Comparative Pharmacology
Head-to-head clinical analysis: LIDOCAINE VISCOUS versus LIDOCATON.
Peer-Reviewed Evidence
Head-to-head clinical analysis: LIDOCAINE VISCOUS versus LIDOCATON.
LIDOCAINE VISCOUS vs LIDOCATON
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Lidocaine is an amide-type local anesthetic that blocks voltage-gated sodium channels (Nav1.7, Nav1.8) in neuronal membranes, inhibiting depolarization and propagation of action potentials, thereby producing local anesthesia. It also has antiarrhythmic properties (class IB) by blocking sodium channels in cardiac myocytes.
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.
15 mL (300 mg) orally every 3 hours as needed for pain; maximum 8 doses per 24 hours.
Lidocaine: Initial IV bolus 1-1.5 mg/kg, then IV infusion 1-4 mg/min. Adjust for arrhythmia suppression.
None Documented
None Documented
Terminal elimination half-life is 1.5–2 hours (up to 3 hours in hepatic impairment). Clinically, redistribution half-life (~6 min) determines duration of action after short infusions.
Terminal half-life 1.5–2 hours (adults); prolonged in heart failure (up to 4–6 hours) or hepatic impairment (up to 8 hours).
Renal excretion of unchanged drug and metabolites accounts for >90% of elimination; <10% biliary/fecal. Metabolites include monoethylglycinexylidide (MEGX) and glycinexylidide (GX).
Renal: ~90% as metabolites (major metabolite 4-hydroxyxylidine) and ~10% unchanged. Biliary/fecal: <5%.
Category A/B
Category C
Local Anesthetic / Antiarrhythmic (Class Ib)
Local Anesthetic