What is the role of Amiodarone (antiarrhythmic medication) in rate control?

From the Guidelines

Amiodarone should be used for rate control in atrial fibrillation when other measures are unsuccessful or contraindicated, due to its potential for serious side effects. For acute rate control, administer 150 mg IV over 10 minutes, followed by 0.5 to 1 mg/min IV 1. For chronic oral therapy, start with a loading dose of 800 mg daily for 1 week, then reduce to 200 mg daily maintenance 1. It is essential to monitor for QT prolongation, bradycardia, and heart block during administration, as well as regular follow-up with thyroid, liver, and pulmonary function tests due to the risk of thyroid dysfunction, hepatotoxicity, and pulmonary fibrosis with long-term use 1.

Key Considerations

• Amiodarone is effective in reducing ventricular rate and is safe in patients with heart failure 1
• Torsades de pointes pro-arrhythmia can occur, and QT interval and TU waves should be monitored on therapy 1
• Amiodarone often causes extracardiac side-effects, especially on long-term therapy, rendering it a second-line treatment in patients who are suitable for other antiarrhythmic drugs 1
• The drug has a very long half-life (40-55 days), so effects and adverse reactions may persist for weeks to months after discontinuation

Administration and Monitoring

• Acute rate control: 150 mg IV over 10 minutes, followed by 0.5 to 1 mg/min IV 1
• Chronic oral therapy: loading dose of 800 mg daily for 1 week, then reduce to 200 mg daily maintenance 1
• Monitor for QT prolongation, bradycardia, and heart block during administration
• Regular follow-up with thyroid, liver, and pulmonary function tests due to the risk of thyroid dysfunction, hepatotoxicity, and pulmonary fibrosis with long-term use 1

From the FDA Drug Label

One of its main effects, with prolonged administration, is to lengthen the cardiac action potential, a class III effect. The negative chronotropic effect of amiodarone in nodal tissues is similar to the effect of class IV drugs. In addition to blocking sodium channels, amiodarone blocks myocardial potassium channels, which contributes to slowing of conduction and prolongation of refractoriness The antisympathetic action and the block of calcium and potassium channels are responsible for the negative dromotropic effects on the sinus node and for the slowing of conduction and prolongation of refractoriness in the atrioventricular (AV) node.

Amiodarone rate control can be achieved through its effects on the cardiac action potential and conduction. The drug's ability to lengthen the cardiac action potential and slow conduction in the AV node makes it useful for controlling heart rate in certain arrhythmias.

• Key effects:
  • Lengthening of the cardiac action potential
  • Slowing of conduction in the AV node
  • Negative dromotropic effects on the sinus node
  • Prolongation of refractoriness in the AV node 2

From the Research

Amiodarone Rate Control

• Amiodarone is an effective antiarrhythmic medication used for both ventricular and atrial arrhythmias 3.
• It is classified as a class III antiarrhythmic but affects all phases of the cardiac action potential.
• The medication has several side effects, including thyroid abnormalities, pulmonary fibrosis, and transaminitis, which require routine monitoring 3.

Thyroid Dysfunction

• Amiodarone can cause thyroid dysfunction, with 15%-20% of patients developing some form of thyroid dysfunction 4, 5, 6.
• The medication can cause both hypothyroidism (amiodarone-induced hypothyroidism, AIH) and hyperthyroidism (amiodarone-induced thyrotoxicosis, AIT) 4, 5, 6.
• AIH is more common in patients with previously diagnosed Hashimoto's thyroiditis, while AIT is more common in patients with underlying thyroid pathology 4.

Management of Thyroid Dysfunction

• Patients treated with amiodarone should be monitored regularly for thyroid dysfunction, including laboratory testing and clinical examinations 4, 5, 6.
• Supplementary levothyroxine therapy is the basis of AIH treatment, and amiodarone therapy may not need to be discontinued 4.
• Type 1 AIT is treated with thyrostatic agents, while type 2 AIT is treated with glucocorticoid therapy 4.