Amiodarone

Neil Turner

WHO essential drug

UNDER REVIEW (April 2017)

Mechanism of Action:

A potassium channel blocker (Class 3 antiarrhythmic drug – Vaughan-Williams Classification). Increases cardiac action potential duration and increases effective refractory period. Normally, potassium enters the cells to repolarise the depolarized membrane.

Lecture and CAL materials:

Drug specifics

Alternative drug name not specified
Effects Increased action potential duration. This decreases re-entry in cardiac tissue which precipitates arrhythmias. Effective at suppressing both ventricular (VT) and supraventricular arrhythmias. Although it is effective amiodarone has a number of unpleasant adverse effects and so it is generally reserved for more refractory or troublesome arrhythmias.
Adverse actions Corneal deposits, photosensitivity, thyroid dysfunction (hypo- and hyper-), hepatitis, pneumonitis leading to pulmonary fibrosis, neuropathy, slate-grey/bluish skin discolouration.
Dose 200mg oral od (after loading dose period of tds then bd doses). Amiodarone can also be given IV for rapid action.
Interactions Digoxin and warfarin’s effects are potentiated by amiodarone. Their doses should be reduced accordingly.
Contraindications not specified
Comments An example of a drug that is extensively tissue bound with very slow onset of action and offset after discontuinuation. It has a ‘half-life’ of around a month! Amiodarone elimination is by shedding of epithelial cells from skin and GI tract and not conventionally by the kidneys or liver. Drugs with long half-luives are usually given as a loading dose to hasten the onset of action. More toxic than other antiarrhythmics but less likely to depress myocardial contractility. Patients should have their thyroid, pulmonary and liver function tested regularly while on amiodarone. As the name suggests amiodarone contains iodine explaining the tendency to disturb thyroid function
Contributors