Cardiac glycosides

Cardiac glycosides

Cardiac glycosides are a group of drugs derived from digitalis, asubstance 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 kid-neys. 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 sub-stantial in some people. Most of the drug is excreted by the kid-neys as unchanged drug. (See Load that dose.)

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 ar-rhythmias (abnormal heart rhythms that originate above the bun-dle branches of the heart’s conduction system), such as atrial fib-rillation and atrial flutter. It also increases the refractory period (the period when the cells of the conduction system can’t conduct an impulse).

Pharmacotherapeutics (how drugs are used)

In addition to treating heart failure and supraventricular arrhyth-mias, digoxin is used to treat paroxysmal atrial tachycardia (an arrhythmia marked by brief periods of tachycardia that alternate with brief periods of sinus rhythm).

Drug interactions

Many drugs can interact with digoxin.

o       Antacids, barbiturates, cholestyramine resin, kaolin and pectin, neomycin, metoclopramide, rifampin, and sulfasalazine reduce the therapeutic effects of digoxin.

o       Calcium preparations, quinidine, verapamil, cyclosporine, tetra-cycline, clarithromycin, propafenone, amiodarone, spironolac-tone, hydroxychloroquine, erythromycin, itraconazole, and omeprazole increase the risk of digoxin toxicity.

o       Amphotericin B, potassium-wasting diuretics, and steroids tak-en with digoxin may cause hypokalemia (low potassium levels) and increase the risk of digoxin toxicity.

o       Beta-adrenergic blockers and calcium channel blockers taken with digoxin may cause an excessively slow heart rate and ar-rhythmias.

o       Succinylcholine and thyroid preparations increase the risk of ar-rhythmias when they’re taken with digoxin.

o       St. John’s wort, an herbal preparation, can increase digoxin lev-els and risk of toxicity.

o       Digoxin can also produce adverse reactions, mostly involving digoxin toxicity. (See Recognizing signs and symptoms of digox-in toxicity, and Adverse reactions to cardiac glycosides.)