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.
DRUG CLASS AND MECHANISM:
Digoxin increases the strength and vigor of heart contractions, and is useful in
the treatment of heart failure. It is extracted from the leaves of a plant
called digitalis lanata. Digoxin increases the force of contraction of the
muscle of the heart by inhibiting the activity
of an enzyme (ATPase) that controls movement of calcium, sodium and potassium
into heart muscle. Calcium
controls the force of contraction. Inhibiting ATPase increases calcium in heart
muscle and therefore increases the force of heart contractions. Digoxin also
slows electrical conduction between the atria and the ventricles of the heart
and is useful in treating abnormally rapid atrial rhythms such as atrial
fibrillation, atrial flutter, and atrial tachycardia.
(Abnormally rapid atrial rhythms can be caused by
heart attacks, excessive
thyroid hormones,
alcoholism, infections, and many other conditions.) During rapid atrial rhythms,
electrical signals from the atria cause rapid contractions of the ventricles.
Rapid ventricular contractions are inefficient in pumping blood containing
oxygen and nutrients to the body, causing symptoms of weakness, shortness of
breath, dizziness, and even chest pain. Digoxin alleviates these symptoms by
blocking the electrical conduction between the atria and ventricles, thus
slowing ventricular contractions. The FDA approved digoxin in 1975.
PRESCRIPTION: Yes
GENERIC AVAILABLE: Yes
PREPARATIONS: Tablets: 0.125, and 0.25 mg; Elixir: 0.05, 0.25, and 0.1
mg/ml.
STORAGE: Digoxin should be stored at room temperature, 59-86 F (15-30 C) and protected from light.
DOSING: Digoxin may be taken
with or without food. Digoxin is primarily eliminated by the kidneys; therefore,
the dose of digoxin should be reduced in patients with kidney dysfunction.
Digoxin blood levels are used for adjusting doses in order to avoid toxicity. The usual starting dose is
0.0625-0.25 mg daily depending on age and kidney function. The dose may be
increased every two weeks to achieve the desired response.
DRUG INTERACTIONS: Drugs such
as verapamil (Calan, Verelan, Verelan PM, Isoptin, Isoptin SR, Covera-HS), quinidine (Quinaglute, Quinide), amiodarone (Cordarone), indomethacin (Indocin, Indocin-SR), alprazolam (Xanax, Xanax XR, Niravam), spironolactone (Aldactone), and itraconazole (Sporanox) can increase digoxin
levels and the risk of toxicity. The co-administration of digoxin and
beta-blockers [for example propranolol (Inderal, Inderal LA) or calcium channel blockers (for example, verapamil),
which also reduces heart rate, can cause serious slowing of the heart rate.
Congestive heart failure (CHF) is a condition in which the heart's function as a pump is inadequate to meet the body's needs. A poor blood supply resulting from congestive heart failure may cause the body's organ systems to fail, leading to a weakened heart muscle and fluid accumulation in the lungs and body tissue. There are many diseases that can impair pumping efficiency and symptoms of congestive heart failure including fatigue, diminished exercise capacity, shortness of breath, and swelling. Treatments include lifestyle modifications, medications, heart transplant, and therapy.
Heart attack happens when a blood clot completely obstructs a coronary
artery supplying blood to the heart muscle. A heart attack can cause chest pain, heart failure, and electrical
instability of the heart.
Chest pain is a common complaint by a patient in the ER. Causes of chest pain include broken or bruised ribs, pleurisy, pneumothorax, shingles, pneumonia, pulmonary embolism, angina, heart attack, costochondritis, pericarditis, aorta or aortic dissection, and reflux esophagitis. Diagnosis and treatment of chest pain depends upon the cause and clinical presentation of the patient's chest pain.
Thrombocytopenia refers to a decreased number of platelets in the blood. There are many causes of thrombocytopenia such as decreased platelet production (viral infections for example rubella, mumps, chickenpox, hepatitis C, and HIV); increased platelet destruction or consumption (for example sulfonamide antibiotics, heparin, blood transfusions, and lupus); or increased splenic sequestration (enlarged spleen due to conditions for example liver disease, blood cancers, and more). Treatment of thrombocytopenia depends on the cause.
Heart rhythm disorders vary from minor palpitations, premature atrial contractions (PACs), premature ventricular contractions (PVCs), sinus tachycardia, and sinus brachycardia, to abnormal heart rhythms such as tachycardia, ventricular fibrillation, ventricular flutter, atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia (PSVT), Wolf-White-Parkinson syndrome, brachycardia, or heart blocks. Treatment is dependant upon the type of heart rhythm disorder.
Heart failure is caused by many conditions including coronary artery disease, heart attack, cardiomyopathy, and conditions that overwork the heart. Symptoms of heart failure include congested lungs, fluid and water retention, dizziness, fatigue and weakness, and rapid or irregular heartbeats.
A heart attack (also known as a myocardial infarction) is the death of heart muscle from the sudden blockage of a coronary artery by a blood clot. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen,causing injury to the heart muscle. Injury to the heart muscle causes chest pain
and chest pressure sensation. If blood flow is not restored to the heart muscle within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to
die for six to eight hours at which time the heart attack usually is "complete." The dead heart muscle is eventually replaced by scar tissue.
Approximately one million Americans suffer a heart attack each year. Four hundred thousand of them die as a result of their heart attack.