Comparative Pharmacology
Head-to-head clinical analysis: ALCAINE versus LIDOCAINE HYDROCHLORIDE 0 2 IN DEXTROSE 5 IN PLASTIC CONTAINER.
Peer-Reviewed Evidence
Head-to-head clinical analysis: ALCAINE versus LIDOCAINE HYDROCHLORIDE 0 2 IN DEXTROSE 5 IN PLASTIC CONTAINER.
ALCAINE vs LIDOCAINE HYDROCHLORIDE 0.2% IN DEXTROSE 5% IN PLASTIC CONTAINER
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Local anesthetic that stabilizes the neuronal membrane by inhibiting sodium ion influx, thereby blocking nerve impulse transmission.
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.
1 to 2 drops of 0.5% solution topically to the eye, repeated as needed for anesthesia.
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.
None Documented
None Documented
Terminal elimination half-life: 0.4–1.2 minutes (rapid enzymatic hydrolysis by plasma esterases); clinical significance: ultra-short duration limits systemic toxicity.
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).
Renal excretion of parent drug and metabolites: <5% unchanged.
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%).
Category C
Category A/B
Local Anesthetic
Local Anesthetic / Antiarrhythmic (Class Ib)