Confirmation of diagnosis required; see Monitor.
0.25 mg/kg of body weight initially (20 mg for the average patient). Some patients may respond to an initial dose of 0.15 mg/kg. A second dose of 0.35 mg/kg may be given in 15 minutes if needed to achieve HR reduction (25 mg for the average patient). Any additional bolus doses used to achieve an appropriate response must be individualized to each patient.
Patients with PSVT may respond to bolus doses and may not require an infusion, but to maintain reduction in HR in patients with atrial fibrillation or atrial flutter, immediately follow with an intravenous infusion at an initial rate of 10 mg/hr. Some patients may maintain response with an initial rate of 5 mg/hr. Infusion may be increased by 5 mg/hr increments to a maximum dose of 15 mg/hr. Discontinue infusion within 24 hours. Duration of infusion longer than 24 hours and infusion rates greater than 15 mg/hr have not been studied.
Transition to other antiarrhythmic agents as appropriate. In clinical trials, therapy with agents to maintain reduced heart rate in atrial fibrillation or atrial flutter or for prophylaxis of PSVT was generally started within 3 hours. Medications that were used included digoxin, quinidine, procainamide, calcium channel blockers (e.g., diltiazem, verapamil), beta-blockers (e.g., atenolol, metoprolol, propranolol). See prescribing information for individual agents.
Specific mg/kg dose must be used for patients with low body weights.
■ Reduced dose may be indicated in impaired hepatic or renal function.
■ Dose selection should be cautious in the elderly. Reduced doses may be indicated based on potential for decreased organ function and concomitant disease or drug therapy.
■ See Drug/Lab Interactions.
Available as a solution in 25-, 50-, or 125-mg vials (5 mg/mL) and, as a 100-mg ADD-Vantage vial. Dilute according to the following chart.
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May be given undiluted through Y-site of tubing containing NS, D5W, or D5/½NS.
May be further diluted for infusion in any of the above solutions; see Dilution Chart above.
No data available from manufacturer.
Store vials containing solution under refrigeration at 2 to 8° C (36 to 46° F). Do not freeze. Some vials may be stored at room temperature for up to 1 month, then discarded. ADD-vantage vials may be stored at CRT. Do not freeze. Following dilution, infusion may be stored at RT or under refrigeration. Use within 24 hours. Discard unused medication and/or solution.
Consider any drug NOT listed as compatible to be INCOMPATIBLE until consulting a pharmacist; specific conditions may apply.
Manufacturer recommends that all formulations not be mixed with any other drugs in the same container and, if possible, that they not be co-infused in the same IV line.
Manufacturer lists Diltiazem for Injection (ADD-Vantage) in NS as compatible at the Y-site with aminophylline, ampicillin, ampicillin/sulbactam, hydrocortisone sodium succinate, insulin (regular U-100), methylprednisolone, nafcillin, and sodium bicarbonate.
Other sources suggest specific compatibilities dependent on concentration and manufacturer; consult a pharmacist.
Each single dose equally distributed over 2 minutes.
5 mg to 15 mg/hr based on patient response. See charts under Dilution for diluent, dose, and infusion rate information. Administer using an infusion pump.
Directly inhibits the influx of calcium ions through slow channels during membrane depolarization of cardiac and vascular smooth muscle. Effective in supraventricular tachycardias because it slows conduction through the AV node and prolongs the effective refractory period. Has little or no effect on normal AV nodal conduction at normal heart rates. Slows ventricular rate in patients with a rapid ventricular response during atrial fibrillation or atrial flutter. Converts paroxysmal supraventricular tachycardia (PSVT) to normal sinus rhythm by interrupting the re-entry circuit in AV nodal re-entrant tachycardias and reciprocating tachycardias (e.g. Wolff-Parkinson-White syndrome [WPW]). Because of its effect on vascular smooth muscle, diltiazem decreases total peripheral resistance, resulting in a decrease in both diastolic and systolic BP. In patients with cardiovascular disease, diltiazem reduces BP, systemic vascular resistance, and coronary vascular resistance and increases coronary blood flow. In studies of patients with compromised myocardium (severe CHF, AMI, hypertrophic cardiomyopathy), administration of diltiazem did not produce a significant effect on contractility, left ventricular end diastolic pressure, or pulmonary capillary wedge pressure. The mean ejection fraction and cardiac output/index remained unchanged or increased. Produces less myocardial depression than verapamil. Effective within 3 minutes; maximum effect should occur within 2 to 5 minutes and last for 1 to 3 hours. 70% to 80% bound to plasma proteins. Metabolized in the liver. Half-life is approximately 3.4 hours following a bolus injection and increases to 4.1 to 4.9 hours with continuous infusion. Excreted in urine and feces. Secreted in breast milk.
Temporary control of rapid ventricular rate in atrial fibrillation or atrial flutter unless associated with an accessory bypass tract (e.g., Wolff-Parkinson-White syndrome or short PR syndrome).
■ Rapid conversion of paroxysmal supraventricular tachycardia (PSVT) to normal sinus rhythm including AV nodal re-entrant tachycardias and reciprocating tachycardias associated with an extranodal accessory pathway (e.g., Wolff-Parkinson-White syndrome or short PR syndrome).
Atrial fibrillation or flutter when associated with an accessory bypass tract (e.g., Wolff-Parkinson-White or short PR syndrome), cardiogenic shock, known hypersensitivity to diltiazem, second- or third-degree AV block or sick sinus syndrome (unless functioning ventricular pacemaker in place), severe hypotension, patients receiving IV beta-adrenergic blocking agents (e.g., atenolol [Tenormin], propranolol [Inderal]) within a few hours, ventricular tachycardia. Not recommended for wide QRS tachycardias of uncertain origin.
For short-term use only.
■ Administration of IV diltiazem should take place in a facility with adequate personnel and emergency drugs and equipment (including a defibrillator) to monitor the patient and respond to any medical emergency.
■ While diltiazem will effectively decrease HR, cardioversion will probably be required to convert atrial fibrillation or atrial flutter to a normal sinus rhythm.
■ Appropriate vagal maneuvers (e.g., Valsalva maneuver) recommended before use of diltiazem in patients with paroxysmal supraventricular tachycardia if clinically appropriate.
■ Use IV diltiazem with caution in patients with pre-existing impaired ventricular function (e.g., congestive heart failure, acute myocardial infarction, or pulmonary congestion documented by x-ray); may exacerbate disease. Use of oral diltiazem in these patients is contraindicated.
■ May cause second- or third-degree AV block in sinus rhythm; discontinue diltiazem if high degree AV block occurs.
■ Can cause life-threatening tachycardia with severe hypotension in atrial fibrillation or flutter in patients with an accessory bypass tract and periods of asystole in patients with sick sinus syndrome; see Contraindications.
■ Use with caution in patients with PSVT who are hemodynamically compromised or are taking other drugs that decrease any or all of the following: peripheral resistance, intravascular volume, myocardial contractility or conduction. Symptomatic hypotension is possible.
■ Use with caution in impaired renal or hepatic function.
■ Ventricular premature beats (VPBs) may occur on conversion of PSVT to sinus rhythm; considered to have no clinical significance.
■ Rare instances of significant liver enzymes and other phenomena consistent with acute hepatic injury have been reported with use of oral diltiazem.
■ Rare cases of dermatologic toxicity progressing to erythema multiforme and/or exfoliative dermatitis has been reported with oral diltiazem.
Accurate pretreatment diagnosis differentiating wide-complex QRS tachycardia of supraventricular origin from ventricular origin is imperative.
■ Continuous ECG monitoring required.
■ Monitor BP and HR closely.
■ See Drug/Lab Interactions.
Use during pregnancy only if potential benefit justifies the potential risk to the fetus.
■ Discontinue breast-feeding.
■ Safety and effectiveness for use in pediatric patients not established.
Overall difference in response between the elderly and younger patients has not been identified, but greater sensitivity of some older individuals cannot be ruled out; see Dose Adjustments.
Diltiazem is both a substrate and inhibitor of CYP3A4. Other drugs that are substrates, inhibitors, or inducers of CYP3A4 may have a significant impact on the efficacy or toxicity of diltiazem. Patients taking drugs that are substrates of CYP3A4 may require dose adjustment when starting or stopping concomitantly administered diltiazem.
■ Do not give concomitantly (within a few hours) with IV beta-adrenergic blocking agents; see Contraindications. May result in bradycardia, AV block, and/or depression of contractility. Use extreme caution if these drugs are administered orally or if patient has received before admission; usually tolerated.
■ May result in additive effects with any agent known to affect cardiac contractility and/or SA or AV node conduction (e.g., digoxin, beta-blockers).
■ Is used with digoxin, but monitor for excessive slowing of HR and/or AV block.
■ Coadministration with amiodarone or clonidine may result in bradycardia. Monitor closely.
■ May increase effects of certain benzodiazepines (e.g., midazolam), buspirone, and methylprednisolone.
■ May increase serum concentrations of carbamazepine, cyclosporine, digoxin, some HMG-CoA reductase inhibitors (e.g., atorvastatin, lovastatin, simvastatin), nifedipine, quinidine, sirolimus, and tacrolimus. Monitor serum levels and/or monitor for S/S of toxicity.
■ May potentiate cardiac effects of anesthetics (e.g., depression of cardiac contractility, conductivity, automaticity, and vascular dilation); titrate both drugs carefully.
■ Metabolism may be decreased and serum concentrations increased by cimetidine and some azole antifungal agents (e.g., itraconazole).
■ Metabolism may be increased and serum concentrations decreased by CYP3A4 inducers (e.g., rifampin). Avoid use if possible and consider alternative therapy.
■ May increase exposure to ivabradine and exacerbate bradycardia and conduction disturbances. Avoid concomitant use.
■ May enhance neurotoxicity of lithium. Variable effects on lithium concentrations have been reported.
Arrhythmia (junctional rhythm or isorhythmic dissociation), flushing, hypotension (asymptomatic and symptomatic), and injection site reactions (burning, itching) occurred most frequently and were most often mild and transient but could have serious potential. Amblyopia, asthenia, asystole, atrial flutter, AV block (first- or second-degree), bradycardia, chest pain, congestive heart failure, constipation, dizziness, dry mouth, dyspnea, edema, elevated alkaline phosphatase and AST, headache, hyperuricemia, nausea, paresthesia, pruritus, sinus node dysfunction, sinus pause, sweating, syncope, ventricular arrhythmias, ventricular fibrillation, ventricular tachycardia, and vomiting have occurred. Additional side effects have been reported with oral diltiazem.
Notify physician promptly of all side effects. Treatment will depend on clinical situation. IV fluids or the Trendelenburg position may be required for BP support. Vasopressors (e.g., dopamine or norepinephrine) may be used, if needed. Administer atropine (0.6 to 1 mg) for bradycardia. If no response, administer isoproterenol cautiously. Discontinue diltiazem if a high-degree AV block occurs. Treat with atropine as above. Fixed-high-degree AV block should be treated with cardiac pacing. Treat cardiac failure with inotropic agents (isoproterenol, dopamine, or dobutamine) and diuretics. Calcium chloride or calcium gluconate have been used to reverse the pharmacologic effects of diltiazem overdose with variable results. Treat hypersensitivity reactions or resuscitate as necessary. Not removed by hemodialysis.