Amiodarone is a voltage-gated potassium channels. It is used in the treatment of acute ventricular tachycardia and persistent (VF) after unsuccessful defibrillation, as well as the long-term treatment of refractory supraventricular arrhythmia (atrial fibrillation). Since amiodarone has a very low negative inotropic effect, it can be used in patients with a reduced ejection fraction (EF). Side effects commonly involve the thyroid, liver, heart, eyes, and central nervous system. Pulmonary side effects, such as lung fibrosis and chronic interstitial pneumonitis, are rare but severe. Because amiodarone is a cytochrome P450 inhibitor, simultaneous administration of other drugs should be considered carefully to minimize the risk of interactions.agent that blocks
- Primary mechanism of action: antiarrhythmic effect via blockage of voltage-gated potassium channels → prolonged repolarization of the cardiac action potential
- Secondary mechanism of action: inhibits β-receptors and sodium and calcium channels → decreases conduction through the AV and sinus node
- Special uses: : only antiarrhythmic agent with (almost) no negative inotropic effect → use in patients with reduced EF
- Amiodarone is highly effective but typically limited to short-term treatment because of its side effect profile.
- Amiodarone accumulation in tissues can cause damage to the thyroid, lungs, nerves, skin, eyes, and heart.
- The lowest effective dose should be administered.
- Before initiating amiodarone therapy, patients should receive a baseline ECG, chest x-ray, ophthalmological exam, and thyroid, liver, and pulmonary function tests.
- Thyroid and liver function should be monitored every 3–6 months and ECG should be performed annually.
|Overview of amiodarone adverse effects |
Amiodarone-induced pulmonary toxicity leads to the most deaths associated with amiodarone therapy.
- Toxicity correlates more closely with cumulative dose than with serum drug levels.
- Treatment: Discontinue amiodarone and initiate corticosteroid therapy.
- Amiodarone causes thyroid dysfunction in ∼ 10% of patients receiving long-term therapy. 
- Amiodarone-induced hypothyroidism
- Type I amiodarone-induced thyrotoxicosis
- Type II amiodarone-induced thyrotoxicosis
"Am-IOD-arone" consists of approx. 37% iodine.
- Asymptomatic rise in AST and ALT is common after initiation of amiodarone therapy.
- Amiodarone should be discontinued if AST and/or ALT rise above 2x higher than the normal range.
- Slows heart rate and AV-node conduction primarily through calcium channel-blocking activity
- Can cause QT prolongation but the risk of progression to torsades de pointes is low
- Corneal micro-deposits occur in > 90% of patients and rarely cause symptoms but have the potential to result in halo vision (especially at night), photophobia, and blurred vision. 
We list the most important adverse effects. The selection is not exhaustive.
- Acute treatment (IV administration)
Long-term treatment: (oral administration): rhythm control in refractory symptomatic atrial fibrillation (supraventricular arrhythmia) and underlying heart disease; → restoration and maintenance of sinus rhythm
Amiodarone is the drug of choice for supraventricular arrhythmias in most heart failure patients (LVEF < 40%).
- Severe sinus node dysfunction with marked sinus bradycardia
- Second- and third-degree heart block (except in patients with a functioning pacemaker)
- Hyperthyroidism and hypothyroidism
- Known allergy to iodine
- Pre-existing lung disease
We list the most important contraindications. The selection is not exhaustive.
- Lipophilic properties → accumulation of amiodarone in myocardium and muscles → long duration of action
- Metabolized in the liver by CYP3A4 with biliary excretion
|Oral treatment||IV bolus|
|Onset of action||2 days to 3 weeks||Within a few hours|
|Time to peak effect||1 week to 5 months||15 minutes|
|Half-life elimination||40–55 days||9–36 days|