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Update Summary
September, 2023
The following table was updated:
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CHAPTER SUMMARY FROM THE PHARMACOTHERAPY HANDBOOK
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For the Chapter in the Schwinghammer Handbook, please go to Chapter 6, Arrhythmias.
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KEY CONCEPTS
The use of antiarrhythmic drugs (AADs) in the United States has declined because clinical trials have shown increased mortality with their use due to proarrhythmic adverse medication reactions and limited efficacy. AADs have been increasingly replaced by nonpharmacologic approaches such as ablation and the implantable cardioverter defibrillator (ICD). However, AADs remain a key tool in the management of many rhythm disorders.
AADs frequently cause adverse medication reactions and are complex in their pharmacokinetic characteristics. Close monitoring is required of all of these medications to assess for adverse reactions as well as potential medication interactions.
The most commonly prescribed AAD is amiodarone, which is effective in terminating and preventing a wide variety of symptomatic supraventricular and ventricular arrhythmias. However, amiodarone is plagued by frequent adverse medication reactions and requires close monitoring. The most concerning toxicity is pulmonary fibrosis. The side effect profiles of the intravenous (IV) (acute, short-term) and oral (chronic, long-term) forms of amiodarone differ substantially.
In patients with atrial fibrillation (AF), therapy is traditionally aimed at controlling the ventricular rate, preventing thromboembolic (TE) complications, and restoring and maintaining sinus rhythm (SR). Traditionally, many have pointed to the AFFIRM trial that maintenance of SR was often not necessary. However, several recent studies challenge this idea, particularly for patients with heart failure with reduced ejection fraction (HFrEF). AADs are also useful in reducing early AF recurrence in the periprocedural period and may improve long-term post-ablation outcomes.
Paroxysmal supraventricular tachycardia (PSVT) is usually a result of either reentry (involving either the atrioventricular [AV] node or incorporating an accessory pathway) or ectopic atrial activity (atrial tachycardia). Common supraventricular tachycardias are often terminated acutely with AV nodal-blocking medications, such as adenosine. For most patients, catheter ablation effectively cures this arrhythmia.
Patients with Wolff-Parkinson-White (WPW) syndrome may have several different tachycardias that are acutely treated by different strategies: orthodromic reentry (adenosine), antidromic reentry (adenosine or procainamide), and AF (procainamide or ibutilide). AV nodal-blocking medications are contraindicated in patients with WPW syndrome and AF. The mainstay of long-term therapy for WPW remains catheter ablation.
AADs (except for β-blockers) should not be used routinely in patients with prior myocardial infarction (MI) or left ventricular (LV) dysfunction for the treatment of premature ventricular complexes (PVCs). More specifically, the routine suppression of asymptomatic PVCs with AADs is not recommended.
Patients with hemodynamically significant ventricular tachycardia (VT) or ventricular fibrillation (VF) not associated with an acute MI who are successfully resuscitated (with electrical cardioversion, epinephrine, amiodarone, and/or lidocaine) are at high risk for sudden cardiac death (SCD). In ...