Lidocaine
Pharmacodynamics
Lidocaine is an anesthetic agent indicated for production of local or regional anesthesia and in the treatment of ventricular tachycardia occurring during cardiac manipulation, such as surgery or catheterization, or which may occur during acute myocardial infarction, digitalis toxicity, or other cardiac diseases. The mode of action of the antiarrhythmic effect of Lidocaine appears to be similar to that of procaine, procainamide and quinidine. Ventricular excitability is depressed and the stimulation threshold of the ventricle is increased during diastole. The sinoatrial node is, however, unaffected. In contrast to the latter 3 drugs, Lidocaine in therapeutic doses does not produce a significant decrease in arterial pressure or in cardiac contractile force. In larger doses, lidocaine may produce circulatory depression, but the magnitude of the change is less than that found with comparable doses of procainamide.
Mechanism of action
Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses thereby effecting local anesthetic action. Lidocaine alters signal conduction in neurons by blocking the fast voltage gated sodium (Na+) channels in the neuronal cell membrane that are responsible for signal propagation. With sufficient blockage the membrane of the postsynaptic neuron will not depolarize and will thus fail to transmit an action potential. This creates the anaesthetic effect by not merely preventing pain signals from propagating to the brain but by aborting their birth in the first place.
Absorption
Information derived from diverse formulations, concentrations and usages reveals that lidocaine is completely absorbed following parenteral administration, its rate of absorption depending, for example, upon various factors such as the site of administration and the presence or absence of a vasoconstrictor agent.
Volume of distribution
0.7 to 2.7 L/kg [healthy volunteers]
Protein binding
60-80%
Metabolism
Primarily hepatic.
Route of elimination
Lidocaine and its metabolites are excreted by the kidneys.
Half life
109 minutes
Clearance
0.64 +/- 0.18 L/min
Toxicity
The oral LD 50 of lidocaine HCl in non-fasted female rats is 459 (346-773) mg/kg (as the salt) and 214 (159-324) mg/kg (as the salt) in fasted female rats. Symptoms of overdose include convulsions, hypoxia, acidosis, bradycardia, arrhythmias and cardiac arrest
Drug drug interaction
Abiraterone + lidocaine= The serum concentration of Lidocaine can be increased when it is combined with Abiraterone.
Acebutolol + lidocaine= The serum concentration of Lidocaine can be increased when it is combined with Acebutolol.
Amiodarone + lidocaine =The serum concentration of Lidocaine can be increased when it is combined with Amiodarone.
Aprepitant + lidocaine =The serum concentration of Lidocaine can be increased when it is combined with Aprepitant.
Adjust dosing interval
Administration with food, particularly dairy products, significantly reduces tetracycline absorption. The calcium content of these foods forms nonabsorbable chelates with tetracycline.
Therapeutic uses
Lidocaine hydrochloride injection, USP is indicated for production of local or regional anesthesia by infiltration techniques such as percutaneous injection and intravenous regional anesthesia by peripheral nerve block techniques such as brachial plexus and intercostal.
Reference- Tripathi KD "Essential of medical pharmacology" 7th edition, page no- 27,360,361,364,366,368,369,370,516,530,531
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