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With the advent of electrical cardioversion, the use of pharmacologic agents to treat arrhythmias has decreased. Pharmacologic cardioversion can result in the development of serious arrhythmias such as torsades de pointes. However, pharmacologic cardioversion does not require conscious sedation or anesthesia, which is necessary for elective electrical cardioversion.

This chapter discusses the actions, indications, pharmacokinetics, dosing, and adverse effect profiles of antiarrhythmic drugs that are pertinent to emergency medicine practice. Specific antiarrhythmics medications also are discussed.

Optimal drug therapy of arrhythmias requires knowledge of the mechanism of action, pharmacokinetics, indications, appropriate dosing and administration, and types of adverse effects that may occur with each medication. Antiarrhythmic drugs are divided into four classes based on their electrophysiologic properties (Table 23-1). Class I drugs are further subdivided into three subgroups (see Chapter 22, Cardiac Rhythm Disturbances).

Table 23-1 Classification of Antiarrhythmic Drugs

Class I Antiarrhythmics: Fast Sodium Channel Blockers



Lidocaine (Xylocaine), a Class Ib antiarrhythmic drug, controls ventricular arrhythmias by binding to fast sodium channels in their inactive state, thereby inhibiting recovery after repolarization in a time- and voltage-dependent manner. Lidocaine suppresses automaticity in the His-Purkinje system and spontaneous depolarization of the ventricles during diastole. Lidocaine appears to act preferentially on ischemic myocardial tissue, causing little or no effect on atrioventricular (AV) nodal or His-Purkinje conduction velocity in normal heart tissue. Lidocaine has local anesthetic effects that stabilize membranes, elevate ventricular fibrillation (Vfib) threshold, and suppress ventricular ectopy in tissues during myocardial ischemia. Unlike quinidine and procainamide, lidocaine has little effect on peripheral vascular tone, myocardial contractility, or cardiac output in normal doses. It does, however, possess central nervous system (CNS) depression activity and can produce sedative, analgesic, and anticonvulsant effects.1

Table 23-2 Electrophysiologic Actions of Class I Antiarrhythmic Agents

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