What is the mechanism of action of amiodarone?

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Mechanism of Action of Amiodarone

Amiodarone works through multiple electrophysiologic mechanisms across all four Vaughan Williams antiarrhythmic classes, primarily acting as a class III agent that prolongs cardiac action potential and refractoriness, while also blocking sodium, potassium, and calcium channels and exerting noncompetitive antisympathetic effects. 1

Primary Electrophysiologic Effects

  • Class III effects: Prolongs cardiac action potential and refractoriness by blocking myocardial potassium channels 2, 1
  • Class I effects: Blocks sodium channels at rapid pacing frequencies 1
  • Class II effects: Exerts noncompetitive antisympathetic action (beta-blocking properties) 1
  • Class IV effects: Blocks calcium channels, contributing to negative chronotropic effects in nodal tissues 1

Specific Cardiac Effects

Conduction System Effects

  • Slows heart rate and atrioventricular nodal conduction through calcium channel and beta-receptor blockade 2
  • Prolongs refractoriness through potassium and sodium channel blockade 2
  • Slows intracardiac conduction through sodium channel blockade 2
  • Prolongs intranodal conduction (Atrial-His) and refractoriness of the atrioventricular node 1

Vascular Effects

  • Acts as a coronary and peripheral vasodilator 3
  • Decreases cardiac workload and consequently myocardial oxygen consumption 1

Unique Pharmacokinetic Properties

  • Highly lipid soluble, stored in high concentrations in fat, muscle, liver, lungs, and skin 2
  • Extremely long elimination half-life (average 58 days) due to slow release from lipid-rich tissues 2
  • Major active metabolite is desethylamiodarone (DEA), which also has antiarrhythmic properties 2, 1
  • Metabolized primarily by cytochrome P450 enzymes (CYP3A4 and CYP2C8) 1

Clinical Implications of Mechanism

  • The complex multi-channel blocking properties make amiodarone effective for both ventricular and supraventricular arrhythmias 3
  • Unlike other class III agents, amiodarone rarely causes torsades de pointes despite QT prolongation 3
  • Can be used in patients with left ventricular dysfunction due to minimal negative inotropic effects 3
  • Initial acute effects after IV administration are predominantly focused on the AV node 1

Important Clinical Considerations

  • The multiple mechanisms of action contribute to amiodarone's effectiveness but also explain its numerous drug interactions and side effects 4
  • Routine monitoring of plasma levels is not recommended due to complex pharmacokinetics 2
  • Drug interactions occur through inhibition of multiple cytochrome P450 pathways (including CYP2C9, CYP2D6, and CYP3A4) 2
  • Despite QT interval prolongation, polymorphic ventricular tachycardia (torsades de pointes) is rare 2

Amiodarone's complex and multifaceted mechanism of action explains both its remarkable efficacy against a wide range of arrhythmias and its extensive side effect profile that requires careful monitoring during long-term therapy.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Amiodarone Therapy

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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