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Adenocard (Adenosine)
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Pharmacology
Adenosine is an endogenous nucleoside occurring in all cells of the body. When injected i.v. adenosine slows atrioventricular (AV) nodal conduction, can interrupt the reentry pathways through the AV 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.
In controlled clinical trials, cumulative 60% and 92% of patients converted to normal sinus rhythm within 1minute after 6mg and 12mg bolus doses of adenosine, respectively. In other controlled clinical trials with bolus doses of 3, 6, 9 and 12mg some patients with paroxysmal supraventricular tachycardia converted to normal sinus rhythm on 3mg of adenosine. Reports in the medical literature indicate success in treating PSVT in pediatric patients (including newborns) with adenosine in doses equivalent by weight to those used in adults.
Adenosine is not effective in converting rhythms other than PSVT, such as atrial flutter, atrial fibrillation, or ventricular tachycardia to normal sinus rhythm.
Hemodynamics: Adenosine is a potent vasodilator in most vascular beds, except in renal afferent arterioles and hepatic veins where it produces vasoconstriction. The i.v. bolus dose of 6or 12mg adenosine usually has no systemic hemodynamic effects. When larger doses are given by infusion, adenosine decreases blood pressure by decreasing peripheral resistance.
Pharmacokinetics: I.V. administered adenosine is rapidly cleared from the circulation via cellular uptake, primarily by erythrocytes and vascular endothelial cells, with a half-life of less than 10seconds. 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. Adenosine monophosphate formed by phosphorylation of adenosine is incorporated into the high-energy phosphate pool. Inosine formed by deamination of adenosine can leave the cell intact or can be metabolized to hypoxanthine, xanthine and ultimately uric acid.
Since neither the kidney nor the liver are required for the metabolism or elimination of adenosine, the activity of adenosine should be unaffected by hepatic or renal insufficiency.
Adenosine is an endogenous nucleoside occurring in all cells of the body. When injected i.v. adenosine slows atrioventricular (AV) nodal conduction, can interrupt the reentry pathways through the AV 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.
In controlled clinical trials, cumulative 60% and 92% of patients converted to normal sinus rhythm within 1minute after 6mg and 12mg bolus doses of adenosine, respectively. In other controlled clinical trials with bolus doses of 3, 6, 9 and 12mg some patients with paroxysmal supraventricular tachycardia converted to normal sinus rhythm on 3mg of adenosine. Reports in the medical literature indicate success in treating PSVT in pediatric patients (including newborns) with adenosine in doses equivalent by weight to those used in adults.
Adenosine is not effective in converting rhythms other than PSVT, such as atrial flutter, atrial fibrillation, or ventricular tachycardia to normal sinus rhythm.
Hemodynamics: Adenosine is a potent vasodilator in most vascular beds, except in renal afferent arterioles and hepatic veins where it produces vasoconstriction. The i.v. bolus dose of 6or 12mg adenosine usually has no systemic hemodynamic effects. When larger doses are given by infusion, adenosine decreases blood pressure by decreasing peripheral resistance.
Pharmacokinetics: I.V. administered adenosine is rapidly cleared from the circulation via cellular uptake, primarily by erythrocytes and vascular endothelial cells, with a half-life of less than 10seconds. 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. Adenosine monophosphate formed by phosphorylation of adenosine is incorporated into the high-energy phosphate pool. Inosine formed by deamination of adenosine can leave the cell intact or can be metabolized to hypoxanthine, xanthine and ultimately uric acid.
Since neither the kidney nor the liver are required for the metabolism or elimination of adenosine, the activity of adenosine should be unaffected by hepatic or renal insufficiency.
Indications
Adenosine Is An Endogenous Nucleoside Occurring In All Cells Of The Body. When Injected I.v. Adenosine Slows Atrioventricular (AV) Nodal Conduction, Can Interrupt The Reentry Pathways Through The AV 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.
In Controlled Clinical Trials, Cumulative 60% And 92% Of Patients Converted To Normal Sinus Rhythm Within 1minute After 6mg And 12mg Bolus Doses Of Adenosine, Respectively. In Other Controlled Clinical Trials With Bolus Doses Of 3, 6, 9 And 12mg Some Patients With Paroxysmal Supraventricular Tachycardia Converted To Normal Sinus Rhythm On 3mg Of Adenosine. Reports In The Medical Literature Indicate Success In Treating PSVT In Pediatric Patients (including Newborns) With Adenosine In Doses Equivalent By Weight To Those Used In Adults.
Adenosine Is Not Effective In Converting Rhythms Other Than PSVT, Such As Atrial Flutter, Atrial Fibrillation, Or Ventricular Tachycardia To Normal Sinus Rhythm.
Hemodynamics: Adenosine Is A Potent Vasodilator In Most Vascular Beds, Except In Renal Afferent Arterioles And Hepatic Veins Where It Produces Vasoconstriction. The I.v. Bolus Dose Of 6or 12mg Adenosine Usually Has No Systemic Hemodynamic Effects. When Larger Doses Are Given By Infusion, Adenosine Decreases Blood Pressure By Decreasing Peripheral Resistance.
Pharmacokinetics: I.V. Administered Adenosine Is Rapidly Cleared From The Circulation Via Cellular Uptake, Primarily By Erythrocytes And Vascular Endothelial Cells, With A Half-life Of Less Than 10seconds. 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. Adenosine Monophosphate Formed By Phosphorylation Of Adenosine Is Incorporated Into The High-energy Phosphate Pool. Inosine Formed By Deamination Of Adenosine Can Leave The Cell Intact Or Can Be Metabolized To Hypoxanthine, Xanthine And Ultimately Uric Acid.
Since Neither The Kidney Nor The Liver Are Required For The Metabolism Or Elimination Of Adenosine, The Activity Of Adenosine Should Be Unaffected By Hepatic Or Renal Insufficiency.
Adenosine Is An Endogenous Nucleoside Occurring In All Cells Of The Body. When Injected I.v. Adenosine Slows Atrioventricular (AV) Nodal Conduction, Can Interrupt The Reentry Pathways Through The AV 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.
In Controlled Clinical Trials, Cumulative 60% And 92% Of Patients Converted To Normal Sinus Rhythm Within 1minute After 6mg And 12mg Bolus Doses Of Adenosine, Respectively. In Other Controlled Clinical Trials With Bolus Doses Of 3, 6, 9 And 12mg Some Patients With Paroxysmal Supraventricular Tachycardia Converted To Normal Sinus Rhythm On 3mg Of Adenosine. Reports In The Medical Literature Indicate Success In Treating PSVT In Pediatric Patients (including Newborns) With Adenosine In Doses Equivalent By Weight To Those Used In Adults.
Adenosine Is Not Effective In Converting Rhythms Other Than PSVT, Such As Atrial Flutter, Atrial Fibrillation, Or Ventricular Tachycardia To Normal Sinus Rhythm.
Hemodynamics: Adenosine Is A Potent Vasodilator In Most Vascular Beds, Except In Renal Afferent Arterioles And Hepatic Veins Where It Produces Vasoconstriction. The I.v. Bolus Dose Of 6or 12mg Adenosine Usually Has No Systemic Hemodynamic Effects. When Larger Doses Are Given By Infusion, Adenosine Decreases Blood Pressure By Decreasing Peripheral Resistance.
Pharmacokinetics: I.V. Administered Adenosine Is Rapidly Cleared From The Circulation Via Cellular Uptake, Primarily By Erythrocytes And Vascular Endothelial Cells, With A Half-life Of Less Than 10seconds. 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. Adenosine Monophosphate Formed By Phosphorylation Of Adenosine Is Incorporated Into The High-energy Phosphate Pool. Inosine Formed By Deamination Of Adenosine Can Leave The Cell Intact Or Can Be Metabolized To Hypoxanthine, Xanthine And Ultimately Uric Acid.
Since Neither The Kidney Nor The Liver Are Required For The Metabolism Or Elimination Of Adenosine, The Activity Of Adenosine Should Be Unaffected By Hepatic Or Renal Insufficiency.
Contraindications
Second- or third-degree AV block (except in patients with a functioning artificial pacemaker). Sick sinus syndrome (except in patients with a functioning artificial pacemaker). Symptomatic bradycardia (except in patients with a functioning artificial pacemaker). Known hypersensitivity to adenosine.
Second- or third-degree AV block (except in patients with a functioning artificial pacemaker). Sick sinus syndrome (except in patients with a functioning artificial pacemaker). Symptomatic bradycardia (except in patients with a functioning artificial pacemaker). Known hypersensitivity to adenosine.
Safety Information / Warning
Heart Block: Adenosine exerts its effect by decreasing conduction through the AV node and may produce a short lasting first-, second- or third-degree heart block. Appropriate therapy should be instituted as needed. Patients who develop high level block on one dose of adenosine should not be given additional doses. Because of the very short half-life of adenosine (<10seconds), these effects are generally self-limiting.
Rarely, ventricular fibrillation/flutter has been reported following adenosine administration, including both resuscitated and fatal events. In most instances, these cases were associated with the concomitant use of digoxin and, less frequently, with digoxin and verapamil. Adenosine should be used with caution in patients receiving digoxin or digoxin and verapamil in combination. Appropriate resuscitative measures should be available.
Patients with atrial fibrillation/flutter and an accessory by-pass tract may develop increased conduction down the anomalous pathway.
Arrhythmias at Time of Conversion: At the time of conversion to normal sinus rhythm, a variety of new rhythms may appear on the ECG. They generally last only a few seconds without intervention, and may take the form of premature ventricular contractions, polymorphic ventricular tachycardia, torsades de pointes, atrial premature contractions, sinus bradycardia, sinus tachycardia, skipped beats, and varying degrees of AV nodal block. These arrhythmias and conduction disturbances were observed in about 55% of patients.
Asystole: Transient or prolonged episodes of asystole have been reported with fatal outcomes in some cases.
Bronchoconstriction: Adenosine has been administered to a limited number of patients with asthma and serious exacerbation of their symptoms has been reported in some patients. Respiratory compromise has occurred during adenosine infusion in patients with chronic obstructive pulmonary disease (COPD). Therefore, the use of adenosine should be avoided in patients with COPD or asthma.
Adenosine therapy should be discontinued in any patient who develops severe respiratory difficulties.
Heart Block: Adenosine exerts its effect by decreasing conduction through the AV node and may produce a short lasting first-, second- or third-degree heart block. Appropriate therapy should be instituted as needed. Patients who develop high level block on one dose of adenosine should not be given additional doses. Because of the very short half-life of adenosine (<10seconds), these effects are generally self-limiting.
Rarely, ventricular fibrillation/flutter has been reported following adenosine administration, including both resuscitated and fatal events. In most instances, these cases were associated with the concomitant use of digoxin and, less frequently, with digoxin and verapamil. Adenosine should be used with caution in patients receiving digoxin or digoxin and verapamil in combination. Appropriate resuscitative measures should be available.
Patients with atrial fibrillation/flutter and an accessory by-pass tract may develop increased conduction down the anomalous pathway.
Arrhythmias at Time of Conversion: At the time of conversion to normal sinus rhythm, a variety of new rhythms may appear on the ECG. They generally last only a few seconds without intervention, and may take the form of premature ventricular contractions, polymorphic ventricular tachycardia, torsades de pointes, atrial premature contractions, sinus bradycardia, sinus tachycardia, skipped beats, and varying degrees of AV nodal block. These arrhythmias and conduction disturbances were observed in about 55% of patients.
Asystole: Transient or prolonged episodes of asystole have been reported with fatal outcomes in some cases.
Bronchoconstriction: Adenosine has been administered to a limited number of patients with asthma and serious exacerbation of their symptoms has been reported in some patients. Respiratory compromise has occurred during adenosine infusion in patients with chronic obstructive pulmonary disease (COPD). Therefore, the use of adenosine should be avoided in patients with COPD or asthma.
Adenosine therapy should be discontinued in any patient who develops severe respiratory difficulties.
Precautions
Pregnancy: Adenosine is a substance naturally present in the body and therefore no fetal effects would be anticipated. However, since it is not known whether adenosine can cause fetal harm when administered to pregnant women, it should not be used during pregnancy unless potential benefits outweigh the potential risks to the fetus.
Children: No controlled studies have been conducted in pediatric patients to establish the safety and efficacy of adenosine for the conversion of paroxysmal supraventricular tachycardia (PSVT). However, open-label studies carried out by independent investigators indicated that i.v. adenosine can be used safely in neonates, infants, children and adolescents (see Dosage, Pediatric Patients).
Drug Interactions : Cardioactive Drugs: Adenosine has been effectively administered in the presence of other cardioactive drugs, such as quinidine, beta-adrenergic blocking agents, calcium channel blocking agents and angiotensin converting enzyme inhibitors, without any change in the adverse reaction profile. Digoxin and verapamil use may be rarely associated with ventricular fibrillation when combined with adenosine (see Warnings). Because of the synergistic depressant effects on the SA and AV nodes, adenosine should be used with caution in the presence of these agents.
Methylxanthines: The effects of adenosine are antagonized by methylxanthines (such as caffeine and theophylline). In the presence of methylxanthines, larger doses of adenosine may be required or adenosine may not be effective.
Dipyridamole: Adenosine effects are potentiated by dipyridamole. Thus, smaller doses of adenosine may be effective in the presence of dipyridamole.
Carbamazepine: Carbamazepine has been reported to increase the degree of heart block produced by other agents. Since the primary effect of adenosine is to decrease conduction through the AV node, higher degrees of heart block may be produced in the presence of carbamazepine.
Pregnancy: Adenosine is a substance naturally present in the body and therefore no fetal effects would be anticipated. However, since it is not known whether adenosine can cause fetal harm when administered to pregnant women, it should not be used during pregnancy unless potential benefits outweigh the potential risks to the fetus.
Children: No controlled studies have been conducted in pediatric patients to establish the safety and efficacy of adenosine for the conversion of paroxysmal supraventricular tachycardia (PSVT). However, open-label studies carried out by independent investigators indicated that i.v. adenosine can be used safely in neonates, infants, children and adolescents (see Dosage, Pediatric Patients).
Drug Interactions : Cardioactive Drugs: Adenosine has been effectively administered in the presence of other cardioactive drugs, such as quinidine, beta-adrenergic blocking agents, calcium channel blocking agents and angiotensin converting enzyme inhibitors, without any change in the adverse reaction profile. Digoxin and verapamil use may be rarely associated with ventricular fibrillation when combined with adenosine (see Warnings). Because of the synergistic depressant effects on the SA and AV nodes, adenosine should be used with caution in the presence of these agents.
Methylxanthines: The effects of adenosine are antagonized by methylxanthines (such as caffeine and theophylline). In the presence of methylxanthines, larger doses of adenosine may be required or adenosine may not be effective.
Dipyridamole: Adenosine effects are potentiated by dipyridamole. Thus, smaller doses of adenosine may be effective in the presence of dipyridamole.
Carbamazepine: Carbamazepine has been reported to increase the degree of heart block produced by other agents. Since the primary effect of adenosine is to decrease conduction through the AV node, higher degrees of heart block may be produced in the presence of carbamazepine.
Side Effects / Adverse Effects
In controlled clinical trials 268patients received adenosine. One hundred and two patients (38%) experienced one or more adverse events. These adverse events appeared immediately after administration of adenosine and usually lasted less than 1minute. The most common adverse reactions were: facial flushing (18%), dyspnea (12%), chest pressure (7%) and nausea (3%).
Cardiovascular: facial flushing (18%), headache (2%), sweating, palpitations, chest pain, hypotension (less than 1%). A variety of arrhythmias and conduction disturbances were observed in about 55% of patients at the time of conversion to normal sinus rhythm.
Respiratory: shortness of breath/dyspnea (12%), chest pressure (7%), hyperventilation, head pressure (less than 1%).
CNS: lightheadedness (2%), dizziness, tingling in arms, numbness (1%), apprehension, blurred vision, burning sensation, heaviness in arms, neck and back pain (less than 1%).
Gastrointestinal: nausea (3%), metallic taste, tightness in throat, pressure in groin (less than 1%).
In postmarketing clinical experience with adenosine, cases of prolonged asystole, ventricular tachycardia including torsades de pointes (see Warnings), ventricular fibrillation, transient increase in blood pressure, bradycardia, atrial fibrillation and bronchospasm have been reported.
In controlled clinical trials 268patients received adenosine. One hundred and two patients (38%) experienced one or more adverse events. These adverse events appeared immediately after administration of adenosine and usually lasted less than 1minute. The most common adverse reactions were: facial flushing (18%), dyspnea (12%), chest pressure (7%) and nausea (3%).
Cardiovascular: facial flushing (18%), headache (2%), sweating, palpitations, chest pain, hypotension (less than 1%). A variety of arrhythmias and conduction disturbances were observed in about 55% of patients at the time of conversion to normal sinus rhythm.
Respiratory: shortness of breath/dyspnea (12%), chest pressure (7%), hyperventilation, head pressure (less than 1%).
CNS: lightheadedness (2%), dizziness, tingling in arms, numbness (1%), apprehension, blurred vision, burning sensation, heaviness in arms, neck and back pain (less than 1%).
Gastrointestinal: nausea (3%), metallic taste, tightness in throat, pressure in groin (less than 1%).
In postmarketing clinical experience with adenosine, cases of prolonged asystole, ventricular tachycardia including torsades de pointes (see Warnings), ventricular fibrillation, transient increase in blood pressure, bradycardia, atrial fibrillation and bronchospasm have been reported.
Overdose
Symptoms and Treatment: No cases of overdosage associated with the use of adenosine have been reported. It is unlikely that the true overdosage will occur because adenosine has a short half-life (<10seconds) and is dosed by a rapid bolus injection. If prolonged adverse events associated with the use of adenosine occur, treatment should be individualized and directed toward the specific event. To date, no patient has required administration of adenosine antagonists such as aminophylline to counteract adverse events associated with the use of adenosine.
In clinical studies on the use of adenosine as a diagnostic agent in imaging, less than 0.1% of the patients exposed to adenosine were described as having severe, prolonged, adverse events. These prolonged adverse events were treated with aminophylline after discontinuation of the adenosine infusion. The usual concentration of aminophylline used was 1.25mg/mL (125mg in 100mL) administered i.v. over 5to 6minutes. An additional 1.25mg/mL (125mg in 100mL) can be administered, but clinical experience has demonstrated that this is rarely required.
Symptoms and Treatment: No cases of overdosage associated with the use of adenosine have been reported. It is unlikely that the true overdosage will occur because adenosine has a short half-life (<10seconds) and is dosed by a rapid bolus injection. If prolonged adverse events associated with the use of adenosine occur, treatment should be individualized and directed toward the specific event. To date, no patient has required administration of adenosine antagonists such as aminophylline to counteract adverse events associated with the use of adenosine.
In clinical studies on the use of adenosine as a diagnostic agent in imaging, less than 0.1% of the patients exposed to adenosine were described as having severe, prolonged, adverse events. These prolonged adverse events were treated with aminophylline after discontinuation of the adenosine infusion. The usual concentration of aminophylline used was 1.25mg/mL (125mg in 100mL) administered i.v. over 5to 6minutes. An additional 1.25mg/mL (125mg in 100mL) can be administered, but clinical experience has demonstrated that this is rarely required.
Recommended Dosage
Adenosine should only be used with appropriate cardiac monitoring.
Adenosine should be given as a rapid bolus i.v. injection. To be certain the solution reaches the systemic circulation, it should be administered either directly into a peripheral vein or, if given into an i.v. line, it should be given as close to the patient as possible and followed by a rapid saline flush.
Adult Patients: The recommended i.v. doses for adults are as follows: Initial dose: 6mg administered as a rapid i.v. bolus given over a 1-to 2-second time period.
Additional Doses: If the initial dose does not terminate supraventricular tachycardia within 1to 2minutes, 12mg dose should be given as a rapid i.v. bolus. This 12mg dose may be repeated a second time if required. Single bolus injections greater than 12mg are not recommended.
Pediatric Patients: Pediatric patients with a body weight <50kg: Initial Dose: Give 0.05 to 0.1mg/kg as a rapid i.v. bolus given either centrally or peripherally.
Additional Doses: 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 0.1mg/kg. Follow each bolus with a saline flush. This process should be continued until sinus rhythm is established or up to a maximum dose of 0.3mg/kg.
For pediatric patients who require single i.v. doses less than 0.6mg (0.2mL), adenosine may be further diluted with normal saline to a final concentration range from 0.3 to 1mg/mL.
Patient with a Body Weight ³50Kg: Administer the adult dose.
Single bolus injections greater than 12mg are not recommended for adult or pediatric patients.
Note: Adenosine injection should be inspected visually for particulate matter and discoloration prior to administration.
The injection should not be refrigerated as crystallization may occur. If crystallization has occurred, dissolve crystals by warming to room temperature. The solution must be clear at the time of use.
Adenosine should only be used with appropriate cardiac monitoring.
Adenosine should be given as a rapid bolus i.v. injection. To be certain the solution reaches the systemic circulation, it should be administered either directly into a peripheral vein or, if given into an i.v. line, it should be given as close to the patient as possible and followed by a rapid saline flush.
Adult Patients: The recommended i.v. doses for adults are as follows: Initial dose: 6mg administered as a rapid i.v. bolus given over a 1-to 2-second time period.
Additional Doses: If the initial dose does not terminate supraventricular tachycardia within 1to 2minutes, 12mg dose should be given as a rapid i.v. bolus. This 12mg dose may be repeated a second time if required. Single bolus injections greater than 12mg are not recommended.
Pediatric Patients: Pediatric patients with a body weight <50kg: Initial Dose: Give 0.05 to 0.1mg/kg as a rapid i.v. bolus given either centrally or peripherally.
Additional Doses: 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 0.1mg/kg. Follow each bolus with a saline flush. This process should be continued until sinus rhythm is established or up to a maximum dose of 0.3mg/kg.
For pediatric patients who require single i.v. doses less than 0.6mg (0.2mL), adenosine may be further diluted with normal saline to a final concentration range from 0.3 to 1mg/mL.
Patient with a Body Weight ³50Kg: Administer the adult dose.
Single bolus injections greater than 12mg are not recommended for adult or pediatric patients.
Note: Adenosine injection should be inspected visually for particulate matter and discoloration prior to administration.
The injection should not be refrigerated as crystallization may occur. If crystallization has occurred, dissolve crystals by warming to room temperature. The solution must be clear at the time of use.
Supplied / Packaging
Each mL of sterile solution for rapid bolus i.v. injection contains: adenosine 3mg and sodium chloride 9mg in water for injection. The pH of the solution is between 5.5 and7.5. Additive-, color- and preservative-free. Single-dose flip-top vials of 2mL. Prefilled sterile syringes of 2and 4mL (with a 22G needle). Any portion of the vial or syringe not used at once should be discarded.
Store at controlled room temperature 15to30°C. Do not refrigerate as crystallization may occur. If crystallization has occurred, dissolve crystals by warming to room temperature. The solution must be clear at the time of use.
Each mL of sterile solution for rapid bolus i.v. injection contains: adenosine 3mg and sodium chloride 9mg in water for injection. The pH of the solution is between 5.5 and7.5. Additive-, color- and preservative-free. Single-dose flip-top vials of 2mL. Prefilled sterile syringes of 2and 4mL (with a 22G needle). Any portion of the vial or syringe not used at once should be discarded.
Store at controlled room temperature 15to30°C. Do not refrigerate as crystallization may occur. If crystallization has occurred, dissolve crystals by warming to room temperature. The solution must be clear at the time of use.
