Comparative Pharmacology
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE versus XYLOCAINE 5 W GLUCOSE 7 5.
Peer-Reviewed Evidence
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE versus XYLOCAINE 5 W GLUCOSE 7 5.
LIDOCAINE HYDROCHLORIDE vs XYLOCAINE 5% W/ GLUCOSE 7.5%
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Lidocaine hydrochloride is a sodium channel blocker that inhibits voltage-gated sodium channels in neuronal and cardiac cell membranes, stabilizing the membrane and preventing depolarization, thereby blocking nerve impulses and exerting local anesthetic and antiarrhythmic effects.
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.
IV: 1-1.5 mg/kg bolus, then 1-4 mg/min continuous infusion. Max: 3 mg/kg (300 mg) loading dose. For ventricular arrhythmias.
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 is 1.5–2 hours in adults. In patients with heart failure, hepatic cirrhosis, or those on CYP-inhibitors, half-life may be prolonged to ≥3 hours; in neonates, up to 3–6 hours.
1.5-2 hours (terminal); prolonged in heart failure, hepatic disease, or elderly; neonates 3-6 hours due to immature hepatic function.
Primarily hepatic metabolism (90% CYP3A4, also CYP1A2) to inactive metabolites (monoethylglycinexylidide, glycinexylidide); <10% excreted unchanged in urine. Renal elimination accounts for the majority of metabolite clearance.
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