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Digoxin is the primary cardiac glycoside in clinical use. Digoxin is used for the treatment of congestive heart failure (CHF) because of its inotropic effects on the myocardium and for the treatment of atrial fibrillation because of its chronotropic effects on the electrophysiological system of the heart. The role of digoxin in the treatment of each of these disease states has changed in recent years as a better understanding of the pathophysiology of these conditions has been gained and new drug therapies have been developed.1,2 For the treatment of chronic CHF, angiotensin I converting enzyme inhibitors (ACE inhibitors) and diuretics are the primary pharmacotherapeutic agents with angiotensin II receptor antagonists, spironolactone, and β-blockers playing key roles.3 For the treatment of acute or severe heart failure, agents that decrease cardiac preload (diuretics, nitrates) or afterload (vasodilators) and ACE inhibitors (decreases both preload and afterload) are used in conjunction with potent intravenously administered inotropic agents (dobutamine, dopamine, adrenergic agonists) to balance the current cardiovascular status of the patient.3 In either the acute or severe heart failure situations, digoxin can be used when a mild inotropic or oral agent is needed.

If a patient presents with severe cardiovascular symptoms due to atrial fibrillation, direct-current cardioversion is a treatment option.4 For the treatment of atrial fibrillation with mild or no cardiovasuclar symptoms, many clinicians prefer to prescribe intravenous calcium channel blockers (diltiazem or verapamil) for the control ventricular rate.4 If atrial fibrillation is due to excessive adrenergic tone, intravenous β-blockers can also be used. Digoxin continues to be prescribed for the control of ventricular rate in patients with atrial fibrillation with no accessory pathway and can be an excellent choice if the patient is sedentary or has heart failure or left ventricular dysfunction. It is also possible to use digoxin in combination with a β-blocker or a calcium channel blocker to treat atrial fibrillation.5 Once ventricular rate is controlled, the patient’s heart may spontaneously revert to normal sinus rhythm, or electrical or pharmacologic cardioversion of atrial fibrillation may be necessary.

The positive inotropic effect of digoxin is caused by binding to sodium- and potassium-activated adenosine triphosphatase, also known as Na,K-ATPase or the sodium pump.6 Digoxin-induced inhibition of Na,K-ATPase leads to decreased transport of sodium out of myocardial cells and increased intracellular sodium concentrations that aid calcium entry and decrease calcium elimination via the sodium-calcium exchanger. The increased intracellular calcium is stored in the endoplasmic reticulum so that action potential–induced calcium release is augmented causing enhanced myocardial contractility. The chronotropic effects of digoxin are mediated via increased parasympathetic activity and vagal tone.

When given as oral or intravenous doses, the serum digoxin concentration–time curve follows a two-compartment model and exhibits a long and large distribution phase of 8–12 hours (Figure 6-1).7–9 During the distribution phase, digoxin in the serum is not in equilibrium with digoxin in the ...

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