Comparative Pharmacology
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE 0 4 IN DEXTROSE 5 IN PLASTIC CONTAINER versus NOVOCAIN.
Peer-Reviewed Evidence
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE 0 4 IN DEXTROSE 5 IN PLASTIC CONTAINER versus NOVOCAIN.
LIDOCAINE HYDROCHLORIDE 0.4% IN DEXTROSE 5% IN PLASTIC CONTAINER vs NOVOCAIN
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.
Procaine, an ester-type local anesthetic, reversibly binds to the intracellular portion of voltage-gated sodium channels, inhibiting sodium influx and blocking nerve impulse conduction.
Intravenous infusion: 1-4 mg/min (20-50 mcg/kg/min) for cardiac arrhythmias. Bolus: 1-1.5 mg/kg IV, then infusion.
Local infiltration: 0.5% solution, up to 20 mL (100 mg) per dose; nerve block: 1-2% solution, 5-10 mL (50-200 mg); maximum single dose: 7 mg/kg or 350 mg (without epinephrine).
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.
Plasma half-life: approximately 30–60 seconds due to rapid hydrolysis by pseudocholinesterases; clinical effects short-lived.
Renal excretion of unchanged drug and metabolites; <10% unchanged in urine, >90% as metabolites (primarily monoethylglycinexylidide and glycinexylidide). Biliary/fecal elimination minimal (<1%).
Renal excretion of para-aminobenzoic acid (PABA) and diethylaminoethanol as major metabolites; <2% excreted unchanged in urine. Biliary/fecal: minimal.
Category A/B
Category C
Local Anesthetic / Antiarrhythmic (Class Ib)
Local Anesthetic