Chalocard 2% Non-Preservative Mechanism of Action

Pharmacology: Pharmacodynamics: Lidocaine Hydrochloride is a local anaesthetic of the amide type. It has a rapid onset and a medium duration of action. Onset and the duration of the local anaesthetic effect of lidocaine depend on the dose and the site of ministration. Lidocaine, like other local anaesthetics, causes a reversible blockade of impulse propagation along nerve fibres by preventing the inward movement of sodium ions through the cell membrane of the nerve fibres. The ion channels of the nerve membrane are considered a receptor for local anaesthetic molecules.
Pharmacokinetics: Absorption: The plasma concentration of lidocaine depends upon the dose, the route of administration and the vascularity of the injection site.
Distribution: The pKa of Lidocaine Hydrochloride is 7.86 and is 60-80% protein-bound (mainly to alpha-1-acid glycoprotein) in plasma, total plasma clearance of 0.95 L/min, Vd is 1.1-2.1 LK; alterable by many patient factors, decrease in CHF and liver disease and crosses blood-brain barrier. Lidocaine readily crosses the placenta. Lidocaine is excreted in breast milk, but in such small quantities that there is no risk of affecting the child with therapeutic doses.
Metabolism: Lidocaine is almost entirely due to liver metabolism 90%. The main metabolites formed from lidocaine are monoethylglycinexylidide (MEGX) and glycinexylidide (GX) can accumulate and may cause CNS toxicity.
Excretion: Lidocaine is metabolism occurs and metabolites are excreted in the urine with less than 10% of unchanged lidocaine. Lidocaine shows biphasic half-life elimination and prolonged with CHF, liver disease, shock, severe renal disease.
Initial: 7-30 minutes; Terminal: Infants, premature 3.2 hours; Adults 1.5-2 hours.