Side effects of beta 1 blockers. Beta-blockers: principles of therapy from the standpoint of evidence-based medicine

Mechanism of action of beta-blockers

The effects of beta-blockers are realized by the blockade of β1 and β2-adrenergic receptors. There are two types of β-adrenergic receptors (β1- and β2-adrenergic receptors), which differ in structural and functional features and distribution in tissues. β1-adrenergic receptors dominate in the structures of the heart, islet tissue of the pancreas, juxtaglomerular apparatus of the kidneys, adipocytes.

Drugs, by binding to β1-adrenergic receptors of the heart, prevent the action of noradrenaline, adrenaline on them, reduce the activity of adenylate cyclase. A decrease in enzyme activity leads to a decrease in cAMP synthesis and inhibition of Ca2+ entry into cardiomyocytes. Thus, the main effects of β-blockers are realized:

• negative inotropic effect (the force of heart contractions decreases);
• negative chronotropic effect(decrease in heart rate)
• negative dromotropic effect (conductivity is suppressed);
• negative bathmotropic effect (automatism decreases).

The antianginal effect of drugs is manifested by a decrease in the strength of heart contractions and heart rate, which reduces myocardial oxygen demand.

Due to the inhibition of conduction and automatism, the drugs have an antiarrhythmic effect.

A decrease in Ca2+ content due to blockade of β1-adrenergic receptors in the cells of the juxtal merular apparatus (JGA) of the kidneys is accompanied by inhibition of renin secretion, and, accordingly, a decrease in the formation of angiotensin II, which leads to a decrease in blood pressure and determines the effectiveness of β-blockers as antihypertensive drugs.

Blockade β2-blockers contributes to the increase:

• bronchial smooth muscle tone;
• contractile activity of the pregnant uterus;
• reduction of smooth muscle cells of the gastrointestinal tract (manifested by abdominal pain, vomiting, nausea, diarrhea, much less often constipation).

In addition, narrowing of arterioles and venules causes an increase in peripheral vascular resistance and can impair blood supply to the extremities up to the development of Raynaud's syndrome.

β-blockers cause changes in lipid and carbohydrate metabolism. They inhibit lipolysis, prevent an increase in the content of free fatty acids in the blood plasma, while the content of TG increases, and the concentration of total cholesterol does not change, the content of HDL cholesterol decreases, LDL cholesterol increases, which leads to an increase in the atherogenic coefficient.

β-blockers cause activation of the synthesis of glycogen from glucose in the liver and inhibit glycogenolysis, which can lead to hypoglycemia, especially against the background of the use of hypoglycemic drugs in patients diabetes. Due to blockade of beta-blockers in the pancreas and inhibition of physiological secretion of insulin, drugs can cause hyperglycemia, however, in healthy people they usually do not affect the concentration of glucose in the blood.

According to their effect on receptors, beta-blockers are divided into non-selective (affecting β1- and β2-adrenergic receptors) and cardioselective (affecting β1-adrenergic receptors), in addition, some of them have internal sympathomimetic activity (ICA).

Beta-blockers with ICA (pindolol, Bopindolol, oxprenolol) reduce heart rate and myocardial contractility to a lesser extent, practically do not affect lipid metabolism, they have a less pronounced withdrawal syndrome.

The vasodilating effect of beta-blockers is due to one of the following mechanisms or a combination of them:

• pronounced ICA in relation to β-blockers of vessels (for example, pindolol, celiprolol);
• a combination of β- and α-adrenergic blocking activity (for example, carvedilol);
• release of nitric oxide from endothelial cells (nebivolol);
• direct vasodilatory effect.

Cardioselective beta-blockers in low doses, unlike non-selective ones, have little effect on bronchial and arterial tone, insulin secretion, glucose mobilization from the liver, and contractile activity of the pregnant uterus, so they can be prescribed for concomitant chronic obstructive pulmonary diseases, diabetes mellitus, and peripheral circulatory disorders ( e.g. Raynaud's syndrome, pregnancy). They practically do not cause vasoconstriction of skeletal muscles, therefore, when using them, increased fatigue and muscle weakness are less likely to be noted.

Pharmacokinetics of beta-blockers

The pharmacokinetic action of various beta-blockers is determined by the degree of their solubility in fats and water. There are three groups of beta-blockers:

• fat-soluble (lipophilic),
• water-soluble (hydrophilic),
• fat and water soluble.

Lipophilic beta-blockers (metoprolol, alprenolol, oxprenolol, propranolol, timolol) are rapidly absorbed in the gastrointestinal tract, easily penetrate the BBB (often cause such side effects like insomnia, general weakness, drowsiness, depression, hallucinations, nightmares). Therefore, single doses and frequency of administration should be reduced in elderly patients, with diseases nervous system. Lipophilic beta-blockers can slow down the elimination from the blood of other drugs that are metabolized in the liver (for example, lidocaine, hydrolasine, theophylline). Lipophilic β-blockers should be prescribed at least 2-3 times a day.

Hydrophilic beta-blockers (atenolol, nadolol, sotalol) are not completely (30-70%) absorbed in the gastrointestinal tract and are slightly (0-20%) metabolized in the liver. Excreted mainly by the kidneys. They have a long half-life (6-24 years). T1 / 2 of hydrophilic drugs increases with a decrease in glomerular filtration rate (for example, with renal failure, in elderly patients). The frequency of application varies from 1 to 4 times a day.

There are beta-blockers that are soluble in fats and water (acebutolol, pindolol, celiprolol, bisoprolol). They have two routes of elimination - hepatic (40-60%) and renal. Fat and water-soluble drugs can be prescribed 1 time per day, with the exception of Pindolol: it is taken 2-3 times. T1 / 2 is 3-12 hours. Most drugs (bisoprolol, pindolol, celiprolol) practically do not interact with drugs that are metabolized in the liver, so they can be prescribed in patients with moderate hepatic or kidney failure(at severe violations functions of the liver and kidneys, the dose of the drug is recommended to be reduced by 1.5 times).

Pharmacokinetic parameters of beta-blockers:

*Note: ? - no data found

Indications for the use of beta-blockers

• angina pectoris,
• acute coronary syndrome,
• AG and primary prevention stroke and ischemic heart disease in patients with hypertension,
• prevention of ventricular and supraventricular arrhythmias,
• prevention of recurrent myocardial infarction,
• prevention of sudden death in patients with long QT syndrome,
• chronic heart failure (carvedilol, metoprolol, bisoprolol, nebivolol),
• systemic diseases with increased influence of the sympathetic nervous system,
• thyrotoxicosis,
• essential tremor,
• alcohol withdrawal,
• dissecting aortic aneurysm,
• hypertrophic cardiomyopathy,
• digitalis intoxication,
• mitral stenosis (tachysystolic form),
• mitral valve prolapse,
• Fallot's tetrad.

Side effects and contraindications of beta-blockers

The main side effects and contraindications of beta-blockers are presented in the table.

Side effects of beta-blockers, contraindications to their use and conditions requiring special care when using beta-blockers:

For β-blockers, withdrawal syndrome is characteristic.

Drug Interactions

The combination of beta-blockers with other drugs exhibits a negative foreign and chronotropic effect, can lead to severe adverse reactions. With the combination of β-blockers with clonidine, a pronounced decrease in blood pressure and bradycardia develops, especially in the horizontal position of patients.

The combination of the appointment of beta-blockers with verapamil, amiodarone, cardiac glycosides can lead to severe bradycardia and AV conduction disturbances.

The combination of beta-blockers with nitrates or calcium channel blockers is justified, since the former reduce myocardial oxygen demand, while others, by reducing the tone of peripheral and coronary vessels, provide hemodynamic unloading of the myocardium and increase coronary blood flow.

Drugs that have the effect of stimulating beta-adrenergic systems are a group of drugs called.

Adrenoblockers were officially recognized and introduced into medical practice in the middle of the twentieth century.

Since then, this class of antiadrenergic substances has been widely and successfully used as antihypertensive, antianginal and other drugs.

However, the features of the pharmacological activity of beta-blockers cause a number of restrictions in their appointment due to the presence of contraindications and the possibility of side effects.

Adrenolytics block the process of nerve impulse transmission by binding to adrenoreceptors instead of catecholamines.

Beta-blockers specifically inhibit the effects of sympathetic nerve impulses and sympathomimetic substances on beta-adrenergic receptors.

Due to the chemical structure, the binding of beta-blockers to receptors causes not a stimulating, but an inhibitory effect.

The totality of physico-chemical properties different drugs from this group provides different features of influence. Beta-blockers are antagonists, when interacting with receptors, they produce an inhibitory effect.

A number of substances combine an antagonistic action with an agonistic one, additionally exerting some stimulating effect. Antagonists slow down heart rate, weaken the force of heart contractions, inhibit automatism and slow down conduction due to the blockade of nerve transmission.

Cardioselective beta-blocker Atenolol

A drug with a joint effect will not affect or even slightly increase it. These drugs differ in the selectivity of their effects on beta 1- or beta 2-adrenergic receptors.

Drugs that specifically bind beta 1 receptors of the heart muscle are considered cardioselective (,).

Others simultaneously act on both types of receptors - cardiac beta 1-adrenergic receptors and beta 2-adrenergic receptors of the bronchi, pancreas, small vessels (Propranolol), due to which the development of bronchospasm may be a concomitant result of exposure to non-selective blockers.

There are drugs with a combined effect on both types of adrenergic receptors - alpha and beta ().

Depending on the solubility in media, adrenolytics are lipophilic (Nebivolol), hydrophilic (Atenolol) and with combined solubility in water and lipids (Bisoprolol).

Beta-blockers have local anesthetic and antiarrhythmic effects on the heart. Due to the antianginal effect of the heart muscle, it needs less oxygen. The mechanism of antiarrhythmic effect is due to the elimination of arrhythmogenic sympathetic action on the conduction system of the heart.

The hypotensive effect is associated with a number of mechanisms: the volume of cardiac output is reduced, the sensitivity of baroreceptors decreases, and the work of the renin-angiotensin system is inhibited to some extent.

Beta-blockers also have a number of other effects:

• inhibit the work of the central nervous system;
• stimulate the contractility of the uterus;
• reduce intraocular pressure;
• interfere with the formation of glucose in the body;
• cause vasoconstriction;
• contribute to the development of insulin resistance, etc.

The variety of effects explains the side effects of beta-blockers and contraindications to their use, which must be considered when using them. In the treatment of cardiac diseases, highly selective drugs should be preferred.

It is necessary to take into account the fact that the selectivity of the effect is not one hundred percent, in high doses and cardioselective blockers can block beta 2-adrenergic receptors, causing serious undesirable effects.

Contraindications for the use of beta-blockers

In the following diseases and conditions, beta-blockers are contraindicated:

• sinus;
• intraventricular block incomplete or complete;
• severe heart failure;
• bronchial asthma and others lung diseases with obstructive syndrome;
• significant violations of peripheral arterial blood flow;
• individual intolerance.

Careful prescription of drugs in this group is required for moderate disorders of peripheral arterial blood flow, COPD without bronchial obstruction, and depressive states.

Side effects of beta blockers

Taking medications may be accompanied by the development of unwanted reactions.

The main side effects when using beta-blockers are directly related to their adrenolytic action:

• increased fatigue, sleep disturbances, depressive states due to the effect on the central nervous system;
• bradycardia, blockade of intracardiac conduction are explained by the blockade of adrenergic receptors of the heart;
• bronchospasm due to blocking of bronchial adrenoreceptors;
• , vomiting, diarrhea, and due to intoxication of the body from the accumulation of the drug (with impaired liver function);
• hypoglycemia due to the suppression of glucose synthesis and the formation of insulin resistance;
• , Raynaud's syndrome, allergic reactions, etc.

It is possible to minimize the side effects of beta-blockers by carefully selecting the appropriate drug at the optimal dosage, because the sensitivity to treatment in patients is extremely individual.

So, to avoid unwanted effects on the central nervous system, it is possible to prefer water-soluble beta-blockers instead of fat-soluble ones, which are not able to penetrate the central nervous system.

It is possible to prevent the development of bronchial obstruction by prescribing the minimum initial dose of the drug with a slow increase until the optimal amount of the drug is reached.

Application during pregnancy

Beta-blockers should not be taken during pregnancy.

These drugs can adversely affect the fetus through indirect and direct effects.

Directly related to hit medicinal product into the bloodstream of the fetus and the implementation of a toxic effect on it: there is a high probability of slowing the heart rate, developing hypoglycemia, and inhibiting the functions of the central nervous system.

The use of beta-blockers during pregnancy is justified only in case of severe cardiac pathology in small doses and under the constant supervision of doctors in a hospital setting.

Indirectly, beta-blockers act on the fetus through a decrease in uteroplacental blood flow, which can manifest as a delay in fetal development, especially when taking drugs in the 1st and 2nd trimester of pregnancy. They also have the property to increase the tone of the uterus and lead to the development of vasoconstriction.

Use in diabetes

Limiting the use of beta-blockers works if the patient has diabetes mellitus due to the potential risk of developing a hypoglycemic state.

This effect is especially characteristic of non-selective beta-blockers.

The drugs inhibit the formation of glucose in the body, contribute to a decrease in insulin sensitivity and mask the clinic of a hypoglycemic state.

The use of beta-blockers against the background of diabetes mellitus should take place with a preference for highly selective, regular monitoring of the amount of blood glucose and, if necessary, with dose adjustment of the hypoglycemic agent.

Beta blockers and erectile dysfunction

When taking beta-blockers, an adverse effect on potency is observed - sexual function is inhibited, up to impotence in 1% of cases.

The exact mechanism of this effect has not been elucidated. The presumable cause is the inhibitory effect of beta-blockers on the central nervous system, on the hormonal background and on the cavernous bodies.

However, taking not every drug from this group is accompanied by the appearance of this undesirable effect, which creates the possibility of choosing beta-blockers instead of refusing to use them.

Related videos

About the mechanism of action and the use of beta-blockers in the video:

Beta-blockers have a wide range of contraindications and adverse reactions, the fear of which reduces the scope of their use. As a result, patients who have direct indications for the appointment of blockers do not receive these drugs.

Careful and gentle selection of the optimal beta-blocker in the optimal dose, taking into account concomitant disorders, will increase the frequency of their use in cardiac diseases and minimize adverse reactions.

Thanks

The site provides reference information for informational purposes only. Diagnosis and treatment of diseases should be carried out under the supervision of a specialist. All drugs have contraindications. Expert advice is required!

general characteristics

Normally, when adrenergic receptors are free, they can be affected by adrenaline or noradrenaline that appears in the bloodstream. Adrenaline, when bound to adrenoreceptors, provokes the following effects:

• Vasoconstrictor (dramatically narrows the lumen of the blood vessels);
• Hypertensive (increased blood pressure);
• Antiallergic;
• Bronchodilator (expands the lumen of the bronchi);
• Hyperglycemic (increases blood glucose levels).

Classification

So, adrenoblockers are classified into the following groups:

1. Alpha blockers:

• Alpha-1-blockers (alfuzosin, doxazosin, prazosin, silodosin, tamsulosin, terazosin, urapidil);
• Alpha-2 blockers (yohimbine);
• Alpha-1,2-blockers (nicergoline, phentolamine, proroxan, dihydroergotamine, dihydroergocristine, alpha-dihydroergocriptine, dihydroergotoxin).

• Beta-1,2-blockers (also called non-selective) - bopindolol, metipranolol, nadolol, oxprenolol, pindolol, propranolol, sotalol, timolol;
• Beta-1-blockers (also called cardioselective or simply selective) - atenolol, acebutolol, betaxolol, bisoprolol, metoprolol, nebivolol, talinolol, celiprolol, esatenolol, esmolol.

This classification contains international titles active substances included in the composition of drugs belonging to each group of adrenergic blockers.

Each group of beta-blockers is also divided into two types - with internal sympathomimetic activity (ISA) or without ICA. However, this classification is auxiliary, and is only necessary for doctors to select the optimal drug.

Adrenoblockers - list

Alpha-adrenergic blockers

To the drugs of the group of alpha-1-adrenergic blockers include the following:

1. Alfuzosin (INN):

• Alfuprost MR;
• Alfuzosin;
• Alfuzosin hydrochloride;
• Dalphaz;
• Dalphaz Retard;
• Dalfaz SR.

• Artezin;
• Artezin Retard;
• doxazosin;
• Doxazosin Belupo;
• Doxazosin Zentiva;
• Doxazosin Sandoz;
• Doxazosin-ratiopharm;
• Doxazosin Teva;
• doxazosin mesylate;
• Zokson;
• Kamiren;
• Kamiren HL;
• Cardura;
• Cardura Neo;
• Tonocardin;
• Urocard.

• Polpressin;
• Prazosin.

• Urorek.

• Hyperprost;
• Glansin;
• Miktosin;
• Omnic Okas;
• Omnic;
• Omsulosin;
• Proflosin;
• Sonizin;
• Tamzelin;
• Tamsulosin;
• Tamsulosin Retard;
• Tamsulosin Sandoz;
• Tamsulosin-OBL;
• Tamsulosin Teva;
• Tamsulosin hydrochloride;
• Tamsulon FS;
• Taniz ERAS;
• Taniz K;
• Tulosin;
• Focusin.

• Cornam;
• Setegis;
• Terazosin;
• Terazosin Teva;
• Khaitrin.

• Urapidil Carino;
• Ebrantil.

To the drugs of the group of alpha-1,2-adrenergic blockers include the following drugs:

1. Dihydroergotoxin (a mixture of dihydroergotamine, dihydroergocristine and alpha-dihydroergocryptine):

• Redergin.

• Ditamine.

• Nilogrin;
• Nicergoline;
• Nicergolin-Ferein;
• Sermion.

• Pyrroxane;
• Proroxan.

• Phentolamine.

Beta blockers - list

Selective beta-blockers (beta-1-blockers, selective blockers, cardioselective blockers). The generally accepted names of this pharmacological group of adrenoblockers are listed in brackets.

So, selective beta-blockers include the following drugs:

1. Atenolol:

• Atenobene;
• Atenova;
• Atenol;
• Athenolan;
• Atenolol;
• Atenolol-Agio;
• Atenolol-AKOS;
• Atenolol-Acre;
• Atenolol Belupo;
• Atenolol Nycomed;
• Atenolol-ratiopharm;
• Atenolol Teva;
• Atenolol UBF;
• Atenolol FPO;
• Atenolol Stada;
• Atenosan;
• Betacard;
• Velorin 100;
• Vero-Atenolol;
• Ormidol;
• Prinorm;
• Sinar;
• Tenormin.

• Acecor;
• Sektral.

• Betak;
• Betaxolol;
• Betalmic EU;
• Betoptik;
• Betoptik C;
• Betoftan;
• Xonef;
• Xonef BK;
• Lokren;
• Optibetol.

• Aritel;
• Aritel Core;
• Bidop;
• Bidop Kor;
• Biol;
• Biprol;
• Bisogamma;
• Bisocard;
• Bisomore;
• bisoprolol;
• Bisoprolol-OBL;
• Bisoprolol LEXVM;
• Bisoprolol Lugal;
• Bisoprolol Prana;
• Bisoprolol-ratiopharm;
• Bisoprolol C3;
• Bisoprolol Teva;
• bisoprolol fumarate;
• Concor Core;
• Corbis;
• Cordinorm;
• Cordinorm Core;
• Coronal;
• Niperten;
• Tirez.

• Betaloc;
• Betalok ZOK;
• Vasocordin;
• Corvitol 50 and Corvitol 100;
• Metozok;
• Metocard;
• Metokor Adifarm;
• Metolol;
• metoprolol;
• Metoprolol Acry;
• Metoprolol Akrikhin;
• Metoprolol Zentiva;
• Metoprolol Organic;
• Metoprolol OBL;
• Metoprolol-ratiopharm;
• metoprolol succinate;
• metoprolol tartrate;
• Serdol;
• Egilok Retard;
• Egilok C;
• Emzok.

• Bivotens;
• Binelol;
• Nebivator;
• Nebivolol;
• Nebivolol NANOLEK;
• Nebivolol Sandoz;
• Nebivolol Teva;
• Nebivolol Chaikapharma;
• Nebivolol STADA;
• Nebivolol hydrochloride;
• Nebicor Adifarm;
• Nebilan Lannacher;
• non-ticket;
• Nebilong;
• OD-Neb.

7. Talinolol:

• Kordanum.

• Celiprol.

• Estekor.

• Breviblock.

1. Bopindolol:

• Sandonorm.

• trimepranol.

• Korgard.

• Trazikor.

• Whisken.

• Anaprilin;
• Vero-Anaprilin;
• Inderal;
• Inderal LA;
• obzidan;
• propranobene;
• propranolol;
• Propranolol Nycomed.

• Darob;
• SotaGEKSAL;
• Sotalex;
• Sotalol;
• Sotalol Canon;
• Sotalol hydrochloride.

• Arutimol;
• Glaumol;
• Glautam;
• Cusimolol;
• Niolol;
• Okumed;
• Okumol;
• Okupres E;
• Optimol;
• Oftan Timogel;
• Oftan Timolol;
• Oftensin;
• TimoGEKSAL;
• Thymol;
• Timolol;
• Timolol AKOS;
• Timolol Betalek;
• Timolol Bufus;
• Timolol DIA;
• Timolol LENS;
• Timolol MEZ;
• Timolol POS;
• Timolol Teva;
• Timolol maleate;
• Timollong;
• Timoptic;
• Timoptic Depot.

Alpha-beta-blockers (drugs that turn off both alpha and beta-adrenergic receptors)

1. Butylmethyloxadiazole:

• Albetor;
• Albetor Long;
• Butylmethyloxadiazole;
• Proxodolol.

• Acridilol;
• Bagodilol;
• Vedicardol;
• Dilatrend;
• Karvedigamma;
• Carvedilol;
• Carvedilol Zentiva;
• Carvedilol Canon;
• Carvedilol Obolensky;
• Carvedilol Sandoz;
• Carvedilol Teva;
• Carvedilol STADA;
• Carvedilol-OBL;
• Carvedilol Pharmaplant;
• Carvenal;
• Carvetrend;
• Carvidil;
• Cardivas;
• Coriol;
• Credex;
• Recardium;
• Talliton.

• Abetol;
• Amipress;
• Labetol;
• Trandol.

Beta-2 blockers

There are only non-selective beta-blockers that simultaneously turn off both beta-1 and beta-2 adrenergic receptors. However, since there are also selective blockers that turn off exclusively beta-1-adrenergic receptors, non-selective ones are often called beta-2-blockers. This name is incorrect, but quite widespread in everyday life. Therefore, when they say "beta-2-blockers", you need to know what is meant by the group of non-selective beta-1,2-blockers.

Action

The action of alpha-blockers

So, drugs of these groups dilate the vessels of all organs, and especially strongly skin, mucous membranes, intestines and kidneys. Due to this, the total peripheral vascular resistance decreases, blood flow and blood supply to peripheral tissues improves, and blood pressure decreases. By reducing peripheral vascular resistance and reducing the amount of blood that returns to the atria from the veins (venous return), the pre- and afterload on the heart is significantly reduced, which greatly facilitates its work and positively affects the state of this organ. Summarizing the above, we can conclude that alpha-1-blockers and alpha-1,2-blockers have the following effect:

• Reduce blood pressure, reduce total peripheral vascular resistance and afterload on the heart;
• Expand small veins and reduce the preload on the heart;
• Improve blood circulation both throughout the body and in the heart muscle;
• Improve the condition of people suffering from chronic heart failure, reducing the severity of symptoms (shortness of breath, pressure surges, etc.);
• Reduce pressure in the pulmonary circulation;
• Reduce the level of total cholesterol and low-density lipoprotein (LDL), but increase the content of high-density lipoprotein (HDL);
• They increase the sensitivity of cells to insulin, so that glucose is used faster and more efficiently, and its concentration in the blood decreases.

In addition, alpha-blockers reduce the severity of symptoms of inflammatory and obstructive processes in the genitourinary organs caused by prostatic hyperplasia. That is, drugs eliminate or reduce the severity incomplete emptying bladder, nocturnal urination, frequent urination and burning sensation when urinating.

Alpha-2-blockers have little effect on the blood vessels of internal organs, including the heart, they mainly affect vascular system genitals. That is why alpha-2-blockers have a very narrow scope - the treatment of impotence in men.

The action of non-selective beta-1,2-blockers

• Reduce heart rate;
• Reduce blood pressure and moderately reduce the total peripheral vascular resistance;
• Reduce myocardial contractility;
• Reduce the need of the heart muscle for oxygen and increase the resistance of its cells to oxygen starvation(ischemia);
• Reduce the degree of activity of foci of excitation in the conduction system of the heart and, thereby, prevent arrhythmias;
• Reduce the production of renin by the kidneys, which also leads to a decrease in blood pressure;
• At the initial stages of application, the tone of the blood vessels is increased, but then it decreases to normal or even lower;
• Prevent platelets from sticking together and forming blood clots;
• Improve the return of oxygen from red blood cells to the cells of organs and tissues;
• Strengthen the contraction of the myometrium (the muscle layer of the uterus);
• Increase the tone of the bronchi and esophageal sphincter;
• Strengthen the motility of the digestive tract;
• Relax the detrusor Bladder;
• Slow down education active forms thyroid hormones in peripheral tissues (only some beta-1,2-blockers).

In women, non-selective beta-blockers increase uterine contractility and reduce blood loss during childbirth or after surgery.

In addition, due to the effect on the vessels of peripheral organs, non-selective beta-blockers reduce intraocular pressure and reduce the production of moisture in the anterior chamber of the eye. This action of drugs is used in the treatment of glaucoma and other eye diseases.

The action of selective (cardioselective) beta-1-blockers

• Reduce the heart rate (HR);
• Reduce the automatism of the sinus node (pacemaker);
• Inhibit impulse conduction through the atrioventricular node;
• Reduce contractility and excitability of the heart muscle;
• Reduce the heart's need for oxygen;
• Suppress the effects of adrenaline and norepinephrine on the heart under conditions of physical, mental or emotional stress;
• Reduce blood pressure;
• Normalize heartbeat with arrhythmias;
• Limit and counteract the spread of the damage zone in myocardial infarction.

In addition, beta-1-blockers eliminate arrhythmia and narrowing of the lumen of small vessels. In people suffering from bronchial asthma, the risk of bronchospasm is reduced, and in diabetes mellitus, the likelihood of developing hypoglycemia is leveled ( low level blood sugar).

The action of alpha-beta-blockers

• Reduce blood pressure and reduce total peripheral vascular resistance;
• Reduce intraocular pressure in open-angle glaucoma;
• Normalize lipid profile indicators (reduce the level of total cholesterol, triglycerides and low density lipoproteins, but increase the concentration of high density lipoproteins).

In addition, alpha-beta-blockers improve myocardial contractility, due to which blood does not remain in the left ventricle after contraction, but is ejected in full into the aorta. This helps to reduce the size of the heart and reduces the degree of its deformation. By improving the work of the heart, the drugs of this group in congestive heart failure increase the severity and volume of endured physical, mental and emotional stress, reduce the frequency of heart contractions and IHD attacks, and also normalize the cardiac index.

The use of alpha-beta-blockers reduces mortality and the risk of re-infarction in people with coronary artery disease or dilated cardiomyopathy.

Application

Indications for the use of alpha-blockers

Alpha-1-adrenergic blockers indicated for use in the following conditions and diseases:

• Hypertension (to lower blood pressure);
• Benign prostatic hyperplasia.

• Peripheral circulatory disorders (for example, Raynaud's disease, endarteritis, etc.);
• Dementia (dementia) due to the vascular component;
• Vertigo and disorders of the vestibular apparatus due to the vascular factor;
• Diabetic angiopathy;
• Dystrophic diseases of the cornea of ​​the eye;
• neuropathy optic nerve due to its ischemia (oxygen starvation);
• prostatic hypertrophy;
• Disorders of urination against the background of a neurogenic bladder.

The use of beta-blockers (indications)

Indications for the use of non-selective beta-1,2-blockers the following:

• Arterial hypertension ;
• Angina pectoris;
• Sinus tachycardia;
• Prevention of ventricular and supraventricular arrhythmias, as well as bigeminy, trigeminy;
• Mitral valve prolapse;
• myocardial infarction;
• Prevention of migraine;
• Increased intraocular pressure.

Cardioselective beta-1-blockers are indicated for use if a person has the following diseases or states:

• Arterial hypertension of moderate or low severity;
• Cardiac ischemia;
• Hyperkinetic cardiac syndrome;
• Various types of arrhythmias (sinus, paroxysmal, supraventricular tachycardia, extrasystole, flutter or atrial fibrillation, atrial tachycardia);
• Hypertrophic cardiomyopathy;
• Mitral valve prolapse;
• Myocardial infarction (treatment of a heart attack that has already occurred and prevention of a second one);
• Prevention of migraine;
• Neurocirculatory dystonia of hypertonic type;
• AT complex therapy pheochromocytoma, thyrotoxicosis and tremor;
• Akathisia provoked by the use of neuroleptics.

Indications for the use of alpha-beta-blockers

• Arterial hypertension;
• stable angina;
• Chronic heart failure (as part of combination therapy);
• Arrhythmia;
• Glaucoma (the drug is administered in the form of eye drops).

Side effects

All alpha-blockers are capable of provoking both the same and different side effects, which is due to the peculiarities of their effect on certain types of adrenergic receptors.

Side effects of alpha blockers

• Headache;
• Orthostatic hypotension (a sharp decrease in pressure when moving to a standing position from a sitting or lying position);
• Syncope (short-term fainting);
• nausea or vomiting;
• Constipation or diarrhea.

• Hypotension (severe decrease in blood pressure);
• Tachycardia (palpitations);
• Arrhythmia;
• Dyspnea;
• Blurred vision (fog before the eyes);
• xerostomia;
• Feeling of discomfort in the abdomen;
• Violations cerebral circulation;
• Decreased libido;
• Priapism (prolonged painful erections);
• Allergic reactions (rash, skin itching, urticaria, Quincke's edema).

• arousal;
• Cold extremities;
• An attack of angina pectoris;
• Increased acidity of gastric juice;
• ejaculation disorder;
• Pain in limbs;
• Allergic reactions (redness and itching of the upper half of the body, urticaria, erythema).

• Tremor;
• Excitation;
• Irritability;
• Increased blood pressure;
• Tachycardia;
• Increased motor activity;
• Abdominal pain;
• Priapism;
• Decreased frequency and amount of urination.

Beta-blockers - side effects

So, the same for selective and non-selective beta-blockers are the following side effects:

• Dizziness;
• Headache;
• Drowsiness;
• Insomnia;
• Nightmares;
• fatigue;
• Weakness;
• Anxiety;
• confusion;
• Brief episodes of memory loss;
• Reaction slowdown;
• Paresthesia (feeling of running "goosebumps", numbness of the limbs);
• Violation of vision and taste;
• Dry mouth and eyes;
• bradycardia;
• palpitations;
• atrioventricular block;
• Violation of conduction in the heart muscle;
• Arrhythmia;
• Deterioration of myocardial contractility;
• Hypotension (lowering blood pressure);
• Heart failure;
• Raynaud's phenomenon;
• Pain in the chest, muscles and joints;
• Thrombocytopenia (a decrease in the total number of platelets in the blood below normal);
• Agranulocytosis (lack of neutrophils, eosinophils and basophils in the blood);
• Nausea and vomiting;
• Abdominal pain;
• diarrhea or constipation;
• Liver disorders;
• Dyspnea;
• Spasm of the bronchi or larynx;
• Allergic reactions (skin itching, rash, redness);
• sweating;
• Cold extremities;
• muscle weakness;
• Deterioration of libido;
• Increase or decrease in the activity of enzymes, the level of bilirubin and glucose in the blood.

• eye irritation;
• Diplopia (double vision);
• Nasal congestion;
• respiratory failure;
• Collapse;
• Exacerbation of intermittent claudication;
• Temporary disorders of cerebral circulation;
• cerebral ischemia;
• fainting;
• Decrease in the level of hemoglobin in the blood and hematocrit;
• Quincke's edema;
• Change in body weight;
• lupus syndrome;
• Impotence;
• Peyronie's disease;
• Thrombosis of the mesenteric artery of the intestine;
• Colitis;
• Increased levels of potassium, uric acid and triglycerides in the blood;
• Blurred and decreased visual acuity, burning, itching and sensation foreign body in the eyes, lacrimation, photophobia, corneal edema, eyelid margin inflammation, keratitis, blepharitis, and keratopathy (eye drops only).

Side effects of alpha-beta blockers

• Dizziness;
• Headache;
• Asthenia (feeling of fatigue, loss of strength, indifference, etc.);
• Syncope (short-term fainting);
• muscle weakness;
• General weakness and fatigue;
• sleep disorders;
• Depression;
• Paresthesia (feeling of running "goosebumps", numbness of the limbs, etc.);
• xerophthalmia (dry eye);
• Decreased production of tear fluid;
• bradycardia;
• Violation of atrioventricular conduction up to blockade;
• Hypotension is postural;
• Pain in the chest, abdomen and limbs;
• angina;
• Deterioration of peripheral circulation;
• Aggravation of the course of heart failure;
• Exacerbation of Raynaud's syndrome;
• swelling;
• Thrombocytopenia (decrease in the number of platelets in the blood below normal);
• Leukopenia (decrease in total;
• Cold extremities;
• Blockade of the legs of the bundle of Hiss.

• bradycardia;
• Decreased blood pressure;
• Bronchospasm;
• Dizziness;
• Weakness;
• Burning sensation or foreign body in the eye;

Contraindications

Contraindications to the use of various groups of alpha-blockers

Beta-blockers - contraindications

Contraindications to the use of alpha-beta blockers

• Increased individual sensitivity to any components of the drugs;
• Atrioventricular block II or III degree;
• Sinoatrial blockade;
• Sick sinus syndrome;
• Chronic heart failure in the stage of decompensation (IV functional class according to NYHA);
• Cardiogenic shock;
• Sinus bradycardia (pulse less than 50 beats per minute);
• Arterial hypotension (systolic pressure below 85 mm Hg);
• Chronic obstructive pulmonary disease;
• Bronchial asthma;
• peptic ulcer of the stomach or duodenum;
• Type 1 diabetes;
• The period of pregnancy and breastfeeding;
• Severe illnesses liver.

Hypotensive beta-blockers

In addition, all beta-blockers are hypotensive, both selective and non-selective. Hypotensive non-selective beta-1,2-blockers containing bopindolol, metipranolol, nadolol, oxprenolol, pindolol, propranolol, sotalol, timolol as active substances. These drugs, in addition to the hypotensive effect, also affect the heart, so they are used not only in the treatment of arterial hypertension, but also in heart disease. The most "weak" antihypertensive non-selective beta-blocker is sotalol, which has a predominant effect on the heart. However, this drug is used in the treatment of arterial hypertension, which is combined with heart disease. All non-selective beta-blockers are optimal for use in hypertension associated with coronary artery disease, angina pectoris and myocardial infarction.

Hypotensive selective beta-1-blockers are drugs containing the following as active substances: atenolol, acebutolol, betaxolol, bisoprolol, metoprolol, nebivolol, talinolol, celiprolol, esatenolol, esmolol. Given the peculiarities of action, these drugs are best suited for the treatment of arterial hypertension, combined with obstructive pulmonary pathologies, peripheral arterial diseases, diabetes mellitus, atherogenic dyslipidemia, as well as for heavy smokers.

Alpha-beta-blockers containing carvedilol or butylmethyloxadiazole as active substances are also hypotensive. But due to a wide range of side effects and a pronounced effect on small vessels, drugs in this group are used less frequently compared to alpha-1-blockers and beta-blockers.

Currently, the drugs of choice for the treatment of arterial hypertension are beta-blockers and alpha-1-blockers.

Alpha-1,2-blockers are used mainly for the treatment of peripheral and cerebral circulation disorders, since they have a more pronounced effect on small blood vessels. Theoretically, drugs of this group can be used to lower blood pressure, but this is ineffective due to a large number side effects that will arise from this.

Adrenoblockers for prostatitis

The most popular and effective adrenoblockers for prostatitis are drugs containing tamsulosin (for example, Hyperprost, Glansin, Miktosin, Omsulosin, Tulosin, Fokusin, etc.).

Beta-blockers called drugs that reversibly (temporarily) block various types (β 1 -, β 2 -, β 3 -) adrenoreceptors.

The value of beta-blockers hard to overestimate. They are the only class of drugs in cardiology for which a . In awarding the prize in 1988, the Nobel Committee called the clinical relevance of beta-blockers " the greatest breakthrough in the fight against heart disease since the discovery of digitalis 200 years ago».

Digitalis preparations (Foxglove plants, lat. Digitalis) are called the group cardiac glycosides (digoxin, strophanthin etc.), which have been used to treat chronic heart failure since about 1785.

Brief classification of beta-blockers

All beta-blockers are divided into non-selective and selective.

Selectivity (cardioselectivity) - the ability to block only beta1-adrenergic receptors and not affect beta2-receptors, since useful action beta-blockers is due mainly to the blockade of beta1 receptors, and the main side effects are beta2 receptors.

In other words, selectivity is selectivity, selectivity of action (from the English. selective- selective). However, this cardioselectivity is only relative - in large doses, even selective beta-blockers can partially block beta2-adrenergic receptors. Note that cardioselective drugs are stronger lower diastolic (lower) pressure than non-selective ones.

Some beta-blockers also have a so-called BCA (intrinsic sympathomimetic activity). It is less often called SSA (own sympathomimetic activity). ICA is the ability of a beta-blocker partially stimulate beta-adrenergic receptors suppressed by it, which reduces side effects (“softens” the effect of the drug).

For example, beta-blockers with ICA reduce heart rate to a lesser extent, and if the heart rate is initially low, then even sometimes it can be increased.

Mixed action beta-blockers:

• Carvedilol- mixed α 1 -, β 1 -, β 2 -blocker without ICA.
• Labetalol- α-, β 1 -, β 2 -blocker and partial agonist (stimulator) of β 2 receptors.

Useful effects of beta-blockers

To understand what we can achieve from the use of beta-blockers, we need to understand the effects that occur when.

Scheme of regulation of cardiac activity.

Adrenoreceptors and catecholamines acting on them [ ], as well as the adrenal glands, which secrete adrenaline and norepinephrine directly into the bloodstream, are combined into sympathoadrenal system(SAS). Activation of the sympathoadrenal system occurs:

• in healthy people under stress,
• in patients with a number of diseases:
  • myocardial infarction,
  • acute and chronic heart failure (the heart is unable to pump blood. With CHF, shortness of breath occurs (in 98% of patients), fatigue (93%), palpitations (80%), edema, cough),
  • arterial hypertension and etc.

Beta1-blockers limit the effects of adrenaline and norepinephrine in the body, thereby leading to 4 major effects:

1. decrease in the force of contractions of the heart,
2. decrease in heart rate (HR),
3. decreased conduction in the conduction system of the heart
4. reducing the risk of arrhythmias.

Now more on each item.

Decreased force of heart contractions

A decrease in the force of heart contractions causes the heart to push blood into the aorta with less force and create a lower level of systolic (upper) pressure there. Decreased contraction force reduces the work of the heart and, accordingly, myocardial oxygen demand.

Decreased heart rate

A decrease in heart rate allows the heart to rest more. This is perhaps the most important of which I wrote about earlier. During contraction (systole), the muscle tissue of the heart is not supplied with blood, since the coronary vessels in the thickness of the myocardium are pinched. Myocardial blood supply only possible during its relaxation (diastole). The higher the heart rate, the shorter the total duration of periods of relaxation of the heart. The heart does not have time to fully rest and may experience ischemia(lack of oxygen).

So, beta-blockers reduce the strength of heart contractions and myocardial oxygen demand, and also lengthen the period of rest and blood supply to the heart muscle. That is why beta-blockers have a pronounced anti-ischemic action and are often used for treatment of angina pectoris, which is a form of coronary artery disease (IHD). Old name for angina pectoris angina pectoris, in Latin angina pectoris, therefore, the anti-ischemic effect is also called antianginal. Now you will know what the antianginal action of beta-blockers is.

Note that among all classes of cardiac drugs beta-blockers without ICA best reduce heart rate ( heart rate). For this reason, when palpitations and tachycardia(heart rate above 90 per minute) they are the first to be prescribed.

Because beta-blockers reduce heart function and blood pressure, they contraindicated in situations where the heart does not cope with its work:

• heavy arterial hypotension(BP is less than 90-100 mm Hg),
• acute heart failure(cardiogenic shock, pulmonary edema, etc.),
• CHF ( chronic heart failure) in the stage decompensation.

Curiously, beta-blockers must be used (in parallel with three other classes of drugs - ACE inhibitors, cardiac glycosides, diuretics) in treatment of the initial stages of chronic heart failure. Beta blockers protect the heart from overactivation of the sympathoadrenal system and increase life expectancy patients. In more detail, I will talk about the modern principles of treating CHF in the topic of cardiac glycosides.

Reduced conductivity

Decreased conductivity ( decrease in the rate of conduction of electrical impulses along) as one of the effects of beta-blockers also has great importance. Under certain conditions, beta-blockers may interfere with atrioventricular conduction(will slow down the conduction of impulses from the atria to the ventricles in AV node), which will cause atrioventricular block (AV block) varying degrees(from I to III).

AV block diagnosis different degrees of severity is put on the ECG and is manifested by one or more signs:

1. permanent or cyclic elongation interval P-Q more than 0.21 s,
2. loss of individual ventricular contractions,
3. a decrease in heart rate (usually from 30 to 60).

Stably increased duration of the P-Q interval from 0.21 s and above.

a) periods of gradual lengthening of the P-Q interval with the loss of the QRS complex;
b) loss of individual QRS complexes without a gradual lengthening of the P-Q interval.

At least half of the ventricular QRS complexes fall out.

No impulses are conducted from the atria to the ventricles.

From here advice: if the patient's pulse has become less than 45 beats per minute or an unusual rhythm irregularity has appeared, it is necessary and most likely to adjust the dose of the drug.

In what cases is increased risk of conduction disorders?

1. If a beta-blocker is given to a patient with bradycardia(heart rate below 60 per minute),
2. if originally present violation of atrioventricular conduction(increased time of conduction of electrical impulses in the AV node by more than 0.21 s),
3. if the patient has an individual high sensitivity to beta blockers
4. if exceeded(incorrectly selected) dose of beta-blocker.

To prevent conduction disorders, you need to start with small doses of a beta blocker and increase dosage gradually. If side effects occur, the beta-blocker should not be discontinued abruptly due to the risk of tachycardia (palpitations). You need to reduce the dosage and stop the drug gradually, within a few days.

Beta-blockers are contraindicated if the patient has dangerous deviations on an ECG, for example:

• conduction disorders(atrioventricular block II or III degree, sinoatrial block, etc.),
• too much rare rhythm(heart rate less than 50 per minute, i.e. severe bradycardia),
• sick sinus syndrome(SSSU).

Reducing the risk of arrhythmias

Taking beta-blockers leads to decrease in myocardial excitability. In the heart muscle, there are fewer foci of excitation, each of which can lead to cardiac arrhythmias. For this reason, beta-blockers are effective in the treatment, as well as for the prevention and treatment and ventricular rhythm disturbances. Clinical studies have shown that beta-blockers significantly reduce the risk of developing fatal (fatal) arrhythmias (for example, ventricular fibrillation) and therefore are actively used for prevention of sudden death, including pathological elongation Q-T interval on the ECG.

Any myocardial infarction due to pain and necrosis (death) of a portion of the heart muscle is accompanied by pronounced activation of the sympathoadrenal system. The appointment of beta-blockers for myocardial infarction (if there are no contraindications mentioned above) significantly reduces the risk of sudden death.

Indications for the use of beta-blockers:

• IHD (angina pectoris, myocardial infarction, chronic heart failure),
• prevention of arrhythmias and sudden death,
• arterial hypertension (treatment of high blood pressure),
• other diseases with increased activity of catecholamines [ adrenaline, norepinephrine, dopamine] in the body:
  1. thyretoxicosis (hyperfunction thyroid gland),
  2. alcohol withdrawal (), etc.

Side effects of beta-blockers

Some of the side effects are due excessive action of beta-blockers on the cardiovascular system:

• sharp bradycardia(heart rate below 45 per minute),
• atrioventricular blockade,
• arterial hypotension(systolic blood pressure below 90-100 mm Hg) - more often with intravenous administration of beta-blockers,
• worsening heart failure up to pulmonary edema and cardiac arrest,
• poor blood circulation in the legs with a decrease in cardiac output - more often in older people with atherosclerosis of peripheral vessels or endarteritis.

If the patient has pheochromocytoma (benign tumor adrenal medulla or nodes of the sympathetic autonomic nervous system, which secretes catecholamines; occurs in 1 per 10 thousand of the population and up to 1% of patients with hypertension), then beta blockers can even raise blood pressure due to stimulation of α 1 -adrenergic receptors and spasm of arterioles. To normalize blood pressure, beta-blockers must be combined with.

In 85-90% of cases, pheochromocytoma is a tumor of the adrenal glands.

Beta-blockers themselves exhibit antiarrhythmic effect, but in combination with other antiarrhythmic drugs, it is possible to provoke seizures ventricular tachycardia or ventricular bigeminy (constant alternation of normal contraction and ventricular extrasystole , from lat. bi- two).

Bigeminy.

Other side effects of beta blockers are extracardiac.

Bronchial constriction and bronchospasm

Beta2-adrenergic receptors dilate the bronchi. Accordingly, beta-blockers acting on beta2-adrenergic receptors narrow the bronchi and can provoke bronchospasm. This is especially dangerous for patients with bronchial asthma, smokers and other people with lung disease. They have increased cough and shortness of breath. To prevent this bronchospasm, risk factors must be taken into account and it is imperative to apply only cardioselective beta-blockers, which in normal doses do not act on beta2-adrenergic receptors.

Decreased sugar levels and worsened lipid profile

Since stimulation of beta2-adrenergic receptors causes the breakdown of glycogen and an increase in glucose levels, beta-blockers may lower sugar levels in the blood with development moderate hypoglycemia. People with normal carbohydrate metabolism have nothing to fear, and patients with should be more careful. Besides, beta blockers mask symptoms of hypoglycemia such as tremor (jitter) and heartbeat (tachycardia), caused by excessive activation of the sympathetic nervous system due to the release of contrainsular hormones during hypoglycemia. note that sweat glands are controlled by the sympathetic nervous system, but they contain M-cholinergic receptors that are not blocked by adrenoblockers. Therefore, hypoglycemia while taking beta-blockers is characterized especially heavy sweating.

Patients with diabetes who are on insulin should be informed of the increased risk of developing when using beta-blockers. For these patients, it is preferable selective beta blockers that do not act on beta2-adrenergic receptors. Patients with diabetes mellitus in an unstable state ( poorly predictable blood glucose levels) beta-blockers are not recommended, otherwise please.

Sexual violations

Possible development impotence(modern name - erectile dysfunction), for example, when receiving propranolol within 1 year it develops in 14% of cases. Also noted was the development fibrous plaques in the body of the penis with its deformation and difficulty in erection when taking propranolol and metoprolol. Sexual dysfunctions are more common in people with (that is, problems with potency when taking beta-blockers usually occur in those who can have them without medication).

To be afraid of impotence and for this reason not to take medication for arterial hypertension is a wrong decision. Scientists have found that long-term high blood pressure leads to erectile dysfunction regardless of the presence of concomitant atherosclerosis. With high blood pressure the walls of blood vessels thicken, become denser and cannot supply the internal organs with the necessary amount of blood.

Other side effects of beta-blockers

Other side effects when taking beta-blockers:

• from the side gastrointestinal tract(in 5-15% of cases): constipation, less often diarrhea and nausea.
• from the side nervous system Key words: depression, sleep disorders.
• from the side skin and mucous: rash, urticaria, eye redness, decreased secretion of tear fluid(relevant for users contact lenses) and etc.
• at the reception propranolol occasionally happens laryngospasm(difficult noisy, wheezing breath) as a manifestation of an allergic reaction. Laryngospasm occurs as a reaction to artificial yellow dye tartrazine about a tablet after 45 minutes after oral administration.

withdrawal syndrome

If you are taking beta blockers long time(several months or even weeks), and then suddenly stop taking, there is withdrawal syndrome. In the days following the cancellation, there is palpitations, anxiety, angina attacks become more frequent, ECG worsens, myocardial infarction and even sudden death may develop.

The development of the withdrawal syndrome is due to the fact that during the time of taking beta-blockers, the body adapts to the reduced effect of (nor)adrenaline and increases the number of adrenergic receptors in organs and tissues. In addition, since propranolol slows down the conversion of thyroid hormone thyroxine(T 4) into hormone triiodothyronine(T 3), some of the withdrawal symptoms (restlessness, trembling, palpitations), especially pronounced after discontinuation of propranolol, may be due to an excess of thyroid hormones.

For the prevention of withdrawal syndrome, it is recommended gradual withdrawal of the drug within 14 days. If surgical manipulations on the heart are necessary, there are other schemes for discontinuing the drug, but in any case, the patient should know your medicines: what, in what dosage, how many times a day and how long he takes. Or at least write them down on a piece of paper and carry them with you.

Features of the most significant beta-blockers

PROPRANOLOL (ANAPRILIN)- non-selective beta-blocker without ICA. it most famous drug from beta blockers. Active briefly- 6-8 hours. Withdrawal syndrome is typical. Fat-soluble, therefore it penetrates into the brain and has calming effect. It is non-selective, therefore it has a large number of side effects caused by beta2 blockade ( narrows the bronchi and increases cough, hypoglycemia, cold extremities).

Recommended for use in stressful situations (for example, before an exam, see). Since sometimes an increased individual sensitivity to a beta-blocker is possible with a rapid and significant decrease in blood pressure, it is recommended that its first appointment be carried out under the supervision of a physician. with a very small dose(for example, 5-10 mg of anaprilin). To increase blood pressure should be administered atropine(not glucocorticoid hormones). For permanent reception propranolol is not suitable, in this case another beta-blocker is recommended - bisoprolol(below).

Atenolol is a cardioselective beta-blocker without ICA. Formerly a popular drug (like metoprolol). It is applied 1-2 times a day. Water-soluble, therefore does not penetrate into the brain. Withdrawal syndrome.

Metoprolol is a non-ICA cardioselective beta-blocker similar to atenolol. It is taken 2 times a day. Atenolol and metoprolol have now lost their importance due to the spread bisoprolol.

BETAXOLOL (LOCREN)- cardioselective beta-blocker without ICA. Mainly used to treat arterial hypertension. It is taken 1 time per day.

BISOPROLOL (CONCOR)- cardioselective beta-blocker without ICA. Perhaps the most important drug to date from the beta-blockers. Convenient form of administration (1 time per day) and reliable smooth 24-hour antihypertensive action. Reduces blood pressure by 15-20%. It does not affect the level of thyroid hormones and blood glucose, therefore it is allowed for diabetes. In bisoprolol, the withdrawal syndrome is less pronounced. There are many on the market bisoprolol different manufacturers, so you can choose an inexpensive one. In Belarus, the cheapest generic today - bisoprolol-lugal(Ukraine).

ESMOLOL - available only in solution for intravenous administration as antiarrhythmic drug. The duration of action is 20-30 minutes.

NEBIVOLOL (NEBILETE)- cardioselective beta-blocker without ICA. It's also a great drug. Causes a gradual decrease in blood pressure. A pronounced antihypertensive effect occurs after 1-2 weeks of administration, the maximum - after 4 weeks. Nebivolol enhances production nitric oxide(NO) in vascular endothelium. The most important function of nitric oxide is vasodilatation. In 1998 was awarded Nobel Prize in medicine with the wording " For discovering the role of nitric oxide as a signaling molecule in the regulation of cardio-vascular system ". Nebivolol has a number additional beneficial effects:

• vasodilating[vasodilating] (from lat. vas- vessel, dilatation- extension),
• antiplatelet(inhibits platelet aggregation and thrombosis),
• angioprotective(protects blood vessels from the development of atherosclerosis).

CARVEDILOL - α 1 -, β-blocker without ICA. Due to the blockade of α 1 receptors, it has vasodilating action and further lowers blood pressure. Less atenolol lowers heart rate. Does not impair tolerance physical activity. Unlike other blockers, it lowers blood glucose levels, so it is recommended for type 2 diabetes. Possesses antioxidant properties, slows down the processes of atherosclerosis. It is taken 1-2 times a day. Particularly recommended for treatment of chronic heart failure(CHF).

LABETALOL is an α-, β-blocker and partially stimulates β 2 receptors. Well reduces blood pressure with a slight increase in heart rate. Has antianginal effect. Can increase blood sugar levels. In high doses, it can cause bronchospasm, as well as cardioselective beta-blockers. Applied intravenously at hypertensive crises and (less commonly) orally twice a day to treat hypertension.

Drug Interactions

As I pointed out above, combination of beta-blockers with other antiarrhythmic drugs potentially dangerous. However, this is a problem for all groups of antiarrhythmic drugs.

Among antihypertensive (antihypertensive) drugs forbidden combination of beta-blockers and calcium channel blockers from the group verapamil and diltiazema. This is associated with an increased risk of cardiac complications, since all these drugs act on the heart, reduce the force of contractions, heart rate and conductivity.

Overdose of beta-blockers

Overdose symptoms beta blockers:

• severe bradycardia (heart rate below 45 per minute),
• dizziness up to loss of consciousness,
• arrhythmia,
• acrocyanosis ( blue fingertips),
• if the beta-blocker is fat-soluble and enters the brain (for example, propranolol), coma and convulsions may develop.

Help with overdose beta-blockers depends on the symptoms:

• at bradycardia - atropine(parasympathetic blocker), β 1 -stimulants ( dobutamine, isoproterenol, dopamine),
• at heart failure - cardiac glycosides and diuretics,
• at low blood pressure(hypotension below 100 mm Hg) - adrenaline, mezaton and etc.
• at bronchospasm - aminophylline (efufillin), isoproterenol.

At topical application (eye drops) beta-blockers reduce the formation and secretion of aqueous humor which lowers intraocular pressure. Local beta blockers ( timolol, proxodolol, betaxolol etc.) are used for glaucoma treatment (progressive eye disease due to increased intraocular pressure). Possible development systemic side effects due to the ingestion of anti-glaucoma beta-blockers through the lacrimal-nasal canal into the nose and from there into the stomach, followed by absorption in the gastrointestinal tract.

Beta-blockers are considered possible doping and should be used by athletes with serious restrictions.

Addition about Koraksan

In connection with frequent questions in the comments about the drug Coraxan (ivabradine) I will highlight its similarities and differences with beta-blockers. Coraxan blocks the I f channels of the sinus node and therefore does NOT belong to beta-blockers.

In this way, coraxan used to slow sinus rhythm with normal (slightly reduced) blood pressure and the absence of arrhythmias. If a BP is elevated or have cardiac arrhythmias, need to use beta blockers. The combination of Coraxan with beta-blockers is allowed.

More about Koraksan: http://www.rlsnet.ru/tn_index_id_34171.htm

Beta-blockers in the treatment of CHF

(addition dated 07/19/2014)

The group of beta-blockers belongs to the basic (mandatory) for treatment CHF (chronic heart failure). Based on the results of clinical trials, currently for the treatment of CHF recommended 4 drugs:

• carvedilol,
• bisoprolol,
• extended form metoprolol succinate,
• in persons over 70 years of age is also allowed nebivolol.

These 4 drugs have proven in clinical research its ability to improve the condition and increase the survival of patients with CHF.

• atenolol,
• metoprolol tartrate.

The goal of treatment with beta-blockers in CHF is to reduce heart rate by at least 15% of baseline to below 70 bpm. per minute (50-60). It has been established that a decrease in heart rate for every 5 strokes reduces mortality by 18%.

The initial dose for CHF is 1/8 of therapeutic and slowly rises every 2-4 weeks. In case of intolerance and inefficiency of beta-blockers, they are combined or completely replaced with a blocker of the I f channels of the sinus node - ivabradine(see above Addition about Koraksan).

Read more about the use of beta-blockers in the treatment of CHF in the National Guidelines for the Diagnosis and Treatment of CHF, 4th revision, approved in 2012-2013. (PDF, 1 Mb, in Russian).

From this article you will learn: what are adrenoblockers, what groups they are divided into. Mechanism of their action, indications, list of adrenoblockers.

Article publication date: 06/08/2017

Article last updated: 05/29/2019

Adrenolytics (blockers) are a group of drugs that block nerve impulses that respond to norepinephrine and adrenaline. medicinal effect they are opposite to the action of adrenaline and norepinephrine on the body. The name of this pharmaceutical group speaks for itself - the drugs included in it “interrupt” the action of adrenoreceptors located in the heart and walls of blood vessels.

Such drugs are widely used in cardiology and therapeutic practice for the treatment of vascular and heart diseases. Often, cardiologists prescribe them to older people who are diagnosed with arterial hypertension, heart rhythm disturbances and other cardiovascular pathologies.

Classification of blockers

There are 4 types of receptors in the walls of blood vessels: beta-1, beta-2, alpha-1, alpha-2-adrenergic receptors. The most common are alpha- and beta-blockers, which “turn off” the corresponding adrenaline receptors. There are also alpha-beta blockers that simultaneously block all receptors.

The means of each of the groups can be selective, interrupting selectively only one type of receptor, for example, alpha-1. And non-selective with simultaneous blocking of both types: beta-1 and -2 or alpha-1 and alpha-2. For example, selective beta-blockers can only affect beta-1.

Subgroups of adrenolytics:

General mechanism of action of adrenergic blockers

When norepinephrine or epinephrine is released into the bloodstream, adrenoceptors instantly react by binding to it. As a result of this process, the following effects occur in the body:

• narrowing of the vessels;
• pulse quickens;
• blood pressure rises;
• increases the level of glucose in the blood;
• bronchi expand.

If there are certain diseases, for example, arrhythmia or hypertension, then such effects are undesirable for a person, because they can provoke or relapse the disease. Adrenoblockers "turn off" these receptors, so they act in the opposite way:

• dilate blood vessels;
• slow down the heart rate;
• prevent an increase in blood sugar;
• narrow the lumen of the bronchi;
• lower BP.

it general actions characteristic of all types of drugs from the group of adrenolytics. But drugs are divided into subgroups depending on the effect on certain receptors. Their actions are slightly different.

Common side effects

Common to all blockers (alpha, beta) are:

1. Headache.
2. Fast fatiguability.
3. Drowsiness.
4. Dizziness.
5. Increased nervousness.
6. Short-term fainting is possible.
7. Violations of the normal activity of the stomach and digestion.
8. Allergic reactions.

Since drugs from different subgroups have slightly different therapeutic effects, the undesirable consequences of taking them also differ.

General contraindications for selective and non-selective beta-blockers:

• bradycardia;
• weak sinus syndrome;
• acute heart failure;
• atrioventricular and sinoatrial blockade;
• hypotension;
• decompensated heart failure;
• allergy to drug components.

Non-selective blockers should not be taken with bronchial asthma and obliterating vascular disease, selective - in the pathology of the peripheral circulation.

Such medications should be prescribed by a cardiologist or therapist. Independent uncontrolled reception can lead to serious consequences up to death due to cardiac arrest, cardiogenic or anaphylactic shock.

Alpha blockers

Action

Alpha-1 receptor blockers dilate blood vessels in the body: peripheral - noticeable by redness skin and mucous; internal organs - in particular the intestines with the kidneys. Due to this, peripheral blood flow increases, microcirculation of tissues improves. The resistance of the vessels along the periphery decreases, and the pressure decreases, and without a reflex increase in heart rate.

By reducing the return of venous blood to the atria and expanding the "periphery", the load on the heart is significantly reduced. Due to the facilitation of his work, the degree characteristic of hypertensive patients and people decreases. old age with heart problems.

Other effects:

• affect fat metabolism. Alpha-ABs lower triglycerides, "bad" cholesterol and increase high-density lipoproteins. Such an additional effect is good for people suffering from hypertension aggravated by atherosclerosis.
• Influence the metabolism of carbohydrates. When taking drugs, the susceptibility of cells to insulin increases. Because of this, glucose is absorbed faster and more efficiently, which means that its level does not increase in the blood. This action is important for diabetics, in whom alpha-blockers reduce blood sugar levels.
• Reduce the severity of signs of inflammation in the organs of the genitourinary system. These funds are successfully used in prostatic hyperplasia to eliminate some characteristic symptoms: partial emptying of the bladder, burning in the urethra, frequent and nocturnal urination.

Blockers of alpha-2 adrenaline receptors have the opposite effect: constrict blood vessels, increase blood pressure. Therefore, they are not used in cardiology practice. But they successfully treat impotence in men.

List of drugs

The table provides a list of international generic names medicines from the group of alpha receptor blockers.

Indications for use

Since the effect of drugs from this subgroup on the vessels is somewhat different, their scope is also different.

There is only one indication for alpha-2 blockers - erectile dysfunction in men.

Side effects of alpha-adrenolytics

In addition to the common side effects listed above in the article, these drugs have the following side effects:

Contraindications

1. Pregnancy.
2. lactation period.
3. Allergy or intolerance to the active ingredient or excipients.
4. Severe disorders (diseases) of the liver, kidneys.
5. Arterial hypotension is low blood pressure.
6. Bradycardia.
7. Severe heart defects, including aortic stenosis.

Beta blockers

Cardioselective beta-1-blockers: principle of action

Medicines from this subgroup are used to treat heart disease, because they mainly have a positive effect on this organ.

Received effects:

• Antiarrhythmic action by reducing the activity of the pacemaker - the sinus node.
• Decreased heart rate.
• Decreased excitability of the myocardium under conditions of psycho-emotional and / or physical activity.
• Antihypoxic effect due to a decrease in the oxygen demand of the heart muscle.
• Lowering blood pressure.
• Prevention of the expansion of the focus of necrosis in a heart attack.

A group of selective drugs, beta-blockers, reduce the frequency and alleviate an attack of angina pectoris. They also improve the tolerance of physical and mental stress on the heart in patients with heart failure, who prolong life. These funds significantly improve the quality of life for patients who have had a stroke or myocardial infarction, suffering from ischemic disease heart, angina pectoris, hypertension.

In diabetics, they prevent an increase in blood sugar levels, reduce the risk of bronchospasm in people with bronchial asthma.

Non-selective beta-1, -2-blockers: action

In addition to antiarrhythmic, hypotensive, antihypoxic effects, such drugs have other actions:

• The antithrombotic effect is possible due to the prevention of platelet aggregation.
• Strengthen the contraction of the muscular layer of the uterus, intestines, esophageal sphincter, at the same time relaxing the sphincter of the bladder.
• During childbirth, blood loss is reduced in the woman in labor.
• Increase the tone of the bronchi.
• Reduce intraocular pressure by reducing fluid in the anterior chamber of the eye.
• Reduce the risk of acute heart attack, stroke, development of coronary artery disease.
• Reduce mortality from heart failure.

List of drugs

There are currently no drugs belonging to the pharmacological subgroup of beta-2-adrenergic receptors.

Indications for use

Side effects

Alpha beta blockers

Action

Drugs from this subgroup lower arterial and intraocular pressure, normalize lipid metabolism, i.e. reduce the level of triglycerides, cholesterol, low density lipoproteins, while increasing high density. The hypotensive effect is achieved without changes in renal blood flow and an increase in total peripheral vascular resistance.

When they are taken, the adaptation of the heart to physical and psycho-emotional stress increases, the contractile function of the heart muscle improves. This leads to a decrease in the size of the heart, normalization of the rhythm, relief from heart disease or congestive insufficiency. If IHD is diagnosed, then the frequency of its attacks against the background of taking alpha-beta-blockers decreases.

List of medicines

1. Carvedilol.
2. Butylmethyloxadiazole.
3. Labetalol.

Contraindications

You can not take adrenoblockers from this subgroup for the same pathologies as described above, supplementing them obstructive disease lungs, diabetes mellitus (type I), peptic ulcer stomach and duodenum 12.