Aritmil (amiodarone hydrochloride) solution for injections 50 mg. 3 ml. ampoules N5

Description

INSTRUCTIONS for the medical use of Aritmil (amiodarone)

Ingredients:

active substance: amiodarone hydrochloride;

1 ml of the drug contains 50 mg of amiodarone hydrochloride;

auxiliary substances: polysorbate 80, benzyl alcohol, water for injections.

Medicinal form. Solution for injections.

Main physico-chemical properties: transparent liquid of light yellow color with a greenish tint or liquid of light yellow color, free of particles.

Pharmacotherapeutic group.

Class III antiarrhythmic drugs. ATX code C01B D01.

Pharmacological properties.

Pharmacodynamics.

Class III antiarrhythmic drug. The antiarrhythmic effect is due to an increase in the 3rd phase of the action potential mainly due to the blockade of potassium channels of cardiomyocyte membranes, as well as calcium channels, slowing down the conduction through the AV node and reducing the automatism of the sinus node. Blocks open and inactivated sodium channels to a small extent and slows the fast sodium influx. The drug non-competitively blocks alpha- and beta-adrenoceptors mainly of the myocardium, which also contributes to the slowing down of sinoatrial, atrial and AV conduction, without affecting intraventricular conduction. Amiodarone increases the refractory period and reduces myocardial excitability. It slows down the conduction of excitation and lengthens the refractory period of additional atrioventricular pathways. The antianginal effect of amiodarone is due to a decrease in oxygen consumption by the myocardium due to a decrease in the heart rate and a decrease in the total peripheral vascular resistance. Amiodarone does not cause a significant negative inotropic effect.

Pharmacokinetics.

Amiodarone has a large volume of distribution. In the first days of the appointment, it accumulates in almost all tissues, especially in adipose tissue, liver, spleen, lungs. The degree of binding to blood plasma proteins is high and is > 95%. The amount of intravenously administered amiodarone in the blood quickly decreases due to tissue saturation and its binding to receptors. The maximum activity is reached after 15 minutes and decreases during 4 hours.

Penetrates through the placental barrier and into breast milk. The half-life of amiodarone is highly variable and is 20-100 days. Metabolized in the liver. Amiodarone contains iodine, during metabolism in the liver iodine is split off and excreted in the urine in the form of salts. Renal excretion of amiodarone is insignificant. The main part of amiodarone and its metabolites is excreted through the intestine. After discontinuation of amiodarone treatment, its elimination from the body continues for several months, and its effective action lasts for several days or even weeks.

Indications.

Severe heart rhythm disturbances, when treatment with oral amiodarone is inappropriate, in particular such as:

• atrial arrhythmia with a high frequency of ventricular contractions;
• achycardia associated with Wolff-Parkinson-White syndrome;
• documented symptomatic ventricular arrhythmia leading to incapacity.
• Cardiopulmonary resuscitation in cardiac arrest due to ventricular fibrillation that is resistant to external electrical impulse therapy.

Contraindications.

• Hypersensitivity to iodine and/or amiodarone, to other components of Aritmil (amiodarone);
• sinus bradycardia (< 50-55 contractions/min), sinoatrial blockade, sinus node weakness syndrome in the absence of an artificial pacemaker (danger of sinus node arrest);
• severe conduction disturbances (II and III degree AV blockade, bifascicular or trifascicular blockade) in the absence of an artificial pacemaker;
• circulatory collapse, severe arterial hypotension, cardiomyopathy, decompensated heart failure, severe respiratory failure are contraindications for the introduction of Aritmil (amiodarone) in the form of an intravenous bolus injection (a sharp deterioration of the patient’s condition is possible);
• dysfunction of the thyroid gland (hypothyroidism, hyperthyroidism). Before starting treatment, it is advisable to check the function of the thyroid gland in all patients;
• simultaneous use with drugs that can cause polymorphic ventricular tachycardia of the “torsade de pointes” type:

1. 1. class Ia antiarrhythmic drugs (quinidine, hydroquinidine, disopyramide);
   2. class III antiarrhythmic drugs (sotalol, dofetilide, ibutilide);
   3. other drugs such as arsenic compounds, bepridil, cisapride, diphemanil, dolasetron IV, domperidone, dronedarone, prucalopride, erythromycin (intravenous), mizolastine, moxifloxacin, levofloxacin, mequitazine, mizolastine, citalopram, escitalopram, spiramycin (intravenous) , vincamine (intravenous), toremifene, some antipsychotics;
   4. telaprevir;
   5. cobicistat