Interpret the Evidence
Why Antiarrhythmics Demand Deliberate Selection
An arrhythmia may arise because an impulse forms too quickly, travels through the wrong pathway, or re enters tissue that should still be refractory.
An arrhythmia may arise because an impulse forms too quickly, travels through the wrong pathway, or re-enters tissue that should still be refractory. Antiarrhythmics change ion movement, autonomic tone, or AV-node conduction to interrupt one of those mechanisms. The same effect that suppresses an arrhythmia can also slow conduction too much, widen the QRS complex, prolong repolarization, or trigger a new dysrhythmia. That is why antiarrhythmics are not interchangeable “rhythm drugs.” Drug selection depends on the rhythm, structural heart disease, ventricular function, conduction status, renal and hepatic function, electrolyte status, concurrent medicines, and whether the patient is stable. A useful distinction in atrial fibrillation (AF) is rate control versus rhythm control: - Rate control slows ventricular response, usually by acting at the AV node. The patient may remain in AF but have a safer, better-tolerated ventricular rate. - Rhythm control attempts to restore and maintain sinus rhythm through cardioversion, antiarrhythmic medication, ablation, or a combination of these approaches. For symptomatic established AF that remains inadequately controlled with rate control, rhythm control is recommended. For newly diagnosed AF, rhythm control should...