Comparative Pharmacology
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE 0 2 IN DEXTROSE 5 IN PLASTIC CONTAINER versus POLOCAINE.
Peer-Reviewed Evidence
Head-to-head clinical analysis: LIDOCAINE HYDROCHLORIDE 0 2 IN DEXTROSE 5 IN PLASTIC CONTAINER versus POLOCAINE.
LIDOCAINE HYDROCHLORIDE 0.2% IN DEXTROSE 5% IN PLASTIC CONTAINER vs POLOCAINE
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Lidocaine is a sodium channel blocker that stabilizes the neuronal membrane by inhibiting the ionic fluxes required for initiation and conduction of impulses, resulting in local anesthetic and antiarrhythmic effects.
Local anesthetic that stabilizes the neuronal membrane by inhibiting the influx of sodium ions, thereby blocking nerve impulse propagation.
Intravenous infusion: 1-4 mg/min (0.2% solution = 2 mg/mL) for antiarrhythmic therapy; loading dose 1-1.5 mg/kg IV bolus, then infusion. Maximum infusion rate 4 mg/min.
100 mg orally every 12 hours
None Documented
None Documented
Terminal elimination half-life is approximately 1.5–2 hours (mean 1.8 h) in adults with normal hepatic function; may be prolonged in patients with hepatic impairment (e.g., cirrhosis) or heart failure (up to 10 h), and in neonates (3–6 h).
Terminal elimination half-life approximately 1.5-2.0 hours in adults; prolonged to 3-5 hours in hepatic impairment and neonates.
Renal excretion of unchanged drug and metabolites accounts for >95% of elimination, with ~10% as unchanged lidocaine and ~90% as metabolites (primarily 4-hydroxy-2,6-xylidine, with minor contribution from monoethylglycinexylidide and glycinexylidide). Biliary/fecal excretion is minimal (<1%).
Hepatic metabolism to 2,6-xylidine and 4-hydroxy-2,6-xylidine; <10% excreted unchanged in urine; approximately 70-80% of metabolites excreted renally, with <5% in feces.
Category A/B
Category C
Local Anesthetic / Antiarrhythmic (Class Ib)
Local Anesthetic