Pharmacologic Therapy for Arrhythmias
Core concepts
Know the Vaughan-Williams classes and their prototypical agents and toxicities. Class I (Na+ channel blockers): IA (quinidine, procainamide - prolong repolarization, torsades risk), IB (lidocaine, mexiletine - shorten repolarization, useful in ischemic VT), IC (flecainide, propafenone - avoid in structural heart disease). Class II: beta-blockers (metoprolol, atenolol) slow AV conduction and reduce sympathetic triggers. Class III: amiodarone, sotalol, dofetilide - prolong refractoriness; amiodarone carries thyroid, pulmonary, hepatic, and corneal toxicity and needs monitoring. Class IV: non-dihydropyridine calcium channel blockers (verapamil, diltiazem) slow the AV node. Other agents: adenosine (transient AV block to terminate PSVT), digoxin (vagotonic, AV nodal slowing; toxicity risk with hypokalemia), and magnesium for torsades.
Anticoagulation is central in atrial fibrillation: use stroke-risk scoring (CHA2DS2-VASc) to guide anticoagulation, and remember that antiarrhythmic drugs do not eliminate stroke risk. Rate control (beta-blocker, calcium channel blocker, digoxin) versus rhythm control is a clinical decision.
Question traps
- Using Class IC agents in patients with structural heart disease or post-MI (proarrhythmic).
- Forgetting amiodarone's broad toxicity profile and need for baseline and periodic monitoring.
- Giving verapamil/diltiazem to a patient with wide-complex tachycardia of uncertain origin - dangerous if it is VT.
- Assuming rhythm control removes the need for anticoagulation.
Rule of thumb
"Structural heart disease + arrhythmia" → avoid Class IC; favor beta-blockade or amiodarone. "Unstable patient" → electricity, not drugs.