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the hydrolysis of the epinephrine. Lidocaine is also available with or without preservatives. Some formulations of lidocaine contain a methylparaben preservative that may cause allergic reactions in PABA-sensitive individuals. The low pKa and medium water solubility provide intermediate duration of topical anesthesia of mucous membranes. Lidocaine can also be used for infiltration, peripheral nerve and plexus blockade, and epidural anesthesia.

The metabolism of lidocaine is typical of the amino amide anesthetics and is shown in Figure 22.16. The liver is responsible for most of the metabolism of lidocaine and any decrease in liver function will decrease metabolism. Lidocaine is primarily metabolized by de-ethylation of the tertiary nitrogen to form monoethylglycinexylidide (MEGX). At low lidocaine concentrations, CYP1A2 is the enzyme responsible for most MEGX formation. At high lidocaine concentrations, both CYP1A2 and CYP3A4 are responsible for the formation of MEGX. The amide functional group is fairly stable because of the steric block provided by the ortho methyl groups although amide hydrolysis products are reported.85-87

The toxicity associated with lidocaine local anesthesia is low when used at appropriate doses. Absorption of lidocaine will be decreased with the addition of epinephrine to the local anesthetic. Toxicity increases in patients with liver disease and those with acidosis, which decreases plasma protein binding of lidocaine. CNS toxicity is low with seizure activity reported with high doses. The cardiac toxicity of lidocaine is manifested by bradycardia, hypotension, and cardiovascular collapse, which may lead to cardiac arrest and death.

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