Alternative to other antiarrhythmic drugs (e.g., amiodarone, procainamide, sotalol) for the acute treatment of hemodynamically compromising ventricular ectopy (e.g., VPCs) that occurs following myocardial ischemia or infarction or during cardiac manipulative procedures such as cardiac surgery or cardiac catheterization.
Prophylactic use to reduce primary VF following AMI is not recommended.
Alternative antiarrhythmic agent to amiodarone in the treatment of cardiac arrest secondary to VF or pulseless VT resistant to CPR, cardioversion (e.g., after 2 to 3 shocks) and a vasopressor (epinephrine, vasopressin).
Alternative to other antiarrhythmic agents or synchronized electrical cardioversion in the treatment of hemodynamically stable monomorphic VT in patients with preserved ventricular function; however, other agents are preferred.
Alternative antiarrhythmic agent in the treatment of hemodynamically stable polymorphic VT in patients with normal baseline QT interval and preserved ventricular function (when ischemia is treated and electrolyte imbalance is corrected) or with prolonged baseline QT interval that suggests torsades de pointes; efficacy not established in torsades de pointes.
Drug-induced cardiovascular emergencies or altered vital signs: May consider use in tachycardia, impaired conduction/ventricular arrhythmias, hypertensive emergencies, or acute coronary syndrome associated with stimulants (e.g., amphetamine, methamphetamine, cocaine, phencyclidine, ephedrine), tricyclic antidepressant, cardiac glycoside, or class I antiarrhythmic (e.g., procainamide, disopyramide, propafenone, flecainide) toxicity; do not use in lidocaine overdose. Safety and efficacy not established in drug-induced polymorphic VT. Efficacy not established in torsades de pointes.
Status Epilepticus
Treatment of status epilepticus†, as a last resort.
Dosage and Administration
General
Ventricular Arrhythmias
Solutions containing epinephrine must not be used to treat arrhythmias.
Adjust dosage carefully according to individual requirements and response; constant ECG monitoring is recommended.
Discontinue therapy for VF or VT (at least temporarily) after 6–24 hours to reassess ongoing need for antiarrhythmic drugs. Terminate infusion as soon as the basic cardiac rhythm appears to be stable or at the earliest sign of toxicity. Immediately stop infusion if signs of excessive cardiac depression occur (e.g., prolongation of PR interval and QRS complex, appearance or aggravation of arrhythmias).
Infusions continued for >24 hours should be rarely necessary.
Administration
Administer IV. Has been administered IM (no longer commercially available in the US); IV infusion is preferred.
For ACLS during CPR, may be administered via endotracheal tube† or by intraosseous injection† when IV administration is not possible. Although endotracheal† administration is possible, IV or intraosseous† administration is preferred because of more predictable drug delivery and pharmacologic effect.
IV Administration
For solution and drug compatibility information, see Compatibility under Stability.
Administer as a bolus IV injection for initial treatment of ventricular arrhythmias. Maintenance IV infusions may be required to maintain normal sinus rhythm if oral antiarrhythmic therapy is not feasible.
Administer via a peripheral vein (antecubital or external jugular in adults and the largest most accessible vein that does not interrupt resuscitation in pediatric patients) during CPR when a vein has not been cannulated prior to the arrest, since central venous access requires interruption of chest compressions, is technically more difficult, and is associated with an increased risk of complications.
Administer via a central venous catheter (if already in place at the time of arrest) because of more rapid onset of drug activity (in adults), more secure access to circulation, and avoidance of tissue infiltration.
Do not use commercially available solutions of lidocaine in 5% dextrose in series connections with other plastic containers; such use could result in air embolism.
Dilution
Lidocaine hydrochloride injections containing 40, 100, or 200 mg/mL are for the preparation of IV infusion solutions and must be diluted prior to administration. Massive overdosage resulting in cardiac arrest, seizures, and/or death may occur if administered by direct IV administration without prior dilution.
Prepare IV infusions by adding 1 g of lidocaine hydrochloride (25 mL of 4% or 5 mL of 20% lidocaine hydrochloride injection) to 1 L of 5% dextrose injection to provide a solution containing 1 mg/mL.
Alternatively, use commercially available 0.4 or 0.8% solutions in 5% dextrose.
If fluid restriction is desirable, up to 8 mg/mL may be used.
Rate of Administration
Administer IV bolus dose at a rate of 25–50 mg/minute (0.35–0.7 mg/kg per minute).
Administer maintenance infusions at a rate of 20–50 mcg/kg per minute in adults or 10–50 mcg/kg per minute in pediatric patients.
For other populations, see Special Populations under Dosage and Administration.
Intraosseous Administration
For intraosseous injection, place a cannula in a noncollapsible marrow venous plexus using a rigid needle, preferably a specially designed intraosseous or Jamshidi-type bone marrow needle; a styleted needle is preferred to prevent obstruction of the needle with cortical bone.
Insert intraosseous needle into the anterior tibial bone marrow; alternatively, the distal femur, medial malleolus, or anterior superior iliac spine can be used. In older children and adults, intraosseous cannulas may be inserted into the distal radius or ulna in addition to the proximal tibia.
Endotracheal Administration
For administration via endotracheal tube, dilute dose in 5–10 mL of 0.9% sodium chloride or sterile water (for adults) or flush with a minimum of 5 mL of 0.9% sodium chloride followed by 5 assisted manual ventilations (for pediatric patients). Dilution in sterile water may increase absorption of lidocaine; however, sterile water may have a more negative effect on arterial oxygen pressure (PaO2).
Dosage
Available as lidocaine hydrochloride; dosage is expressed in terms of the salt.
Pediatric Patients
Ventricular Arrhythmias
IV
Initially, 0.5–1 mg/kg as a rapid IV injection (i.e., bolus); dose may be repeated according to patient response, up to a maximum total dose of 3–5 mg/kg. Maintenance infusion of 10–50 mcg/kg per minute.
For ACLS, 1 mg/kg initially, up to maximum initial dose of 100 mg. If VT or VF is not corrected following defibrillation (or cardioversion) and initial lidocaine dose, give 20–50 mcg/kg per minute as an IV infusion. If the time between initial IV bolus dose and onset of IV infusion exceeds 15 minutes, give an additional IV bolus of 0.5–1 mg/kg.
Intraosseous
Initially, 1 mg/kg, up to maximum initial dose of 100 mg. If VT or VF is not corrected following defibrillation (or cardioversion) and initial lidocaine dose, give infusion of 20–50 mcg/kg per minute.
Endotracheal
Optimal dose not established.
Initially, 2–3 mg/kg; however, 2–2.5 times the recommended IV dosage may be recommended.
Adults
Ventricular Arrhythmias
IV
Initial doses ranging from 0.5–0.75 mg/kg and up to 1–1.5 mg/kg (about 50–100 mg) administered as rapid IV injection may be used. If desired response is not achieved, 25–50 mg may be administered 5 minutes after completion of the first injection, or 0.5–0.75 mg/kg as rapid IV injection may be repeated at 5- to 10-minute intervals as necessary, up to a total of 3 doses (or up to 3 mg/kg).
Cardiac arrest secondary to VF or pulseless VT: 1–1.5 mg/kg as initial loading dose, then 0.5–0.75 mg/kg as rapid IV injection repeated at 5- to 10-minute intervals as necessary, up to a total of 3 doses (or up to 3 mg/kg).
Maintenance infusion of 30–50 mcg/kg per minute (1–4 mg/minute in an average 70-kg adult).
If arrhythmias recur during maintenance infusion, administer 0.5 mg/kg as a bolus dose while maintaining or increasing infusion rate simultaneously up to a maximum rate of 4 mg/minute.
Intraosseous
Cardiac arrest secondary to VF or pulseless VT: 1–1.5 mg/kg as initial loading dose, then 0.5–0.75 mg/kg repeated at 5- to 10-minute intervals as necessary, up to a total of 3 doses (or up to 3 mg/kg).
Endotracheal
Optimal dose not established.
Usually, 2–2.5 times the recommended IV dosage.
Status Epilepticus
IV
Initially, 1 mg/kg. After 2 minutes, administer 0.5 mg/kg if seizure is not terminated. Maintenance infusion of 30 mcg/kg per minute for prevention of seizure recurrence.†
Prescribing Limits
Pediatric Patients
Ventricular Arrhythmias
IV
Maximum 3–5 mg/kg for initial treatment.
ACLS: 1 mg/kg initially up to maximum initial dose of 100 mg.
Intraosseous
ACLS: 1 mg/kg initially up to maximum initial dose of 100 mg.
Adults
Ventricular Arrhythmias
IV
Maximum 3 mg/kg as total dose for initial treatment.
Maximum total dose of 200–300 mg over a 1-hour period.
Maximum 4 mg/minute as maintenance infusion.
Special Populations
Hepatic Impairment
Careful and individualized dosing recommended.
Slower infusion rates (e.g., 50% of usual maintenance infusion) recommended.
Reduce infusion rate after 24 hours to 1–2 mg/minute; dosage reduction may be guided by plasma lidocaine concentrations.
Renal Impairment
Dosage modification not required.
Geriatric Patients
Slower infusion rates (e.g., 50% of usual maintenance infusion) recommended in patients >70 years of age.
Decreased Cardiac Output
Smaller bolus doses may be required.
Slower infusion rates (e.g., 50% of usual maintenance infusion) recommended in patients with decreased cardiac output (e.g., hypotension or shock associated with AMI, poor peripheral perfusion states, CHF).
Maximum infusion rate of 20 mcg/kg per minute in patients with persistently poor cardiac output and hepatic or renal failure; <30 mcg/kg per minute in patients with CHF.
Reduce infusion rate after 24 hours to 1–2 mg/minute; dosage reduction may be guided by plasma lidocaine concentrations.
Patients Requiring Prolonged Therapy
Possible increased half-life following infusions lasting>24 hours; reduce dosage accordingly (e.g., by 50%) to avoid accumulation of the drug and potential toxicity.
Cautions
Contraindications
Adams-Stokes syndrome; severe degrees of SA, AV, or intraventricular heart block (unless a functioning pacemaker is present). Some manufacturers state that lidocaine is contraindicated in patients with Wolff-Parkinson-White syndrome.
Constant ECG monitoring is necessary during IV administration. Discontinue infusion if signs of excessive cardiac depression occur (e.g., prolongation of PR interval and QRS complex, appearance or aggravation of arrhythmias).
Severe Reactions
Resuscitative equipment and drugs should be immediately available for the management of severe adverse cardiovascular, respiratory, or CNS effects. Discontinue therapy if severe reactions occur; institute emergency resuscitative procedures and other supportive measures as required.
Severe reactions may be preceded by somnolence and paresthesia.
Possible increased half-life following infusions lasting >24 hours; reduce dosage accordingly (see Patients Requiring Prolonged Therapy under Dosage and Administration).
Possible muscle twitching or tremors, seizures, unconsciousness, and coma; may be associated with high doses or overdosage.
Possible drowsiness, disorientation, slurred speech, and altered consciousness.
Cardiovascular Effects
Possible hypotension, arrhythmias, heart block, cardiovascular collapse, and bradycardia, which may lead to cardiac arrest in patients with high plasma lidocaine concentrations or myocardial conduction defects.
Possible serious ventricular arrhythmias or heart block in patients with sinus bradycardia; potentially life-threatening adverse effects in patients with symptomatic bradycardia.
Possible increased sensitivity to cardiac depressant effects in patients with a diseased or abnormal sinus node.
Possible increased coronary blood flow in patients with recent MI.
Possible myocardial and circulatory depression.
Cautious use recommended in patients with any form of heart block, CHF, marked hypoxia, severe respiratory depression, hypovolemia, or shock.
Respiratory Effects
Possible respiratory depression and arrest; may be associated with high doses or overdosage.
Local Effects
Possible local thrombophlebitis in patients receiving prolonged IV infusions.
Tissue infiltration may lead to local ischemia, tissue injury, and ulceration.
Laboratory Test Interference
Possible increased serum CK (CPK) concentrations associated with IM injections. Isoenzyme separation is necessary when CK determinations are used in the diagnosis of AMI.
Specific Populations
Pregnancy
Category B.
Lactation
Distributed into milk. Use with caution.
Pediatric Use
Safety and efficacy not established in controlled clinical studies; however, lidocaine has been used for treatment of ventricular arrhythmias in infants and children.
Use may be considered in children as an alternative antiarrhythmic agent, if amiodarone is unavailable, in the treatment of cardiac arrest secondary to VF or pulseless VT resistant to CPR, cardioversion, and epinephrine.
Hepatic Impairment
Use with caution. (See Pharmacokinetics and also see Hepatic Impairment under Dosage and Administration.)
Renal Impairment
Use with caution in severe renal impairment. (See Elimination: Special Populations, under Pharmacokinetics.)
Appears to be important only at lidocaine doses higher than those used clinically
Pharmacokinetics
Absorption
Bioavailability
Absorbed from the GI tract, but passes into hepatic circulation and only about 35% of an oral dose reaches the systemic circulation unchanged. Toxic effects appear at oral doses that fail to produce therapeutic plasma concentrations.
Following IM (deltoid) injection, peak plasma concentrations are achieved in 10 minutes.
Onset
Following direct IV (bolus) administration of 50–100 mg, onset of action is 45–90 seconds.
Duration
Following direct IV (bolus) administration of 50–100 mg, duration is 10–20 minutes.
Plasma Concentrations
Plasma lidocaine concentrations of 1–5 mcg/mL are required to suppress ventricular arrhythmias; concentrations exceeding 5 mcg/mL associated with toxicity.
Distribution
Extent
Widely distributed into body tissues. Readily crosses the blood-brain barrier. Crosses the placenta and is distributed into milk.
Early, rapid decline in plasma concentrations is associated with distribution into highly perfused tissues (e.g., kidneys, lungs, liver, heart); slower elimination phase associated with metabolism and redistribution into skeletal muscle and adipose tissue.
Plasma Protein Binding
Binding is variable and concentration dependent; 60 –80% bound to plasma proteins at concentrations of 1–4 mcg/mL. Partially bound to α1-acid glycoprotein.
Special Populations
Volume of distribution is decreased in patients with CHF and increased in patients with liver disease.
Elimination
Metabolism
Approximately 90% of a parenteral dose is metabolized rapidly in the liver by de-ethylation to the active metabolites monoethylglycinexylidide (MEGX) and glycinexylidide (GX). Rate of metabolism appears to be limited by hepatic blood flow.
Elimination Route
Excreted in urine principally as metabolites.
Half-life
Lidocaine has an initial half-life of 7–30 minutes and a terminal half-life of 1.5–2 hours. Elimination half-lives of MEGX and GX are 2 and 10 hours, respectively.
Special Populations
Rate of metabolism of lidocaine may be decreased and the half-life increased in patients with liver disease. Major differences may exist in pharmacokinetics for different types of liver disease (e.g., cirrhosis, hepatitis); no consistent correlation established between clearance and severity of liver disease (as determined by liver function tests).
Drugs that require low pH for stability (e.g., dopamine, epinephrine, norepinephrine, isoproterenol) may be adversely affected by the pH of lidocaine (5–7). Use such mixtures promptly after preparation or consider separate administration of the drugs. The manufacturers state that commercially available solutions of lidocaine hydrochloride in 5% dextrose should not be mixed with other drugs.
Membrane-stabilizing antiarrhythmic agent. Combines with fast sodium channels in their inactive state and inhibits recovery after repolarization in a time- and voltage-dependent manner. Exhibits rapid rates of attachment to and dissociation from transmembrane sodium channels.
Controls ventricular arrhythmias by suppressing automaticity in His-Purkinje system and by suppressing spontaneous depolarization of the ventricles during diastole.
Little effect on AV node conduction and His-Purkinje conduction in normal heart at therapeutic concentrations. Affects conducting tissues of ventricles more than atria. Variable effect on the effective refractory period (ERP) of the AV node; ERP and action potential duration of the His-Purkinje system are shortened.
Cardiac actions appear to be similar to those of phenytoin.
Produces little effect on autonomic tone; generally does not produce a substantial fall in BP, decreased myocardial contractility, or diminished cardiac output. Usually has little effect on heart rate.
Advice to Patients
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, and of concomitant illnesses.
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.
Importance of advising patients of other important precautionary information. (See Cautions.)
Preparations
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
† Use is not currently included in the labeling approved by the US Food and Drug Administration.
Remember, keep this and all other medicines out of the reach of children,
never share your medicines with others, and use this medication only for the indication prescribed.
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