| Indication |
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 and by central neural techniques such as lumbar and
caudal epidural blocks. |
| 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 |
|
| 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. |
| Affected organisms |
|
