Comparative Pharmacology
Head-to-head clinical analysis: LIDOCATON versus NOVOCAIN.
Peer-Reviewed Evidence
Head-to-head clinical analysis: LIDOCATON versus NOVOCAIN.
LIDOCATON vs NOVOCAIN
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Lidocaine is a class IB antiarrhythmic agent that blocks voltage-gated sodium channels, inhibiting the inward sodium current, thereby stabilizing cardiac membranes, decreasing automaticity, and increasing the fibrillation threshold. It also acts as a local anesthetic by reversibly blocking nerve impulse propagation.
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.
Lidocaine: Initial IV bolus 1-1.5 mg/kg, then IV infusion 1-4 mg/min. Adjust for arrhythmia suppression.
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 half-life 1.5–2 hours (adults); prolonged in heart failure (up to 4–6 hours) or hepatic impairment (up to 8 hours).
Plasma half-life: approximately 30–60 seconds due to rapid hydrolysis by pseudocholinesterases; clinical effects short-lived.
Renal: ~90% as metabolites (major metabolite 4-hydroxyxylidine) and ~10% unchanged. Biliary/fecal: <5%.
Renal excretion of para-aminobenzoic acid (PABA) and diethylaminoethanol as major metabolites; <2% excreted unchanged in urine. Biliary/fecal: minimal.
Category C
Category C
Local Anesthetic
Local Anesthetic