenosine kinase, or via deamination to inosine by adenosine deaminase in the cytosol.  Since adenosine kinase has a lower K _m and V _max than adenosine deaminase, deamination plays a significant role only when cytosolic adenosine saturates the phosphorylation pathway.  Inosine formed by deamination of adenosine can leave the cell intact or can be degraded to hypoxanthine, xanthine, and ultimately uric acid.  Adenosine monophosphate formed by phosphorylation of adenosine is incorporated into the high-energy phosphate pool.  While extracellular adenosine is primarily cleared by cellular uptake with a half-life of less than 10 seconds in whole blood, excessive amounts may be deaminated by an ecto-form of adenosine deaminase.  As adenosine requires no hepatic or renal function for its activation or inactivation, hepatic and renal failure would not be expected to alter its effectiveness or tolerability.

In controlled studies in the United States, bolus doses of 3, 6, 9, and 12 mg were studied.  A cumulative 60% of patients with paroxysmal supraventricular tachycardia had converted to normal sinus rhythm within one minute after an intravenous bolus dose of 6 mg adenosine injection (some converted on 3 mg and failures were given 6 mg), and a cumulative 92% converted after a bolus dose of 12 mg.  Seven to sixteen percent of patients converted after 1 to 4 placebo bolus injections.  Similar responses were seen in a variety of patient subsets, including those using or not using digoxin, those with Wolff-Parkinson-White Syndrome, males, females, blacks, Caucasians, and Hispanics.

Adenosine is not effective in converting rhythms other than PSVT, such as atrial flutter, atrial fibrillation, or ventricular tachycardia, to normal sinus rhythm.