Comparative Pharmacology
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE 0 4 IN DEXTROSE 5 IN PLASTIC CONTAINER versus XYLOCAINE 5 W GLUCOSE 7 5.
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE 0 4 IN DEXTROSE 5 IN PLASTIC CONTAINER versus XYLOCAINE 5 W GLUCOSE 7 5.
LIDOCAINE HYDROCHLORIDE 0.4% IN DEXTROSE 5% IN PLASTIC CONTAINER vs XYLOCAINE 5% W/ GLUCOSE 7.5%
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Lidocaine is a sodium channel blocker that inhibits depolarization of cardiac myocytes and nerve axons by binding to voltage-gated sodium channels and stabilizing the neuronal membrane, thereby preventing the propagation of action potentials.
Lidocaine is an amide-type local anesthetic that stabilizes the neuronal membrane by inhibiting sodium ion channels, thereby blocking the initiation and conduction of nerve impulses.
Intravenous infusion: 1-4 mg/min (20-50 mcg/kg/min) for cardiac arrhythmias. Bolus: 1-1.5 mg/kg IV, then infusion.
Adult: 5-25 mL (250-1250 mg lidocaine) of 5% lidocaine with glucose 7.5% solution, administered by caudal or lumbar epidural injection, single dose. Max total dose: 1250 mg.
None Documented
None Documented
Terminal elimination half-life approximately 1.5-2 hours after bolus, prolonged to 2-4 hours in heart failure or hepatic impairment; continuous infusion may show context-sensitive half-life.
1.5-2 hours (terminal); prolonged in heart failure, hepatic disease, or elderly; neonates 3-6 hours due to immature hepatic function.
Renal excretion of unchanged drug and metabolites; <10% unchanged in urine, >90% as metabolites (primarily monoethylglycinexylidide and glycinexylidide). Biliary/fecal elimination minimal (<1%).
Hepatic metabolism (90% N-dealkylation by CYP1A2/CYP3A4 to monoethylglycinexylidide and glycinexylidide); renal excretion of metabolites and parent drug (<10% unchanged); <1% biliary/fecal.
Category A/B
Category C
Local Anesthetic / Antiarrhythmic (Class Ib)
Local Anesthetic