Lycan Mechanism of Action

Pharmacotherapeutic group: Anaesthetics, local, amides.
Pharmacology: Pharmacodynamics: Lidocaine is used to provide anaesthesia by nerve blockade at various sites in the body and in the control of dysrhythmias.
It has a rapid onset of action (about one minute following intravenous injection and fifteen minutes following intramuscular injection) and rapidly spreads through the surrounding tissues.
The effect lasts about ten to twenty minutes and about sixty to ninety minutes following intravenous and intramuscular injection respectively.
Pharmacokinetics: The concentration of Lidocaine in the blood will be determined by its rate of absorption from the site of injection, the rate of tissue distribution and the rate of metabolism and excretion.
Absorption: The systemic absorption of Lidocaine is determined by the site of injection, the dosage and its pharmacological profile. The maximum blood concentration occurs following intercostal nerve blockade followed in order of decreasing concentration, the lumbar epidural space, brachial plexus site and subcutaneous tissue. The total dose injected regardless of the site is the primary determinant of the absorption rate and blood levels achieved. There is a linear relationship between the amount of Lidocaine injected and the resultant peak anaesthetic blood levels. The lipid solubility and vasodilator activity will also influence its rate of absorption.
Distribution: Lidocaine is distributed throughout the total body water. Its rate of disappearance from the blood can be described by a two or three compartment model.
There is a rapid disappearance (Alpha phase) which is believed to be related to uptake by rapidly equilibrating tissues (i.e. tissues with a high vascular perfusion). The slower phase is related to distribution, to slowly equilibrating tissues (Beta phase) and to its metabolism and excretion (Gamma phase). In general, the more highly perfused organs will show higher concentrations of Lidocaine. The highest percentage of this drug will be found in skeletal muscle.
This is because of the mass of muscle rather than an affinity.
Biotransformation: Lidocaine undergoes enzymatic degradation primarily in the liver. Some degradation may take in tissues other than liver. The main pathway involves oxidative de-ethylation to monoethylglycinexylidide followed by a subsequent hydrolysis to xylidine.
Elimination: The excretion occurs via the kidney with less than 5% in the unchanged form appearing in the urine. The renal clearance is inversely related to its protein binding affinity and the pH of the urine. This suggests by the latter that excretion of Lidocaine occurs by non-ionic diffusion.