Version May 2024
Paroxysmal supraventricular tachycardia (PSVT): Adenocard: Rapid IV: Initial dose: 0.05 to 0.1 mg/kg; if not effective within 1 to 2 minutes, increase dose by 0.05 to 0.1 mg/kg increments every 1 to 2 minutes to a maximum dose of 0.3 mg/kg or until termination of PSVT; follow each bolus with NS flush.
Supraventricular tachycardia: Adenocard:
Hemodynamically unstable:
Infants, Children, and Adolescents: Rapid IV, Intraosseous: Initial: 0.1 mg/kg (maximum initial dose: 6 mg/dose); if not effective, increase to 0.2 mg/kg (maximum dose: 12 mg/dose); follow each bolus with NS flush (Ref).
Hemodynamically stable:
Infants, Children, and Adolescents <50 kg: Rapid IV: Initial dose: 0.05 to 0.1 mg/kg via peripheral or central line; maximum initial dose: 6 mg/dose; if not effective within 1 to 2 minutes, increase dose by 0.05 to 0.1 mg/kg increments every 1 to 2 minutes to a maximum single dose of 0.3 mg/kg or 12 mg (whichever is less) or until termination of paroxysmal supraventricular tachycardia (PSVT); follow each bolus with NS flush.
Heart transplant patients: Limited data available: Infants ≥6 months, Children, and Adolescents <50 kg: Rapid IV: Initial dose: 0.025 mg/kg; repeat dosing with gradual dose escalation has been reported (Ref).
Children and Adolescents ≥50 kg: Rapid IV: Initial: 6 mg via peripheral line, if not effective within 1 to 2 minutes, 12 mg may be given; may repeat 12 mg bolus if needed; follow each bolus with NS flush. Note: In adults, lower initial doses of 3 mg have been suggested for administration via central line (Ref).
Heart transplant patients: Limited data available: Rapid IV: Initial dose: 0.025 mg/kg (maximum initial dose: 1.5 mg/dose); repeat dosing with gradual dose escalation has been reported (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling. However, adenosine is not renally eliminated.
There are no dosage adjustments provided in the manufacturer's labeling. However, adenosine is not hepatically eliminated.
(For additional information see "Adenosine: Drug information")
Paroxysmal supraventricular tachycardia:
Note: Recommended for hemodynamically stable patients who do not respond to vagal maneuvers or for hemodynamically unstable patients. Preparations should be made for synchronized direct-current cardioversion in case adenosine is ineffective. For patients whose arrhythmia persists despite successful adenosine-induced AV block, switch to an alternative therapy. Do not use in patients with a known accessory pathway that exhibits retrograde conduction; this can lead to ventricular arrhythmias (Ref).
IV: Initial: 6 mg over 1 to 2 seconds via a peripheral line, followed immediately by an NS flush; if initial dose does not terminate the arrhythmia or cause AV block within 1 to 2 minutes, administer a second dose of 12 mg using the same procedures; if second dose does not terminate the arrhythmia or cause AV block, may administer a third dose of 12 or 18 mg using the same procedures. If supraventricular tachycardia terminates then recurs, may repeat the last effective dose as needed for a total of 3 doses (Ref).
Central line administration: Initial dose should be reduced to 3 mg with subsequent doses of 6 mg, then 9 mg, if needed (Ref).
Heart transplant patients: Initial dose should be reduced to 1 mg; may increase subsequent doses up to 3 mg, if needed (Ref).
Pharmacologic cardiac stress testing, diagnostic aid: Continuous infusion: IV (via peripheral line): 140 mcg/kg/minute for 6 minutes using syringe or volumetric infusion pump; total dose: 840 mcg/kg. Thallium-201 is injected at midpoint (3 minutes) of adenosine infusion.
Fractional flow reserve testing, diagnostic aid (off- label use):
Continuous infusion: IV (via peripheral line): 140 mcg/kg/minute during testing (Ref).
Intracoronary: 40 mcg into the right coronary artery or 80 mcg into the left coronary artery; dilute dose in 10 mL of NS and administer rapidly through the guiding catheter (Ref).
Tachyarrhythmia, diagnostic aid in hemodynamically stable patients (off-label use):
Note: May administer to hemodynamically stable patients as a diagnostic aid when trying to decipher the type of arrhythmia (eg, ventricular tachycardia vs supraventricular tachycardia with aberrancy). Do not administer to hemodynamically unstable patients or for irregular or polymorphic wide complex tachycardia (Ref).
IV: Initial: 6 mg over 1 to 2 seconds via a peripheral line, followed immediately by an NS flush; if initial dose does not terminate the arrhythmia or cause AV block within 1 to 2 minutes, administer a second dose of 12 mg using the same procedures; if second dose does not terminate the arrhythmia or cause AV block, may administer a third dose of 12 or 18 mg using the same procedures (Ref).
Central line administration: Initial dose should be reduced to 3 mg with subsequent doses of 6 mg, then 9 mg, if needed (Ref).
Heart transplant patients: Initial dose should be reduced to 1 mg; may increase subsequent doses up to 3 mg, if needed (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling. Adenosine is not renally eliminated.
There are no dosage adjustments provided in the manufacturer's labeling. Adenosine is not hepatically eliminated.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Frequency varies based on use and is not always defined; higher frequency of infusion-related effects, such as flushing and lightheadedness/dizziness, were reported with continuous infusion (Adenoscan).
>10%:
Cardiovascular: Cardiac arrhythmia (transient and new arrhythmia after cardioversion; eg, atrial premature contractions, atrial fibrillation, premature ventricular contractions; 55%), chest pressure (and discomfort; 7% to 40%)
Central nervous system: Headache (2% to 18%), dizziness (≤12%)
Dermatologic: Facial flushing (18% to 44%)
Gastrointestinal: Gastrointestinal distress (13%)
Neuromuscular & skeletal: Neck discomfort (includes throat, jaw; <1% to 15%)
Respiratory: Dyspnea (12% to 28%)
1% to 10%:
Cardiovascular: Atrioventricular block (infusion 6%; third-degree <1%), depression of ST segment on ECG (3%), hypotension (<1% to 2%), chest pain, palpitations
Central nervous system: Nervousness (2%), paresthesia (≤2%), numbness (1%), apprehension
Dermatologic: Diaphoresis
Gastrointestinal: Nausea (3%)
Neuromuscular & skeletal: Upper extremity discomfort (≤4%)
Respiratory: Hyperventilation
<1%, postmarketing, and/or case reports: Asystole (prolonged), atrial fibrillation, blurred vision, bradycardia, bronchospasm, burning sensation, cardiac arrest (fatal and nonfatal), increased intracranial pressure, injection site reaction, loss of consciousness, metallic taste, myocardial infarction, respiratory arrest, seizure, torsades de pointes, transient hypertension, ventricular arrhythmia, ventricular fibrillation, ventricular tachycardia
Hypersensitivity to adenosine or any component of the formulation; second- or third-degree AV block, sick sinus syndrome, or symptomatic bradycardia (except in patients with a functioning artificial pacemaker); known or suspected bronchoconstrictive or bronchospastic lung disease, asthma (manufacturer's labeling).
Concerns related to adverse effects:
• Atrial fibrillation/flutter: There have been reports of atrial fibrillation/flutter when administered to patients with paroxysmal supraventricular tachycardia (PSVT) and may be especially problematic in patients with PSVT and underlying Wolff-Parkinson-White syndrome; has also been reported in patients with or without a history of atrial fibrillation undergoing myocardial perfusion imaging with adenosine infusion.
• Cardiovascular events: Cardiac arrest (fatal and nonfatal), myocardial infarction, cerebrovascular accident (hemorrhagic and ischemic), and sustained ventricular tachycardia (requiring resuscitation) have occurred when used for pharmacologic stress testing. Avoid use in patients with signs or symptoms of unstable angina, acute myocardial ischemia, or cardiovascular instability due to possible increased risk of significant cardiovascular consequences. Appropriate measures for resuscitation should be available during use.
• Conduction disturbances: Adenosine decreases conduction through the AV node and may produce first-, second-, or third-degree heart block. Patients with preexisting SA nodal dysfunction may experience prolonged sinus pauses after adenosine; use caution in patients with first-degree atrioventricular (AV) block or bundle branch block; use is contraindicated in patients with high-grade AV block, sinus node dysfunction, or symptomatic bradycardia (unless a functional artificial pacemaker is in place). Rare, prolonged episodes of asystole have been reported, with fatal outcomes in some cases. Discontinue adenosine in any patient who develops persistent or symptomatic high-grade AV block.
• Hypersensitivity: Hypersensitivity reactions (including dyspnea, pharyngeal edema, erythema, flushing, rash, or chest discomfort) have been reported.
• Hypertension: Systolic and diastolic pressure increases have been observed. In most instances, blood pressure increases resolved spontaneously within several minutes; occasionally, hypertension lasted for several hours.
• Hypotension: May produce profound vasodilation with subsequent hypotension. When used as a bolus dose (PSVT), effects are generally self-limiting (due to the short half-life of adenosine). However, when used as a continuous infusion (pharmacologic stress testing), effects may be more pronounced and persistent, corresponding to continued exposure. Use infusions with caution in patients with autonomic dysfunction, carotid stenosis (with cerebrovascular insufficiency), hypovolemia, pericarditis, pleural effusion and/or stenotic valvular heart disease; discontinue infusion in patients who develop persistent or symptomatic hypotension.
• Proarrhythmic effects: Monitor for proarrhythmic effects (eg, polymorphic ventricular tachycardia) during and shortly after administration/termination of arrhythmia. The benign transient occurrence of atrial and ventricular ectopy is common upon termination of arrhythmia.
• Seizures: Seizures (new-onset or recurrent) have been reported; risk may be increased with concurrent use of aminophylline. Concomitant use of any methylxanthine (eg, aminophylline, caffeine, theophylline) is not recommended.
Disease-related concerns:
• Arrhythmia (wide-complex tachycardia): Avoid use in irregular or polymorphic wide-complex tachycardias; may cause degeneration to ventricular fibrillation (AHA [Neumar 2010]).
• Heart transplant recipients: Use with extreme caution in heart transplant recipients; adenosine may cause prolonged asystole; reduction of initial adenosine dose is recommended (AHA [Neumar 2010]); considered by some to be contraindicated in this setting (Delacrétaz 2006).
• Pulmonary artery hypertension: Acute vasodilator testing (not an approved use): Use with extreme caution in patients with concomitant heart failure (LV systolic dysfunction with significantly elevated left heart filling pressures) or pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis; significant decompensation has occurred with other highly selective pulmonary vasodilators resulting in acute pulmonary edema.
• Respiratory disease: Avoid use in patients with bronchoconstriction or bronchospasm (eg, asthma); dyspnea, bronchoconstriction, and respiratory compromise have occurred during use. Use caution in patients with obstructive lung disease not associated with bronchoconstriction (eg, emphysema, bronchitis). Immediately discontinue therapy if severe respiratory difficulty is observed. Appropriate measures for resuscitation should be available during use.
• Wolff-Parkinson-White (WPW) syndrome: Adenosine should not be used in patients with WPW syndrome and preexcited atrial fibrillation/flutter since ventricular fibrillation may result (AHA/ACC/HRS [January 2014]).
Concurrent drug therapy issues:
• Caffeine: Pharmacologic stress testing: Since caffeine antagonizes the activity of adenosine, withhold for 5 half-lives prior to adenosine use; avoid dietary caffeine for at least 12 hours prior to pharmacologic stress testing (ASNC [Henzlova 2016]).
• Dipyridamole: Concomitant use potentiates the effects of adenosine; reduction of initial adenosine dose is recommended when used for SVT (AHA [Neumar 2010]); withhold dipyridamole-containing medications for at least 48 hours prior to pharmacologic stress testing (ASNC [Henzlova 2016]).
• Theophylline or aminophylline: Pharmacologic stress testing: Since methylxanthines antagonizes the activity of adenosine, withhold for 5 half-lives prior to adenosine use whenever possible.
Special populations:
• Older adult: Use with caution in older patients; may be at increased risk of hemodynamic effects, bradycardia, and/or AV block.
Dosage form specific issues:
• Atrioventricular block: Transient AV block is expected when administered as an IV bolus for treatment of paroxysmal supraventricular tachycardia (PSVT). When used for PSVT, at the time of conversion to normal sinus rhythm, a variety of new rhythms may appear on the ECG. Administer as a rapid bolus, either directly into a vein or (if administered into an IV line), as close to the patient as possible (followed by saline flush). Dose reduction recommended when administered via central line (AHA [Neumar 2010]).
Other warnings/precautions:
• Appropriate use: ECG monitoring is required during use. Equipment for resuscitation and trained personnel experienced in handling medical emergencies should always be immediately available. Adenosine does not convert atrial fibrillation/flutter to normal sinus rhythm; however, may be used diagnostically in these settings if the underlying rhythm is not apparent.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution, Intravenous:
Generic: 3 mg/mL (20 mL, 30 mL); 6 mg/2 mL (2 mL); 12 mg/4 mL (4 mL)
Solution, Intravenous [preservative free]:
Adenocard: 12 mg/4 mL (4 mL [DSC])
Generic: 3 mg/mL (20 mL, 30 mL); 6 mg/2 mL (2 mL); 12 mg/4 mL (4 mL)
Yes
Solution (Adenosine (Diagnostic) Intravenous)
3 mg/mL (per mL): $6.68 - $7.80
Solution (Adenosine Intravenous)
6 mg/2 mL (per mL): $3.60 - $9.60
12 mg/4 mL (per mL): $3.00 - $7.80
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution, Intravenous:
Adenocard: 3 mg/mL ([DSC])
Generic: 3 mg/mL (2 mL, 4 mL); 6 mg/2 mL (2 mL); 12 mg/4 mL (4 mL)
Not effective in atrial flutter, atrial fibrillation, or ventricular tachycardia; short duration of action is an advantage as adverse effects are usually rapidly self-limiting; effects may be prolonged in patients with denervated transplanted hearts.
Parenteral: Adenocard: For rapid bolus IV use, administer over 1 to 2 seconds at peripheral IV site closest to patient's heart (IV administration into lower extremities may result in therapeutic failure or requirement of higher doses); follow each bolus with NS flush (infants and children: 5 to 10 mL; adults: 20 mL); Note: The use of 2 syringes (one with adenosine dose and the other with NS flush) connected to a T-connector or stopcock is recommended for IV and intraosseous administration (Ref).
IV: For rapid IV bolus use; administer IV push over 1 to 2 seconds at a peripheral IV site as proximal as possible to trunk (not in lower arm, hand, lower leg, or foot); immediately after each bolus, administer an NS flush. Use of 2 syringes (one with adenosine dose and the other with NS flush) connected to a T-connector or stopcock is recommended. Alternatively, if no stopcock is available or the patient only has a single-port IV, prepare a single syringe with adenosine 6 mg and 18 mL of NS and administer at a peripheral IV site (Ref).
Fractional flow reserve testing (off-label use): Intracoronary: Administer rapidly followed by a 10 mL NS flush (Ref).
For IV continuous infusion: Only administer via a peripheral line.
Store at 20°C to 25°C (68°F to 77°F); excursions permitted between 15°C and 30°C (59°F and 86°F). Do not refrigerate; crystallization may occur (may dissolve by warming to room temperature).
Adenocard: Treatment of paroxysmal supraventricular tachycardia (PSVT), including that associated with accessory bypass tracts (eg, Wolff-Parkinson-White syndrome) (FDA approved in all ages); Note: When clinically advisable, appropriate vagal maneuvers should be attempted prior to adenosine administration.
Has also been used according to PALS algorithm for probable supraventricular tachycardia with a pulse and wide-complex ventricular tachycardia with a pulse as a therapeutic (if arrhythmia supraventricular) and as a diagnostic maneuver.
Adenoscan: Pharmacologic stress agent used in myocardial perfusion thallium-201 scintigraphy (FDA approved in adults).
This medication is in a class the Institute for Safe Medication Practices (ISMP) includes among its list of drug classes that have a heightened risk of causing significant patient harm when used in error.
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Risk C: Monitor therapy
Caffeine and Caffeine Containing Products: May diminish the therapeutic effect of Adenosine. Management: Monitor for decreased effect of adenosine if patient is receiving caffeine; significantly higher adenosine doses or alternative agents may be required. Discontinue caffeine 24 hours in advance of scheduled diagnostic use of adenosine if possible. Risk D: Consider therapy modification
CarBAMazepine: May enhance the adverse/toxic effect of Adenosine. Specifically, the risk of higher degree heart block may be increased. Management: Monitor for increased degrees of heart block and bradycardia when these agents are combined. Consider using a lower initial dose of adenosine (3 mg) for the treatment of supraventricular tachycardia in patients who are receiving carbamazepine. Risk C: Monitor therapy
Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider therapy modification
Digoxin: May enhance the adverse/toxic effect of Adenosine. Risk C: Monitor therapy
Dipyridamole: May enhance the adverse/toxic effect of Adenosine. Specifically, cardiovascular effects of adenosine may be enhanced. Adenosine dose reduction may be needed. Management: For patients requiring pharmacologic stress testing with adenosine, hold dipyridamole tablets for 48 hours. Hold aspirin/dipyridamole capsules for 24 to 48 hours. For treatment of SVT, monitor for prolonged adenosine effects, consider lower initial doses. Risk D: Consider therapy modification
Etrasimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Fexinidazole: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole. Risk X: Avoid combination
Fingolimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider therapy modification
Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Risk C: Monitor therapy
Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Risk C: Monitor therapy
Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Nicotine: May enhance the AV-blocking effect of Adenosine. Nicotine may enhance the tachycardic effect of Adenosine. Risk C: Monitor therapy
Ozanimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Ponesimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider therapy modification
Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider therapy modification
Theophylline Derivatives: May diminish the therapeutic effect of Adenosine. Management: Consider alternatives to this combination if possible. Theophylline may decrease adenosine efficacy and higher adenosine doses may be required. When using adenosine for diagnostic studies, discontinue theophylline derivatives 5 half-lives prior to test. Risk D: Consider therapy modification
Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy
Avoid dietary caffeine for at least 12 hours prior to pharmacologic stress testing.
Animal reproduction studies have not been conducted. Adenosine is an endogenous substance and adverse fetal effects would not be anticipated. Adenosine is recommended for the acute treatment of SVT in pregnant women. The usual recommended doses may be used, although higher doses may be needed in some cases (ACC/AHA/HRS [Page 2016]). AHA guidelines suggest use is safe and effective in pregnancy (AHA [Neumar 2010]).
Continuous ECG, heart rate, blood pressure, respirations.
Antiarrhythmic actions: Slows conduction time through the AV node, interrupting the re-entry pathways through the AV node, restoring normal sinus rhythm
Myocardial perfusion scintigraphy: Adenosine also causes coronary vasodilation and increases blood flow in normal coronary arteries with little to no increase in stenotic coronary arteries; thallium-201 uptake into the stenotic coronary arteries will be less than that of normal coronary arteries revealing areas of insufficient blood flow.
Onset of action: Rapid
Duration: Very brief
Metabolism: Removed from systemic circulation primarily by vascular endothelial cells and erythrocytes (by cellular uptake); rapidly metabolized intracellularly; phosphorylated by adenosine kinase to adenosine monophosphate (AMP) which is then incorporated into high-energy pool; intracellular adenosine is also deaminated by adenosine deaminase to inosine; inosine can be metabolized to hypoxanthine, then xanthine and finally to uric acid.
Half-life elimination: <10 seconds
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