Class I - sodium channel blockers (membrane stabilizing agents). Antiarrhythmic drugs - a list of the most effective with a description of the composition, indications and prices Sodium channel blockers drugs

Cardiac arrhythmia is a broad concept. It includes various types of pathology and some physiological conditions. Treatment requires heart rhythm failure, which most often represents a symptom of cardiac, as well as any other disease. An important part of therapeutic measures in this case is the prescription of appropriate medications. Treatment of cardiac arrhythmia with tablets depends on its type, and it is aimed, first of all, at the cause of abnormal myocardial function. Medicines eliminate severe symptoms of an unpleasant condition, and also prevent the development of complications of diseases of the cardiovascular system.

A heart rate of 60-90 beats per 60 seconds is considered normal. Arrhythmia refers to a series of myocardial contractions that occur at the wrong frequency or out of sequence. In accordance with this definition, the following types of abnormal rhythm can be distinguished:

• bradycardia (decreased heart rate per minute);
• tachycardia (increased heart rate during the same time);
• extrasystole (the rhythm becomes erratic, certain areas of the myocardium contract prematurely).

When classifying arrhythmia, the area of ​​origin of the pathology must also be taken into account. The source of the disturbances may be in the atria, ventricles, sinus or atrioventricular nodes.

Another sign of dividing irregular heart rhythms into subtypes is the duration over time.

1. Paroxysmal arrhythmia lasts a maximum of a week. It develops unexpectedly and stops on its own, as suddenly as it began.
2. The persistent form of rhythm disturbance lasts longer (sometimes over 12 months). To eliminate symptoms, you have to resort to drug therapy.
3. With chronic arrhythmia, a person constantly feels pathological symptoms. In this case, it is not possible to restore the correct functioning of the ventricles and atria. The doctor chooses tactics to maintain the existing rhythm and prescribes medications that support the heart muscle.

The following types of abnormal contractions pose the greatest danger to life:

• Ventricular and atrial flutter, which often leads to atrial fibrillation. This is a severe pathology characterized by randomly occurring excitation of various parts of the myocardium. They contract on their own, without the participation of the sinus node. At the same time, the heart rhythm becomes chaotic and accelerated.
• Atrioventricular complete block is a disorder in which the electrical impulse from the AV node to the ventricles is not conducted at all. In the latter case, the pacemaker becomes the His bundle with its branches. This arrhythmia is characterized by severe bradycardia. Such disorders lead to heart failure or cerebral ischemia.
• Sick sinus syndrome can cause sudden cardiac arrest. Drug treatment, as a rule, does not have the desired effect. To save life, the patient is asked to install a pacemaker. Signals from the sinus center are sent weakly or at irregular intervals. Characteristic symptoms of cardiac arrhythmia: significant slowing of the rhythm or alternation of bradycardia and tachycardia.

Separately, we can highlight arrhythmia that develops with the arrival of night. It is often associated with a phenomenon called apnea. A person suffering from this pathology experiences periodic pauses in breathing during sleep. This usually happens during night snoring: the walls of the pharynx and larynx close tightly during breathing movements, and air cannot pass through them.

As a result of apnea, the myocardium does not receive the oxygen it needs, and the load on the heart muscle increases. Holding your breath in most cases leads to the development of a type of arrhythmia such as severe sinus bradycardia (the pulse ranges from 30 to 50 beats per minute). The more often these sleep disorders occur, and the longer these attacks last, the more severe the arrhythmia takes.

Tablets for cardiac arrhythmia: treatment features

• Cardiac glycosides (Digoxin) restore sinus rhythm, treat atrial fibrillation and supraventricular tachycardia.
• "Magnesium sulfate" is used for paroxysms of ventricular tachycardia.
• Potassium preparations (“Potassium Chloride”) help in the treatment of ventricular and supraventricular arrhythmias.
• Adenosine preparations (“Sodium adenosine triphosphate”) are effective for fibrillation and heart failure.

• Iron-containing agents (“Actiferrin”) are used for severe hypoxia of heart cells.
• Preparations with iodine (Iodofol, Iodbalance) and thyroid hormones (Eutirox) are prescribed when the thyroid gland is not functioning well.
• Vitamins (group B, rutin, biotin, folic acid, ascorbic acid, vitamin E, lipoic and pantothenic acids, lecithin).
• A drug for normalizing metabolic processes in the myocardium, the name is “Riboxin”.

Special age categories

These include children and old age. Selecting treatment for such categories should be done with caution. Many drugs have side effects, which, due to the special vulnerability of such patients, can significantly worsen the patient’s condition if the dosage is incorrectly selected.

Tablets used to treat arrhythmia in a child:

• "Adenosine";
• "Bretylium";
• "Digoxin";
• "Labetalol".

Medicines to eliminate rhythm disturbances in an elderly person:

• "Cordaron";
• "Ritmonorm";
• "Lidocaine";
• Cardiplant.

Rating of antiarrhythmics by price

1. “Atenolol”, “Verapamil”, “Riboxin” - from 19.50 rubles. up to 56 rub.
2. “Novacainomide”, “Diltiazem”, “Bisoprolol”, “Amiodoron”, “Amlodipine”, “Panangin” - from 72 rubles. up to 149 rub.
3. “Concor”, “Egilok”, “Kordaron” - from 79 rubles. up to 300 rub.
4. “Ritmonorm”, “Nebilet”, “Propanorm”, “Allapinin” - 496 rubles. up to 568 rub.

Description of common tablets for cardiac arrhythmia:

Elimination of arrhythmia with special tablets should be carried out under the supervision of a physician. He will make the correct diagnosis, select the dose and take into account the individual characteristics of the body. Self-medication can cause irreparable damage. At home, you can use traditional medicine methods, but only as an additional measure. When conservative treatment does not bring the desired effect, the doctor decides to install a pacemaker.

Atrial fibrillation (AF) is a common heart rhythm disorder. With this pathology, normal atrial contraction is replaced by flutter, which leads to a general disturbance of cardiac activity and harms the entire body.

Atrial fibrillation: treatment with tablets is the main type of help.

The choice of therapy depends on the form of AF:

• acute - occurs once with an excessive dose of alcohol or caffeine, etc.;
• - short-term attacks often go away on their own and alternate with normal heart activity;
• persistent - long-term fibrillations that do not go away on their own, but can be stopped;
• - chronic heartbeat disorder, in which it is not advisable to perform cardioversion (restoration of sinus rhythm).

General principles of drug treatment

All medications for atrial fibrillation - a list with a huge number of items. The choice of drugs is difficult even for an experienced doctor.

Atrial fibrillation is dangerous due to complications, so the treatment of the pathology should be selected by a doctor.

1. Among the general principles that determine which medicine to use for atrial fibrillation, several main directions can be distinguished.
2. Treatment of the disease that caused fibrillation, if any (hypertension, thyroid dysfunction, pulmonary pathologies, diabetes mellitus). Sometimes you need to stop taking medications. For example, if Vasobral is prescribed, atrial fibrillation may be more likely to occur due to caffeine.
3. Prevention of AF is prescribed for paroxysmal and persistent forms.
4. Termination of an attack of fibrillation that has already begun - the medication is achieved more effectively.
5. Maintaining sinus rhythm with a constant type of fibrillation does not always make sense; the need for this treatment is determined by the doctor.
6. Prevention of such a dangerous complication as thrombosis is carried out in any type of AF.

Antiarrhythmic drugs

Medicines for atrial fibrillation belong to the group of antiarrhythmic drugs. When selecting these funds, you must consider:

• condition of various structures of the heart;
• compatibility of drugs with each other and with other drugs used by the patient.

Thus, patients with diabetes need to clarify whether it is possible to take Siofor for atrial fibrillation within the limits of the selected treatment, since this drug reduces the effectiveness of indirect anticoagulants. In addition, the concentration in the blood of the main substance “Siofor” is increased by quinidine.

Antiarrhythmic drugs for atrial fibrillation are classified in various ways, but the generally accepted classification includes 4 classes. They differ in the type of effect on the excitation of the cardiomyocyte and the conduction of the cardiac impulse.

Drugs that block fast sodium channels

Drugs for the treatment of atrial fibrillation belonging to this class are divided into 3 subclasses depending on the intensity of the effect on the conductive channels of the cell wall of cardiomyocytes:

• IA moderately affects phase 0 (depolarization), can also block potassium channels, prolonging phase 1 (rapid repolarization) - quinidine, procainamide, rhythmylene;
• IB weakly slow down depolarization and slightly accelerate phase 1 - phenytoin;
• ICs intensively slow down depolarization and do not affect repolarization - lappaconitine, propafenone, etacizine.

The active ingredient of this drug is the compound lappaconitine.

It not only suppresses depolarization, but also blocks beta-adrenergic receptors. Allapinin also has an analgesic and sedative effect.

It should be taken 25 mg every 6-8 hours after meals. Sometimes the dosage is increased.

Novocainamide

In tablet form for the treatment of atrial fibrillation it is used as follows:

• at the first dose, a maximum of 6 tablets containing 0.25 g of novocainamide are prescribed;
• if a single dose is ineffective - 2 more tablets, and every 2 hours - 2-4 tablets.

In case of heart failure of the 2nd degree, the dosage of the drug should be reduced by at least a third.

Propaphenone

An attack of AF can be stopped with a single dose of 600 mg of propafenone. The initiation of treatment should be carried out in a hospital setting; in the future, the drug can be used by the patient to block AF independently at the prescribed dosage. It is recommended to always have it with you.

To maintain heart rhythm, 150 mg is often prescribed 3 times a day at regular intervals.

Analogs are Propanorm and Ritmonorm, which are available in the form of tablets containing 150 or 300 g of propafenone hydrochloride.

Phenytoin

Patients with cardiogenic shock, sinoatrial block, bronchial asthma, bradycardia, pheochromocytoma, or metoprolol intolerance are prohibited from taking the drug. There is no clinical data on the effect of the drug on patients under 18 years of age.

As a rule, Egilok tablets are tolerated quite well by patients. Unpleasant symptoms from taking it are extremely rare. Sometimes patients experience severe fatigue, bradycardia, paresthenia, anxiety, shortness of breath, nausea, allergies, decreased sexual desire, and arthralgia.

Metoprolol

A popular beta-blocker, which includes the active substance metoprolol tartrate. Prescribed for the treatment of arrhythmia, coronary heart disease, arterial hypertension, hyperthyroidism, as well as for the prevention of migraines.

Metoprolol tablets are taken during or after meals. It is recommended to take the drug with a sufficient amount of water. First, patients are prescribed 1-2 tablets twice a day; if no therapeutic effect is observed, the dose is increased. Do not exceed the established maximum daily dose (200 mg).

Patients with cardiogenic shock, bradycardia, weak sinus node syndrome, heart failure, Prinzmetal's angina, arterial hypertension, and metoprolol intolerance are prohibited from taking tablets. They are also contraindicated for patients under 18 years of age and breastfeeding women.

The appearance of unpleasant symptoms while taking Metoprolol is associated with the individual sensitivity of each patient. Sometimes the following may appear: tinnitus, blurred vision, weakness, depression, poor attention, conjunctivitis, vomiting, pain in the abdomen, headaches, allergies.

Bisoprolol

A popular drug against arrhythmia, which includes bisoprolol fumarate. It is also used to treat angina pectoris, especially during attacks.

The initial dose of Bisoprolol is 5 mg per 24 hours. In this case, the tablet should be taken before breakfast with a sufficient amount of liquid. If necessary, the attending physician may increase the daily dose to 10 mg.

Patients with cardiogenic shock, collapse, pulmonary edema, chronic heart failure, sinoatrial block, bradycardia, Prinzmetal's angina, cardiomegaly, bronchial asthma, metabolic acidosis, bisoprolol intolerance are prohibited from taking tablets.

Quite often, after taking Bisoprolol, patients experience diarrhea, headaches, insomnia, depression, weakness and fatigue, conjunctivitis, pain in the chest, liver and kidney dysfunction, hyperglycemia, allergies, fetal bradycardia, delayed fetal development, increased sweating .

Verapamil

A popular calcium channel blocker, which contains the active substance verapamine hydrochloride. It has antihypertensive, antiarrhythmic and antianginal effects. Reduces myocardial oxygen demand.

The dosage and duration of treatment are prescribed individually by the attending physician. The drug is often used as a prophylaxis for arrhythmia and angina. In this case, patients are prescribed 80 mg of the drug three times a day.

Patients with cardiogenic shock, bradycardia, weak sinus node syndrome, Morgagni-Adams-Stokes syndrome, Wolff-Parkinson-White syndrome, heart failure and intolerance to verapamine are prohibited from taking the drug. Quite rarely, patients after taking Verapamil tablets may experience the following unpleasant symptoms: headaches, dizziness, vomiting, nausea, redness of the facial skin, bradycardia, constipation, allergies, peripheral edema.

Amlodipine

A popular drug from the group of calcium channel blockers. The active ingredient is amlodipine in the form of besylate, which is 10 mg per tablet.

Take on an empty stomach or after meals. Initially, the dose is 5 mg of the drug every 24 hours. Over seven to fourteen days, the dose is gradually increased to 10 mg per day. Do not exceed the maximum daily dose (10 mg).

Patients with collapse, bradycardia, unstable angina, arterial hypertension, and intolerance to amlodipine are contraindicated to take the drug. This product is also prohibited for patients under 18 years of age and pregnant women.

Quite often, after taking the drug, patients experience side effects: dizziness, increased heart rate, headaches, swelling, pain in the abdomen, nausea, tachycardia, pollakiuria, arthralgia, xeroderma, allergies, conjunctivitis.

Amlodak

A drug from the group of selective calcium channel blockers. Amlodac tablets contain a substance derived from dihydropyridine.

In the initial stages of therapy, the attending physician usually prescribes a minimum dose of 5 mg once a day. Over the course of a week, the dose is increased to 10 mg per day. Do not exceed the maximum possible daily dose of 10 mg.

Patients with intolerance to dihydropyridine and severe arterial hypertension should not take Amlodac tablets. It has not been established whether the drug is safe to use during pregnancy and breastfeeding.

In some patients, taking the drug may lead to the following side effects: headaches, peripheral edema, drowsiness, excessive fatigue, arrhythmia, shortness of breath, skin flushing, paresthesia, allergies, pain in the extremities.

Amiodarone

A popular antiarrhythmic drug, which contains the active substance amiodarone hydrochloride. The drug is a repolarization inhibitor. It also has a pronounced coronary dilation, antianginal and thyroid stimulating effect.

As a rule, it is prescribed for the treatment of severe ventricular arrhythmia, as well as supraventicular and atrial fibrillation. The dose and duration of treatment are established and adjusted (if necessary) by a specialist. Take the tablets before or after meals with a sufficient amount of liquid.

Amiodarone tablets have many contraindications that should be carefully studied before taking the drug. Patients with weak sinus node syndrome, atrioventricular block, arterial hypertension, hyper- and hypothyroidism, hypokalemia, hypomagnesemia, interstitial lung diseases, intolerance to amiodarone, lactose or iodine are completely prohibited from taking the drug. It also cannot be used to treat patients under 18 years of age. Pregnant women should not take it, as the drug contains iodine.

Often, patients taking Amiodarone may experience side effects: moderate bradycardia, vomiting, taste disturbances, acute toxic hepatitis, pneumonitis, fatal acute respiratory syndrome), photosensitivity, tremor, allergies.

Cordaron

The drug with antiarrhythmic effect contains the active substance amiodarone hydrochloride. The drug is taken only as prescribed by a specialist. However, the dosage and duration of therapy are individual. There is a loading and maintenance dose. Do not exceed the maximum possible daily dose of 400 mg.

Patients with hypomagnesemia, hypokalemia, sinus bradycardia, thyroid dysfunction, interstitial lung diseases, iodine, amiodarone or lactose intolerance should not use the drug. Also, it should not be taken by patients under 18 years of age, during pregnancy and breastfeeding.

Very often, patients who take Cordarone tablets for arrhythmia may experience the following side effects: bradycardia, dysgeusia, vomiting, chronic liver disease (sometimes fatal), bronchospasm, hypothyroidism, photosensitivity, epididymitis, Quincke's edema.

Mexiletine

In terms of its chemical structure, this drug and its pharmacological characteristics are similar to lidocaine. It is a popular antiarrhythmic drug, which is included in class IB. Used to treat various heart rhythm disorders.

First, the drug is used as an injection. After obtaining the required therapeutic effect, switch to Mexiletine tablets. They are swallowed whole with a sufficient amount of water. First, two tablets (400 mg) are taken once every six to eight hours, after the patient’s condition improves, the dose is reduced to one tablet every six to eight hours.

Patients with sinus node weakness, bradycardia, hypotension, heart failure, liver or kidney failure, or intolerance to mexiletine should not take tablets. Not for pregnant women and breastfeeding women.

With long-term use of Mexiletine, some patients experience changes in taste sensations, nystagmus, vomiting, visual impairment, ataxia, paresthesia, tremor, confusion, drowsiness, and allergies.

Tablets for atrial fibrillation

One of the popular drugs for the treatment of atrial fibrillation is Quinidine tablets. They have a well-defined antiarrhythmic effect.

For the treatment of adult patients, a minimum dose (no more than 0.3 g) is first prescribed. This will reveal how sensitive the patient’s body is to the substance quinidine. If necessary, the dose can be increased to 0.4 g once every six hours. If the therapeutic effect has not been achieved, add 0.2 g of the drug every 60 minutes until the paroxysm stops.

To treat frequent attacks of ventricular arrhythmia, it is necessary to take 0.4 g Quinidine tablets every three hours.

Patients with thrombocytopenic purpura, hypersensitivity, glycoside intoxication, cardiogenic shock, and myasthenia gravis are prohibited from taking Quinidine. Pregnant and breastfeeding women should use with extreme caution.

When taking the drug, the following symptoms may occur: headaches, ringing in the ears, dizziness, hemolytic anemia, poor appetite, vomiting, constipation, diarrhea, sinus bradycardia, quinidine shock, allergies.

Tablets for sinus arrhythmia

Sinus arrhythmia is a disease that is almost always asymptomatic. If this type of arrhythmia is not combined with another, more serious type of rhythm disorder, then no treatment is required. In some cases, a cardiologist may prescribe therapy based on sedative medications. As a rule, tablets for sinus arrhythmia are medicines based on plant extracts.

If vagotonia is severe, the patient can take Atropine Sulfate. The standard dose is 300 mg every four to six hours. If the patient suffers from glaucoma and obstructive diseases of the gastrointestinal tract, atropine sulfate is contraindicated for use. During treatment, the following side effects may occur: a feeling of dry mouth, mydriasis, rapid heartbeat, difficulty urinating, atonic constipation, vertigo, headaches. Tablets for high blood pressure and arrhythmia

If a patient's arrhythmia is accompanied by high blood pressure, complications may develop in the form of myocardial ischemia, negative neurological. Reducing blood pressure during arrhythmia is very important. The following tablets are used for this:

1. Hydrochlorothiazide – Each tablet contains 25 mg of hydrochlorothiazide. Take one or two tablets once every 24 hours. Patients with arterial hypertension, edema syndrome, glaucoma, and diabetes insipidus are prohibited from taking it. Tablets can disrupt, lead to headaches, drowsiness, dizziness, paresthesia and allergies.
2. Indapamide is a popular diuretic. It is best to take it in the morning on an empty stomach with a sufficient amount of liquid. Do not exceed the maximum dose – 1 tablet per 24 hours. Do not use in patients with galactosemia, renal failure, hypokalemia, encephalopathy, lactose intolerance, or during pregnancy. Taking it can cause nausea, headaches, nocturia, pharyngitis, anorexia, loss of appetite, and allergies.

A pathological persistent change in heart rate is most often not an independent disease, but only indicates an underlying cardiovascular disease. However, any type of arrhythmia requires its elimination, and the leading method for this is the prescription of drugs through intravenous infusions in case of a sharp deterioration in health, and tablets for long-term therapy.

Arrhythmia is conventionally considered to be any heartbeat rhythm that differs from normal. In a healthy person, the pulsation is even, in the range of 60-75 beats per minute, the tones are heard clearly, loudly, rhythmically without background sounds. Pathological contractions of the atria or ventricles of the heart are:

• changed frequency: stable slow or accelerated pulse;
• altered rhythm pattern: flickering, fluttering, premature muscle contraction.

One that is natural and does not require medical care or a thorough examination is a short-term change in the speed of contractions under the influence of heavy physical activity, adrenaline release, endurance tests, stress, or activation of the underlying disease. In this case, the arrhythmia is physiological in nature and stops when the provoking factor is eliminated. Also, the frequency and quality of the rhythm may change due to the use of certain medications, as well as in women during pregnancy.

The occurrence of arrhythmia may be an individual reaction to a particular drug. If the phenomenon causes significant discomfort, then immediate discontinuation of the drug and selection of a more suitable analogue is recommended.

Non-physiologically caused arrhythmia always indicates the presence of more serious heart problems than superficial rhythm disharmony. A person who notices a persistent change in heartbeat often experiences decreased endurance, pain in the heart area, shortness of breath, difficulty breathing, and in this case should consult a doctor for an ECG and ultrasound of the heart.

The most commonly diagnosed types of arrhythmia are bradycardia, tachycardia, atrial fibrillation and extrasystole.

Treatment of cardiac arrhythmia with tablets

The treatment of cardiac arrhythmia primarily includes medical care for the patient regarding his underlying disease that caused the cardiac arrhythmia. At the same time, medications suitable for the specific type of arrhythmia are prescribed. For the treatment of organic bradycardia, angioprotectors and low-dose acetylsalicylic acid are often prescribed. These drugs improve blood flow in the vessels supplying the heart muscle by reducing atherosclerotic phenomena.

Low-dose aspirin is taken long-term. A small dose does not have an ulcerogenic effect and does not increase the risk of bleeding.

In case of arrhythmia caused by taking medications, reduce the dosage or discontinue the drug completely. In case of such a reaction to antihypertensive drugs, it is necessary to select a replacement.

Video - How to treat cardiac arrhythmia

Antiarrhythmic drugs

Sodium channel blockers

This group of drugs includes drugs that normalize heart rate by blocking Na channels and improve impulse conduction. The higher the pulse, the more active the blockade is created. In this case, drugs are isolated with different effects on the repolarization time.

Repolarization is a physiological process that denotes the transition of cardiac muscle cells to a relaxed state after they perform a contractile function.

If any drug from the group of sodium blockers is not suitable for the patient, you can replace the medication within the same group with a drug from the same group, but with a different effect on the repolarization process:

Potassium channel blockers

Due to the blockade of K channels, this group of drugs is successfully used among patients at high risk of ventricular fibrillation. Unlike the sodium channel group, in which it is possible to replace one drug with another within the same class, this is unacceptable with potassium channel blockers due to the difference in their mechanism.

Beta blockers

Beta blockers are unique in preventing the unwanted effects that result from fight-or-flight responses. It is relevant to use such antiarrhythmic drugs to reduce myocardial excitation in case of tachycardia, various types of arrhythmia in which the functioning of the central nervous system is damaged. This group of drugs includes Esmolol, Timolol, Nadolol, Carvedilol, but more common are:

Calcium channel blockers

Electrolytes - Panangin

Panangin can also be used in the treatment of arrhythmia as an electrolyte that replenishes missing microelements for the heart. In hospital settings or in cases of severe potassium deficiency, magnesium is used intravenously. Then the drug is prescribed in the form of tablets 3 times a day. An absolute analogue of Panangin is Asparkam.

Additional drugs

In addition to classical antiarrhythmic drugs, other medications may be prescribed, taking into account the medical history and type of arrhythmia. If a heart rhythm disturbance is associated with a decrease or overexcitation of the central nervous system, then various sedatives and sedatives, including tranquilizers, are prescribed.

Iron supplements

If there is a suspicion of insufficient oxygen supply to the cells, the doctor orders the patient to evaluate the level of ferritin in the blood. In case of deficiency, preparations with iron are prescribed, where the choice depends on the body’s sensitivity to a particular remedy and tolerance.

Injectable iron preparations are practically not used to treat arrhythmia.

Thyroid hormones

If the cause of tachycardia or bradycardia is thyroid dysfunction, then the following are prescribed:

1. Thyroid hormones - L-thyroxine or Euthyrox, the dosage of which is selected individually taking into account the level of free thyroxine in the blood and thyroid-stimulating hormone. Hormones are prescribed for a long time and are taken in the morning on an empty stomach 20-30 minutes before breakfast from 5 to 8 am.
2. Iodine-containing preparations 100-200 mcg - Iodofol, Iodomarin or Iodine balance. These drugs are complete analogues of each other (but folic acid is added to Iodofol).

Digoxin

A cardiac glycoside and cardiotonic of plant origin - Digoxin - has proven itself in the treatment of atrial fibrillation, as well as heart failure. Prescribed 0.25 mg from one to several times a day, but must be discontinued if extrasystole occurs. Digoxin has the ability to inhibit sodium and potassium channels, which should be taken into account when concomitantly prescribing antiarrhythmic drugs. Digoxin should not be prescribed for tachycardia, ventricular fibrillation, or myocardial infarction.

If you suspect a persistent arrhythmia - and repeated, caused by a natural physiological need in certain conditions - you must immediately contact a cardiologist to assess the work of the heart. A sudden severe attack of arrhythmia requires calling an ambulance, since in many cases the first signs of organ dysfunction were ignored, and this situation can be critical. But when diagnosing a heart rate rhythm disorder, as well as clarifying the cause of the arrhythmia, the doctor will select a highly effective course of treatment that will not only improve the quality of life, but also help to avoid serious complications in the future.

Sodium channel blockers (“fast”) are drugs that block sodium channels of cardiomyocyte membranes (reducing the rate of depolarization of the cardiac fiber) and have membrane-stabilizing and antiarrhythmic effects.

• A - ajmaline, disopyramide, procainamide (Novocainamide), quinidine (Kinidin Durules).
• B – lidocaine (Lidocaine hydrochloride, mexiletine, phenytoin.
• C – lippaconitine hydrobromide (Allapinin), propafenone (Propanorm, Ritmonorm).

• Mechanism of action

  Sodium channel blockers cause blockade of sodium channels in cardiomyocyte membranes, which leads to inhibition of transmembrane sodium current, reduce the rate of depolarization and have membrane stabilizing and antiarrhythmic effects (class I antiarrhythmic drugs).

  These processes lead to suppression of the excitability of cardiomyocyte membranes, prolongation of the effective refractory period in the atria and ventricles of the heart, inhibition of impulse transmission through the atrioventricular node and in the His-Purkinje system.

  During the use of sodium channel blockers, the following signs can be detected on the ECG:

  • Slight increase in sinus rhythm.
  • Widening of the P wave (slowing of atrial conduction).
  • Prolongation of the P–Q(R) interval (mainly due to deterioration of conductivity in the His–Purkinje system).
  • Expansion of the QRS complex (slowing down the depolarization of the ventricular myocardium).
  • Increasing the duration of the QT interval (slowing ventricular repolarization).

  If the concentration of drugs of this group in the blood is high (toxic) or the patient has sinus node dysfunction, then the following effects are possible:

  • Inhibition of the function of the sinoatrial node with the development of sinus bradycardia and sick sinus syndrome.
  • Bundle branch blocks and distal atrioventricular blocks.

  There are class IA, IB and IC sodium channel blockers.

  Sodium channel blockers, included in the subgroup of class IA antiarrhythmic drugs, cause a moderately pronounced inhibition of initial depolarization (moderate kinetics of binding to sodium channels), occupying an intermediate position in this indicator between class IB and IC drugs. In addition, class IA drugs can lead to an increase in the duration of repolarization due to blockade of potassium channels.

  As a result, a significant slowdown in conduction is observed in tissues with a “fast” response: in the His–Purkinje conduction system and in the myocardium of the atria and ventricles.

  Sodium channel blockers, which are part of the subgroup of class IA antiarrhythmic drugs, can also have an inhibitory effect on M-cholinergic receptors. Quinidine exhibits α-adrenergic blocking activity.

  Sodium channel blockers, which are included in the subgroup of class IB antiarrhythmic drugs, in contrast to sodium channel blockers, which are included in the subgroup of class IA antiarrhythmic drugs, are characterized by rapid binding kinetics to sodium channels.

  The severity of the effect of sodium channel blockers, included in the subgroup of class IB antiarrhythmic drugs, on the rate of depolarization in the His-Purkinje system and ventricular myocardium depends on the degree of damage to these tissues. With unchanged myocardium, this effect is weakly manifested; with organic changes in the heart muscle, a pronounced inhibition of the rapid depolarization phase is observed.

  With the use of sodium channel blockers, which are included in the subgroup of class IB antiarrhythmic drugs, a decrease in the duration of repolarization is also noted.

  Lidocaine, which belongs to the group of sodium channel blockers, included in the subgroup of class IB antiarrhythmic drugs, has a local anesthetic effect. Phenytoin can have an anticonvulsant effect.

  Sodium channel blockers, included in the subgroup of class IC antiarrhythmic drugs, are characterized by slow binding kinetics to sodium channels. Against the background of their use, there is a pronounced inhibition of initial depolarization and no effect on repolarization. These drugs can also block calcium channels.

  Propafenone has β-adrenergic blocking activity. Lappaconitine hydrobromide is a β-adrenergic receptor agonist.

  Aymalin is poorly absorbed when taken orally. The time for the onset of the clinical effect with i.v. administration of aimalinamine, with i.m., with oral administration is 1 hour. Duration of the effect. The half-life is 15 hours.

  After oral administration, disopyramide is quickly and almost completely absorbed from the gastrointestinal tract. The maximum concentration in the blood plasma is reached after almost 0.5-3 hours. Plasma protein binding is 50-65%. Disopyramide is partially metabolized in the liver with the participation of the CYP3A4 isoenzyme. Disopyramide passes through the placental barrier and passes into breast milk. Excreted mainly by the kidneys. About 10% of the drug is excreted in the feces. The half-life from plasma is 4-10 hours and increases with impaired renal function and liver failure.

  When taken orally and with intramuscular administration of procainamide, absorption of this drug occurs quickly. Protein binding is 15-20%. Procainamide is metabolized in the liver. The half-life is 2.5-4.5 hours, and in case of impaired renal function. Excreted by the kidneys: 50-60% unchanged, the rest as a metabolite.

  Quinidine, when taken orally, is absorbed in the small intestine. Bioavailability is 70-80%. The half-life is 6-7 hours. It undergoes biotransformation in the liver. Excreted by the kidneys.

  Mexiletine after oral administration is quickly and almost completely (90%) absorbed from the gastrointestinal tract. The maximum concentration is achieved within 2-4 hours. Plasma protein binding is 55%. Passes through the placental barrier and enters breast milk. Metabolized in the liver to form inactive metabolites. The half-life is hours. Excreted by the kidneys (70-80%), mainly in the form of metabolites.

  When taken orally and with intramuscular injection, phenytoin is absorbed slowly. The maximum concentration is achieved after 3-15 hours. The drug penetrates into the cerebrospinal fluid, saliva, semen, gastric and intestinal juice, bile, and is excreted in breast milk. Phenytoin crosses the placental barrier. Binding to blood plasma proteins is more than 90%. Metabolized in the liver. Excreted by the kidneys in the form of metabolites and through the intestines. Half-life – hours.

  The bioavailability of lippaconitine hydrobromide is 40%. The drug undergoes a “first pass” effect through the liver. When taken orally, the volume of distribution is 690 l. Penetrates the blood-brain barrier. The half-life is 1-1.2 hours. Excreted by the kidneys.

  After oral administration, propafenone is absorbed quickly and almost completely (90%). The maximum concentration of the drug in the blood plasma is achieved after 1-3.5 hours. Protein binding is 97%. It is subjected to intensive metabolism during the “first pass” through the liver with the formation of active metabolites. Half-life in patients with intensive metabolism (more than 90% of cases) hours, with slow metabolism (less than 10% of cases) hours. Excreted by the kidneys - 38% in the form of metabolites, 1% - unchanged. 53% of the drug is excreted through the intestines (in the form of metabolites).

  Indications for the use of sodium channel blockers included in the subgroup of class IB antiarrhythmic drugs:

  • Ventricular extrasystole.
  • Arrhythmias of central origin.
  • Heart rhythm disturbances that occur during anesthesia and heart surgery.

  Indications for the use of sodium channel blockers included in the subgroup of class IC antiarrhythmic drugs:

  • Prevention and treatment of supraventricular and ventricular arrhythmias.
  • Bradycardia.
  • Arterial hypotension.
  • Atrioventricular block of the second degree, type II and type III.
  • Sinoatrial block.
  • Severe heart failure.
  • Prolongation of the QT interval.
  • Sick sinus syndrome.

  Drugs from this group are used with caution in the following clinical situations:

  • Bundle branch block.
  • Arrhythmias due to intoxication with cardiac glycosides.
  • Myasthenia.
  • Liver failure.
  • Kidney failure.
  • Systemic lupus erythematosus.
  • Bronchial asthma.
  • Atherosclerosis.
  • First degree atrioventricular block.
  • Emphysema.
  • Thyrotoxicosis.
  • Hypokalemia.
  • Acute infectious diseases.
  • Thrombocytopenia.
  • Prostatic hyperplasia.
  • Angle-closure glaucoma.
  • Psoriasis.
  • Elderly age.
  • Pregnancy.
  • Lactation.
  • From the cardiovascular system:
    • Bradycardia.
    • Slowing of sinoatrial, atrioventricular and intraventricular conduction.
    • Decreased myocardial contractility.
    • Orthostatic hypotension.
    • Arrhythmogenic effect.
  • From the digestive system:
    • Nausea.
    • Anorexia.
    • Feeling of heaviness in the epigastrium.
    • Constipation.
    • Liver dysfunction.
  • From the side of the central nervous system:
    • Headache.
    • Dizziness.
    • Visual impairment.
    • Depression.
    • Psychotic reactions with productive symptoms.
    • Ataxia.
  • From the hematopoietic system:
    • Leukopenia.
    • Agranulocytosis.
    • Thrombocytopenia.
    • Neutropenia.
    • Hypoplastic anemia.
  • From the reproductive system:
    • Oligospermia.
  • Allergic reactions:
    • Skin rash.
  • From the urinary system:
    • Difficulty urinating.
    • Urinary retention.

  Sodium channel blockers are used with caution in cases of liver dysfunction, severe renal dysfunction, and also in combination with other antiarrhythmic drugs.

  Patients taking drugs in this group should avoid potentially hazardous activities that require increased attention and speed of psychomotor reactions.

  Treatment with sodium channel blockers must be carried out in a hospital setting, under constant monitoring of blood pressure, heart rate, ECG (QT and PQ intervals, QRS complex), peripheral blood patterns, and hemodynamic parameters.

  Due to the possible inhibition of myocardial contractility and a decrease in blood pressure, procainamide should be used with great caution during myocardial infarction. In cases of severe atherosclerosis, procainamide is not recommended.

  When using propafenone or when prescribing procainamide, the risk of developing the arrhythmogenic effect of these drugs increases.

  The use of mexiletine may increase the symptoms of parkinsonism.

  In elderly patients, as well as in patients weighing less than 70 kg, propafenone is used in doses lower than recommended.

  Sodium channel blockers are not prescribed concomitantly with antiarrhythmic drugs of other classes.

  When combining drugs from this group with other drugs, the following reactions are possible:

  • With antihypertensive drugs – the hypotensive effect of these drugs is enhanced.
  • With anticholinesterase drugs, the effectiveness of these drugs is reduced.
  • With m-anticholinergic blockers, the anticholinergic effect of these drugs is enhanced.
  • With amiodarone and cisapride, the QT interval prolongs and the risk of developing ventricular arrhythmia of the “pirouette” type increases.
  • With rifampicin - the concentration of sodium channel blockers in the blood plasma decreases.
  • With phenobarbital - the concentration of sodium channel blockers in the blood plasma decreases.
  • With verapamil, the risk of developing arterial hypotension and collapse increases.

  When disopyramide is used simultaneously with other drugs, the following effects are possible:

  • With antibiotics from the macrolide group (erythromycin, clarithromycin, azithromycin, josamycin), the concentration of disopyramide in the blood plasma increases, and there is a risk of prolongation of the QT interval and the development of ventricular arrhythmia of the “pirouette” type.
  • With beta-blockers, the risk of developing severe bradycardia and increasing the QT interval increases.
  • With hypoglycemic agents, the risk of developing hypoglycemia increases.
  • With cyclosporine, the risk of developing nephrotoxicity increases and the anticholinergic effects of disopyramide are enhanced.

  When quinidine is used simultaneously with other drugs, the following effects are possible:

  • With laxatives - a decrease in the concentration of quinidine in the blood plasma and a decrease in its effectiveness.
  • With sodium bicarbonate, acetazolamide, the likelihood of developing the toxic effects of quinidine increases.
  • With tricyclic antidepressants, the excretion of desipramine, imipramine, nortriptyline, and trimipramine from the body is reduced, which leads to an increase in their concentrations in the blood plasma.
  • With amiloride, the effectiveness of quinidine decreases.
  • With warfarin, the anticoagulant effect of this drug is enhanced.
  • With haloperidol - the concentration of this drug in the blood plasma increases and the risk of side effects increases.
  • With hydroxyzine, the risk of developing severe heart rhythm disturbances increases.
  • With dextromethorphan - the concentration of this drug in the blood plasma increases.
  • With digoxin, the concentration of this drug in the blood serum increases.
  • With disopyramide - the concentration of quinidine in the blood plasma increases, the QT interval lengthens.
  • With dicumarol, the concentration of its effectiveness increases.
  • With itraconazole, ketoconazole - the concentration of quinidine in the blood plasma increases.
  • With codeine - the concentration of the analgesic effect of this drug increases.
  • With mefloquine – the QT interval is prolonged.
  • With propranolol, the β-adrenergic blocking effect of this drug is enhanced, and the risk of developing orthostatic hypotension increases.

  When procainamide is used simultaneously with other drugs, the following effects are possible:

  • With captopril - increased risk of developing leukopenia.
  • With ofloxacin - an increase in the concentration of procainamide in the blood plasma.
  • With cimetidine - an increase in the concentration of procainamide in the blood plasma and the risk of increased side effects.

  When mexiletine is used simultaneously with other drugs, the following effects are possible:

  • With diamondylate, atropine and morphine - slowing down the absorption of mexiletine.
  • With metoclopramide - acceleration of mexiletine absorption.
  • With theophylline - an increase in the concentration of this drug in the blood plasma and an increase in its side effects.

  When using propafenone simultaneously with other drugs, the following effects are possible:

  • With β-blockers, tricyclic antidepressants, local anesthetics - enhanced antiarrhythmic effect of propafenone in ventricular arrhythmias.
  • With indirect anticoagulants - potentiation of the effect of these drugs.
  • With propranolol, metoprolol, cyclosporine, digoxin - an increase in the concentrations of these drugs in the blood.
  • With theophylline - an increase in the concentration of this drug in the blood and an increase in the likelihood of developing its toxic effects.
  • With cimetidine - an increase in the concentration of propafenone in the blood plasma and an expansion of the QRS complex on the ECG.
  • With erythromycin – inhibition of propafenone metabolism.

  Sodium channel blockers

  1C - flecainide, propafenone.

  The main differences between these subgroups are indicated in Table. 6.

  Subgroup IA drugs - quinidine, procainamide, disopyramide. Quinidine is a dextrorotatory isomer of quinine (an alkaloid of cinchona bark; genus Cinchona). Acting on cardiomyocytes, quinidine blocks sodium channels and therefore slows down the depolarization processes. In addition, quinidine blocks potassium channels and therefore slows down repolarization.

  Purkinje fibers ventricles of the heart. The following phases are distinguished in the action potential of Purkinje fibers (Fig. 31):

  Phase 4 - spontaneous slow depolarization (diastolic depolarization); once the spontaneous slow depolarization reaches the threshold level, a new action potential is generated; the rate of reaching the threshold level determines the frequency of potentials, i.e. automaticity of Purkinje fibers.

  Table 6. Properties of subgroups of sodium channel blockers

  1 Vmax - speed of fast depolarization (phase 0).

  These phases are associated with the movement of ions through the ion channels of the cell membrane (Fig. 32).

  Rice. 31. Purkinje fiber action potentials.

  Phase 0 - rapid depolarization; phase 1 - early repolarization;

  phase 2 - “plateau”; phase 3 - late repolarization; phase 4 - spontaneous slow

  depolarization (diastolic depolarization).

  Phase 0 is associated with the rapid entry of Na + ions.

  Phase 1 is associated with the release of K + ions.

  Phase 2 - output of K + ions, input of Ca 2+ ions and partly Na +.

  Phase 3 - release of K + ions.

  Phase 4 - K + output (decreases) and Na + input (increases). Quinidine blocks Na + channels and slows down fast depolarization (phase 0) and spontaneous slow depolarization (phase 4).

  Quinidine blocks potassium channels and slows down repolarization (phase 3) (Fig. 33).

  Due to the slowdown of fast depolarization, quinidine reduces excitability and conductivity, and due to the slowdown of spontaneous slow depolarization, it reduces the automaticity of Purkinje fibers.

  Due to phase 3 inhibition, quinidine increases the duration of the action potential of Purkinje fibers.

  Due to an increase in the duration of the action potential and a decrease in excitability, the effective refractory period (ERP - the period of non-excitability between two propagating impulses) increases (Fig. 34).

  Obviously, reducing excitability and automaticity is useful in the treatment of tachyarrhythmias and extrasystoles.

  Reducing conduction may be useful in “reentry” type arrhythmias, which are associated with the formation of a unidirectional block (Fig. 35). Quinidine completely blocks the conduction of impulses in the area of ​​the unidirectional block (translates the unidirectional block into a complete block) and stops the re-entry of excitation.

  An increase in ERP may be useful for tachyarrhythmias associated with the circulation of excitation along closed circuits of cardiomyocytes (for example, with atrial fibrillation); as the ERP increases, the circulation of excitation stops.

  Fig.35. Effect of quinidine in arrhythmias of the reentry type.

  On the cells sinoatrial node quinidine has a weak inhibitory effect, since the resting potential in these cells is much lower than in Purkinje fibers (Table 7) and depolarization processes are associated mainly with the entry of Ca 2+ (Fig. 36). At the same time, quinidine blocks the inhibitory effect of the vagus nerve on the sinoatrial node (vagolytic effect) and therefore can cause minor tachycardia.

  In fibers atrioventricular node depolarization processes (phases 0 and 4) are caused mainly by the entry of Ca 2+ and, to a lesser extent, by the entry of Na + (Fig. 37). Quinidine slows down phases 0 and 4 of the action potential and, accordingly, reduces the conductivity and automaticity of the fibers of the atrioventricular node. At the same time, quinidine eliminates the inhibitory effect of the vagus on atrioventricular conduction. As a result, in therapeutic doses, quinidine has a moderate inhibitory effect on atrioventricular conduction.

  Table 7. Electrophysiological characteristics of cells of the cardiac conduction system

  In fibers working myocardium atria and ventricles, quinidine disrupts depolarization and weakens myocardial contractions. Quinidine reduces excitability and increases ERP of working myocardial fibers, which also prevents pathological impulse circulation.

  Quinidine dilates peripheral blood vessels (a-adrenergic blocking effect). Due to a decrease in cardiac output and a decrease in total peripheral vascular resistance, quinidine reduces blood pressure.

  Quinidine is prescribed orally for persistent and paroxysmal forms of atrial fibrillation, ventricular and supraventricular paroxysmal tachycardia, ventricular and atrial extrasystoles.

  Side effects of quinidine: decreased strength of heart contractions, decreased blood pressure, dizziness, impaired atrioventricular conduction, cinchonism (tinnitus, hearing loss, dizziness, headache, visual disturbances, disorientation), nausea, vomiting, diarrhea, thrombocytopenia, allergic reactions. Quinidine, like many other antiarrhythmic drugs, can cause cardiac arrhythmias in some patients (on average 5%) - an arrhythmogenic (proarrhythmic) effect.

  Procainamide (procainamide), unlike quinidine, has less effect on myocardial contractility and does not have α-adrenergic blocking properties. The drug is prescribed orally, and in emergency cases it is administered intravenously or intramuscularly, mainly for ventricular, less often for supraventricular tachyarrhythmias (to stop atrial flutter or fibrillation) and extrasystole.

  Side effects of procainamide: arterial hypotension (associated with the ganglion-blocking properties of procainamide), flushing of the face, neck, atrioventricular conduction disturbances, nausea, vomiting, headache, insomnia. With long-term use of procainamide, hemolytic anemia, leukopenia, agranulocytosis, and the development of systemic lupus erythematosus syndrome are possible (initial symptoms are skin rashes, arthralgia).

  Disopyramide (rhythmilen) is prescribed orally. Effective for atrial and especially ventricular tachyarrhythmias and extrasystoles. Among the side effects, the inhibitory effect of disopyramide on myocardial contractility and M-anticholinergic effect (mydriasis, impaired near vision, dry mouth, constipation, difficulty urinating) is expressed. Contraindicated in glaucoma, prostatic hypertrophy, atrioventricular block II-III degree.

  Subgroup IB drugs- lidocaine, mexiletine, phenytoin, unlike drugs of subgroup IA, have less effect on conductivity, do not block potassium channels (“pure” sodium channel blockers), do not increase, but decrease the duration of the action potential (ERP decreases accordingly).

  Lidocaine (xicaine) is a local anesthetic and at the same time an effective antiarrhythmic agent. Due to low bioavailability, the drug is administered intravenously. The effect of lidocaine is short-term (t 1/2 1.5-2 hours), so usually solutions of lidocaine are administered intravenously.

  In Purkinje fibers, lidocaine slows the rate of rapid depolarization (phase 0) to a lesser extent than quinidine. Lidocaine slows diastolic depolarization (phase 4). Unlike drugs of subgroup IA, lidocaine does not increase, but rather decreases, the duration of the action potential of Purkinje fibers. This is due to the fact that, by blocking Na + channels in the “plateau” phase (phase 2), lidocaine shortens this phase; phase 3 (repolarization) begins earlier (Fig. 38).

  Lidocaine reduces excitability and conductivity (less than quinidine), reduces automaticity and reduces ERP of Purkinje fibers (the ratio of ERP to action potential duration increases).

  Lidocaine does not have a significant effect on the sinoatrial node; has a weak inhibitory effect on the atrioventricular node. In therapeutic doses, lidocaine has little effect on myocardial contractility, blood pressure, and atrioventricular conduction.

  Lidocaine is used only for ventricular tachyarrhythmias and extrasystole. Lidocaine is the drug of choice for the treatment of ventricular arrhythmias associated with myocardial infarction. At the same time, long-term administration of lidocaine is considered inappropriate for the prevention of arrhythmias during myocardial infarction (possible proarrhythmic effect of lidocaine, weakening of heart contractions, disruption of atrioventricular conduction).

  Side effects of lidocaine: moderate inhibition of atrioventricular conduction (contraindicated in atrioventricular block II-III degree), increased excitability, dizziness, paresthesia, tremor.

  An overdose of lidocaine may cause drowsiness, disorientation, bradycardia, atrioventricular block, arterial hypotension, respiratory depression, coma, cardiac arrest.

  Phenytoin (diphenin) is an antiepileptic drug that also has antiarrhythmic properties similar to those of lidocaine. Phenytoin is especially effective for arrhythmias caused by cardiac glycosides.

  Subgroup 1C drugs- propafenone, flecainide - significantly slow down the rate of fast depolarization (phase 0), slow down spontaneous slow depolarization (phase 4) and have little effect on the repolarization (phase 3) of Purkinje fibers. Thus, these substances clearly inhibit excitability and conductivity, having little effect on the duration of the action potential. By reducing excitability, the ERP of Purkinje fibers and fibers of the working myocardium is increased. Inhibits atrioventricular conduction. Propafenone has weak β-adrenergic blocking activity.

  The drugs are effective for supraventricular arrhythmias, ventricular extrasystoles and tachyarrhythmias, but have pronounced arrhythmogenic properties (can cause arrhythmias in

  10-15% of patients), reduce myocardial contractility. Therefore, they are used only when other antiarrhythmic drugs are ineffective. Prescribed orally and intravenously.

  β-Adrenergic blockers, by blocking β-adrenergic receptors, eliminate the stimulating effect of sympathetic innervation on the heart and, therefore, reduce: 1) automaticity of the sinoatrial node, 2) automaticity and conductivity of the atrioventricular node, 3) automaticity of Purkinje fibers (Fig. 39).

  P-blockers are used mainly for supraventricular tachyarrhythmias and extrasystoles. In addition, these drugs may be effective in ventricular extrasystoles associated with increased automaticity.

  Side effects of β-blockers: heart failure, bradycardia, impaired atrioventricular conduction, increased fatigue, increased bronchial tone (contraindicated in bronchial asthma), narrowing of peripheral vessels, increased effect of hypoglycemic agents (elimination of the hyperglycemic effect of adrenaline).

  15.1.3. Drugs that increase the duration of the action potential (drugs that slow down repolarization; blockers of potassium channels)

  Drugs in this group include amiodarone, sotalol, bretilium, ibutilide, and dofetilide.

  Amiodarone (cordarone) is an iodine-containing compound (similar in structure to thyroid hormones). Highly effective for various forms of tachyarrhythmias and extrasystoles, including those resistant to other antiarrhythmic drugs. In particular, amiodarone is highly effective in converting atrial fibrillation and flutter into sinus rhythm and in preventing ventricular fibrillation. The drug is prescribed orally, less often - intravenously.

  Amiodarone blocks K + channels and slows down repolarization in the fibers of the cardiac conduction system and in the fibers of the working myocardium. In this regard, the duration of the action potential and ERP increases.

  In addition, amiodarone has some inhibitory effects on Na + channels and Ca 2+ channels, and also has non-competitive β -adrenergic blocking properties. Therefore, amiodarone can be classified not only as III, but also as 1a, II and IV classes of antiarrhythmic drugs.

  Due to the blockade of Ca 2+ channels and β-adrenergic receptors, amiodarone weakens and slows down heart contractions (reduces the heart's need for oxygen), and due to the blockade of α-adrenergic receptors, it dilates coronary and peripheral vessels and moderately reduces blood pressure. Therefore, amiodarone is effective for angina pectoris, for the prevention of exacerbations of coronary insufficiency after myocardial infarction.

  Amiodarone is highly lipophilic, is deposited in tissues for a long time (adipose tissue, lungs, liver) and is very slowly excreted from the body, mainly with bile ( t 60-100 days). With long-term systematic use of amiodarone, light brown deposits (promelanin and lipofuscin) are noted along the perimeter of the cornea (usually do not interfere with vision), as well as deposits in the skin, due to which the skin acquires a gray-blue tint and becomes highly sensitive to ultraviolet rays (photosensitization) .

  Arrhythmias torsade de pointes (“twisting of peaks”; ventricular tachyarrhythmia with periodic changes in the direction of QRS waves; associated with a slowdown in repolarization and the occurrence of early post-depolarization - before the end of the 3rd phase) in 2-5% of patients;

  Increased bronchial tone; :

  Tremor, ataxia, paresthesia;

  Hyperfunction of the thyroid gland or hypofunction of the thyroid gland (amiodarone interferes with the conversion of T4 to T3);

  Liver dysfunction;

  Interstitial pneumonitis (associated with the formation of toxic oxygen radicals, inhibition of phospholipases and the development of lipophospholipidosis); possible pulmonary fibrosis;

  Nausea, vomiting, constipation.

  Sotalol (betapece) is a β-adrenergic blocker, which at the same time increases the duration of the action potential, i.e. belongs to classes II and III of antiarrhythmic drugs. It is used for ventricular and supraventricular tachyarrhythmias (in particular, for atrial fibrillation and flutter to restore the sinus rhythm of atrial contractions), as well as for extrasystole. It is devoid of many side effects characteristic of amiodarone, but exhibits side effects characteristic of β-blockers. When using the drug, torsade de pointes arrhythmias are possible (1.5-2%).

  Bretylium (ornid) increases the duration of the action potential mainly in ventricular cardiomyocytes and is used for ventricular tachyarrhythmias (can be administered intravenously to relieve arrhythmias). It also has sympatholytic properties.

  Drugs that increase the duration of the action potential and, accordingly, the ERP in the atria are effective for converting atrial fibrillation into sinus rhythm.

  Compounds have been synthesized that selectively block K + channels and increase the duration of the action potential and ERP without affecting other properties of cardiomyocytes - “pure” class III drugs ibutilidium dofetild. These drugs have a selective antifibrillatory effect. They are used to convert atrial fibrillation to sinus rhythm and to prevent subsequent atrial fibrillation. Torsade de pointes arrhythmias are possible when using ibutilide and dofetilide.

  Sodium channel blockers

  Sodium channel blockers are divided into 3 subgroups:

  IA - quinidine, procainamide, disopyramide,

  IB - lidocaine, mexiletine, phenytoin,

  1C - flecainide, propafenone.

  Subgroup IA drugs - quinidine, procainamide, disopyramide.

  Quinidine is a dextrorotatory isomer of quinine (an alkaloid of cinchona bark; genus Cinchona). Acting on cardiomyocytes, quinidine blocks sodium channels and therefore slows down the depolarization processes. In addition, quinidine blocks potassium channels and therefore slows down repolarization.

  The effect of quinidine on Purkinje fibers ventricles of the heart. The following phases are distinguished in the action potential of Purkinje fibers:

  Phase 0 - rapid depolarization,

  Phase 1 - early repolarization,

  Phase 3 - late repolarization,

  Phase 4 - spontaneous slow depolarization (diastolic depolarization); once the spontaneous slow depolarization reaches the threshold level, a new action potential is generated; the rate of reaching the threshold level determines the frequency of potentials, i.e. automaticity of Purkinje fibers.

  Due to the slowdown of fast depolarization, quinidine reduces excitability and conductivity, and due to the slowdown of spontaneous slow depolarization, it reduces the automaticity of Purkinje fibers.

  Quinidine increases the duration of the action potential of Purkinje fibers.

  On the cells sinoatrial node quinidine has a weak inhibitory effect, since the resting potential in these cells is much lower than in Purkinje fibers and depolarization processes are associated mainly with the entry of Ca 2+. At the same time, quinidine blocks the inhibitory effect of the vagus nerve on the sinoatrial node (vagolytic effect) and therefore can cause minor tachycardia.

  In fibers working myocardium atria and ventricles, quinidine disrupts depolarization and weakens myocardial contractions. Quinidine reduces the excitability of the fibers of the working myocardium, which also prevents the pathological circulation of impulses.

  Quinidine dilates peripheral blood vessels (a-adrenergic blocking effect). Due to a decrease in cardiac output and a decrease in total peripheral vascular resistance, quinidine reduces blood pressure.

  Quinidine is prescribed orally for persistent and paroxysmal forms of atrial fibrillation, ventricular and supraventricular paroxysmal tachycardia, ventricular and atrial extrasystoles.

  Side effects of quinidine: decreased strength of heart contractions, decreased blood pressure, dizziness, impaired atrioventricular conduction, cinchonism (tinnitus, hearing loss, dizziness, headache, visual disturbances, disorientation), nausea, vomiting, diarrhea, thrombocytopenia, allergic reactions. Quinidine, like many other antiarrhythmic drugs, can cause cardiac arrhythmias in some patients (on average 5%) - an arrhythmogenic (proarrhythmic) effect.

  Procainamide (procainamide), unlike quinidine, has less effect on myocardial contractility and does not have α-adrenergic blocking properties. The drug is prescribed orally, and in emergency cases it is administered intravenously or intramuscularly, mainly for ventricular, less often for supraventricular tachyarrhythmias (to stop atrial flutter or fibrillation) and extrasystole.

  Side effects of procainamide: arterial hypotension (associated with the ganglion-blocking properties of procainamide), flushing of the face, neck, atrioventricular conduction disturbances, nausea, vomiting, headache, insomnia. With long-term use of procainamide, hemolytic anemia, leukopenia, agranulocytosis, and the development of systemic lupus erythematosus syndrome are possible (initial symptoms are skin rashes, arthralgia).

  Disopyramide (rhythmilen) is prescribed orally. Effective for atrial and especially ventricular tachyarrhythmias and extrasystoles. Among the side effects, the inhibitory effect of disopyramide on myocardial contractility and M-anticholinergic effect (mydriasis, impaired near vision, dry mouth, constipation, difficulty urinating) is expressed. Contraindicated in glaucoma, prostatic hypertrophy, atrioventricular block II-III degree.

  Subgroup IB drugs - lidocaine, mexiletine, phenytoin unlike drugs of subgroup IA, they have less effect on conductivity, do not block potassium channels (“pure” sodium channel blockers), and do not increase, but decrease, the duration of the action potential (ERP decreases accordingly).

  Lidocaine (xicaine) is a local anesthetic and at the same time an effective antiarrhythmic agent. Due to low bioavailability, the drug is administered intravenously. The effect of lidocaine is short-term (t 1/2 1.5-2 hours), so usually solutions of lidocaine are administered intravenously.

  In Purkinje fibers, lidocaine slows the rate of rapid depolarization (phase 0) to a lesser extent than quinidine. Lidocaine slows diastolic depolarization (phase 4). Unlike drugs of subgroup IA, lidocaine does not increase, but rather decreases, the duration of the action potential of Purkinje fibers. This is due to the fact that, by blocking Na + channels in the “plateau” phase (phase 2), lidocaine shortens this phase; phase 3 (repolarization) begins earlier.

  Lidocaine reduces excitability and conductivity (less than quinidine), reduces automaticity and reduces ERP of Purkinje fibers (the ratio of ERP to action potential duration increases).

  Lidocaine does not have a significant effect on the sinoatrial node; has a weak inhibitory effect on the atrioventricular node. In therapeutic doses, lidocaine has little effect on myocardial contractility, blood pressure, and atrioventricular conduction.

  Lidocaine is used only for ventricular tachyarrhythmias and extrasystole. Lidocaine is the drug of choice for the treatment of ventricular arrhythmias associated with myocardial infarction. At the same time, long-term administration of lidocaine is considered inappropriate for the prevention of arrhythmias during myocardial infarction (possible proarrhythmic effect of lidocaine, weakening of heart contractions, disruption of atrioventricular conduction).

  Side effects of lidocaine: moderate inhibition of atrioventricular conduction (contraindicated in atrioventricular block II-III degree), increased excitability, dizziness, paresthesia, tremor.

  An overdose of lidocaine may cause drowsiness, disorientation, bradycardia, atrioventricular block, arterial hypotension, respiratory depression, coma, cardiac arrest.

  Mexiletine is an analogue of lidocaine, effective when taken orally.

  Phenytoin (diphenin) is an antiepileptic drug that also has antiarrhythmic properties similar to those of lidocaine. Phenytoin is especially effective for arrhythmias caused by cardiac glycosides.

  Subgroup 1C drugs - propafenone, flecainide - significantly slow down the rate of fast depolarization (phase 0), slow down spontaneous slow depolarization (phase 4) and have little effect on the repolarization (phase 3) of Purkinje fibers. Thus, these substances clearly inhibit excitability and conductivity, having little effect on the duration of the action potential. By reducing excitability, the ERP of Purkinje fibers and fibers of the working myocardium is increased. Inhibits atrioventricular conduction.

  Propafenone has weak adrenergic blocking activity.

  The drugs are effective for supraventricular arrhythmias, ventricular extrasystoles and tachyarrhythmias, but have pronounced arrhythmogenic properties (can cause arrhythmias in 10-15% of patients) and reduce myocardial contractility. Therefore, they are used only when other antiarrhythmic drugs are ineffective. Prescribed orally and intravenously.

  Of the β-blockers, propranolol, metoprolol, atenolol, etc. are used as antiarrhythmic drugs.

  β-Adrenergic blockers, by blocking β-adrenergic receptors, eliminate the stimulating effect of sympathetic innervation on the heart and, therefore, reduce: 1) automaticity of the sinoatrial node, 2) automaticity and conductivity of the atrioventricular node, 3) automaticity of Purkinje fibers.

  B-blockers are used mainly for supraventricular tachyarrhythmias and extrasystoles. In addition, these drugs may be effective in ventricular extrasystoles associated with increased automaticity.

  Side effects of β-blockers: heart failure, bradycardia, impaired atrioventricular conduction, increased fatigue, increased bronchial tone (contraindicated in bronchial asthma), constriction of peripheral vessels, increased effect of hypoglycemic agents (elimination of the hyperglycemic effect of adrenaline).

  Drugs that increase the duration of the action potential (drugs that slow down repolarization; potassium channel blockers)

  Drugs in this group include amiodarone, sotalol, bretylium, ibutilide, and dofetilide.

  Amiodarone (cordarone) is an iodine-containing compound (similar in structure to thyroid hormones). Highly effective for various forms of tachyarrhythmias and extrasystoles, including those resistant to other antiarrhythmic drugs. In particular, amiodarone is highly effective in converting atrial fibrillation and flutter into sinus rhythm and in preventing ventricular fibrillation. The drug is prescribed orally, less often - intravenously.

  Amiodarone blocks K + channels and slows down repolarization in the fibers of the cardiac conduction system and in the fibers of the working myocardium. In this regard, the duration of the action potential and ERP increases.

  In addition, amiodarone has some inhibitory effects on Na + channels and Ca 2+ channels, and also has non-competitive β -adrenergic blocking properties. Therefore, amiodarone can be classified not only as III, but also as 1a, II and IV classes of antiarrhythmic drugs.

  Amiodarone has non-competitive α-adrenergic blocking properties and dilates blood vessels.

  Due to the blockade of Ca 2+ channels and β-adrenergic receptors, amiodarone weakens and slows down heart contractions (reduces the heart's need for oxygen), and due to the blockade of α-adrenergic receptors, it dilates coronary and peripheral vessels and moderately reduces blood pressure. Therefore, amiodarone is effective for angina pectoris, for the prevention of exacerbations of coronary insufficiency after myocardial infarction.

  Amiodarone is highly lipophilic, is deposited in tissues for a long time (adipose tissue, lungs, liver) and is very slowly excreted from the body, mainly with bile ( t 60-100 days). With long-term systematic use of amiodarone, light brown deposits (promelanin and lipofuscin) are noted along the perimeter of the cornea (usually do not interfere with vision), as well as deposits in the skin, due to which the skin acquires a gray-blue tint and becomes highly sensitive to ultraviolet rays (photosensitization) .

  Other side effects of amiodarone:

  Decreased myocardial contractility;

  Difficulty in atrioventricular conduction;

  Arrhythmias torsade de pointes (“twisting of peaks”; ventricular tachyarrhythmia with periodic changes in the direction of QRS waves; associated with a slowdown in repolarization and the occurrence of early afterdepolarization - before the end of the 3rd phase) in 2-5% of patients;

  Increased bronchial tone; :

  Tremor, ataxia, paresthesia;

  Hyperfunction of the thyroid gland or hypofunction of the thyroid gland (amiodarone interferes with the conversion of T4 to T3);

  Liver dysfunction;

  Interstitial pneumonitis (associated with the formation of toxic oxygen radicals, inhibition of phospholipases and the development of lipophospholipidosis); possible pulmonary fibrosis;

  Nausea, vomiting, constipation.

  Sotalol (betapece) is a β-adrenergic blocker, which at the same time increases the duration of the action potential, i.e. belongs to classes II and III of antiarrhythmic drugs. It is used for ventricular and supraventricular tachyarrhythmias (in particular, for atrial fibrillation and flutter to restore the sinus rhythm of atrial contractions), as well as for extrasystole. It is devoid of many side effects characteristic of amiodarone, but exhibits side effects characteristic of β-blockers. When using the drug, torsade de pointes arrhythmias are possible (1.5-2%).

  Bretylium (ornid) increases the duration of the action potential mainly in ventricular cardiomyocytes and is used for ventricular tachyarrhythmias (can be administered intravenously to relieve arrhythmias). It also has sympatholytic properties.

  Drugs that increase the duration of the action potential and, accordingly, the ERP in the atria are effective for converting atrial fibrillation into sinus rhythm.

  Compounds have been synthesized that selectively block K + channels and increase the duration of the action potential and ERP without affecting other properties of cardiomyocytes - “pure” class III drugs ibutilid dofetilide. These drugs have a selective antifibrillatory effect. They are used to convert atrial fibrillation to sinus rhythm and to prevent subsequent atrial fibrillation. Torsade de pointes arrhythmias are possible when using ibutilide and dofetilide.

In medicine, antiarrhythmic drugs are used to normalize the rhythm of heart contractions. Such drugs are intended only to control the clinical symptoms of diseases in which the functioning of the heart muscle is impaired. Antiarrhythmics have no effect on life expectancy. Depending on the nature of changes in heart rhythm, antiarrhythmic drugs from different pharmacological groups and classes are prescribed. Their use should be long-term and under strict control of electrocardiography.

Indications for the use of antiarrhythmic drugs

The muscle cells of the heart, called cardiomyocytes, are riddled with a large number of ion channels. Arrhythmia is directly related to their work. It develops as follows:

1. Sodium, potassium and chlorine ions move through cardiomyocytes.
2. Due to the movement of these particles, an action potential is formed - an electrical signal.
3. In a healthy state, cardiomyocytes contract synchronously, so the heart works normally.
4. With arrhythmia, this established mechanism malfunctions, which leads to disruption of the propagation of nerve impulses.

Antiarrhythmic drugs are used to restore normal heart contraction. Medicines help reduce the activity of the ectopic pacemaker. Literally, ectopia means the appearance of something in the wrong place. With an ectopic rhythm, electrical excitation of the heart occurs in any part of the conducting fibers of the myocardium, but not in the sinus node, which is an arrhythmia.

Drugs against arrhythmia act by blocking certain ion channels, which helps stop the circulation of the pathological impulse. The main indications for the use of such drugs are tachyarrhythmias and bradyarrhythmias. Certain medications are prescribed taking into account the clinical symptoms of the pathology and the presence or absence of structural pathologies of the heart. Arrhythmias for which antiarrhythmics are prescribed are associated with the following diseases:

• coronary heart disease (CHD);
• central nervous system (CNS) disorders;
• stress;
• hormonal disorders during pregnancy, menopause;
• inflammatory heart diseases (rheumatic carditis, myocarditis);
• imbalance of electrolytes with hypercalcemia and hypokalemia;
• hyperfunction of the thyroid gland and other endocrine pathologies;
• cardiopsychoneurosis.

Classification of antiarrhythmic drugs

The criterion for classifying antiarrhythmic drugs is their main effect on the production of electrical impulses in cardiomyocytes. Different antirhythmics show certain effectiveness only in relation to specific types of arrhythmia. Taking this factor into account, the following groups of antiarrhythmic drugs are distinguished:

• Class 1 antiarrhythmics are membrane-stabilizing sodium channel blockers. They directly affect the functional abilities of the myocardium.
• Class 2 antiarrhythmics - beta blockers. They act by reducing the excitability of the heart muscle.
• Class 3 antiarrhythmics are potassium channel blockers. These are new generation antiarrhythmic drugs. They slow down the flow of potassium ions, thereby lengthening the time of excitation of cardiomyocytes. This helps stabilize the electrical activity of the heart.
• Class 4 antiarrhythmics are calcium antagonists, or slow calcium channel blockers. Helps prolong the time of heart insensitivity to pathological impulses. As a result, the abnormal contraction is eliminated.
• Other antiarrhythmic drugs. These include tranquilizers, antidepressants, cardiac glycosides, sedatives, and neurotropic drugs. They have a complex effect on the myocardium and its innervation.
• Plant-based drugs with antiarrhythmogenic effects. These medications have a milder effect and fewer side effects.

Membrane-stabilizing sodium channel blockers

These are class 1 antiarrhythmic drugs. Their main effect is to stop the flow of sodium ions into cardiomyocytes. As a result, the excitation wave passing through the myocardium slows down. This eliminates the conditions for rapid circulation of ectopic signals in the heart. The result is that the arrhythmia stops. Sodium channel blockers are divided into 3 more subclasses depending on the effect on the repolarization time (returning the potential difference that occurs during depolarization to the original level):

• 1A – lengthen repolarization time;
• 1B – shorten the repolarization time;
• 1C – do not affect the repolarization time in any way.

1A class

These antiarrhythmic drugs are used for extrasystole - ventricular and supraventricular. Atrial fibrillation is also an indication for their use. This is a heart rhythm disorder in which the atria contract frequently and chaotically and fibrillation of individual groups of atrial muscle fibers is observed. The main effect of class 1A drugs is inhibition of rapid depolarization (extension of repolarization) of the action potential in the myocardium. Due to this, the normal sinus rhythm of heart contractions is restored. Examples of such drugs:

• Quinidine. Reduces the tone of veins and arteries, blocks the penetration of sodium ions into myocardial cells, exhibits antipyretic and analgesic effects. Indications: atrial fibrillation, paroxysmal supraventricular tachycardia, frequent extrasystole. Quinidine should be taken half an hour before meals. The standard dosage is 200–300 mg up to 4 times a day. contraindications: cardiac decompensation, pregnancy, idiosyncrasy. Side effects include nausea, vomiting, diarrhea, allergies, and cardiac depression.
• Novocainamide. Reduces the excitability of the heart, suppresses ectopic foci of excitation, and exhibits a local anesthetic effect. Indicated for extrasystole, paroxysmal atrial fibrillation, paroxysmal tachycardia. Initial dose – 1 tablet 1 hour before or 2 hours after meals. Then the dose is increased to 2-3 pieces per day. Maintenance dosage – 1 tablet every 6 hours. Novocainamide is prohibited in cases of cardiac conduction disturbances and severe heart failure. Its side effects include general weakness, insomnia, nausea, headache, and a sharp drop in blood pressure.

1B class

These antiarrhythmic drugs are ineffective for atrial fibrillation because they have little effect on the sinus node, the degree of conduction and contractility of the myocardium. In addition, such drugs shorten the repolarization time. For this reason, they are not used for supraventricular arrhythmia. Indications for their use:

• extrasystole;
• paroxysmal tachycardia;
• arrhythmias caused by an overdose of cardiac glycosides.

A representative of class 1B antiarrhythmics is the local anesthetic Lidocaine. Its active component increases the permeability of membranes to potassium ions and at the same time blocks sodium channels. Lidocaine affects cardiac contractility in significant dosages. Indications for use:

• ventricular arrhythmias;
• relief and prevention of repeated ventricular fibrillation in patients with acute coronary syndrome;
• repeated paroxysms of ventricular tachycardia, including in the post-infarction and early postoperative period.

To stop an arrhythmic attack, 200 mg of lidocaine is administered intramuscularly. If there is no therapeutic effect, the procedure is repeated after 3 hours. In severe cases of arrhythmia, intravenous injection followed by intramuscular injection is indicated. Lidocaine contraindications:

• sinoatrial block;
• severe bradycardia;
• cardiogenic shock;
• Adam-Stokes syndrome;
• pregnancy;
• lactation;
• sick sinus syndrome;
• heart failure;
• intraventricular conduction disorders.

Intravenous and intramuscular injections of Lidocaine are used with caution in chronic heart failure, sinus bradycardia, arterial hypotension, hepatic and renal dysfunction. Side effects of the drug:

• euphoria;
• dizziness;
• headache;
• disorientation;
• disturbances of consciousness;
• vomiting, nausea;
• collapse;
• bradycardia;
• decrease in pressure.

1C class

The arrhythmogenic effect of antiarrhythmic drugs in this group has led to restrictions on their use. Their main effect is to lengthen intracardiac conduction. A representative of such antiarrhythmics is the drug Ritmonorm based on propafenone. This active component slows down the blood flow of sodium ions into cardiomyocytes, thereby reducing their excitability. Indications for use of Ritmonorm:

• severe ventricular paroxysmal tachyarrhythmia, which poses a threat to life;
• supraventricular paroxysmal tachyarrhythmias;
• AV nodal and supraventricular tachycardia in persons with paroxysmal atrial fibrillation.

Ritmonorm tablets are taken orally, swallowed whole, so as not to feel their bitter taste. Adults weighing over 70 kg are prescribed 150 mg up to 3 times a day. After 3–4 days, the dosage can be increased to 300 mg 2 times. If the patient's weight is less than 70 kg, treatment begins with a lower dose. It is not increased if therapy lasts less than 3–4 days. Common side effects of Ritmonorm include nausea, vomiting, metallic taste in the mouth, dizziness, and headache. Contraindications to the use of this drug:

• myocardial infarction in the last 3 months;
• Brugada syndrome;
• changes in water and electrolyte balance;
• age under 18 years;
• myasthenia gravis;
• obstructive chronic pulmonary disease;
• combined use with Ritonavir;
• pronounced changes in the myocardium.

Beta blockers

Class 2 antiarrhythmics are called beta blockers. Their main actions are lowering blood pressure and dilating blood vessels. For this reason, they are often used for hypertension, myocardial infarction, and circulatory failure. In addition to lowering blood pressure, beta-blockers help normalize the pulse, even if the patient has resistance to cardiac glycosides.

Drugs in this group are effective in increasing the tone of the sympathetic nervous system against the background of stress, autonomic disorder, hypertension, and ischemia. Due to these pathologies, the level of catecholamines in the blood increases, including adrenaline, which acts on beta-adrenergic receptors of the myocardium. Beta blockers interfere with this process, preventing overstimulation of the heart. They have the described properties:

• Anaprilin. Based on propranolol, which is a non-selective adrenergic blocker. Reduces heart rate, reduces contractile force of the myocardium. Indications: sinus, atrial fibrillation and supraventricular tachycardia, arterial hypertension, angina pectoris, prevention of migraine attacks. Start taking 40 mg 2 times a day. The dose should not exceed 320 mg per day. For heart rhythm disturbances, it is recommended to take 20 mg 3 times a day with a gradual increase to 120 mg, divided into 2-3 doses. Contraindications: arterial hypotension, sinus bradycardia, sinotrial block, heart failure, bronchial asthma, metabolic acidosis, tendency to bronchospasm, vasomotor rhinitis. Adverse reactions may include the development of muscle weakness, Raynaud's syndrome, heart failure, vomiting, and abdominal pain.
• Metoprolol. This is a cardioselective adrenergic blocker with antianginal, hypotensive and antiarrhythmic effects. The drug is indicated for hypertension, myocardial infarction, supraventricular, ventricular, and atrial fibrillation, sinus and atrial tachycardia, atrial flutter and fibrillation, ventricular extrasystole. Daily dosage – 50 mg 1–2 times. The side effects of Metoprolol are numerous, so they should be clarified in the detailed instructions for the drug. The medicine is contraindicated for cardiogenic shock, acute heart failure, lactation, intravenous infusion of Verapamil, arterial hypotension.

Potassium channel blockers

These are class 3 antiarrhythmic drugs. They slow down electrical processes in cardiomyocytes by blocking the penetration of potassium ions into these cells. Amiodarone is most often used in this category of antiarrhythmics. It is based on the component of the same name, which exhibits coronary vasodilating, antiarrhythmic and antianginal effects. The latter is due to the blockade of b-adrenergic receptors. Additionally, Amiodarone reduces heart rate and blood pressure. Indications for use:

• paroxysm of flickering;
• prevention of ventricular fibrillation;
• ventricular tachycardia;
• atrial flutter;
• parasystole;
• ventricular and atrial extrasystoles;
• arrhythmias due to coronary and chronic heart failure;
• ventricular arrhythmias.

The initial dose of Amiodarone is 600–800 mg per day, divided into several doses. The total dosage should be 10 g, it is achieved in 5–8 days. After administration, dizziness, headaches, auditory hallucinations, pulmonary fibrosis, pleurisy, vision problems, sleep and memory disturbances may occur. Amiodron is contraindicated for:

• cardiogenic shock;
• collapse;
• hypokalemia;
• sinus bradycardia;
• insufficient secretion of thyroid hormones;
• thyrotoxicosis;
• taking MAO inhibitors;
• weak sinus node syndrome;
• under the age of 18.

Calcium antagonists

Class 4 antiarrhythmics are slow calcium channel blockers. Their action is to block the slow flow of calcium, which helps suppress ectopic foci in the atria and reduce the automaticity of the sinus node. These drugs are often used for hypertension because they can lower blood pressure. Examples of such drugs:

• Verapamil. It has antianginal, hypotensive and antiarrhythmic effects. Indications: atrial fibrillation, sinus, supraventricular tachycardia, supraventricular extrasystole, stable angina pectoris, hypertension. Verapamil is prohibited during pregnancy, lactation, severe bradycardia, and arterial hypotension. The dosage is 40–80 mg per day. After administration, facial flushing, bradycardia, nausea, constipation, dizziness, headache, and weight gain may occur.
• Diltiazem. It acts in the same way as Verapamil. Additionally improves coronary and cerebral blood flow. Diltiazem is used after myocardial infarction, for hypertension, diabetic retinopathy, angina pectoris, supraventricular tachycardia, and attacks of atrial fibrillation. The dosage is selected individually depending on the indications. Contraindications for Diltiazem: atrioventricular block, severe hypertension, atrial fibrillation and flutter, renal failure, lactation. Possible side effects: paresthesia, depression, dizziness, fatigue, bradycardia, constipation, nausea, dry mouth.

Other drugs for arrhythmia

There are drugs that are not antiarrhythmics, but have this effect. They help with paroxysmal tachycardia, mild attacks of atrial fibrillation, ventricular and supraventricular extrasystoles. Examples of such drugs:

• Cardiac glycosides: Korglykon, Strophanthin, Digoxin. They are used to restore sinus rhythm and relieve supraventricular tachycardia.
• Preparations containing magnesium and potassium ions: Panangin, Asparkam. They help reduce the speed of electrical processes in the myocardium. Indicated for ventricular and supraventricular rhythm disturbances.
• Anticholinergics: Atropine, Metacin. These are antiarrhythmic drugs for bradycardia.
• Magnesium sulfate. Used for pirouette-type arrhythmia that occurs after a liquid protein meal, long-term use of certain antiarrhythmics and severe electrolyte disturbances.

Antiarrhythmic drugs of plant origin

Herbal preparations, including antiarrhythmic ones, are safer. In addition to normalizing heart rate, most of them exhibit sedative, analgesic and antispasmodic effects. Examples of such drugs:

• Valerian. Contains extract of the plant of the same name. It has sedative, antiarrhythmic, choleretic and analgesic effects. You need to take 1 per day – 2 tablets or 20–40 drops 3 times. Contraindications: first trimester of pregnancy, deficiency of lactase, sucrase or isomaltase, age under 3 years, glucose-galactose absorption. Side effects include drowsiness, constipation, lethargy, and muscle weakness. Price – 50 tablets – 56 rub.
• Motherwort. Based on an extract of the plant of the same name. Shows hypotensive and sedative effects. The dosage is 14 mg 3-4 times a day. Contraindication – high sensitivity to the composition of the drug. Adverse reactions: rash, irritation and redness on the skin. The price of tablets is 17 rubles.
• Novo-passit. Contains extracts of hops, lemon balm, St. John's wort, hawthorn and guaifenesin. Has a sedative effect. The drug is taken 1 tablet 3 times a day. Adverse reactions: dizziness, vomiting, constipation, cramps, nausea, increased drowsiness. The drug is prohibited for myasthenia gravis, under the age of 12 years. Price – 660 rub. for 60 tablets.
• Persen. Contains extracts of lemon balm, peppermint, valerian. Shows calming, sedative and antispasmodic properties. Take the medicine 2-3 times a day, 2-3 tablets. After administration, constipation, skin rash, bronchospasm, and hyperemia may develop. Contraindications for Persen: arterial hypotension, fructose intolerance, pregnancy, lactation, age less than 12 years, cholelithiasis.

Video

Almost all of the cardiologist’s patients have experienced arrhythmias of various kinds in one way or another. The modern pharmacological industry offers many antiarrhythmic drugs, the characteristics and classification of which will be discussed in this article.

Antiarrhythmic drugs are divided into four main classes. Class I is further divided into 3 subclasses. This classification is based on the effect of drugs on the electrophysiological properties of the heart, that is, on the ability of its cells to produce and conduct electrical signals. Drugs of each class act on their own “points of application”, so their effectiveness for different arrhythmias differs.

There are a large number of ion channels in the cell wall of the myocardium and the conduction system of the heart. Through them there is a movement of potassium, sodium, chlorine and other ions into and out of the cell. The movement of charged particles forms an action potential, that is, an electrical signal. The action of antiarrhythmic drugs is based on the blockade of certain ion channels. As a result, the flow of ions stops and the production of pathological impulses that cause arrhythmia is suppressed.

Classification of antiarrhythmic drugs:

• Class I - fast sodium channel blockers:

1. IA – quinidine, procainamide, disopyramide, gilurythmal;
2. IB – lidocaine, pyromecaine, trimecaine, tocainide, mexiletine, diphenin, aprindin;
3. IC – etacizin, ethmozin, bonnecor, propafenone (ritmonorm), flecainide, lorcainide, allapinin, indecainide.

• Class II - beta-blockers (propranolol, metoprolol, acebutalol, nadolol, pindolol, esmolol, alprenolol, trazicor, cordanum).
• Class III - potassium channel blockers (amiodarone, bretylium tosylate, sotalol).
• Class IV - slow calcium channel blockers (verapamil).
• Other antiarrhythmic drugs (sodium adenosine triphosphate, potassium chloride, magnesium sulfate, cardiac glycosides).

Fast sodium channel blockers

These medications block sodium ion channels and stop sodium from entering the cell. This leads to a slowdown in the passage of the excitation wave through the myocardium. As a result, the conditions for rapid circulation of pathological signals in the heart disappear, and the arrhythmia stops.

Class IA drugs

Class IA drugs are prescribed for supraventricular and, as well as to restore sinus rhythm during atrial fibrillation () and to prevent its repeated attacks. They are indicated for the treatment and prevention of supraventricular and ventricular tachycardias.
The most commonly used drugs from this subclass are quinidine and procainamide.

Quinidine

Lidocaine can cause dysfunction of the nervous system, manifested by convulsions, dizziness, blurred vision and speech, and disturbances of consciousness. When large doses are administered, a decrease in cardiac contractility, slowing of the rhythm or arrhythmia is possible. Allergic reactions are likely to develop (skin lesions, urticaria, Quincke's edema, itchy skin).

The use of lidocaine is contraindicated in atrioventricular block. It is not prescribed for severe supraventricular arrhythmias due to the risk of developing atrial fibrillation.

IC class drugs

These drugs prolong intracardiac conduction, especially in the His-Purkinje system. These drugs have a pronounced arrhythmogenic effect, so their use is currently limited. Of the medications in this class, rhythmonorm (propafenone) is mainly used.

This drug is used to treat ventricular and supraventricular arrhythmias, including. Due to the risk of arrhythmogenic effects, the medicine should be used under the supervision of a physician.

In addition to arrhythmias, the drug can cause worsening of cardiac contractility and progression of heart failure. Nausea, vomiting, and a metallic taste in the mouth are likely. Dizziness, blurred vision, depression, insomnia, and changes in blood tests are possible.

Beta blockers

When the tone of the sympathetic nervous system increases (for example, during stress, autonomic disorders, hypertension, coronary heart disease), a large amount of catecholamines, in particular adrenaline, is released into the blood. These substances stimulate myocardial beta-adrenergic receptors, leading to electrical instability of the heart and the development of arrhythmias. The main mechanism of action of beta blockers is to prevent overstimulation of these receptors. Thus, these drugs protect the myocardium.

In addition, beta-blockers reduce the automaticity and excitability of the cells that make up the conduction system. Therefore, under their influence, the heart rate slows down.

By slowing atrioventricular conduction, beta blockers reduce the heart rate in atrial fibrillation.

Beta-blockers are used in the treatment of atrial fibrillation and flutter, as well as for the relief and prevention of supraventricular arrhythmias. They also help cope with sinus tachycardia.

Ventricular arrhythmias are less responsive to treatment with these drugs, except in cases clearly associated with an excess of catecholamines in the blood.

Anaprilin (propranolol) and metoprolol are most often used to treat rhythm disturbances.
Side effects of these drugs include a decrease in myocardial contractility, a slower pulse, and the development of atrioventricular block. These medications can cause deterioration of peripheral blood flow and coldness of the extremities.

The use of propranolol leads to a deterioration of bronchial obstruction, which is important for patients with bronchial asthma. In metoprolol, this property is less pronounced. Beta blockers can worsen the course of diabetes mellitus, leading to an increase in blood glucose levels (especially propranolol).
These medications also affect the nervous system. They can cause dizziness, drowsiness, memory loss and depression. In addition, they change neuromuscular conduction, causing weakness, fatigue, and decreased muscle strength.

Sometimes, after taking beta blockers, skin reactions (rash, itching, alopecia) and blood changes (agranulocytosis, thrombocytopenia) are observed. Taking these drugs in some men leads to the development of erectile dysfunction.

Be aware of the possibility of beta blocker withdrawal syndrome. It manifests itself in the form of anginal attacks, ventricular arrhythmias, increased blood pressure, increased heart rate, and decreased exercise tolerance. Therefore, these medications should be discontinued slowly, over two weeks.

Beta-blockers are contraindicated in acute heart failure (cardiogenic shock), as well as in severe forms of chronic heart failure. They should not be used for bronchial asthma and insulin-dependent diabetes mellitus.

Sinus bradycardia, second degree atrioventricular block, and a decrease in systolic blood pressure below 100 mm Hg are also contraindications. Art.

Potassium channel blockers

These drugs block potassium channels, slowing down electrical processes in heart cells. The most commonly used drug from this group is amiodarone (cordarone). In addition to blocking potassium channels, it acts on adrenergic and M-cholinergic receptors and inhibits the binding of thyroid hormone to the corresponding receptor.

Cordarone slowly accumulates in tissues and is released from them just as slowly. The maximum effect is achieved only 2 – 3 weeks after the start of treatment. After discontinuation of the drug, the antiarrhythmic effect of cordarone also persists for at least 5 days.

Cordarone is used for the prevention and treatment of supraventricular and ventricular arrhythmias, atrial fibrillation, and rhythm disturbances associated with Wolff-Parkinson-White syndrome. It is used to prevent life-threatening ventricular arrhythmias in patients with acute myocardial infarction. In addition, cordarone can be used for persistent atrial fibrillation to reduce the heart rate.

With long-term use of the drug, the development of interstitial fibrosis of the lungs, photosensitivity, and changes in skin color (purple coloring is possible). Thyroid function may change, so thyroid hormone levels should be monitored while taking this drug. Sometimes visual disturbances, headaches, sleep and memory disturbances, paresthesia, and ataxia appear.

Cordarone may cause sinus bradycardia, slowing of intracardiac conduction, as well as nausea, vomiting and constipation. An arrhythmogenic effect develops in 2–5% of patients taking this medicine. Cordarone is embryotoxic.

This drug is not prescribed for initial bradycardia, intracardiac conduction disorders, or prolongation of the QT interval. It is not indicated for arterial hypotension, bronchial asthma, thyroid diseases, or pregnancy. When combining cordarone with cardiac glycosides, the dose of the latter must be halved.

Slow calcium channel blockers

These drugs block the slow flow of calcium, reducing the automaticity of the sinus node and suppressing ectopic foci in the atria. The main representative of this group is verapamil.

Verapamil is prescribed for the relief and prevention of paroxysms of supraventricular tachycardia, in the treatment, as well as to reduce the frequency of ventricular contractions during fibrillation and atrial flutter. For ventricular arrhythmias, verapamil is ineffective. Side effects of the drug include sinus bradycardia, atrioventricular block, arterial hypotension, and in some cases, decreased cardiac contractility.

Verapamil is contraindicated in atrioventricular block, severe heart failure and cardiogenic shock. The drug should not be used in Wolff-Parkinson-White syndrome, as this will increase the frequency of ventricular contractions.

Other antiarrhythmic drugs

Sodium adenosine triphosphate slows conduction in the atrioventricular node, which makes it possible to use it to stop supraventricular tachycardias, including against the background of Wolff-Parkinson-White syndrome. When it is administered, redness of the face, shortness of breath, and pressing pain in the chest often occur. In some cases, nausea, a metallic taste in the mouth, and dizziness appear. Some patients may develop ventricular tachycardia. The drug is contraindicated in case of atrioventricular block, as well as in case of poor tolerability of this drug.

Potassium preparations help reduce the rate of electrical processes in the myocardium and also suppress the re-entry mechanism. Potassium chloride is used for the treatment and prevention of almost all supraventricular and ventricular rhythm disturbances, especially in cases of hypokalemia during myocardial infarction, alcoholic cardiomyopathy, and intoxication with cardiac glycosides. Side effects are slowing of pulse and atrioventricular conduction, nausea and vomiting. One of the early signs of potassium overdose is paresthesia (sensitivity disturbances, “pins and needles” in the fingers). Potassium supplements are contraindicated in renal failure and atrioventricular block.

Cardiac glycosides can be used to relieve supraventricular tachycardias, restoring sinus rhythm or reducing the frequency of ventricular contractions in atrial fibrillation. These drugs are contraindicated in bradycardia, intracardiac blockade, paroxysmal ventricular tachycardia and Wolff-Parkinson-White syndrome. When using them, it is necessary to monitor the appearance of signs of digitalis intoxication. It can manifest itself as nausea, vomiting, abdominal pain, sleep and vision disturbances, headache, and nosebleeds.

Antagonists (from Greek antagonisma– rivalry), or blockers .

Blockers (antagonists) bind to molecular receptors instead of natural control substances and interfere with the normal action of normal mediators and hormones on these receptors. Unlike agonists, antagonists are only partially similar in structure to the signaling molecule, i.e. to a mediator, modulator or hormone. Therefore, they “idlely” bind to the receptor and form a kind of “protective screen”, preventing the action of the body’s natural signaling molecules on this receptor. In this regard, the natural mediator or hormone remains “out of work”.

Examples of pharmaceutical blocking drugs are antihistamines drugs (for example, diphenhydramine, suprastin, claritin and others) that block histamine receptors on cells and prevent histamine from triggering an allergic reaction.

Another example is the opioid agonist nalorphine, which is used particularly for respiratory disorders caused by high doses of morphine and other similar drugs. Nalorphine (Nalorphini hydrochchloridum - N-allylnormorphine hydrochloride) is an agonist-antagonist of opioid receptors, in contrast to the “pure” morphine antagonist - naloxone. Therefore, nalorphine not only blocks receptors, but also has some activating effect on them as an agonist.

Finally, in the treatment of arterial hypertension, beta-blockers (atenolol, obzidan, inderal and others) are widely used, which block certain adrenergic receptors and cause a slowdown in the heartbeat.

We will look at specific blockers using the example of adrenergic blockers.

Blockers - these are also substances that interfere with the operation of ion channels and, therefore, disrupt the control of the channels, blocking or inhibiting their activity.

1. Blockers of voltage-gated ion channels

1.1. Sodium voltage-gated ion channel blockers

Sodium voltage-gated ion channels can be blocked by water-soluble heterocyclic guanidines, fat-soluble polycyclic compounds, and low-molecular polypeptide poisons of animal origin.

1.1.1. Ion conductivity blocker toxins

1. Tetrodotoxin- an animal poison of a non-protein nature, an alkaloid contained in the body of fish of the Tetraodontidae family (synonyms: pufferfish, four-toothed, cleavers) of the order of pufferfish, in which there are 19 genera and more than 90 species. This poison is better known by the name of the Japanese fish dish - fugu, for the preparation of which poisonous pufferfish is used. Tetrodotoxin has also been found in the California newt (Taricha torosa) and in the eggs of the frog Atepolus chiriquensis.

2. Saxitoxin.

3. Neotoxin.

4. Conotoxin.

Alpha conotoxin (DL50 = 0.012 mg/kg)
Component of the complex venom of the mollusk Conus geographus
A neurotoxin that blocks H-cholinergic receptors in muscles and peripheral nerves.
Cones are very active when touched in their habitat. Their toxic apparatus consists of a poisonous gland connected by a duct to a hard proboscis by a radula-grater located at the wide end of the shell, with sharp spines that replace the mollusk’s teeth. If you take the shell in your hands, the mollusk instantly extends the radula and thrusts spines into the body. The injection is accompanied by acute pain leading to loss of consciousness, numbness of the fingers, strong heartbeat, shortness of breath, and sometimes paralysis. In the Pacific Islands, cases of shell collectors dying from cone stings have been recorded.
The cone shells are 15–20 cm long. Habitat is the eastern and northern coasts of Australia, the eastern coast of Southeast Asia and China, and the Central Pacific region.

1.1.2. Inactivation blocking toxins

1. Toxins of scorpions Androctonus, Buthus, Leiurus.

2. Anemonotoxins from the sea anemone Anemonia sulcata.

2. Blockers of ligand-gated ion channels

For example, the action of acetylcholine is blocked by anticholinergic drugs; norepinephrine with adrenaline - adrenergic blockers; histamine - histamine blockers, etc. Many blockers are used for therapeutic purposes as medications.

3. Sodium-potassium pump blockers

3.1. Palytoxin (DL50 = 0.00015 mg/kg - the average lethal dose, causing death in half of the experimental mice.)
Contained in the rays of six-rayed coral polyps Palythoa toxica, P. tuberculosa, P. сaribacorum. Cytotoxic poison. Damages the sodium-potassium pump of cell membranes, disrupting the gradient of ion concentrations between the cell and the intercellular environment. Causes pain in the chest, as with angina pectoris, tachycardia, difficulty breathing, hemolysis. Death occurs within the first few minutes after the injection into the polyp.

Video:Anticholinergics

Video:Adrenergic blockers