Dr. Ogbru received his Doctorate in Pharmacy from the University of the Pacific School of Pharmacy in 1995. He completed a Pharmacy Practice Residency at the University of Arizona/University Medical Center in 1996. He was a Professor of Pharmacy Practice and a Regional Clerkship Coordinator for the University of the Pacific School of Pharmacy from 1996-99.
Jay W. Marks, MD, is a board-certified internist and gastroenterologist. He graduated from Yale University School of Medicine and trained in internal medicine and gastroenterology at UCLA/Cedars-Sinai Medical Center in Los Angeles.
Combining sotalol with beta-blockers such as atenolol (Tenormin),
propranolol (Inderal), metoprolol (Lopressor), or calcium channel blockers
such as verapamil (Calan, Isoptin, Verelan, Covera-HS) or diltiazem
(Cardizem, Dilacor, Tiazac), may excessively slow heart rate or cause a
block in the conduction of electrical impulses through the heart.
Additionally, these combinations may further reduce blood pressure, possibly
leading to hypotension.
Digoxin and beta-blockers slow conduction of impulses in the heart and
decrease heart rate. Combining them can increase the risk of slow heart
Sotalol may cause high blood glucose, and the dosage of insulin or
antidiabetic drugs may require adjustment. It also may mask symptoms of low
blood glucose (hypoglycemia).
Administration of sotalol within 2 hours of antacids containing aluminum
oxide and magnesium hydroxide may reduce blood concentrations of sotalol by
26%. This reduces the effect of sotalol. This combination should be avoided
or the antacid should be taken two hours after the sotalol.
PREGNANCY AND BREASTFEEDING SAFETY: Sotalol crosses the
placenta and is found in amniotic fluid. Safe use by pregnant women has not been
established. Sotalol is excreted in human milk. A decision should be made
whether to discontinue nursing or to discontinue the drug due to risk of adverse
effects in the infant.
STORAGE: Store at room temperature, 15 C - 30 C (59 F - 86 F).
For ventricular arrhythmias and supraventricular arrhythmias the
recommended dose is 80 to 160 mg orally every 12 hours or 75 to 150 mg given
intravenously every 12 hours.
The recommended dose for refractory life-threatening ventricular
arrhythmias is 80 to 160 mg orally every 12 hours. Doses of 160 to 640
mg/day given in divided doses every 8 to 12 hours may be required.
The recommended dose for atrial fibrillation or flutter is 80 to 160 mg
orally every 12 hours or 75 to 150 mg given intravenously every 12 hours.
To reduce the risk of induced arrhythmia, patients should be observed
for a minimum of 3 days in a facility that can provide cardiac resuscitation
and continuous electrocardiographic monitoring while on their maintenance
The different formulations and brands of sotalol are not
DRUG CLASS AND MECHANISM:
Sotalol is a beta-adrenergic
blocking drug that is used to treat abnormal heart rhythms. Sotalol is a first
generation beta blocker in a class that includes propranolol (Inderal,
InnoPran), nadolol (Corgard), penbutolol sulfate (Levatol), timolol (Blocadren),
and pindolol (Visken).
These drugs differ from other beta blocking drugs because
they are non-selective in nature, meaning that they block both beta-1 and beta-2
receptors on nerves and, therefore, will affect not only the heart but also the
kidneys, lungs, gastrointestinal tract, liver, uterus, muscles surrounding blood
vessels, and skeletal muscle.
Norepinephrine and epinephrine (adrenaline) are chemicals released within the
body that attach to receptors on several types of cells, including nerves and
some muscles. Attachment changes the way the cells function, either stimulating
the cells or suppressing them, in part through beta receptors.
Sotalol prevents norepinephrine and epinephrine from binding to beta
receptors on nerves. By blocking the effect of norepinephrine and epinephrine,
beta blockers reduce heart rate, reduce the force of the heart's contractions,
and reduce blood pressure by relaxing the muscles surrounding the blood vessels.
Sotalol also directly reduces the rate at which the heart beats by reducing the
rapidity of firing of the normal generator of electrical impulses in the heart
(the heart's pacemaker).