Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

The following summarises the contents of both this review and its predecessor in this journal (Iisalo, 1977). The two reviews should be read in conjunction with each other. Digoxin is absorbed mostly from the proximal part of the small intestine. About 67% is absorbed from tablets, 80% from elixir and up to 100% from encapsulated elixir. Protein binding of digoxin and its metabolites is low and of little clinical significance. Digoxin is widely distributed throughout body tissues and has a high apparent volume of distribution (about 6L/kg). Although most of the digoxin in the body is in skeletal muscle it is found in highest concentrations in the heart, kidneys and brain. The apparent volume of distribution is reduced in patients with renal impairment and in the elderly. Plasma digoxin concentrations do not closely reflect myocardial whole tissue concentrations. The half-time of elimination in healthy subjects averages 40 hours. In most patients, more than 80% of digoxin is excreted unchanged in the urine but in about 12% of patients between 20% and 55% is excreted as metabolites, mostly dihydrodigoxin, which is relatively inactive. In a few subjects other, more active, metabolites may be found in the urine. Renal elimination is mainly by glomerular filtration but some passive tubular reabsorption and active secretion occur. The relationships between plasma digoxin concentrations and its pharmacodynamic or therapeutic effects are not clear. However, plasma digoxin concentrations may relate well to the slowing of ventricular rate from pre-treatment values in atrial fibrillation but not to resting ventricular rates. In cardiac failure in sinus rhythm, plasma digoxin concentrations may relate well to the inotropic effect of the drug but theoretical tissue digoxin concentrations may be more closely related. Digoxin passes across the placenta and into breast milk but not in sufficient quantities to prove harmful to the fetus or neonate. In renal impairment, the half-time of digoxin is prolonged and its apparent volume of distribution reduced. The pharmacokinetics of digoxin in different states of thyroid function are complex and do not fully explain, for example, the apparent ‘resistance’ to digoxin in hyperthyroidism. The most important digoxin-drug interactions are those involving quinidine and drugs which deplete the body of potassium. Plasma (or serum) digoxin concentration measurement may be of value in the diagnosis of toxicity or undertreatment, in overdose and in changing treatment in patients with renal impairment or on long term therapy. © 1980, ADIS Press Australasia Pty Ltd.. All rights reserved.

Original publication




Journal article


Clinical Pharmacokinetics

Publication Date





137 - 149