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Digitalis is the oldest cardiovascular compound still in use today.1 More than 200 years ago, Sir William Withering observed that foxglove flower derivative (digitalis purpura) could be used for “cardiac dropsy.”2 Since that time, the positive hemodynamic, neurohormonal, and electrophysiologic effects of digoxin have been well explored.1

The pharmacodynamic effects of digoxin include increased cardiac output, decreased pulmonary capillary wedge pressure, and increased ejection fraction. The neurohormonal effects of digoxin include improved baroreceptor sensitivity, decreased norepinephrine concentration, decreased renin-angiotensin activations, sympathoinhibitory effect, and increase release of atrial natriuretic peptide and brain natriuretic peptide. The electrophysiological effects are primarily mediated through the interaction of digoxin with the sodium-potassium-ATPase pump.1,2

Digoxin increases contractility by inhibiting the sodium-potassium exchange in the sodium-potassium-ATPase pump leading to an increase of sodium in the myocytes. This increase results in decreased outflow of calcium from the myocyte and greater contractile force of the myocardium.1,2

Digoxin also has electrophysiological effects. It has the ability to slow conduction through the AV node and it can slow the sinus rate via the S-A node. It is these effects that allow it to be used for atrial fibrillation.3


The bioavailability of digoxin can range from 70 percent to nearly 100 percent, depending on the type of oral formulation. The elixir and tablet formulations are approximately 80 percent and 70 percent bioavailable, respectively.4 Encapsulated digoxin solution is close to 100 percent bioavailable, but no longer manufactured. The bioavailability of intravenous digoxin is always complete. The estimated elimination half-life of digoxin can take as long as 48 hours.5

Digoxin is roughly 30 percent protein bound in the plasma and has a large volume of distribution (VD) of nearly 7 L/kg in healthy adults.5,6 It follows a two-compartment kinetic model with an initial distribution phase into the central compartment consisting primarily of plasma and highly perfused tissues, such as the liver. A second, slower distribution phase soon occurs and moves the drug out of the central compartment and into the peripheral, deep tissue compartment.5 The target site, the myocardium, is affected by drug concentration in the peripheral compartment and, therefore, clinical effect may not be seen until sufficient drug has accumulated at that site, which may take several hours after a loading dose. Serum drug concentrations early after a loading dose may not represent the true drug concentration at the site of action and may lead to inappropriate dosage adjustments.

The VD in obese patients best correlates with ideal body weight, rather than actual body weight.7 Due to digoxin's hydrophilic nature, it does not significantly distribute into adipose tissue. However, actual body weight should be used in underweight patients, whose ideal body weight is greater than their actual body weight. Pediatric patients have ...

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