Overview
Amiodarone is a very effective, but highly toxic, class III antiarrhythmic.
- Mechanism of action
- Blocks potassium channels → prolongs repolarisation
- Increased QTc → increased action potential duration → increased effective refractory period
- This suppresses re-entry arrhythmias and decreases ectopic automaticity
- Amiodarone also blocks Na+ channels, Ca2+ channels, and β-adrenergic receptors to cause:
- Decreased SA node automaticity
- Decreased AV node conduction
- Bradycardia
- Indications
- Ventricular fibrillation
- Pulseless ventricular tachycardia
- Malignant ventricular arrhythmias
- Wide-complex tachycardia in ACLS
- Atrial fibrillation with rapid ventricular response
- Adverse effects
- Pneumonitis
- Hypothyroidism
- Hyperthyroidism
- Bradycardia
- AV block
- AT prolongation
- Corneal microdeposits
- Visual halos
- Photophobia
- Optic neuropathy
- Hepatotoxicity
- Neurotoxicity
- Photosensitivity
- Blue-gray skin discoloration
- Contraindications
- 2nd or 3rd degree heart block without a pacemaker
- Severe sinus node dysfunction
- Baseline QT prolongation
- Congenital long QT syndrome
- Wolff-Parkinson-White (WPW) with atrial fibrillation
Amiodarone-induced Hypothyroidism (AIH)
The pathophysiology of hypothyroidism is due to the Wolff-Chaikoff effect – thyroxine formation is inhibited due to high levels of circulating iodine.
Amiodarone-induced Thyrotoxicosis (AIT)
| AIT type 1 | AIT type 2 | |
|---|---|---|
| Pathophysiology | Excess iodine-induced thyroid hormone synthesis | Amiodarone-related destructive thyroiditis |
| Goitre | Present | Absent |
| Management | Carbimazole or potassium perchlorate | Corticosteroids |