Comparative Pharmacology
Head-to-head clinical analysis: ALPHACAINE versus LIDOCAINE HYDROCHLORIDE 0 4 AND DEXTROSE 5 IN PLASTIC CONTAINER.
Peer-Reviewed Evidence
Head-to-head clinical analysis: ALPHACAINE versus LIDOCAINE HYDROCHLORIDE 0 4 AND DEXTROSE 5 IN PLASTIC CONTAINER.
ALPHACAINE vs LIDOCAINE HYDROCHLORIDE 0.4% AND 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 a amide-type local anesthetic that blocks voltage-gated sodium channels in neuronal membranes, inhibiting the initiation and conduction of nerve impulses. Dextrose provides calories and does not have pharmacological activity.
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. Maximum total dose: 3 mg/kg bolus; infusion for up to 24 hours. Note: 0.4% concentration = 4 mg/mL, 5% dextrose as diluent.
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: 1.5–2 hours after a single dose in healthy adults. In patients with hepatic impairment, heart failure, or prolonged infusion, half-life can increase to >3 hours due to reduced clearance. Neonates: 3–6.3 hours.
Renal: ~60-70% unchanged; Hepatic metabolism: ~20-30% via CYP3A4 and CYP2C9; Fecal: <10%.
Renal: Approximately 90% of lidocaine is metabolized in the liver, and less than 10% is excreted unchanged in urine. The major metabolites (monoethylglycinexylidide and glycinexylidide) are excreted renally. Biliary/fecal excretion is minimal (<1%).
Category C
Category A/B
Local Anesthetic
Local Anesthetic / Antiarrhythmic (Class Ib)