Continuing Education Activity

Sotalol has the following are the FDA and non-FDA indications: premature ventricular contractions, hemodynamically stable ventricular tachycardia, pharmacological cardioversion of atrial fibrillation, maintaining sinus rhythm, postoperative atrial fibrillation after cardiac surgery, supraventricular tachycardia, and others. This activity outlines the indications, mechanisms of action, methods of administration, significant adverse effects, contraindications, and monitoring, of sotalol, so providers can direct patient therapy in treating indicated disorders as part of the interprofessional team, with a basis on the current knowledge for optimal utilization.


  • Describe the mechanism of action of sotalol.
  • Outline the indicated uses, both approved and off label, for imitating therapy with sotalol.
  • Identify the adverse effects and contraindications associated with sotalol therapy.
  • Review interprofessional team strategies for improving care coordination and communication to advance sotalol when indicated and improve patient outcomes.


 The following are the FDA and non-FDA indications for sotalol:

  1. Premature ventricular contractions-sotalol has been superior to placebo for the suppression of premature ventricular contractions.[1] 
  2. Hemodynamically stable ventricular tachycardia.[2] (FDA indicated)
  3. Pharmacological cardioversion of atrial fibrillation-less effective.[3]
  4. Maintaining sinus rhythm-especially in paroxysmal atrial fibrillation.[4] (FDA indicated)
  5. Postoperative atrial fibrillation after cardiac surgery.[5]
  6. Supraventricular tachycardia-especially when administered intravenously.
  7. Transplacental isolated sotalol or along with digoxin used to treat fetal SVT and atrial fibrillation with 85% complete or partial resolution.[6]

There is no difference between sotalol and amiodarone when it comes to the pharmacological conversion of atrial fibrillation.[7][8] The recurrence rate of atrial fibrillation is higher for sotalol as compare to amiodarone, except in patients with ischemic heart disease.[7][8]

Sotalol has not demonstrated any beneficial effect as prophylaxis with AICD for prevention of ventricular arrhythmias to stop appropriate or inappropriate ICD shocks; in this scenario, amiodarone is better than sotalol. 

Mechanism of Action

Sotalol is a non-cardioselective beta-blocker that also possesses potassium channel blocker properties. It classifies as a class III agent in the Vaughan-Williams classification system for antiarrhythmic medications due to its predominant potassium channel blocking effect.  Sotalol prolongs the action potential duration and effective refractory period in atrium and ventricle, and in nodal and extranodal tissue as it is a potent competitive inhibitor for potassium current. Sotalol exhibits reverse use-dependent effects, meaning that the maximal potassium current blocking effect occurs when the heart rate is slow, increasing the risk of QT prolongation and torsades de pointes in bradycardic conditions.  A low dose is enough to exert a beta-blocking effect. For example, 25 mg offers good beta-blocking activity, but for class III antiarrhythmic effects, a higher dose is necessary, in the range of 80 mg.


The bioavailability is 95% to 100% without the hepatic first-pass effect (metabolism). After a single oral dosage, it takes about 2.5 to 3 hours to reach its maximal (peak) concentration in serum. On the other hand, the intravenous (IV) infusion takes around 2 hours to attain peak serum levels. The drug is water-soluble, which results in minimal blood-brain barrier penetration. Sotalol has no active metabolites. Sotalol distributes to the heart, liver, and kidneys. It is excreted maximally from kidneys with up 20%  excreted in the feces. Its half-life is 10 to 20 hours in a population with normal renal function.[9] However, its half-life is decreased to 10 hours in pregnancy due to increased glomerular filtration rate during pregnancy. Data show that sotalol should be avoided in pregnancy and during lactation.[10]

As stated, sotalol is excreted mainly through kidneys. Therefore dose adjustment is required if the eGFR is less than 60 ml/min. The recommended initial dose of sotalol is 80 mg given twice daily if GFR is more than 60 ml/min, with the dose increased (generally allowing 2 to 3 days between dosing increments), if necessary, up to 320 mg, given in 2 or 3 divided doses.[11] Sotalol should be prescribed once daily if the creatinine clearance is between 40 to 60 ml/min. Data suggest that the patient population with heart failure also needs a dose adjustment.[12] The most effective dosage for the prevention of atrial fibrillation is 120 mg up to twice daily, depending on renal function. 

There is a dosage conversion between oral and intravenous sotalol. Oral sotalol 80 mg is equivalent to 75 mg of IV, and similarly, 160mg oral is equivalent to 150 mg of IV. If infusing intravenously, the recommendation is to administer the drug slowly as a rapid infusion can cause hypotension.[13]

There is no statistically significant difference between intravenous and oral sotalol in different parameters like a prolongation of QT interval, atrial effective refractory period and right ventricular effective refractory period, sinus cycle length, and atrioventricular node relative and functional refractory periods.[14]

Adverse Effects

Sotalol's adverse effect profile is inherent in its mechanisms of action as both a potassium-channel blocker and a non-cardioselective beta-blocker. The potassium channel blockade, primarily in phase 3 of the cardiac action potential, serves to prolong the QTc. Thus the ECG must be monitored upon initiation of sotalol or addition of other QTc-prolonging medications. Prolongation of the QT interval occurs in 1% to 2% of cases, which could lead to torsades de pointes or new ventricular tachycardia/ventricular fibrillation. 

The adverse effect of sotalol on QT prolongation is directly related to its serum levels.[13] Its side effects, especially torsades de pointes, are also dose-dependent; the rate of torsades is 1% with doses less than 320 mg and increases up to 5% at doses of more than 320mg. Higher doses are possible if a patient has an implantable cardioverter-defibrillator. The incidence of QT prolongation occurs more frequently with the  IV formulation. 

Other adverse effects associated with its non-cardioselective beta-blockade include bradycardia, fatigue, dyspnea, and worsening heart failure.


Contraindications related to its non-cardioselective beta-blockade:

  • Bronchial asthma or other bronchospamsmodic conditions
  • Sinus bradycardia
  • 2nd or 3rd degree AV block absent a functioning pacemaker
  • Cardiogenic shock
  • Decompensated heart failure due to a negative inotropic effect
  • Sick sinus syndrome (without a pacemaker)
  • Labile diabetes (due to hypoglycemia)
  • Left ventricular hypertrophy (which also increases the risk of arrhythmia) 

Contraindications related to QTc prolonging effects:

  • CrCl < 40 ml/min when used for atrial fibrillation or flutter
  • Acquired or congenital long QTc syndromes
  • Uncorrected hypokalemia or hypomagnesemia (increased risk of prolonging QT  and causing torsades de pointes)

Other contraindications

  • Previous evidence of sotalol hypersensitivity or allergy


Patients initiated on sotalol should be in the hospital for at least three days with facilities for cardiac rhythm monitoring and assessment. Do not initiate sotalol with a baseline QTc greater than 450 msec. Providers should have magnesium over 2 mEq/L and potassium greater than 4 mEq/L available when a patient receives sotalol. The dose requires adjustment according to renal function. The recommendation that the dose of sotalol gradually is increased over a three-day interval. Most cardiologists recommend observing the patient in a hospital for at least three days after starting sotalol with serial EKGs. 


Sotalol toxicity is inherent due to its mechanisms of action as both a potassium channel blocker and a non-cardioselective beta-blocker and mirrors its adverse effect profile. The most obvious and potentially problematic sign of toxicity is concentration-related QTc prolongation. If QTc is is over 500 msec during initiation, the sotalol dose should be reduced or discontinued. If QTc exceeds 520 msec during the maintenance phase of dosing, the clinician should either reduce the dose or discontinue sotalol.

Enhancing Healthcare Team Outcomes

Managing sotalol initiation and monitoring requires an interprofessional team of healthcare professionals that includes a cardiologist, nurse, and pharmacist. Without proper management, the risk of toxicity can increase.[12] Coordination of care consists of the following:

  • Assess both blood pressure and heart rate before and following the first dose and with any change in dosage (Level II)
  • Obtain serum creatinine, magnesium, and potassium (Level II)
  • Cardiac monitoring to observe for QT changes and arrhythmias (Level II)
  • Assess cardiac and pulmonary status. 
  • Advise patients with diabetes to monitor glucose levels closely (beta-blockers may alter glucose tolerance)
  • Assess other medicines a patient may be taking; alternate therapy or dosage adjustments may be needed.
  • Ensure to utilize a pharmacist to assess drug interactions, renal dose adjustments, and medication education 

A cardiology board-certified pharmacist can assist the clinician team with sotalol dosing and monitoring. Nursing will need to understand the signs of adverse events associated with the use of this drug, as well as report the therapeutic effectiveness of the regimen to the team to enable therapy modifications if necessary. An interprofessional team approach to sotalol use allows for optimal outcomes while minimizing adverse effects. [Level 5]

Article Details

Article Author

Ateeq Mubarik

Article Author

Connor Kerndt

Article Editor:

Manouchkathe Cassagnol


12/5/2020 7:38:23 PM

PubMed Link:




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