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Class Explorer · Cardiovascular

Antiarrhythmics

Drugs that alter cardiac conduction or refractoriness. Every one of them can also cause the arrhythmia it treats, which is the single most important fact about the class.

Members

Also in this class: Sotalol · Flecainide · Propafenone · Adenosine. Full pages arrive as the library grows.

Compare the members

Amiodarone
Role
Rhythm control, refractory VT
Signature toxicity
Thyroid, lung, liver, cornea
Monitoring anchor
TSH, LFTs, chest imaging
Digoxin
Role
Rate control at rest; symptomatic HFrEF
Signature toxicity
Narrow index; nausea, visual halos, arrhythmia
Monitoring anchor
K, renal function

Shared across the class

Indications
Atrial fibrillation, rate or rhythm control · Ventricular arrhythmia
Adverse effects
Proarrhythmia · Bradycardia · Organ-specific toxicity
Contraindications
Untreated high-grade AV block · Known QT prolongation (for the QT-prolonging members)
Monitoring
ECG including QT · Amiodarone: thyroid and liver every 6 months, chest imaging and pulmonary symptoms, ophthalmology if visual change · Digoxin: potassium, renal function, and level only when toxicity is suspected

What makes each agent different

  • Amiodarone works everywhere and damages everywhere: thyroid, lung, liver, eye, skin. Its efficacy is unmatched and its toxicity is cumulative, so the question is always how long, not just whether.
  • Digoxin is not really an antiarrhythmic so much as a vagal tone amplifier: it controls rate at rest and fails during exertion, which is why it is a second agent rather than a first.
  • Sotalol and flecainide are structural-heart-disease-dependent choices: flecainide is contraindicated after myocardial infarction, and forgetting that has killed people.

In atrial fibrillation, rate control and rhythm control are not a hierarchy; they are different answers to different patients' symptoms.

The most common cause of digoxin toxicity is not a dosing error, it is a kidney that got worse or a potassium that fell.

Last reviewed 2026-08-16 · Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed.