The following are the FDA and non-FDA indications for sotalol:
There is no difference between sotalol and amiodarone when it comes to the pharmacological conversion of atrial fibrillation. The recurrence rate of atrial fibrillation is higher for sotalol as compare to amiodarone, except in patients with ischemic heart disease.
Sotalol has not been shown to have 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.
Sotalol is a non-cardioselective beta-blocker that also possesses potassium channel blocker properties. It is classified 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 required 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. However, its half-life is decreased to 10 hours in pregnancy due to increased glomerular filtration rate in pregnancy. Data show that sotalol should be avoided in pregnancy and during lactation.
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. 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. 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 80mg is equivalent to 75 mg of IV, and similarly, 160mg oral is equivalent to 150mg of IV. If infusing intravenously, the recommendation is that the drug is administered slowly as a rapid infusion can cause hypotension.
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.
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 and 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. 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 can be used 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:
Contraindications related to QTc prolonging effects:
Patients initiated on sotalol should be hospitalized 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 dose should be reduced, or sotalol should be discontinued.
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. Coordination of care includes the following:
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 so that therapy modifications can be made if necessary. An interprofessional team approach to sotalol use allows for optimal outcomes while minimizing adverse effects. [Level 5]
|||Anderson JL,Askins JC,Gilbert EM,Miller RH,Keefe DL,Somberg JC,Freedman RA,Haft LR,Mason JW,Lessem JN, Multicenter trial of sotalol for suppression of frequent, complex ventricular arrhythmias: a double-blind, randomized, placebo-controlled evaluation of two doses. Journal of the American College of Cardiology. 1986 Oct [PubMed PMID: 2428852]|
|||deSouza IS,Martindale JL,Sinert R, Antidysrhythmic drug therapy for the termination of stable, monomorphic ventricular tachycardia: a systematic review. Emergency medicine journal : EMJ. 2015 Feb [PubMed PMID: 24042252]|
|||McNamara RL,Tamariz LJ,Segal JB,Bass EB, Management of atrial fibrillation: review of the evidence for the role of pharmacologic therapy, electrical cardioversion, and echocardiography. Annals of internal medicine. 2003 Dec 16 [PubMed PMID: 14678922]|
|||Zimetbaum PJ,Josephson ME, Amiodarone versus sotalol for atrial fibrillation. The New England journal of medicine. 2005 Aug 11 [PubMed PMID: 16094764]|
|||Gomes JA,Ip J,Santoni-Rugiu F,Mehta D,Ergin A,Lansman S,Pe E,Newhouse TT,Chao S, Oral d,l sotalol reduces the incidence of postoperative atrial fibrillation in coronary artery bypass surgery patients: a randomized, double-blind, placebo-controlled study. Journal of the American College of Cardiology. 1999 Aug [PubMed PMID: 10440141]|
|||Shah A,Moon-Grady A,Bhogal N,Collins KK,Tacy T,Brook M,Hornberger LK, Effectiveness of sotalol as first-line therapy for fetal supraventricular tachyarrhythmias. The American journal of cardiology. 2012 Jun 1 [PubMed PMID: 22444730]|
|||Sotalol versus Amiodarone in Treatment of Atrial Fibrillation., Somberg Md J,Molnar Md J,, Journal of atrial fibrillation, 2016 Feb 29 [PubMed PMID: 27909477]|
|||Singh BN,Singh SN,Reda DJ,Tang XC,Lopez B,Harris CL,Fletcher RD,Sharma SC,Atwood JE,Jacobson AK,Lewis HD Jr,Raisch DW,Ezekowitz MD, Amiodarone versus sotalol for atrial fibrillation. The New England journal of medicine. 2005 May 5 [PubMed PMID: 15872201]|
|||Hanyok JJ, Clinical pharmacokinetics of sotalol. The American journal of cardiology. 1993 Aug 12 [PubMed PMID: 8346722]|
|||O'Hare MF,Murnaghan GA,Russell CJ,Leahey WJ,Varma MP,McDevitt DG, Sotalol as a hypotensive agent in pregnancy. British journal of obstetrics and gynaecology. 1980 Sep [PubMed PMID: 7426541]|
|||Anderson JL,Prystowsky EN, Sotalol: An important new antiarrhythmic. American heart journal. 1999 Mar [PubMed PMID: 10047618]|
|||Finks SW,Rogers KC,Manguso AH, Assessment of sotalol prescribing in a community hospital: opportunities for clinical pharmacist involvement. The International journal of pharmacy practice. 2011 Aug [PubMed PMID: 21733016]|
|||Samanta R,Thiagalingam A,Turner C,Lakkireddy DJ,Kovoor P, The Use of Intravenous Sotalol in Cardiac Arrhythmias. Heart, lung & circulation. 2018 Nov [PubMed PMID: 29853342]|
|||Kopelman HA,Woosley RL,Lee JT,Roden DM,Echt DS, Electrophysiologic effects of intravenous and oral sotalol for sustained ventricular tachycardia secondary to coronary artery disease. The American journal of cardiology. 1988 May 1 [PubMed PMID: 3284316]|