2016A Question 09

Describe the mechanism of action, pharmacokinetics and major side effects of amiodarone.

Examiner Report

43% of candidates achieved a pass in this question.

Simply stating the Vaughan-Williams classification is not a description of mechanism of action. Relating the K+ channel blocking effects to the action potential and effective refractory period, with some mention of the other mechanisms, would have achieved a pass on this section. Full marks required more detail on the various mechanisms, with the overall effects on the AV node, SA node and speed of conduction.

Describing the high plasma protein binding, high tissue binding and large Vd, with consequent need for a prolonged loading dose schedule and comment on the elimination kinetics would have earned a pass for the second section.

Almost every candidate listed corneal micro-deposits as a major side-effect, yet many did not mention the pulmonary complications and those who did rarely commented on their incidence, or their high morbidity and mortality.

Many candidates wrote an extensive preamble to their answer, with details on indications, contra-indications and its use in an arrest situation, none of which was asked for. A few candidates confused amiodarone with adenosine and digoxin.

Model Answer


  • PC
  • PK
  • PD


Factor Description

- Iodine-containing

- Similar appearance to thyroxine


- Tablets

- Aqueous solution


Factor Description

- Arrest 300mg push

- IV loading 150mg 1/24 then 850mg 23/24

- PO loading 10-20mg.kg-1/day for 7-10 days

- Maintenance: ~100-200mg daily

Time course

- IV onset 5 minutes

- IV duration 30 mins for bolus


- Variable


- VD 70L/kg

- Plasma protein binding >95% (can displace other highly bound drugs e.g. Warfarin)

- Tissue protein binding very high

- Lipid solubility high


- Hepatic CYP

- Cl 1.5-11mL.kg-1.min-1

- t1/2β 15-140 days

- Active metabolite desethylamiodarone


- Bile, skin, tears


Factor Description
Antiarrhythmic class

- Broad spectrum: Class 3 > 1,2,4

- ↓ K+ rectifier conductance → Prolongs phase 3 of ventricular action potential


- Ablation of supraventricular and ventricular tachyarrhythmias

- Rate control in AF

CVS toxicity

Increased with rapid infusion:

- Hypotension

- Bradycardia (atropine resistant)

- ↑ QTc → ↑ Risk torsades de pointes

Tissue toxicity

- Cirrhosis

- Pulmonary fibrosis

- Thyroid disease (hypo > hyper)

- Corneal disease

Last updated 2021-08-23

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