Lidocaine ampoules 2% 2 ml. №10


Manufacturer: Ukraine

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



Lidocaine ampoules Composition
Active ingredient: lidocaine, 1 ml of solution contains lidocaine hydrochloride in terms of 100% anhydrous substance 20 mg.

Excipients: sodium chloride, 1 M sodium hydroxide solution, water for injection.

Lidocaine ampoules Dosage form

Basic physical and chemical properties: transparent, colorless or slightly colored liquid.

Lidocaine ampoules Release form
2 ml in an ampoule; 10 ampoules per pack.
Active substance

The mechanism of the local anesthetic action of lidocaine is to stabilize the neuronal membrane by reducing its permeability to sodium ions, which prevents the emergence of an action potential and the conduction of impulses by nerve fibers. Antagonism with calcium ions is possible. Suppresses the conduction of not only pain impulses, but also impulses of a different modality. It is rapidly hydrolyzed in a weakly alkaline environment of tissues and after a short latency period it acts for 60-90 minutes. The anesthetic effect of lidocaine is 2-6 times stronger than procaine. When applied topically, it dilates blood vessels, does not have a local irritating effect. With inflammation (tissue acidosis), the anesthetic activity decreases. Effective for all types of local anesthesia. Expands blood vessels. Does not irritate fabrics.

In addition to the main local anesthetic effect, it has an antiarrhythmic effect. Antiarrhythmic activity is due to the inhibition of phase 4 (diastolic depolarization) in Purkin’s fibers, a decrease in automatism, and suppression of ectopic foci of arousal. The rate of rapid depolarization (phase 0) is not affected or slightly reduced. Increases the permeability of membranes for potassium ions, accelerates the repolarization process and shortens the action potential. When used in moderate therapeutic doses, it does not change the excitability of the sinus-atrial node, has little effect on the conductivity and contractility of the myocardium. When administered intravenously, it acts quickly and shortly (10-20 minutes).
With intravenous administration, the maximum concentration in the blood (Cmax) is reached practically at the moment of administration (“on the needle”) and is 45-90 s, with intramuscular administration – after 5-15 minutes.

Distribution. In plasma, it binds to proteins by 50-80%. Plasma protein binding of lidocaine is highly dependent on the concentration of the drug and alpha-1-acid glycoprotein (AAG) in plasma. Plasma protein binding increases in patients with uremia and renal transplant recipients and increases after acute myocardial infarction, characterized by an increase in AAG levels. High protein binding can reduce the effect of free lidocaine or cause a general increase in the concentration of the drug in the blood plasma.

A stable concentration in the blood is established after 3-4 hours with continuous intravenous administration (in patients with acute myocardial infarction – after 8-10 hours). The therapeutic effect develops at a concentration of 1.5-5 μg / ml. The distribution is fast, the volume of distribution is 1 l / kg. Easily penetrates histohematogenous barriers, including the BBB. First, it enters tissues with a high rate of blood supply: heart, brain, kidneys, lungs, liver, spleen. Then – into adipose and muscle tissue. Penetrates through the placenta, 40-55% of the concentration of the drug in the mother’s body is found in the newborn’s body.

Metabolism. Lidocaine is metabolized with the participation of liver microsomal enzymes. The metabolic rate is determined by the blood flow in the liver and, as a result, can be impaired in patients after myocardial infarction and / or congestive heart failure. As a result of biotransformation, lidocaine metabolites are formed – monoethyl-glcinexylidide (MEGKS) and glicinexylidide, which have a much less pronounced antiarrhythmic activity.

Output. About 90% is excreted in the form of metabolites and 10% – unchanged by the kidneys. Excretion of unchanged drug in the urine depends in part on the ph of the urine. Acidic urine leads to an increase in the proportion excreted in the urine.

The half-life (T1 / 2) after an intravenous bolus is 1.5-2 hours (in newborns – 3 hours). With intravenous infusion – up to 3 hours or more. Metabolites have a T1 / 2 of 2 hours and 10 hours, respectively.

Conclusion in special conditions. In case of impaired liver function, T1 / 2 may increase 2 times or more.
All types of conduction anesthesia: including in dentistry, intercostal block, cervical vagosympathetic block. Intravenous regional anesthesia. Caudal or lumbar epidural block.

Ventricular premature beats and tachyarrhythmias, including in acute myocardial infarction, in the postoperative period.
Hypersensitivity to the components of the drug, as well as to other amide local anesthetic drugs.

Severe bleeding, infection of the site of the intended injection.

Diseases of the cardiovascular system:

– WPW syndrome;

– AV block II and III degree and intraventricular conduction disorders;

– Morgagni-Adams-Stokes syndrome;

– severe bradycardia;

– weakness syndrome with