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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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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 drowsiness,
dizziness, ...