Indication |
For the treatment and management of congestive cardiac insufficiency, arrhythmias and heart failure. |
Pharmacodynamics |
Digitoxin is a cardiac glycoside sometimes used in place of
DIGOXIN. It has a longer half-life than digoxin; toxic effects, which
are similar to those of digoxin, are longer lasting (From Martindale,
The Extra Pharmacopoeia, 30th ed, p665). Unlike digoxin (which is
eliminated from the body via the kidneys), it is eliminated via the
liver, so could be used in patients with poor or erratic kidney
function. However, it is now rarely used in current UK medical practice.
While there have been several controlled trials which have shown
digoxin to be effective in a proportion of patients treated for heart
failure, there is not the same strong evidence base for digitoxin,
although it is presumed to be similarly effective. |
Mechanism of action |
Digitoxin inhibits the Na-K-ATPase membrane pump, resulting in an
increase in intracellular sodium and calcium concentrations. Increased
intracellular concentrations of calcium may promote activation of
contractile proteins (e.g., actin, myosin). Digitoxin also acts on the
electrical activity of the heart, increasing the slope of phase 4
depolarization, shortening the action potential duration, and decreasing
the maximal diastolic potential. |
Absorption |
Not Available |
Volume of distribution |
Not Available |
Protein binding |
Not Available |
Metabolism |
Hepatic. |
Route of elimination |
Not Available |
Half life |
Not Available |
Clearance |
Not Available |
Toxicity |
Digitoxin exhibits similar toxic effects to the more-commonly used
digoxin, namely: anorexia, nausea, vomiting, diarrhoea, confusion,
visual disturbances, and cardiac arrhythmias. |
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