Comparative Pharmacology
Head-to-head clinical analysis: CHLOROPROCAINE HYDROCHLORIDE versus LIDOCAINE HYDROCHLORIDE 0 2 IN DEXTROSE 5.
Peer-Reviewed Evidence
Head-to-head clinical analysis: CHLOROPROCAINE HYDROCHLORIDE versus LIDOCAINE HYDROCHLORIDE 0 2 IN DEXTROSE 5.
CHLOROPROCAINE HYDROCHLORIDE vs LIDOCAINE HYDROCHLORIDE 0.2% IN DEXTROSE 5%
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Blocks voltage-gated sodium channels in nerve cell membranes, inhibiting conduction of nerve impulses. Exhibits rapid onset and short duration due to hydrolysis by plasma pseudocholinesterase.
Lidocaine is a local anesthetic that stabilizes neuronal membranes by inhibiting sodium ion influx, thereby blocking initiation and conduction of nerve impulses.
10-30 mL of 1% solution infiltrated locally; epidural: 15-25 mL of 2% or 3% solution, repeated as needed, not to exceed 800 mg total dose.
1-1.5 mg/kg IV bolus over 2-3 minutes, followed by continuous IV infusion of 1-4 mg/min for ventricular arrhythmias; maximum 3 mg/kg (or 200-300 mg) over 1 hour.
None Documented
None Documented
Terminal elimination half-life of chloroprocaine is approximately 0.1-0.2 hours (6-12 minutes) in adults with normal pseudocholinesterase activity. This extremely short half-life accounts for its rapid clearance and short duration of action.
Terminal elimination half-life: 1.5-2 hours (adults); prolonged in heart failure (up to 4-6 hours) or hepatic impairment (up to 5-7 hours).
Primarily renal excretion of metabolites; unchanged drug undergoes rapid hydrolysis by plasma pseudocholinesterase, producing 2-chloro-4-aminobenzoic acid and diethylaminoethanol. Less than 2% excreted unchanged in urine. Biliary/fecal elimination is negligible.
Renal: ~90% as metabolites and <10% unchanged. Biliary/fecal: minor (<1%).
Category C
Category A/B
Local Anesthetic
Local Anesthetic / Antiarrhythmic (Class Ib)