Lidocaine For Horses

Lidocaine HCl Injection, USP is a sterile, nonpyrogenic, aqueous solution that contains a local anesthetic agent and is administered parenterally by injection. See INDICATIONS for specific uses.

Lidocaine HCl Injection, USP solution contains Lidocaine HCl, which is chemically designated as acetamide, 2-(diethylamino)-N-(2,6-dimethylphenyl)-, monohydrochloride and has the molecular wt. 270.8.Â Lidocaine HCl (C14H22N2O â€¢ HCl) has the following structural formula:

Lidocaine HCl Injection, USP solution is for single dose usage, and is Methyl Paraben Free (Preservative-Free).

Lidocaine HCl Injection, USP is a sterile, nonpyrogenic, isotonic solution containing sodium chloride. The pH of this solution is adjusted to approximately 6.5 (5.0 to 7.0) with sodium hydroxide and/or hydrochloric acid.

Lidocaine – 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.Â 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. 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.Â 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.Â At concentrations of 1 to 4 mcg of free base per mL 60 to 80 percent of Lidocaine HCl is protein bound.Â 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.Â Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the amide linkage, and conjugation.Â N-dealkylation, a major pathway of biotransformation, yields the metabolites monoethylglycinexylidide and glycinexylidide.Â The pharmacological/toxicological actions of these metabolites are similar to, but less potent than, those of Lidocaine HCl.Â Approximately 90% of Lidocaine HCl administered is excreted in the form of various metabolites, and less than 10% is excreted unchanged.Â 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.Â Because of the rapid rate at which Lidocaine HCl is metabolized, any condition that affects liver function may alter Lidocaine HCl kinetics.Â The half-life may be prolonged two-fold or more in patients with liver dysfunction.Â Renal dysfunction does not affect Lidocaine HCl kinetics but may increase the accumulation of metabolites.

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

Indications and Usage for Lidocaine

Lidocaine HCl Injection, USP is indicated for production of local or regional anesthesia by infiltration techniques such as percutaneous injection and intravenous regional anesthesia by peripheral nerve block techniques such as brachial plexus and intercostal and by central neural techniques such as lumbar and caudal epidural blocks, when the accepted procedures for these techniques as described in standard textbooks are observed.