Lidocaine (CHEM002158)
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| Version | 1.0 | ||||||||
| Creation Date | 2009-07-21 20:26:27 UTC | ||||||||
| Update Date | 2026-05-14 16:25:09 UTC | ||||||||
| Accession Number | CHEM002158 | ||||||||
| Identification | |||||||||
| Common Name | Lidocaine | ||||||||
| Class | Small Molecule | ||||||||
| Description | Lidocaine is only found in individuals that have used or taken this drug. It is a local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of procaine but its duration of action is shorter than that of bupivacaine or prilocaine. 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. | ||||||||
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| Chemical Structure |  | ||||||||
| Synonyms | Not Available | ||||||||
| Chemical Formula | C14H22N2O | ||||||||
| Average Molecular Mass | 234.337 g/mol | ||||||||
| Monoisotopic Mass | 234.173 g/mol | ||||||||
| CAS Registry Number | 137-58-6 | ||||||||
| IUPAC Name | 2-(diethylamino)-N-(2,6-dimethylphenyl)acetamide | ||||||||
| Traditional Name | Not Available | ||||||||
| SMILES | CCN(CC)CC(O)=NC1=C(C)C=CC=C1C | ||||||||
| InChI Identifier | InChI=1S/C14H22N2O/c1-5-16(6-2)10-13(17)15-14-11(3)8-7-9-12(14)4/h7-9H,5-6,10H2,1-4H3,(H,15,17) | ||||||||
| InChI Key | InChIKey=NNJVILVZKWQKPM-UHFFFAOYSA-N | ||||||||
| Chemical Taxonomy | |||||||||
| Classification | Not classified | ||||||||
| Biological Properties | |||||||||
| Status | Detected and Not Quantified | ||||||||
| Origin | Exogenous | ||||||||
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| Biofluid Locations | Not Available | ||||||||
| Tissue Locations | Not Available | ||||||||
| Pathways | Not Available | ||||||||
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| Biological Roles | Not Available | ||||||||
| Chemical Roles | Not Available | ||||||||
| Physical Properties | |||||||||
| State | Solid | ||||||||
| Appearance | White powder. | ||||||||
| Experimental Properties |
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| Predicted Properties | Not Available | ||||||||
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| Toxicity Profile | |||||||||
| Route of Exposure | Intravenous, Topical, Oral, Buccal, Dental, Intramuscular, or Urethral injection , Infiltration. 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. | ||||||||
| Mechanism of Toxicity | 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. | ||||||||
| Metabolism | Primarily hepatic. Route of Elimination: Lidocaine and its metabolites are excreted by the kidneys. Half Life: 109 minutes | ||||||||
| Toxicity Values | LD50: 459 (346-773) mg/kg (oral, non-fasted female rats) LD50: 214 (159-324) mg/kg (oral, fasted female rats) | ||||||||
| Lethal Dose | Not Available | ||||||||
| Carcinogenicity (IARC Classification) | No indication of carcinogenicity to humans (not listed by IARC). | ||||||||
| Uses/Sources | 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. | ||||||||
| Minimum Risk Level | Not Available | ||||||||
| Health Effects | Systemic exposure to excessive quantities of lidocaine mainly result in central nervous system (CNS) and cardiovascular effects. CNS effects may include CNS excitation(nervousness, tingling around the mouth) followed by depression. [Wikipedia] | ||||||||
| Symptoms | Symptoms of overdose include convulsions, hypoxia, acidosis, bradycardia, arrhythmias and cardiac arrest. | ||||||||
| Treatment | The first step in the management of systemic toxic reactions consists of immediate attention to the establishment and maintenance of a patent airway and assisted or controlled ventilation with oxygen and a delivery system capable of permitting immediate positive airway pressure by mask. If convulsions occur, the objective of the treatment is to maintain ventilation and oxygenation and support the circulation. Oxygen must be given and ventilation assisted if necessary (mask and bag or tracheal intubation). Should convulsions not stop spontaneously after 15-20 seconds, an anticonvulsant should be given i.v. to facilitate adequate ventilation and oxygenation. Thiopental sodium 1-3 mg/kg i.v. is the first choice. Alternatively diazepam 0.1 mg/kg bw i.v. may be used, although its action will be slow. Prolonged convulsions may jeopardise the patient's ventilation and oxygenation. If so, injection of a muscle relaxant (e.g. succinylcholine 1 mg/kg bw) will facilitate ventilation, and oxygenation can be controlled. Early endotracheal intubation must be considered in such situations. If cardiovascular depression is evident (hypotension, bradycardia), ephedrine 5-10 mg i.v. should be given and may be repeated, if necessary, after 2-3 minutes. Should circulatory arrest occur, immediate cardiopulmonary resuscitation should be instituted. Continual oxygenation and ventilation and circulatory support as well as treatment of acidosis are of vital importance. (4) | ||||||||
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| Identifiers | Not Available | ||||||||
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| MSDS | Link | ||||||||
| General References | Not Available | ||||||||
