Mechanism of Action of Amiodarone in Ventricular Tachycardia
Amiodarone works to correct ventricular tachycardia through multiple mechanisms, primarily by blocking sodium, potassium, and calcium channels while also exerting noncompetitive antisympathetic effects, making it uniquely effective for life-threatening ventricular arrhythmias. 1
Electrophysiologic Properties
Amiodarone is classified as a class III antiarrhythmic drug but possesses characteristics of all four Vaughan Williams classes:
- Class I effect: Blocks sodium channels at rapid pacing frequencies
- Class II effect: Exerts noncompetitive antisympathetic action
- Class III effect: Lengthens cardiac action potential (primary effect with prolonged administration)
- Class IV effect: Produces negative chronotropic effects in nodal tissues similar to calcium channel blockers 1
This multi-channel blocking activity explains why amiodarone is effective in situations where other antiarrhythmics fail.
Specific Actions on Cardiac Tissue
Amiodarone affects the heart through several mechanisms:
- Prolongs intranodal conduction (Atrial-His, AH)
- Increases refractoriness of the atrioventricular node (ERP AVN)
- Blocks myocardial potassium channels, contributing to slowing of conduction and prolongation of refractoriness
- Vasodilatory action decreases cardiac workload and myocardial oxygen consumption 1
These combined effects make amiodarone particularly effective for ventricular tachycardia by:
- Preventing re-entry circuits that sustain VT
- Slowing conduction in abnormal pathways
- Increasing the refractory period of cardiac tissue
Onset of Action
The antiarrhythmic effect of intravenous amiodarone occurs rapidly, with rhythmic effects appearing in less than 30 minutes 2. This makes it suitable for emergency treatment of ventricular tachyarrhythmias where rapid control is essential.
Clinical Application for V-Tach
For ventricular tachycardia, amiodarone is administered:
- IV administration for acute treatment: 150 mg IV bolus over 10 minutes (may be repeated in 10-30 minutes if necessary), followed by 1 mg/minute for 6 hours, then 0.5 mg/minute for 18 hours 2
- Oral administration for maintenance: 800-1,600 mg/day in divided doses until a total of 10 g has been given, then 200-400 mg/day 2
Important Clinical Considerations
Efficacy: Amiodarone substantially improves survival and hospital admission rates in patients with shock-resistant ventricular fibrillation compared to other treatments 2
Adverse effects: Common side effects include:
- Hypotension (particularly with IV administration)
- Bradycardia and AV block
- QT prolongation
- GI upset and constipation
- Rarely, torsades de pointes 2
Long-term toxicity: With prolonged use, amiodarone can cause:
- Pulmonary toxicity (most serious)
- Thyroid dysfunction
- Liver function abnormalities
- Visual disturbances
- Neurological effects (tremor, ataxia) 2
Comparison to Other Antiarrhythmics
Amiodarone is particularly valuable for ventricular tachycardia because:
- It works when other antiarrhythmics have failed
- It can be used in patients with structural heart disease or left ventricular dysfunction, unlike many other antiarrhythmics 2
- It has a broader spectrum of activity due to its multiple mechanisms of action
For refractory ventricular tachycardia, amiodarone has shown efficacy rates of 63-71% in patients who failed conventional antiarrhythmic agents 3, 4.
In summary, amiodarone's effectiveness in treating ventricular tachycardia stems from its unique multi-channel blocking properties and antisympathetic effects, allowing it to disrupt the abnormal electrical circuits that sustain the arrhythmia while also modulating autonomic influences on the heart.