Lidocain

Gefahreninformationscode (GHS)

• Bildanzeige (GHS)

  

• Alarmwort

  Warnung

• Gefahrenhinweise

  H302：Gesundheitsschädlich bei Verschlucken.

Lidocaine Chemische Eigenschaften,Einsatz,Produktion Methoden

• R-Sätze Betriebsanweisung:

  R22:Gesundheitsschädlich beim Verschlucken.

• S-Sätze Betriebsanweisung:

  S22:Staub nicht einatmen.
  S26:Bei Berührung mit den Augen sofort gründlich mit Wasser abspülen und Arzt konsultieren.
  S36:DE: Bei der Arbeit geeignete Schutzkleidung tragen.

• Beschreibung

  Lidocaine [2-(diethylamino)-N-(2, 6-dimethylphenyl) acetamide monohydrochloride] is the most commonly used amino amide-type local anesthetic. Lidocaine is very lipid soluble and, thus, has a more rapid onset and a longer duration of action than most amino ester-type local anesthetics, such as procaine and tetracaine. It can be administered parenterally (with or without epinephrine) or topically either by itself or in combination with prilocaine or etidocaine as a eutectic mixture that is very popular with pediatric patients. The use of lidocaine–epinephrine mixtures should be avoided, however, in areas with limited vascular supply to prevent tissue necrosis. Lidocaine also frequently is used as a class IB antiarrhythmic agent for the treatment of ventricular arrhythmias, both because it binds and inhibits sodium channels in the cardiac muscle and because of its longer duration of action than amino ester-type local anesthetics.
  Central nervous system changes are the most frequently observed systemic toxicities of lidocaine. The initial manifestations are restlessness, vertigo, tinnitus, slurred speech, and eventually, seizures. Subsequent manifestations include CNS depression with a cessation of convulsions and the onset of unconsciousness and respiratory depression or cardiac arrest. This biphasic effect occurs because local anesthetics initially block the inhibitory GABAergic pathways, resulting in stimulation, and eventually block both inhibitory and excitatory pathways (i.e., block the sodium channels associated with the NMDA receptors, resulting in overall CNS inhibition).

• Chemische Eigenschaften

  solid

• Originator

  Xylocaine,Astra,US,1949

• Verwenden

  Lidocaine is used in creams and lotions to soothe areas of inflamed skin or for example in hemorrhoid preparations to reduce discomfort; used by doctors to anesthetise areas prior to surgery, often avoiding the need for a general anesthetie; used by injection after a heart attack to treat some rhythm disturbances.

• Verwenden

  Lidocaine (Alphacaine)is a selective inverse peripheral histamine H1-receptor agonist with an IC50 of >32 μM. [1] Histamine is responsible for many features of allergic reactions. Lidocaine (Alphacaine)is a second-generation antihistamine agent closely st

• Verwenden

  Antiarrhythmic Agents, Anesthetics；Anticonvulsant；antihypertensive

• Definition

  ChEBI: Lidocaine is the monocarboxylic acid amide resulting from the formal condensation of N,N-diethylglycine with 2,6-dimethylaniline. It has a role as a local anaesthetic, an anti-arrhythmia drug, an environmental contaminant, a xenobiotic and a drug allergen. It is a monocarboxylic acid amide, a tertiary amino compound and a member of benzenes. It derives from a glycinamide.

• Indications

  Experimentally, lidocaine has been found to prevent VF arising during myocardial ischemia or infarction by preventing the fragmentation of organized largewavefronts into heterogeneous wavelets. Although lidocaine is of proven benefit in preventing VF early after clinical myocardial infarction, there is no evidence that it reduces mortality. To the contrary, lidocaine may increase mortality after myocardial infarction by approximately 40% to 60%.There are no controlled studies of lidocaine in secondary prevention of recurrence of VT or VF.
  Lidocaine terminates organized monomorphic spontaneous VT or induced sustained VT in only approximately 20% of cases and is less effective than many other antiarrhythmic drugs. In a blinded, randomized study of intravenous lidocaine versus intravenous amiodarone in out-of-hospital VF resistant to defibrillation, lidocaine was associated with half the likelihood of survival to hospital admission compared with amiodarone.

• Manufacturing Process

  One mol of 2,6-xylidine is dissolved in 800 ml glacial acetic acid. The mixture is cooled to 10°C, after which 1.1 mol chloracetyl chloride is added at one time. The mixture is stirred vigorously during a few moments after which 1,000 ml half-saturated sodium acetate solution, or other buffering or alkalizing substance, is added at one time. The reaction mixture is shaken during half an hour. The precipitate formed which consists of ω-chloro-2,6- dimethyl-acetanilide is filtered off, washed with water and dried. The product is sufficiently pure for further treatment. The yield amounts to 70 to 80% of the theoretical amount.
  One mole of the chloracetyl xylidide thus prepared and 2.5 to 3 mols diethyl amine are dissolved in 1,000 ml dry benzene. The mixture is refluxed for 4 to 5 hours. The separated diethyl amine hydrochloride is filtered off. The benzene solution is shaken out two times with 3N hydrochloric acid, the first time with 800 ml and the second time with 400 ml acid. To the combined acid extracts is added an approximately 30% solution of sodium hydroxide until the precipitate does not increase.
  The precipitate, which sometimes is an oil, is taken up in ether. The ether solution is dried with anhydrous potassium carbonate after which the ether is driven off. The remaining crude substance is purified by vacuum distillation. During the distillation practically the entire quantity of the substance is carried over within a temperature interval of 1° to 2°C. The yield approaches the theoretical amount. MP 68° to 69°C. BP 180° to 182°C at 4 mm Hg; 159° to 160°C at 2 mm Hg. (Procedure is from US Patent 2,441,498.)

• Trademarks

  Alphacaine (Carlisle); Lidoderm (Teikoku); Xylocaine (AstraZeneca）.

• Therapeutic Function

  Local anesthetic, Antiarrhythmic

• Allgemeine Beschreibung

  Lidocaine was the first amino amide synthesized in 1948and has become the most widely used local anesthetic. Thetertiary amine has a pKa of 7.8 and it is formulated as thehydrochloride salt with a pH between 5.0 and 5.5. When lidocaineis formulated premixed with epinephrine the pH ofthe solution is adjusted to between 2.0 and 2.5 to prevent the hydrolysis of the epinephrine. Lidocaine is also availablewith or without preservatives. Some formulations of lidocainecontain a methylparaben preservative that maycause allergic reactions in PABA-sensitive individuals. Thelow pKa and medium water solubility provide intermediateduration of topical anesthesia of mucous membranes.Lidocaine can also be used for infiltration, peripheral nerveand plexus blockade, and epidural anesthesia.

• Biologische Aktivität

  Anasthetic and class Ib antiarrhythmic agent. Blocks voltage-gated sodium channels in the inactivated state.

• Kontakt-Allergie

  Lidocaine is an anesthetic of the amide group, like articaine or bupivacaine. Immediate-type IgE-dependent reactions are rare, and delayed-type contact dermatitis is exceptional. Cross-reactivity between the different amide anesthetics is not systematic.

• Biochem/physiol Actions

  Na+ channel blocker; class IB antiarrhythmic that is rapidly absorbed after parenteral administration.

• Pharmakologie

  Lidocaine is the most widely used local anaesthetic. It has a rapid onset and short duration of action. Lidocaine is rapidly and extensively metabolised in the liver and is safe at recommended doses. Efficacy is enhanced markedly and duration of action prolonged by addition of adrenaline. Lidocaine is less toxic than bupivacaine; a testament to this relative safety is that lidocaine is used intravenously as a class 1b antiarrhythmic and as an i.v. infusion to treat refractory chronic pain. Lidocaine solutions for injection are available in concentrations of 1% and 2%, with or without adrenaline. It is also available as a spray (4% or 10%), cream (2% or 4%), ointment or medicated plaster (both 5%) for topical application.

• Pharmakokinetik

  Lidocaine is administered intravenously because extensive first-pass transformation by the liver prevents clinically effective plasma concentrations orally. The drug is dealkylated and eliminated almost entirely by the liver; therefore, dosage adjustments are necessary in the presence of hepatic disease or dysfunction. Lidocaine clearance exhibits the time dependency common to high-clearance agents. With a continuous infusion lasting more than 24 hours, there is a decrease in total lidocaine clearance and an increase in elimination half-life compared with a single dose. Lidocaine free plasma levels can vary in certain patients owing to binding with albumin and the acutephase reactant a1-acid glycoprotein. Levels of a1-acid glycoprotein are increased in patients after surgery or acute myocardial infarction, whereas levels of both a1-acid glycoprotein and serum albumin are decreased in chronic hepatic disease or heart failure and in those who are malnourished. This is an essential consideration because it is the unbound fraction that is pharmacologically active.

• Clinical Use

  The metabolism of lidocaine is typical of the amino amideanesthetics . The liver is responsiblefor most of the metabolism of lidocaine and any decreasein liver function will decrease metabolism. Lidocaineis primarily metabolized by de-ethylation of the tertiary nitrogento form monoethylglycinexylidide (MEGX). At lowlidocaine concentrations, CYP1A2 is the enzyme responsiblefor most MEGX formation. At high lidocaine concentrations,both CYP1A2 and CYP3A4 are responsible for the formationof MEGX.

• Nebenwirkungen

  Central nervous system side effects such as drowsiness, slurred speech, paresthesias, agitation, and confusion predominate. These symptoms may progress to convulsions and respiratory arrest with higher plasma concentrations. A rare adverse effect is malignant hyperthermia.
  Cimetidine significantly reduces the systemic clearance of lidocaine as well as the volume of distribution at steady state and the degree of plasma protein binding. Beta blockers also reduce lidocaine clearance owing to a decrease in hepatic blood flow. For the same reason, clearance is reduced in congestive heart failure or low-output states.
  Amiodarone may also influence the pharmacokinetics of lidocaine. In patients receiving amiodarone, single doses of intravenous lidocaine do not influence the pharmacokinetics of either agent. When amiodarone treatment is started in patients who are already receiving lidocaine infusion, there is a decrease in lidocaine clearance, which can result in toxic lidocaine levels.

• Sicherheitsprofil

  Poison by ingestion, intravenous, intraperitoneal, and subcutaneous routes. Human systemic effects: blood pressure lowering, changes in heart rate, coma, convulsions, dlstorted perceptions, dyspnea, excitement, hallucinations, muscle contraction or spasticity, pulse rate, respiratory depression, toxic psychosis. An experimental teratogen. Other experimental reproductive effects. A local anesthetic. Mutation data reported. When heated to decomposition it emits toxic fumes of NOx.

• Synthese

  Lidocaine, 2-(diethylamino)-N-(2,6-dimethylphenyl)acetamide (2.2.2), is synthesized from 2,6-dimethylaniline upon reaction with chloroacetic acid chloride, which gives |á-chloro-2,6-dimethylacetanilide (2.1.1), and its subsequent reaction with diethylamine [11].
  
  Synthesis of Lidocaine

• Veterinary Drugs and Treatments

  Besides its use as a local and topical anesthetic agent, lidocaine is used to treat ventricular arrhythmias, principally ventricular tachycardia and ventricular premature complexes in all species. Cats may be more sensitive to the drug and some clinicians feel that it should not be used in this species as an antiarrhythmic, but this remains controversial. In horses, lidocaine may be useful to prevent postoperative ileus and reperfusion injury.

• Elektrophysiologische Effekte

  Experimentally, lidocaine has been found to prevent VF arising during myocardial ischemia or infarction by preventing the fragmentation of organized largewavefronts into heterogeneous wavelets. Although lidocaine is of proven benefit in preventing VF early after clinical myocardial infarction, there is no evidence that it reduces mortality. To the contrary, lidocaine may increase mortality after myocardial infarction by approximately 40% to 60%.There are no controlled studies of lidocaine in secondary prevention of recurrence of VT or VF.
  Lidocaine terminates organized monomorphic spontaneous VT or induced sustained VT in only approximately 20% of cases and is less effective than many other antiarrhythmic drugs. In a blinded, randomized study of intravenous lidocaine versus intravenous amiodarone in out-of-hospital VF resistant to defibrillation, lidocaine was associated with half the likelihood of survival to hospital admission compared with amiodarone.

• Arzneimittelwechselwirkung

  The concurrent administration of lidocaine with cimetidine but not ranitidine may cause an increase (15%) in the plasma concentration of lidocaine. This effect is a manifestation of cimetidine reducing the clearance and volume of distribution of lidocaine. The myocardial depressant effect of lidocaine is enhanced by phenytoin administration.

• Stoffwechsel

  Lidocaine is extensively metabolized in the liver by N-dealkylation and aromatic hydroxylations catalyzed by CYP1A2 isozymes. Lidocaine also possesses a weak inhibitory activity toward the CYP1A2 isozymes and, therefore, may interfere with metabolism of other medications.

• Lager

  Store at RT

• Toxicity evaluation

  The potency of lidocaine depends on various factors including age of the subject, weight, physique including obesity, vascularity of the site, and indication for use, as this would determine the absorption and excretion rate. Physiologically, lidocaine blocks neuronal transmission by interfering with the flow of sodium across excitable membranes. A single lidocaine molecule binds to a single voltage-gated sodium channel impeding the movement of sodium ions across neuronal membranes. Consequently repolarization is prevented and further depolarization is not possible. Toxicity is dose related and results from excessive quantities of lidocaine.

• Vorsichtsmaßnahmen

  Contraindications include hypersensitivity to local anesthetics of the amide type (a very rare occurrence), severe hepatic dysfunction, a history of grand mal seizures due to lidocaine, and age 70 or older. Lidocaine is contraindicated in the presence of second- or thirddegree heart block, since it may increase the degree of block and can abolish the idioventricular pacemaker responsible for maintaining the cardiac rhythm.

Lidocaine Upstream-Materialien And Downstream Produkte

Lidocain Anbieter Lieferant Produzent Hersteller Vertrieb Händler.

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