Comparative Pharmacology
Head-to-head clinical analysis: ALPHACAINE versus LIDOCAINE HYDROCHLORIDE 0 8 IN DEXTROSE 5 IN PLASTIC CONTAINER.
Peer-Reviewed Evidence
Head-to-head clinical analysis: ALPHACAINE versus LIDOCAINE HYDROCHLORIDE 0 8 IN DEXTROSE 5 IN PLASTIC CONTAINER.
ALPHACAINE vs LIDOCAINE HYDROCHLORIDE 0.8% IN DEXTROSE 5% IN PLASTIC CONTAINER
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
ALPHACAINE is a local anesthetic that binds to the intracellular portion of voltage-gated sodium channels, blocking sodium influx and preventing depolarization and conduction of nerve impulses.
Lidocaine is an amide-type local anesthetic that acts by blocking voltage-gated sodium channels in neuronal cell membranes, thereby inhibiting the initiation and conduction of nerve impulses. This stabilizes the neuronal membrane and produces a reversible loss of sensation.
10-20 mg IM or IV every 4-6 hours as needed; maximum 80 mg/day.
Intravenous administration: 1-1.5 mg/kg bolus, followed by 1-4 mg/min continuous infusion for ventricular arrhythmias. Max dose: 3 mg/kg bolus, 4 mg/min infusion.
None Documented
None Documented
Terminal elimination half-life: 3.5-5.0 hours (prolonged in hepatic impairment; requires dose adjustment in Child-Pugh B or C).
Terminal elimination half-life is approximately 1.5–2.0 hours after a single IV dose. In patients with heart failure or hepatic impairment, it may be prolonged to >3 hours. After continuous infusion, the half-life may increase due to accumulation.
Renal: ~60-70% unchanged; Hepatic metabolism: ~20-30% via CYP3A4 and CYP2C9; Fecal: <10%.
Lidocaine is primarily metabolized in the liver by CYP1A2 and CYP3A4 to active metabolites (MEGX, GX). Less than 10% is excreted unchanged in urine. Renal excretion accounts for about 20% of total clearance as metabolites and parent drug; fecal elimination is minimal (<5%).
Category C
Category A/B
Local Anesthetic
Local Anesthetic / Antiarrhythmic (Class Ib)