Sotalol is a medicine for irregular heart rhythms (an antiarrhythmic). It calms the heart's rhythm and is used when other treatments have not worked. It requires close medical monitoring, including ECGs, because it can change the heart's electrical conduction.
Also known as: Sotalex
Sotalol antagonises the effect of formoterol and may cause bronchospasm in predisposed patients.
Formoterol is a long-acting beta2-agonist (LABA) and sotalol a non-selective beta-blocker with class III antiarrhythmic activity (QT prolongation). Sotalol blocks beta2 receptors, opposing the bronchodilator effect of formoterol (risk of asthma/COPD exacerbation), and beta2-agonists "may produce significant hypokalaemia in some patients, possibly through intracellular potassium shunting, with the potential to produce adverse cardiovascular effects" (formoterol label) — and hypokalaemia "can exaggerate the degree of QT prolongation, and increase the potential for Torsade de Pointes" (sotalol label). The combination is particularly risky in patients with underlying heart disease or long QT. Whenever possible, avoid non-selective beta-blockers in patients using a LABA; if unavoidable, monitor respiratory function, potassium/magnesium and ECG.
Formoterol + sotalol: sotalol blocks beta2 receptors (antagonises the LABA) and formoterol-induced hypokalaemia may potentiate sotalol QT. Avoid or monitor ECG and potassium.
β2-receptor antagonism between formoterol (LABA) and sotalol (non-selective beta-blocker).
Monitor respiratory function and bronchodilator response.
Bronchospasm, worsening of airway obstruction.
Do not use non-selective beta-blockers in patients with obstructive airways disease.
DailyMed (FDA) — approved Formoterol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=35538d89-a984-4335-acdf-85a893f51eee ; approved Sotalol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9a36d95c-6e93-4e57-befe-b5274f359244 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Sotalol may reduce the bronchodilator effect of salmeterol and increase the risk of bronchospasm.
Salmeterol is a LABA (long-acting beta2-agonist) and sotalol a non-selective beta-blocker with QT prolongation (class III). Sotalol blocks bronchial beta2 receptors, opposing the bronchodilation of salmeterol, and beta-agonists "may produce significant hypokalaemia in some patients, possibly through intracellular shunting, with the potential to produce adverse cardiovascular effects" (salmeterol label). Hypokalaemia, in turn, "can exaggerate the degree of QT prolongation, and increase the potential for Torsade de Pointes" (sotalol label). In patients with asthma/COPD and cardiovascular disease, the combination adds bronchoconstriction, hypokalaemia and arrhythmogenic risk. Avoid non-selective beta-blockers in patients using a LABA; if unavoidable, monitor respiratory symptoms, potassium/magnesium and ECG.
Salmeterol + sotalol: beta2 antagonism (sotalol opposes the LABA) + salmeterol hypokalaemia potentiating sotalol QT. Avoid or monitor ECG and electrolytes.
β2-receptor antagonism between the LABA and the non-selective beta-blocker.
Monitor for bronchospasm and bronchodilator efficacy.
Bronchospasm, lack of response to salmeterol.
Avoid the combination in asthma; monitor respiratory function.
DailyMed (FDA) — approved Salmeterol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=12d9728e-6b5c-4aee-bfb0-745e542ed2e4 ; approved Sotalol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9a36d95c-6e93-4e57-befe-b5274f359244 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Thiazide-induced hypokalaemia raises the risk of torsades with sotalol.
Sotalol prolongs the QT interval (class III) and the risk of torsades de pointes rises as serum potassium and magnesium fall. Hydrochlorothiazide depletes these electrolytes and creates the electrophysiological environment for potentially fatal polymorphic ventricular arrhythmias. The combination is common in hypertensive and cardiac patients, which demands discipline: keep serum potassium at least at 4.0 mEq/L, correct hypomagnesaemia, monitor the ECG (QT) and electrolytes during treatment and avoid other QT-prolonging drugs.
Thiazide + sotalol: diuretic-induced hypokalaemia (and hypomagnesaemia) increases the risk of torsades de pointes. Correct electrolytes before and during treatment and monitor the QT.
The thiazide depletes potassium and amplifies sotalol's QT prolongation.
Potassium, magnesium, ECG (QT).
Ventricular arrhythmia or syncope.
Monitor potassium and ECG; correct the hypokalaemia first.
DailyMed (FDA) — approved Sotalol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9a36d95c-6e93-4e57-befe-b5274f359244 ; approved Hydrochlorothiazide label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=0789baef-3424-43ab-a3fb-4908172da565 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Non-selective beta-blockers such as sotalol antagonise the bronchodilator effect of salbutamol and may trigger bronchospasm.
Sotalol is a non-selective beta-blocker that also prolongs the QT interval (class III); it blocks bronchial beta2 receptors, directly opposing the bronchodilator effect of salbutamol, and the sotalol label warns that "uncorrected hypokalaemia or hypomagnesaemia can exaggerate the degree of QT prolongation, and increase the potential for Torsade de Pointes", recommending correction before initiation. Salbutamol, like other beta2-agonists, "may produce significant hypokalaemia in some patients, possibly through intracellular shunting, with the potential to produce adverse cardiovascular effects" (salbutamol label). The combination therefore adds bronchial antagonism to the arrhythmogenic risk (hypokalaemia + QT). Avoid whenever possible in patients with asthma and cardiovascular disease; if unavoidable, use the lowest salbutamol dose, correct potassium/magnesium and monitor ECG and respiratory function.
Salbutamol + sotalol: sotalol (non-selective beta-blocker) opposes the bronchodilator effect of salbutamol, and beta2-agonist-induced hypokalaemia may exaggerate sotalol QT prolongation. Avoid or monitor ECG and potassium.
Sotalol blocks bronchial β2 receptors, opposing salbutamol.
Monitor respiratory function and response to the bronchodilator.
Bronchospasm, worsening dyspnoea.
Avoid non-selective beta-blockers in asthmatic patients; if unavoidable, use cardioselective agents with caution.
DailyMed (FDA) — approved Salbutamol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=3236f82c-14e9-dfd4-e063-6294a90ac43d ; approved Sotalol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9a36d95c-6e93-4e57-befe-b5274f359244 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Loop-diuretic hypokalaemia raises the risk of torsades de pointes with sotalol.
Sotalol prolongs the QT interval and the risk of torsades de pointes rises as serum potassium (and magnesium) fall. Furosemide, by depleting these electrolytes, creates the electrophysiological environment for potentially fatal polymorphic ventricular arrhythmias. The combination is not prohibited but demands discipline: correct potassium to at least 4.0 mEq/L before starting sotalol, correct hypomagnesaemia, monitor the QT and electrolytes during treatment and avoid other QT-prolonging drugs.
Loop diuretic + sotalol: diuretic-induced hypokalaemia/hypomagnesaemia increases the risk of torsades de pointes with a QT-prolonging drug. Correct electrolytes first and monitor the ECG.
Potassium/magnesium depletion by furosemide predisposes to ventricular arrhythmias on sotalol.
Potassium, magnesium, ECG (QT).
Syncope or ventricular tachycardia (torsades).
Correct the hypokalaemia before combining and monitor electrolytes.
DailyMed (FDA) — approved Sotalol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9a36d95c-6e93-4e57-befe-b5274f359244 ; approved Furosemide label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=6d9caaab-d874-4cf1-b9fe-408452a18998 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
The combination raises the risk of bradycardia and AV-node dysfunction.
Sotalol combines beta blockade (negative chronotropic and dromotropic effects) with class III activity (QT prolongation): with digoxin, the effects on heart rate and AV conduction add up, increasing the risk of bradycardia and block. Hypokalaemia/hypomagnesaemia (which digoxin can favour) potentiates sotalol torsades de pointes risk. This combination arises in atrial fibrillation, requiring ECG monitoring (rate, PR, QT), electrolytes and renal function, with dose adjustment.
Sotalol + digoxin: additive bradycardia and AV block; sotalol prolongs the QT and digoxin increases the arrhythmia risk. Monitor ECG and electrolytes.
Sotalol and digoxin depress AV conduction; sotalol also prolongs the QT.
Heart rate, ECG (PR/QT interval).
High-degree AV block, syncope or severe bradycardia.
Monitor heart rate and ECG; titrate with caution.
DailyMed (FDA) — approved Sotalol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9a36d95c-6e93-4e57-befe-b5274f359244 ; approved Digoxin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=e61d2108-d871-44c0-b12a-2e61fbb56967 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Alcohol may disturb the heart rhythm and potentiate the hypotensive effects of sotalol; limit intake.
Limit alcohol intake during treatment.
DailyMed/FDA (NIH/NLM) — approved Sotalol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9a36d95c-6e93-4e57-befe-b5274f359244
Food reduces sotalol absorption by about 20%; taking it consistently on an empty stomach reduces variability.
Take sotalol on an empty stomach, 1 hour before or 2 hours after meals.
DailyMed/FDA (NIH/NLM) — approved Sotalol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9a36d95c-6e93-4e57-befe-b5274f359244
Sotalol has beta-blocking activity and is contraindicated in bronchial asthma or COPD because of the risk of bronchospasm.
Do not use in asthma or COPD; consider a class III antiarrhythmic without beta-blockade.
EMC-UK (MHRA) — approved Sotalol SmPC: https://www.medicines.org.uk/emc/product/7039/smpc
Sotalol prolongs the QT interval and is contraindicated in congenital QT prolongation or a history of torsades de pointes.
Do not use; check baseline QT on ECG before starting and monitor QT during treatment.
EMC-UK (MHRA) — approved Sotalol SmPC: https://www.medicines.org.uk/emc/product/7039/smpc
Sotalol crosses the placenta and may cause beta-blocking effects in the fetus (bradycardia, hypoglycaemia); data do not indicate teratogenicity.
Use only if the benefit outweighs the risk; monitor fetal growth and heart rate.
Sotalol is excreted into breast milk; monitor the infant for signs of beta-blockade.
No specific contraception is required, but chronic therapy in women of childbearing age should be reviewed before conception.
EMC-UK (MHRA) — approved Sotalol SmPC: https://www.medicines.org.uk/emc/product/7039/smpc
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Antiarrhythmic with class II (non-cardioselective beta-adrenergic blockade) and class III (action potential duration prolongation) properties. With oral doses of 160 to 640 mg/day it prolongs the QT and QTc intervals dose-dependently (mean 40 to 100 ms and 10 to 40 ms), without significantly changing the QRS.
The l-isomer accounts for virtually all of the beta-blocking activity; both isomers share the class III antiarrhythmic effects. Beta-blockade is half maximal at about 80 mg/day and maximal between 320 and 640 mg/day; significant class III effects appear from 160 mg/day. It has no partial agonist or membrane-stabilising activity.
Oral bioavailability of 90 to 100%; peak plasma concentrations are reached 2.5 to 4 hours after dosing and steady state within 2 to 3 days. It does not bind to plasma proteins. Administration with a standard meal reduces absorption by about 20%.
Not metabolised and does not inhibit or induce cytochrome P450 enzymes. Eliminated predominantly unchanged by the kidneys (glomerular filtration and, to a small degree, tubular secretion), so lower doses are required in renal impairment.
The mean elimination half-life is about 12 hours. Renal impairment prolongs the half-life (up to 69 hours in anuric patients), requiring dose or interval adjustment based on creatinine clearance.
