Lidocaine ampoules 2% 2 ml. №100


Manufacturer: Hungary

Use for local anesthesia (terminal, infiltration, conduction) in surgery, ophthalmology, dentistry, otorhinolaryngology; as a solvent for antibacterial agents of the cephalosporin group.



Lidocaine ampoules 2% Storage
active substance: lidocaine;

1 ampoule (2 ml) of solution contains lidocaine hydrochloride anhydrous (in the form of lidocaine hydrochloride monohydrate) 40 mg;

Excipients: sodium chloride, water for injections.

Lidocaine ampoules 2% Dosage form
Solution for injection.

Main physical and chemical properties: clear colorless or almost colorless aqueous solution, odorless.

Lidocaine ampoules 2% Pharmacotherapeutic group
Means for local anesthesia. ATX code N01B B02.

Lidocaine ampoules 2% Pharmacological properties

Lidocaine is a membrane stabilizing agent of the amide group for local anesthesia. It inhibits the sensitive nerve endings of the skin and mucous membranes, ie causes reversible inhibition of the conduction of tissue elements of nerve cells (neuron, axon, synapses).

The mechanism of action of local anesthetics is the inhibition of ion fluxes, which are necessary for the formation of the stimulus – through neuronal membranes.

Lidocaine inhibits the stimulus-activated transient increase in permeability to sodium ions and to a lesser extent reduces the delayed permeability to potassium and sodium ions, thereby stabilizing neuronal membranes. Lidocaine reduces the degree of depolarization that occurs in response to a physiological stimulus, as well as the amplitude of the action potential, and inhibits nerve conduction.

Among the various sensory modes of action, local anesthetics primarily suppress pain sensitivity, accompanied by the suppression of heat and tactile sensations. Lidocaine absorbed after topical administration may cause central nervous system agitation or depression. Its effect on the cardiovascular system can manifest itself in the form of impaired conduction and peripheral vasodilation.


After parenteral administration, lidocaine is completely absorbed. The degree of absorption depends on the site of administration of the drug, the presence or absence of a vasoconstrictor.

In addition to intravascular administration, the highest plasma levels of lidocaine are observed with intercostal nerve block, and the lowest – with subcutaneous injection. Plasma protein binding is 60-80%. Lidocaine crosses the placental and blood-brain barriers.

Lidocaine is rapidly metabolized in the liver, mainly by oxidative N-dealkylation. Its metabolites have the same pharmacological and toxicological effects as the unchanged compound, but they are less potent. Almost 90% of the administered dose of lidocaine is excreted as metabolites. Approximately 10% of the administered dose of the drug is excreted unchanged by the kidneys. The half-life is 1.5-2 hours. In patients with liver disease, the half-life is longer.

Use for local anesthesia (terminal, infiltration, conduction) in surgery, ophthalmology, dentistry, otorhinolaryngology; as a solvent for cephalosporin antibacterial agents.

Hypersensitivity to the components of the drug, other amide local anesthetics, a history of epileptiform seizures after lidocaine, severe bradycardia, severe hypotension, cardiogenic shock, severe chronic heart failure (II-III degree weakness) , Wolf – Parkinson – White syndrome, Adams – Stokes syndrome, atrioventricular (AV) blockade of II and III degree, hypovolemia, severe hepatic / renal dysfunction, porphyria, myasthenia, retrobulbar administration to patients with glaucoma; contraindicated in patients in the first three months after myocardial infarction with reduced cardiac output of the left ventricle (less than 35% of normal); blood clotting disorders, anticoagulant therapy; Injection site infections are contraindicated in non-contact patients. significant decrease in left ventricular function.

Interaction with other medicinal products and other forms of interaction
When combined with lidocaine with drugs such as chlorpromazine, pethidine, bupivacaine, quinidine, disopyramide, amitriptyline, imipramine, nottriptyline, the concentration of lidocaine in blood plasma increases due to decreased hepatic metabolism.

Antiarrhythmic drugs (including amiodarone, verapamil, disopyramide, aimalin) and class IA antiarrhythmic drugs (including quinidine, procainamide, disopyramide) or certain antipsychotics (including olanzapine, quetiapine) or antagonists (including tropisetron, dolasetron) – increased cardiodepressant effect (QT interval is prolonged, and in isolated cases the development of AV blockade or ventricular fibrillation is possible); concomitant use with amiodarone may lead to seizures.

Novocaine, novocainamide, procainamide – possible excitation of the central nervous system, delirium, hallucinations.

Curare-like drugs – increased muscle relaxation (possible paralysis of the respiratory muscles).

Ethanol enhances the respiratory inhibitory effect of lidocaine.

Vasoconstrictors (epinephrine, methoxamine, phenylephrine) help to slow down the absorption of lidocaine and prolong the effect of the latter.