Cardiac glycosides are a group of drugs derived from digitalis, a substance that occurs naturally in foxglove plants and in certain toads. The most frequently used cardiac glycoside is digoxin.
Pharmacokinetics (how drugs circulate)
The intestinal absorption of digoxin varies greatly; the capsules are absorbed most efficiently, followed by the elixir form, and then tablets. Digoxin is distributed widely throughout the body, with highest concentrations in the heart muscle, liver, and kidneys. Digoxin binds poorly to plasma proteins.
In most patients, a small amount of digoxin is metabolized in the liver and gut by bacteria. This effect varies and may be substantial in some people. Most of the drug is excreted by the kidneys as unchanged drug.
Pharmacodynamics (how drugs act)
Digoxin is used to treat heart failure because it strengthens the contraction of the ventricles by boosting intracellular calcium at the cell membrane, enabling stronger heart contractions.
Digoxin may also enhance the movement of calcium into the myocardial cells and stimulate the release, or block the reuptake, of norepinephrine at the adrenergic nerve terminal.
Stop that impulse
Digoxin acts on the central nervous system (CNS) to slow the heart rate, thus making it useful for treating supraventricular arrhythmias (abnormal heart rhythms that originate above the bundle branches of the heart’s conduction system), such as atrial fibrillation and atrial flutter. It also increases the refractory period (the period when the cells of the conduction system can’t conduct an impulse).
Load that dose
Because digoxin has a long half-life, a loading dose must be given to a patient who requires immediate drug effects, as in supraventricular arrhythmia.
By giving a larger initial dose, a minimum effective concentration of the drug in the blood may be reached faster.
Note: Avoid giving a loading dose to a patient with heart failure to avoid toxicity.
Pharmacotherapeutics (how drugs are used)
Many drugs can interact with digoxin.
- Antacids, barbiturates, cholestyramine resin, kaolin and pectin, neomycin, metoclopramide, rifampin, and sulfasalazine reduce the therapeutic effects of digoxin.
- Calcium preparations, quinidine, verapamil, cyclosporine, tetracycline, clarithromycin, propafenone, amiodarone, spironolactone, hydroxychloroquine, erythromycin, itraconazole, and omeprazole increase the risk of digoxin toxicity.
- Amphotericin B, potassium-wasting diuretics, and steroids taken with digoxin may cause hypokalemia (low potassium levels) and increase the risk of digoxin toxicity.
- Beta-adrenergic blockers and calcium channel blockers taken with digoxin may cause an excessively slow heart rate and arrhythmias.
- Succinylcholine and thyroid preparations increase the risk of arrhythmias when they’re taken with digoxin.
- St. John’s wort, an herbal preparation, can increase digoxin levels and risk of toxicity.
Digoxin can also produce adverse reactions, mostly involving digoxin toxicity.
Adverse reactions to cardiac glycosides
Because cardiac glycosides have a narrow therapeutic index (margin of safety), they may produce digoxin toxicity. To prevent digoxin toxicity, the dosage should be individualized based on the patient’s serum digoxin concentration.
Adverse reactions to digoxin include:
Safe and sound
Recognizing signs and symptoms of digoxin toxicity
Digoxin toxicity usually produces cardiac, gastrointestinal, and neurologic signs and symptoms. To prevent severe or even life-threatening effects, be prepared to recognize the signs and symptoms listed below. Also assess the patient for the most common early indicators of toxicity, which are usually GI-related.
- Accelerated junctional rhythms
- Atrial tachycardia with atrioventricular (AV) block
- Second-degree AV block (Wenckebach)
- Sinoatrial arrest or block
- Third-degree AV block (complete)
- Ventricular arrhythmias
- Abdominal pain
- Blue-yellow color blindness
- Blurred vision
- Colored dots in vision
- Flickering lights
- Personality changes
- White halos on dark objects