What Is Metoprolol Succinate?

Physical and chemical properties of Metoprolol succinate (English name: Metoprolol succinate): white or almost white crystalline powder API for the treatment of angina pectoris and hypertension. Metoprolol is a selective 1 receptor blocker and is one of the commonly used drugs for the treatment of hypertension, chronic heart failure and coronary heart disease.

Metoprolol succinate

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Physical and chemical properties of Metoprolol succinate (English name: Metoprolol succinate): white or almost white crystalline powder API for the treatment of angina pectoris and hypertension.

Chinese name: metoprolol succinate

Chinese alias: 1-isopropylamino-3- [p- (2-methoxyethyl)

Chemical composition of metoprolol succinate

Metoprolol succinate.

Indications of metoprolol succinate

hypertension. Angina pectoris. Chronic heart failure with stable symptoms of left ventricular systolic dysfunction.

Pharmacological effects of metoprolol succinate

Metoprolol is a selective 1 receptor blocker, which requires a lower dose of 1 receptor on the heart than the dose of 2 receptor on the peripheral blood vessels and bronchus. The selectivity of metoprolol succinate is dose-dependent. Because the peak plasma concentration of the sustained-release tablets is significantly lower than that of ordinary flat tablets of the same dose, this dosage form has a relatively higher 1 receptor selectivity. Metoprolol has no beta receptor agonism and almost no membrane activation. Beta blockers have a negative inotropic and time-varying effect. Metoprolol treatment can reduce the effects of catecholamines related to physiological and psychological load, reducing heart rate, cardiac output and blood pressure. Under stress, the adrenaline secreted by the adrenal glands increases, and metoprolol does not hinder physiological vasodilation. At the therapeutic dose, metoprolol has a weaker contraction effect on bronchial smooth muscle than non-selective beta blockers. This feature makes it possible to use it in combination with beta 2 agonists to treat bronchial asthma or other obvious obstructions. With pulmonary disease. The effect of metoprolol on insulin release and glucose metabolism is less than that of non-selective beta blockers, so it can be used in patients with diabetes. Compared with non-selective beta-blockers, metoprolol has a lesser effect on the cardiovascular response to hypoglycemia, such as tachycardia, and the blood glucose returns to normal levels faster. For patients with hypertension, metoprolol succinate can significantly reduce blood pressure in the upright, supine, and exercise positions, and the effect lasts for more than 24 hours. An increase in peripheral vascular resistance was observed at the beginning of metoprolol treatment; however, the decrease in blood pressure obtained with long-term treatment may be due to a decrease in peripheral vascular resistance and constant cardiac output. For men with moderate / severe hypertension, metoprolol reduces the risk of cardiovascular death. Metoprolol does not cause electrolyte disturbances. Effect on chronic heart failure: In a study involving 3991 heart failure patients with NYHA class -IV heart function and decreased ejection fraction (0.40) (called MERIT-HF), metoprolol succinate Increase survival and reduce the number of hospital admissions. Improved overall symptoms in patients receiving long-term treatment (New York Heart Association rating and overall treatment assessment score). In addition, metoprolol succinate can increase ejection fraction and decrease end-systolic and end-diastolic volume of left ventricle. For patients with tachyarrhythmia, this product can block the effect of increased sympathetic nerve activity and slow the heart rate. This is mainly through reducing the autonomy of the pacing cells and extending the time of supraventricular conduction. In patients after myocardial infarction, metoprolol can reduce the risk of another myocardial infarction and reduce the risk of cardiac death, especially sudden death after myocardial infarction.

Metoprolol succinate drug interactions

This product should be avoided in combination with the following drugs: Barbiturates: Barbiturates (researched on pentobarbital) can increase the metabolism of metoprolol through enzyme induction. Propafenone: In 4 patients who have been treated with metoprolol, the plasma concentration of metoprolol increased 2 to 5 times after the administration of propafenone, of which 2 patients had side effects related to metoprolol. This interaction was confirmed in 8 healthy volunteers. A possible explanation for this interaction is that propafenone is similar to quinidine and inhibits metoprolol metabolism through the cytochrome P4502D6 pathway. Since propafenone also has a b-blocker effect, its combined use with metoprolol is difficult to grasp. Verapamil: When Verapamil is used in combination with b-blockers (it has been reported in combination with atenolol, propranolol, and indololol), it may cause bradycardia and lower blood pressure. Verapamil and b-blockers have additive inhibitory effects on atrioventricular conduction and sinus node function. This product may require dose adjustment when used in combination with the following drugs: Amiodarone: One case report shows that when using amiodarone and metoprolol, significant sinus bradycardia may occur. Amiodarone has a long half-life (approximately 50 days), which means that the use of metoprolol may still cause interactions between the two drugs for a long period of time after amiodarone treatment is stopped. Class I antiarrhythmic drugs: Class I antiarrhythmic drugs have a negative inotropic effect with b-blockers, so they may cause severe hemodynamics in patients with impaired left ventricular function side effect. Patients with sick sinus node syndrome and pathological atrioventricular block should also avoid the simultaneous use of metoprolol and Class I antiarrhythmic drugs. There is clear data on the interaction between propiamine and metoprolol. Non-steroidal anti-inflammatory / anti-rheumatic drugs (NSAID): NSAID anti-inflammatory analgesics have been found to counteract the antihypertensive effects of beta blockers. In this regard, the drugs studied are mainly indomethacin. B-blockers are likely not to interact with sulindac. In a study of diclofenac, no b-blockers were found to interact with diclofenac. Diphenhydramine: In a rapidly hydroxylated population, diphenhydramine reduces the clearance of metoprolol through CYP2D6 to alpha-hydroxymetolol by 2.5 times. The role of metoprolol is thus enhanced. Diphenhydramine may inhibit the metabolism of other CYP2D6 substrates. Diltiazem: Calcium antagonists and b-blockers have additive inhibitory effects on atrioventricular conduction and sinus node function. Significant bradycardia has been reported when b-blockers are used in combination with diltiazem. Adrenaline: Approximately 10 reports have shown that patients receiving non-selective b-blockers (including indolol and propranolol) develop significant hypertension and bradycardia after adrenaline administration . These clinical observations have been confirmed in studies on healthy volunteers. Adrenaline in local anesthetics may cause this response when administered intravascularly. Presumably, the risk of this response is lower when using a cardiac selective b-blocker. Phenylpropanolamine: A single dose of 50mg of phenylpropanolamine can increase the diastolic blood pressure of healthy volunteers to pathological levels. Propranolol usually antagonizes this increase in blood pressure caused by phenylpropanolamine. However, in patients receiving high-dose phenylpropanolamine, b-blockers can abnormally cause hypertension. Hypertension reactions have also been reported during phenylpropanolamine treatment alone. Quinidine: Quinidine can inhibit the metabolism of metoprolol in so-called "rapid hydroxylators" (more than 90% of this type in Sweden), resulting in a significant increase in the latter's plasma concentration and b-receptor blockade. Stagnation effect is enhanced. Other b-blockers that metabolize via the same enzymatic pathway (cytochrome P4502D6) may also interact with quinidine. Clonidine: b-blockers may aggravate the rebound hypertension that occurs when clonidine is suddenly discontinued: rifampicin can induce the metabolism of metoprolol, leading to a decrease in the plasma concentration of the latter . When combined with cimetidine, hydralazine, and selective serotonin reuptake inhibitors (SSRIs) such as paroxetine, fluoxetine, and sertraline, plasma levels of metoprolol increase. Patients receiving other beta-blockers (eg, eye drops) or monoamine oxidase (MAO) inhibitors should be closely monitored. In patients receiving b-blockers, inhaled anesthesia increases cardiac suppression. YCZ has 2 children, N

Metoprolol succinate overdose

Toxicity: Metoprolol 7.5g causes fatal poisoning in adults. A 5-year-old child took 100mg by mistake and had no symptoms after gastric lavage. A 12-year-old child was given 450 mg to cause moderate poisoning, an adult was given 1.4 g to cause moderate poisoning, 2.5 g to cause severe poisoning, and 7.5 g to cause extremely severe poisoning. Symptoms: Symptoms of the cardiovascular system are most pronounced, but in some cases, especially children and young patients, central nervous system symptoms and respiratory depression may be the main manifestations. The main symptoms of poisoning are bradycardia, I-III degree atrioventricular block, cardiac arrest, decreased blood pressure, poor peripheral circulation perfusion, cardiac insufficiency, cardiogenic shock, respiratory depression and asphyxia. Other symptoms include fatigue, confusion, loss of mind, frequent tremors, cramps, sweating, paresthesia, bronchospasm, nausea, vomiting, possible esophageal spasm, hypoglycemia (especially in children), or hyperglycemia, high potassium Bloodemia, effects on the kidneys, and transient weakness syndrome. Treatment: Those with a clear diagnosis are given gastric lavage and activated carbon, and closely observe the changes in the condition. note! In order to reduce the risk of vagus nerve stimulation, atropine should be given intravenously (0.25 to 0.5 mg for adults and 10 to 20 mg / kg for children) before gastric lavage. When indicated, perform endotracheal intubation and respiratory support. Appropriate volume replacement therapy, glucose infusion, and ECG monitoring. Atropine is 1.0-2.0 mg intravenously and can be repeated if necessary (mainly controlling vagus nerve symptoms). For patients with myocardial function inhibition, dobutamine or dopamine, calcium glucuronate (9mg / ml) 10-20ml can be instilled. Another alternative method is glucagon 50-150mg / kg, intravenous injection within 1 minute, followed by intravenous drip, or amrinone. Epinephrine is effective in some patients. Patients with widened QRS waves and arrhythmias can be infused with sodium chloride or sodium bicarbonate. A pacemaker may need to be installed. For patients with cardiac arrest, sometimes several hours of resuscitation are needed. When treating bronchospasm, terbutaline (injection or inhalation) can be used. In addition, symptomatic treatment is performed. ^[1-2]