Lidocaine Hydrochloride and Epinephrine

LIDOCAINE HYDROCHLORIDE AND EPINEPHRINE- lidocaine hydrochloride and epinephrine injection, solution
Cardinal Health 107, LLC

For Infiltration and Nerve Block

Ampul
Fliptop Vial
Multiple-dose Fliptop Vial

Protect from light.

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Rx only

DESCRIPTION

Lidocaine Hydrochloride and Epinephrine Injection, USP is a sterile, nonpyrogenic solution of lidocaine hydrochloride and epinephrine in water for injection for parenteral administration in various concentrations with characteristics as follows:

Concentration

Lidocaine HCl

Epinephrine

Lidocaine HCl

(anhyd.) mg/mL

Epinephrine

mcg/mL

Sodium Chloride

mg/mL

0.5%

1:200,000

5

5

8

1%

1:200,000

10

5

7

1.5%

1:200,000

15

5

6.5

2%

1:200,000

20

5

6

1%

1:100,000

10

10

7

2%

1:100,000

20

10

6

Sodium metabisulfite 0.5 mg/mL and citric acid, anhydrous 0.2 mg/mL added as stabilizers. The headspace of Lists 1209, 3177, 3178, 3181, 3182 and 3183 are nitrogen gassed. May contain sodium hydroxide and/or hydrochloric acid to adjust pH; pH is 4.5 (3.3 to 5.5). See HOW SUPPLIED section for various sizes and strengths.

Multiple-dose vials contain methylparaben 1 mg/mL added as preservative.

Single-dose ampuls and vials contain no bacteriostat or antimicrobial agent. Discard unused portion.

Lidocaine is a local anesthetic of the amide type.

Lidocaine Hydrochloride, USP is chemically designated 2-(diethyl-amino)-2′,6′-acetoxylidide monohydrochloride monohydrate, a white powder freely soluble in water. It has the following structural formula:

structural formula lidocaine hydrochloride usp
(click image for full-size original)

Epinephrine, USP is a sympathomimetic (adrenergic) agent designated chemically as 4-[1-hydroxy-2 (methylamino) ethyl]-1,2 benzenediol, a white, microcrystalline powder. It has the following structural formula:

structrual formula epinephrine, uspstructural formula lidocaine hydrochloride uspstructrual formula epinephrine, usp

CLINICAL PHARMACOLOGY

Mechanism of Action Lidocaine HCl stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses thereby effecting local anesthetic action.

Hemodynamics Excessive blood levels may cause changes in cardiac output, total peripheral resistance, and mean arterial pressure. With central neural blockade these changes may be attributable to block of autonomic fibers, a direct depressant effect of the local anesthetic agent on various components of the cardiovascular system, and/or the beta-adrenergic receptor stimulating action of epinephrine when present. The net effect is normally a modest hypotension when the recommended dosages are not exceeded.

Pharmacokinetics and Metabolism Information derived from diverse formulations, concentrations and usages reveals that lidocaine HCl is completely absorbed following parenteral administration, its rate of absorption depending, for example, upon various factors such as the site of administration and the presence or absence of a vasoconstrictor agent. Except for intravascular administration, the highest blood levels are obtained following intercostal nerve block and the lowest after subcutaneous administration.

The plasma binding of lidocaine HCl is dependent on drug concentration, and the fraction bound decreases with increasing concentration. At concentrations of 1 to 4 mcg of free base per mL, 60 to 80 percent of lidocaine HCl is protein bound. Binding is also dependent on the plasma concentration of the alpha-1-acid glycoprotein.

Lidocaine HCl crosses the blood-brain and placental barriers, presumably by passive diffusion.

Lidocaine HCl is metabolized rapidly by the liver, and metabolites and unchanged drug are excreted by the kidneys. Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the amide linkage, and conjugation. N-dealkylation, a major pathway of biotransformation, yields the metabolites monoethylglycinexylidide and glycinexylidide. The pharmacological/toxicological actions of these metabolites are similar to, but less potent than, those of lidocaine HCl. Approximately 90% of lidocaine HCl administered is excreted in the form of various metabolites, and less than 10% is excreted unchanged. The primary metabolite in urine is a conjugate of 4-hydroxy-2,6-dimethylaniline.

The elimination half-life of lidocaine HCl following an intravenous bolus injection is typically 1.5 to 2 hours. Because of the rapid rate at which lidocaine HCl is metabolized, any condition that affects liver function may alter lidocaine HCl kinetics. The half-life may be prolonged two-fold or more in patients with liver dysfunction. Renal dysfunction does not affect lidocaine HCl kinetics but may increase the accumulation of metabolites.

Factors such as acidosis and the use of central nervous system (CNS) stimulants and depressants affect the CNS levels of lidocaine HCl required to produce overt systemic effects. Objective adverse manifestations become increasingly apparent with increasing venous plasma levels above 6 mcg free base per mL. In the rhesus monkey arterial blood levels of 18 to 21 mcg/mL have been shown to be threshold for convulsive activity.

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