Version July 2025
To minimize the risk of drug-induced arrhythmia, initiate, reinitiate, or uptitrate sotalol in a facility that can provide cardiac resuscitation and continuous ECG monitoring. Sotalol can cause life threatening ventricular tachycardia associated with QT interval prolongation. Do not initiate sotalol therapy if the baseline QTc is longer than 450 msec. If the QT interval prolongs to 500 msec or greater, reduce the dose, lengthen the dosing interval, or discontinue the drug. Calculate CrCl to determine appropriate dosing.
Note: Baseline QTc interval and CrCl must be determined prior to initiation. If CrCl ≤60 mL/minute, dosing interval adjustment is necessary. When initiating sotalol, patients should be hospitalized for at least 3 days in order to monitor cardiac rhythm and assess for QT prolongation. Maintain potassium and magnesium in the normal range prior to initiation and during therapy. Proarrhythmic events can occur after initiation of therapy and with each upward dosage adjustment.
Atrial fibrillation/flutter, maintenance of sinus rhythm:
Maintenance dose:
Oral:
Initial: 80 mg twice daily.
Dose adjustment: If initial dose does not reduce frequency of relapse and excessive QTc prolongation does not occur (eg, QTc <500 msec) after 3 days, may increase dose to 120 mg twice daily; may increase dose further after another 3 days to a maximum dose of 160 mg twice daily if response is inadequate and QTc prolongation is not excessive (eg, QTc <500 msec).
IV (as substitution for oral sotalol):
Initial dose: 75 mg infused over 5 hours twice daily.
Dose adjustment: If initial dose does not reduce frequency of relapse and excessive QTc prolongation does not occur (eg, QTc <500 msec) after 3 days, may increase dose to 112.5 mg twice daily; may increase dose further after another 3 days to a maximum dose of 150 mg twice daily if response is inadequate and QTc prolongation is not excessive (eg, QTc < 500 msec).
Loading dose to initiate therapy or for dose escalation: Not routinely required. This approach consists of a single, initial IV dose administered over 1 hour, followed by oral maintenance dosing beginning 4 to 12 hours later (see table). The IV loading dose is used to quickly achieve maximum steady-state concentrations similar to the targeted oral maintenance dose in order to observe how patients respond in a setting with continuous ECG monitoring. Achieving maximum steady-state concentrations quickly with an IV loading dose may help facilitate faster patient discharge (Ref):
Note: Dosing derived from pharmacokinetic/pharmacodynamic modeling in 15 healthy volunteers (Ref).
|
CrCl (mL/minute)a |
Therapy initiationb: IV loading dose (mg) when oral maintenance is planned to be: |
Therapy escalationb: IV loading dose (mg) when increasing the oral maintenance dose from: |
Minimum delay to start of oral dose (hour) |
Oral dosing interval (hour) | ||
|---|---|---|---|---|---|---|
|
80 mgc |
120 mg |
80 to 120 mg |
120 to 160 mg | |||
|
a Calculate using Cockcroft-Gault formula. | ||||||
|
b Monitor QTc interval every 15 minutes during the 1-hour infusion and around the Tmax (2 to 4 hours post dose) of oral doses given within the first 24 hours of therapy. If QTc interval prolongs to >500 msec or increases ≥20% from baseline, discontinue sotalol when targeting an oral maintenance dose of 80 mg. When targeting an oral maintenance dose of 120 mg, discontinue sotalol and consider reinitiating to target 80 mg; when reinitiating to target 80 mg, wait at least 1 day in patients with CrCl ≥60 mL/minute (Somberg 2020; manufacturer’s labeling). | ||||||
|
c Recommended starting dose. | ||||||
|
>90 mL/minute |
60 mg |
90 mg |
75 mg |
90 mg |
4 hours |
12 hours |
|
60 to 90 mL/minute |
82.5 mg |
125 mg |
82.5 mg |
105 mg |
4 hours |
12 hours |
Fetal tachycardia, sustained (maternal/transplacental administration) (off-label use): Oral: Initial: 80 to 160 mg twice daily; may increase dose as needed up to 480 mg/day in 2 to 3 divided doses based on response and tolerability (Ref).
Supraventricular tachycardia (off-label use): Oral: Initial: 40 to 80 mg every 12 hours; maximum maintenance dose: 160 mg every 12 hours (Ref).
Ventricular arrhythmias:
Maintenance dose:
Oral:
Initial dose: 80 mg twice daily.
Dose adjustment: If initial dose does not reduce frequency of relapse and excessive QTc prolongation does not occur (eg, QTc <500 msec) after 3 days, may increase dose to 120 mg twice daily; may increase dose further after another 3 days to a usual maximum dose of 160 mg twice daily if response is inadequate and QTc prolongation is not excessive (eg, QTc <500 msec).
IV (as substitution for oral sotalol):
Initial dose: 75 mg infused over 5 hours twice daily.
Dose adjustment: If initial dose does not reduce frequency of relapse and excessive QTc prolongation does not occur (eg, QTc <500 msec) after 3 days, may increase dose to 112.5 mg twice daily; may increase dose further after another 3 days to a usual maximum dose of 150 mg twice daily if response is inadequate and QTc prolongation is not excessive (eg, QTc <500 msec).
Loading dose to initiate therapy or for dose escalation: Not routinely required. This approach consists of a single, initial IV dose administered over 1 hour, followed by oral maintenance dosing beginning 4 to 12 hours later (see table). The IV loading dose is used to quickly achieve maximum steady-state concentrations similar to the targeted oral maintenance dose in order to observe how patients respond in a setting with continuous ECG monitoring. Achieving maximum steady-state concentrations quickly with an IV loading dose may help facilitate faster patient discharge (Ref):
Note: Dosing derived from pharmacokinetic/pharmacodynamic modeling in 15 healthy volunteers (Ref).
|
CrCl (mL/minute)a |
Therapy initiationb: IV loading dose (mg) when oral maintenance is planned to be: |
Therapy escalationb: IV loading dose (mg) when increasing the oral maintenance dose from: |
Minimum delay to start of oral dose (hour) |
Oral dosing interval (hour) | ||
|---|---|---|---|---|---|---|
|
80 mgc |
120 mg |
80 to 120 mg |
120 to 160 mg | |||
|
a Calculate using Cockcroft-Gault formula. | ||||||
|
b Monitor QTc interval every 15 minutes during the 1-hour infusion and around the Tmax (2 to 4 hours post dose) of oral doses given within the first 24 hours of therapy. If QTc interval prolongs to >500 msec or increases ≥20% from baseline, discontinue sotalol when targeting an oral maintenance dose of 80 mg. When targeting an oral maintenance dose of 120 mg, discontinue sotalol and consider reinitiating to target 80 mg; when reinitiating to target 80 mg, wait at least 1 day in patients with CrCl ≥60 mL/minute. | ||||||
|
c Recommended starting dose. | ||||||
|
>90 mL/minute |
60 mg |
90 mg |
75 mg |
90 mg |
4 hours |
12 hours |
|
60 to 90 mL/minute |
82.5 mg |
125 mg |
82.5 mg |
105 mg |
4 hours |
12 hours |
Sustained monomorphic ventricular tachycardia, hemodynamically stable (off-label use): IV: 1.5 mg/kg or 100 mg over 5 minutes (Ref).
Ventricular premature beats, symptomatic (off-label use): Oral: Initial: 80 mg twice daily; dose may be increased gradually in increments of 80 mg/day up to a maximum dose of 160 mg twice daily; allow 3 days between dose adjustments in order to attain steady-state plasma concentrations and to allow for monitoring of QT intervals (Ref).
Conversion from oral sotalol to IV sotalol:
Note: Conversion only applies when substituting an oral maintenance dose with an IV dose administered as a 5-hour infusion.
80 mg oral equivalent to 75 mg IV.
120 mg oral equivalent to 112.5 mg IV.
160 mg oral equivalent to 150 mg IV.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function:
Maintenance dose:
Atrial fibrillation/flutter: Oral, IV:
CrCl >60 mL/minute: Administer every 12 hours.
CrCl 40 to 60 mL/minute: Administer every 24 hours.
CrCl <40 mL/minute: Use is contraindicated.
Ventricular arrhythmia: Oral, IV:
CrCl >60 mL/minute: Administer every 12 hours.
CrCl 30 to 60 mL/minute: Administer every 24 hours.
CrCl 10 to 29 mL/minute: Administer every 36 to 48 hours.
CrCl <10 mL/minute: Avoid use (Ref).
Loading dose to initiate therapy or for dose escalation: Atrial fibrillation/flutter or ventricular arrhythmia: IV: Not routinely required. This approach consists of a single, initial IV dose administered over 1 hour, followed by oral maintenance dosing beginning 4 to 12 hours later depending on kidney function (see table). The IV loading dose is used to quickly achieve maximum steady-state concentrations similar to the targeted oral maintenance dose in order to observe how patients respond in a setting with continuous ECG monitoring. Achieving maximum steady-state concentrations quickly with an IV loading dose may help facilitate faster patient discharge (Ref):
Note: Dosing derived from pharmacokinetic/pharmacodynamic modeling in 15 healthy volunteers. Doses for CrCl <40 mL/minute only apply to patients with ventricular arrhythmias since use of oral therapy is contraindicated in patients with atrial fibrillation/flutter and CrCl <40 mL/minute. Patients with kidney dysfunction will require a higher initial IV dose to test safety and efficacy of the oral sotalol regimen because these patients tend to have higher sotalol concentrations at steady state despite proper dosage adjustments (Ref).
|
CrCl (mL/minute)a |
Therapy initiationb: IV loading dose (mg) when oral maintenance is planned to be: |
Therapy escalationb: IV loading dose (mg) when increasing the oral maintenance dose from: |
Minimum delay to start of oral dose (hour) |
Oral dosing interval (hour) | ||
|---|---|---|---|---|---|---|
|
80 mgc |
120 mg |
80 to 120 mg |
120 to 160 mg | |||
|
a Calculate using Cockcroft-Gault formula. | ||||||
|
b Monitor QTc interval every 15 minutes during the 1-hour infusion and around the Tmax (2 to 4 hours post dose) of oral doses given within the first 24 hours of therapy. If QTc interval prolongs to >500 msec or increases ≥20% from baseline, discontinue sotalol when targeting an oral maintenance dose of 80 mg. When targeting an oral maintenance dose of 120 mg, discontinue sotalol and consider reinitiating to target 80 mg; when reinitiating to target 80 mg, wait at least 1 day in patients with CrCl ≥60 mL/minute, at least 3 days in patients with CrCl 30 to <60 mL/minute, and at least 7 days in patients with CrCl 10 to <30 mL/minute (manufacturer’s labeling). | ||||||
|
c Recommended starting dose. | ||||||
|
>90 mL/minute |
60 mg |
90 mg |
75 mg |
90 mg |
4 hours |
12 hours |
|
60 to 90 mL/minute |
82.5 mg |
125 mg |
82.5 mg |
105 mg |
4 hours |
12 hours |
|
30 to <60 mL/minute |
75 mg |
112.5 mg |
82.5 mg |
105 mg |
6 hours |
24 hours |
|
10 to <30 mL/minute |
75 mg |
112.5 mg |
82.5 mg |
105 mg |
12 hours |
48 hours |
Hemodialysis , intermittent (thrice weekly): Dialyzable (20% to 43%) (Ref): Oral, IV:
Avoid use; consider alternative agent (Ref). Multiple cases of torsades de pointes have been reported when sotalol was used, even at low dosages (eg, 80 mg daily orally) in patients with end-stage kidney disease treated with hemodialysis (Ref). In at least one case, QT interval was not corrected by several days of dialysis, suggestive of widely fluctuating and unpredictable tissue and plasma drug concentrations (Ref).
Peritoneal dialysis: Oral, IV: Avoid use; consider alternative agent (Ref). Cases of torsades de pointes have been reported when sotalol was used even at low dosages (eg, 80 mg daily orally) in patients with end-stage kidney disease treated with peritoneal dialysis (Ref).
CRRT:
Note: Drug clearance is dependent on the effluent flow rate, filter type, and method of renal replacement. Recommendations are based on high-flux dialyzers and effluent flow rates of 20 to 25 mL/kg/hour (or ~1,500 to 3,000 mL/hour) unless otherwise noted.
Oral, IV: Avoid use; consider alternative agent(s), as no pharmacokinetic data are available in this population. Additionally, removal by CRRT can be interrupted by clotting, filter changes, etc. (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration):
Oral, IV: Avoid use, consider alternative agent(s), as no pharmacokinetic data are available in the population. Additionally, clearance will vary on PIRRT versus non-PIRRT days (Ref).
There are no dosage adjustments provided in the manufacturer's labeling. However, dosage adjustment unlikely because sotalol is not metabolized by the liver.
QTc ≥500 msec:
Tablets, oral solution: Reduce dose, prolong the dosing interval, or discontinue sotalol
Injection:
Substitution for oral: Reduce dose, prolong the infusion time by decreasing the infusion rate, prolong the dosing interval, or discontinue sotalol.
Loading dose to initiate therapy or for dose escalation: Refer to table in adult or renal dosing sections.
Refer to adult dosing.
Dosage guidance:
Safety: Baseline QTc interval and CrCl must be determined prior to initiation; use with caution if QTc is >500 msec. Measure baseline serum potassium and magnesium; normalize prior to initiating therapy. Dosage must be adjusted to individual response and tolerance; doses should be initiated and preferably increased in a hospital facility that can provide continuous ECG monitoring and cardiac resuscitation.
Dosing: In pediatric patients, dosing may be based on either BSA (mg/m2) or weight (mg/kg); use extra caution to verify dosing parameters during calculations.
Clinical considerations: For infants and children ≤2 years of age, the manufacturer recommends a dosage reduction based on an age factor determined from an age factor nomogram.
Arrhythmias, treatment (eg, ventricular arrhythmias, atrial fibrillation, atrial flutter, supraventricular tachycardia, junctional ectopic tachycardia):
Oral:
BSA-directed dosing:
Infants and Children ≤2 years: The manufacturer-recommended pediatric dosage of 30 mg/m2/dose every 8 hours must be REDUCED using an age-related factor that is obtained from the graph (see graph). First, obtain the patient's age in months; use the graph to determine where the patient's age (on the logarithmic scale) intersects the age factor curve; read the age factor from the Y-axis; then multiply the age factor by the pediatric dose of 30 mg/m2/dose; this will result in the proper reduction in dose for age. For example, the age factor for an infant 2 months of age is 0.8, so the initial dose would be (0.8 × 30 mg/m2/dose) = 24 mg/m2/dose given every 8 hours. Increase dosage gradually as needed; allow adequate time between dosage increases to achieve new steady-state plasma concentration and to monitor clinical response, heart rate, and QTc interval; half-life is prolonged with decreasing age (<2 years), so time to reach new steady-state plasma concentration is increased (Ref). Refer to manufacturer's labeling for more information.
Children >2 years and Adolescents: Initial: 30 mg/m2/dose given every 8 hours; increase dosage gradually if needed; allow at least 36 hours between dosage increases to achieve new steady-state plasma concentration and to monitor clinical response, heart rate, and QTc intervals; may increase gradually to a maximum of 60 mg/m2/dose given every 8 hours; not to exceed adult doses (usual maximum adult daily dose: 320 mg/day) (Ref).
Weight-directed dosing:
Infants and Children ≤2 years: The manufacturer-recommended pediatric dosage of 1.2 mg/kg/dose every 8 hours must be REDUCED using an age-related factor that is obtained from the graph (see graph). First, obtain the patient's age in months; use the graph to determine where the patient's age (on the logarithmic scale) intersects the age factor curve; read the age factor from the Y-axis; then multiply the age factor by the pediatric dose of 1.2 mg/kg/dose; this will result in the proper reduction in dose for age. For example, the age factor for an infant 2 months of age is 0.8, so the initial dose would be (0.8 × 1.2 mg/kg/dose) = 0.96 mg/kg/dose given every 8 hours. Increase dosage gradually as needed; allow adequate time between dosage increases to achieve new steady-state plasma concentration and to monitor clinical response, heart rate, and QTc interval; half-life is prolonged with decreasing age (<2 years), so time to reach new steady-state plasma concentration is increased (Ref). Refer to manufacturer's labeling for more information.
Children >2 years and Adolescents: Initial: Oral: 0.67 to 1.2 mg/kg/dose every 8 hours; increase dose based on clinical response, heart rate, and QTc interval, allow 36 hours between dosage increases to achieve steady-state plasma concentration, maximum daily dose: 8 mg/kg/day, not to exceed adult doses (usual maximum adult daily dose: 320 mg/day) (Ref).
IV: Note: May be used in place of oral sotalol in patients unable to take oral medications or to achieve steady-state plasma concentration faster.
Loading dose (acute treatment):
BSA-directed dosing:
Infants, Children, and Adolescents: IV: 30 to 40 mg/m2/dose over 15 to 60 minutes, maximum dose: 80 mg/dose (Ref).
Weight-directed dosing:
Infants, Children, and Adolescents: Usual reported dose: 1 mg/kg/dose over 30 to 60 minutes, maximum dose: 80 mg/dose (Ref).
The manufacturer recommends loading dose based on age:
Infants and Children <6 years: IV: Initial: 1.2 mg/kg/dose over 60 minutes.
Children ≥6 years: IV: Initial: 1.1 mg/kg/dose over 60 minutes.
Adolescents: IV: Initial: 0.95 mg/kg/dose over 60 minutes.
Maintenance dose (eg, unable to take oral medications): Very limited data available; reported regimens variable and ideal dose response not established:
BSA-directed dosing:
Infants, Children, and Adolescents: IV: 50 mg/m2/day divided every 8 to 12 hours (Ref), maximum dose: 80 mg/dose; administer each dose over 2 to 5 hours (Ref).
Weight-directed dosing:
Infants, Children, and Adolescents: IV: 3 mg/kg/day divided every 8 to 12 hours (Ref), maximum dose: 80 mg/dose, administer each dose over 2 to 5 hours (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Dosing adjustment for toxicity:
Infants, Children, and Adolescents:
QTc ≥500 msec:
Oral: Reduce dose, increase dosing interval, or discontinue sotalol.
IV: Reduce dose or discontinue sotalol.
Altered kidney function:
Infants, Children, and Adolescents:
Oral: There are no pediatric-specific dosage adjustments provided in manufacturer's labeling; dosing in children with kidney impairment has not been studied. In adults, a lower dose or increased dosing interval is recommended; closely monitor clinical response, heart rate, and QTc interval; allow adequate time between dosage increases to achieve new steady-state plasma concentration, since half-life will be prolonged with kidney impairment.
IV: Initiate at a lower dose and increase dose less frequently; allow adequate time between dosage increases to achieve new steady-state plasma concentration, since half-life will be prolonged. Closely monitor clinical response, heart rate, and QTc interval.
Hemodialysis: IV, Oral: Hemodialysis would be expected to reduce sotalol plasma concentrations because sotalol is not bound to plasma proteins and does not undergo extensive metabolism. According to the manufacturers, extreme caution should be employed if sotalol is used in patients with kidney failure undergoing hemodialysis. In adults, multiple cases of torsades de pointes have been reported when sotalol was used even at low adult dosages (eg, 80 mg daily) in patients with end-stage kidney disease treated with hemodialysis (Ref).
Peritoneal dialysis: IV, Oral: There are no pediatric-specific dosage adjustments provided in manufacturer's labeling. Peritoneal dialysis does not remove sotalol; in adults, supplemental dose is not necessary (Ref). Cases of torsades de pointes have been reported when sotalol was used even at low adult dosages (eg, 80 mg daily) in patients with end-stage kidney disease treated with peritoneal dialysis (Ref).
All patients: There are no dosage adjustments provided in the manufacturer's labeling; however, clearance is not affected by liver impairment.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. There is minimal clinical experience with IV sotalol; however, since exposure is similar between IV and oral sotalol, adverse reactions are expected to be similar.
>10%:
Cardiovascular: Bradycardia (dose related; 8% to 13%), chest pain (8%), palpitations (8%)
Nervous system: Dizziness (13% to 16%), fatigue (dose related; 19% to 26%), headache (12%)
Neuromuscular & skeletal: Asthenia (5% to 11%)
Respiratory: Dyspnea (dose related; 9% to 18%)
1% to 10%:
Cardiovascular: Complete atrioventricular block (1%), second degree atrioventricular block (1%), torsades de pointes (dose related; ≤4%), ventricular tachycardia (new or worsened: ≤1%)
Dermatologic: Diaphoresis (5%)
Gastrointestinal: Abdominal pain (4%), diarrhea (5% to 6%), nausea and vomiting (6% to 8%)
Neuromuscular & skeletal: Musculoskeletal pain (4%)
Ophthalmic: Visual disturbance (5%)
<1%:
Cardiovascular: Sinoatrial arrest, sinus node dysfunction, sinus pause
Nervous system: Peripheral neuropathy
Frequency not defined: Cardiovascular: Cardiac failure, hypotension, prolonged QT interval on ECG, sinus bradycardia
Postmarketing:
Dermatologic: Alopecia, pruritus, skin photosensitivity
Endocrine & metabolic: Hyperlipidemia
Hematologic & oncologic: Eosinophilia, leukopenia, thrombocytopenia
Nervous system: Altered mental status, ataxia, emotional lability, paralysis, vertigo
Neuromuscular & skeletal: Myalgia
Respiratory: Pulmonary edema
Miscellaneous: Fever
Hypersensitivity to sotalol or any component of the formulation; bronchial asthma or related bronchospastic conditions; sinus bradycardia (<50 bpm during waking hours); second- or third-degree AV block (unless a functioning pacemaker is present); congenital or acquired long QT syndromes; cardiogenic shock; decompensated heart failure; sick sinus syndrome; serum potassium <4 mEq/L; when used for atrial fibrillation/flutter, initiation of oral tablet is contraindicated if baseline QTc interval >450 msec; when used for atrial fibrillation/flutter or ventricular arrhythmias, oral solution is contraindicated if baseline QTc interval >450 msec.
Canadian labeling: Additional contraindications (not in the US labeling): Allergic rhinitis; severe sinus node dysfunction; concurrent use with anesthetics that produce myocardial depression.
Concerns related to adverse effects:
• Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.
• Bradycardia/hypotension: May cause bradycardia (including heart block) and hypotension. Dose adjustments of agents that slow AV nodal conduction may be necessary when sotalol is initiated.
• Proarrhythmic effects: Severe and potentially fatal ventricular arrhythmias (eg, sustained ventricular tachycardia [VT]/ventricular fibrillation [VF], primarily Torsade de Pointes) may occur; females and patients with reduced creatinine clearance, reduced heart rate, higher doses, and history of sustained VT/VF or heart failure may be at increased risk. Calculation of CrCl must occur prior to administration of the first dose. Dosage should be adjusted gradually with 3 days between dosing increments to achieve steady-state concentrations, and to allow time to monitor QT intervals. Monitor and adjust dose to prevent QTc prolongation.
Disease-related concerns:
• Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; if used at all, should be used cautiously with close monitoring. Sotalol is contraindicated in patients with bronchial asthma or related bronchospastic conditions.
• Conduction abnormality: Consider preexisting conditions such as sick sinus syndrome before initiating.
• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms.
• Electrolyte imbalances: Correct electrolyte imbalances before initiating (especially hypokalemia and hypomagnesemia) because these conditions increase the risk of torsades de pointes.
• Heart failure: New onset or worsening heart failure may occur during initiation or titration. Use with caution in patients with compensated heart failure; monitor for a worsening of the condition and discontinue if symptoms of heart failure occur. Use is contraindicated in patients with uncontrolled (or decompensated) heart failure.
• Myasthenia gravis: Use with caution in patients with myasthenia gravis; may worsen disease.
• Myocardial infarction: Use with caution within the first 2 weeks post myocardial infarction (MI), especially in patients with markedly impaired ventricular function (experience limited).
• Peripheral vascular disease and Raynaud disease: Can precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease and Raynaud disease. Use with caution and monitor for progression of arterial obstruction.
• Pheochromocytoma (untreated): Adequate alpha-blockade is required prior to use of any beta-blocker.
• Renal impairment: CrCl must be calculated with dose initiation and dose increases. When used for atrial fibrillation/flutter, sotalol is contraindicated in patients with CrCl <40 mL/minute.
• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If thyrotoxicosis is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm.
Special populations:
• Older adult: Bradycardia may be observed more frequently in older adult patients (>65 years of age); dosage reductions may be necessary.
Other warnings/precautions:
• Abrupt withdrawal: Beta-blocker therapy should not be withdrawn abruptly (particularly in patients with coronary artery disease), but gradually tapered over 1 to 2 weeks to avoid acute tachycardia, hypertension, and/or ischemia. Severe exacerbation of angina, ventricular arrhythmias, and MI have been reported following abrupt withdrawal of beta-blocker therapy. Temporary but prompt resumption of beta-blocker therapy may be indicated with worsening of angina or acute coronary insufficiency. When QTc prolongation occurs, consider weighing the risk of abrupt withdrawal of sotalol with the risk of QTc prolongation. Use of an alternative beta-blocker may be indicated if worsening angina or acute coronary insufficiency occurs when sotalol is withdrawn abruptly due to QTc prolongation.
• Appropriate use: Discontinue other antiarrhythmic therapy prior to initiation and monitor patient for ≥2 to 3 plasma half-lives prior to initiating sotalol if patient’s clinical condition permits.
• Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution, Intravenous, as hydrochloride:
Generic: 150 mg/10 mL (10 mL)
Solution, Oral, as hydrochloride:
Sotylize: 5 mg/mL (250 mL, 480 mL) [contains sodium benzoate; grape flavor]
Tablet, Oral, as hydrochloride:
Betapace: 80 mg, 120 mg, 160 mg [scored; contains fd&c blue #2 (indigo carm) aluminum lake]
Betapace AF: 80 mg, 120 mg, 160 mg [scored]
Sorine: 80 mg [DSC], 120 mg [DSC], 160 mg [DSC], 240 mg [DSC] [scored]
Generic: 80 mg, 120 mg, 160 mg, 240 mg
Yes
Solution (Sotalol HCl Intravenous)
150 mg/10 mL (per mL): $434.76
Solution (Sotylize Oral)
5 mg/mL (per mL): $2.82
Tablets (Betapace AF Oral)
80 mg (per each): $18.22
120 mg (per each): $24.32
160 mg (per each): $30.41
Tablets (Betapace Oral)
80 mg (per each): $30.52
120 mg (per each): $40.73
160 mg (per each): $50.91
Tablets (Sotalol HCl Oral)
80 mg (per each): $0.23 - $2.56
120 mg (per each): $0.31 - $3.42
160 mg (per each): $0.39 - $4.27
240 mg (per each): $5.09 - $5.56
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.
Tablet, Oral, as hydrochloride:
Generic: 80 mg, 160 mg, 240 mg
Oral: Administer without regard to meals.
When used for the management of fetal tachycardia (maternal/transplacental administration; off-label use), oral doses are administered to the mother.
IV:
Loading dose to initiate therapy or for dose escalation: Must be diluted prior to administration. Administer over 1 hour.
Substitution for oral: Must be diluted prior to administration. Administer over 5 hours; may prolong duration of infusion if QT interval prolongs to ≥500 msec.
Hemodynamically stable monomorphic VT: Administer IV push over 5 minutes; use with caution because of increased risk of adverse events (eg, bradycardia, hypotension, torsade de pointes) (Ref).
Oral: May be administered without regard to meals, but should be administered at the same time each day.
Parenteral:
Loading dose (acute treatment): Must be diluted prior to administration; administer over 15 to 60 minutes (Ref).
Maintenance dose (unable to take oral medications): Must be diluted prior to administration; administer over 2 to 5 hours (Ref).
Missed dose: Oral: Administer next dose at next scheduled time; do not double dose or shorten dosing interval.
Atrial fibrillation/flutter, maintenance of sinus rhythm: Maintenance of normal sinus rhythm (delay in time to recurrence of atrial fibrillation/atrial flutter) in patients with symptomatic atrial fibrillation/atrial flutter who are currently in sinus rhythm.
Ventricular arrhythmias: Treatment of documented, life-threatening ventricular arrhythmias (ie, sustained ventricular tachycardia)
Fetal tachycardia, sustained; Supraventricular tachycardia; Sustained monomorphic ventricular tachycardia, hemodynamically stable; Ventricular premature beats, symptomatic
Sotalol may be confused with Stadol, Sudafed
Betapace may be confused with Betapace AF
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drug classes (antiarrhythmic agent, IV) which have a heightened risk of causing significant patient harm when used in error (High-Alert Medications in Acute Care Settings).
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 drug interactions program by clicking on the “Launch drug interactions program” link above.
Acetylcholinesterase Inhibitors: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Alfuzosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Alpha2-Agonists: Beta-Blockers may increase rebound hypertensive effects of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Alpha2-Agonists may increase AV-blocking effects of Beta-Blockers. Sinus node dysfunction may also be enhanced. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Risk D: Consider Therapy Modification
Amifostine: Blood Pressure Lowering Agents may increase hypotensive effects of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider Therapy Modification
Amiodarone: QT-prolonging Class III Antiarrhythmics (Highest Risk) may increase QTc-prolonging effects of Amiodarone. Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Amisulpride (Oral): QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Amisulpride (Oral). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even greater risk. Risk D: Consider Therapy Modification
Antacids: May decrease serum concentration of Sotalol. Management: Avoid simultaneous administration of sotalol and antacids. Administer antacids 2 hours after sotalol. Risk D: Consider Therapy Modification
Antidiabetic Agents: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Antidiabetic Agents. Beta-Blockers (Nonselective) may increase adverse/toxic effects of Antidiabetic Agents. Specifically, beta-blockers may mask the hypoglycemic symptoms of antidiabetic agents. Risk C: Monitor
Antipsychotic Agents (Phenothiazines): May increase hypotensive effects of Beta-Blockers. Beta-Blockers may decrease metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease metabolism of Beta-Blockers. Risk C: Monitor
Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may increase hypotensive effects of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor
Arginine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Azithromycin (Systemic): QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Azithromycin (Systemic). Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Barbiturates: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Benperidol: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Beta2-Agonists: Beta-Blockers (Nonselective) may decrease bronchodilatory effects of Beta2-Agonists. Risk X: Avoid
Blood Pressure Lowering Agents: May increase hypotensive effects of Hypotension-Associated Agents. Risk C: Monitor
Bradycardia-Causing Agents: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Brimonidine (Topical): May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Bromperidol: May decrease hypotensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase hypotensive effects of Bromperidol. Risk X: Avoid
Cafedrine: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Cafedrine. Risk C: Monitor
Cannabis: Beta-Blockers may increase adverse/toxic effects of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor
Carbetocin: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Ceritinib: May increase QTc-prolonging effects of Sotalol. Ceritinib may increase bradycardic effects of Sotalol. Management: Avoid coadministration if possible. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Chloroquine: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Chloroquine. Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Chlorprothixene: May increase QTc-prolonging effects of Antiarrhythmic Agents (Class III). Risk X: Avoid
Cholinergic Agonists: Beta-Blockers may increase adverse/toxic effects of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Risk C: Monitor
Citalopram: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Citalopram. Risk X: Avoid
Clarithromycin: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Clarithromycin. Risk X: Avoid
Clofazimine: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Clofazimine. Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
ClomiPRAMINE: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
CloZAPine: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of CloZAPine. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Dabrafenib: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Dasatinib: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Dasatinib. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Diazoxide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Dipyridamole: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor
DOBUTamine: Beta-Blockers may decrease therapeutic effects of DOBUTamine. Risk C: Monitor
Domperidone: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Domperidone. Risk X: Avoid
Doxepin-Containing Products: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Doxepin-Containing Products. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
DroPERidol: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of DroPERidol. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
DULoxetine: Blood Pressure Lowering Agents may increase hypotensive effects of DULoxetine. Risk C: Monitor
Encorafenib: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Entrectinib: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Risk X: Avoid
EPHEDrine (Systemic): Beta-Blockers may decrease therapeutic effects of EPHEDrine (Systemic). Risk C: Monitor
EPINEPHrine (Nasal): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Nasal). Risk C: Monitor
EPINEPHrine (Oral Inhalation): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Oral Inhalation). Risk C: Monitor
EPINEPHrine (Systemic): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Systemic). Risk C: Monitor
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may increase vasoconstricting effects of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor
Erythromycin (Systemic): QT-prolonging Class III Antiarrhythmics (Highest Risk) may increase QTc-prolonging effects of Erythromycin (Systemic). Erythromycin (Systemic) may increase QTc-prolonging effects of QT-prolonging Class III Antiarrhythmics (Highest Risk). Management: Avoid concomitant use of erythromycin and class III antiarrhythmic agents. Use of erythromycin with dronedarone is specifically contraindicated. Risk X: Avoid
Escitalopram: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Escitalopram. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Etelcalcetide: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Etilefrine: Beta-Blockers may decrease therapeutic effects of Etilefrine. Etilefrine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Etofylline: Beta-Blockers may decrease therapeutic effects of Etofylline. Risk X: Avoid
Etrasimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Fexinidazole: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Risk X: Avoid
Fingolimod: May increase QTc-prolonging effects of QT-prolonging Class III Antiarrhythmics (Highest Risk). Risk X: Avoid
Flecainide: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Flecainide. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Fluorouracil Products: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Fluorouracil Products. Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Flupentixol: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Flupentixol. Risk X: Avoid
Gadobenate Dimeglumine: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Gadobenate Dimeglumine. Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Gemifloxacin: May increase QTc-prolonging effects of QT-prolonging Class III Antiarrhythmics (Highest Risk). Risk X: Avoid
Gilteritinib: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this combination. If use is necessary, monitor for QTc interval prolongation and arrhythmias. Risk D: Consider Therapy Modification
Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may increase adverse/toxic effects of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider Therapy Modification
Halofantrine: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Halofantrine. Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Haloperidol: QT-prolonging Class III Antiarrhythmics (Highest Risk) may increase QTc-prolonging effects of Haloperidol. Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Herbal Products with Blood Pressure Lowering Effects: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
HydrOXYzine: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Risk C: Monitor
Hypotension-Associated Agents: Blood Pressure Lowering Agents may increase hypotensive effects of Hypotension-Associated Agents. Risk C: Monitor
Iloperidone: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Imipramine: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Inotuzumab Ozogamicin: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Inotuzumab Ozogamicin. Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Insulin: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Insulin. Beta-Blockers (Nonselective) may decrease therapeutic effects of Insulin. Risk C: Monitor
Isoproterenol: Beta-Blockers may decrease therapeutic effects of Isoproterenol. Risk C: Monitor
Ivabradine: Bradycardia-Causing Agents may increase bradycardic effects of Ivabradine. Risk C: Monitor
Lacosamide: Antiarrhythmic Agents (Class III) may increase adverse/toxic effects of Lacosamide. Specifically the risk for bradycardia, ventricular tachyarrhythmias, or a prolonged PR interval may be increased. Risk C: Monitor
Lacosamide: Bradycardia-Causing Agents may increase AV-blocking effects of Lacosamide. Risk C: Monitor
Landiolol: Bradycardia-Causing Agents may increase bradycardic effects of Landiolol. Risk X: Avoid
Levodopa-Foslevodopa: Blood Pressure Lowering Agents may increase hypotensive effects of Levodopa-Foslevodopa. Risk C: Monitor
Levofloxacin-Containing Products (Systemic): May increase QTc-prolonging effects of QT-prolonging Class III Antiarrhythmics (Highest Risk). Risk X: Avoid
Levoketoconazole: QT-prolonging Class III Antiarrhythmics (Highest Risk) may increase QTc-prolonging effects of Levoketoconazole. Risk X: Avoid
Lofexidine: May increase QTc-prolonging effects of Sotalol. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Lormetazepam: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Mavacamten: Beta-Blockers may increase adverse/toxic effects of Mavacamten. Specifically, negative inotropic effects may be increased. Risk C: Monitor
Meglumine Antimoniate: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Metergoline: May decrease antihypertensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase orthostatic hypotensive effects of Metergoline. Risk C: Monitor
Methacholine: Beta-Blockers may increase adverse/toxic effects of Methacholine. Risk C: Monitor
Methadone: QT-prolonging Class III Antiarrhythmics (Highest Risk) may increase QTc-prolonging effects of Methadone. Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Midodrine: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Midostaurin: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Midostaurin. Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Mivacurium: Beta-Blockers may increase therapeutic effects of Mivacurium. Risk C: Monitor
Molsidomine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Moxifloxacin (Systemic): QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Moxifloxacin (Systemic). Risk X: Avoid
Naftopidil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Nicergoline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Nicorandil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
NIFEdipine (Topical): May increase adverse/toxic effects of Beta-Blockers. Risk C: Monitor
NIFEdipine: May increase hypotensive effects of Beta-Blockers. NIFEdipine may increase negative inotropic effects of Beta-Blockers. Risk C: Monitor
Nilotinib: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Nilotinib. Risk X: Avoid
Nitrendipine: May increase therapeutic effects of Beta-Blockers. Risk C: Monitor
Nitroprusside: Blood Pressure Lowering Agents may increase hypotensive effects of Nitroprusside. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents (Topical): May decrease therapeutic effects of Beta-Blockers. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents: May decrease antihypertensive effects of Beta-Blockers. Risk C: Monitor
Obinutuzumab: May increase hypotensive effects of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider Therapy Modification
OLANZapine: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of OLANZapine. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Ondansetron: QT-prolonging Class III Antiarrhythmics (Highest Risk) may increase QTc-prolonging effects of Ondansetron. Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Opipramol: Beta-Blockers may increase serum concentration of Opipramol. Opipramol may increase serum concentration of Beta-Blockers. Risk C: Monitor
Osimertinib: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Osimertinib. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Oxytocin: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Ozanimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Pacritinib: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Pacritinib. Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor
PAZOPanib: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of PAZOPanib. Risk X: Avoid
Pentamidine (Systemic): QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Pentamidine (Systemic). Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Pentoxifylline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Pholcodine: Blood Pressure Lowering Agents may increase hypotensive effects of Pholcodine. Risk C: Monitor
Phosphodiesterase 5 Inhibitors: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Pilsicainide: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Pilsicainide. Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Pimozide: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Pimozide. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk X: Avoid
Piperaquine: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Piperaquine. Risk X: Avoid
Ponesimod: Bradycardia-Causing Agents may increase bradycardic effects 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
Probucol: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Probucol. Risk X: Avoid
Propafenone: May increase QTc-prolonging effects of QT-prolonging Class III Antiarrhythmics (Highest Risk). Risk X: Avoid
Propofol: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Prostacyclin Analogues: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
QT-prolonging Agents (Indeterminate Risk - Avoid): May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor
QT-prolonging Agents (Indeterminate Risk - Caution): May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Monitor for QTc interval prolongation and ventricular arrhythmias when these agents are combined. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk C: Monitor
QT-prolonging Class IA Antiarrhythmics (Highest Risk): May increase QTc-prolonging effects of QT-prolonging Class III Antiarrhythmics (Highest Risk). Risk X: Avoid
QT-prolonging Class III Antiarrhythmics (Highest Risk): May increase QTc-prolonging effects of QT-prolonging Class III Antiarrhythmics (Highest Risk). Risk X: Avoid
QT-Prolonging Inhalational Anesthetics (Moderate Risk): May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
QT-prolonging Kinase Inhibitors (Highest Risk): May increase QTc-prolonging effects of QT-prolonging Class III Antiarrhythmics (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
QT-prolonging Miscellaneous Agents (Highest Risk): QT-prolonging Class III Antiarrhythmics (Highest Risk) may increase QTc-prolonging effects of QT-prolonging Miscellaneous Agents (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
QT-prolonging Moderate CYP3A4 Inhibitors (Moderate Risk): QT-prolonging Class III Antiarrhythmics (Highest Risk) may increase QTc-prolonging effects of QT-prolonging Moderate CYP3A4 Inhibitors (Moderate Risk). QT-prolonging Moderate CYP3A4 Inhibitors (Moderate Risk) may increase serum concentration of QT-prolonging Class III Antiarrhythmics (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
QT-prolonging Strong CYP3A4 Inhibitors (Highest Risk): QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of QT-prolonging Strong CYP3A4 Inhibitors (Highest Risk). Management: Consider alternatives to this combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
QT-prolonging Strong CYP3A4 Inhibitors (Moderate Risk): QT-prolonging Class III Antiarrhythmics (Highest Risk) may increase QTc-prolonging effects of QT-prolonging Strong CYP3A4 Inhibitors (Moderate Risk). QT-prolonging Strong CYP3A4 Inhibitors (Moderate Risk) may increase serum concentration of QT-prolonging Class III Antiarrhythmics (Highest Risk). Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
QUEtiapine: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of QUEtiapine. Risk X: Avoid
Quinagolide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Quizartinib: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Reserpine: May increase hypotensive effects of Beta-Blockers. Reserpine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Ribociclib: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Ribociclib. Risk X: Avoid
RisperiDONE: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of RisperiDONE. QT-prolonging Agents (Highest Risk) may increase CNS depressant effects of RisperiDONE. Management: Consider alternatives to this drug combination. If combined, monitor for QTc interval prolongation and ventricular arrhythmias. Patients with additional risk factors for QTc prolongation may be at even higher risk. Risk D: Consider Therapy Modification
Rivastigmine: May increase bradycardic effects of Beta-Blockers. Risk X: Avoid
ROPivacaine: Antiarrhythmic Agents (Class III) may increase arrhythmogenic effects of ROPivacaine. Risk C: Monitor
Sertindole: May increase QTc-prolonging effects of QT-prolonging Agents (Highest Risk). Risk X: Avoid
Silodosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Siponimod: Bradycardia-Causing Agents may increase bradycardic effects 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
Sparfloxacin: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Sparfloxacin. Risk X: Avoid
Succinylcholine: Beta-Blockers may increase neuromuscular-blocking effects of Succinylcholine. Risk C: Monitor
Sulfonylureas: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Sulfonylureas. Beta-Blockers (Nonselective) may decrease therapeutic effects of Sulfonylureas. Risk C: Monitor
SUNItinib: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of SUNItinib. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Tasimelteon: Beta-Blockers may decrease therapeutic effects of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider Therapy Modification
Terbutaline: Sotalol may decrease therapeutic effects of Terbutaline. Terbutaline may increase QTc-prolonging effects of Sotalol. Risk X: Avoid
Theodrenaline: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Theodrenaline. Risk C: Monitor
Theophylline Derivatives: Beta-Blockers (Nonselective) may decrease bronchodilatory effects of Theophylline Derivatives. Risk C: Monitor
Thioridazine: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Thioridazine. Risk X: Avoid
Toremifene: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Toremifene. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
Vemurafenib: QT-prolonging Agents (Highest Risk) may increase QTc-prolonging effects of Vemurafenib. Management: Consider alternatives to this combination. Patients with other risk factors (eg, older age, female sex, bradycardia, hypokalemia, hypomagnesemia, heart disease, and higher drug concentrations) are likely at greater risk for these toxicities. Risk D: Consider Therapy Modification
White Birch Allergen Extract: Beta-Blockers may increase adverse/toxic effects of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid
Sotalol peak serum concentrations may be decreased if taken with food. Management: Administer without regard to meals.
Erectile dysfunction is noted in product labeling following use of sotalol. As a class, outcomes from available studies evaluating beta-blockers and sexual dysfunction are inconsistent, and the negative effects on erectile function are considered controversial. A clear relationship between use of beta-blockers and erectile dysfunction has not been established. Patients on a beta-blocker presenting with sexual dysfunction should be evaluated for underlying disease (Farmakis 2021; Levine 2012; Semet 2017; Terentes-Printzios 2022; Viigimaa 2020).
Sotalol crosses the placenta.
Adverse fetal/neonatal events have been reported with beta-blockers as a class. If maternal use of a beta-blocker is needed, monitor fetal growth during pregnancy; monitor the newborn for 48 hours after delivery for bradycardia, hypoglycemia, and respiratory depression (ESC [Regitz-Zagrosek 2018]).
Due to pregnancy-induced physiologic changes, renal clearance of sotalol is increased during pregnancy (O’Hare 1983).
Because sotalol crosses the placenta in concentrations similar to maternal serum, it has been studied for the treatment of sustained fetal tachycardia. Sotalol may be considered for the in utero management of fetal supraventricular tachycardia (SVT) or atrial flutter with hydrops or ventricular dysfunction. In cases of SVT without hydrops or ventricular dysfunction, sotalol may be considered if fetal heart rate is ≥200 bpm. Sotalol may also be used for in utero treatment of atrial flutter, and other rare tachycardias with an average fetal heart rate of ≥200 bpm. In addition, sotalol may be considered for fetal ventricular tachycardia (VT) with normal QTc with or without hydrops but is contraindicated for the treatment of fetal VT when long QT syndrome is suspected or confirmed (AHA [Donofrio 2014]).
Sotalol may be used for the treatment of maternal ventricular arrhythmias, atrial fibrillation/atrial flutter, or supraventricular tachycardia during pregnancy; consult current guidelines for specific recommendations (ACC/AHA/HRS [Page 2015]; ESC [Regitz-Zagrosek 2018]).
Sotalol is present in breast milk.
Multiple reports summarize data related to the presence of sotalol in breast milk:
• Sotalol concentrations in breast milk were evaluated in 5 patients receiving sotalol during pregnancy and continuing postpartum. Sotalol therapy started at 200 mg/day and was adjusted as required for maternal BP control (range: 200 to 800 mg/day). Twenty simultaneous milk and maternal serum concentrations were obtained (sampling times not specified). Sotalol concentrations in the breast milk ranged from 4.8 to 20.2 mcg/mL (mean: 10.5 mcg/mL) and maternal serum concentrations ranged from 0.8 to 5 mcg/mL (mean: 2.3mcg/mL). The estimated daily infant dose of sotalol via breast milk calculated by the authors of the study was 0.8 to 3.4 mg/kg/day. Bradycardia was not observed in a breastfeeding infant exposed to the highest concentration of sotalol (≤20.2 mcg/mL; fed twice at 12 days of age and monitored over a period of 8 hours); this infant was noted to have mild bradycardia at birth prior to the start of breastfeeding (maternal dose 600 mg/day) (O’Hare 1980). Using a milk concentration of 20.2 mcg/mL the relative infant dose (RID) of sotalol is 35% compared to a weight-adjusted maternal oral dose of 600 mg/day.
• Sotalol breast milk concentrations were evaluated in a case report. The mother received sotalol 80 mg 3 times/day during pregnancy; this dose was decreased to 80 mg 2 times/day 14 days postpartum. Maternal serum and breast milk samples were obtained on postpartum days 5 and 105. Maternal serum concentrations on day 5 were 0.72 mcg/mL, 6.5 hours after the dose. Corresponding milk concentrations were 4.06 mcg/mL (prefeed: 6.3 hours after the dose) and 3.65 mcg/mL (postfeed: 7 hours after the dose). Maternal serum concentrations on day 105 were 0.97 mcg/mL (2.8 hours after the dose) and milk concentrations ranged from 2.36 mcg/mL (2.8 hours after the dose) to 3.16 mcg/mL (3.3 hours after the dose). The estimated daily infant dose of sotalol via breast milk calculated by the authors of the study was 0.41 to 0.58 mg/kg/day, providing a RID of 20% to 23% compared to a weight adjusted maternal dose of 2.29 to 4.57 mg/kg/day. Adverse events were not observed in the breastfed infant (Hackett 1990).
• Sotalol was measurable in breast milk following maternal use of sotalol 80 mg in combination with flecainide. Both medications were administered twice daily prior to and throughout pregnancy. Breast milk was sampled 3 hours after the second dose on postpartum days 5 and 7. Breast milk concentrations were 5 mcg/mL (postpartum day 5) and 4.4 mcg/mL (postpartum day 7) (Wagner 1990).
• Product labeling estimates the RID of sotalol to be 22% to 22.5% of a weight adjusted maternal dose. In general, breastfeeding is considered acceptable when the RID of a medication is <10%; when the RID is >25% breastfeeding should generally be avoided (Anderson 2016; Ito 2000). Additional considerations can include the gestational and postnatal age of the infant, the actual amount of milk being ingested (less in the first couple days of life and when weaning), properties of the specific maternal medication, medical conditions of the infant, and medications the infant is receiving therapeutically
The manufacturer recommends breastfeeding be discontinued during sotalol therapy. Closely monitor infants exposed to sotalol via breast milk for adverse events such as bradycardia, hypotension, respiratory distress, hypoglycemia (Hackett 1990) as well as diarrhea, constipation, and dry mouth, skin, or eyes.
Serum creatinine (creatinine clearance), magnesium, potassium; heart rate, blood pressure; ECG (eg, QTc interval, PR interval); serum glucose (in patients with diabetes); signs and symptoms of heart failure.
Oral: During initiation and titration period, monitor QTc interval 2 to 4 hours after each dose. If QTc interval is ≥500 msec, reduce dose, prolong the dosing interval, or discontinue sotalol. If the QTc interval is <500 msec after 3 days (after fifth or sixth dose if patient receiving once-daily dosing), patient may be discharged on current regimen. Monitor QTc interval periodically thereafter.
IV:
Loading dose to initiate therapy or for dose escalation: Refer to table in adult or renal dosing sections.
Substitution for oral: Measure QTc interval after completion of each infusion.
Consult individual institutional policies and procedures.
Beta-blocker which contains both beta-adrenoreceptor-blocking (Vaughan Williams Class II) and cardiac action potential duration prolongation (Vaughan Williams Class III) properties
Class II effects: Increased sinus cycle length, slowed heart rate, decreased AV nodal conduction, and increased AV nodal refractoriness Sotalol has both beta1- and beta2-receptor blocking activity. The beta-blocking effect of sotalol is a noncardioselective (half maximal at about 80 mg/day and maximal at doses of 320 to 640 mg/day). Significant beta-blockade occurs at oral doses as low as 25 mg/day.
Class III effects: Prolongation of the atrial and ventricular monophasic action potentials, and effective refractory prolongation of atrial muscle, ventricular muscle, and atrioventricular accessory pathways in both the antegrade and retrograde directions. Sotalol is a racemic mixture of d- and l-sotalol; both isomers have similar Class III antiarrhythmic effects while the l-isomer is responsible for virtually all of the beta-blocking activity. The Class III effects are seen only at oral doses ≥160 mg/day.
Onset of action:
Oral: Rapid; at 1 to 2 hours post dosing (steady-state), reductions in heart rate and cardiac index seen (Winters 1993).
IV: When administered IV over 5 minutes for ongoing VT, onset of action is ~5 to 10 minutes (Ho 1994).
Absorption: Oral: Well absorbed (Hanyok 1993); decreased ~20% by meals compared with fasting.
Distribution: Vd: 1.2 to 2.4 L/kg (Hanyok 1993).
Protein binding: None.
Metabolism: None.
Bioavailability: Oral: 90% to 100%.
Half-life elimination:
Oral:
Neonates ≤1 month: 8.4 ± 0.3 hours (Saul 2001).
Infants and Children >1 month to 24 months: 7.4 ± 1.8 hours (Saul 2001).
Children >2 years to <7 years: 9.1 ± 2.9 hours (Saul 2001).
Children 7 to 12 years: 9.2 ± 3 hours (Saul 2001).
Adults: 12 hours; adults with renal failure (anuric): Up to 69 hours.
IV: Pharmacokinetics of the IV formulation (administered over 5 hours) are similar to the oral formulations (Somberg 2010).
Time to peak, serum: Oral: Infants and Children 3 days to 12 years: Mean range: 2 to 3 hours; Adults: 2.5 to 4 hours.
Excretion: Urine (as unchanged drug).
Clearance (apparent) (Saul 2001):
Neonates ≤1 month: 11 ± 2 mL/minute.
Infants and Children >1 month to 24 months: 32 ± 14 mL/minute.
Children >2 years to <7 years: 63 ± 21 mL/minute.
Children 7 to 12 years: 95 ± 32 mL/minute.
Altered kidney function: Terminal half-life increases with renal impairment.
