Comparative Pharmacology
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE 0 2 IN DEXTROSE 5 versus SENSORCAINE.
Peer-Reviewed Evidence
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE 0 2 IN DEXTROSE 5 versus SENSORCAINE.
LIDOCAINE HYDROCHLORIDE 0.2% IN DEXTROSE 5% vs SENSORCAINE
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Lidocaine is a local anesthetic that stabilizes neuronal membranes by inhibiting sodium ion influx, thereby blocking initiation and conduction of nerve impulses.
SENSORCAINE (bupivacaine) is an amide-type local anesthetic that blocks sodium ion channels in nerve cell membranes, thereby inhibiting depolarization and propagation of action potentials, resulting in reversible local anesthesia.
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.
Epidural or caudal block: 15-30 mL of 0.5% to 1% solution (75-150 mg) every 2-4 hours as needed. Maximum single dose: 225 mg.
None Documented
None Documented
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).
The terminal elimination half-life of bupivacaine is approximately 2.7 hours in adults (range 1.5–5.5 hours). In neonates, the half-life is significantly prolonged (~8–12 hours) due to immature hepatic function, leading to an increased risk of toxicity.
Renal: ~90% as metabolites and <10% unchanged. Biliary/fecal: minor (<1%).
SENSORCAINE (bupivacaine) is primarily metabolized in the liver via conjugation with glucuronic acid and undergoes hepatic dealkylation. Approximately 6% of the drug is excreted unchanged in the urine. The majority of the dose (about 95%) is excreted as metabolites in the urine (<10% unchanged) and the remainder in feces via biliary elimination.
Category A/B
Category C
Local Anesthetic / Antiarrhythmic (Class Ib)
Local Anesthetic