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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