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  • CLASSES

    Anti-arrhythmics, Class II
    Anti-arrhythmics, Class III

    BOXED WARNING

    Apheresis, AV block, bradycardia, cardiogenic shock, cardiomyopathy, celiac disease, diarrhea, females, fever, heart failure, human immunodeficiency virus (HIV) infection, hyperparathyroidism, hypocalcemia, hypokalemia, hypomagnesemia, hypothermia, hypothyroidism, long QT syndrome, myocardial infarction, pheochromocytoma, QT prolongation, requires a specialized care setting, requires an experienced clinician, rheumatoid arthritis, sick sinus syndrome, sickle cell disease, sleep deprivation, stroke, systemic lupus erythematosus (SLE), ventricular arrhythmias, ventricular fibrillation, ventricular tachycardia

    Sotalol is contraindicated in patients with sinus bradycardia (less than 50 beats per minute), sick sinus syndrome, second or third-degree AV block without a pacemaker, congenital or acquired long QT syndrome, cardiogenic shock, decompensated heart failure, and/or serum potassium less than 4 mEq/L (hypokalemia). Sotalol is also contraindicated in patients with a baseline QT interval of more than 450 milliseconds; for Betapace/Betapace AF and Sorine, this contraindication only applies for the treatment of atrial fibrillation or atrial flutter. Sotalol has proarrhythmic effects and may induce or worsen cardiac arrhythmias, primarily ventricular arrhythmias. Use has been associated with QT prolongation, which can lead to sustained ventricular fibrillation (VF), sustained ventricular tachycardia (VT), and/or torsade de pointes (TdP). To minimize the risk of drug-induced arrhythmia, the initiation or up-titration of intravenous sotalol and initiation or reinitiation of oral sotalol requires a specialized care setting, specifically a facility that can provide continuous ECG monitoring and cardiac resuscitation, and requires an experienced clinician who is trained in the management of serious ventricular arrhythmias. Hospitalize patients initiated or reinitiated on sotalol for at least 3 days or until steady-state concentrations are achieved. Correct hypokalemia and hypomagnesemia before initiating sotalol. Assess electrolyte and acid-base balance in patients experiencing severe or prolonged diarrhea or those receiving concomitant diuretics. Use sotalol with caution in patients with conditions that may increase the risk of QT prolongation including bradycardia, AV block, heart failure, stress-related cardiomyopathy, myocardial infarction, stroke, hypocalcemia, or in patients receiving medications known to prolong the QT interval or cause electrolyte imbalances. Females, people 65 years and older, patients with sleep deprivation, pheochromocytoma, sickle cell disease, hypothyroidism, hyperparathyroidism, hypothermia, systemic inflammation (e.g., human immunodeficiency virus (HIV) infection, fever, and some autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus (SLE), and celiac disease) and patients undergoing apheresis procedures (e.g., plasmapheresis [plasma exchange], cytapheresis) may also be at increased risk for QT prolongation. Reduced renal function, higher doses, bradycardia, history of sustained VT/VF, and atrial fibrillation with sinus node dysfunction can also increase the risk of TdP. Adjust the sotalol dosage according to renal function and monitor the ECG for excessive increases in the QT interval.[28432] [28457] [36213] [36512] [56592] [58335] [60784]

    DEA CLASS

    Rx

    DESCRIPTION

    Nonselective beta-adrenergic blocking agent and class III antiarrhythmic
    Used for the treatment of atrial fibrillation, atrial flutter, and life-threatening ventricular arrhythmias
    May induce QT prolongation and torsade de pointes

    COMMON BRAND NAMES

    BETAPACE, BETAPACE AF, Sorine, SOTYLIZE

    HOW SUPPLIED

    BETAPACE/BETAPACE AF/Sorine/Sotalol/Sotalol Hydrochloride Oral Tab: 80mg, 120mg, 160mg, 240mg
    Sotalol/Sotalol Hydrochloride Intravenous Inj Sol: 1mL, 15mg
    SOTYLIZE Oral Sol: 1mL, 5mg

    DOSAGE & INDICATIONS

    For the maintenance of normal sinus rhythm in patients with symptomatic atrial fibrillation or atrial flutter who are currently in sinus rhythm.
    For the maintenance of normal sinus rhythm in adults.
    Oral dosage
    Adults

    80 mg PO twice daily, initially. May increase dose by 80 mg/day every 3 days if the QTc interval is less than 500 milliseconds. Most patients will have a satisfactory response with 120 mg PO twice daily.[58335] [60784]

    Intravenous dosage (substituting for oral sotalol therapy)
    Adults

    75 mg IV for 80 mg PO, 112.5 mg IV for 120 mg PO, or 150 mg IV for 160 mg PO at the same oral dosing frequency.

    Intravenous dosage (initiation)

    NOTE: The intravenous loading dose depends on the target oral dose.

    Adults

    60 mg IV once when initiating 80 mg PO every 12 hours or 90 mg IV once when initiating 120 mg PO every 12 hours. Delay first oral dose for at least 4 hours after IV loading dose.

    Intravenous dosage (escalation)

    NOTE: The intravenous loading dose depends on the target oral dose.

    Adults

    75 mg IV once when escalating from 80 to 120 mg PO every 12 hours or 90 mg IV once when escalating from 120 to 160 mg PO every 12 hours. Delay first oral dose for at least 4 hours after IV loading dose.

    For the maintenance of normal sinus rhythm in pediatric patients†.
    Oral dosage
    Children and Adolescents 6 to 17 years

    30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily titrated up as needed at intervals of 36 hours or more (Max: 60 mg/m2/dose or 2.4 mg/kg/dose PO 3 times daily) is recommended by FDA-approved labeling. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day).[24916] [24917] [36233] A target dose of 4 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.[36233] An absolute maximum dose for pediatric patients has not been specified; FDA-approved labeling recommends a maximum dose of 320 mg/day PO for adult patients.[60784]

    Children 2 to 5 years

    30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily titrated up as needed at intervals of 36 hours or more (Max: 60 mg/m2/dose or 2.4 mg/kg/dose PO 3 times daily) is recommended by FDA-approved labeling. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day).[24916] [24917] [36233] A target dose of 6 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.[36233] An absolute maximum dose for pediatric patients has not been specified; FDA-approved labeling recommends a maximum dose of 320 mg/day PO for adult patients.[60784]

    Infants and Children younger than 2 years

    Reducing the usual starting dose recommended for a child 2 years or older (30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily) by an age-specific reduction factor, which is determined by plotting the child's age on the manufacturer-provided logarithmic scale (see complete prescribing information), is recommended by FDA-approved product labeling. Use similar calculations for dose titration. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day).[24916] [24917] [36233] A target dose of 6 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.[36233]

    Neonates

    Reducing the usual starting dose recommended for a child 2 years or older (30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily) by an age-specific reduction factor, which is determined by plotting the child's age on the manufacturer-provided logarithmic scale (see complete prescribing information), is recommended by FDA-approved product labeling. Use similar calculations for dose titration. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day).[24916] [24917] [36233] A target dose of 4 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.[36233]

    Intravenous dosage
    Adolescents

    0.95 mg/kg IV as a starting dose.

    Children 6 to 12 years

    1.1 mg/kg IV as a starting dose.

    Infants and Children 1 month to 5 years

    1.2 mg/kg IV as a starting dose.

    Neonates 3 weeks

    1 mg/kg IV as a starting dose.

    Neonates 2 weeks

    0.9 mg/kg IV as a starting dose.

    Neonates 12 to 13 days

    0.81 mg/kg IV as a starting dose.

    Neonates 9 to 11 days

    0.69 mg/kg IV as a starting dose.

    Neonates 6 to 8 days

    0.51 mg/kg IV as a starting dose.

    Neonates 3 to 5 days

    0.32 mg/kg IV as a starting dose.

    For the treatment of life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia.
    For the treatment of life-threatening ventricular arrhythmias in adult patients.
    Oral dosage
    Adults

    80 mg PO twice daily, initially. May increase dose by 80 mg/day every 3 days if the QTc interval is less than 500 milliseconds. Most patients will have a satisfactory response with 160 to 320 mg/day PO in 2 or 3 divided doses. Doses as high as 480 to 640 mg/day PO have been used in refractory life-threatening arrhythmias.[36512] [60784]

    Intravenous dosage (substituting for oral sotalol therapy)
    Adults

    75 mg IV for 80 mg PO, 112.5 mg IV for 120 mg PO, or 150 mg IV for 160 mg PO at the same oral dosing frequency.

    Intravenous dosage (initiation)

    NOTE: The intravenous loading dose depends on the target oral dose.

    Adults

    60 mg IV once when initiating 80 mg PO every 12 hours or 90 mg IV once when initiating 120 mg PO every 12 hours. Delay first oral dose for at least 4 hours after IV loading dose.

    Intravenous dosage (escalation)

    NOTE: The intravenous loading dose depends on the target oral dose.

    Adults

    75 mg IV once when escalating from 80 to 120 mg PO every 12 hours or 90 mg IV once when escalating from 120 to 160 mg PO every 12 hours. Delay first oral dose for at least 4 hours after IV loading dose.

    For the treatment of life-threatening ventricular arrhythmias in pediatric patients†.
    Oral dosage
    Children and Adolescents 6 to 17 years

    30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily titrated up as needed at intervals of 36 hours or more (Max: 60 mg/m2/dose or 2.4 mg/kg/dose PO 3 times daily) is recommended by FDA-approved labeling. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day).[24916] [24917] [36233] A target dose of 4 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.[36233] An absolute maximum dose for pediatric patients has not been specified; FDA-approved labeling recommends a maximum dose of 320 mg/day PO for adult patients.[60784]

    Children 2 to 5 years

    30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily titrated up as needed at intervals of 36 hours or more (Max: 60 mg/m2/dose or 2.4 mg/kg/dose PO 3 times daily) is recommended by FDA-approved labeling. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day).[24916] [24917] [36233] A target dose of 6 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.[36233] An absolute maximum dose for pediatric patients has not been specified; FDA-approved labeling recommends a maximum dose of 320 mg/day PO for adult patients.[60784]

    Infants and Children younger than 2 years

    Reducing the usual starting dose recommended for a child 2 years or older (30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily) by an age-specific reduction factor, which is determined by plotting the child's age on the manufacturer-provided logarithmic scale (see complete prescribing information), is recommended by FDA-approved product labeling. Use similar calculations for dose titration. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day).[24916] [24917] [36233] A target dose of 6 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.[36233]

    Neonates

    Reducing the usual starting dose recommended for a child 2 years or older (30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily) by an age-specific reduction factor, which is determined by plotting the child's age on the manufacturer-provided logarithmic scale (see complete prescribing information), is recommended by FDA-approved product labeling. Use similar calculations for dose titration. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day).[24916] [24917] [36233] A target dose of 4 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.[36233]

    Intravenous dosage
    Adolescents

    0.95 mg/kg IV as a starting dose.

    Children 6 to 12 years

    1.1 mg/kg IV as a starting dose.

    Infants and Children 1 month to 5 years

    1.2 mg/kg IV as a starting dose.

    Neonates 3 weeks

    1 mg/kg IV as a starting dose.

    Neonates 2 weeks

    0.9 mg/kg IV as a starting dose.

    Neonates 12 to 13 days

    0.81 mg/kg IV as a starting dose.

    Neonates 9 to 11 days

    0.69 mg/kg IV as a starting dose.

    Neonates 6 to 8 days

    0.51 mg/kg IV as a starting dose.

    Neonates 3 to 5 days

    0.32 mg/kg IV as a starting dose.

    For the maintenance of sinus rhythm in patients with supraventricular arrhythmias†, including paroxysmal supraventricular tachycardia (PSVT)†, Wolff-Parkinson-White (WPW) syndrome†, junctional ectopic tachycardia†, and atrioventricular node reentrant tachycardia†.
    Oral dosage
    Children and Adolescents 6 to 17 years

    30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily titrated up as needed at intervals of 36 hours or more (Max: 60 mg/m2/dose or 2.4 mg/kg/dose PO 3 times daily) is recommended by FDA-approved labeling. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day PO). A target dose of 4 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study. An absolute maximum dose for pediatric patients has not been specified; FDA-approved labeling recommends a maximum dose of 320 mg/day PO for adult patients treated for atrial fibrillation/atrial flutter and 640 mg/day PO for adult patients treated for ventricular arrhythmias.

    Children 2 to 5 years

    30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily titrated up as needed at intervals of 36 hours or more (Max: 60 mg/m2/dose or 2.4 mg/kg/dose PO 3 times daily) is recommended by FDA-approved labeling. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day PO). A target dose of 6 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study. An absolute maximum dose for pediatric patients has not been specified; FDA-approved labeling recommends a maximum dose of 320 mg/day PO for adult patients treated for atrial fibrillation/atrial flutter and 640 mg/day PO for adult patients treated for ventricular arrhythmias.

    Infants and Children younger than 2 years

    Reducing the usual starting dose recommended for a child 2 years or older (30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily) by an age-specific reduction factor, which is determined by plotting the child's age on the manufacturer-provided logarithmic scale (see complete prescribing information), is recommended by FDA-approved product labeling. Use similar calculations for dose titration. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day). A target dose of 6 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.

    Neonates

    Reducing the usual starting dose recommended for a child 2 years or older (30 mg/m2/dose or 1.2 mg/kg/dose PO 3 times daily) by an age-specific reduction factor, which is determined by plotting the child's age on the manufacturer-provided logarithmic scale (see complete prescribing information), is recommended by FDA-approved product labeling. Use similar calculations for dose titration. [58335] Alternatively, initial doses of 1 to 2 mg/kg/day PO given in 2 to 3 divided doses have been studied in pediatric patients with various tachyarrhythmias (combined n from 3 studies = 213). The dose was increased as needed by 1 to 2 mg/kg/day PO every 3 days (Max: 10 mg/kg/day). A target dose of 4 mg/kg/day PO given in 3 divided doses has been recommended based on the results of a population pharmacokinetic/pharmacodynamic study.

    For primary atrial fibrillation prophylaxis† in patients undergoing cardiac surgery†.
    Oral dosage
    Adults

    80 mg PO twice daily.[33410] [33411] [33412] [33413] [33414] Individualize dose based on CrCl, QTc, and clinical response. Prophylactic administration of sotalol may be considered for patients at risk of developing atrial fibrillation after cardiac surgery.[56966]

    †Indicates off-label use

    MAXIMUM DOSAGE

    Adults

    320 mg/day PO for atrial fibrillation/atrial flutter; 640 mg/day PO for life-threatening ventricular arrhythmias; 600 mg/day IV.

    Geriatric

    320 mg/day PO for atrial fibrillation/atrial flutter; 640 mg/day PO for life-threatening ventricular arrhythmias; 600 mg/day IV.

    Adolescents

    Safety and efficacy have not been established; 180 mg/m2/day or 7.2 mg/kg/day PO is the maximum dosage recommended by FDA-approved labeling; alternatively, doses up to 10 mg/kg/day PO have been used for the management of various tachyarrhythmias.

    Children

    2 to 12 years: Safety and efficacy have not been established; 180 mg/m2/day or 7.2 mg/kg/day PO is the maximum dosage recommended by FDA-approved labeling; alternatively, doses up to 10 mg/kg/day PO have been used for the management of various tachyarrhythmias.
    1 year: Safety and efficacy have not been established; see full prescribing information for age-specific dosing chart; doses up to 10 mg/kg/day PO have been used for the management of various tachyarrhythmias.

    Infants

    Safety and efficacy have not been established; see full prescribing information for age-specific dosing chart; doses up to 10 mg/kg/day PO have been used for the management of various tachyarrhythmias.

    Neonates

    Safety and efficacy have not been established; see full prescribing information for age-specific dosing chart; doses up to 10 mg/kg/day PO have been used for the management of various tachyarrhythmias.

    DOSING CONSIDERATIONS

    Hepatic Impairment

    Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.

    Renal Impairment

    Sotalol has not been studied in pediatric patients with renal impairment; although lower doses, increased dosing intervals, and/or slower titration are recommended, specific dosage adjustments are not available. It will take longer to reach steady-state in pediatric patients with renal impairment; closely monitor heart rate and QTc interval. Recommended dose adjustments for adult patients are dependent on the formulation and/or indication:
     
    Betapace/Betapace AF (all indications) and Sorine (ventricular arrhythmias):
    CrCl 60 mL/minute or more: No dosage adjustment needed.
    CrCl 30 to 59 mL/minute: Extend dosage interval to every 24 hours. Dose may be titrated after at least 5 doses.
    CrCl 10 to 29 mL/minute: Extend dosage interval to every 36 to 48 hours according to clinical response. Dose may be titrated after at least 5 doses.
    CrCl less than 10 mL/minute: Individualize dosage. [60784]
     
    Sorine (atrial fibrillation/atrial flutter) and Sotylize (all indications):
    CrCl 60 mL/minute or more: No dosage adjustment needed.
    CrCl 40 to 59 mL/minute: Extend dosage interval to every 24 hours. Dose may be titrated after at least 5 doses.
    CrCl less than 40 mL/minute: Use is contraindicated. [58335]
     
    Intravenous Load DosingNOTE: The intravenous loading dose depends on the target oral dose.[36213]InitiationCrCl 60 to 90 mL/minute: 82.5 mg IV once followed by 80 mg PO every 12 hours or 125 mg IV once followed by 120 mg PO every 12 hours. Delay first oral dose for at least 4 hours after IV loading dose.
    CrCl 30 to 60 mL/minute: 75 mg IV once followed by 80 mg PO every 24 hours or 112.5 mg IV once followed by 120 mg PO every 24 hours. Delay first oral dose for at least 6 hours after IV loading dose.
    CrCl 10 to 30 mL/minute: 75 mg IV once followed by 80 mg PO every 48 hours or 112.5 mg IV once followed by 120 mg PO every 48 hours. Delay first oral dose for at least 12 hours after IV loading dose.[36213]EscalationCrCl 60 to 90 mL/minute: 82.5 mg IV once when escalating from 80 to 120 mg PO every 12 hours or 105 mg IV once when escalating from 120 to 160 mg PO every 12 hours. Delay first oral dose for at least 4 hours after IV loading dose.
    CrCl 30 to 60 mL/minute: 82.5 mg IV once when escalating from 80 to 120 mg PO every 24 hours or 105 mg IV once when escalating from 120 to 160 mg PO every 24 hours. Delay first oral dose for at least 6 hours after IV loading dose.
    CrCl 10 to 30 mL/minute: 82.5 mg IV once when escalating from 80 to 120 mg PO every 48 hours or 105 mg IV once when escalating from 120 to 160 mg PO every 48 hours. Delay first oral dose for at least 12 hours after IV loading dose.[36213]
    Intermittent hemodialysis
    Sorine for atrial fibrillation/atrial flutter and Sotylize are contraindicated in patients with CrCl less than 40 mL/minute. [58335] The half-life of sotalol is prolonged up to 69 hours in anuric patients. While sotalol is partially removed by hemodialysis, subsequent partial rebound in sotalol concentrations will occur once the dialysis session is completed. Both heart rate and QT interval, as well as efficacy (arrhythmia control), must be carefully monitored.[58335] [60784]

    ADMINISTRATION

    Oral Administration

    May administer without regard to meals.

    Oral Liquid Formulations

    Measure dosage with calibrated measuring device.
    Extemporaneous Oral Suspension: Shake well prior to use.

    Extemporaneous Compounding-Oral

    Extemporaneous 5 mg/mL Oral Suspension Preparation
    NOTE: A 5 mg/mL oral solution is commercially available.
    Measure 120 mL of Simple Syrup containing 0.1% sodium benzoate (Syrup, NF).
    Transfer the syrup to a 6-ounce amber plastic bottle.
    Add five 120 mg sotalol tablets to the bottle. The tablets may be added intact or they may be crushed.
    If the tablets are crushed, carefully transfer the entire amount of powder to the bottle and shake the bottle until dispersion of the fine particles in the syrup is obtained.
    If the tablets are intact, shake the bottle to wet the entire surface of the tablet and allow to hydrate for approximately 2 hours. The tablets may also be hydrated overnight to allow for easier disintegration.
    Shake the bottle intermittently over the next 2 hours until the tablets are completely disintegrated and dispersion of fine particles in the syrup is achieved.
    Storage: The resulting suspension is stable for 3 months at 15 to 30 degrees C (59 to 86 degrees F).[36512] [60784]

    Injectable Administration

    Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
    Initiate or titrate intravenous sotalol in a facility that can provide continuous ECG monitoring and cardiac resuscitation.[36213]

    Intravenous Administration

    Dilution
    Dilute in 0.9% Sodium Chloride Injection, Dextrose 5% Injection, or Lactated Ringer's Injection.
    Choose a volume convenient for administration and consistent with fluid restriction.[36213]
     
    IV Infusion
    Use a volumetric infusion pump.
    The infusion rate varies by indication:
    For substitution of oral sotalol: Infuse over 5 hours.
    For loading dose: Infuse over 1 hour. Measure and normalize serum potassium and magnesium concentrations before initiation. Monitor QTc interval every 15 minutes during infusion.[36213]
    For emergent situations: Infuse 100 mg over 5 minutes.[45649] [60266]

    STORAGE

    Generic:
    - Protect from freezing
    - Protect from light
    - Store at controlled room temperature (between 68 and 77 degrees F)
    - Store in carton until time of use
    BETAPACE:
    - Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
    BETAPACE AF:
    - Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
    Sorine :
    - Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F
    SOTYLIZE:
    - Store between 68 to 77 degrees F, excursions permitted 59 to 86 degrees F

    CONTRAINDICATIONS / PRECAUTIONS

    General Information

    Sotalol is contraindicated in patients with a known hypersensitivity to sotalol. Use sotalol with caution in patients with a history of anaphylactic reactions. These patients may have a more severe reaction if rechallenge to the allergen occurs while receiving a beta-blocker, such as sotalol. The patient also may be unresponsive to the usual doses of epinephrine used to treat the reaction.

    Abrupt discontinuation

    Abrupt discontinuation of beta-blockers can exacerbate angina and precipitate a heart attack. Further, abrupt discontinuation of sotalol may unmask latent coronary insufficiency. When discontinuing chronically administered sotalol, gradually reduce the dose over 1 to 2 weeks, if possible, and monitor the patient. Consider use of an alternative beta-blocker if angina worsens or acute coronary ischemia develops. Advise patient's not to interrupt therapy without their health care provider's advice.[36512] [60784]

    Hyperthyroidism, thyroid disease

    Beta-blockade may mask certain clinical signs (e.g., tachycardia) of hyperthyroidism. Avoid abrupt withdrawal of beta-blockade in patients with thyroid disease because it may lead to an exacerbation of symptoms of hyperthyroidism, including thyroid storm.[36213] [60784]

    Apheresis, AV block, bradycardia, cardiogenic shock, cardiomyopathy, celiac disease, diarrhea, females, fever, heart failure, human immunodeficiency virus (HIV) infection, hyperparathyroidism, hypocalcemia, hypokalemia, hypomagnesemia, hypothermia, hypothyroidism, long QT syndrome, myocardial infarction, pheochromocytoma, QT prolongation, requires a specialized care setting, requires an experienced clinician, rheumatoid arthritis, sick sinus syndrome, sickle cell disease, sleep deprivation, stroke, systemic lupus erythematosus (SLE), ventricular arrhythmias, ventricular fibrillation, ventricular tachycardia

    Sotalol is contraindicated in patients with sinus bradycardia (less than 50 beats per minute), sick sinus syndrome, second or third-degree AV block without a pacemaker, congenital or acquired long QT syndrome, cardiogenic shock, decompensated heart failure, and/or serum potassium less than 4 mEq/L (hypokalemia). Sotalol is also contraindicated in patients with a baseline QT interval of more than 450 milliseconds; for Betapace/Betapace AF and Sorine, this contraindication only applies for the treatment of atrial fibrillation or atrial flutter. Sotalol has proarrhythmic effects and may induce or worsen cardiac arrhythmias, primarily ventricular arrhythmias. Use has been associated with QT prolongation, which can lead to sustained ventricular fibrillation (VF), sustained ventricular tachycardia (VT), and/or torsade de pointes (TdP). To minimize the risk of drug-induced arrhythmia, the initiation or up-titration of intravenous sotalol and initiation or reinitiation of oral sotalol requires a specialized care setting, specifically a facility that can provide continuous ECG monitoring and cardiac resuscitation, and requires an experienced clinician who is trained in the management of serious ventricular arrhythmias. Hospitalize patients initiated or reinitiated on sotalol for at least 3 days or until steady-state concentrations are achieved. Correct hypokalemia and hypomagnesemia before initiating sotalol. Assess electrolyte and acid-base balance in patients experiencing severe or prolonged diarrhea or those receiving concomitant diuretics. Use sotalol with caution in patients with conditions that may increase the risk of QT prolongation including bradycardia, AV block, heart failure, stress-related cardiomyopathy, myocardial infarction, stroke, hypocalcemia, or in patients receiving medications known to prolong the QT interval or cause electrolyte imbalances. Females, people 65 years and older, patients with sleep deprivation, pheochromocytoma, sickle cell disease, hypothyroidism, hyperparathyroidism, hypothermia, systemic inflammation (e.g., human immunodeficiency virus (HIV) infection, fever, and some autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus (SLE), and celiac disease) and patients undergoing apheresis procedures (e.g., plasmapheresis [plasma exchange], cytapheresis) may also be at increased risk for QT prolongation. Reduced renal function, higher doses, bradycardia, history of sustained VT/VF, and atrial fibrillation with sinus node dysfunction can also increase the risk of TdP. Adjust the sotalol dosage according to renal function and monitor the ECG for excessive increases in the QT interval.[28432] [28457] [36213] [36512] [56592] [58335] [60784]

    Renal failure, renal impairment

    Sorine for atrial fibrillation/atrial flutter and Sotylize are contraindicated in patients with a creatinine clearance less than 40 mL/minute (i.e., renal failure or renal impairment). Adjustments to sotalol dosage are necessary based on creatinine clearance.[36213] [36512] [58335] [60784]

    Laboratory test interference

    The presence of sotalol in the urine may cause laboratory test interference and result in falsely elevated concentrations of urinary metanephrine when measured by fluorimetric or photometric method.[36213]

    Surgery

    The impaired ability of the heart to respond to reflex adrenergic stimuli due to beta-blocking therapy may augment the risks of general anesthesia and surgical procedures. In general, do not routinely withdraw chronically administered beta-blocking therapy before major surgery.[36213] [36512] [60784]

    Acute bronchospasm, asthma, bronchitis, chronic lung disease (CLD)

    Sotalol is contraindicated in patients with bronchial asthma or related bronchospastic conditions (e.g., acute bronchospasm). Avoid sotalol in patients with bronchospastic diseases (e.g., chronic lung disease (CLD), like emphysema or chronic bronchitis). If sotalol is to be administered, use the smallest effective dose to minimize inhibition of bronchodilation produced by endogenous or exogenous catecholamine stimulation of beta-2 receptors.[36213] [36512] [58335] [60784]

    Diabetes mellitus

    Beta-blockers prolong or enhance hypoglycemia by interfering with catecholamine-induced glycogenolysis, glyconeogenesis, and lipolysis. Additionally, they can mask signs of hypoglycemia, including tachycardia, palpitations, and tremors. In addition to acute blood glucose effects, beta-blockers have been shown to increase the risk of developing diabetes mellitus in adult hypertensive patients. The risk in pediatric patients is undefined.

    Peripheral vascular disease, Raynaud's phenomenon

    Avoid sotalol in patients with Raynaud's phenomenon or peripheral vascular disease because reduced cardiac output and the relative increase in alpha stimulation can exacerbate symptoms.

    Acute myocardial infarction

    Use sotalol with caution and careful dosage titration in the first 2 weeks after acute myocardial infarction, especially in patients with markedly impaired ventricular function. Sotalol (320 mg/day PO; non-titrated) did not significantly affect mortality in a large double-blind, placebo-controlled secondary prevention (post-infarction) trial including 1,456 adults; however, there was a suggestion of early (within the first 10 days of treatment) excess mortality in sotalol-treated patients. In a second smaller trial (n = 17 randomized to sotalol), 4 fatalities and 3 serious hemodynamic/electrical events occurred within 2 weeks of sotalol initiation in high-risk post-infarction patients (ejection fraction less than 40% and either more than 10 VPC/hour or VT on Holter) receiving high dose sotalol (320 mg PO twice daily).[60784] During investigation of the d-isomer of sotalol (virtually devoid of beta-blocking activity and considered a pure Class III antiarrhythmic) as an antiarrhythmic in high-risk patients post-MI, a higher mortality rate was observed with d-sotalol vs. placebo, presumably due to increased arrhythmic deaths.[26285]

    Geriatric

    In general, geriatric patients may be at increased risk for QT prolongation from drugs such as sotalol.[28432] [28457] [56592] The federal Omnibus Budget Reconciliation Act (OBRA) regulates medication use in residents (e.g., geriatric adults) of long-term care facilities. The OBRA guidelines caution that antiarrhythmics can have serious adverse effects (e.g., impairment of mental function, appetite, behavior, heart function, or falls) in older individuals.

    Labor, neonates, obstetric delivery, pregnancy

    Both the use of sotalol and the untreated underlying condition in pregnancy cause adverse outcomes to the mother and fetus/neonate. The incidence of ventricular tachycardia is increased and may be more symptomatic during pregnancy. Breakthrough arrhythmias may also occur during pregnancy, as therapeutic drug concentrations may be difficult to maintain due to the increased volume of distribution and increased drug metabolism during pregnancy. Sotalol crosses the placenta and is found in amniotic fluid. From published observational studies, potential fetal adverse effects include growth restriction, transient fetal bradycardia, hyperbilirubinemia, hypoglycemia, maternal uterine contractions, and intrauterine death. Sotalol may have a greater effect on QT prolongation in the immature heart, and therefore, there may be an increased risk of serious fetal arrhythmia and/or intrauterine death. Monitor exposed neonates for symptoms of beta-blockade. Monitor mothers treated with sotalol continuously during labor and obstetric delivery; the risk of arrhythmias increases during the labor and delivery process. In animal reproduction studies in rats, early resorptions were increased at 15 to 18 times the maximum recommended human dose (MRHD), while no increase in early resorptions was noted at 2 to 2.5 times the MRHD. In rabbits, an increase in fetal death was observed at 2 times the MRHD administered as single dose (50 mg/kg) on gestation day 4. A slight increase in fetal death and maternal toxicity occurred in rabbits that received 6 times the MRHD. No teratogenic effects were noted in rats and rabbits that received sotalol at 9 the 7 times the MRHD, respectively, during organogenesis.[36213] [36512] [60784]

    Breast-feeding

    Because of the potential for serious adverse reactions in the breast-fed child and the high concentration of sotalol in breast milk, advise women to discontinue breast-feeding during sotalol therapy. Sotalol is present in human milk. The estimated daily infant dose of sotalol received from breastmilk is 0.8 to 3.4 mg/kg/day (22% to 25.5% of the maternal weight-adjusted dosage), which is similar to the neonatal therapeutic dosage. Therefore, there is potential for bradycardia and other symptoms of beta-blockade (e.g., dry mouth, skin, or eyes, diarrhea, or constipation) in the breast-fed child. There is no information on the effects of sotalol on milk production.[36213] [60784]

    Infertility, reproductive risk

    Beta-blockers, including sotalol, may be associated with reproductive risk and cause erectile dysfunction resulting in male infertility.[36213]

    ADVERSE REACTIONS

    Severe

    bradycardia / Rapid / 1.0-13.1
    torsade de pointes / Rapid / 0.6-4.0
    AV block / Early / 1.0-1.0
    muscle paralysis / Delayed / 0-1.0
    heart failure / Delayed / Incidence not known
    ventricular fibrillation / Early / Incidence not known
    ventricular tachycardia / Early / Incidence not known
    visual impairment / Early / Incidence not known
    bronchospasm / Rapid / Incidence not known

    Moderate

    chest pain (unspecified) / Early / 4.0-15.4
    QT prolongation / Rapid / 4.0-12.0
    depression / Delayed / 2.0-2.0
    confusion / Early / 0-1.0
    thrombocytopenia / Delayed / 0-1.0
    eosinophilia / Delayed / 0-1.0
    hyperlipidemia / Delayed / 0-1.0
    leukopenia / Delayed / 0-1.0
    hyperglycemia / Delayed / Incidence not known
    hypoglycemia / Early / Incidence not known
    diabetes mellitus / Delayed / Incidence not known
    peripheral neuropathy / Delayed / Incidence not known
    dyspnea / Early / Incidence not known
    withdrawal / Early / Incidence not known

    Mild

    asthenia / Delayed / 10.5-20.5
    abdominal pain / Early / 7.0-7.0
    fatigue / Early / 2.0-6.0
    dizziness / Early / 3.0-3.0
    headache / Early / 2.0-2.0
    vertigo / Early / 0-1.0
    emotional lability / Early / 0-1.0
    myalgia / Early / 0-1.0
    pruritus / Rapid / 0-1.0
    photosensitivity / Delayed / 0-1.0
    alopecia / Delayed / 0-1.0
    nausea / Early / Incidence not known
    diarrhea / Early / Incidence not known
    vomiting / Early / Incidence not known
    hyperhidrosis / Delayed / Incidence not known
    fever / Early / Incidence not known
    musculoskeletal pain / Early / Incidence not known
    weakness / Early / Incidence not known
    cough / Delayed / Incidence not known

    DRUG INTERACTIONS

    Abarelix: (Contraindicated) Since abarelix can cause QT prolongation, abarelix should be used cautiously, if at all, with other drugs that are associated with QT prolongation, including sotalol.
    Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Acetaminophen; Aspirin: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Acetaminophen; Aspirin; Diphenhydramine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Albiglutide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Aldesleukin, IL-2: (Moderate) Beta blockers may potentiate the hypotension seen with aldesleukin, IL 2.
    Alfentanil: (Moderate) Alfentanil may cause bradycardia. The risk of significant hypotension and/or bradycardia during therapy with alfentanil is increased in patients receiving beta-blockers.
    Alfuzosin: (Major) Use caution during concurrent administration. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Based on electrophysiology studies performed by the manufacturer, alfuzosin has a slight effect to prolong the QT interval. The QT prolongation appeared less with alfuzosin 10 mg than with 40 mg. The manufacturer warns that the QT effect of alfuzosin should be considered prior to administering the drug to patients taking other medications known to prolong the QT interval.
    Aliskiren; Amlodipine: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Aliskiren; Amlodipine; Hydrochlorothiazide, HCTZ: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Alogliptin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Alpha-blockers: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
    Alpha-glucosidase Inhibitors: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Alprostadil: (Minor) The concomitant use of systemic alprostadil injection and antihypertensive agents, such as beta-clockers, may cause additive hypotension. Caution is advised with this combination. Systemic drug interactions with the urethral suppository (MUSE) or alprostadil intracavernous injection are unlikely in most patients because low or undetectable amounts of the drug are found in the peripheral venous circulation following administration. In those men with significant corpora cavernosa venous leakage, hypotension might be more likely. Use caution with in-clinic dosing for erectile dysfunction (ED) and monitor for the effects on blood pressure. In addition, the presence of medications in the circulation that attenuate erectile function may influence the response to alprostadil. However, in clinical trials with alprostadil intracavernous injection, anti-hypertensive agents had no apparent effect on the safety and efficacy of alprostadil.
    Ambrisentan: (Moderate) Although no specific interactions have been documented, ambrisentan has vasodilatory effects and may contribute additive hypotensive effects when given with other antihypertensive agents. Patients receiving ambrisentan in combination with other antihypertensive agents should be monitored for decreases in blood pressure.
    Amifostine: (Major) Patients receiving beta-blockers should be closely monitored during amifostine infusions due to additive effects. Patients receiving amifostine at doses recommended for chemotherapy should have antihypertensive therapy interrupted 24 hours preceding administration of amifostine. If the antihypertensive cannot be stopped, patients should not receive amifostine.
    Amiodarone: (Major) Sotalol administration is associated with a well-established risk of QT prolongation and torsades de pointes (TdP). Drugs that prolong the QT interval should be used with extreme caution in combination with sotalol. Ventricular tachycardia, including torsade de pointes and monomorphic ventricular tachycardia can occur with excessive prolongation of the QT interval. Before initiating sotalol, the previous Class I and Class III antiarrhythmic therapy should be withdrawn under careful monitoring for a minimum of (2-3) plasma half-lives for the discontinued drug. Class III antiarrhythmics (e.g., amiodarone, dofetilide) are associated with QT prolongation and ventricular arrhythmias; concurrent exposure with sotalol could increase the risk of drug-induced proarrhythmias. Because of unpredictable pharmacokinetics with amiodarone, sotalol should not be initiated following discontinuation of amiodarone therapy until the QTc interval has normalized. In clinical trials, patients were not allowed to receive sotalol if they had received amiodarone for > 1 month in the previous 3 months.
    Amisulpride: (Major) Monitor ECGs for QT prolongation when amisulpride is administered with sotalol. Amisulpride causes dose- and concentration- dependent QT prolongation. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Amlodipine: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Amlodipine; Atorvastatin: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Amlodipine; Benazepril: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Amlodipine; Celecoxib: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Amlodipine; Olmesartan: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Amlodipine; Valsartan: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Amlodipine; Valsartan; Hydrochlorothiazide, HCTZ: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Amoxicillin; Clarithromycin; Omeprazole: (Major) Use caution if coadministering clarithromycin and sotalol. Clarithromycin is associated with an established risk for QT prolongation and torsades de pointes (TdP). Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Anagrelide: (Major) Torsades de pointes (TdP) and ventricular tachycardia have been reported during post-marketing use of anagrelide. A cardiovascular examination, including an ECG, should be obtained in all patients prior to initiating anagrelide therapy. Monitor patients during anagrelide therapy for cardiovascular effects and evaluate as necessary. Drugs with a possible risk for QT prolongation and TdP that should be used cautiously and with close monitoring with anagrelide include sotalol.
    Antacids: (Moderate) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Antacid administration two hours after the sotalol dose does not alter sotalol pharmacokinetics or pharmacodynamics. Instruct patients to avoid using antacids containing aluminum hydroxide or magnesium hydroxide within 2 hours of taking sotalol.
    Antithyroid agents: (Minor) Hyperthyroidism may cause increased clearance of beta blockers that possess a high extraction ratio. A dose reduction of some beta-blockers may be needed when a hyperthyroid patient treated with methimazole becomes euthyroid.
    Apomorphine: (Major) Use apomorphine and sotalol together with caution due to the risk of additive QT prolongation. Dose-related QTc prolongation is associated with therapeutic apomorphine exposure. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Apraclonidine: (Moderate) Theoretically, additive blood pressure reductions could occur when apraclonidine is combined with antihypertensive agents.
    Aripiprazole: (Major) Concomitant use of aripiprazole and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Arsenic Trioxide: (Major) If possible, drugs that are known to prolong the QT interval should be discontinued prior to initiating arsenic trioxide therapy. QT prolongation should be expected with the administration of arsenic trioxide. Torsade de pointes (TdP) and complete atrioventricular block have been reported. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Artemether; Lumefantrine: (Major) Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. The administration of artemether; lumefantrine is associated with prolongation of the QT interval. Although there are no studies examining the effects of artemether; lumefantrine in patients receiving other QT prolonging drugs, coadministration of such drugs may result in additive QT prolongation and should be avoided. Consider ECG monitoring if sotalol must be used with or after artemether; lumefantrine treatment.
    Asenapine: (Major) Asenapine has been associated with QT prolongation. According to the manufacturer of asenapine, the drug should be avoided in combination with other agents also known to have this effect. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Aspirin, ASA: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Butalbital; Caffeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Butalbital; Caffeine; Codeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Caffeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Caffeine; Orphenadrine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Carisoprodol: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Carisoprodol; Codeine: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Citric Acid; Sodium Bicarbonate: (Major) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer magnesium hydroxide two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics. (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Dipyridamole: (Major) Beta-blockers should generally be withheld before dipyridamole-stress testing. Monitor the heart rate carefully following the dipyridamole injection. (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Omeprazole: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Oxycodone: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Aspirin, ASA; Pravastatin: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Atomoxetine: (Major) Concomitant use of atomoxetine and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Azithromycin: (Major) Concomitant use of azithromycin and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Bedaquiline: (Major) Due to the potential for QT prolongation and torsade de pointes (TdP), caution is advised when administering bedaquiline with sotalol. Bedaquiline has been reported to prolong the QT interval. Prior to initiating bedaquiline, obtain serum electrolyte concentrations and a baseline ECG. An ECG should also be performed at least 2, 12, and 24 weeks after starting bedaquiline therapy. Sotalol administration is also associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Betaxolol: (Contraindicated) Using sotalol with other beta-blockers would be illogical as it would represent duplicate therapy; additive effects on AV nodal conduction and blood pressure would be expected. The risk of additive inhibition of AV conduction is symptomatic bradycardia with hypotension or advanced AV block; whereas additive negative inotropic effects could precipitate overt heart failure in some patients.
    Bismuth Subcitrate Potassium; Metronidazole; Tetracycline: (Major) Concomitant use of metronidazole and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Bismuth Subsalicylate: (Moderate) Concurrent use of beta-blockers with bismuth subsalicylate and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Bismuth Subsalicylate; Metronidazole; Tetracycline: (Major) Concomitant use of metronidazole and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary. (Moderate) Concurrent use of beta-blockers with bismuth subsalicylate and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Bretylium: (Major) Discontinue bretylium at least 3 half-lives before dosing with sotalol. Class III antiarrhythmics, such as bretylium, are not recommended as concomitant therapy with sotalol due to the potential to prolong refractoriness. In addition, concomitant use may result in excessive reduction of resting sympathetic nervous tone increasing the risk for hypotension and marked bradycardia, which may produce syncope.
    Buprenorphine: (Major) Concomitant use of sotalol and buprenorphine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Buprenorphine; Naloxone: (Major) Concomitant use of sotalol and buprenorphine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Cabergoline: (Moderate) Cabergoline should be used cautiously with antihypertensive agents, including beta-blockers. Cabergoline has been associated with hypotension. Initial doses of cabergoline higher than 1 mg may produce orthostatic hypotension. It may be advisable to monitor blood pressure.
    Cabotegravir; Rilpivirine: (Major) Supratherapeutic doses of rilpivirine (75 to 300 mg/day) have caused QT prolongation; caution is advised when administering rilpivirine with other drugs that may prolong the QT or PR interval. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Calcium Carbonate: (Moderate) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer antacids two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
    Calcium Carbonate; Famotidine; Magnesium Hydroxide: (Moderate) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer antacids two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
    Calcium Carbonate; Magnesium Hydroxide: (Moderate) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer antacids two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
    Calcium Carbonate; Magnesium Hydroxide; Simethicone: (Moderate) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer antacids two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
    Calcium Carbonate; Risedronate: (Moderate) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer antacids two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
    Calcium Carbonate; Simethicone: (Moderate) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer antacids two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
    Calcium; Vitamin D: (Moderate) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer antacids two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
    Canagliflozin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Carbidopa; Levodopa: (Moderate) Concomitant use of beta-blockers with levodopa can result in additive hypotensive effects.
    Carbidopa; Levodopa; Entacapone: (Moderate) Concomitant use of beta-blockers with levodopa can result in additive hypotensive effects.
    Carbonic anhydrase inhibitors: (Major) Diuretics should be used cautiously with sotalol and should be accompanied by close monitoring of electrolyte balance because hypokalemia and hypomagnesemia have been associated with an increased risk of proarrhythmia.
    Cardiac glycosides: (Moderate) Sotalol and digoxin should be used together cautiously. Digoxin and sotalol slow AV conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia. In addition, digoxin used concomitantly with sotalol can increase the possibility of proarrhythmia. Proarrhythmic events were more common in sotalol-treated patients also receiving digoxin; it is not clear whether this represents an interaction or is related to the presence of CHF, a known risk factor for proarrhythmia. Single and multiple doses of sotalol do not appear to interfere substantially with digoxin serum concentrations.
    Cariprazine: (Moderate) Orthostatic vital signs should be monitored in patients who are at risk for hypotension, such as those receiving cariprazine in combination with antihypertensive agents. Atypical antipsychotics may cause orthostatic hypotension and syncope, most commonly during treatment initiation and dosage increases. Patients should be informed about measures to prevent orthostatic hypotension, such as sitting on the edge of the bed for several minutes prior to standing in the morning, or rising slowly from a seated position. Consider a cariprazine dose reduction if hypotension occurs.
    Ceritinib: (Major) Avoid concomitant use of sotalol and ceritinib due to the risk of additive QT prolongation and bradycardia. Ceritinib causes concentration-dependent QT prolongation. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Both ceritinib and timolol can cause bradycardia.
    Cevimeline: (Major) Cevimeline should be administered with caution to patients taking beta adrenergic antagonists, because of the possibility of conduction disturbances. Cevimeline can potentially alter cardiac conduction and/or heart rate. Patients with significant cardiovascular disease treated with beta-blockers may potentially be unable to compensate for transient changes in hemodynamics or rhythm induced by cevimeline. If use of these drugs together cannot be avoided, close monitoring of blood pressure, heart rate and cardiac function is advised.
    Charcoal: (Major) Charcoal exerts a nonspecific effect, and many medications can be adsorbed by activated charcoal. While the reduction in absorption is beneficial in treating overdoses of drugs and toxins, activated charcoal dietary supplements used for flatulence or other purposes may reduce the effectiveness of certain beta-blocking agents (e.g., atenolol, sotalol, nadolol, pindolol). Use together is best limited to situations of drug overdose. Activated charcoal (single dose, 50-gram) reduced the absorption of therapeutic doses of atenolol, pindolol, and sotalol by > 90%. Repeat charcoal doses may decrease the entero-hepatic recycling of some of these agents. Repeated doses increased the elimination of sotalol and nadolol.
    Chloroquine: (Major) Avoid coadministration of chloroquine with sotalol due to the increased risk of QT prolongation. If use together is necessary, obtain an ECG at baseline to assess initial QT interval and determine frequency of subsequent ECG monitoring, avoid any non-essential QT prolonging drugs, and correct electrolyte imbalances. Chloroquine is associated with an increased risk of QT prolongation and torsade de pointes (TdP); the risk of QT prolongation is increased with higher chloroquine doses. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Chlorpromazine: (Major) Use caution during concurrent administration of chlorpromazine and sotalol. Phenothiazines have been associated with a risk of QT prolongation and/or torsade de pointes (TdP). This risk is generally higher at elevated drugs concentrations of phenothiazines. Chlorpromazine is specifically associated with an established risk of QT prolongation and TdP; case reports have included patients receiving therapeutic doses of chlorpromazine. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Chlorthalidone; Clonidine: (Moderate) Monitor heart rate in patients receiving concomitant clonidine and agents known to affect sinus node function or AV nodal conduction (e.g., beta-blockers). Severe bradycardia resulting in hospitalization and pacemaker insertion has been reported during combination therapy with clonidine and other sympatholytic agents. Concomitant use of clonidine with beta-blockers can also cause additive hypotension. Beta-blockers should not be substituted for clonidine when modifications are made in a patient's antihypertensive regimen because beta-blocker administration during clonidine withdrawal can augment clonidine withdrawal, which may lead to a hypertensive crisis. If a beta-blocker is to be substituted for clonidine, clonidine should be gradually tapered and the beta-blocker should be gradually increased over several days to avoid the possibility of rebound hypertension; administration of beta-blockers during withdrawal of clonidine can precipitate severe increases in blood pressure as a result of unopposed alpha stimulation.
    Choline Salicylate; Magnesium Salicylate: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Ciprofloxacin: (Major) Concomitant use of ciprofloxacin and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Cisapride: (Contraindicated) Avoid concomitant use of sotalol and cisapride due to an increased risk for torsade de pointes (TdP) and QT/QTc prolongation.
    Citalopram: (Major) Concomitant use of citalopram and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Clarithromycin: (Major) Use caution if coadministering clarithromycin and sotalol. Clarithromycin is associated with an established risk for QT prolongation and torsades de pointes (TdP). Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Class IA Antiarrhythmics: (Major) Sotalol administration is associated with a well-established risk of QT prolongation and torsades de pointes (TdP). Drugs that prolong the QT interval should be used with extreme caution in combination with sotalol. Ventricular tachycardia, including torsade de pointes and monomorphic ventricular tachycardia can occur with excessive prolongation of the QT interval. Examples of agents that may prolong the QT interval include: Class IA antiarrhythmics (disopyramide, procainamide, quinidine). Before initiating sotalol, the previous Class I antiarrhythmic therapy should be withdrawn under careful monitoring for a minimum of (2-3) plasma half-lives for the discontinued drug.
    Clofazimine: (Major) Concomitant use of clofazimine and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Clonidine: (Moderate) Monitor heart rate in patients receiving concomitant clonidine and agents known to affect sinus node function or AV nodal conduction (e.g., beta-blockers). Severe bradycardia resulting in hospitalization and pacemaker insertion has been reported during combination therapy with clonidine and other sympatholytic agents. Concomitant use of clonidine with beta-blockers can also cause additive hypotension. Beta-blockers should not be substituted for clonidine when modifications are made in a patient's antihypertensive regimen because beta-blocker administration during clonidine withdrawal can augment clonidine withdrawal, which may lead to a hypertensive crisis. If a beta-blocker is to be substituted for clonidine, clonidine should be gradually tapered and the beta-blocker should be gradually increased over several days to avoid the possibility of rebound hypertension; administration of beta-blockers during withdrawal of clonidine can precipitate severe increases in blood pressure as a result of unopposed alpha stimulation.
    Clozapine: (Major) Treatment with clozapine has been associated with QT prolongation, torsade de pointes (TdP), cardiac arrest, and sudden death. The manufacturer of clozapine recommends caution during concurrent use with medications known to cause QT prolongation. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Codeine; Phenylephrine; Promethazine: (Major) Concomitant use of sotalol and promethazine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Codeine; Promethazine: (Major) Concomitant use of sotalol and promethazine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Crizotinib: (Major) Avoid coadministration of crizotinib with sotalol due to the risk of QT prolongation. If concomitant use is unavoidable, monitor ECGs for QT prolongation and monitor electrolytes. An interruption of therapy, dose reduction, or discontinuation of therapy may be necessary for crizotinib if QT prolongation occurs. Crizotinib has been associated with concentration-dependent QT prolongation. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP); proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Dapagliflozin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Dasabuvir; Ombitasvir; Paritaprevir; Ritonavir: (Major) The use of ritonavir could result in QT prolongation. Drugs with a possible risk for QT prolongation and TdP that should be used cautiously and with close monitoring with ritonavir include sotalol.
    Dasatinib: (Minor) Use caution during concurrent use of sotalol and dasatinib. In vitro studies have shown that dasatinib has the potential to prolong cardiac ventricular repolarization (prolong QT interval). Cautious dasatinib administration is recommended to patients who have or may develop QT prolongation such as patients taking drugs that lead to QT prolongation. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Dasiglucagon: (Minor) A temporary increase in both blood pressure and pulse rate may occur following the administration of glucagon. Patients taking beta-blockers might be expected to have a greater increase in both pulse and blood pressure. Glucagon exerts positive inotropic and chronotropic effects and may, therefore, cause tachycardia and hypertension in some patients. The increase in blood pressure and pulse rate may require therapy in some patients with coronary artery disease.
    Degarelix: (Major) Consider whether the benefits of androgen deprivation therapy outweigh the potential risks in patients receiving other QT prolonging agents. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Androgen deprivation therapy (i.e., degarelix) may also prolong the QT/QTc interval.
    Desflurane: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Severe, protracted hypotension and difficulty in restarting the heart have been reported after surgery on patients receiving beta-blockers. In addition, sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Drugs with a possible risk for QT prolongation and TdP, such as halogenated anesthetics, should be used cautiously with sotalol.
    Deutetrabenazine: (Major) The risk of QT prolongation may be increased with coadministration of deutetrabenazine and sotalol. Deutetrabenazine may prolong the QT interval, but the degree of QT prolongation is not clinically significant when deutetrabenazine is administered within the recommended dosage range. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Dexmedetomidine: (Major) In general, the concomitant administration of dexmedetomidine with antihypertensive agents could lead to additive hypotensive effects. Dexmedetomidine can produce bradycardia or AV block and should be used cautiously in patients who are receiving antihypertensive drugs that lower the heart rate such as beta-blockers.
    Dextromethorphan; Quinidine: (Major) Sotalol administration is associated with a well-established risk of QT prolongation and torsades de pointes (TdP). Drugs that prolong the QT interval should be used with extreme caution in combination with sotalol. Ventricular tachycardia, including torsade de pointes and monomorphic ventricular tachycardia can occur with excessive prolongation of the QT interval. Examples of agents that may prolong the QT interval include: Class IA antiarrhythmics (disopyramide, procainamide, quinidine). Before initiating sotalol, the previous Class I antiarrhythmic therapy should be withdrawn under careful monitoring for a minimum of (2-3) plasma half-lives for the discontinued drug.
    Diazoxide: (Moderate) Additive hypotensive effects can occur with the concomitant administration of diazoxide with other antihypertensive agent. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly. The manufacturer advises that IV diazoxide should not be administered to patients within 6 hours of receiving beta-blockers.
    Dihydroergotamine: (Moderate) Concurrent use of beta-blockers and ergot alkaloids should be approached with caution. Concomitant administration with beta-blockers may enhance the vasoconstrictive action of certain ergot alkaloids including dihydroergotamine, ergotamine, methylergonovine, and methysergide. The risk of peripheral ischemia, resulting in cold extremities or gangrene, has been reported to be increased when ergotamine or dihydroergotamine is coadministered with selected beta-blockers, including propranolol, a beta-blocker commonly used for migraine prophylaxis. However, the precise mechanism of these interactions remains elusive. Additionally, because of the potential to cause coronary vasospasm, these ergot alkaloids could antagonize the therapeutic effects of anti-anginal agents including beta-blockers; clinicians should keep in mind that ergot alkaloids are contraindicated for use in patients with coronary heart disease or hypertension.
    Diltiazem: (Moderate) Monitor blood pressure and heart rate during concomitant diltiazem and sotalol use; dosage adjustments may be needed. Concomitant use may result in additive effects in prolonging AV conduction and additive antihypertensive effects.
    Dipeptidyl Peptidase-4 Inhibitors: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Dipyridamole: (Major) Beta-blockers should generally be withheld before dipyridamole-stress testing. Monitor the heart rate carefully following the dipyridamole injection.
    Disopyramide: (Major) Sotalol administration is associated with a well-established risk of QT prolongation and torsades de pointes (TdP). Drugs that prolong the QT interval should be used with extreme caution in combination with sotalol. Ventricular tachycardia, including torsade de pointes and monomorphic ventricular tachycardia can occur with excessive prolongation of the QT interval. Examples of agents that may prolong the QT interval include: Class IA antiarrhythmics (disopyramide, procainamide, quinidine). Before initiating sotalol, the previous Class I antiarrhythmic therapy should be withdrawn under careful monitoring for a minimum of (2-3) plasma half-lives for the discontinued drug.
    Dofetilide: (Major) Coadministration of dofetilide and sotalol is not recommended as concurrent use may increase the risk of QT prolongation. Class III antiarrhythmic agents, such as sotalol, should be withheld for at least 3 half-lives prior to initiating dofetilide therapy. Dofetilide, a Class III antiarrhythmic agent, is associated with a well-established risk of QT prolongation and torsade de pointes (TdP). Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Dolasetron: (Major) Use caution during concurrent use of dolasetron and sotalol. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Dolasetron has been associated with a dose-dependant prolongation in the QT, PR, and QRS intervals on an electrocardiogram. Use of dolasetron injection for the prevention of chemotherapy-induced nausea and vomiting is contraindicated because the risk of QT prolongation is higher with the doses required for this indication; when the injection is used at lower doses (i.e., those approved for post-operative nausea and vomiting) or when the oral formulation is used, the risk of QT prolongation is lower and caution is advised.
    Dolutegravir; Rilpivirine: (Major) Supratherapeutic doses of rilpivirine (75 to 300 mg/day) have caused QT prolongation; caution is advised when administering rilpivirine with other drugs that may prolong the QT or PR interval. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Donepezil: (Major) Monitor for evidence of QT prolongation and torsade de pointes (TdP) if concurrent use of donepezil and sotalol is necessary. Both drugs are associated with a risk of QT prolongation and TdP; these effects may be additive during coadministration. In addition, the increase in vagal tone induced by some cholinesterase inhibitors may produce bradycardia, hypotension, or syncope. The vagotonic effect of these drugs may be increased when given with other medications known to cause bradycardia such as beta-blockers. These interactions are pharmacodynamic in nature rather than pharmacokinetic.
    Donepezil; Memantine: (Major) Monitor for evidence of QT prolongation and torsade de pointes (TdP) if concurrent use of donepezil and sotalol is necessary. Both drugs are associated with a risk of QT prolongation and TdP; these effects may be additive during coadministration. In addition, the increase in vagal tone induced by some cholinesterase inhibitors may produce bradycardia, hypotension, or syncope. The vagotonic effect of these drugs may be increased when given with other medications known to cause bradycardia such as beta-blockers. These interactions are pharmacodynamic in nature rather than pharmacokinetic.
    Doxazosin: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
    Dronedarone: (Contraindicated) Avoid concomitant use of sotalol and dronedarone due to an increased risk for torsade de pointes (TdP) and QT/QTc prolongation.
    Droperidol: (Major) Use caution during concurrent use of droperidol and sotalol. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.Droperidol should be administered with extreme caution to patients receiving other agents that may prolong the QT interval. Droperidol administration is associated with an established risk for QT prolongation and TdP. In December 2001, the FDA issued a black box warning regarding the use of droperidol and its association with QT prolongation and potential for cardiac arrhythmias based on post-marketing surveillance data. According to the revised 2001 labeling for droperidol, any drug known to have potential to prolong the QT interval should not be coadministered with droperidol.
    Dulaglutide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Dutasteride; Tamsulosin: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents
    Efavirenz: (Major) Coadministration of efavirenz and sotalol may increase the risk for QT prolongation and torsade de pointes (TdP). QT prolongation has been observed with use of efavirenz. Although data are limited, the manufacturer of efavirenz recommends an alternative antiretroviral be considered for patients receiving medications with a known risk for TdP. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Efavirenz; Emtricitabine; Tenofovir Disoproxil Fumarate: (Major) Coadministration of efavirenz and sotalol may increase the risk for QT prolongation and torsade de pointes (TdP). QT prolongation has been observed with use of efavirenz. Although data are limited, the manufacturer of efavirenz recommends an alternative antiretroviral be considered for patients receiving medications with a known risk for TdP. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Efavirenz; Lamivudine; Tenofovir Disoproxil Fumarate: (Major) Coadministration of efavirenz and sotalol may increase the risk for QT prolongation and torsade de pointes (TdP). QT prolongation has been observed with use of efavirenz. Although data are limited, the manufacturer of efavirenz recommends an alternative antiretroviral be considered for patients receiving medications with a known risk for TdP. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Eliglustat: (Major) Coadministration of sotalol and eliglustat is not recommended. If coadministration is necessary, use extreme caution and close monitoring. Sotalol is associated with a well-established risk of QT prolongation and torsades de pointes (TdP). Eliglustat is predicted to cause PR, QRS, and/or QT prolongation at significantly elevated plasma concentrations. Coadministration may result in additive effects on the QT interval, further increasing the risk of serious adverse events (e.g., cardiac arrhythmias).
    Empagliflozin; Linagliptin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Empagliflozin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Emtricitabine; Rilpivirine; Tenofovir alafenamide: (Major) Supratherapeutic doses of rilpivirine (75 to 300 mg/day) have caused QT prolongation; caution is advised when administering rilpivirine with other drugs that may prolong the QT or PR interval. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Emtricitabine; Rilpivirine; Tenofovir Disoproxil Fumarate: (Major) Supratherapeutic doses of rilpivirine (75 to 300 mg/day) have caused QT prolongation; caution is advised when administering rilpivirine with other drugs that may prolong the QT or PR interval. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Enalapril; Felodipine: (Moderate) The concomitant use of felodipine and sotalol can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Encainide: (Major) There is limited experience when using class 1C antiarrhythmics, like encainide, in combination with sotalol. Pharmacologically, sotalol causes AV nodal conduction depression and additive effects are possible when used in combination with encainide. Patients should be monitored closely if encainide used in combination with sotalol, and the dose should be adjusted according to clinical response. In addition, sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Encorafenib: (Major) Avoid coadministration of encorafenib and sotalol due to the potential for additive QT prolongation. If concurrent use cannot be avoided, monitor ECGs for QT prolongation and monitor electrolytes; correct hypokalemia and hypomagnesemia prior to treatment. Encorafenib is associated with dose-dependent prolongation of the QT interval. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Entrectinib: (Major) Avoid coadministration of entrectinib with sotalol due to the risk of QT prolongation. Entrectinib has been associated with QT prolongation. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Epoprostenol: (Moderate) Epoprostenol can have additive effects when administered with other antihypertensive agents, including beta-blockers. These effects can be used to therapeutic advantage, but dosage adjustments may be necessary.
    Ergonovine: (Major) Whenever possible, concomitant use of beta-blockers and ergot alkaloids should be avoided, since propranolol has been reported to potentiate the vasoconstrictive action of ergotamine. The risk of peripheral ischemia, resulting in cold extremities or gangrene, has been reported to be increased when ergot alkaloids are coadministered with selected beta-blockers, including propranolol, a beta-blocker commonly used for migraine prophylaxis. However, the precise mechanism of these interactions remains elusive. Additionally, because of the potential to cause coronary vasospasm, ergot alkaloids could antagonize the therapeutic effects of anti-anginal agents including beta-blockers; clinicians should keep in mind that ergot alkaloids are contraindicated for use in patients with coronary heart disease or hypertension.
    Ergotamine: (Moderate) Monitor blood pressure during concomitant beta-blocker and ergotamine use. Beta-blockers may potentiate the vasoconstrictive action of ergotamine by blocking the vasodilating property of epinephrine.
    Ergotamine; Caffeine: (Moderate) Monitor blood pressure during concomitant beta-blocker and ergotamine use. Beta-blockers may potentiate the vasoconstrictive action of ergotamine by blocking the vasodilating property of epinephrine.
    Eribulin: (Major) Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.Drugs with a possible risk for QT prolongation and TdP that should be used cautiously with sotalol include eribulin. If eribulin and sotalol must be coadministered, ECG monitoring is recommended; closely monitor the patient for QT interval prolongation.
    Ertugliflozin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Erythromycin: (Major) Concomitant use of sotalol and erythromycin increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Escitalopram: (Major) Concomitant use of sotalol and escitalopram increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Estradiol Cypionate; Medroxyprogesterone: (Minor) Estrogens can induce fluid retention and may increase blood pressure in some patients; patients who are receiving antihypertensive agents concurrently with hormonal contraceptives should be monitored for antihypertensive effectiveness.
    Estradiol: (Minor) Estrogens can induce fluid retention and may increase blood pressure in some patients; patients who are receiving antihypertensive agents concurrently with hormonal contraceptives should be monitored for antihypertensive effectiveness.
    Etomidate: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension.
    Exenatide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Felodipine: (Moderate) The concomitant use of felodipine and sotalol can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Fenoldopam: (Major) Avoid concomitant use of fenoldopam with beta-blockers due to the risk of hypotension. If used together, monitor blood pressure frequently. Beta-blockers may inhibit the sympathetic reflex response to fenoldopam.
    Fingolimod: (Contraindicated) Avoid concomitant use of sotalol and fingolimod due to an increased risk for torsade de pointes (TdP) and QT/QTc prolongation.
    Flecainide: (Major) Concomitant use of flecainide and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Fluconazole: (Major) Concomitant use of sotalol and fluconazole increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Fluorescein: (Moderate) Patients on beta-blockers are at an increased risk of adverse reaction when administered fluorescein injection. It is thought that beta-blockers may worsen anaphylaxis severity by exacerbating bronchospasm or by increasing the release of anaphylaxis mediators; alternately, beta-blocker therapy may make the patient more pharmacodynamically resistance to epinephrine rescue treatment.
    Fluoxetine: (Major) Concomitant use of fluoxetine and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Fluphenazine: (Minor) Use caution during concurrent administration of fluphenazine and sotalol. Fluphenazine, a phenothiazine, is associated with a possible risk for QT prolongation. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Fluvoxamine: (Major) There may be an increased risk for QT prolongation and torsade de pointes (TdP) during concurrent use of fluvoxamine and sotalol. Cases of QT prolongation and TdP have been reported during postmarketing use of fluvoxamine. Sotalol is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Foscarnet: (Major) When possible, avoid concurrent use of foscarnet with other drugs known to prolong the QT interval, such as sotalol. Foscarnet has been associated with postmarketing reports of both QT prolongation and torsade de pointes (TdP). Sotalol administration is also associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. If these drugs are administered together, obtain an electrocardiogram and electrolyte concentrations before and periodically during treatment.
    Fostemsavir: (Major) Avoid coadministration of sotalol with fostemsavir as concomitant use may increase the risk of QT prolongation. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Supratherapeutic doses of fostemsavir (2,400 mg twice daily, four times the recommended daily dose) have been shown to cause QT prolongation. Fostemsavir causes dose-dependent QT prolongation.
    Galantamine: (Moderate) The increase in vagal tone induced by cholinesterase inhibitors such as galantamine may produce bradycardia or syncope. The vagotonic effect of galantamine may theoretically be increased when given with beta-blockers.
    Gemifloxacin: (Major) Concurrent use of sotalol and gemifloxacin should be avoided due to an increased risk for QT prolongation and torsade de pointes (TdP). Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Gemifloxacin may also prolong the QT interval in some patients, with the maximal change in the QTc interval occurring approximately 5 to 10 hours following oral administration. The likelihood of QTc prolongation may increase with increasing dose of gemifloxacin; therefore, the recommended dose should not be exceeded especially in patients with renal or hepatic impairment where the Cmax and AUC are slightly higher.
    Gemtuzumab Ozogamicin: (Major) Use gemtuzumab ozogamicin and sotalol together with caution due to the potential for additive QT interval prolongation and risk of torsade de pointes (TdP). If these agents are used together, obtain an ECG and serum electrolytes prior to the start of gemtuzumab and as needed during treatment. Although QT interval prolongation has not been reported with gemtuzumab, it has been reported with other drugs that contain calicheamicin. Sotalol administration is also associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of sotalol and after each upward dosage adjustment.
    Gilteritinib: (Major) Use caution and monitor for additive QT prolongation if concurrent use of gilteritinib and sotalol is necessary. Gilteritinib has been associated with QT prolongation. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Glasdegib: (Major) Avoid coadministration of glasdegib with sotalol due to the potential for additive QT prolongation. If coadministration cannot be avoided, monitor patients for increased risk of QT prolongation with increased frequency of ECG monitoring. Glasdegib therapy may result in QT prolongation and ventricular arrhythmias including ventricular fibrillation and ventricular tachycardia. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Glipizide; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Glucagon: (Minor) A temporary increase in both blood pressure and pulse rate may occur following the administration of glucagon. Patients taking beta-blockers might be expected to have a greater increase in both pulse and blood pressure. Glucagon exerts positive inotropic and chronotropic effects and may, therefore, cause tachycardia and hypertension in some patients. The increase in blood pressure and pulse rate may require therapy in some patients with coronary artery disease.
    Glyburide; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Goserelin: (Major) Consider whether the benefits of androgen deprivation therapy (i.e., goserelin) outweigh the potential risks of QT prolongation in patients receiving sotalol. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Androgen deprivation therapy may also prolong the QT/QTc interval.
    Granisetron: (Major) Granisetron has been associated with QT prolongation. According to the manufacturer, use of granisetron in patients concurrently treated with drugs known to prolong the QT interval and/or are arrhythmogenic, may result in clinical consequences. Drugs with a possible risk for QT prolongation and TdP, such as granisetron, should be used cautiously with sotalol. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Guanabenz: (Moderate) Guanabenz can have additive effects when administered with other antihypertensive agents, including beta-blockers. These effects can be used to therapeutic advantage, but dosage adjustments may be necessary.
    Guanfacine: (Moderate) Guanfacine can have additive effects when administered with other antihypertensive agents, including beta-blockers. These effects can be used to therapeutic advantage, but dosage adjustments may be necessary.
    Halogenated Anesthetics: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Severe, protracted hypotension and difficulty in restarting the heart have been reported after surgery on patients receiving beta-blockers. In addition, sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Drugs with a possible risk for QT prolongation and TdP, such as halogenated anesthetics, should be used cautiously with sotalol.
    Haloperidol: (Major) QT prolongation and torsade de pointes (TdP) have been observed during haloperidol treatment. Excessive doses (particularly in the overdose setting) or IV administration of haloperidol may be associated with a higher risk of QT prolongation. According to the manufacturer of haloperidol, caution is advisable when prescribing the drug concurrently with medications known to prolong the QT interval. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Histrelin: (Major) Consider whether the benefits of androgen deprivation therapy (i.e., histrelin) outweigh the potential risks of QT prolongation in patients receiving sotalol. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Androgen deprivation therapy may also prolong the QT/QTc interval.
    Hydroxychloroquine: (Major) Concomitant use of hydroxychloroquine and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Hydroxyzine: (Major) Concomitant use of hydroxyzine and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Ibutilide: (Contraindicated) Combined use of antiarrhythmic drugs can have additive, antagonistic, or synergistic electrophysiologic, pharmacodynamic, or toxic effects. Because of their potential to prolong refractoriness, other Class III antiarrhythmics (e.g., amiodarone, dofetilide and sotalol) are not recommended for use concurrently or within 4 hours after an infusion of ibutilide. In general, combination therapy with Class III antiarrhythmics has been reported to increase the risk of proarrhythmias. The manufacturer reported that during clinical trials, other Class III antiarrhythmics were not given for at least 5 half-lives prior to ibutilide infusion or 4 hours after ibutilide dosing. If sotalol is to be initiated in a patient previously receiving ibutilide, ibutilide should be withdrawn under careful monitoring for a minimum of (2-3) plasma half-lives.
    Iloperidone: (Major) Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. loperidone has been associated with QT prolongation; however, TdP has not been reported. According to the manufacturer, since iloperidone may prolong the QT interval, it should be avoided in combination with other agents also known to have this effect.
    Iloprost: (Moderate) Additive reductions in blood pressure may occur when inhaled iloprost is administered to patients receiving other antihypertensive agents.
    Incretin Mimetics: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Inotuzumab Ozogamicin: (Major) Avoid coadministration of inotuzumab ozogamicin with sotalol due to the potential for additive QT prolongation and risk of torsade de pointes (TdP). If coadministration is unavoidable, obtain an ECG and serum electrolytes prior to the start of treatment, after treatment initiation, and periodically during treatment. Inotuzumab has been associated with QT interval prolongation. Sotalol administration is also associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of sotalol and after each upward dosage adjustment.
    Insulin Degludec; Liraglutide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Insulin Glargine; Lixisenatide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Insulins: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Isoflurane: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Severe, protracted hypotension and difficulty in restarting the heart have been reported after surgery on patients receiving beta-blockers. In addition, sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Drugs with a possible risk for QT prolongation and TdP, such as halogenated anesthetics, should be used cautiously with sotalol.
    Isradipine: (Moderate) Although concomitant therapy with beta-blockers and isradipine is generally well tolerated and can even be beneficial in some cases, coadministration of these agents can induce excessive bradycardia or hypotension. Isradipine when used in combination with beta-blockers, especially in heart failure patients, can result in additive negative inotropic effects. Finally, angina has been reported when beta-adrenergic blocking agents are withdrawn abruptly when isradipine therapy is initiated. A gradual downward titration of the beta-adrenergic blocking agent dosage during initiation of isradipine therapy can minimize or eliminate this potential interaction. Patients should be monitored carefully, however, for excessive bradycardia, cardiac conduction abnormalities, or hypotension when these drugs are given together. In general, these reactions are more likely to occur with other non-dihydropyridine calcium channel blockers than with isradipine.
    Itraconazole: (Major) Itraconazole has been associated with prolongation of the QT interval. Drugs with a possible risk for QT prolongation and TdP that should be used cautiously and with close monitoring with itraconazole include sotalol.
    Ivabradine: (Moderate) Monitor heart rate if ivabradine is coadministered with other negative chronotropes like beta-blockers. Most patients receiving ivabradine will receive concomitant beta-blocker therapy. Coadministration of drugs that slow heart rate increases the risk for bradycardia.
    Ivosidenib: (Major) Avoid coadministration of ivosidenib with sotalol due to an increased risk of QT prolongation. If concomitant use is unavoidable, monitor ECGs for QTc prolongation and monitor electrolytes; correct any electrolyte abnormalities as clinically appropriate. An interruption of therapy and dose reduction of ivosidenib may be necessary if QT prolongation occurs. Prolongation of the QTc interval and ventricular arrhythmias have been reported in patients treated with ivosidenib. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Ketamine: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension.
    Ketoconazole: (Contraindicated) Avoid concomitant use of ketoconazole and sotalol due to an increased risk for QT/QTc prolongation and torsade de pointes (TdP).
    Lacosamide: (Moderate) Use lacosamide with caution in patients taking concomitant medications that affect cardiac conduction, such as Class III antiarrhythmics, because of the risk of AV block, bradycardia, or ventricular tachyarrhythmia. If use together is necessary, obtain an ECG prior to lacosamide initiation and after treatment has been titrated to steady-state. In addition, monitor patients receiving lacosamide via the intravenous route closely.
    Lanreotide: (Moderate) Concomitant administration of bradycardia-inducing drugs such as sotalol may have an additive effect on the reduction of heart rate associated with lanreotide. Adjust the dose of sotalol if necessary.
    Lansoprazole; Amoxicillin; Clarithromycin: (Major) Use caution if coadministering clarithromycin and sotalol. Clarithromycin is associated with an established risk for QT prolongation and torsades de pointes (TdP). Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Lapatinib: (Major) Monitor ECGs for QT prolongation and monitor electrolytes if coadministration of lapatinib with sotalol is necessary; correct electrolyte abnormalities prior to treatment. Lapatinib has been associated with concentration-dependent QT prolongation; ventricular arrhythmias and torsade de pointes (TdP) have been reported in postmarketing experience with lapatinib. Sotalol administration is also associated with QT prolongation and TdP; proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Lasmiditan: (Moderate) Monitor heart rate if lasmiditan is coadministered with beta-blockers as concurrent use may increase the risk for bradycardia. Lasmiditan has been associated with lowering of heart rate. In a drug interaction study, addition of a single 200 mg dose of lasmiditan to a beta-blocker (propranolol) decreased heart rate by an additional 5 beats per minute.
    Lefamulin: (Major) Avoid coadministration of lefamulin with sotalol as concurrent use may increase the risk of QT prolongation. If coadministration cannot be avoided, monitor ECG during treatment. Lefamulin has a concentration dependent QTc prolongation effect. The pharmacodynamic interaction potential to prolong the QT interval of the electrocardiogram between lefamulin and other drugs that effect cardiac conduction is unknown. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Lenvatinib: (Major) Avoid coadministration of lenvatinib with sotalol due to the risk of QT prolongation. Prolongation of the QT interval has been reported with lenvatinib therapy. Sotalol administration is also associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of sotalol therapy and after each upward dosage adjustment.
    Leuprolide: (Major) Consider whether the benefits of androgen deprivation therapy (i.e., leuprolide) outweigh the potential risks of QT prolongation in patients receiving sotalol. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Androgen deprivation therapy may also prolong the QT/QTc interval.
    Leuprolide; Norethindrone: (Major) Consider whether the benefits of androgen deprivation therapy (i.e., leuprolide) outweigh the potential risks of QT prolongation in patients receiving sotalol. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Androgen deprivation therapy may also prolong the QT/QTc interval.
    Levamlodipine: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Levodopa: (Moderate) Concomitant use of beta-blockers with levodopa can result in additive hypotensive effects.
    Levofloxacin: (Major) Concomitant use of levofloxacin and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Levoketoconazole: (Contraindicated) Avoid concomitant use of ketoconazole and sotalol due to an increased risk for QT/QTc prolongation and torsade de pointes (TdP).
    Levothyroxine: (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
    Levothyroxine; Liothyronine (Porcine): (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
    Levothyroxine; Liothyronine (Synthetic): (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
    Linagliptin; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Liothyronine: (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
    Liraglutide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Lithium: (Major) Concomitant use of lithium and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Lixisenatide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Lofexidine: (Major) Because both lofexidine and sotalol can cause hypotension and bradycardia, concurrent use should be avoided if possible. In addition, both drugs have been associated with QT prolongation and torsade de pointes (TdP) and additive effects are possible. If coadministration is necessary, monitor the ECG during treatment. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Patients being given lofexidine in an outpatient setting should be capable of and instructed on self-monitoring for hypotension, orthostasis, bradycardia, and associated symptoms. If clinically significant or symptomatic hypotension and/or bradycardia occur, the next dose of lofexidine should be reduced in amount, delayed, or skipped.
    Loperamide: (Major) Concomitant use of sotalol and loperamide increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Loperamide; Simethicone: (Major) Concomitant use of sotalol and loperamide increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Lopinavir; Ritonavir: (Major) Avoid coadministration of lopinavir with sotalol due to the potential for additive QT prolongation. If use together is necessary, obtain a baseline ECG to assess initial QT interval and determine frequency of subsequent ECG monitoring, avoid any non-essential QT prolonging drugs, and correct electrolyte imbalances. Lopinavir is associated with QT prolongation. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. (Major) The use of ritonavir could result in QT prolongation. Drugs with a possible risk for QT prolongation and TdP that should be used cautiously and with close monitoring with ritonavir include sotalol.
    Lovastatin; Niacin: (Moderate) Cutaneous vasodilation induced by niacin may become problematic if high-dose niacin is used concomitantly with other antihypertensive agents. This effect is of particular concern in the setting of acute myocardial infarction, unstable angina, or other acute hemodynamic compromise.
    Macimorelin: (Major) Avoid concurrent administration of macimorelin with drugs that prolong the QT interval, such as sotalol. Use of these drugs together may increase the risk of developing torsade de pointes-type ventricular tachycardia. Sufficient washout time of drugs that are known to prolong the QT interval prior to administration of macimorelin is recommended. Treatment with macimorelin has been associated with an increase in the corrected QT (QTc) interval. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Magnesium Salicylate: (Moderate) Concurrent use of beta-blockers with aspirin and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Mannitol: (Major) Diuretics should be used cautiously with sotalol and should be accompanied by close monitoring of electrolyte balance because hypokalemia and hypomagnesemia have been associated with an increased risk of proarrhythmia.
    Maprotiline: (Major) Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Drugs with a possible risk for QT prolongation and TdP should be used cautiously with sotalol. Maprotiline has been reported to prolong the QT interval, particularly in overdose or with higher-dose prescription therapy (elevated serum concentrations). Cases of long QT syndrome and TdP tachycardia have been described with maprotiline use, but rarely occur when the drug is used alone in normal prescribed doses and in the absence of other known risk factors for QT prolongation. Limited data are available regarding the safety of maprotiline in combination with other QT-prolonging drugs.
    Mavacamten: (Moderate) Expect additive negative inotropic effects during concomitant use of mavacamten and sotalol. If concomitant therapy with sotalol is initiated, or if the dose is increased, monitor left ventricular ejection fraction closely until stable doses and clinical response have been achieved.
    Mefloquine: (Moderate) Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Mefloquine is associated with a possible risk for QT prolongation and TdP and should be used cautiously with sotalol. In addition, the concurrent use of mefloquine and beta-blockers can result in ECG abnormalities or cardiac arrest.
    Meglitinides: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Meperidine; Promethazine: (Major) Concomitant use of sotalol and promethazine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Metformin; Repaglinide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Metformin; Rosiglitazone: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Metformin; Saxagliptin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Metformin; Sitagliptin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Methacholine: (Moderate) Beta-blockers may impair reversal of methacholine-induced bronchoconstriction with an inhaled rapid-acting beta-agonist.
    Methadone: (Major) The need to coadminister methadone with sotalol should be done with extreme caution and a careful assessment of treatment risks versus benefits. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Methadone is considered to be associated with an increased risk for QT prolongation and TdP, especially at higher doses (> 200 mg/day but averaging approximately 400 mg/day in adult patients). Laboratory studies, both in vivo and in vitro, have demonstrated that methadone inhibits cardiac potassium channels and prolongs the QT interval. Most cases involve patients being treated for pain with large, multiple daily doses of methadone, although cases have been reported in patients receiving doses commonly used for maintenance treatment of opioid addiction.
    Methohexital: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension.
    Methylergonovine: (Moderate) Concurrent use of beta-blockers and ergot alkaloids should be approached with caution. Concomitant administration with beta-blockers may enhance the vasoconstrictive action of certain ergot alkaloids including dihydroergotamine, ergotamine, methylergonovine, and methysergide. The risk of peripheral ischemia, resulting in cold extremities or gangrene, has been reported to be increased when ergotamine or dihydroergotamine is coadministered with selected beta-blockers, including propranolol, a beta-blocker commonly used for migraine prophylaxis. However, the precise mechanism of these interactions remains elusive. Additionally, because of the potential to cause coronary vasospasm, these ergot alkaloids could antagonize the therapeutic effects of anti-anginal agents including beta-blockers; clinicians should keep in mind that ergot alkaloids are contraindicated for use in patients with coronary heart disease or hypertension.
    Metronidazole: (Major) Concomitant use of metronidazole and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Midostaurin: (Major) The concomitant use of midostaurin and sotalol may lead to additive QT interval prolongation. If these drugs are used together, consider electrocardiogram monitoring. Consider sotalol dose reduction or discontinuation if the QTc interval is greater than 500 milliseconds (msec); serious consideration to dose reduction or drug discontinuation should occur in patients with a QTc interval greater than 550 msec. In clinical trials, QT prolongation has been reported in patients who received midostaurin as single-agent therapy or in combination with cytarabine and daunorubicin. QT prolongation and torsade de pointes have been reported with sotalol in clinical trials.
    Mifepristone: (Major) Concomitant use of sotalol and mifepristone increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Milrinone: (Moderate) Concurrent administration of antihypertensive agents could lead to additive hypotension when administered with milrinone. Titrate milrinone dosage according to hemodynamic response.
    Mirtazapine: (Major) Concomitant use of sotalol and mirtazapine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Mobocertinib: (Major) Concomitant use of mobocertinib and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Moxifloxacin: (Major) Prolongation of the QT interval has been reported with administration of moxifloxacin. Post-marketing surveillance has identified very rare cases of ventricular arrhythmias including torsade de pointes (TdP), usually in patients with severe underlying proarrhythmic conditions. The likelihood of QT prolongation may increase with increasing concentrations of moxifloxacin, therefore the recommended dose or infusion rate should not be exceeded. According to the manufacturer, moxifloxacin should be avoided in patients taking drugs that can result in prolongation of the QT interval, such as sotalol. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Nebivolol: (Major) Avoid concomitant use of nebivolol and other beta-blockers, such as sotalol. Concomitant use may result in additive risk for hypotension and bradycardia.
    Nebivolol; Valsartan: (Major) Avoid concomitant use of nebivolol and other beta-blockers, such as sotalol. Concomitant use may result in additive risk for hypotension and bradycardia.
    Nefazodone: (Minor) Although relatively infrequent, nefazodone may cause orthostatic hypotension in some patients; this effect may be additive with antihypertensive agents. Blood pressure monitoring and dosage adjustments of either drug may be necessary.
    Neuromuscular blockers: (Moderate) Concomitant use of neuromuscular blockers and beta-blockers may prolong neuromuscular blockade.
    Niacin, Niacinamide: (Moderate) Cutaneous vasodilation induced by niacin may become problematic if high-dose niacin is used concomitantly with other antihypertensive agents. This effect is of particular concern in the setting of acute myocardial infarction, unstable angina, or other acute hemodynamic compromise.
    Niacin; Simvastatin: (Moderate) Cutaneous vasodilation induced by niacin may become problematic if high-dose niacin is used concomitantly with other antihypertensive agents. This effect is of particular concern in the setting of acute myocardial infarction, unstable angina, or other acute hemodynamic compromise.
    Nicardipine: (Moderate) Although concomitant therapy with nicardipine and sotalol generally is well tolerated and can even be beneficial in some cases (by inhibiting reflex tachycardia induced by nicardipine), sotalol can induce excessive bradycardia or hypotension. This combination also can cause additive negative inotropic effects. Finally, angina has been reported when beta-adrenergic blocking agents are withdrawn abruptly and nicardipine therapy is initiated. A gradual downward titration of the beta-adrenergic blocking agent dosage during initiation of nicardipine therapy can minimize or eliminate this potential interaction. Patients should be monitored carefully, however, for excessive bradycardia, cardiac conduction abnormalities, or hypotension when these drugs are given together. In general, these reactions are more likely to occur with verapamil or diltiazem than with nicardipine.
    Nifedipine: (Moderate) In general, concomitant therapy of nifedipine with beta-blockers is well tolerated and can even be beneficial in some cases (i.e., inhibition of nifedipine-induced reflex tachycardia by beta-blockade). Negative inotropic and/or chronotropic effects can be additive when these drugs are used in combination. Finally, angina has been reported when beta-adrenergic blocking agents are withdrawn abruptly and nifedipine therapy is initiated. A gradual downward titration of the beta-adrenergic blocking agent dosage during initiation of nifedipine therapy may minimize or eliminate this potential interaction. Hypotension and impaired cardiac performance can occur during coadministration of nifedipine with beta-blockers, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis. Monitor clinical response during coadministration; adjustment of nifedipine dosage may be needed during concurrent beta-blocker therapy.
    Nilotinib: (Major) Avoid the concomitant use of nilotinib and sotalol; significant prolongation of the QT interval may occur. Sudden death and QT prolongation have occurred in patients who received nilotinib therapy. Sotalol administration is associated with QT prolongation and torsades de pointes. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Nimodipine: (Moderate) Nimodipine, a selective calcium-channel blocker, can enhance the antihypertensive effects of beta-blockers. Although often used together, concurrent use of calcium-channel blockers and beta-blockers may result in additive hypotensive, negative inotropic, and/or bradycardic effects in some patients.
    Nirmatrelvir; Ritonavir: (Major) The use of ritonavir could result in QT prolongation. Drugs with a possible risk for QT prolongation and TdP that should be used cautiously and with close monitoring with ritonavir include sotalol.
    Nisoldipine: (Moderate) Concurrent use of nisoldipine with sotalol can be beneficial (i.e., inhibition of vasodilation-induced reflex tachycardia by beta-blockade); however, the additive negative inotropic and/or chronotropic effects can cause adverse effects, especially in patients with compromised ventricular function or conduction defects (e.g., sinus bradycardia or AV block).
    Nitroprusside: (Moderate) Additive hypotensive effects may occur when nitroprusside is used concomitantly with other antihypertensive agents. Dosages should be adjusted carefully, according to blood pressure.
    Non-Ionic Contrast Media: (Moderate) Use caution when administering non-ionic contrast media to patients taking beta-blockers. Beta-blockers lower the threshold for and increase the severity of contrast reactions and reduce the responsiveness of treatment of hypersensitivity reactions with epinephrine.
    Nonsteroidal antiinflammatory drugs: (Moderate) Monitor blood pressure during concomitant beta-blocker and nonsteroidal anti-inflammatory drug (NSAID) use. The antihypertensive effect of beta-blockers may be diminished by NSAIDs.
    Octreotide: (Major) Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Octreotide should be used cautiously with sotalol. Arrhythmias, sinus bradycardia, and conduction disturbances have occurred during octreotide therapy warranting more cautious monitoring during octreotide administration in higher risk patients with cardiac disease. Since bradycardia is a risk factor for development of TdP, the potential occurrence of bradycardia during octreotide administration could theoretically increase the risk of TdP in patients receiving drugs that prolong the QT interval.
    Ofloxacin: (Major) Concomitant use of ofloxacin and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Olanzapine: (Major) Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Drugs with a possible risk for QT prolongation and TdP, such as olanzapine, should be used cautiously with sotalol. Limited data, including some case reports, suggest that olanzapine may be associated with a significant prolongation of the QTc interval in rare instances.
    Olanzapine; Fluoxetine: (Major) Concomitant use of fluoxetine and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary. (Major) Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Drugs with a possible risk for QT prolongation and TdP, such as olanzapine, should be used cautiously with sotalol. Limited data, including some case reports, suggest that olanzapine may be associated with a significant prolongation of the QTc interval in rare instances.
    Olanzapine; Samidorphan: (Major) Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Drugs with a possible risk for QT prolongation and TdP, such as olanzapine, should be used cautiously with sotalol. Limited data, including some case reports, suggest that olanzapine may be associated with a significant prolongation of the QTc interval in rare instances.
    Olmesartan; Amlodipine; Hydrochlorothiazide, HCTZ: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Ombitasvir; Paritaprevir; Ritonavir: (Major) The use of ritonavir could result in QT prolongation. Drugs with a possible risk for QT prolongation and TdP that should be used cautiously and with close monitoring with ritonavir include sotalol.
    Omeprazole; Sodium Bicarbonate: (Major) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer magnesium hydroxide two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
    Ondansetron: (Major) Concomitant use of ondansetron and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Osilodrostat: (Major) Monitor ECGs in patients receiving osilodrostat with sotalol. Osilodrostat is associated with dose-dependent QT prolongation. Sotalol administration is associated with QT prolongation and torsade de pointes. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Osimertinib: (Major) Avoid coadministration of sotalol with osimertinib if possible due to the risk of QT prolongation and torsade de pointes (TdP). If concomitant use is unavoidable, periodically monitor ECGs for QT prolongation and monitor electrolytes; an interruption of osimertinib therapy with dose reduction or discontinuation of therapy may be necessary if QT prolongation occurs. Concentration-dependent QTc prolongation occurred during clinical trials of osimertinib. Sotalol administration is associated with QT prolongation and TdP; proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Oxaliplatin: (Major) Monitor electrolytes and ECGs for QT prolongation if coadministration of sotalol with oxaliplatin is necessary; correct electrolyte abnormalities prior to administration of oxaliplatin. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. QT prolongation and ventricular arrhythmias including fatal TdP have also been reported with oxaliplatin use in postmarketing experience.
    Oxymetazoline: (Major) The vasoconstricting actions of oxymetazoline, an alpha adrenergic agonist, may reduce the antihypertensive effects produced by beta-blockers. If these drugs are used together, closely monitor for changes in blood pressure.
    Ozanimod: (Major) In general, do not initiate ozanimod in patients taking sotalol due to the risk of additive bradycardia, QT prolongation, and torsade de pointes (TdP). If treatment initiation is considered, seek advice from a cardiologist. Ozanimod initiation may result in a transient decrease in heart rate and atrioventricular conduction delays. Ozanimod has not been studied in patients taking concurrent QT prolonging drugs; however, QT prolonging drugs have been associated with TdP in patients with bradycardia. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Pacritinib: (Major) Concomitant use of pacritinib and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Paliperidone: (Major) Paliperidone has been associated with QT prolongation; torsade de pointes (TdP) and ventricular fibrillation have been reported in the setting of overdose. According to the manufacturer, since paliperidone may prolong the QT interval, it should be avoided in combination with other agents also known to have this effect. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. If coadministration is necessary and the patient has known risk factors for cardiac disease or arrhythmias, close monitoring is essential.
    Panobinostat: (Major) QT prolongation has been reported with panobinostat therapy in patients with multiple myeloma in a clinical trial; use of panobinostat with other agents that prolong the QT interval is not recommended. Obtain an electrocardiogram at baseline and periodically during treatment. Hold panobinostat if the QTcF increases to >= 480 milliseconds during therapy; permanently discontinue if QT prolongation does not resolve. Antiarrhythmic medicines with a possible risk for QT prolongation and torsade de pointes that should be used cautiously and with close monitoring with panobinostat include sotalol.
    Pasireotide: (Major) Cautious use of pasireotide and drugs that prolong the QT interval is needed, as coadministration may have additive effects on the prolongation of the QT interval. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. In addition, pasireotide may cause a decrease in heart rate. Closely monitor patients who are also taking drugs associated with bradycardia such as beta-blockers. Dose adjustments of beta-blockers may be necessary.
    Pazopanib: (Major) Coadministration of pazopanib and other drugs that prolong the QT interval, such as sotalol, is not advised; pazopanib has been reported to prolong the QT interval. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. If pazopanib and sotalol must be continued, closely monitor the patient for QT interval prolongation.
    Pentamidine: (Major) Pentamidine has been associated with QT prolongation. Drugs with a possible risk for QT prolongation and torsades de pointes (TdP), such as sotalol, should be used cautiously with pentamidine. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Perindopril; Amlodipine: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Perphenazine: (Minor) Use caution during concurrent administration of perphenazine and sotalol. Perphenazine, a phenothiazine, is associated with a possible risk for QT prolongation. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Perphenazine; Amitriptyline: (Minor) Use caution during concurrent administration of perphenazine and sotalol. Perphenazine, a phenothiazine, is associated with a possible risk for QT prolongation. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Phenoxybenzamine: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
    Phentolamine: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
    Pilocarpine: (Moderate) Systemically administered pilocarpine (e.g., when used for the treatment of xerostomia or xerophthalmia) should be administered with caution in patients taking beta-blockers because of the possibility of cardiac conduction disturbances. The risk of conduction disturbances with beta-blockers and ophthalmically administered pilocarpine is low.
    Pimavanserin: (Major) Pimavanserin may cause QT prolongation and should generally be avoided in patients receiving other medications known to prolong the QT interval, such as sotalol. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Pimozide: (Contraindicated) Avoid concomitant use of sotalol and pimozide due to an increased risk for torsade de pointes (TdP) and QT/QTc prolongation.
    Pioglitazone; Metformin: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Pitolisant: (Major) Avoid coadministration of pitolisant with sotalol as concurrent use may increase the risk of QT prolongation. Pitolisant prolongs the QT interval. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Ponesimod: (Major) In general, do not initiate ponesimod in patients taking sotalol due to the risk of additive bradycardia, QT prolongation, and torsade de pointes (TdP). If treatment initiation is considered, seek advice from a cardiologist. Ponesimod initiation may result in a transient decrease in heart rate and atrioventricular conduction delays. Ponesimod has not been studied in patients taking concurrent QT prolonging drugs; however, QT prolonging drugs have been associated with TdP in patients with bradycardia. Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Posaconazole: (Major) Use caution during concurrent administration of sotalol and posaconazole. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Posaconazole has been associated with prolongation of the QT interval as well as rare cases of torsade de pointes.
    Pramlintide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Prazosin: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
    Primaquine: (Major) Due to the potential for QT interval prolongation with primaquine, caution is advised with other drugs that prolong the QT interval. Drugs with a possible risk for QT prolongation and TdP that should be used cautiously and with close monitoring with primaquine include sotalol.
    Procainamide: (Major) Sotalol administration is associated with a well-established risk of QT prolongation and torsades de pointes (TdP). Drugs that prolong the QT interval should be used with extreme caution in combination with sotalol. Ventricular tachycardia, including torsade de pointes and monomorphic ventricular tachycardia can occur with excessive prolongation of the QT interval. Examples of agents that may prolong the QT interval include: Class IA antiarrhythmics (disopyramide, procainamide, quinidine). Before initiating sotalol, the previous Class I antiarrhythmic therapy should be withdrawn under careful monitoring for a minimum of (2-3) plasma half-lives for the discontinued drug.
    Prochlorperazine: (Minor) Phenothiazines have been reported to prolong the QT interval. Concurrent use of drugs that are associated with a possible risk for QT prolongation and torsade de pointes (TdP), such as sotalol, with prochlorperazine should be approached with caution. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. If coadministration is considered necessary, and the patient has known risk factors for cardiac disease or arrhythmia, then close monitoring is essential.
    Promethazine: (Major) Concomitant use of sotalol and promethazine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Promethazine; Dextromethorphan: (Major) Concomitant use of sotalol and promethazine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Promethazine; Phenylephrine: (Major) Concomitant use of sotalol and promethazine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Propafenone: (Major) Concomitant use of propafenone and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary. Class III antiarrhythmics generally should be withheld for at least five half-lives prior to initiating propafenone.
    Propofol: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension.
    Quetiapine: (Major) Concomitant use of sotalol and quetiapine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Quinidine: (Major) Sotalol administration is associated with a well-established risk of QT prolongation and torsades de pointes (TdP). Drugs that prolong the QT interval should be used with extreme caution in combination with sotalol. Ventricular tachycardia, including torsade de pointes and monomorphic ventricular tachycardia can occur with excessive prolongation of the QT interval. Examples of agents that may prolong the QT interval include: Class IA antiarrhythmics (disopyramide, procainamide, quinidine). Before initiating sotalol, the previous Class I antiarrhythmic therapy should be withdrawn under careful monitoring for a minimum of (2-3) plasma half-lives for the discontinued drug.
    Quinine: (Major) Concurrent use of quinine and sotalol should be avoided due to an increased risk for QT prolongation and torsade de pointes (TdP). Quinine has been associated with prolongation of the QT interval and rare cases of TdP. Sotalol administration is also associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of sotalol therapy and after each upward dosage adjustment.
    Ranolazine: (Major) Ranolazine is associated with dose- and plasma concentration-related increases in the QTc interval. The mean increase in QTc is about 6 milliseconds, measured at the tmax of the maximum dosage (1000 mg PO twice daily). However, in 5% of the population studied, increases in the QTc of at least 15 milliseconds have been reported. Although there are no studies examining the effects of ranolazine in patients receiving other QT prolonging drugs, such as sotalol, coadministration may result in additive QT prolongation. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Rasagiline: (Moderate) Limited data suggest that bradycardia is worsened when monoamine oxidase inhibitors (MAOIs) are administered to patients receiving beta-blockers. Although the sinus bradycardia observed was not severe, until more data are available, clinicians should use MAOIs cautiously in patients receiving beta-blockers.
    Relugolix: (Major) Consider whether the benefits of androgen deprivation therapy outweigh the potential risks in patients receiving other QT prolonging agents. Androgen deprivation therapy (i.e., relugolix) may prolong the QT/QTc interval. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Relugolix; Estradiol; Norethindrone acetate: (Major) Consider whether the benefits of androgen deprivation therapy outweigh the potential risks in patients receiving other QT prolonging agents. Androgen deprivation therapy (i.e., relugolix) may prolong the QT/QTc interval. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Remifentanil: (Moderate) The risk of significant hypotension and/or bradycardia during therapy with remifentanil may be increased in patients receiving beta-blockers or calcium-channel blockers due to additive hypotensive effects.
    Reserpine: (Major) Use caution when adminstering sotalol together with catecholamine-depleting agents, such as reserpine or other rauwolfia alkaloids, as concomitant use may cause excessive reductions in resting sympathetic tone can produce hypotension or bradycardia, precipitating a syncopal episode.
    Ribociclib: (Major) Avoid coadministration of ribociclib with sotalol due to an increased risk for QT prolongation and torsade de pointes (TdP). Ribociclib has been shown to prolong the QT interval in a concentration-dependent manner. Sotalol administration is also associated with QT prolongation and TdP, with proarrhythmic events anticipated after initiation of therapy and after each upward dosage adjustment. Concomitant use may increase the risk for QT prolongation.
    Ribociclib; Letrozole: (Major) Avoid coadministration of ribociclib with sotalol due to an increased risk for QT prolongation and torsade de pointes (TdP). Ribociclib has been shown to prolong the QT interval in a concentration-dependent manner. Sotalol administration is also associated with QT prolongation and TdP, with proarrhythmic events anticipated after initiation of therapy and after each upward dosage adjustment. Concomitant use may increase the risk for QT prolongation.
    Rilpivirine: (Major) Supratherapeutic doses of rilpivirine (75 to 300 mg/day) have caused QT prolongation; caution is advised when administering rilpivirine with other drugs that may prolong the QT or PR interval. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Risperidone: (Major) Risperidone has been associated with a possible risk for QT prolongation and/or torsade de pointes; however, data are currently lacking to establish causality in association with torsades de pointes (TdP). Reports of QT prolongation and torsades de pointes during risperidone therapy are noted by the manufacturer, primarily in the overdosage setting. Since risperidone may prolong the QT interval, it should be used cautiously with other agents also known to have this effect, such as sotalol, taking into account the patient's underlying disease state(s) and additional potential risk factors. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. If coadministration is chosen, and the patient has known risk factors for cardiac disease or arrhythmia, then the patient should be closely monitored clinically.
    Ritonavir: (Major) The use of ritonavir could result in QT prolongation. Drugs with a possible risk for QT prolongation and TdP that should be used cautiously and with close monitoring with ritonavir include sotalol.
    Rivastigmine: (Moderate) The increase in vagal tone induced by some cholinesterase inhibitors may produce bradycardia, hypotension, or syncope. The vagotonic effect of these drugs may theoretically be increased when given with other medications known to cause bradycardia such as beta-blockers.
    Romidepsin: (Major) Romidepsin has been reported to prolong the QT interval. Sotalol also prolongs the QT interval. If romidepsin and sotalol must be continued, appropriate cardiovascular monitoring precautions should be considered, such as the monitoring of electrolytes and ECGs at baseline and periodically during treatment.
    Salsalate: (Moderate) Concurrent use of beta-blockers with salsalate and other salicylates may result in loss of antihypertensive activity due to inhibition of renal prostaglandins and thus, salt and water retention and decreased renal blood flow.
    Saquinavir: (Major) Concurrent use of saquinavir boosted with ritonavir and sotalol should be avoided if possible due to the risk of life threatening cardiac arrhythmias such as torsade de pointes (TdP). Saquinavir boosted with ritonavir causes dose-dependent QT and PR prolongation; if possible, avoid use with other drugs that may prolong the QT or PR interval, such as all Class III antiarrhythmics. If no alternative therapy is acceptable, perform a baseline ECG prior to initiation of concomitant therapy and follow recommended ECG monitoring.
    Selpercatinib: (Major) Monitor ECGs more frequently for QT prolongation if coadministration of selpercatinib with sotalol is necessary due to the risk of additive QT prolongation. Concentration-dependent QT prolongation has been observed with selpercatinib therapy. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Semaglutide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Sertraline: (Major) Concomitant use of sertraline and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Sevoflurane: (Major) General anesthetics can potentiate the antihypertensive effects of beta-blockers and can produce prolonged hypotension. Severe, protracted hypotension and difficulty in restarting the heart have been reported after surgery on patients receiving beta-blockers. In addition, sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Drugs with a possible risk for QT prolongation and TdP, such as halogenated anesthetics, should be used cautiously with sotalol.
    SGLT2 Inhibitors: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Siponimod: (Major) In general, do not initiate treatment with siponimod in patients receiving sotalol due to the potential for QT prolongation. Consult a cardiologist regarding appropriate monitoring if siponimod use is required. Siponimod therapy prolonged the QT interval at recommended doses in a clinical study. Sotalol administration is associated with QT prolongation and torsade de pointes. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Sodium Bicarbonate: (Major) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer magnesium hydroxide two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
    Sodium Stibogluconate: (Major) Concomitant use of sodium stibogluconate and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Solifenacin: (Major) Due to the potential for QT prolongation and torsade de pointes (TdP), caution is advised when administering solifenacin with sotalol. Solifenacin has been associated with dose-dependent prolongation of the QT interval; TdP has been reported during post-marketing use, although causality was not determined. Sotalol administration is also associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Sorafenib: (Major) Avoid coadministration of sorafenib with sotalol due to the risk of additive QT prolongation. If concomitant use is unavoidable, monitor electrocardiograms and correct electrolyte abnormalities. An interruption or discontinuation of sorafenib therapy may be necessary if QT prolongation occurs. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP); proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Sorafenib is also associated with QTc prolongation.
    Sufentanil: (Moderate) The incidence and degree of bradycardia and hypotension during induction with sufentanil may be increased in patients receiving beta-blockers.
    Sulfonylureas: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Sunitinib: (Major) Monitor patients for QT prolongation if coadministration of sotalol with sunitinib is necessary. Sotalol administration is associated with QT prolongation and torsade de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment. Sunitinib can also cause dose-dependent QT prolongation, which may increase the risk for ventricular arrhythmias, including TdP.
    Sympathomimetics: (Moderate) Monitor hemodynamic parameters and for loss of efficacy during concomitant sympathomimetic agent and beta-blocker use; dosage adjustments may be necessary. Concomitant use may antagonize the cardiovascular effects of either drug.
    Tacrolimus: (Major) Concomitant use of tacrolimus and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Tamoxifen: (Major) Concomitant use of tamoxifen and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Tamsulosin: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents
    Tasimelteon: (Moderate) Advise patients to administer the beta-blocker in the morning if tasimelteon is used concomitantly. Nighttime administration of a beta-blocker may reduce the efficacy of tasimelteon by decreasing the production of melatonin via inhibition of beta1 receptors.
    Telavancin: (Major) Concomitant use of telavancin and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Telithromycin: (Major) Concomitant use of telithromycin and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Telmisartan; Amlodipine: (Moderate) Coadministration of amlodipine and beta-blockers can reduce angina and improve exercise tolerance. When these drugs are given together, however, hypotension and impaired cardiac performance can occur, especially in patients with left ventricular dysfunction, cardiac arrhythmias, or aortic stenosis.
    Terazosin: (Moderate) Orthostatic hypotension may be more likely if beta-blockers are coadministered with alpha-blockers.
    Tetrabenazine: (Major) Concomitant use of tetrabenazine and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Thalidomide: (Moderate) Thalidomide and other agents that slow cardiac conduction such as beta-blockers should be used cautiously due to the potential for additive bradycardia.
    Thiazolidinediones: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Thioridazine: (Contraindicated) Avoid concomitant use of thioridazine and sotalol due to an increased risk for torsade de pointes (TdP) and QT/QTc prolongation.
    Thyroid hormones: (Minor) Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone is given to the patient.
    Tirzepatide: (Moderate) Increased frequency of blood glucose monitoring may be required when a beta blocker is given with antidiabetic agents. Since beta blockers inhibit the release of catecholamines, these medications may hide symptoms of hypoglycemia such as tremor, tachycardia, and blood pressure changes. Other symptoms, like headache, dizziness, nervousness, mood changes, or hunger are not blunted. Beta-blockers also exert complex actions on the body's ability to regulate blood glucose. Some beta-blockers, particularly non-selective beta-blockers such as propranolol, have been noted to potentiate insulin-induced hypoglycemia and a delay in recovery of blood glucose to normal levels. Hyperglycemia has been reported as well and is possibly due to beta-2 receptor blockade in the beta cells of the pancreas. A selective beta-blocker may be preferred in patients with diabetes mellitus, if appropriate for the patient's condition. Selective beta-blockers, such as atenolol or metoprolol, do not appear to potentiate insulin-induced hypoglycemia. While beta-blockers may have negative effects on glycemic control, they reduce the risk of cardiovascular disease and stroke in patients with diabetes and their use should not be avoided in patients with compelling indications for beta-blocker therapy when no other contraindications are present.
    Tolterodine: (Major) Due to the potential for QT prolongation and torsade de pointes (TdP), caution is advised when administering tolterodine with sotalol. Tolterodine has been associated with dose-dependent prolongation of the QT interval, especially in poor CYP2D6 metabolizers. Sotalol administration is also associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Toremifene: (Major) Concomitant use of toremifene and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Trandolapril; Verapamil: (Moderate) Monitor blood pressure and heart rate if concomitant use of verapamil and sotalol is necessary. Concomitant use can increase the risk of bradycardia or hypotension.
    Tranylcypromine: (Major) Avoid concomitant use of beta-blockers and tranylcypromine due to the risk of additive hypotension and/or severe bradycardia. Potential for this interaction persists for up to 10 days after discontinuation of tranylcypromine (or 4 to 5 half-lives after discontinuation of the beta-blocker). If a medication-free interval is not feasible, initiate therapy at the lowest appropriate dose and monitor blood pressure and heart rate closely.
    Trazodone: (Major) Concomitant use of sotalol and trazodone increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Triclabendazole: (Major) Concomitant use of triclabendazole and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Trifluoperazine: (Minor) Trifluoperazine, a phenothiazine, is associated with a possible risk for QT prolongation and should be used cautiously with sotalol. Sotalol administration is associated with QT prolongation and torsades de pointes (TdP). Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Triptorelin: (Major) Concomitant use of triptorelin and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Urea: (Major) Diuretics should be used cautiously with sotalol and should be accompanied by close monitoring of electrolyte balance because hypokalemia and hypomagnesemia have been associated with an increased risk of proarrhythmia.
    Vandetanib: (Major) Concomitant use of vandetanib and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Vardenafil: (Major) Concomitant use of vardenafil and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Vemurafenib: (Major) Concomitant use of vemurafenib and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Venlafaxine: (Major) Concomitant use of sotalol and venlafaxine increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Verapamil: (Moderate) Monitor blood pressure and heart rate if concomitant use of verapamil and sotalol is necessary. Concomitant use can increase the risk of bradycardia or hypotension.
    Voclosporin: (Major) Concomitant use of voclosporin and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary. The degree of QT prolongation associated with voclosporin is not clinically significant when administered within the recommended dosage range; QT prolongation has been described at 3 times the maximum recommended dose.
    Vonoprazan; Amoxicillin; Clarithromycin: (Major) Use caution if coadministering clarithromycin and sotalol. Clarithromycin is associated with an established risk for QT prolongation and torsades de pointes (TdP). Sotalol administration is associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of therapy and after each upward dosage adjustment.
    Voriconazole: (Major) Due to the potential for QT prolongation and torsade de pointes (TdP), caution is advised when administering voriconazole with sotalol. Voriconazole has been associated with prolongation of the QT interval and rare cases of arrhythmias, including TdP. Sotalol is also associated with QT prolongation and TdP. Proarrhythmic events should be anticipated after initiation of sotalol therapy and after each upward dosage adjustment.
    Vorinostat: (Major) Concomitant use of vorinostat and sotalol increases the risk of QT/QTc prolongation and torsade de pointes (TdP). Avoid concomitant use if possible, especially in patients with additional risk factors for TdP. Consider taking steps to minimize the risk for QT/QTc interval prolongation and TdP, such as electrolyte monitoring and repletion and ECG monitoring, if concomitant use is necessary.
    Ziprasidone: (Contraindicated) Avoid concomitant use of ziprasidone and sotalol due to an increased risk for torsade de pointes (TdP) and QT/QTc prolongation.

    PREGNANCY AND LACTATION

    Pregnancy

    Both the use of sotalol and the untreated underlying condition in pregnancy cause adverse outcomes to the mother and fetus/neonate. The incidence of ventricular tachycardia is increased and may be more symptomatic during pregnancy. Breakthrough arrhythmias may also occur during pregnancy, as therapeutic drug concentrations may be difficult to maintain due to the increased volume of distribution and increased drug metabolism during pregnancy. Sotalol crosses the placenta and is found in amniotic fluid. From published observational studies, potential fetal adverse effects include growth restriction, transient fetal bradycardia, hyperbilirubinemia, hypoglycemia, maternal uterine contractions, and intrauterine death. Sotalol may have a greater effect on QT prolongation in the immature heart, and therefore, there may be an increased risk of serious fetal arrhythmia and/or intrauterine death. Monitor exposed neonates for symptoms of beta-blockade. Monitor mothers treated with sotalol continuously during labor and obstetric delivery; the risk of arrhythmias increases during the labor and delivery process. In animal reproduction studies in rats, early resorptions were increased at 15 to 18 times the maximum recommended human dose (MRHD), while no increase in early resorptions was noted at 2 to 2.5 times the MRHD. In rabbits, an increase in fetal death was observed at 2 times the MRHD administered as single dose (50 mg/kg) on gestation day 4. A slight increase in fetal death and maternal toxicity occurred in rabbits that received 6 times the MRHD. No teratogenic effects were noted in rats and rabbits that received sotalol at 9 the 7 times the MRHD, respectively, during organogenesis.[36213] [36512] [60784]

    MECHANISM OF ACTION

    Sotalol is a racemic mixture of isomers. The levorotatory isomer has all of the beta-blocking activity and both the levorotatory and dextrorotatory isomers possess Class III antiarrhythmic activity. Significant beta-blockade occurs with oral doses as low as 25 mg; the half maximal beta-blocking effect of sotalol is seen with daily doses of 80 mg, and maximal beta-blocking effects are observed with daily doses between 320 mg and 640 mg. Significant class III antiarrhythmic effects are observed with daily doses of 160 mg and more.
     
    The beta-blocker activity of sotalol increases sinus cycle length, decreases AV nodal conduction, and increases AV nodal refractoriness. Hemodynamic effects of sotalol include reduced heart rate and cardiac index as well as increased systemic vascular resistance, stroke volume, and pulmonary capillary wedge pressure. Significant reductions in systolic and diastolic blood pressure are also seen in hypertensive patients. In general, beta-blockers without intrinsic sympathomimetic activity (ISA), like sotalol, exert detrimental effects on left ventricular hypertrophy and the lipid profile.
     
    The antiarrhythmic activity is exerted by a combination of Class II activity and Class III activity, which lengthens repolarization or the plateau phase of the action potential and lengthens the refractory period in all cardiac tissues. In addition, sotalol prolongs the QT interval (a Class III effect), which must be carefully monitored to avoid predisposing patients to proarrhythmic events.

    PHARMACOKINETICS

    Sotalol is administered orally or intravenously. Distribution occurs to a central (plasma) and peripheral compartment. Sotalol does not bind to plasma proteins and has poor penetration of the blood-brain barrier. Sotalol is not metabolized and is excreted primarily unchanged by the kidneys via glomerular filtration and tubular secretion. The plasma half-life in patients with normal renal function is 12 hours.[60784]
     
    Affected cytochrome P450 isoenzymes and drug transporters: none

    Oral Route

    After oral administration, bioavailability is 90% to 100%. Food reduces the rate of absorption by approximately 20%, but sotalol may be taken with or without food. Peak plasma concentrations after oral administration are reached within 2 to 3 hours in pediatric patients (3 days to 12 years) and 2.5 to 4 hours in adult patients. Steady-state plasma concentrations are reached within 1 to 2 days in pediatric patients and 2 to 3 days in adult patients.