Instructions for use METOPROLOL
In case of 1st degree AV block, the drug is prescribed with caution, taking into account the dromotropic effect it has. In Prinzmetal's angina, beta blockers may increase the number and duration of attacks. In patients with peripheral arterial diseases, the administration of beta-blockers may lead to an exacerbation of the course of these diseases. For elderly people, the drug is prescribed with caution in low doses and under constant medical supervision with regular monitoring of kidney function indicators. In patients with non-insulin-dependent diabetes mellitus, plasma glucose levels should be monitored. If it is necessary to prescribe Metoprolol to patients with pheochromocytoma, alpha-blockers should be prescribed simultaneously. In patients with psoriasis, while taking Metoprolol, an exacerbation of the disease is possible. If you are predisposed to severe anaphylactic reactions, regardless of their origin (especially after the administration of iodinated contrast agents or during desensitizing treatment), the use of beta-blockers may lead to increased allergic reactions and to the lack of effect from the use of epinephrine in medium doses. Before conducting a radiological examination with iodinated contrast agents, treatment with Metoprolol should be discontinued in advance. In cases where the use of metoprolol is absolutely necessary and cannot be discontinued, appropriate treatment must be prescribed. When performing general anesthesia while taking beta-blockers, the risk of developing arterial hypotension increases. If surgical intervention is necessary, the anesthesiologist should be informed about the therapy being carried out in order to select an anesthetic agent with minimal negative inotropic effect, however, discontinuation of the drug before surgery in patients with coronary artery disease is not recommended. When prescribing the drug to patients with impaired renal function, periodic monitoring of heart rate is necessary. The use of the drug may mask the symptoms of hypoglycemia and thyrotoxicosis. Patients who use contact lenses should take into account that during treatment with beta-blockers, there may be a decrease in the production of tear fluid.
Effect on driving a car and working with machinery
Use with caution while working for vehicle drivers and people whose profession involves increased concentration.
Metoprolol retard-akrikhin tablet p/o film prolong. 25 mg 30 pcs
Drugs that reduce catecholamine reserves (for example, reserpine, MAO inhibitors), when used simultaneously with metoprolol, can enhance the hypotensive effect or cause severe bradycardia. The break in treatment between taking MAO inhibitors and metoprolol should be at least 14 days. Metoprolol is a substrate of the CYP2D6 isoenzyme. Medicines that inhibit or induce the activity of the CYP2D6 isoenzyme may affect the plasma concentrations of metoprolol. Inhibitors of the CYP2D6 isoenzyme: some antidepressants and antipsychotics, quinidine, terbinafine, celecoxib, propafenone, difehydramine, hydroxychlorine, cimetidine increase the concentration of metoprolol in the blood plasma. Inducers of the CYP2D6 isoenzyme: barbituric acid derivatives, rifampicin reduce the concentration of metoprolol in the blood plasma. The combined use of Metoprolol retard-Akrikhin with the following drugs should be avoided: Barbituric acid derivatives: barbiturates (the study was carried out with pentobarbital) increase the metabolism of metoprolol due to enzyme induction.
Propafenone: When propafenone was prescribed to four patients treated with metoprolol, an increase in plasma concentrations of metoprolol was observed by 2-5 times, while two patients experienced side effects characteristic of metoprolol. This interaction was confirmed in a study on 8 volunteers. The interaction is likely due to the inhibition by propafenone, like quinidine, of the metabolism of metoprolol via the CYP2D6 isoenzyme. Taking into account the fact that propafenone has beta-blocker properties, the co-administration of metoprolol and propafenone does not seem appropriate.
Verapamil: The combination of beta-blockers (atenolol, propranolol and pindolol) and verapamil can cause bradycardia and lead to a decrease in blood pressure. Verapamil and beta-blockers have a complementary inhibitory effect on atrioventricular conduction and sinus node function. The combination of Metoprolol retard-Akrikhin with the following drugs may require dose adjustment:
Amiodarone: Concomitant use of amiodarone and metoprolol may result in severe sinus bradycardia. Given the extremely long half-life of amiodarone (50 days), a possible interaction should be considered long after discontinuation of amiodarone. Class I antiarrhythmic drugs:
Class I antiarrhythmics and beta-blockers may result in additive negative inotropic effects, which can lead to serious hemodynamic side effects in patients with impaired left ventricular function. This combination should also be avoided in patients with sick sinus syndrome and impaired AV conduction. The interaction is described using disopyramide as an example.
Nonsteroidal anti-inflammatory drugs (NSAIDs): NSAIDs reduce the antihypertensive effect of beta-blockers. This interaction has been documented for indomethacin. It is likely that the described interaction will not be observed with sulindac. Negative interactions have been noted in studies with diclofenac. Diphenhydramine: Diphenhydramine reduces the clearance of metoprolol to alpha-hydroxymetoprolol by 2.5 times. At the same time, an increase in the effect of metoprolol is observed.
Diltiazem: Diltiazem and beta-blockers mutually enhance the inhibitory effect on AV conduction and sinus node function. Cases of severe bradycardia have been reported when combining metoprolol with diltiazem.
Epinephrine (adrenaline): 10 cases of severe hypertension and bradycardia have been reported in patients taking non-selective beta blockers (including pindolol and propranolol) and receiving epinephrine (adrenaline). An interaction was also noted in a group of healthy volunteers. It is assumed that similar reactions can be observed when epinephrine is used together with local anesthetics if it accidentally enters the vascular bed. It is assumed that this risk is much lower with the use of cardioselective beta-blockers.
Phenylpropanolamine: Phenylpropanolamine (norephedrine) in a single dose of 50 mg can cause an increase in diastolic blood pressure to pathological values in healthy volunteers. Propranolol mainly prevents the increase in blood pressure caused by phenylpropanolamine. However, beta-blockers may cause paradoxical hypertension reactions in patients receiving high doses of phenylpropanolamine. Several cases of hypertensive crisis have been reported while taking phenylpropanolamine. Quinidine: Quinidine inhibits the metabolism of metoprolol in a special group of patients with rapid hydroxylation (approximately 90 of the population in Sweden), causing mainly a significant increase in plasma concentrations of metoprolol and an increase in beta-blockers metabolized by the CYP2D6 isoenzyme.
Clonidine: Hypertensive reactions following abrupt discontinuation of clonidine may be exacerbated by concomitant use of beta-blockers. When used together, if clonidine is discontinued, discontinuation of beta-blockers should begin several days before discontinuation of clonidine. Rifampicin: Rifampicin may increase the metabolism of metoprolol, reducing plasma concentrations of metoprolol. Patients concomitantly taking metoprolol and other beta-blockers (eye drops) or monoamine oxidase inhibitors (MAOIs) should be closely monitored. While taking beta-blockers, inhalational anesthetics enhance the cardio-depressive effect. While taking beta-blockers, patients receiving oral hypoglycemic agents may require dose adjustment of the latter. Plasma concentrations of metoprolol may increase when taking cimetidine or hydralazine. Cardiac glycosides, when used together with beta-blockers, can increase atrioventricular conduction time and cause bradycardia. Ergot alkaloids increase the risk of peripheral circulatory disorders. When taken together with insulin - increases the risk of developing hypoglycemia, prolonging and increasing its severity, masking some symptoms of hypoglycemia (tachycardia, sweating, increased blood pressure). Reduces the clearance of xanthines (except diaphylline), especially in patients with initially increased clearance of theophylline under the influence of smoking . Reduces the clearance of lidocaine, increases the concentration of lidocaine in plasma. Strengthens and prolongs the effect of non-depolarizing muscle relaxants: prolongs the anticoagulant effect of coumarins. Allergens used for immunotherapy or allergen extracts for skin testing when used in combination with metoprolol increase the risk of systemic allergic reactions or anaphylaxis; Iodine-containing x-ray contrast agents for intravenous administration increase the risk of developing anaphylactic reactions. When used together with ethanol, the risk of a pronounced decrease in blood pressure increases.
Metoprolol, 25 mg, extended-release film-coated tablets, 30 pcs.
Co-administration of Metoprolol with the following drugs should be avoided:
Barbituric acid derivatives: barbiturates (study conducted with phenobarbital) slightly increase the metabolism of metoprolol due to enzyme induction.
Propafenone: it is possible to increase the plasma concentration of metoprolol by 2-5 times and develop side effects characteristic of metoprolol. The interaction is likely due to propafenone's inhibition, like quinidine, of the metabolism of metoprolol via the cytochrome P4502D6 system. Taking into account the fact that propafenone has the properties of a beta-blocker, the joint administration of metoprolol and propafenone does not seem appropriate.
Verapamil: The combination of beta-blockers (atenolol, propranolol and pindolol) and verapamil can cause bradycardia and lead to a decrease in blood pressure. Verapamil and β-blockers have a complementary inhibitory effect on atrioventricular conduction and sinus node function.
The combination of Metoprolol with the following drugs may require dose adjustment:
Class I Antiarrhythmics: Class I antiarrhythmics and β-blockers may result in additive negative inotropic effects, which can lead to serious hemodynamic side effects in patients with impaired left ventricular function. This combination should also be avoided in patients with sick sinus syndrome and atrioventricular conduction disorder. The interaction is described using disopyramide as an example.
Amiodarone: Concomitant use of amiodarone and metoprolol may result in severe sinus bradycardia. Given the extremely long half-life of amiodarone (50 days), a possible interaction should be considered long after discontinuation of amiodarone.
Diltiazem: Diltiazem and β-blockers mutually enhance the inhibitory effect on atrioventricular conduction and sinus node function. When metoprolol was combined with diltiazem, cases of severe bradycardia were observed.
Nonsteroidal anti-inflammatory drugs (NSAIDs): NSAIDs reduce the antihypertensive effect of beta-blockers. This interaction is best documented for indomethacin and celecoxib. There is no reported interaction observed for sulindac. In studies with diclofenac, the described reaction was not observed.
Diphenhydramine: Diphenhydramine reduces the clearance of metoprolol to α-hydroxymetoprolol by 2.5 times. At the same time, an increase in the effect of metoprolol is observed.
Epinephrine (adrenaline): Severe hypertension and bradycardia may develop in patients taking non-selective beta-blockers (including pindolol and proprapolol) and receiving epinephrine (adrenaline). It is assumed that similar reactions can be observed when epinephrine is used together with local anesthetics if it accidentally enters the vascular bed. It is assumed that this risk is much lower with the use of cardioselective beta-blockers.
Phenylpropanolamine: Phenylpropanolamine (norephedrine) in a single dose of 50 mg may cause an increase in diastolic blood pressure. Propranolol mainly prevents the increase in blood pressure caused by phenylpropanolamine. However, beta-blockers may cause paradoxical hypertension reactions in patients receiving high doses of phenylpropanolamine. It is possible to develop a hypertensive crisis while taking phenylpropanolamine.
Quinidine: Quinidine inhibits the metabolism of metoprolol in a special group of patients with rapid hydroxylation (in Sweden, approximately 90% of the population), causing mainly a significant increase in plasma concentrations of metoprolol and increased β-blockade. It is believed that a similar interaction is typical for other β-blockers in the metabolism of which cytochrome P4502D6 is involved.
Clonidine: Hypertensive reactions during abrupt withdrawal of clonidine may be exacerbated by concomitant use of beta-blockers. When used together, if clonidine is discontinued, discontinuation of β-blockers should begin several days before discontinuation of clonidine.
Rifampicin: Rifampicin may increase the metabolism of metoprolol, reducing plasma concentrations of metoprolol.
Cimetidine, hydralazine, selective serotonin reuptake inhibitors (including paroxetine, fluoxetine, sertraline) increase the concentration of metoprolol in the blood plasma.
Medicines for inhalation anesthesia enhance the cardiodepressive effect of metoprolol.
Patients concomitantly taking metoprolol and other β-blockers (eye drops) or monoamine oxidase inhibitors (MAOIs) should be closely monitored.
While taking β-blockers, inhalational anesthetics enhance the cardiodepressive effect.
While taking β-blockers, patients receiving oral hypoglycemic agents may require dose adjustment of the latter.
Cardiac glycosides, when used together with beta-blockers, can increase atrioventricular conduction time and cause bradycardia.
Allergens used for immunotherapy or allergen extracts for skin testing increase the risk of severe systemic allergic reactions or anaphylaxis in patients receiving metoprolol.
Iodine-containing radiocontrast agents for intravenous administration increase the risk of anaphylactic reactions.
Metoprolol tablets 25 mg No. 15x4
Name
Metoprolol.
Release form
Pills.
Dosage
25 mg. Quantity per package: 60 pcs.
Manufacturer
Lekpharm sooo.
INN
Metoprolol.
FTG
Beta1-adrenergic blocker selective.
Description
Tablets are white, flat-cylindrical in shape, with a bevel (dosages 25 mg and 50 mg). Tablets are white, flat-cylindrical in shape, beveled and scored (dosage 100 mg).
Compound
Each tablet contains: active substance: metoprolol tartrate – 25 mg, 50 mg or 100 mg; excipients: colloidal anhydrous silicon dioxide, microcrystalline cellulose, sodium starch glycolate (type A), talc, magnesium stearate, lactose monohydrate.
Pharmacotherapeutic group
Beta blockers. Selective beta blockers. Metoprolol. ATX code: C07A B02
Pharmacological properties
Pharmacodynamics Metoprolol is a beta-blocker. It does not have internal sympathomimetic activity. High blood pressure is reduced both in a standing and lying position. Does not cause orthostatic hypotension and does not affect the electrolyte composition of the blood. It has antianginal, antihypertensive and antiarrhythmic effects. Reduces the stimulating effect of catecholamines on the heart during physical and psychoemotional stress, leading to a decrease in heart rate, myocardial contractility, and cardiac output. In the first days of use, the drug increases peripheral vascular resistance, which normalizes or even decreases with long-term use. Reduces myocardial oxygen demand (due to a decrease in heart rate and reduced myocardial contractility), reduces the number and severity of angina attacks and increases exercise tolerance. With supraventricular tachycardia, atrial fibrillation, sinus tachycardia, functional heart disease and hyperthyroidism, it reduces heart rate and can lead to restoration of sinus rhythm. The antiarrhythmic effect is due to a decrease in the rate of spontaneous excitation of the sinus and ectopic pacemaker and a slowdown in AV conduction. Prevents the development of headaches of vascular origin. To a lesser extent than non-selective beta-blockers, it affects the release of insulin and carbohydrate metabolism, masks the symptoms of hypoglycemia in patients with diabetes, increases the content of triglycerides in the blood, reduces the content of free fatty acids and high-density lipoproteins. Pharmacokinetics Absorption and distribution After taking the drug orally, metoprolol is almost completely (approximately 95%) absorbed from the gastrointestinal tract. The maximum concentration in the blood plasma is reached after 1.5–2 hours. The bioavailability of metoprolol is approximately 50% with a single dose and approximately 70% with multiple doses. Concomitant food intake can increase the bioavailability of metoprolol by 30–40%. Plasma protein binding – 10%. Penetrates through the BBB and placental barrier, excreted in breast milk. Metoprolol is widely distributed in tissues and has a large volume of distribution (5.6 l/kg). Metabolism and excretion Metoprolol is intensively biotransformed in the liver with the formation of inactive metabolites. The plasma half-life ranges from 1 to 9 hours (average 3.5 hours). The total clearance of the drug is about 1 l/min. It is excreted mainly by the kidneys (95%), about 5% - unchanged, the rest - in the form of metabolites. Separate groups of patients There were no significant differences in the pharmacokinetics of metoprolol in elderly patients. If renal function is impaired, the excretion of metabolites decreases and the excretion of unchanged metoprolol remains virtually unchanged. In severe renal failure (GFR 5 ml/min), a significant accumulation of metabolites is observed, but the degree of beta-adrenergic blockade does not increase. Impaired liver function has little effect on the pharmacokinetics of metoprolol. However, in severe liver cirrhosis and/or after a portacaval shunt, bioavailability may increase and total clearance may decrease. After portacaval shunting, the total clearance of the drug is approximately 0.3 L/min, and the area under the concentration-time curve increases approximately 6-fold compared with healthy individuals.
Indications for use
Arterial hypertension; Angina; stable symptomatic chronic heart failure with impaired left ventricular systolic function (as an adjuvant therapy to the main treatment of chronic heart failure); reduction in mortality and recurrent infarction after the acute phase of myocardial infarction; heart rhythm disturbances, including supraventricular tachycardia, decreased ventricular contraction frequency with atrial fibrillation and ventricular extrasystoles; functional disorders of cardiac activity accompanied by tachycardia; prevention of migraine attacks; as an adjuvant for hyperthyroidism.
Directions for use and doses
The dosage is selected individually according to the symptoms of the disease. The tablets are taken orally during or after meals, without chewing and with a sufficient amount of drinking water. During dose selection, heart rate should be monitored to prevent bradycardia. The duration of the course of therapy is determined by the doctor individually and depends on the characteristics of the disease. If, after long-term use of the drug, it is necessary to stop treatment, then this should be done gradually and slowly, since sudden discontinuation of the drug can lead to a sharp increase in blood pressure. Arterial hypertension. For moderate to moderate arterial hypertension, the initial dose is 25–50 mg twice a day (morning and evening). If necessary, the daily dose can be gradually increased to 200 mg (100 mg in the morning and evening) or another antihypertensive agent can be added. Angina pectoris. The initial dose is 25–50 mg two to three times a day. Depending on the effect, this dose can be gradually increased to 200 mg per day in two divided doses or another antianginal drug can be added. Secondary prevention of myocardial infarction. The usual dose is 50–100 mg twice daily (morning and evening). Arrhythmias. The initial dose is 25–50 mg two to three times a day. If necessary, the daily dose can be gradually increased to 200 mg or another antiarrhythmic agent can be added. Hyperthyroidism. The dose should be set individually. Recommendations for use: at the beginning of treatment, 50 mg 3-4 times a day; the dose can be increased to 100 mg 3–4 times a day if the heart rate is higher than 75 beats/min after 3–4 days of treatment with the initial dose of the drug. In hyperthyroidism, the biotransformation of metoprolol is increased, so it may be necessary to use a higher dose of the drug. The drug is usually used during the period of withdrawal from another drug. Functional heart disorders accompanied by tachycardia. The usual dose is 50 mg twice daily (morning and evening); if necessary, the single dose can be increased to 100 mg, maintaining the same dosage regimen. Prevention of migraine attacks. The usual dose is 50 mg twice daily (morning and evening); if necessary, it can be increased to 100 mg per day. Special groups of patients Renal dysfunction. There is no need to change the dosage of the drug in case of impaired renal function. Liver dysfunction. For patients suffering from liver disease, metoprolol is prescribed in the same doses as for patients whose liver function is not impaired. However, in cases of significant impairment of liver function (for example, after bypass surgery), it may be necessary to reduce the dose of metoprolol. Elderly patients. No dose adjustment is required. Children. Clinical experience with metoprolol in children is limited.
Side effect
The frequency of adverse reactions listed below was determined using the following notation: very common (> 1/10), common (> 1/100 - 1/1000 - 1/10,000 -
Contraindications
Hypersensitivity to metoprolol tartrate, other beta-adrenolytic agents or any other excipients. Second or third degree atrioventricular node block. Heart failure in the stage of decompensation (pulmonary edema, circulatory disorders or hypotension) and constant or periodic use of drugs that increase myocardial contractile function (beta-adrenergic receptor agonists). Symptomatic and clinical sinus bradycardia (heart rate 0.24 seconds or systolic pressure
Overdose
Symptoms: hypotension, sinus bradycardia, atrioventricular block, heart failure, cardiogenic shock, asystole, nausea, vomiting, bronchospasm, cyanosis, hypoglycemia, loss of consciousness, coma. The symptoms listed above may increase with the simultaneous use of alcohol, antihypertensive drugs, quinidine and barbiturates. The first symptoms of an overdose appear 20 minutes to 2 hours after taking the drug. Treatment: intensive care and monitoring of the patient's vital functions (circulatory and respiratory, renal, glycemic, serum electrolytes) are necessary. If the drug was taken not too long ago, gastric lavage is mandatory; if lavage is not possible and the patient is conscious, vomiting can be induced (in the presence of medical personnel), followed by the administration of activated charcoal and an osmotic laxative. Atropine (0.25–0.5 mg IV for adults, 10–20 mcg/kg for children) should be given before gastric lavage (due to the risk of vagus nerve stimulation). For severe hypotension, bradycardia and risk of heart failure, beta1-agonists (dobutamine) should be administered intravenously at intervals of 2–5 minutes or by infusion until the desired effect is achieved. If selective beta1-agonists are not available, administer atropine or dopamine intravenously. In the absence of the desired effect, it is possible to use other adrenergic agonists (isoprenaline or norepinephrine). Administration of glucagon in doses of 1–10 mg is useful in achieving reversibility of the effects of beta-receptor blockade. In cases of severe bradycardia that are resistant to pharmacotherapy, implantation of a cardiac pacemaker may be required. Bronchospasm can be relieved by IV administration of a beta2-agonist (eg, salbutamol or terbutaline). These antidotes can be used in doses exceeding therapeutic ones. Hemodialysis is ineffective.
Use during pregnancy and lactation
Metoprolol should not be prescribed during pregnancy and breastfeeding, unless the expected benefit to the mother outweighs the potential risk to the fetus and/or child. Pregnancy Beta-adrenolytic drugs may impair placental perfusion and cause fetal death and preterm birth. Intrauterine growth retardation has been observed after long-term use of metoprolol for pregnant women with mild to moderately elevated blood pressure. Beta-adrenolytic drugs can prolong labor and cause bradycardia in the fetus and newborn. There are also reports of hypoglycemia, hypotension, increased bilirubinemia, as well as a difficult response to tissue hypoxemia in the newborn. Treatment with the drug must be interrupted 48–72 hours before the planned date of birth. When this is not possible, the newborn should be monitored for 48 to 72 hours after birth for subjective and objective symptoms of beta-adrenergic blockade (eg, cardiac and pulmonary complications). Breastfeeding The concentration of metoprolol in milk is approximately three times higher than in blood plasma. Although the risk of harm to the nursing infant following therapeutic dosage is low (except in those with slow metabolisms), the breastfed infant should be monitored for signs of beta-adrenergic blockade.
Precautions and application features
If bradycardia increases, the dose of the drug must be reduced or the drug discontinued, gradually reducing the dose. Beta-adrenolytic drugs should be used cautiously in patients with bronchial asthma. If a patient with asthma is taking a beta2-agonist drug (in the form of tablets or inhalations), then, when starting treatment with metoprolol, the dose of the beta2-agonist should be monitored and increased if necessary. Metoprolol may interfere with glycemic control in the treatment of diabetes mellitus and mask signs of hypoglycemia. In patients with non-insulin-dependent diabetes mellitus, plasma glucose levels should be monitored. Disorders of atrioventricular conduction may sometimes intensify during treatment with metoprolol (possibility of atrioventricular node blockade). Metoprolol may lead to exacerbation of peripheral arterial disease such as intermittent claudication. In Prinzmetal's angina, beta blockers may increase the number and duration of attacks. In patients with psoriasis, an exacerbation of the disease may occur while taking metoprolol. Beta-adrenolytic drugs may worsen or cause the symptoms of lichen planus. In the case when metoprolol is prescribed to patients with tumors arising from chromaffin tissue (pheochromocytoma), it is necessary to first use an alpha-adrenolytic drug and continue its use simultaneously with metoprolol. Treatment with metoprolol may mask signs of thyroid hyperfunction. When performing general anesthesia while taking beta-blockers, the risk of developing arterial hypotension increases. If surgical intervention is necessary, the anesthesiologist should be informed about the therapy being carried out in order to select an anesthetic agent with minimal negative inotropic effect, however, discontinuation of the drug before surgery in patients with coronary artery disease is not recommended. Before conducting a radiological examination with iodinated contrast agents, treatment with metoprolol should be discontinued in advance. In cases where the use of metoprolol is absolutely necessary and cannot be discontinued, appropriate treatment must be prescribed. Avoid prescribing high doses of metoprolol immediately without prior titration to patients undergoing non-cardiac surgery, as it has been associated with bradycardia, hypotension and stroke, including death, in patients with cardiovascular risk factors. Just like other beta-adrenolytic drugs, metoprolol can increase both sensitivity to allergens and intensify anaphylactic reactions. Epinephrine does not always produce the desired therapeutic result in patients treated with beta-adrenolytic drugs. Patients with severe renal impairment, severe acute conditions involving metabolic acidosis, and patients receiving combination treatment with digitalis should be given special attention. For elderly people, the drug is prescribed with caution in low doses and under constant medical supervision with regular monitoring of kidney function indicators. Patients who use contact lenses should take into account that during treatment with beta-blockers, there may be a decrease in the production of tear fluid. The drug Metoprolol contains lactose monohydrate. It should not be used in patients with rare hereditary galactose intolerance, hereditary lactase deficiency or glucose-galactose malabsorption syndrome.
Impact on the ability to drive vehicles or potentially dangerous mechanisms
Use with caution while working for vehicle drivers and people whose profession involves increased concentration. Dizziness and fatigue may occur during treatment with metoprolol, so patients should assess their response to the medication before driving or operating mechanical devices while in motion. The described symptoms may intensify if you drink alcohol at the same time or after changing medications.
Interaction with other drugs
Metoprolol is a CYP2D6 substrate, and therefore drugs that inhibit CYP2D6 (quinidine, terbinafine, paroxetine, fluoxetine, sertraline, celecoxib, propafenone and diphenhydramine) may affect the plasma concentrations of metoprolol tartrate. The combined use of Metoprolol with the following drugs should be avoided: barbituric acid derivatives. Barbiturates increase the metabolism of metoprolol due to enzyme induction. Propaphenone. When propafenone was prescribed to four patients treated with metoprolol, an increase in plasma concentrations of metoprolol was observed by 2-5 times, while two patients experienced side effects characteristic of metoprolol. This interaction was confirmed in a study on 8 volunteers. The interaction is likely due to propafenone's inhibition, like quinidine, of the metabolism of metoprolol via the cytochrome P4502D6 system. Taking into account the fact that propafenone has beta-blocker properties, the co-administration of metoprolol and propafenone does not seem appropriate. Verapamil. The combination of beta-blockers (atenolol, propranolol and pindolol) and verapamil can cause bradycardia and lead to a decrease in blood pressure. Verapamil and beta-blockers have a complementary inhibitory effect on atrioventricular conduction and sinus node function. The combination of Metoprolol with the following drugs may require dose adjustment of Amiodarone. The combined use of amiodarone and metoprolol can lead to severe sinus bradycardia. Given the extremely long half-life of amiodarone (50 days), a possible interaction should be considered long after discontinuation of amiodarone. Class I antiarrhythmic drugs. Class I antiarrhythmics and beta-blockers may result in additive negative inotropic effects, which can lead to serious hemodynamic side effects in patients with impaired left ventricular function. This combination should also be avoided in patients with sick sinus syndrome and impaired AV conduction. The interaction is described using disopyramide as an example. Nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs weaken the antihypertensive effect of beta-blockers. Studies have focused primarily on indomethacin. This effect will not occur when interacting with sulindac. In studies with diclofenac, no such interaction was found. Diphenhydramine. Diphenhydramine reduces the clearance of metoprolol to α-hydroxymetoprolol by 2.5 times. At the same time, an increase in the effect of metoprolol is observed. Diltiazem: Diltiazem and beta-blockers mutually enhance the inhibitory effect on AV conduction and sinus node function. When metoprolol was combined with diltiazem, cases of severe bradycardia were observed. Epinephrine. Ten cases of severe hypertension and bradycardia have been reported in patients taking non-selective beta blockers (including pindolol and propranolol) and receiving epinephrine. The interaction was also observed in the group of healthy volunteers. It is assumed that similar reactions can be observed when epinephrine is used together with local anesthetics if it accidentally enters the vascular bed. It is assumed that this risk is much lower with the use of cardioselective beta-blockers. Phenylpropanolamine. Phenylpropanolamine (norephedrine) in a single dose of 50 mg can cause an increase in diastolic blood pressure to pathological values in healthy volunteers. Propranolol mainly prevents the increase in blood pressure caused by phenylpropanolamine. However, beta-blockers may cause paradoxical hypertension reactions in patients receiving high doses of phenylpropanolamine. Several cases of hypertensive crisis have been reported while taking phenylpropanolamine. Quinidine. Quinidine inhibits the metabolism of metoprolol in a special group of patients with rapid hydroxylation, mainly causing a significant increase in plasma concentrations of metoprolol and increased beta blockade. It is believed that a similar interaction is typical for other beta-blockers, the metabolism of which involves cytochrome P4502D6. Clonidine. Hypertensive reactions during abrupt withdrawal of clonidine may be exacerbated by concomitant use of beta-blockers. When used together, if clonidine is discontinued, discontinuation of beta-blockers should begin several days before discontinuation of clonidine. Rifampicin. Rifampicin may increase the metabolism of metoprolol, reducing plasma concentrations of metoprolol. Patients concomitantly taking metoprolol and other beta-blockers (eye drops) or monoamine oxidase inhibitors should be closely monitored. While taking beta-blockers, inhalational anesthetics enhance the cardiodepressive effect. While taking beta-blockers, patients receiving oral hypoglycemic agents may require dose adjustment of the latter. Plasma concentrations of metoprolol may increase when taking cimetidine or hydralazine. Cardiac glycosides, when used together with beta-blockers, can increase atrioventricular conduction time and cause bradycardia. Metoprolol may cause a decrease in the elimination of other drugs (eg lidocaine).
Storage conditions
In a place protected from moisture and light at a temperature not exceeding 25 °C. Keep out of the reach of children.
Best before date
2 years. Do not use after the expiration date stated on the packaging.
Package
10 tablets with a dosage of 25 mg, 50 mg and 100 mg in a blister pack made of polyvinyl chloride film and aluminum foil. Three blister packs for dosages of 50 mg and 100 mg, six blister packs for dosages of 25 mg and 50 mg along with instructions for use in a cardboard pack.
Release from pharmacies
By doctor's prescription.
Buy Metoprolol tablets 25 mg No. 15x4 in a pharmacy
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