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  1. Pharmacology

    1. Lidocaine is a local anesthetic and a type Ib antiarrhythmic agent. It inhibits fast sodium channels and depresses automaticity within the His-Purkinje system and the ventricles but has a variable effect and may shorten the effective refractory period and action potential duration. Conduction within ischemic myocardial areas is depressed, abolishing reentrant circuits. Unlike quinidine and related drugs, lidocaine exerts a minimal effect on the automaticity of the sinoatrial node and on conduction through the AV node, and it does not decrease myocardial contractility or blood pressure in usual doses. It also has rapid “on-off” binding to sodium channels (to allow reactivation of the channel) and competes with other sodium channel blockers (that are slow to release and block the channel throughout the cardiac cycle). This may account for its antiarrhythmic effect with poisonings from other sodium channel blockers (type 1a antiarrhythmics, tricyclic antidepressants).

    2. The oral bioavailability of lidocaine is poor owing to extensive first-pass hepatic metabolism (although systemic poisoning is possible from ingestion). After intravenous administration of a single dose, the onset of action is within 60–90 seconds and the duration of effect is 10–20 minutes. The elimination half-life of lidocaine is approximately 1.5–2 hours; active metabolites have elimination half-lives of 2–10 hours. Lidocaine clearance declines with continuous infusions, which may be attributable to its metabolite monoethylglycinexylidide (MEGX). Drug accumulation may occur in patients with congestive heart failure or with liver or renal disease.

  2. Indications. Lidocaine is used for the control of ventricular arrhythmias arising from poisoning by a variety of cardioactive drugs and toxins (eg, digoxin, cyclic antidepressants, stimulants, and theophylline). Patients with atrial arrhythmias usually do not respond to this drug.

  3. Contraindications

    1. The presence of nodal or ventricular rhythms in the setting of third-degree AV or intraventricular block. These are usually reflex escape rhythms that may provide lifesaving cardiac output, and abolishing them may result in asystole.

    2. Hypersensitivity to lidocaine or other amide-type local anesthetics (rare).

  4. Adverse effects

    1. Excessive doses produce dizziness, confusion, agitation, and seizures.

    2. Conduction defects, bradycardia, and hypotension may occur in patients with extremely high serum concentrations or in those with underlying conduction disease.

    3. Use in pregnancy. FDA Category B. Fetal harm is extremely unlikely (See Introduction in Section III).

  5. Drug or laboratory interactions

    1. Cimetidine and propranolol may decrease the hepatic clearance of lidocaine.

    2. Lidocaine may produce additive effects with other local anesthetics. In severe cocaine intoxication, lidocaine theoretically may cause additive neuronal depression.

  6. Dosage and method of administration (adults and children)

    1. Administer 1- to 1.5-mg/kg (usual adult dose: 50–100 mg; children: 1 mg/kg) IV bolus at a rate of 25–50 mg/min, followed by infusion of 1–4 mg/min (20–50 mcg/kg/min) to maintain serum concentrations of 1.5–5 mg/L. Can also be administered by intraosseous infusion.

    2. If significant ectopy persists after the initial bolus, repeat doses of 0.5 mg/kg IV can be given if needed at 5- to 10-minute intervals (to a maximum 300-mg or 3-mg/kg total dose in any 1-hour period; children may be given repeated 1-mg/kg doses every 5–10 minutes to ...

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