Lidocaine bufus, 100 mg/ml 2 ml 10 pcs

It has antiarrhythmic (class Ib) action. Stabilizes cell membranes, blocks sodium channels, increases membrane permeability to potassium ions.

With almost no effect on the electrophysiological state of the atria, lidocaine accelerates repolarization in the ventricles, inhibits phase IV depolarization in Purkinje fibers (especially in ischemic myocardium), reducing their automaticity and duration of action potential, increases the minimum potential difference at which myofibrils respond to premature stimulation.

Shortens the duration of the action potential and the effective refractory period. It has no significant effect on myocardial conduction and contractility (suppression of conduction is observed only when administered in large doses, close to toxic) – the duration of intervals PQ , QT and the width of the QRS complex on the electrocardiogram does not change. Negative inotropic effect is also expressed insignificantly and appears transiently only when administered in high doses.

Pharmacokinetics

Absorption

The main factor determining the absorption rate and concentration in the blood is the total dose administered, regardless of the site of administration. There is a linear relationship between the amount of lidocaine administered and the resulting maximum concentration of the drug in the blood.

Distribution

Lidocaine binds to plasma proteins, including α1-acid glycoprotein (ACG) and albumin. The degree of binding is variable and is approximately 66%. Plasma concentration of AKG in newborns is low, so they have relatively high content of free bioactive fraction of lidocaine.
Lidocaine penetrates through the blood-brain and placental barriers, probably by passive diffusion.

Metabolism

Lidocaine is metabolized in the liver, with about 90% of the administered dose undergoing N-dealkylation to form monoethylglycincylidide (MEGX) and glycincylidide (GX), both contributing to the therapeutic and toxic effects of lidocaine. The pharmacological and toxic effects of MEGX and GX are comparable to those of lidocaine, but are weaker. GX has a longer half-life than lidocaine (about 10 hours) and may cumulate with repeated administration.

Metabolites resulting from subsequent metabolism are excreted with urine, the content of unchanged lidocaine in urine does not exceed 10%.

Excretion

The terminal elimination half-life of lidocaine after intravenous bolus injection in healthy adult volunteers is 1-2 hours. The terminal half-life of GX is approximately 10 hours, MEGX 2 hours.

Special patient groups

Due to rapid metabolism, the pharmacokinetics of lidocaine may be affected by conditions that impair hepatic function. In patients with hepatic dysfunction, the elimination half-life of lidocaine may increase two or more times.

Impaired renal function does not affect the pharmacokinetics of lidocaine, but may lead to cumulation of its metabolites.

Newborns have a low concentration of ACG, so binding to plasma proteins may be reduced. Due to the potentially high concentration of the free fraction, the use of lidocaine in neonates is not recommended.

Indications

Active ingredient

Composition

How to take, the dosage

Interaction

It is undesirable to combine lidocaine with the following drugs:
With beta-adrenoblockers because of increased toxic properties of lidocaine, with digitoxin because of weakened cardiotonic effect, with curare-like drugs – increased muscle relaxation.

Lidocaine should not be administered together with aymalin, amiodarone, verapamil or quinidine due to increased cardiodepressant effect.
Concomitant use of lidocaine and novocainamide may cause CNS agitation and hallucinations.

In intravenous administration of hexenal or thiopental sodium with lidocaine may cause respiratory depression.

MoA inhibitors may increase the local anesthetic effect of lidocaine. Patients taking MAO inhibitors should not administer lidocaine parenterally.

The simultaneous administration of lidocaine and polymyxin-B may increase the inhibitory effect on neuromuscular transmission, so the respiratory function of the patient should be monitored in this case.

The simultaneous use of lidocaine with hypnotics or sedatives may increase their CNS depressant effect. When lidocaine is administered intravenously to patients taking cimetidine such unwanted effects as stunned state, somnolence, bradycardia, parasthesias and others are possible. This is associated with increased plasma levels of lidocaine, which is explained by the release of lidocaine from bonding with blood proteins, as well as a slowdown of its inactivation in the liver. If combination therapy with these drugs is necessary, the dose of lidocaine should be reduced.

Pharmaceutical interaction
When used concomitantly, the following drugs increase the concentration of lidocaine in blood serum: aminazin, cimetidine, propranolol, pethidine, bupivacaine, quinidine, disopyramide, amitriptyline, imipramine, nortriptyline.

Special Instructions

Contraindications

Side effects

Overdose

Pregnancy use

Similarities