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Lidocaine is a local anesthetic agent that also has antiarrhythmic effects. It is classified as a type IB antiarrhythmic agent and is a treatment for ventricular tachycardia or ventricular fibrillation.1,2 For episodes of sustained ventricular tachycardia with signs or symptoms of hemodynamic instability (angina, pulmonary edema, hypotension, hemodynamic collapse), electrical cardioversion is the treatment of choice. However, for patients who are more hemodynamically stable, sustained monomorphic ventricular tachycardia due to myocardial ischemia or infarction may be successfully treated using lidocaine therapy. Lidocaine therapy can also be considered for the treatment of polymorphic ventricular tachycardia due to myocardial ischemia or infarction.3

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The primary treatment for ventricular fibrillation is also direct-current cardioversion. Lidocaine is an alternative antiarrhythmic drug treatment to amiodarone for patients that are not converted using electrical shock and intravenous epinephrine or vasopressin.4

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Lidocaine inhibits transmembrane sodium influx into the His-Purkinje fiber conduction system thereby decreasing conduction velocity.2 It also decreases the duration of the action potential and as a result decreases the duration of the absolute refractory period in Purkinje fibers and bundle of His. Automaticity is decreased during lidocaine therapy. The net effect of these cellular changes is that lidocaine eradicates ventricular reentrant arrhythmias by abolishing unidirectional blocks via increased conduction through diseased fibers.

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When given intravenously, the serum lidocaine concentration/time curve follows a two-compartment model.5,6 This is especially apparent when initial loading doses of lidocaine are given as rapid intravenous injections over 1–5 minutes (maximum rate: 25–50 mg/min) and a distribution phase of 30–40 minutes is observed after drug administration (Figure 7-1). Unlike digoxin, the myocardium responds to the higher concentrations achieved during the distribution phase because lidocaine moves rapidly from the blood into the heart, and the onset of action for lidocaine after a loading dose is within a few minutes after completion of the intravenous injection.1,2 Because of these factors, the heart is considered to be located in the central compartment of the two-compartment model for lidocaine.

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Figure 7-1
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Lidocaine serum concentrations initially drop rapidly after an intravenous bolus as drug distributes from blood into the tissues during the distribution phase. During the distribution phase, drug leaves the blood due to tissue distribution and elimination. After 0.5–1 hour, an equilibrium is established between the blood and tissues, and serum concentrations drop more slowly since elimination is the primary process removing drug from the blood. This type of serum concentration/time profile is described by a two-compartment model. The conduction system of the heart responds to the high concentrations of lidocaine present during the distribution phase, so lidocaine has a quick onset of action.

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The generally accepted therapeutic range for lidocaine is 1.5–5 μg/mL. In the upper end of the therapeutic range (>3 μg/mL), some patients will experience minor side effects including ...

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