A β blocker used with rhythm disturbances of the heart, and to treat hypertension in some individuals.
A non-selective competitive β-adrenergic receptor blocker that also exhibits Class III antiarrhythmic properties by its inhibition of potassium channels.
Prolongs both the PR interval and the QT interval.
Due to the dual action of sotalol, it is often used preferentially to other β-blockers as treatment for both ventricular fibrillation and ventricular tachycardia.
Patients to be started on or reinitiated to this drug should be placed for a minimum of three days in a facility that can provide cardiac resuscitation and continuous electrocardiographic monitoring.
Creatinine clearance should be established prior to dosing.
Also indicated for the maintenance of normal sinus rhythm in patients with symptomatic atrial fibrillation currently in sinus rhythm.
Beta-blocking effect is non-cardioselective, half maximal at about 80 mg/day and maximal at doses between 320 and 640 mg/day.
Significant beta-blockade occurs at oral doses as low as 25 mg, while Class III effects are seen at daily doses of 160 mg and above.
Prolongs the plateau phase of the cardiac action potential in the myocyte.
Class II , beta-blockade, electrophysiological effects slows heart rate, decreases AV nodal conduction and increases AV nodal refractoriness.
Class III effects include prolongation of the atrial and ventricular monophasic action potentials, and effective refractory period prolongation of atrial muscle, ventricular muscle, and atrio-ventricular accessory pathways.
With oral doses of 160 to 640 mg/day,associated with increases of 40 to 100 msec in QT and 10 to 40 msec in QTc, but does not significantly alter QRS interval.
Reduces systolic and diastolic blood pressure in hypertensive patients.
May precipitate heart failure in poorly compensated patients.
Oral bioavailability is 90 to 100%.
After oral administration, peak plasma concentrations are reached in 2.5 to 4 hours, and steady-state plasma concentrations are attained within 2 to 3 days.
Does not bind to plasma proteins and is not metabolized.
Excretion is predominantly via the kidney in the unchanged form, and therefore lower doses are necessary in conditions of renal impairment.
Absorption reduced by approximately 20% compared to fasting when it was administered with a standard meal.
A medication used to treat heart arrhythmias.
Should only be used for serious arrhythmias, because its prolongation of the QT interval carries a small risk of life-threatening torsade de pointes.
Trade name Betapace,
Pregnancy category AU: C
Oral agent.
Drug class beta blocker.
Bioavailability 90–100%.
Not metabolized.
Biological half-life 12 hours.
Excretion by the kidney.
A non-selective competitive beta-adrenergic receptor blocker that also exhibits Class III antiarrhythmic properties.
Can be used to maintain normal heart rhythm in people with life-threatening ventricular arrhythmias, or very symptomatic atrial fibrillation or flutter.
Due to the risk of serious side effects, should generally be reserved for people whose ventricular arrhythmias are life-threatening, or whose fibrillation/flutter cannot be resolved using the Valsalva maneuver or another simple method.
Should not be used in people with a heart rate lower than 50 beats per minute., sick sinus syndrome, long QT syndrome, cardiogenic shock, uncontrolled heart failure, bronchial asthma or a related bronchospastic condition, or people with serum potassium below 4 meq/L.
It should only be used in people with a second and third degree AV block if a functioning pacemaker is present.
It should not be used in people with a creatinine clearance rate below 40 mL/min, as it is cleared by the kidney.
It is also excreted in breast milk.
Because it prolongs the QT interval it should not be used in conjunction with other drugs that prolong QT interval.
Serious side effects are more common in patients also taking digoxin.
As with other beta blockers, it may interact with calcium channel blockers, catecholamine-depleting drugs, insulin or antidiabetic drugs, beta2-adrenergic agonists, and clonidine.
Should be avoided in the setting of decreased ejection fraction due to an increased risk of death.
Adverse effects: over 10% of oral sotalol users experience fatigue, dizziness, lightheadedness, headache, weakness, nausea, shortness of breath, bradycardia, palpitations, or chest pain.
Averse risks increases with dosage.
Rarely, QT prolongation can lead to the development of life-threatening torsade de pointes ventricular tachycardia
0.6% of oral sotalol patients with supraventricular arrhythmias develop torsade de pointes.
In patients with a history of sustained ventricular tachycardia 4% develop torsade de pointes.
Torsade de pointes risk increases with dosage, female sex, or having a history of cardiomegaly or congestive heart failure.
The incidence of torsade de pointes in sustained ventricular tachycardia patients was 0% with an 80 mg daily dose, 0.5% at 160 mg, 1.6% at 320 mg, 4.4% at 480 mg, 3.7% at 640 mg, and 5.8% at doses greater than 640 mg.
FDA requires patients to be hospitalized for at least three days in a facility that can provide cardiac resuscitation and continuous electrocardiographic monitoring upon starting or restarting sotalol.
Non-selectively binds to both β1- and β2-adrenergic receptors preventing activation of the receptors by their stimulatory ligand.
Results in a decrease in activation of calcium channels with a decrease in intracellular calcium.
In cardiac cells, calcium is important in generating electrical signals for contraction, as well as generating force for contraction.
In consideration of these important properties of calcium, two conclusions can be drawn. Firstly,
When there is less calcium in the cell, there is a decrease in electrical signals for contraction, thus allowing time for the heart’s natural pacemaker to rectify arrhythmic contractions..
When there is less calcium in the cell there is a decrease in strength and rate of heartvcontractions, which can be helpful in treatment of abnormally high heart rates in patients with tachycardia.
Also acts on potassium channels and causes a delay in relaxation of the ventricles.
It blocks potassium channels, inhibiting efflux of K+ ions, resulting in an increase in the time before another electrical signal can be generated in ventricular myocytes.
This delay helps correct arrhythmias by reducing the potential for premature or abnormal contraction of the ventricles but also prolongs the frequency of ventricular contraction to help treat tachycardia.