Covers antiarrhythmic drugs by mechanism, starting with the action potential of myocardial, nodal and Purkinje tissue and the ECG changes each block produces. It then sets out the Vaughan Williams classes in a table, followed by a 2018 expanded scheme, and gives drug-by-drug dosing tables for classes I to IV and other agents. It closes with digoxin toxicity, proarrhythmia risks and a table matching drug choice to arrhythmia type.
Topic 33 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 10 sections, about 899 words (15 min of reading), with 13 flashcards.
In this note
Definition and principles
Action potential reminder
Vaughan Williams classification
Class I: sodium-channel blockers
Class II: beta-blockers
Class III: potassium-channel blockers
Class IV: calcium-channel blockers
Other antiarrhythmic drugs
Proarrhythmia and safety
Choice by arrhythmia
Definition and principles
Antiarrhythmic drugs (AADs): drugs that prevent or terminate arrhythmias by acting on cardiac ion channels, receptors or autonomic tone.
They work against the three mechanisms of arrhythmia: they suppress abnormal automaticity and triggered activity, and break re-entry by slowing conduction or by prolonging the refractory period.
All of them can cause arrhythmias themselves (proarrhythmia); apart from beta-blockers, none improves survival. Electrical treatment (cardioversion, catheter ablation, an implantable cardioverter-defibrillator, ICD) is often more effective.
Action potential reminder
Working myocardium and Purkinje fibres: phase 0 — fast sodium inflow; phase 1 — early repolarisation (transient potassium outflow); phase 2 — plateau (L-type calcium inflow balanced by potassium outflow); phase 3 — repolarisation (delayed rectifier potassium currents IKr and IKs); phase 4 — resting potential (inward rectifier).
Sinoatrial (SA) and atrioventricular (AV) nodes: phase 0 depends on calcium channels; phase 4 rises spontaneously (funny current, If), faster with sympathetic and slower with vagal stimulation.
On the electrocardiogram (ECG): sodium-channel block widens the QRS, potassium-channel block lengthens the QT, and nodal block (classes II and IV, digoxin) lengthens the PR and slows the rate.
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