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An antiarrhythmic agent for PSVT including those associated with WPW; is an effective "diagnostic aid" in wide complex tachycardias where it is preferred over verapamil because its effects are more transient; adenosine effectiveness in PSVT is equal to verapamil; not effective in managing atrial arrhythmias such as a. flutter/fib, atrial ectopic foci or in converting v. tach.
Adenocard/Adenoscan/Adenosine Intravenous Inj Sol: 1mL, 3mgAdenocard/Adenoscan/Adenosine Intravenous Sol: 1mL, 3mg
6 mg by rapid IV/IO bolus followed immediately by a 20 mL saline flush. If conversion does not occur within 1 to 2 minutes, then administer 12 mg by rapid IV/IO bolus. May repeat the 12 mg dose once if needed. Single doses greater than 12 mg are not recommended. The initial dose should be decreased to 3 mg in patients taking carbamazepine or dipyridamole, in those with a transplanted heart, or in those receiving the drug by central venous access.
0.1 mg/kg/dose by rapid IV/IO bolus followed immediately by a saline flush. If conversion does not occur within 1 to 2 minutes, then administer 0.2 mg/kg/dose by rapid IV/IO bolus. The manufacturer recommends an initial dose of 0.05 to 0.1 mg/kg IV, with the dose increased in 0.05 to 0.1 mg/kg increments, up to 0.3 mg/kg IV (Max: 12 mg/dose). However, studies have shown that initial doses of 0.05 mg/kg/dose and 0.1 mg/kg/dose terminated the arrhythmia in less than 10% and less than 37% of pediatric patients who received these doses, respectively. The median effective dose was approximately 0.2 mg/kg in infants and 0.1 to 0.15 mg/kg in children, leading some experts to recommend higher initial doses of 0.2 mg/kg/dose. Although no specific recommendations are available in children, a 50% initial dose reduction is recommended in adolescents/adults receiving carbamazepine or dipyridamole, in those with a transplanted heart, or in those receiving the drug by central venous access.
0.05 to 0.1 mg/kg/dose by rapid IV/IO bolus followed immediately by a saline flush. If conversion does not occur within 1 to 2 minutes, additional boluses may be administered at incrementally higher doses increasing by 0.05 to 0.1 mg/kg with each dose up to a maximum of 0.3 mg/kg/dose. Studies have shown that initial doses of 0.05 mg/kg/dose and 0.1 mg/kg/dose terminated the arrhythmia in less than 10% and less than 37% of pediatric patients who received these doses, respectively. The median effective dose was approximately 0.2 mg/kg in neonates and infants, leading some experts to recommend higher initial doses of 0.2 mg/kg/dose.
NOTE: The adenosine infusion rate can be calculated from the following formula: Infusion rate (mL/min) = [0.140 (mg/kg/min) x total body weight (kg)] divided by the Adenoscan concentration (3 mg/mL).
140 mcg/kg/minute IV infused for 6 minutes for a total dose of 0.84 mg/kg. The dose of thallium-201 should be injected after the first 3 minutes of adenosine infusion. The thallium injection should be made as close as possible to the venous access to prevent an inadvertent increase in the dose of adenosine.
See adult dosage. In general, use adenosine with caution in the elderly since older patients may have cardiac dysfunction, nodal dysfunction, or concomitant diseases or drug therapy that may alter hemodynamic function and increase risk for severe bradycardia or AV block.
50 mcg/kg/minute IV titrated by 50 mcg/kg/minute every 2 minutes up to a maximum of 250 mcg/kg/minute. Clinical practice guidelines suggest that patients with pulmonary arterial hypertension undergo acute vasoreactivity testing with a short-acting agent in the absence of contraindications, including low systemic blood pressure, low systemic cardiac output, or the presence of functional class (FC) IV symptoms. Acute vasoreactivity is defined as a fall in mean pulmonary artery pressure (mPAP) more than 10 mmHg, to an mPAP less than 40 mmHg, with an unchanged or increased cardiac output.
0.1 mg/kg/dose rapid IV/IO push (Max: 6 mg/dose) followed immediately by a saline flush. If necessary, may administer a second dose of 0.2 mg/kg/dose rapid IV/IO push (Max: 12 mg/dose) followed by a saline flush. When IV access is available, administer through IV access that is closest to the heart. Consider adenosine use only if the rhythm is regular and the QRS is monomorphic. Do not use adenosine in patients with Wolff-Parkinson-White syndrome and wide-complex tachycardia.
†Indicates off-label use
12 mg/dose IV, with maximum total dosage up to 30 mg for PSVT.
>= 50 kg: 12 mg/dose IV, with maximum total dosage up to 30 mg for PSVT.< 50 kg: 0.3 mg/kg/dose IV or 12 mg/dose IV, whichever is less, for PSVT.
0.3 mg/kg/dose IV or 12 mg/dose IV, whichever is less, for PSVT.
0.3 mg/kg/dose IV for PSVT.
No dosage adjustment is needed.
No dosage adjustment is needed. Intermittent hemodialysisNo dosage adjustment is needed.
NOTE: Prior to administration of the stress test, screen all candidates for their suitability to receive the drug and have ready access to cardiac resuscitation equipment and a trained medical staff. NOTE: Appropriate vagal maneuvers should be instituted prior to the initiation of adenosine, unless otherwise contraindicated (i.e. carotid massage in patient with carotid artery atherosclerotic disease).
Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
Adenocard injection:Vials are for single-dose use; discard any unused portion.Administer undiluted by rapid intravenous bolus (over 1—2 seconds).To be certain the solution reaches the systemic circulation, inject directly into either a peripheral vein or into an IV line (one that is placed as proximal to the systemic circulation as possible). If injected into an IV line, immediately follow adenosine injection with a rapid saline flush (>= 5mL). If injected into the antecubital vein, the ACLS guidelines suggest a saline flush of 20 mL following dose administration, followed by elevation of the arm.Adenoscan injection:Vials are for single-dose use; discard any unused portion.Administer undiluted by peripheral intravenous infusion using a syringe pump or a volumetric infusion pump (see Dosage for infusion rate calculation).
Intraosseous administration:NOTE: Adenocard is not approved by the FDA for intraosseous administration.During cardiopulmonary resuscitation, the same dosage of adenosine (Adenocard) may be given via the intraosseous route when IV access is not available (see Dosage).
Adenocard:- Discard product if it contains particulate matter, is cloudy, or discolored- Discard unused portion. Do not store for later use.- Do not refrigerate- Store at controlled room temperature (between 68 and 77 degrees F)Adenoscan:- Discard product if it contains particulate matter, is cloudy, or discolored- Discard unused portion. Do not store for later use.- Do not refrigerate- Store at controlled room temperature (between 68 and 77 degrees F)
Prior to receiving adenosine for stress imaging, patients should avoid intake of products containing caffeine, aminophylline, theophylline, and dipyridamole for at least 24 hours. Methylxanthines block the effects of adenosine. Dipyridamole potentiates the effects of adenosine.
Cases of hemodynamically unstable proarrhythmic events have been reported in patients with Wolff-Parkinson-White syndrome (WPW) after adenosine treatment. Although adenosine has been shown to be safe and effective in treating tachyarrhythmias in patients with WPW syndrome, it should be used with caution in patients with WPW syndrome who present with atrial fibrillation with rapid ventricular response. Adenosine is not effective in managing atrial flutter, atrial fibrillation, or ventricular tachycardia, and it should not be used to control these arrhythmias.
Adenosine is contraindicated in patients with sinus node disease, such as sick sinus syndrome or symptomatic bradycardia, and in patients with second- or third-degree AV block, except in patients with a functioning artificial pacemaker in place. Adenosine should be given cautiously to patients with pre-existing first-degree AV block or bundle-branch block. Because adenosine decreases conduction through the AV node, first-, second-, or third-degree heart block are possible effects. If a patient develops a high-level block after the initial dose of adenosine, subsequent doses should not be given. In addition, new rhythms commonly result from adenosine administration (approximately 55% of patients); new rhythms are usually transient and self-limiting due to adenosine's short half-life. However, serious, even fatal rhythm disturbances have occurred; electrocardiogram monitoring, appropriate resuscitative measures, and trained personnel must be available at the time of adenosine administration. New rhythms may include premature ventricular contractions, atrial fibrillation, sinus tachycardia, sinus bradycardia, varying degrees of AV block, ventricular fibrillation, and transient or prolonged asystole (some cases have resulted in death).
Use adenosine cautiously in patients with autonomic neuropathy, stenotic valvular heart disease, pericarditis or pericardial effusion, stenotic carotid artery disease with cerebrovascular insufficiency, or uncorrected hypovolemia. Due to potent peripheral vasodilatory effects, adenosine can cause significant hypotension in susceptible patients. Patients with any of the above conditions may not have an intact baroreceptor response (increased heart rate and cardiac output) to maintain blood pressure and tissue perfusion. Discontinue adenosine in any patient who develops symptomatic or persistent hypotension. Cerebrovascular accidents have been reported with adenosine; these adverse reactions may be associated with the hemodynamic effects of the drug.
Prior to administration of adenosine as part of a cardiac nuclear stress test, screen all candidates for their suitability to receive the drug; rare cases of myocardial infarction and death have occurred. Avoid adenosine use in patients with signs/symptoms of unstable angina or cardiovascular instability because they may be at increased risk for cardiovascular adverse events. Cardiac resuscitation equipment and a trained medical staff must be readily available. If a serious reaction occurs, consider use of theophylline (an adenosine antagonist) to shorten the duration of increased coronary blood flow. Adenosine induces arterial vasodilation, resulting in increased blood flow to unblocked/unobstructed arteries and decreased blood flow to obstructed arteries. In some patients, reduced blood flow within obstructed arteries can result in myocardial infarction (MI), which may be fatal. An analysis of the FDA Adverse Event Reporting System (FAERS) has associated the use of adenosine administered as part of a cardiac nuclear stress test with 6 cases of MI and 27 cases of death; the majority occurred within 6 hours of drug administration. Of the 27 deaths, the most commonly reported adverse events were cardiorespiratory arrest, dyspnea, cardiac arrest, respiratory arrest, and ventricular arrhythmias (tachycardia).
The use of adenosine for myocardial perfusion imaging is contraindicated in patients with bronchoconstrictive or bronchospastic lung disease (e.g., asthma). When considering other uses, adenosine should be avoided in patients with bronchoconstriction or acute bronchospasm. Adenosine is a respiratory stimulant and IV administration has been shown to increase minute ventilation and reduce arterial PCO2, causing respiratory alkalosis. Use of adenosine in patients with asthma has resulted in mild to moderate exacerbation of their symptoms. In addition, respiratory compromise has occurred during adenosine infusion in patients with chronic obstructive pulmonary disease (COPD). Therefore, adenosine should be used with caution in patients with COPD that is not associated with bronchoconstriction (e.g., emphysema, chronic bronchitis). Discontinue adenosine if a patient develops severe respiratory symptoms.
Clinical studies of adenosine did not include sufficient numbers of geriatric subjects to determine whether they respond differently compared to younger subjects. In general, use adenosine use with caution in geriatric patients since this population may have a diminished cardiac function, nodal dysfunction, or concomitant diseases that may alter hemodynamic function and increase the risk of severe bradycardia or AV block. The federal Omnibus Budget Reconciliation Act (OBRA) regulates medication use in residents of long-term care facilities; adenosine is not typically given in the skilled care setting. The OBRA guidelines caution that antiarrhythmics can have serious adverse effects (e.g., impairment of mental function, appetite, behavior, heart function, or falls) in older individuals.
Adenosine is classified as FDA pregnancy risk category C. There are no adequate human studies of the effects of this drug on the fetus; however, adenosine is a naturally occurring material and dispersed widely in the body; fetal effects are not anticipated. Adenosine should be used during pregnancy only if clearly needed.
It is not known if adenosine is excreted into human milk. No specific precautions for breast-feeding are provided by the manufacturer given its intended use, rapid IV bolus administration, and rapid elimination from the body (see Pharmacokinetics). Because of adenosine's extremely short half-life (< 10 seconds), clinically relevant breast milk concentrations are not expected. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally administered drug, healthcare providers are encouraged to report the adverse effect to the FDA.
Use adenosine with caution and careful monitoring in heart transplant recipients. Adult data has shown a supersensitivity of the transplanted heart to adenosine. While not a contraindication documented by the manufacturer, some experts warn against use in heart transplant patients. Other experts recommend an initial dosage reduction in this population.
Use adenosine with caution in patients with a history of seizure disorder. During post-market use, adenosine has been associated with the development of new-onset and recurrent convulsive type seizures (tonic-clonic or grand mal seizures). In some cases, the seizures were prolonged and required emergent anticonvulsive treatment. Advise patients who experience an adenosine-associated seizure to avoid use of methylxanthines (caffeine, aminophylline, theophylline), as these drugs may increase the seizure risk.
AV block / Early / 3.0-3.0arrhythmia exacerbation / Early / 1.0-1.0ventricular fibrillation / Early / 0-1.0bradycardia / Rapid / 0-1.0myocardial infarction / Delayed / 0-1.0atrial fibrillation / Early / Incidence not knownstroke / Early / Incidence not knownseizures / Delayed / Incidence not knownintracranial bleeding / Delayed / Incidence not knownbronchospasm / Rapid / Incidence not knownrespiratory arrest / Rapid / Incidence not knownheart failure / Delayed / Incidence not knowncardiac arrest / Early / Incidence not known
chest pain (unspecified) / Early / 40.0-40.0dyspnea / Early / 28.0-28.0hypotension / Rapid / 2.0-2.0sinus tachycardia / Rapid / 0-1.0palpitations / Early / 0-1.0hypertension / Early / 0-1.0blurred vision / Early / 0-1.0vaginal pain / Early / 0-1.0scotomata / Delayed / 0-1.0
flushing / Rapid / 44.0-44.0headache / Early / 18.0-18.0dizziness / Early / 12.0-12.0paresthesias / Delayed / 2.0-2.0anxiety / Delayed / 2.0-2.0syncope / Early / 0-1.0back pain / Delayed / 0-1.0weakness / Early / 0-1.0tremor / Early / 0-1.0drowsiness / Early / 0-1.0cough / Delayed / 0-1.0diaphoresis / Early / 0-1.0urinary urgency / Early / 0-1.0xerostomia / Early / 0-1.0metallic taste / Early / 0-1.0nasal congestion / Early / 0-1.0otalgia / Early / 0-1.0nausea / Early / Incidence not knowninjection site reaction / Rapid / Incidence not knownvomiting / Early / Incidence not known
Aspirin, ASA; Dipyridamole: (Major) Adenosine effects are potentiated by dipyridamole; consider reducing the dose of adenosine in patients taking dipyridamole. When adenosine is used in adult patients for supraventricular tachycardia, reduce the initial dose to 3 mg (50% dosage reduction). Dipyridamole inhibits the metabolism of adenosine and blocks its uptake by erythrocytes, thereby enhancing the actions of adenosine when administered concomitantly. Although adenosine's duration of action is short and therefore not likely to cause a considerable interaction, serious adverse events have been reported. Beta-adrenergic blockers: (Moderate) Because the pharmacologic effects of beta-blockers include depression of AV nodal conduction and myocardial function, additive effects are possible when used in combination with adenosine. The risk of additive inhibition of AV conduction is symptomatic bradycardia with hypotension or advanced AV block; whereas additive negative inotropic effects could precipitate overt heart failure in some patients. Caffeine: (Major) Methylxanthines, such as caffeine, competitively block the effects of adenosine. Patients receiving adenosine should be monitored for decreased efficacy of adenosine. Carbamazepine: (Major) Carbamazepine can increase the degree of heart block precipitated by other cardioactive agents including adenosine. Colesevelam: (Moderate) Colesevelam may decrease the absorption of adenosine if coadministered. To minimize potential for interactions, consider administering adenosine at least 1 hour before or at least 4 hours after colesevelam; monitor drug response and/or serum drug concentrations. Digoxin: (Major) Adenosine has been safely administered with digoxin, but should be used with caution and monitoring. Because of the potential for additive or synergistic depressant effects on SA and AV nodes, however, adenosine should be used with caution in the presence of agents that slow cardiac conduction, especially digoxin. Digoxin and less frequently digoxin with verapamil may be rarely associated with ventricular fibrillation when combined with adenosine. Appropriate resuscitative measures should be available during combined therapy. Dipyridamole: (Major) Adenosine effects are potentiated by dipyridamole; consider reducing the dose of adenosine in patients taking dipyridamole. When adenosine is used in adult patients for supraventricular tachycardia, reduce the initial dose to 3 mg (50% dosage reduction). Dipyridamole inhibits the metabolism of adenosine and blocks its uptake by erythrocytes, thereby enhancing the actions of adenosine when administered concomitantly. Although adenosine's duration of action is short and therefore not likely to cause a considerable interaction, serious adverse events have been reported. Ginger, Zingiber officinale: (Minor) In vitro studies have demonstrated the positive inotropic effects of ginger, Zingiber officinale. It is theoretically possible that ginger could affect the action of antiarrhythmics, however, no clinical data are available. Green Tea: (Major) Some, but not all, green tea products contain caffeine. Methylxanthines, such as caffeine, competitively block the effects of adenosine, although this action may only occur at doses of caffeine higher than are usually administered in clinical practice. Nevertheless, larger doses of adenosine may be required for therapeutic effect if administered to patients with high daily caffeine intakes. Guarana: (Major) Methylxanthines, such as caffeine, theophylline, and theobromine, which are all found in guarana, competitively block the effects of adenosine. Larger doses of adenosine may be required for therapeutic effect if administered to patients who are using guarana. Inotersen: (Moderate) Use caution with concomitant use of inotersen and adenosine due to the potential risk of bleeding from thrombocytopenia. Consider discontinuation of adenosine in a patient taking inotersen with a platelet count of less than 50,000 per microliter. Methylxanthines: (Major) Methylxanthines, such as theophylline, aminophylline, or caffeine, competitively block the effects of adenosine. If possible, stop use of methylxanthines at least 5 half-lives prior to administering adenosine. Patients receiving theophylline, aminophylline and adenosine should be monitored for adenosine efficacy; larger doses of adenosine may be required to achieve antiarrhythmic goals in some patients. In addition, larger doses of adenosine may be required for therapeutic effect if administered to patients with high daily caffeine intake (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate). Theophylline, aminophylline may increase the risk of seizures associated with adenosine; avoid methylxanthine use in patients who have experienced an adenosine-associated seizure. Methylxanthines, such as caffeine, theophylline, and theobromine, are also found in guarana. Nicotine: (Major) Nicotine has been reported to enhance the cardiovascular effects of adenosine; an increase in angina-like chest pains, heart rate or a decrease in blood pressure may be noted. While no special cautions are recommended when adenosine is used therapeutically to treat supraventricular tachycardia, it may be advisable for patients to avoid nicotine products or tobacco prior to electrophysiologic studies or stress testing where adenosine will be administered. Tobacco: (Major) Nicotine has been reported to enhance the cardiovascular effects of adenosine; an increase in angina-like chest pains, heart rate or a decrease in blood pressure may be noted. While no special cautions are recommended when adenosine is used therapeutically to treat supraventricular tachycardia, it may be advisable for patients to avoid nicotine products or tobacco prior to electrophysiologic studies or stress testing where adenosine will be administered.
Mechanism of Action: Adenosine is a metabolic product of adenosine monophosphate (which also occurs as a diphosphorylated (ADP) or triphosphorylated (ATP) compound) and is found in all human cells. During periods of hypoxia, nucleotidases in the cardiac myocytes increase the concentration of adenosine in the cell by inducing the hydrolysis of AMP. Endogenous adenosine may be involved in mediating the balance between oxygen delivery and oxygen consumption in the heart. The drug's vasodilatory, antiadrenergic, and negative chronotropic properties act to decrease cardiac oxygen demand, possibly protecting the myocardium during hypoxic episodes.Adenosine produces electrophysiologic changes by stimulating adenosine-sensitive potassium channels in the atrial and sinoatrial node, causing an outward flow of potassium from the cardiac myocytic membrane, which acts to induce sinus bradycardia. Thus, the drug hyperpolarizes atrial tissues, reducing the duration of the atrial action potential. Adenosine reduces the diastolic depolarization phase of the sinoatrial nodal pacemaker cells, but, unlike calcium-channel blocking agents, adenosine does not affect the upstroke phase of the action potential of sinus-node cells. The drug does, however, reduce the upstroke phase of the action potential of atrioventricular ("N") cells, resulting in atrioventricular nodal blockade and reduction of accessory-pathway antegrade refractoriness. The ionic mechanism of the drug's action on the atrioventricular node is unknown.Adenosine's use as a adjunct to thallium-201 scintigraphy stems from adenosine's ability to increase blood flow in normal coronary arteries with little or no change in stenotic arteries. The myocardial uptake of thallium-201 is directly proportional to the coronary blood flow. During myocardial imaging with adenosine and thallium-201, areas supplied by stenotic arteries show less uptake of thallium-201 as compared to normal arteries.Methylxanthines competitively block the effects of adenosine, but the activity of adenosine is not antagonized by atropine. Dipyridamole, a nucleoside transport blocking agent, inhibits the cellular uptake of adenosine, thereby enhancing its effects. There appear to be no clinically significant adverse reactions when adenosine is administered concomitantly with other cardioactive agents including digitalis, quinidine, beta-adrenergic blocking agents, calcium-channel blocking agents, and angiotensin converting agent inhibitors.
Adenosine is administered intravenously. Rapid metabolism of adenosine results in an extremely short plasma half-life (less than 10 seconds with intravenous doses). Due to this short half-life, it is not known how adenosine is excreted.
Following rapid intravenous administration, adenosine is promptly taken up by erythrocytes and cells of the vascular endothelium, then deaminated to inosine and phosphorylated to adenosine monophosphate (AMP) by cellular enzymes. Inosine may remain unchanged or degraded to hypoxanthine, xanthine, and eventually uric acid. AMP is added to the high-energy phosphate pool.