Amiodarone

• Due to amiodarone's high iodine content and structural similarity to thyroid hormones, it can disrupt thyroid function, leading to both hyperthyroidism and hypothyroidism:

  • Hyperthyroidism - excess iodine can stimulate thyroid hormone production (usually in iodine deficient areas). Amiodarone can be directly toxic to thyroid follicular cells, leading to destructive thyroiditis and release of preformed thyroid hormones
  • Hypothyroidism - excess iodine can initially suppress thyroid hormone production
• Amiodarone is given in cardiac arrest, where the patient is in a shockable rhythm.

  300mg given after 3 unsuccessful shocks

  Further 150mg given after 5 shocks
• MOA:

  • Class III anti-arrhythmic drug
  • Blocks sodium and potassium channels
  • Lengthens the cardiac action potential and prolonging the QT interval
  • Reduces electrical irritability of the cardiac muscle
  • Also blocks alpha and beta adrenergic receptors - decreases heart rate and blood pressure
• Indications:

  • Cardiopulmonary resuscitation - shockable rhythms
  • Rhythm control in AF
  • Atrial flutter and tachyarrhythmias in WPW
• Contraindications:

  • Severe conduction disturbances
  • Sinus node disease
  • Iodine sensitivity
  • Sino-atrial heart block (except in cardiac arrest)
  • Sinus bradycardia (except in cardiac arrest)
  • Thyroid dysfunction
• Amiodarone inhibits CYP450 enzymes, so can interact with:

  • Warfarin - increased anticoagulation
  • Digoxin - increased plasma levels
  • Beta blockers - increased risk of bradycardia
  • Simvastatin - increased plasma levels
  • Amiodarone has a long half life and drug interactions may occur for several weeks after treatment cessation
• Monitoring:

  • Baseline CXR before treatment - risk of pulmonary fibrosis
  • TFTs and LFTs before treatment and every 6 months
  • Serum potassium should be measured before treatment - taking amiodarone if have hypokalaemia is very dangerous and can trigger ventricular arrhythmias - especially torsades de pointes
• Common side effects:

  • Bradycardia
  • Thyroid dysfunction
  • Pulmonary fibrosis
  • Photosensitivity
  • Corneal microdeposits
  • Peripheral neuropathy
  • Jaundice
  • Hepatotoxicity
  • Vomiting
  • Tremor
• Corneal microdeposits:

  • Results from the secretion of amiodarone by the lacrimal gland with accumulation on, and absorption by the corneal epithelium
  • Blurred vision, halos, glare and light sensitivity
  • Especially at night
  • Reversible on withdrawal of treatment
  • If vision is impaired, if optic neuritis or optic neuropathy occur - amiodarone must be stopped
• Hepatotoxicity:

  • Amiodarone is associated with hepatotoxicity and treatment should be discontinued if severe liver function abnormalities or clinical signs of liver disease develop
  • LFTs taken before treatment and every 6 months after starting
• Pulmonary toxicity:

  • Amiodarone is associated with pulmonary toxicity/fibrosis
  • Suspect if new or progressive shortness of breath or cough develops
  • Usually reversible following early withdrawal of amiodarone
• Patient advice:

  • Phototoxicity - advise to shield skin from light and use sunscreen due to risk of phototoxic reactions
  • Patient should be given an alert card
  • Caution on the effects on driving and operating heavy machinery - corneal microdeposits may cause blurred vision