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Dif diagnostics of atrial fibrillation and atrial tachycardia. Differential diagnosis and treatment of cardiac arrhythmias and conduction disorders. Measures for the treatment of chronic functional constipation in children

Heart cough refers to a much discussed and rather conventional term in the clinic for heart disease. It is used by both physicians and patients to denote a manifestation that signals diseases of the cardiovascular system.

The primary concept - cough in heart disease - meant a symptom of left ventricular failure of the heart and arose as a result of the accumulation and stagnation of fluid in the pulmonary circulation (in the lungs). The consequences of this pathological process are cardiac asthma and swollen lungs, transudate (fluid) in which it causes a protective mechanism - cough.

Therefore, the symptoms and treatment of cardiac cough constitute an urgent and demanded problem in the healthcare system.

Provoking factors

The causes of the appearance of a heart cough are diseases that disrupt and exhaust the robot's heart to the stage of decompensation and the development of heart failure. The main ones are:

• ischemic disease hearts;
• cardiosclerosis after a heart attack;
• cardiomyopathy;
• myocarditis;
• arterial hypertension;
• arrhythmias;
• defeat and congenital defects of the heart valves (especially the mitral valve);
• heart defects, often acquired.

Often, simultaneous problems with the respiratory system are the cause of the aggravation of the heart cough.

Features and Symptoms

The symptoms of a heart cough are manifested in certain conditions and are in direct proportion to physical activity. In the initial stage of the disease, the cough becomes more intense with muscular exertion, with the progression of the pathological process - with any physical exertion.

Distinctive features of the heart cough from other types of cough illustrate the question "heart cough - what is it?":

1. Causes discomfort and pain in the heart and chest area during coughing.
2. It is inherently accompanied by a strong heartbeat in most cases.
3. As a rule, it is dry, without phlegm, as opposed to bronchial cough and in smokers. The appearance of bloody discharge indicates an acute course or an advanced form of heart failure (disruption of the left ventricle).
4. In patients, hoarse and ineffective breathing is observed, which is manifested by shortness of breath, a feeling of lack of oxygen and cyanosis. At first, this condition occurs with significant exertion, followed by the appearance with minimal physical activity (climbing stairs, accelerating steps) or a significant monologue during a conversation.
5. Loss of consciousness (fainting) and possible swelling of the cervical veins reveal poor circulation and an increase in chest pressure.

Heart failure cough has special characteristics. With a left ventricular lesion, it is loud, exhausting, mostly dry and irritable, occurs mainly in the evening and interferes with sleep. The position of the patient during sleep in the horizontal plane also provokes a cough, he instinctively sits down and lowers his legs down to reduce the load on the heart and lungs. Over time, hemoptysis joins.

Such a set of signs will help distinguish it from a cough of a different nature and send it to a cardiologist for consultation.

Treatment

The basic principles and methods of therapy include:

• detailed examination of the patient and carrying out differential diagnostics with the pathology of the respiratory system;
• identification and elimination of the underlying cardiac disease that provokes a cough;
• an integrated approach to treatment instead of symptomatic cough suppression, which clears fluid from the bronchi.

Treatment for cardiac cough includes a combination of optimal work and rest, a diet appropriate to the underlying disease, a healthy lifestyle, and medication. To reduce pressure on the small (pulmonary) circulation, diuretics and vasodilators are used. If necessary, antitussive and expectorant medications are used. The combination with oxygen therapy and drugs to strengthen the myocardium and improve its function leads to visible results.

Treatment of cardiac cough with folk remedies in the acute period of the disease and in severe cases is not recommended. Decoctions and infusions, which include mint, lemon balm, valerian root, yarrow, are used under the supervision of a doctor with full courses at the stage of recovery and for the purpose of prevention.

Thus, the answer to the question "how to treat a heart cough?" is an integrated approach, which is based on drug treatment of the underlying disease, maintaining the structure and function of the heart muscle and relieving the load on the circulatory system in combination with a healthy lifestyle and nutrition. The use of traditional medicine is possible with the permission of the attending physician.

As a result, "is there a heart cough," we can say that it not only exists, but its presence acts as a signal to immediately seek medical advice without self-medication.

Symptoms and treatment of paroxysmal atrial fibrillation

The heart works constantly, without stopping. Strong muscular walls of the heart - the atria and ventricles - help him pump blood. During contractions muscle tissue the heart contracts and pushes the blood stream.

• Atrial fibrillation - concept
• Classification of the disease
• Causes of atrial fibrillation
• The clinical picture of pathology
• Diagnosing atrial fibrillation
• Emergency care for an arrhythmia attack
• Atrial fibrillation treatment
• Conservative treatment
• Electro-impulse therapy
• Surgical intervention
• Traditional methods of therapy
• Complications of the disease
• Prevention measures
• Prognosis for atrial fibrillation

A clear rhythm for heart contractions is set by the sinus (sinus-atrial) node located in the right atrium. This pacemaker sends impulses to the atrioventricular node located between the atria and ventricles.

When too many impulses are sent to the AV node, the person experiences an irregular heartbeat and paroxysmal atrial fibrillation is diagnosed.

Atrial fibrillation - concept

PMA - paroxysmal atrial fibrillation (synonym - atrial fibrillation, or AF) - is understood as a type of arrhythmia, a widespread violation of atrial contraction.

This form of arrhythmia is distinguished by the occurrence of tachycardic attacks (paroxysms) with a heart rate of 350 - 700 beats per minute.

With this type of atrial fibrillation, the upper heart chambers contract at a high frequency and irregularly, and the attack can last from a couple of minutes to several days.

The specific rate of contraction of the heart will depend on individual indicators:

• the level of activity of the nervous system;
• physiological properties of the atrioventricular node;
• taking medications;
• presence / absence of organic pathologies of the heart, etc.

Paroxysmal atrial fibrillation (PFP) is a common diagnosis, among other HPCs (cardiac arrhythmias). The disease occurs in 1 - 2% of the population, and after 80 years - already in 8%, the risk of developing arrhythmias in men and women is approximately the same. In stroke survivors, such a heart rhythm disorder is recorded in 20% of cases.

The risk of sudden death in atrial fibrillation increases 2 times compared with a healthy person. The lethal outcome is due to severe hemodynamic and thromboembolytic complications. A person with AF receives an exemption from military service.

Classification of the disease

Depending on the specific heart rate per minute, the following types of pathology are distinguished:

1. Flutter with a frequency of contractions up to 200 beats.
2. Flicker with a contraction rate of 200 beats or more.

Since the ventricles against the background of arrhythmia begin to contract in an enhanced mode, the classification takes into account the following forms of the disease:

1. Tachysystolic (tachyform) - the ventricles contract above 90 times per minute.
2. Bradystolic - the indicator is less than 60 times per minute.
3. Normosystolic - the rate of contractions is in the range of 60 - 90.

Another classification subdivides arrhythmia into the following forms:

• ventricular, with severe heart rhythm disturbances, pronounced on the ECG;
• atrial, with a change in the conduction of the His bundle;
• mixed, with a combination of the two indicated forms.

The first detected episode of the disease should be distinguished from the actual paroxysmal fibrillation, in which the paroxysm is repeated and lasts up to 7 days (more often up to 2 days).

The disease can persist (last more than a week) or turn into a long-term persistent type (the attack lasts up to a year).

With frequent exacerbations of cardiac arrhythmias, they speak of a recurrent type. A persistent type of disease implies the persistence of symptoms of atrial fibrillation for more than a year with the ineffectiveness of the therapy.

On the basis of the FP is divided into classes:

1. First, there is no clinical picture.
2. Second, the quality of life does not suffer, but there are mild signs of the disease.
3. Third - there are numerous complaints, the patient has to limit himself in life.
4. Fourth, the clinic is bright, there are disabling complications.

Causes of atrial fibrillation

Young people often develop an idiopathic form of the disease, the cause of which cannot be established. In other cases, drug addiction and alcoholism, hereditary predisposition and genetic diseases can disrupt the work of the heart in a patient under 30 years of age.

In older people, coronary artery disease (coronary artery disease) is considered the main cause of atrial fibrillation.

The etiology of paroxysms of atrial fibrillation can be as follows:

• diseases of the thyroid gland, especially thyrotoxicosis;
• rheumatism;
• valvular heart failure;
• cardiomyopathies of various types;
• inflammation of the heart membrane - pericarditis;
• long-term current hypertension;
• obstructive sleep apnea syndrome;
• suffered ischemic stroke, heart attack;
• amyloidosis;
• myxoma and sarcoma of the heart;
• hemochromatosis;
• serious types of anemia;
• low levels of potassium in the body;
• lung cancer, emphysema, pneumonia, pulmonary embolism;
• severe poisoning;
• electric shock;
• SVC syndrome (Wolff-Parkinson-White syndrome).

Paroxysmal arrhythmias sometimes become a consequence of unsuccessful heart surgery. Risk factors against which a situational arrhythmia with paroxysm may occur:

• smoking;
• abuse of coffee, energy drinks;
• severe stress.

The pathogenesis of paroxysmal heart contractions is associated with a combination of the appearance of multiple waves and focal changes. Several centers of rhythm are formed in the atria, and impulses are formed in them, and not in the pacemaker. Due to the presence of additional conduction pathways, the atria contract in an enhanced mode, transmitting impulses to the ventricles.

The clinical picture of pathology

Symptoms in milder forms of heart disease may be absent altogether. Episodes of atrial fibrillation can proceed without obvious manifestations, or a person notes a slight discomfort in the chest. Symptoms are not the same in everyone specific case arrhythmia attacks.

The clinic of cardiac arrhythmia can be very variable and include the following components:

• chest pain;
• hypotension (pressure drop);
• feeling of a rapid heartbeat;
• general weakness, dizziness;
• feeling short of breath and shortness of breath;
• cold hands and feet;
• the appearance of cold sweats;
• chills, trembling;
• light-headedness, loss of consciousness;
• increased urination;
• arrhythmia (unevenness) of the pulse on the arm, neck;
• panic, fear, a feeling of imminent death;
• pallor of the skin, blueness of the lips.

The main symptom of atrial fibrillation with paroxysmal manifestations in a number of patients is the sudden development of a stroke, which can occur after a long asymptomatic course of atrial fibrillation. This variant of AF development is the most severe and can be fatal.

Diagnosing atrial fibrillation

If a patient is admitted to the hospital with an acute attack of arrhythmia, the examination is carried out in the hospital. Diagnostics at the prehospital stage is performed when a person seeks help from a cardiologist for a routine examination with a number of complaints.

A cardiogram (ECG) is the main method for detecting atrial fibrillation. The procedure should be done once a year, even if there are no complaints over the age of 45. According to the ECG, signs of atrial fibrillation with attacks of paroxysms are the absence of a P wave in all leads, which is replaced by chaotic waves of tachysystoles f. R-R intervals are not uniform in duration.

If the patient indicates a history of characteristic symptoms, but there are no obvious ECG changes, Holter monitoring is performed. Exercise ECG can help identify AF.

Organic causes of atrial fibrillation are detected after ultrasound of the heart. Transesophageal ultrasound is indicated if a blood clot in the heart is suspected and is rarely performed.

Differential diagnosis is made with other types of arrhythmias and heart block. An example of the formulation of the diagnosis: paroxysm of atrial fibrillation, tachysystolic form.

Emergency care for an arrhythmia attack

With the development of an attack of cardiac arrhythmia, the task of the patient and his relatives is to see a doctor as early as possible, no later than 48 hours. After 2 days, the risk of blood clots inside the heart and the development of heart attack and stroke is high.

Algorithm for providing emergency care at home:

1. Lay the person on the bed, sofa, floor.
2. Open the window, provide air access.
3. Give the patient advice to take a deep breath, then puff out the cheeks with a closed mouth and a pinched nose. This attempt is designed to act on the vagus nerve and is aimed at stopping the attack. You can press on the eyeballs, on the abdominal press.
4. Give the person warfarin or another prescription anticoagulant to reduce the risk of blood clots.

In parallel, the ambulance team should be called. To stop the paroxysm of arrhythmia, the doctor urgently injects a cardiac glycoside (Korglikon, Strofantin) or a solution of Novocainomide, a solution of Lidocaine on glucose (intravenously).

Atrial fibrillation treatment

After receiving the conclusion, the patient is selected the necessary therapy, recommendations are given on healthy way life, elimination of heavy physical exertion, proper nutrition... It is important to find the cause of the pathology and act on it, for example, to treat the hyperfunction of the thyroid gland, inflammation of the pericardium, etc.

In milder forms, treatment is permissible on an outpatient basis. The indications for hospitalization are:

• first episode of atrial fibrillation;
• heart rate - more than 200 per minute;
• signs of heart failure;
• a sharp drop in pressure;
• the presence of thrombotic complications.

Conservative treatment

The goal of treatment is to restore the rhythm or maintain arrhythmia, but with a normal heart rate. It is important to eliminate the symptoms of the disease and reduce the risk of blood clots and further complications. For everyone who has a paroxysmal form of arrhythmia, the doctor must write a prescription for anticoagulants and antiplatelet agents.

If a person is under 60 years of age and there is no organic lesion of the myocardium, drug treatment should include constant intake of acetylsalicylic acid (Aspirin-Cardio, Cardiomagnyl).

In the presence of coronary artery disease and other aggravating diseases, Warfarin is indicated with regular monitoring of tests. In acute cases, low molecular weight heparins are prescribed for short term.

To restore the rhythm, medical assistance (cardioversion) is prescribed, which can be pharmacological or instrumental.

There are a number of effective antiarrhythmic drugs that prevent recurrent attacks of paroxysmal fibrillation:

• Kordaron;
• Nibentan;
• Propafenone;
• Amiodarone;
• Allapinin;
• Sotalex.

If a strategy for controlling heart rate without eliminating arrhythmia is chosen, then these funds are not prescribed, but are replaced by beta-blockers (Carvedilol, Metoprolol, Betalok), calcium channel blockers (Lerkamen, Amlodipine).

Electro-impulse therapy

Electrical cardioversion involves bringing the heart rhythm back to normal by exposure to an electric current. Due to the high pain, the procedure is performed under anesthesia. A device (cardioverter-defibrillator) with electrodes is installed in the region of the right clavicle, which sends an impulse to the heart, which reboots the organ.

Cardioversion can be done on an emergency or routine basis. If the procedure is planned, a person should drink Warfarin within a month before and after it. Before emergency cardioversion, heparin is urgently administered to the patient.

Surgical intervention

With a recurrent form of the disease and the ineffectiveness of other techniques, the operation is indicated - radiofrequency catheter ablation. This is a minimally invasive intervention.

The electrode is inserted through the femoral vein into the heart, with the help of an electric shock, pathological foci of excitation are destroyed. If it is necessary to destroy an AV node or a bundle of His, a pacemaker must be installed during the operation.

Traditional methods of therapy

Paroxysmal forms of arrhythmia are very life-threatening, therefore, their treatment should be carried out only under the supervision of a physician. Folk remedies can only serve as auxiliary measures for maintaining and strengthening the heart muscle.

For this purpose, the reception of infusions of hawthorn, rose hips is shown, it is useful to eat lemons with honey, add natural vegetable oils to food.

Complications of the disease

The transition of the disease to a permanent form threatens a serious decrease in the quality of life.

The most common complication is the appearance of blood clots in the heart, because the blood does not come out in full from the atria, so it stagnates. With a thrombus embolism, it can cause an ischemic stroke.

Prevention measures

In order not to face atrial fibrillation in its paroxysmal form, it is important:

• give up a lot of coffee, energy drinks;
• do not abuse alcohol, do not smoke;
• do not take medicines with pseudoephedrine without a doctor's prescription;
• eat right;
• take vitamins, omega-3,6,9 acids;
• treat hypertension, ischemic heart disease.

Prognosis for atrial fibrillation

The prognosis will depend on the severity of the heart or other medical condition that caused the arrhythmia. With AF, the risk of stroke is 1.5% before the age of 60, and 25% after the age of 80.

The risk of sudden death increases from year to year. With proper therapy, patients live for 10 - 20 years, after a successful operation, a person can live a full life.

Atrial fibrillation is one of the forms of rhythm disturbances caused by the occurrence of a pathological focus of pulse circulation in the sinus node or in the atrial tissue, characterized by the occurrence of an irregular, rapid and chaotic contraction of the atrial myocardium, and manifested by a sensation of a frequent and irregular heartbeat.

Forms of atrial fibrillation; paroxysmal, constant

In the general concept of atrial fibrillation, fibrillation (flickering) and atrial flutter are distinguished. In the first type, the atrial contractions are "small-wave", with a pulse of about 500 per minute, providing a rapid contraction of the ventricles. In the second type of atrial contraction of about 300-400 per minute, "large-wave", but also forcing the ventricles to contract more often. In both the first and the second type, ventricular contractions can reach more than 200 per minute, but with atrial flutter, the rhythm can be regular - this is the so-called rhythmic, or correct form of atrial flutter.

In addition, atrial fibrillation and atrial flutter can occur simultaneously in one patient for a certain period of time, for example, with paroxysmal atrial fibrillation - atrial flutter. Often during atrial flutter, the ventricular rate can remain within normal limits, and then a more accurate analysis of the cardiogram is required for a correct diagnosis.

In addition to such a division of atrial fibrillation, according to the principle of the course of this disease, the following forms are distinguished:

• Paroxysmal, characterized by the occurrence of interruptions in the work of the heart and recorded by ECG during the first 24-48 hours (up to seven days), which can be stopped independently or with the help of medications,
• Persistent, characterized by rhythm disturbances such as atrial fibrillation or atrial flutter for more than seven days, but capable of spontaneous or medication restoration of the rhythm,
• Long-term persistent, existing for more than one year, but capable of restoring rhythm with the introduction of drugs or electrocardioversion (restoration of sinus rhythm using a defibrillator),
• Constant - a form characterized by the inability to restore sinus rhythm, which has existed for years.

Depending on the frequency of ventricular contractions, brady-, normo- and tachysystolic variants of atrial fibrillation are distinguished. Accordingly, in the first case, the frequency of ventricular contractions is less than 55-60 per minute, in the second - 60-90 per minute and in the third - 90 or more per minute.

Statistical data

According to studies carried out in Russia and abroad, atrial fibrillation occurs in 5% of the population over the age of 60 and in 10% of the population over 80. At the same time, women suffer from atrial fibrillation 1.5 times more often than men. The danger of arrhythmia is that in patients with paroxysmal or permanent forms, strokes and other thromboembolic complications occur 5 times more often.

In patients with heart defects, atrial fibrillation occurs in more than 60% of all cases, and in people with coronary heart disease - in almost 10% of cases.

What happens with atrial fibrillation?

Pathogenetic changes in this rhythm disturbance are due to the following processes. In normal myocardial tissue, the electrical impulse moves unidirectionally - from the sinus node towards the atrioventricular junction. In the presence of any blocks on the path of the impulse (inflammation, necrosis, etc.), the impulse cannot bypass this obstacle and is forced to move in the opposite direction, again causing excitation of the myocardial sections that have just contracted. Thus, a pathological focus of constant circulation of impulses is created.

Constant stimulation of certain areas of atrial tissue leads to the fact that these areas spread excitation to the remaining atrial myocardium, and its fibers contract separately, chaotically and irregularly, but often.

In the future, impulses are conducted through the atrioventricular junction, but due to its relatively small "throughput" capacity, only a part of the impulses reaches the ventricles, which begin to contract at different frequencies and also irregularly.

Video: Atrial Fibrillation - Medical Animation

What causes atrial fibrillation?

In the overwhelming majority of cases, atrial fibrillation occurs as a result of organic damage to the myocardium. Diseases of this type include, first of all, heart defects. As a result of stenosis or valve failure, over time, the patient develops cardiomyopathy - a change in the structure and morphology of the myocardium. Cardiomyopathy leads to the fact that some of the normal muscle fibers in the heart are replaced by hypertrophied (thickened) fibers, which lose their ability to conduct impulses normally. Areas of hypertrophied tissue are pathological foci of impulses in the atria, if it comes about stenosis and / or insufficiency of the mitral and tricuspid valves.

The next disease, which ranks second in the incidence of atrial fibrillation, is ischemic heart disease, including acute and postponed myocardial infarction. The path of development of arrhythmia is similar to defects, only areas of normal muscle tissue are replaced not by hypertrophied, but by necrotic fibers.

Also a significant cause of arrhythmia is cardiosclerosis - the proliferation of connective (scar) tissue instead of ordinary muscle cells. Cardiosclerosis can form within a few months or years after heart attacks or myocarditis (inflammatory changes in the heart tissue of a viral or bacterial nature). Atrial fibrillation often occurs in the acute period of myocardial infarction or in acute myocarditis.

In some patients, atrial fibrillation occurs in the absence of organic damage to the heart due to diseases of the endocrine system. The most common cause in this case is thyroid disease, accompanied by an increased release of thyroid hormones into the blood. This condition is called hyperthyroidism and occurs with nodular or autoimmune goiter. In addition, the constant stimulating effect of thyroid hormones on the heart leads to the formation of dyshormonal cardiomyopathy, which in itself can lead to impaired conduction in the atria.

In addition to the main reasons, risk factors can be identified that increase the likelihood of developing atrial fibrillation in a particular patient. These include age over 50, female sex, obesity, hypertension, endocrine pathology, including diabetes mellitus, a history of heart disease.

The factors that provoke the onset of paroxysm of atrial fibrillation in persons with a history of arrhythmia include conditions that cause changes in the autonomic regulation of cardiac activity.

For example, with the predominant influence of the vagus nerve (vagal, parasympathetic effects), an attack of arrhythmia can begin after an abundant meal, when turning the body, at night or during daytime rest, etc. occurs as a result of stress, fright, strong emotions or physical exertion - that is, all those conditions that are accompanied by increased secretion of adrenaline and norepinephrine into the blood.

Atrial fibrillation symptoms

Symptoms of atrial fibrillation may vary from patient to patient. Moreover, clinical manifestations are largely determined by the form and variant of atrial fibrillation.

For example, the clinic of paroxysmal atrial fibrillation is striking and characteristic. The patient, against the background of complete health or minor precursors (shortness of breath when walking, painful sensations in the heart region), experiences sudden unpleasant symptoms - a sharp feeling of rapid heartbeat, a feeling of shortness of breath, an attack of suffocation, a feeling of a coma in the chest and throat, inability to breathe in or out. At the same time, according to the description of the patients themselves, the heart flutters like a "hare's tail", is ready to jump out of the chest, etc. In addition to this most characteristic symptom, some patients develop vegetative manifestations - excessive sweating, a feeling of internal trembling throughout the body, redness or pale skin, nausea, feeling lightheaded. This symptom complex on simple language called "breakdown" of the rhythm.
But the menacing signs that should alert relatives and the doctor examining the patient are a sharp jump in blood pressure upward (more than 150 mm Hg) or, conversely, a significant decrease in pressure (less than 90 mm Hg), since there is a high risk against the background of high blood pressure development of a stroke, and low blood pressure is a sign of acute heart failure or arrhythmogenic shock.

The clinical manifestations are brighter, the higher the heart rate. Although there are exceptions when a patient tolerates a frequency of 120-150 per minute more than satisfactory, and, conversely, a patient with a bradystolic variant experiences heart interruptions and dizziness more pronounced than with normo- and tachysystole.

With an uncompensated constant form of atrial fibrillation or atrial flutter, the heart rate is usually 80-120 per minute. Patients get used to this rhythm, and practically do not feel interruptions in the work of the heart, only with physical exertion. But here, due to the development of chronic heart failure, complaints of shortness of breath during physical exertion come to the fore, and often with minimal household activity and at rest.

Diagnostics

The algorithm for diagnosing atrial fibrillation consists of the following points:

1. Examination and questioning of the patient. So, even in the process of collecting complaints and anamnesis, it is possible to establish that the patient has any rhythm disturbance. Counting the pulse per minute and determining its irregularity can lead the doctor to think about atrial fibrillation.
2. ECG diagnostics is a simple, accessible and informative method for confirming atrial fibrillation. The cardiogram is performed already when the ambulance team is called or during the initial treatment of the patient with interruptions to the clinic.

The criteria for atrial fibrillation are:

1. After the ECG, the indications for hospitalization are determined (see below). In case of hospitalization, further examination is carried out in the department of cardiology, therapy or arrhythmology, in case of refusal of hospitalization, the patient is sent for additional examination to the polyclinic at the place of residence.
2. Of the additional diagnostic methods, the most often prescribed and informative is daily monitoring of the ECG and blood pressure. This method allows you to register even short runs of arrhythmias that are not "caught" on a standard cardiogram, and also helps to assess the quality of the treatment.
3. Ultrasound of the heart, or echo-CS (echo-cardioscopy). Is the "gold standard" in the imaging diagnosis of heart disease, as it allows you to detect
   significant violations of myocardial contractility, its structural disorders and to evaluate the left ventricular ejection fraction, which is a decisive criterion for evaluating the effectiveness of therapy for heart failure with a constant form of atrial fibrillation.
4. A transesophageal electrophysiological study (PEEPI) is a method based on artificial stimulation of the myocardium and on provoking flicker, which can be immediately recorded on an ECG. It is carried out in order to register arrhythmias, which clinically disturb the patient with subjective sensations, and was not registered on the ECG (including with the help of Holter monitoring).
5. Chest X-ray is used to examine patients with a paroxysmal form (suspected pulmonary embolism) and with a permanent form (to assess venous stasis in the lungs due to chronic heart failure).
6. General and biochemical blood tests, study of the level of thyroid hormones in the blood, ultrasound of the thyroid gland - helps in the differential diagnosis of cardiomyopathies.

In principle, for the diagnosis of atrial fibrillation, characteristic complaints (interruptions in the heart, chest pain, dyspnea), anamnesis (acute or long-lasting), and an ECG with signs of atrial fibrillation or flutter are sufficient. However, it is necessary to find out the cause of such rhythm disturbance only in the process of careful examination of the patient.

Tactics for the treatment of atrial fibrillation

Therapy for paroxysmal and persistent forms of atrial fibrillation is different. The purpose of care in the first form is to provide emergency care and to conduct rhythm-restoring therapy. In the second form, the priority is the appointment of rhythm-reducing therapy with the constant use of medications. The persistent form can be subject to both rhythm-restoring therapy and, in case of unsuccessful implementation of the latter, the transfer of the persistent form to a permanent one using rhythm-reducing drugs.

Treatment of paroxysmal atrial fibrillation

The relief of a paroxysm of flickering or flutter is carried out already at the prehospital stage - by an ambulance or in a polyclinic.

Of the main drugs for an attack of arrhythmia, the following are used intravenously:

• The polarizing mixture is a solution of potassium chloride 4% + glucose 5% 400 ml + insulin 5 ED. In patients with diabetes mellitus instead of a glucose-insulin mixture, physical is used. solution (sodium chloride 0.9%) 200 or 400 ml.
• Panangin or asparkam solution 10 ml intravenously.
• A solution of novocainamide 10% 5 or 10 ml in saline. In case of a tendency to hypotension (low pressure), it should be administered simultaneously with Mesatone to prevent drug hypotension, collapse and loss of consciousness.
• Cordaron at a dosage of 5 mg / kg of body weight is injected in a 5% glucose solution intravenously slowly or by drip. Should be used in isolation from other antiarrhythmic drugs.
• Strofantin 0.025% 1 ml in 10 ml of saline intravenously slowly or in 200 ml of saline by intravenous drip. It can be used only in the absence of glycosidic intoxication (chronic overdose with drugs of digoxin, korglikon, strophanthin, etc.).

After the administration of the drugs, after 20-30 minutes, the patient has an ECG taken and, in the absence of sinus rhythm, he must be taken to the admission department of the hospital to resolve the issue of hospitalization. Restoring the rhythm at the level of the admission department is not carried out, the patient is hospitalized in the department, where the started treatment continues.

Indications for hospitalization:

1. First identified paroxysmal arrhythmia,
2. Prolonged paroxysm (from three to seven days), since the likelihood of thromboembolic complications is high,
3. Paroxysm uncropped at the prehospital stage,
4. Paroxysm with developing complications (acute heart failure, pulmonary edema, pulmonary embolism, heart attack or stroke),
5. Decompensation of heart failure with a constant form of flicker.

Treatment of persistent atrial fibrillation

In the case of persistent flicker, the physician should seek to restore sinus rhythm with medication and / or cardioversion. This is due to the fact that with a restored sinus rhythm, the risk of thromboembolic complications is much lower than with a permanent form, and chronic heart failure progresses less. In case of successful restoration of sinus rhythm, the patient should constantly take antiarrhythmic drugs, for example, amiodarone, cordarone or propafenone (propanorm, rhythmonorm).

Thus, the tactics for a persistent form is as follows - the patient is observed in a polyclinic with atrial fibrillation more than seven days old, for example, after discharge from the hospital with unsuccessful relief of paroxysm and with ineffectiveness of the pills taken by the patient. If the doctor decides to try to restore sinus rhythm, he again sends the patient to the hospital for planned hospitalization for the purpose of medication to restore the rhythm or for cardioversion. If the patient has contraindications (past heart attacks and strokes, blood clots in the heart cavity according to the results of echocardioscopy, untreated hyperthyroidism, severe chronic heart failure, arrhythmia more than two years ago), the persistent form is transferred to a permanent form with the administration of other groups of drugs.

Treatment of a permanent form of atrial fibrillation

With this form, the patient is prescribed pills that slow down the heart rate. The main ones here are the group of beta-blockers and cardiac glycosides, for example, Concor 5 mg x 1 time per day, Coronal 5 mg x 1 time per day, egilok 25 mg x 2 times a day, Betaloc ZOK 25-50 mg x 1 time per day and others. From cardiac glycosides used digoxin 0.025 mg 1/2 tablet x 2 times a day - 5 days, a break - 2 days (Sat, Sun).

It is imperative to prescribe anticoagulants and antiplatelet agents, for example, cardiomagnyl 100 mg at lunchtime, or clopidogrel 75 mg at lunchtime, or warfarin 2.5-5 mg x 1 time per day (it is mandatory under the control of INR - the parameter of the blood coagulation system, usually 2.0-2.5 is recommended). These drugs prevent increased blood clots and reduce the risk of heart attacks and strokes.

Chronic heart failure should be treated with diuretics (indapamide 1.5 mg in the morning, veroshpiron 25 mg in the morning) and ACE inhibitors (prestarium 5 mg in the morning, enalapril 5 mg x 2 times a day, lisinopril 5 mg in the morning), which have an organoprotective effect on blood vessels and the heart.

When is cardioversion indicated?

Cardioversion is the restoration of the original heart rate in a patient with atrial fibrillation using medication (see above) or electric current passed through the chest and affecting the electrical activity of the heart.

Electrical cardioversion is performed on an emergency or routine basis using a defibrillator. This view care should be provided only in the intensive care unit with the use of anesthesia.

Indication for emergency cardioversion is a paroxysm of atrial fibrillation not more than two days old with the development of arrhythmogenic shock.

The indication for elective cardioversion is a paroxysm more than two days old, not stopped with medication, in the absence of blood clots in the atrial cavity, confirmed by transesophageal ultrasound of the heart. If a thrombus is found in the heart, the patient takes warfarin on an outpatient basis for a month, during which, in most cases, the thrombus dissolves, and then, after repeated ultrasound of the heart, in the absence of a thrombus, is sent back to the hospital to decide on cardioversion.

Thus, planned cardioversion is carried out mainly when the doctor strives to restore sinus rhythm with a persistent form of atrial fibrillation.

Technically, cardioversion is performed by placing defibrillator electrodes on the anterior chest wall after the patient is anesthetized with intravenous drugs. After that, the defibrillator delivers a shock, which affects the heart rate. The success rate is very high and accounts for over 90% of successful restoration of sinus rhythm. However, cardioversion is not suitable for all patient populations, and in many cases (eg, in the elderly), MA will rapidly reappear.

Thromboembolic complications after cardioversion account for about 5% among patients who did not take anticoagulants and antiplatelet agents, as well as about 1% among patients who receive such drugs from the onset of arrhythmia.

When is surgical treatment indicated?

Surgical treatment for atrial fibrillation can serve several purposes. So, for example, with heart defects as the main cause of arrhythmia, surgical correction of the defect as an independent operation prevents further recurrence of atrial fibrillation in a greater percentage of cases.

For other heart diseases, radiofrequency or laser ablation of the heart is justified in the following cases:

• Ineffectiveness of antiarrhythmic therapy with frequent paroxysms of atrial fibrillation,
• A persistent form of flicker with rapid progression of heart failure
• Intolerance to antiarrhythmic drugs.

Radiofrequency ablation consists in the action of an electrode with a radio sensor at the end of the atria involved in the pathological circulation of the impulse. The electrode is inserted into the patient under general anesthesia through the femoral artery under X-ray television control. The operation is safe and low-traumatic, takes a short period of time and is not a source of unpleasant sensations for the patient. RFA can be performed according to quotas from the Ministry of Health of the Russian Federation or at the patient's own money.

Is treatment with folk remedies acceptable?

Some patients may ignore the recommendations of their attending physician and begin to heal themselves using traditional medicine methods. As an independent therapy, the intake of herbs and decoctions, of course, is not recommended. But as an auxiliary method, in addition to the main drug therapy, the patient can take decoctions of soothing plants, which have a beneficial effect on the nervous and cardiovascular system. For example, decoctions and infusions of valerian, hawthorn, clover, chamomile, mint and lemon balm are often used. In any case, the patient should inform the treating doctor about taking such herbs.

Are complications of atrial fibrillation possible?

The most common complications are pulmonary embolism (PE), acute heart attack and acute stroke, as well as arrhythmogenic shock and acute heart failure (pulmonary edema).

The most significant complication is stroke. Ischemic stroke, caused by a shot of a blood clot into the vessels of the brain (for example, when the paroxysm stops), occurs in 5% of patients in the first five years after the onset of atrial fibrillation.

Prevention of thromboembolic complications (stroke and PE) is the constant intake of anticoagulants and antiplatelet agents. However, there are some nuances here as well. So, for example, with an increased risk of bleeding in a patient, there is a likelihood of hemorrhage in the brain with the development of a hemorrhagic stroke. The risk of developing such a condition is more than 1% in patients in the first year from the start of anticoagulant therapy. Prevention of increased bleeding is regular monitoring of INR (at least once a month) with timely correction of the anticoagulant dose.

Video: how a stroke occurs due to atrial fibrillation

Forecast

The prognosis for life with atrial fibrillation is determined primarily by the causes of the disease. So, for example, in survivors of acute myocardial infarction and with significant cardiosclerosis, the short-term prognosis for life can be favorable, and for health and in the medium term, unfavorable, since in a short period of time the patient develops chronic heart failure, which worsens the quality of life and shortens it. duration.

Nevertheless, with the regular use of prescribed medications, the prognosis for life and health will undoubtedly improve. And patients with a permanent form of MA registered at a young age, with proper compensation, live with it for up to 20-40 years.

Video: atrial fibrillation - expert opinion

Video: atrial fibrillation in the "Living Healthy" program

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Characteristics of persistent atrial fibrillation

Persistent atrial fibrillation is a serious disorder of the heart, which is characterized by chaotic, frequent, disturbed pace of excitation and contraction of the atria. Often, the disease manifests itself as twitching or fibrillation of individual fibers of the heart, which is called an attack of atrial fibrillation. With the development of pathology, the patient's heart rate reaches 350-600 times per minute, which is considered critical for a person.

Is it possible to get rid of the disease forever, what to do when detecting malfunctions in the work of the heart, how to recognize the signs, symptoms and causes of the disease, is the pathology dangerous for a person's life and what kind of life should be pursued with the development of chaotic contraction of the heart muscles? These questions worry patients who are faced with a disease and are just beginning to treat it.

Important: the disease manifests itself with characteristic and obvious signs, therefore, it is not difficult to detect the development of pathology in the body. The main thing is to start treatment on time, since the prognosis for life will be disappointing - a permanent chronic or persistent form is considered life-threatening and often leads the patient to death.

Atrial fibrillation - a description of the disease

Today, atrial fibrillation is considered a pathology that most often occurs in patients with an irregular heart rhythm. As the diagnosis and prognosis of the disease show, 30% of patients undergo urgent hospitalization, since a permanent persistent form develops rapidly in the human body, while disrupting the work of the heart and causing the appearance of blood clots. If the disease is present in the body for more than 48 hours, this process is considered inevitable, therefore, to eliminate complications, the patient should undergo a full course of treatment.

Doctors say that the patient's drug treatment depends on the form of atrial fibrillation, therefore, before prescribing a group of drugs, a person will need diagnostics, the prognosis of which will show the state of the atria, heart muscle and its fibers. If the restoration of tissues and fibers of the heart with the help of drugs is not possible, the doctor prescribes surgical treatment of the disease, which helps to get rid of the flickering impulses in the heart and restore its functionality.

Important: it is not difficult to notice a violation of the antiarrhythmic of the heart, however, the symptoms of arrhythmia begin to manifest themselves a little later - if the disease is recognized in time, you can achieve fast and high-quality treatment until the pathology has passed into chronic form... If atrial fibrillation is promptly cured, it is possible to:

• return to the old way of life;
• quickly restore the work of the heart;
• facilitate your own quality of life;
• restore the pulse;
• overcome unpleasant symptoms and signs of illness.

But not always atrial fibrillation has pronounced causes and symptoms - in this case, the patient only complains of malaise, weakness and pain in the chest. In this case, only diagnostics will help to make the correct diagnosis thanks to the delivery of tests and ECG, where manifestations of atrial fibrillation will be noticeable. In any case, it is better not to delay the treatment of the disease, then it will not be difficult to cure and completely get rid of this pathology, dangerous to health.

Important: the restoration of the body after treatment is carried out from 1 to 6 months, so you should not hope for a quick result of treatment. If there is no prevention of arrhythmia, the disease manifests itself within a couple of weeks after treatment.

With a long progression of the disease (more than 48 hours), the patient's risk of ischemic stroke and thrombus formation greatly increases. If atrial fibrillation becomes chronic, the progression of circulatory failure will begin in the human body, which will not allow organs and systems to receive nutrients from the blood stream - this leads to serious disruptions in the body's work.

The development of this disease in the human body increases with age - you can get sick with arrhythmia after 40 years. At the same time, treatment with age will only be more difficult, since every year it becomes more difficult for the body to make blood flow, which will certainly affect the quality of treatment. However, the disease cannot be called a common disease, since diagnostics show that the disease is classified in only 6% of patients with heart dysfunction.

Arrhythmia classification

The classification of such a disease has 2 types of clinical course, which include:

• etiological factors;
• electrophysiological mechanisms.

Forms of atrial fibrillation, according to doctors, in our time are divided into three types:

• chronic (or, in other words, permanent);
• persistent;
• transitory.

In a transient form, the disease is characterized by seizures that last in the patient's body for less than 7 days. The rest (advanced) forms of arrhythmia last more than a week and are determined using ecg. Important: the persistent and chronic form are often recurrent, that is, the signs and symptoms of the disease regularly overtake the patient and are expressed in severe pain.

Today, there are 2 types of arrhythmias - newly diagnosed and recurrent. It is important to get rid of them in a short time, since recurrent pathology greatly worsens the condition of the body, so the patient often needs surgery, after which recovery is long and difficult. If you start treating the disease on time and identify its symptoms, you can shorten the treatment, restore the pulse, prevent the onset of coronary heart disease and protect yourself from complications.

As the ECG shows, during atrial fibrillation in the body, certain groups of heart fibers contract, which causes a chaotic muscle contraction. As a result of the uncoordinated work of the atria, an increase in electrical impulses occurs, most of which begin to linger in the body, and the other quickly spread to the ventricles. In this case, the ventricles are forced to contract with a different rhythm. This frequency also has its own types:

• tachysystolic - when the contraction of the ventricles exceeds more than 90 beats per minute;
• normomystolic - contractions are from 60 to 90 beats;
• bradystolic - contractions are less than 60 beats.

Important: each of these types significantly increases the human heart rate and causes the development of coronary heart disease, which carries a dangerous prognosis for life and worsens its image.

With the development of advanced forms of the disease during ECG, the doctor notices atrial flutter. This is a contraction of the heart muscle up to 200-400 beats per minute, which is characterized by a regular and undisturbed heartbeat. Moreover, such flutter occurs in the patient's body without interruption, which does not allow the atria to relax and rest. In this case, the ventricles quickly fill with blood and prevent it from spreading to all parts of the heart. In this case, the patient requires immediate hospitalization and surgery.

The reasons for the development of atrial fibrillation

The restoration and treatment of the body, as well as the normalization of the usual way of life, is possible only if the reason for which atrial fibrillation has struck the human body is identified. Diseases of the heart and other internal organs lead to the development of this disease.

Doctors say that the causes of arrhythmia are:

• arterial hypertension;
• increased heart rate;
• heart failure;
• heart defects caused by rheumatism;
• cardiosclerosis;
• improper lifestyle (lack of physical activity, obesity, sedentary lifestyle);
• myocardial infarction.

Sometimes pathology develops in the body due to the intake of large doses of alcohol, in the presence of thyrotoxicosis, nervous disorders and hypokalemia. In this case, the patient will need surgery, since drug treatment does not always help.

Important: today another type of arrhythmia is known - idiopathic. The causes, signs and symptoms of this form have not yet been able to be identified by doctors even after conducting thorough examinations (ecg, testing, and so on).

Symptoms of the disease

In order to get rid of the disease forever, it is important to identify the symptoms of atrial fibrillation in time, since delay in this case leads to an aggravation of the situation. Symptoms of pathology depend not only on its form, but also on the mental state of the patient, the state of the myocardium, as well as the valve apparatus.

An untreated form of arrhythmia has the following symptoms:

• fast heartbeat;
• pain in the region of the heart;
• interruptions in his work;
• dyspnea;
• discomfort when performing physical activity or excessive physical activity.

Usually, these signs and symptoms affect the human body paroxysm - that is, the patient does not always feel unwell, but only during a certain period. At the same time, the frequency of relapse in each patient is different, since it depends on the characteristics of the organism and the general condition of the patient. For example, some patients can catch the chronic form after 3 attacks, while others throughout their lives feel short flickering, which does not bring any discomfort and does not disrupt the lifestyle.

Important: the signs and symptoms of the disease are not always pronounced - often many people learn about the development of atrial fibrillation only after undergoing an ecg. Therefore, it is important to regularly do ecg in order to diagnose pathology in time.

If the disease has already become chronic, it has the following symptoms:

• sweating;
• polyuria;
• frequent fainting;
• dizziness;
• general weakness;
• disturbed pulse;
• signs of ischemic heart disease;
• trembling, fear.

Patients with a permanent form of the disease during treatment begin to gradually ignore these signs and symptoms of pathology, since recurrent pains become stronger over time.

When a disease is detected, the pulse plays an important role, since it manifests itself with different amplitudes. It is important to note that atrial fibrillation is characterized by a pulse deficit, which is caused by dangerous consequences for the body - the pulse causes a chaotic reduction in the release of blood into the aorta. As a result, there is a violation of the blood flow, which is considered dangerous to human health.

Pulsing in the veins of the neck, shortness of breath and a sensation of atrial flutter are all characteristic symptoms of the disease. What to do if they are found? The patient should immediately consult a doctor in order to conduct an ecg and measure the pulse - after that, the doctor will decide how the treatment will be carried out, by taking medications or in a hospital.

Complications of atrial fibrillation

Arrhythmia not cured in time leads to serious complications, which are not very easy to get rid of. These include:

• heart failure;
• blood clots;
• blockage of the left heart opening;
• thromboembolism of internal organs;

If the patient has diabetes mellitus or arterial hypertension, such pathologies cause pulmonary edema and cardiac asthma - in this case, the patient needs urgent surgical intervention, since the patient's condition will only worsen every day.

Important: if a person develops arrhythmogenic shock, this leads to a sharp cardiac arrest. Such a shock can appear with a long absence of treatment, therefore, it is important to pay close attention to the symptoms and signs of atrial fibrillation.

Diagnostics of the persistent arrhythmia of the heart

Usually, the diagnosis of pathology is established even during a physical examination - the doctor, with the help of palpation, measures the pulse, which, with arrhythmia, has a strong tension and chaos. Also, the patient is assigned auscultation of the heart, thanks to which it is possible to listen to the irregularity of the heart.

It is especially important during diagnostics to conduct an examination of the ecg, where you can accurately listen to all atrial waves. Also, ECG allows you to control the heart rate, understand the form of arrhythmia and establish the load on the body. If a person is suspected of having coronary heart disease, exercise tests should be performed to understand the damage to the heart muscle.

Echocardiography allows the doctor to determine the size of the ventricles and atria of the heart, to understand whether blood clots have formed in the muscle, whether the valves have been damaged, and also to assess the function of the ventricles.

It is possible to conduct a detailed examination of the heart muscle and see violations in its work using MRI or MSCT of the heart, which are often prescribed to patients with suspected atrial fibrillation.

If the patient requires surgery to introduce catheter ablation or an artificial rhythm normalizer, the doctor prescribes an HPECG, which allows to identify the mechanism of the disease development. Such an operation is performed with advanced forms of the disease, as well as with the development of complications that are dangerous to the patient's health and life.

Treatment

Treatment of atrial fibrillation in Israel will be of better quality and more reliable, since this country has everything you need to diagnose and treat the disease. However, our treatment is carried out at a high level - only 3% of patients cannot completely cure the pathology, while the rest, although for a long time, still effectively treat the disease.

Therapeutic tactics for any form of arrhythmia is aimed at restoring the work of the heart and maintaining the sinus rhythm, on which the permeability of the blood flow in the body depends. At the same time, during treatment, the patient will prevent attacks of atrial fibrillation and prevent the appearance of blood clots. During the treatment, the doctor will constantly monitor the heart rate with the help of an ecg and regularly measure the patient's pulse in order to understand whether the treatment helps to overcome the attacks of arrhythmias.

Today, the treatment of pathology is carried out by ingestion or intravenous administration of the following drugs (each remedy must be prescribed by a doctor):

• Propanorm;
• Novocainamide;
• Quinidine;
• Cordaron.

With self-treatment, the patient is prescribed Anaprilin, Digoxin and Verapamil, but they are considered weaker than the above drugs. Each medicinal composition prescribed by a doctor improves the patient's condition, reduces and tidies up the work of the heart, normalizes its contraction and eliminates unpleasant symptoms of the disease (shortness of breath, high pulse, pain in the heart).

If the treatment does not completely get rid of the flickering, the patient undergoes electrical cardioversion, which consists in applying a current to the heart muscle to restore the rhythm. At this time, the drug prescribed by the doctor for treatment must be stopped so as not to disrupt the result of the procedure.

Neglected types of disease, the prognosis of which is disappointing, are treated by performing an operation, after which positive result seen in 90% of patients.

Year of issue: 2000

Genre: Cardiology

Format: DjVu

Quality: Scanned pages

Description: Heart rhythm and conduction disorders are one of the most difficult areas of modern cardiology and therapy. Diagnosis of arrhythmias and blockages is carried out almost exclusively by electrocardiography data, and in difficult cases - using transesophageal and endocardial electrograms. This manual presents 250 electrocardiograms recorded in patients with cardiac arrhythmias and conduction disorders, covering most types of arrhythmias. Almost all of them were registered synchronously with intracardiac electrograms - of the atria, Tis's bundle, less often - with transesophageal electrocardiograms. Since most practicing doctors in their daily activities do not come across such records, the beginning of the book provides basic information that allows you to more freely navigate in them. Comparison of a conventional ECG with intracardiac electrograms will allow the reader to understand the features of the formation of a conventional surface ECG in complex rhythm disturbances.
The book is divided into several chapters, each of which is devoted to a separate group of arrhythmias. All chapters are structured in the same way: first, the main electrocardiographic (and electrophysiological) characteristics of arrhythmias and blockages are given, then electrocardiograms are given, after which detailed comments are given for each of these electrocardiograms. ECG number and comment number are the same. All ECGs were recorded at a speed of 50mm / s, on each electrocardiogram the intervals are indicated in fractions of a second and in milliseconds (ms). Each ECG has a scale bar that allows, if desired, to measure any interval independently.
When working with the book, first it is advisable to familiarize yourself with the ECG characteristics of the arrhythmias included in this chapter, then make your own impression on each electrocardiogram, and only then compare your conclusion with the comments given to each specific electrocardiogram.
The book is intended for therapists, cardiologists, doctors of functional diagnostics, as well as for electrophysiologists. I hope this guide will be useful in improving the diagnosis and, therefore, the treatment of cardiac arrhythmias and conduction disorders.

Chapter 1. Violations of the formation (formation) of the heart impulse
Sinus node automatism disorders
Sinus tachycardia
Sinus bradycardia
Sinus arrhythmia
Rigid sinus rhythm
Manifestations of automatism of latent pacemakers
Slip-out (replacement) complexes and rhythms
Atrial escape complexes and rhythms
Escaping complexes and rhythms from the AV junction

Idioventricular (ventricular) replacement complexes and rhythms
Accelerated slip complexes and rhythms
Migration of the supraventricular pacemaker
Atrioventricular dissociation
Electrocardiograms from No. 1.1 to No. 1.16

Heart rhythm disturbances are one of the most common types of disturbances, and their frequency cannot be accurately estimated. Transient rhythm disturbances occur in most healthy people. When diseases of internal organs occur, conditions are created for the development of cardiac arrhythmias.

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PAGE 2

State budgetary educational institution

higher professional education

"Stavropol State Medical University"

Ministry of Health Russian Federation

Approved by the head. chair

hospital therapy

A.V. Berry

"___" _____________ 2013

METHODOLOGICAL DEVELOPMENT

to a practical lesson for students

5 courses of the specialty "General Medicine"

by academic discipline"internal illnesses"

TOPIC №2. DIFFERENTIAL DIAGNOSTICS AND TREATMENT OF HEART RATE AND CONDUCTIVITY DISORDERS

LESSON # 1. CLINIC, DIAGNOSTICS AND TREATMENT OF HEART RATE DISORDERS

Discussed at the meeting

Department of Hospital Therapy

"___" _____________ 2013

Protocol No. ___

Methodical development compiled

Shnyukova T.V.

Stavropol, 2013

Topic number 2. Differential diagnosis and treatment of cardiac arrhythmias and conduction disorders

Lesson number 1. Clinic, diagnosis and treatment of cardiac arrhythmias.

Study questions of the lesson:

Questions for independent work(self-study) students:

- - etiology, pathogenesis and classification of cardiac arrhythmias.

Clinic, diagnosis and treatment of extrasystole.

Clinical picture, diagnosis and treatment of paroxysmal tachycardia.

Clinical picture, diagnosis and treatment of atrial fibrillation and flutter.

Clinical picture, diagnosis and treatment of ventricular pre-excitation syndrome (Wolff-Parkinson-White). Indications for surgical treatment.

Clinical picture, diagnosis and treatment of ventricular fibrillation.

Electric pulse therapy for cardiac arrhythmias: indications, technique.

Questions for self-study students:

Clinical examination and examination of working capacity in case of cardiac arrhythmias.

List of studied diseases and conditions:

Extrasystole;

Paroxysmal tachycardia;

Atrial fibrillation and flutter;

Ventricular fibrillation;

Wolff-Parkinson-White syndrome.

Location of the lesson:Clinical base of the Department of Internal Diseases No. 1 with a course of polyclinic therapy - cardiology department No. 2 of the State Healthcare Institution SKKKD.

Material and laboratory support:

Training tables;

Sets of electrocardiograms;

Sets of test items;

Sets of situational tasks.

Educational and educational goals:

A) general purpose - the student needs to master the algorithm for differential diagnosis of various forms of heart rhythm disturbances, study the differential diagnostic signs of various forms of heart rhythm disturbances and learn to apply the knowledge gained in his future profession.

B) private goals - as a result of studying the educational issues of the lesson, the student must

KNOW:

Etiology, pathogenesis, clinical picture and diagnosis of various forms of cardiac arrhythmias;

Algorithm for differential diagnosis of cardiac arrhythmias;

Diagnostic capabilities of direct research methods and modern methods of laboratory and instrumental research (chest x-ray, electrocardiography, echocardiography with Doppler analysis) in case of cardiac arrhythmias;

Basic principles of medical care (drug and electro-pulse therapy) in case of emergency conditions arising against the background of cardiac arrhythmias.

BE ABLE TO:

Draw up a program for examining a patient with cardiac arrhythmias;

Conduct a physical examination of the patient (examination, palpation, auscultation, measurement of blood pressure, determination of the properties of the pulse) and identify the main signs of diseases that led to heart rhythm disturbances;

Establish and substantiate the clinical diagnosis of a patient with cardiac arrhythmias;

Decipher the ECG in 12 leads with the identification of cardiac arrhythmias;

Evaluate the results of a biochemical blood test (electrolytes, indicators of the blood coagulation system, indicators of the activity of the inflammatory process) of patients with cardiac arrhythmias;

Draw up a plan for examining a patient with cardiac arrhythmias;

Provide emergency care for conditions that complicate the course of cardiac arrhythmias;

Conduct resuscitation measures in cases of clinical death;

OWN:

Methods of auscultation of the heart and blood vessels;

Interpretation of the results of laboratory and instrumental examination of a patient with cardiac arrhythmias;

Algorithm for setting a preliminary and detailed clinical diagnosis (main, concomitant, complications) of a patient with cardiac arrhythmias;

Implementation of basic medical treatment measures for the provision of first aid for paroxysmal tachyarrhythmias, ventricular fibrillation;

HAVE A SET OF COMPETENCIES:

Ability and willingness to implement primary and secondary prevention of cardiac arrhythmias;

The ability and willingness to establish deviations in the health of a patient with rhythm disturbances, taking into account the laws of the course of pathology in systems, regions and the body as a whole; using knowledge of fundamental and clinical disciplines;

Ability to comply with the requirements of medical ethics and deontology when communicating with patients, as well as their relatives and friends;

The ability and willingness to conduct a qualified diagnostic search to identify rhythm disturbances and their causes in the early stages, typical, as well as low-symptom and atypical manifestations of the disease, using clinical, laboratory and instrumental methods in an adequate volume;

The ability and willingness to correctly formulate the established diagnosis, taking into account the ICD-10, with an additional examination and the appointment of adequate treatment;

The ability and willingness to assess the need to choose an outpatient or inpatient treatment regimen, to resolve issues of examination of working capacity; draw up primary and current documentation, evaluate the effectiveness of dispensary observation.

The ability and willingness to assess the possibilities of using drugs for the treatment and prevention of cardiac arrhythmias; analyze the action of drugs in terms of the totality of their pharmacological properties; possible toxic effects of drugs;

Ability and willingness to interpret the results of modern diagnostic technologies, to understand the strategy of a new generation of therapeutic and diagnostic drugs;

The ability and willingness to perform basic diagnostic and therapeutic measures, as well as to make the optimal choice of drug therapy for providing first aid in urgent and life-threatening conditions that complicate the course of cardiac arrhythmias;

Ability and readiness to analyze the performance indicators of health care facilities different types in order to optimize their functioning, to the use of modern organizational technologies for diagnosis, treatment, rehabilitation, prevention in the provision of medical services in the main types of medical institutions;

Ability and willingness to maintain accounting and reporting medical documentation;

Ability for independent analytical work with various sources of information, willingness to analyze the results of their own activities to prevent professional mistakes;

HAVE REPRESENTATIONS:

About clinical examination and examination of working capacity in case of cardiac arrhythmias.

Integrative relationships (elements of a unified lifelong learning program):

- normal anatomy: the structure of the cardiovascular system;

- normal physiology: the conduction system of the heart is normal;

- pathological physiology: congenital and acquired disorders of the functioning of the conducting system of the heart;

- propedeutics of internal diseases: methods of research of the cardiovascular system;

Pharmacology : antiarrhythmic drugs, cardiac glycosides, metabolic drugs.

main:

1. Internal diseases: textbook / Ed. S.I. Ryabova, V.A. Almazova, E.V. Shlyakhtova. - SPb., 2001.
2. Internal diseases: textbook: in 2 volumes / Ed. N.L. Mukhina, V.S. Moiseeva, A.I. Martynov. - 2nd ed., Rev. and add. - M: GEOTAR-Media, 2004.
3. Internal diseases: textbook: in 2 volumes / Ed. N.L. Mukhina, V.S. Moiseeva, A.I. Martynov. - 1st ed. - M: GEOTAR-Media, 2001.
4. Internal diseases: textbook: in 2 volumes / Ed. N.L. Mukhina, V.S. Moiseeva, A.I. Martynov. - 2nd ed., Rev. and add. - M: GEOTAR-Media, 2005.
5. Internal diseases: textbook / Ed. IN AND. Makolkin, S.I. Ovcharenko. - 5th ed. - M: Medicine, 2005.

additional:

1. 2000 diseases from A to Z / Ed. I.N. Denisova, Yu.L. Shevchenko. - M., 2003.
2. Mukhin, N.A. Selected lectures on internal medicine / N.A. Mukhin. - M., 2006.
3. Cardiology: A Guide for Physicians / Ed. R.G. Oganova, I. G. Fomina. - M .: Medicine, 2004.
4. Diagnosis in cardiovascular diseases. Formulation, classification. Practice. manual / Ed. I.N. Denisova, S.G. Gorokhovoy. - M .: Geotar-Media, 2005.

Familiarize yourself with the educational (general and specific) objectives and educational questions of the lesson;

Restore the acquired knowledge of basic disciplines within the framework of integrative relations on the studied topic of the lesson;

Analyze the work done by answering questions for self-study (self-study) and self-study;

Complete test tasks (Appendix 2) and solve situational tasks (Appendix 3).

Appendix 1. Abstract (current state of the art):

Heart rhythm disordersare one of the most common types of violations, their frequency cannot be accurately estimated. Transient rhythm disturbances occur in most healthy people. When diseases of internal organs occur, conditions are created for the development of cardiac arrhythmias, which sometimes become the main manifestation in the clinical picture of the disease, as, for example, with thyrotoxicosis, coronary artery disease. Arrhythmias complicate the course of many cardiovascular diseases.

The term "cardiac arrhythmias" refers to arrhythmias and heart block. Arrhythmias are abnormalities in the frequency, regularity, and consistency of heartbeats. Disturbances in the conduction of arousal cause the development of heart block.

All arrhythmias are the result of changes in the basic functions of the heart: automatism, excitability and conduction. They develop when the formation of the action potential of the cell is disturbed and the rate of its conduction changes as a result of changes in potassium, sodium and calcium channels. Disruption of the activity of potassium, sodium and calcium channels depends on sympathetic activity, the level of acetylcholine, muscarinic M 2 -receptors, ATP.

Mechanisms of heart rhythm disturbance:

1. Violations of impulse formation:

- violations of the automatism of the sinus node (SS);

- abnormal automatism and trigger activity (early and late depolarization).

2. Circulation of the excitation wave ( re-entry).

3. Violations of impulse conduction.

4. Combinations of these changes.

Impulse formation disorders... Ectopic foci of automatic activity (abnormal automatism) can be located in the atria, coronary sinus, along the perimeter of the atrioventricular valves, in the AV node, in the system of the His bundle and Purkinje fibers. The emergence of ectopic activity is facilitated by a decrease in the automatism of SU (bradycardia, dysfunction, sick sinus syndrome (SSS)).

Violation of impulse conduction... Impulse conduction disorders can occur in any part of the cardiac conduction system. Blockade on the path of impulse conduction is manifested by asystole, bradycardia, sinoatrial, AV and intraventricular blockade. This creates conditions for a circular motion. re-entry.

Circular motion... To form re-entry it is necessary to have a closed conduction loop, a unidirectional blockade in one of the sections of the circuit and a delayed propagation of excitation in another section of the circuit. The impulse slowly spreads along the knee of the circuit with preserved conductivity, makes a turn and enters the knee where there was a conduction block. If conductivity is restored, then the impulse, moving in a closed circle, returns to the place of its origin and repeats its movement again. Waves re-entry can occur in the sinus and AV nodes, atria and ventricles, in the presence of additional pathways and in any part of the cardiac conduction system, where dissociation of excitation conduction may occur. This mechanism plays an important role in the development of paroxysmal tachycardia, atrial flutter and atrial fibrillation.

Trigger Activity... With trigger activity, trail depolarization develops at the end of repolarization or the beginning of the resting phase. This is due to the disruption of transmembrane ion channels.

Factors contributing to the development of cardiac arrhythmias.

Exogenous and endogenous factors play an important role in the development of arrhythmias arising from various diseases and conditions, such as psychosocial stress preceding life-threatening arrhythmias in 20-30% of cases, neurovegetative imbalance, with a predominance of activity of the sympathetic or parasympathetic divisions of the autonomic nervous system, toxic effects (alcohol, nicotine, drugs, drugs, industrial poisons, etc.), diseases of internal organs.

Etiology of cardiac arrhythmias:

• Myocardial damage of any etiology: atherosclerosis of the coronary arteries, myocarditis, dilated and hypertrophic cardiomyopathies, heart defects, diabetes mellitus, thyroid diseases, menopause, amyloidosis, sarcoidosis, hemochromatosis, myocardial hypertrophy in arterial hypertension and chronic pulmonary heart disease, intoxication drugs, industrial substances (mercury, arsenic, cobalt, organochlorine and organophosphorus compounds), closed heart injuries, involutive processes during aging.
• Lesions of the SU and the cardiac conduction system of congenital and acquired genesis, for example, SSS, sclerosis and calcification of the fibrous skeleton of the heart and primary sclerodegenerative damage to the cardiac conduction system with the development of AV and intraventricular blockade, additional pathways (for example, WPW, CLC syndromes).
• Heart valve prolapse.
• Tumors of the heart (myxoma, etc.).
• Pericardial diseases: pericarditis, pleuropericardial adhesions, pericardial metastases, etc.
• Electrolyte disturbances (disturbances in the balance of potassium, calcium, sodium, magnesium).
• Mechanical irritation of the heart (catheterization, angiography, heart surgery).
• Reflex influences from the internal organs when swallowing, straining, changing the position of the body, etc.
• Violations of the nervous regulation of the heart (vegetative dystonia syndrome, organic lesions of the central nervous system).
• Under stress (with the development of hyperadrenalinemia, hypokalemia, stress ischemia).
• Idiopathic heart rhythm disorders.

Examination of a patient with cardiac arrhythmias

includes questioning the patient, clinical and instrumental research methods. It is aimed at identifying the reasons for the development of arrhythmias, those unfavorable factors that can contribute to their progression in the future, accurately determining the types of arrhythmias, diagnosing the state of the heart (valve apparatus, the size of the heart chambers, wall thickness, contractility).

When questioning the patient, pay attention toanamnestic data: the first appearance of unpleasant sensations in the area of ​​the heart and related phenomena; diagnosis (if carried out) of objective disorders of the cardiovascular system and other organs and systems that could lead to the development of cardiac arrhythmias; previous treatment and its effectiveness; the dynamics of the development of symptoms up to the moment the patient goes to the doctor. It is very important to find out if the patient had bad habits, occupational hazards, what diseases he suffered, and also know the family history.

Identification of complaints the patient is of great importance, since heart rhythm disturbances are often accompanied by the appearance of unpleasant sensations. They are determined by the type of rhythm disturbance, the degree of hemodynamic disorders, and the nature of the underlying disease. The most frequent complaints of patients with arrhythmias are unpleasant sensations in the region of the heart: palpitations (sensations of rhythmic or irregular heartbeats), interruptions, sensations of fading and "stopping" of the heart, pain of various nature or a feeling of compression, a feeling of heaviness in the chest, etc. can have different duration and frequency, develop suddenly or gradually, periodically or without a certain pattern. In addition, there may be severe weakness, headache, dizziness, nausea, syncope, which is an indicator of the development of hemodynamic disorders. With a decrease in the contractile ability of the left heart, shortness of breath, cough, suffocation are noted. The appearance or progression of heart failure with arrhythmias is prognostically unfavorable.

Heart rhythm disturbances in many cases are accompanied by a feeling of fear and anxiety. In some patients, arrhythmias are asymptomatic.

Clinical studies reveal:the patient's condition can be different (from satisfactory to severe) depending on the type of disorder and the initial condition of the patient. Lethargy, loss of consciousness (fainting), manifestations of hypoxic encephalopathy up to coma are possible. Disorders of the autonomic nervous system are manifested in the form of anxiety, anxious behavior, discoloration of the skin, sweating, polyuria, bowel movements, etc. Skin coloration can be either pale or hyperemic, especially in the presence of arterial hypertension, cyanotic in heart failure. With left ventricular heart failure, changes are revealed during a physical examination of the respiratory system - weakening of vesicular breathing or hard breathing, moist non-voiced wheezing, sometimes in combination with dry wheezing. In this case, the emphasis of the II tone on the pulmonary artery can be determined. The study of the cardiovascular system often reveals changes in heart rate (HR) and pulse rate - an increase or decrease, disturbance of the rhythm of heart sounds and pulse waves. The volume of the tones changes, for example, different loudness of the I tone with atrial fibrillation (MA), an increase in the I tone with a ventricular extrasystole, its weakening with paroxysmal supraventricular tachycardia (PNT). A decrease in pulse filling is determined with vascular insufficiency; with MA, a pulse deficit often occurs. Changes in blood pressure are often observed - hypo- or hypertension. With right ventricular heart failure - enlargement of the liver and its soreness. With a decrease in renal blood flow - oliguria. Thromboembolic syndrome may also develop.

Instrumental research methods... Electrocardiography remains the leading method in recognizing cardiac arrhythmias. Both a one-stage study and a longer one are used: within 3 minutes, 1 and 24 hours. For example, in patients with coronary artery disease, ventricular extrasystoles on a conventional ECG are detected in 5% of cases, with a 3-minute registration - in 14%, with a 1-hour - in 38% of patients, within 24 hours - in 85% of patients. Daily Holter ECG monitoring provides a study in various conditions (during exercise, during sleep, while eating, etc.), which allows you to identify provoking factors in the development of arrhythmias. Holter monitoring allows you to give a qualitative and quantitative assessment of cardiac arrhythmias. Samples with dosed physical activity are used to clarify the diagnosis of coronary artery disease, to identify the relationship of rhythm disturbances with angina pectoris and physical activity, to assess the effectiveness of therapy, as well as the arrhythmogenic effect of drugs. In case of insufficient efficiency of the ECG study for the diagnosis of the syndrome of premature excitation of the ventricles, a transesophageal ECG is used for the diagnosis and treatment of transient or permanent CVS. It is not always possible to obtain the necessary information using this method, therefore the most reliable method is an intracardiac electrophysiological study, which includes an endocardial ECG recording and programmed cardiac pacing (PAS).

Classification of rhythm disturbances

Arrhythmias are divided into supraventricular and ventricular arrhythmias. There are a large number of classifications of heart rhythm disturbances, of which the most convenient in practical application is the classification proposed by M.S. Kushakovsky, N.B. Zhuravleva modified by A.V. Strutynsky et al .:

I. Violation of impulse formation.

A. Violation of SA-node automatism (nomotopic arrhythmias):

sinus tachycardia,

sinus bradycardia,

sinus arrhythmia,

SSSU.

B. Ectopic (heterotopic) rhythms due to the predominance of the automatism of ectopic centers:

1) Slow (replacement) escape rhythms: atrial, from the AV-junction, ventricular.

2) Accelerated ectopic rhythms (non-paroxysmal tachycardia): atrial, from the AV junction, ventricular.

3) Migration of the supraventricular pacemaker.

B. Ectopic (heterotopic) rhythms, mainly due to the mechanism of re-entry of the excitation wave:

1) Extrasystole (atrial, from the AV-connection, ventricular.

2) Paroxysmal tachycardia (atrial, from the AV junction, ventricular).

3) Atrial flutter.

4) Atrial fibrillation (fibrillation).

5) Flutter and fibrillation (fibrillation) of the ventricles.

II. Conduction disorders:

1) Sinoatrial blockade.

2) Intra-atrial (interatrial) block.

3) Atrioventricular block: I degree, II degree, III degree (complete blockade).

4) Intraventricular blockade (blockade of the branches of the His bundle): one branch, two branches, three branches.

5) Ventricular asystole.

6) Syndrome of premature excitation of the ventricles (PRV): Wolff-Parkinson-White syndrome (WPW), syndrome of a shortened P – Q interval (R) (CLC).

III. Combined rhythm disturbances:

1) Parasystole.

2) Ectopic rhythms with blockage of the exit.

3) Atrioventricular dissociation.

Principles of antiarrhythmic therapy.

Treatment tactics depend on the severity of the disease, the prognostic value of heart rhythm disturbances, and the presence of burdened heredity. The patient does not need antiarrhythmic therapy for asymptomatic rhythm disturbances, in the presence of normal heart size and contractility, and high exercise tolerance. These are, for example, such disorders as sinus bradycardia (in the absence of heart disease and normal hemodynamic parameters), pacemaker migration, sinus arrhythmia, slow ectopic rhythms. In this case, dispensary observation, preventive measures, exclusion of bad habits are necessary. Etiotropic treatment of arrhythmias (treatment of the underlying disease that causes the development of rhythm disturbances) in some cases is effective to eliminate them. "Basic" therapy is aimed at creating a favorable electrolyte background for exposure to antiarrhythmic drugs (AAT). In the treatment of paroxysmal supraventricular tachyarrhythmias, the use of reflex stimulation of the vagus - "vagal tests" is effective. In severe rhythm disturbances, accompanied by a progressive deterioration of hemodynamic parameters (heart failure, vascular insufficiency), there is a real threat of death of the patient, electric pulse therapy (EIT) and pacemaker are used. There are methods of surgical treatment of some types of arrhythmias (ventricular tachyarrhythmias resistant to antiarrhythmic drugs, MA, PVI syndrome with treatment-resistant attacks of supraventricular and ventricular tachycardia, a combination of PVI and CVS syndromes) and radiofrequency catheter ablation.

Pharmacotherapy of cardiac arrhythmias is widespread and is used in 85-90% of patients with arrhythmia. A wide range of drugs with different mechanisms of action allows you to choose the most effective for the treatment of specific types of arrhythmias. The mechanism of action of AAP is the blockade of sodium, calcium, potassium ion channels, which leads to a change in the electrophysiological properties of the myocardium. Many AAPs act simultaneously on different types of transmembrane ion channels. Currently, it is considered a generally accepted classification, which includes 4 classes of AARP. If any antiarrhythmic drug is ineffective, the next drug is selected from another group. When prescribing an AAP, the indications for prescribing a specific drug should be clearly defined. It is necessary to consider the possibility of an arrhythmogenic effect of AAP

Extrasystole (ES)

Extrasystole is a premature contraction of the whole heart or any part of it under the influence of an ectopic impulse.
Extrasystolic arrhythmia is the most frequent rhythm disturbance that one has to deal with in a medical
practice.

By etiology, there are:

• functional extrasystoles occurring in persons with a practically healthy heart, but impaired activity of the autonomic nervous system;
• organic extrasystoles appear in heart disease,
  as well as when the heart is exposed to various toxic agents
  (caffeine, alcohol, nicotine, benzene, etc.);
• mechanical extrasystoles, which occur during mechanical stimulation of the myocardium during the period of its vigorous activity. Such an irritant can be an endo- or myocardial electrode of an implanted prosthetic valve pacemaker, an atrioventricular valve leaflet, which occurs in the syndrome of atroventricular leaflet prolapse.

Classification of extrasystole

1. By localization - sinus, atrial, from the AV junction, ventricular.
2. By the time of appearance in diastole - early, middle, late.
3. By frequency - rare (less than 5 in 1 min), medium (from 6 to 15 in 1 min) and frequent (more than 15 in 1 min).
4. By density - single and double.
5. By frequency - sporadic and allorhythmic (bigeminia, trigeminia, quadrigymenia).
6. By the hidden nature of extrasystoles - hidden extrasystoles.
7. On carrying out extrasystoles - blockade of conduction (antero- and retrograde), "gap" in conduction, abnormal conduction.

Extrasystole nomenclature

Early extrasystoles- ES with a very small adhesion interval, when the initial part of the extrasystole is layered on the T wave of the previous ES the next QRST complex.

Group (salvo) extrasystole is the presence of three or more ES in a row on the ECG.

Monotopic extrasystole- E S emanating from one ectopic source.

Polytopic extrasystole- ES emanating from different ectopic foci.

Allorhythmy - correct alternation ES and normal (eg sinus) P-QRST complexes (bigeminia, trigeminia, quadrheminia).

Clutch interval – the distance from the next P-QRST cycle of the main rhythm preceding the extrasystole to the extrasystole.

Compensatory pause – the distance from the extrasystole to the following P-QRST cycle of the main rhythm.

Incomplete compensatory pause – this is a pause that occurs after an atrial extrasystole or an extrasystole from the AV connection, the duration of which is slightly longer than the usual P-P (R-R) interval of the main rhythm. Incomplete compensatory pause includes the time required for the ectopic impulse to reach CA -node and "discharged" it, as well as the time it takes to prepare the next sinus pulse in it.

Full compensatory pause – a pause that occurs after a ventricular extrasystole, the duration of which is twice the R-R interval of the main rhythm.

Blocked atrial ES - extrasystoles emanating from the atria, which are presented on ECG only by the P wave, after which there is no extrasystolic ventricular complex QRST ".

Insert (interpolated)extrasystole - ES , which is, as it were, inserted between two ordinary ventricular QRS complexes without any compensatory pause.

Threatening ventricular extrasystoles ( ZhE ) - extrasystoles, which are often harbingers of more severe rhythm disturbances (paroxysmal ventricular tachycardia, fibrillation or ventricular flutter). To threatening ventricular extrasystoles ( ZhE ) include: 1) frequent; 2) polytopic; 3) paired (group) and 4) early ZhE.

Atrial extrasystoles

arise from the focus of excitation in the atria. ECG they are characterized by the presence of an extrasytolic P wave occupying a premature place, usually deformed or with a reversed polarity. In cases where the extrasystole occurs in the upper atria, close to the sinus node, the P wave in the II standard lead in shape may differ little from the sinus. The P-Q interval with atrial extrasystoles can be normal, shortened, or lengthened. Sometimes an extrasystolic impulse from the atria may not pass into the ventricles, causing the appearance of an extrasystolic P wave and the absence of a ventricular complex. The QPS complex with atrial extrasystoles in most cases is not changed. However, if one of the branches of the His bundle is caught by an impulse in a refractory state, deformation of the ventricular complex is possible. Such an extrasystole is called atrial with an aberrant ventricular complex and is observed more often in violation of conduction along the right leg of the bundle of His. Due to the time spent on discharging the sinus node with an extrasystolic impulse, with atrial
in extrasystoles, an incomplete compensatory pause is more often observed.

Extrasystoles from the atrioventricular junction

They differ in that the extrasystolic impulse arising in the atrioventricular junction propagates in two directions: anterograde along the conduction system to the ventricles and retrograde to the atria, reaching and discharging the sinus node. Since the atrial vector is directed from bottom to top, the ECG
the atrial complex is negative. Depending on the conditions of coverage by excitation of the atria and ventricles with extrasystole from the atrioventricular connection, several electrocardiographic options are distinguished:

1.with simultaneous excitation of the atria and ventricles
(there is no scar P on the ECG),

2.with simultaneous excitation of the atria (on the ECG, the negative P wave is located at a short distance in front of the QRS
complex),
3.with premature excitation of the ventricles (on the ECG, the negative P wave is located behind the QRS complex at the RS-T interval or the T wave).

Nodal extrasystoles can be accompanied as incomplete,
and a full compensatory pause. The QRS complex can also
be aberrant, as in the case of atrial extrasystoles.

Ventricular extrasystoles

- one of the most common forms of extrasystole, along with the phenomenon of premature, there is a broadening of the QRS complex for more than 0.1 seconds, the absence of an extrasystolic wave P. full compensatory pause. In clinical practice, sometimes it is necessary to evaluate the topic of ventricular extrasystoles and compare it with the state of the cardiac chambers. For example,extrasystole from the left ventricleaccompanied by a deviation of the electrical axis of the heart to the right, and in the chest leads V there are high and serrated R teeth. In leads V there are low R teeth and deep S ".Extrasystoles from the right ventricledeflect the electrical axis of the heart to the left. In the chest leads - a deep and wide S "wave with high and positive T and V waves. In leads V, there are high, widened and split R waves with negative and asymmetric T waves.
Ventricular extrasystoles from the same ectopic focus of the same shape on the ECG are called monomorphic, in contrast to polymorphic extrasystoles, which on the ECG have a different direction and shape of the ventricular complex. The polymorphic nature of ventricular extrasystole always indicates more
severe myocardial damage. Provided that the cardiac cycle slows down and the ventricular extrasystole coupling time is short, the impulse originating in the sinus node, having excited the atrium, can find the ventricles in a state of excitability, i.e. when they left the state
refractoriness due to extrasystole. In such situation
there may be no compensatory pause. Ventricular extra-
systole without compensatory pause is calledinterpolated or interpolated.Another type of ventricular extrasystoles are early forms in which the QRS complex of the extrasystole is layered on the T wave of the previous sinus contraction - so
called extrasystoles "R to T". The criterion for premature is a distance of less than 0.05 seconds, measured from the end
the T wave of sinus contraction before the onset of the ventricular complex of the extrasystole. It was believed that early extrasystoles are usually of organic origin and the prognosis for them is serious. In research recent years found that early ventricular extrasystoles are by no means more often, and sometimes less often than late ventricular extrasystoles, cause ventricular tachycardia, flutter or fibrillation of the ventricles.

The correct alternation of extrasystoles with normal sinus cycles P-QRST indicatesallorhythmic extrasystole,or about allorhythmy. Usually alloarrhythmia
accompanies myocardial damage. More often in clinical practice
there is extrasystolic bigeminy, characterized by
constant alternation of sinus contraction with extrasystolic.

Classification of ventricular extrasystoles

(after B.Lown, M. Wolf, M. Ryan, 1975):

0. absence of ventricular extrasystoles within 24 hours of monitoring;

1. not more than 30 ventricular extrasystoles for any hour of monitoring;

2. more than 30 ventricular extrasystoles for any hour of monitoring; 3. polymorphic ventricular extrasystoles;

4 A. monomorphic paired ventricular extrasystoles;

4 B. - polymorphic paired ventricular extrasystoles;

5. ventricular tachycardia (more than 3 in a row extrasystoles).

The likelihood of an unfavorable prognosis increases with an increase in the class of extrasystole.

Paroxysmal supraventricular tachycardia

The electrophysiological mechanism of PNT is the re-entry of the excitation wave, in some cases - increased automatism of ectopic foci.

ECG signs: a suddenly starting and just as suddenly ending attack of tachycardia with a heart rate of 140-250 per minute while maintaining the correct rhythm, changes in the shape, size, polarity and localization of the P wave (with PNT from the AV junction, P is located behind the ventricular complex), unchanged ventricular QRS complexes, except in cases with ventricular conduction aberration. Sometimes there is a deterioration in AV conduction with the development of AV block of I or II degree. The type of PNT depends on various electrophysiological mechanisms, which determines the choice of AARP in each specific case. All four classes of drugs are used.

Ventricular paroxysmal tachycardia

Ventricular paroxysmal tachycardia is a frequent and mostly regular rhythm, characterized by the presence of three or more complexes on the ECG, originating from a) the contractile myocardium of the ventricles, b) the Purkinje network, c) the bundle branch. Seizures lasting less than 30 seconds are called unstable (unstable), and seizures longer than 30 seconds are called persistent (persistent). Ventricular tachycardias are:

1. Reciprocal,
2. Focal automatic,
3. Focal trigger.

In 90% or more cases of ventricular paroxysmal tachycardia, there are organic changes in the myocardium. With this form
tachycardia, hemodynamic disturbance occurs much more often,
than with supraventricular paroxysmal tachycardia. With ventricular tachycardia of high frequency (over 220 in 1 min.) And organic damage to the myocardium, due to an acute
circulatory disorders arrhythmic shock develops, sometimes
accompanied by loss of consciousness or clinical death.

ECG with ventricular tachycardiacelebrated
three or more consecutive wide (more than 0.12 s) QRS complexes with a frequency of 100-250 per minute with a discordant displacement of the ST segment and the T wave in the direction opposite to the main tooth of the QRS complex.
Possibly periodic appearance of QRS complexes
normal width, or different QRS complexes with polyfocal
tachycardia.
It should also be noted the form of "bidirectional-fusiform" ventricular paroxysmal tachycardia, which occurs against the background of an extended QT interval on the ECG. During an attack, the QRS complexes are significantly expanded, and their direction changes after 5-20 cycles, which gives the impression of their "rotation" around the isoelectric line. The intervals between the beats vary, and the T waves are opposite to the beats. This kind
ventricular tachycardia can often progress to atrial fibrillation
or ventricular fibrillation.

Flicker (atrial fibrillation)

The frequency of MA is about 80% of all supraventricular arrhythmias. According to the Framingham Study, MA occurs in 0.3-0.4% of the adult population, and its frequency increases with age. It is customary to distinguish three main forms of MA: permanent (permanent), persistent (at least 2 days of atrial fibrillation and no more than 6 months) and paroxysmal. In about 90% of patients with permanent MA, the cause is organic heart disease, among them the most common are organic heart defects (30%) and coronary artery disease (20%). In the paroxysmal form, up to 60% of patients are persons with idiopathic MA. Among diseases that do not cause gross morphological changes in the atrial myocardium and lead to the development of MA, thyrotoxicosis and dysfunction of the autonomic nervous system, in particular, vagotonia, play an important role. The mechanism of MA development is the re-entry of the excitation wave, while several re-entry loops are functioning.

ECG signs of atrial fibrillationcharacterized by the absence of a P wave in all leads, the presence of random f waves of various shapes and amplitudes with a frequency of 350-700 per minute, an irregular rhythm of QRS complexes, which, as a rule, have an unchanged appearance. The frequency of ventricular contractions in most cases is 100-160 per minute, but there are also normosystolic and bradystolic forms. According to modern ideas about the mechanisms of MA, AAD is used for its treatment, blocking potassium and sodium channels (I and III class of drugs).

Atrial flutter (AT)

The frequency of this type of rhythm disturbance is about 10% of all supraventricular tachyarrhythmias. Electrophysiological mechanism of TP - re-entry. The most common etiological factors are organic heart defects, coronary artery disease, arterial hypertension.

ECG signs: atrial F waves of a regular sawtooth shape, similar to each other, rhythmic (not always) with a frequency of 200-400 per minute, in most cases, a correct ventricular rhythm, the presence of unchanged ventricular complexes, each of which is preceded by a certain, more often constant, number of atrial F waves (2: 1, 3: 1, etc.). For the treatment of LT, blockers of sodium (class I) and potassium channels (class III AAP) are used.

Ventricular fibrillation (VF)

is the most common cause of sudden death. There are primary, secondary and late ventricular fibrillation.

Primary VF occurs in the first hours of acute myocardial infarction due to transient electrical instability in the ischemic zone. It is the cause of high out-of-hospital mortality from acute coronary occlusion. In the absence of prophylactic administration of lidocaine, it occurs in 3-7% of cases of acute myocardial infarction. Primary VF is successfully treated.

Secondary VF develops in patients with severe left ventricular dysfunction with low ejection fraction (less than 30%) and heart failure. It develops in the preterminal and terminal periods. Defibrillation and antiarrhythmic drugs are sometimes effective, but the prognosis is more commonbad due to severe irreversible changes in the heart. Secondary VF can be mediated by drugs or metabolic changes. With the correction of etiological factors, successful treatment and a more favorable prognosis are possible.

Late VF is the leading cause of sudden death after myocardial infarction. It can occur due to recurrence of myocardial ischemia or electrical instability in the re-infarction zone. If precursors are diagnosed in a timely manner, more often it is ventricular premature beats, then late VF is often eliminated by defibrillation. But it can arise without precursors.

WPW syndrome

The phenomenon of WPW (asymptomatic, does not require treatment) and the manifest WPW syndrome are distinguished. WPW syndrome is caused by the congenital presence of accessory pathways (AP) connecting the atria and ventricles bypassing the AV node.

WPW syndrome is differentiated from AV nodal tachycardia by the value of the RP "interval on the intracardiac or transesophageal endogram. In WPW, it is more than 100 ms.

With WPW syndrome, there are:

• paroxysmal reciprocal AV orthodromic tachycardia (anterograde impulse is conducted through the AV node, retrograde - through the DPP),
• paroxysmal reciprocal AV antidromic tachycardia (anterograde - through the DPP, retrograde - through the AV node).

Routine treatment for WPW syndrome is RPP catheter ablation. Prophylactic antiarrhythmic therapy for reciprocal tachycardia is carried out only with contraindications or refusal of the patient from radiofrequency ablation.

application 2. Test tasks:

1. With bigeminy, extrasystole occurs after:

1) two sinus complexes

2) each sinus complex

3) three sinus complexes

2. Pulse deficiency is:

1) the number of heart contractions is less than the number of pulse waves on the radial artery

2) the number of heart contractions is greater than the number of pulse waves on the radial artery

3) the number of heart contractions is equal to the number of pulse waves on the radial artery

3. Reflex methods of arrhythmia relief are effective for:

1) paroxysmal atrial fibrillation

2) paroxysmal atrial flutter

3) paroxysmal supraventricular tachycardia

4) sinus tachycardia

5) paroxysmal ventricular tachycardia

4. Contraindications to the use of reflex methods of relief of supraventricular tachycardia are:

1) ischemic heart disease, including acute myocardial infarction, postinfarction cardiosclerosis

2) sick sinus syndrome

3) chronic heart failure II - III stages

4) everything is correct

5. Antiarrhythmic therapy is not performed for the following cardiac arrhythmias:

1) persistent atrial fibrillation

2) sinus arrhythmias

3) sinus tachycardia

6. How does the presystolic murmur change in patients with mitral stenosis when atrial fibrillation occurs?

1) increases significantly

2) slightly increases

3) does not change

4) disappears

5) decreases

7. What antiarrhythmic drug is the least safe and sufficiently effective in the treatment of tachyarrhythmias caused by digitalis intoxication?

1) novocainamide

2) lidocaine

3) isoptin

4) inderal

5) quinidine

8. A patient with ischemic heart disease - acute transmural anterior septal myocardial infarction developed frequent ventricular extrasystoles. Which of the following drugs should he inject?

1) strophanthin

2) lidocaine

3) obzidan

4) finoptin

5) digoxin

9. A patient with coronary artery disease - acute transmural anterior-septal myocardial infarction, developed ventricular fibrillation. Your tactics:

1) introduce strophanthin

2) perform cardioversion

3) enter obzidan

4) introduce cordaron

10. A patient with ischemic heart disease has postinfarction cardiosclerosis. The syndrome of weakness of the sinus node was revealed, for the last 2 weeks, attacks of atrial fibrillation occur every day, episodes of bradycardia, accompanied by dizziness, are noted. Your tactics:

1) prescribe quinidine

2) prescribe novocainamide

3) to implant a permanent artificial pacemaker

4) prescribe digoxin

5) carry out temporary pacing

11. What is typical for atrial fibrillation?

1. the frequency of ventricular complexes is more than 120 per minute;
2. absence of P waves;
3. the presence of premature QRS complexes;
4. shortening of PQ intervals;
5. the presence of a delta wave.

12. What ECG criteria are typical for ventricular premature beats?

1. the extrasystolic QRS complex is expanded, deformed;
2. the presence of a complete compensatory pause;
3. altered P wave in front of the extrasystolic complex;
4. correct 1, 2, 3.

13. What ECG criteria are typical for supraventricular extrasystole?

1. premature QRS complex;
2. the extrasystolic complex is similar to the main one;
3. the presence of an incomplete compensatory pause;
4. the presence of a deformed P wave in front of the extrasystolic complex;
5. everything is correct.

14. In what diseases is atrial fibrillation most common?

1. hypertrophic cardiomyopathy;
2. mitral stenosis;
3. thyrotoxicosis;
4. myocarditis;
5. correct 2 and 3.

15. What drugs are indicated for the relief of paroxysmal supraventricular tachycardia?

1. rhythmilen;
2. finoptin;
3. gilurithmal;
4. cordaron;
5. all of the above.

16. What drugs are indicated for the relief of paroxysmal ventricular tachycardia?

1. rhythmilen;
2. digoxin;
3. finoptin.

4) gilurhythmal.

17. What complication is observed in atrial fibrillation?

1. thromboembolic syndrome;
2. myocardial infarction;
3. hypertensive crisis.

18. The most unfavorable prognostic sign in patients with acute myocardial infarction:

1. atrial fibrillation;
2. early ventricular premature beats;
3. group ventricular extrasystoles;
4. polytopic ventricular extrasystoles;
5. supraventricular extrasystoles.

19. For the treatment of paroxysmal supraventricular tachycardia in Wolff-Parkinson-White syndrome the best remedy it is considered:

1) digoxin

3) novocainamide

4) cordaron

20. Indications for electro-impulse therapy are:

1) rapid progression against the background of an attack of tachyarrhythmia of signs of heart failure, insufficiency of the coronary or cerebral circulation

2) bradystolic form of atrial fibrillation

3) tachyarrhythmias that developed against the background of intoxication with cardiac glycosides

Answers to test tasks: 1 - 2; 2 - 2; 3 - 3; 4 - 2; 5 - 2; 6 - 3; 7 - 4; 8 - 2; 9 - 4; 10 - 3; 11 - 2; 22 - 5; 13 - 5; 14 - 5; 15 - 5; 16 - 4; 17 - 1; 18 - 3; 19 - 4; 20 - 1.

Appendix 3. Situational tasks:

Objective 1.

Objective 2.

1. Describe the changes on the ECG.
2. Name possible reasons this rhythm disturbance.
3. Is antiarrhythmic therapy indicated and why?
4. Does the patient need surgical correction of arrhythmias?

Objective 3.

1. Describe the changes on the ECG.
2. What are the possible causes of this rhythm disturbance?
3. Is antiarrhythmic therapy indicated and why?
4. Does the patient need surgical correction of arrhythmias?

Task 4.

1. Describe the changes on the ECG.
2. What are the possible causes of this rhythm disturbance?
3. Is antiarrhythmic therapy indicated and why?
4. Does the patient need surgical correction of arrhythmias?

Task 5.

1. Describe the changes on the ECG.
2. What are the possible causes of this rhythm disturbance?
3. Is antiarrhythmic therapy indicated and why?
4. Does the patient need surgical correction of arrhythmias?

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“My pulse, like yours, sounds the same measured
sound music ... "(W. Shakespeare" Hamlet ")
DIFFERENTIAL
DIAGNOSTICS AND TREATMENT
HEART RATE DISORDERS

Arrhythmias (in a broad sense) are
changes in normal frequency,
regularity and source of excitement
heart, as well as disorders of
impulse, communication failure and / or
sequences between activation
atria and ventricles. (Kushakovsky
M.S., 1998)

Signs:
1. Change in heart rate above or below normal
(60 - 80 per minute)
2. Irregular rhythm (wrong
rhythm)
3. Changing the localization of the source
excitement (pacemaker) -
non-sinus rhythm
4. Violation of the impulse conductivity
conduction system of the heart

BASIC HEART FUNCTIONS:
1. AUTOMATION
2. CONDUCTIVITY
3. EXCITABILITY
4. REDUCTION
5. FINE
6. REFRACTION
7. ABBERANCE

AUTOMATISM
This is the ability of the heart to produce
electrical impulses in the absence
external irritations. This function
have only conductive cells
systems of the heart, which are called
pacemakers or pacemakers

First order centers of automatism (SA node) generate pulses with a frequency of 60 - 80
per minute. Centers of automatism of the second
order (the conduction system of the atria and
AB connection - the zone of transition of the AV node to
His bundle) generate pulses with a frequency
40 - 60 per minute. Automatism centers
third order (the lower part of the His bundle,
its branches and Purkinje fibers) generate
impulses with a frequency of 25 - 45 per minute.

CONDUCTIVITY
This is the ability to conduct
excitement arising in any
area of ​​the heart, to other departments
heart muscle. This property
the fibers of the conductive system also have
heart, and contractile myocardium,
however, it has the speed of
the impulse is much less. CA AB

EXCITABILITY
This is the ability of the heart to get excited under
the influence of impulses. This property
possess cells as a conducting system
heart and contractile myocardium.

REDUCTION
This is the ability of the heart muscle
contract in response to arousal. it
the function of the contractile myocardium, and this,
in fact, a mechanical result
electrical processes, allowing in
the result of consistent
contractions of different parts of the heart
carry out its main - pumping
function.

FINE
This is the ability of the heart to keep its
form in diastole

REFRACTION
This is the impossibility of excited cells
myocardium reactivate when
the emergence of additional
pulse. (absolute and relative)

ABBERANCE
This is a pathological impulse conduction
along the atria and ventricles.

Diagnostic Criteria for Normal Sinus Rhythm

Positive P wave in II standard
abduction
Constant and normal PQ interval
Permanent P wave shape in each
abduction
Constant distance P-P or R-R

Classification of heart rhythm and conduction disorders (according to M.S. Kushakovsky and N.B. Zhuravleva, 1981)

I. Arrhythmias due to violation
pulse formation
II. Conduction disturbances
III. Combined rhythm disturbances

A. Violation of the automatism of the CA-node (nomotopic arrhythmias)
1. Sinus tachycardia.
2. Sinus bradycardia.
3. Sinus arrhythmia.
4. Syndrome of weakness of the sinus node.
B. Ectopic (heterotopic) rhythms caused by
the predominance of automatism of ectopic centers
1. Slow (replacement) slip out complexes and rhythms
but. Atrial.
b. From the AV connection.
in. Ventricular.
2. Accelerated ectopic rhythms (non-paroxysmal tachycardia)
but. Atrial
b. From the AV connection.
in. Ventricular.
3. Migration of the supraventricular pacemaker.

I Arrhythmias due to impaired impulse formation
B. Ectopic (heterotopic) rhythms, mostly not
associated with violation of automatism (mechanism of repeated
excitation wave input)
1. Extrasystole
but. Atrial.
b. From the AV connection.
in. Ventricular.
2. Paroxysmal tachycardia
but. Atrial.
b. From the AV connection.
in. Ventricular.
3. Atrial flutter
4. Atrial fibrillation (fibrillation).
5. Flutter and fibrillation (fibrillation) of the ventricles

II Conduction disturbances
1. Sinoatrial blockade.
2. Intra-atrial blockade.
3. Atrioventricular block.
but. First degree.
b. Second degree - Mobitz type I, Mobitz type II,
in. Third degree (complete).
4. Intraventricular blockade.
but. Single branch (single-beam or monofascicular)
b. Two branches (two-beam or bifascicular)
in. Three branches (three-beam or trifascicular)
5. Ventricular asystole.
6. Syndromes of premature excitement
but. Wolff-Parkinson-White syndrome
b. Short PQ Interval Syndrome (CLC)

III. Combined rhythm disturbances
1. Parasystole
2. Ectopic rhythms with exit block.
3. Atrioventricular dissociation

Non-sinus rhythms

Atrial rhythms (from the lower atria)
- the presence of negative P waves in II and III
standard leads and the following
unchanged QRS complexes.
Rhythms from the AV junction - no P wave,
merging with the unaltered QRS complex, or
the presence of negative P waves after unchanged
complexes of QRS. Atrial complexes and rhythms and
complexes and rhythms from the AV junction are combined
the term supraventricular
Ventricular (idioventricular) rhythm -
slow (less than 40 per minute), with extended and
deformed QRS complexes and lack of
the natural connection of QRS complexes and P waves.

Classification of antiarrhythmic drugs

Class I - fast sodium channel blockers
cell membrane (membrane stabilizers)
IA - quinidine, novocainamide, disopyramide, aymalin
IB - local anesthetics (lidocaine, trimecaine,
pyromecaine, mexiletine, diphenine)
IC - etmozin, etacizin, allapinin, propafenone,
flecainide
Class II - beta-blockers
Class III - potassium channel blockers, evenly
lengthening all phases of repolarization (amiodarone,
bretilium, sotalol, dofetilide, ibutilide, nibentan)
Class IV - slow calcium channel blockers
cell membrane (verapamil, diltiazem) Diagnosis of cardiac arrhythmias
based on data:
History and physical examination
Resting ECG
24-hour ECG monitoring
Exercise ECG (VEM, treadmill test)
High resolution ECG
Pharmacological tests
Transesophageal atrial stimulation
(CPES)
Intracardiac electrophysiological
research (EPI) Indication for the appointment of antiarrhythmic
LS serves:
The presence of severe clinical symptoms, incl.
caused by hemodynamic disorders
Increased risk of sudden death:
with malignant arrhythmias (condition after
resuscitation for VF, sustained VT);
potentially malignant arrhythmias
(ventricular arrhythmias of high
grades in patients with severe damage
myocardium and decreased systolic function
LV)

Treatment for arrhythmias includes:
Elimination of the causes of arrhythmia
Symptomatic treatment: general measures
(sedatives,
oxygen therapy, vagal techniques and
etc.), the use of antiarrhythmic drugs,
electro-pulse therapy, catheter
destruction, cardiac surgery
interference

Violation of hemodynamics requires urgent
measures to correct heart rate
(intravenous administration of antiarrhythmic drugs, increasing
CPES or electro-impulse therapy)

Sinus arrhythmia

Interval duration fluctuations
R-R exceeds 15%
Allocate respiratory CA and unrelated
with breathing phases
Clinical manifestations are more common
absent
Treatment is usually not required

Sinus bradycardia

Correct heart rate rhythm< 60 мин–1 Синусовые зубцы P
PQ interval - 0.12 s
The reasons:
increased parasympathetic tone (often in healthy
persons, especially during sleep; in athletes; heart attack
myocardium (especially the lower one); taking medications
(beta-blockers, verapamil, diltiazem,
cardiac glycosides, class Ia antiarrhythmics,
Ib, Ic, amiodarone, clonidine, methyldopa, reserpine,
guanethidine, cimetidine, lithium); verapamil,
diltiazem, amiodarone clonidine, methyldopa, reserpine
guanethidine cimetidine lithium; hypothyroidism, hypothermia,
obstructive jaundice, hyperkalemia, increased ICP,
sick sinus syndrome. Against the background of bradycardia
sinus arrhythmia is often observed (scatter
intervals PP exceeds 0.16 s).

Treatment

Only if it is proven that it causes
angina pectoris, arterial hypotension,
fainting, heart failure,
ventricular arrhythmias!
With hemodynamically significant
bradycardia:
ATROPINE 0.6-2.0 mg IV
ISOPRENALINE 2-20 μg / min IV ECS
atrial in the absence of AV block.

Sinus tachycardia

Correct rhythm. Sinus P waves of conventional
configuration (their amplitude can be increased).
Heart rate 100-180 min – 1, in young people up to 200 min – 1.
Gradual start and stop.
The reasons:
physiological response to stress, including
emotional, pain, fever, hypovolemia,
arterial hypotension, anemia, thyrotoxicosis,
myocardial ischemia, myocardial infarction, cardiac
failure, myocarditis, pulmonary embolism,
pheochromocytoma, arteriovenous fistulas,
the effect of drugs and other drugs (caffeine,
alcohol, nicotine, catecholamines, hydralazine,
thyroid hormones, atropine, aminophylline).

Treatment:

Treatment of the main
diseases. If the tachycardia itself is
itself serves as a pathogenetic factor
(for example, with angina pectoris, heart attack
myocardium), BETAADRENO BLOCKERS are prescribed.

Pacemaker migration

Correct or incorrect heart rate rhythm< 100
min Sinus and non-sinus P waves
PQ interval varies, maybe< 0,12 с
The reasons:
It is observed in healthy individuals, athletes with
organic lesions of the heart Occurs
moving the pacemaker out of the sinus
node in the atrium or AV node
No treatment required

SSSU-Sick sinus syndrome

it is a descriptive term coined by Lown (1966)
to designate a set of features,
symptoms and electrocardiographic changes,
determining dysfunction of the sinus node
in a clinical setting.
The syndrome is characterized by fainting or other
manifestations of cerebral dysfunction,
accompanied by: sinus bradycardia,
stopping the sinus node (sinus arrest),
sinoatrial blockade, alternating
bradyarrhythmias and tachyarrhythmias (tachybradi syndrome),
hypersensitivity of the carotid
sinus.

To determine the tactics of treatment, it is necessary
differential diagnosis:
between sick sinus syndrome and
autonomic dysfunction of the sinus node.
The main criterion is the result of the sample with
atropine or drug tests
denervation of the heart.
The patient is injected intravenously (or subcutaneously)
atropine sulfate solution at a dose of 0.025 mg / kg
body weight of the patient. Increase in heart rate after
the introduction of atropine and the disappearance of clinical
symptoms speak in favor of vegetative
sinus node dysfunction
Treatment of sick sinus syndrome
consists of implantation
pacemaker (ECS).

Atrial extrasystoles

Extraordinary non-sinus P wave, followed by
followed by normal or aberrant
complex QRS. PQ interval 0.12 0.20 s.
PQ interval of early extrasystole can
exceed 0.20 s. Compensatory pause
usually incomplete.
Causes: are in healthy individuals, with
fatigue, stress, smokers, under
the action of caffeine and alcohol, with
organic lesions of the heart, pulmonary
a heart.

AV nodal extrasystoles

Extraordinary QRS complex with retrograde
(negative in leads II, III, aVF)
P wave, which can be recorded up to
or after the QRS complex or layering
on him. The shape of the QRS complex is normal; at
aberrant conduct may resemble
ventricular premature beats. A source
extrasystoles AV node. Compensatory
the pause can be complete or incomplete.
Reasons: there are healthy individuals and
organic lesions of the heart.

Ventricular extrasystoles

Extraordinary, wide (> 0.12 s) and
deformed QRS complex. ST segment
and the T wave are discordant to the QRS complex. Barb
P may not be associated with extrasystoles (AV dissociation) or be negative and
follow the QRS complex (retrograde
P wave). Compensatory pause is usually
complete

Classification of ventricular extrasystoles (according to B.Lown, M. Wolf, M. Ryan, 1975)

0. - the absence of ventricular extrasystoles in 24 hours.
Monitoring
1. - no more than 30 ventricular extrasystoles per
any hour of monitoring
2.- more than 30 ventricular extrasystoles for any
monitoring hour
3. - polymorphic ventricular extrasystoles
4. A - monomorphic paired ventricular
extrasystoles
4.B - polymorphic paired ventricular
extrasystoles
5.ventricular tachycardia (more than 3 in a row
extrasystoles).

Treatment

In most cases, specific
antiarrhythmic therapy for extrasystole
not required
In case of deteriorating well-being of patients
NZhES in the absence of organic pathology
hearts as the drug of choice are prescribed BB.
As alternative drugs are prescribed
calcium antagonists (verapamil, diltiazem)
Less often, in such cases,
antiarrhythmic drugs of IA, IC classes
(disopyramide, allapinin, hanadin, etacizin and
etc.)

In the absence of clinical manifestations of VES
antiarrhythmic drugs are not required.
With a worsening well-being of patients with VES in
lack of organic pathology of the heart
prescribe antiarrhythmic drugs IА, IС classes
Patients with heart disease need
treatment of the underlying disease, correction
electrolyte disturbances, the appointment of BB.
Prognostically most unfavorable
ventricular extrasystoles of high gradations in
B. Lown - Grade 2 and above. Preventive treatment
high-grade ventricular premature beats
corresponds to the treatment of ventricular tachycardia

With high grade VES in patients with
organic heart disease
drug of choice amiodarone.

Paroxysmal atrial tachycardia

Possible complaints about the feeling of increased frequency.
palpitations, weakness, shortness of breath, pain in
breasts. Can provoke an attack
angina pectoris, aggravation of heart failure, up to edema
lungs. Dizziness, loss of consciousness.
ECG: tachycardia with normal narrow
QRS complexes preceded by ZR
non-sinus origin. Heart rate 150-200 in
min In atrial tachycardia with acute
hemodynamic disorders are necessary
electrical cardioversion
In the absence of hemodynamic disturbances
it is possible to use BB (propranolol,
esmolol, as well as radical
radio frequency catheter destruction
ectopic focus
With polytopic PT, treatment is performed
underlying disease + metoprolol,
verapamil or amiodarone

Reciprocal AV nodal tachycardia

ECG: tachycardia with narrow QRS complexes
at a heart rate of 180-2220 per minute or more. P waves not
are identified. At the moment of development
an attack is registered a sharp (2-3 times)
elongation interval P-Q(jump phenomenon)
In case of hemodynamic disturbance -
electrical cardioversion
In the absence of hemodynamic disturbances -
vagal tests, if ineffective -
adenosine phosphate, verapamil, or digoxin
In the absence of effect - procainamide,
propafenone
Possibly CPPS

Prevention of paroxysms

Constant use of drugs that depress
conducting in the AV node: BB (atenolol,
bisoprolol, metoprolol, pindolol, timolol,
propranolol), verapamil
Class IC antiarrhythmic drugs (allapinin,
etacizin, etmozin)
In case of inefficiency +
Class IA drugs: procainamide, disopyramide,
quinidine sulfate, quinidine gluconate

Atrial flutter

ECG criteria
1. F waves of sawtooth shape with a frequency of 230-400
in 1 min
2. Waves F pass one into another without
isoelectric line in II, III, AVF
3. Absence of P waves
4. QRS complex is not changed
5. HRF is usually about 150 per 1 min.
6. Distinguish between regular and irregular forms of TP
Diagnostics
With 1: 1 AV conduction, the ventricular rate
contractions can reach 300 min – 1, while
due to aberrant conduct it is possible
expansion of the QRS complex acute violation hemodynamics is shown
emergency electrical cardioversion
With stable hemodynamics, you can
resort to ultra-frequent stimulation
atria using a food electrode.
Drug treatment includes
the use of drugs that inhibit AV conduction to reduce the ventricular rate:
(bisoprolol, verapamil, digoxin, diltiazem,
metoprolol, timolol, etc.) nibentan
(efficiency 80-90%)
For paroxysms lasting more than 48 hours
- prevention of systemic thromboembolism.

Prevention of recurrent TP

Antiarrhythmic drugs IА, IС, III classes:
Disopyramide, lappoconitine
hydrobromide, procainamide, propafenone,
quinidine gluconate, hanadine sulfate,
etacizin.
The combination is effective
class I antiarrhythmic drugs and BB:
Sotalol + amiodarone

ATRIAL FIBRILLATION

Supraventricular tachycardia,
characterized by uncoordinated
electrical activity of the atria with
subsequent deterioration of their contractile
function
Most common violation
heart rate, occurring in 1-2% of the total
populations (more than 6 million Europeans have AF)
Increased prevalence projected
AF at least twice within
the next 50 years as the population ages
(AF prevalence increases with
age from less than 0.5% at 40-50 years old to 5-15% at 80
years)
Men are more likely to have AF than women

ATRIAL FIBRILLATION Associated with
an increase in mortality, the risk of developing
heart failure and increase
hospitalization rate, deterioration in quality
life, decreased tolerance to physical
load and development of left dysfunction
ventricle
Having AF increases the risk of developing
ischemic stroke 5 times (paroxysmal
the form of AF suggests the same risk of developing
stroke, as well as persistent or permanent
forms)

Cardiac and extracardiac factors in the development of AF

AGE (65 and over)
ARTERIAL HYPERTENSION (AS
A FACTOR OF THE OCCURRENCE OF AF AND
A FACTOR OF AF COMPLICATIONS, SUCH AS
STROKE AND SYSTEMIC THROMBOEMBOLES)
HEART FAILURE (II-IV FC
NYHA). MAY PERFORM AS IN QUALITY
AF COMPLICATIONS, AS WELL AS CAUSES
AF (INCREASED ATRIAL PRESSURE AND
OVERLOADING VOLUME, SECONDARY
VALVE DYSFUNCTION OR CHRONIC
NEUROHORMONAL STIMULATION)
VALVE HEART DISEASES MEET IN
30% OF CASES OF OP

Atrial septum defect
ARITHMOGENIC CARDIOMYOPATHY IN THE BACKGROUND
TACHYCARDIA (LEFT DYSFUNCTION
VENTRICLE WITH HIGH HR WITHOUT
SIGNS OF ORGANIC DAMAGE
HEART)
CARDIOMYOPATHIES OF ANOTHER GENESIS
(ESPECIALLY IN YOUNG PATIENTS)
IHD (present in 20% or more patients with AF)
Dysfunction of thyroid gland

OBESITY (present in 25% of patients with AF)
DIABETES
COPD (present in 10-15% of patients with AF)
SLEEPY APNEA SYNDROME (in
especially in combination with arterial
hypertension, diabetes mellitus and
organic heart disease)
CHRONIC KIDNEY DISEASES
(present in 10-15% of patients with AF)

Mechanisms of AF development

Myocardial remodeling with the development of electrical heterogeneity and
the formation of multiple foci of re-entry
Focal triggering activity of myocardial cells in the orifice
pulmonary veins
Ion channel gene expression
Changing the distribution of vulnerable areas
Atrial dilatation
Pulmonary vein dilation
Apoptosis of atrial myocytes and interstitial fibrosis
Shortening of the effective refractory period of atrial myocytes
Calcium overload of atrial myocytes
Trigger activity or automatism of atrial myocytes
Decreased atrial conduction velocity
Atrial refractoriness heterogeneity
Dispersion of conductivity
Hypersensitivity to catecholamines and acetylcholine
Hereditary predisposition

AF classification

1. Course: paroxysmal, persistent,
long-term persistent,
constant
2. Anamnesis: newly diagnosed,
recurrent
3. The severity of symptoms according to EHRA (European
Heart Rhythm Association): Class I - no
symptoms class II - mild symptoms,
daily activity is not limited to class III
- severe symptoms, everyday
activity is limited to IV class -
disabling symptoms, everyday
activity is impossible

AF classification

Newly diagnosed AF - in the case of
the first treatment of the patient about AF outside
depending on the duration of the violation
rhythm or symptoms caused by
arrhythmia
Recurrent AF - if the patient has had 2
and more episodes of AF.

Paroxysmal AF - self-relieving
usually within 48 hours. Although paroxysmal AF can
last up to 7 days, the 48 hour mark is
clinically significant indicator - after
this time the probability of spontaneous cardioversion
low and it is necessary to consider the issue of
anticoagulant therapy.
Persistent AF - in case of duration
episode of AF for more than 7 days or if there is
the need for pharmacological or
electrical cardioversion
Long-term persistent AF -
lasting from 1 year or more by the time of adoption
decisions to restore rhythm
Constant AF - in the case when the cadioversion turned out to be
ineffective or has not been attempted.

AF classification (continued)

Mute (asymptomatic) AF - may
manifest as complications of AF
(ischemic stroke, arrhythmogenic
cardiomyopathy due to tachycardia) or
diagnosed by accidental registration
ECG. The terms defined above refer to
episodes of AF longer than
30 seconds for no reversible reason.

AF classification

Secondary AF is atrial fibrillation that occurs when
acute myocardial infarction, cardiac surgery,
pericarditis, myocarditis, hyperthyroidism or acute
pulmonary diseases, with appropriate treatment
the underlying disease usually stops the arrhythmia.
applicable to patients under 60 years of age without clinical or






mortality increases. Lone FP is applicable to
patients under 60 years of age without clinical or
echocardiographic evidence of cardiopulmonary
pathology, including hypertension. Such patients have
a favorable prognosis for the risk of thromboembolism and
mortality. Over time, patients leave this category in
as a result of aging or the development of heart disease, such
both left ventricular hypertrophy and the risk of thromboembolism and
mortality increases.

Management of patients with AF

MAIN GOALS OF THERAPY:
1.Treatment of the arrhythmia itself
Cardioversion
Antiarrhythmic therapy
Ablation
2.Prevention of severe complications associated
with FP
Antithrombotic therapy
Ventricular rate control
Treatment of concomitant cardiac pathology
Both therapeutic goals must be addressed
parallel

cardioversion

Antiarrhythmic drugs I (excluding IV) and III
classes. The effectiveness of most of them
depends on the duration of the episode of continuous
FP:
less than 48 hours - 70-90% efficiency;
more than 48 hours - efficiency 30%;
more than 7 days - efficiency tends to
zero.

With paroxysms of AF

Amiodarone. Procainamide, propafenone,
sotalol, quinidine sulfate.
The exception is
nitrop
(nibentan), the effectiveness of which
comparable to the efficiency of electrical
cardioversion
With an increase in the phenomena of acute heart failure against the background
paroxysmal AF, ineffectiveness or
impossibility of carrying out medicinal
emergency cardioversion
electrical cardioversion

Prevention of relapses (paroxysms of AF or permanent AF after cardioversion)

Class I antiarrhythmic drugs: disopyramide,
lappaconitine hydrobromide, procainamide,
propafenone, quinidine gluconate, quinidine
sulfate, etacizin, etmozin.
They also use Antiarrhythmic drugs III
class: amiodarone, sotalol
Combination of class I antiarrhythmic drugs and BB

Ventricular rate control

They use drugs that inhibit conduction in the AV node - digoxin, BB, calcium antagonists
(diltiazem, verapamil)
For AF in patients with WPW syndrome, verapamil
and digoxin are contraindicated.

Risk factors for endocardial thrombosis and
systemic thromboembolism in patients with AF:
Recurrent protracted paroxysms of AF and
permanent form of AF
Age over 65
Ischemic stroke and / or others
history of thromboembolism
AG
History of myocardial infarction
SD
Cardiomegaly, HF
Dilation of the drug

Based on risk factors, a convenient
scale that allows the doctor to assess the risk
ischemic stroke in every patient with
atrial fibrillation. The scale received
CHADS2 name

Prevention of systemic thromboembolism in patients with AF

Anticoagulants are indicated for patients over 65 years of age.
with lingering paroxysms or constant form
AF, as well as younger people,
having other risk factors for development
thromboembolism
Anticoagulants are indicated for all patients with
permanent form of AF, which is planned
cardioversion
Anticoagulants should be used under
INR control (2.0-3.0)
Acetisalicylic acid can be used in individuals
under 65 years of age who have no other developmental risk factors
thromboembolism, and if there are contraindications to
use of anticoagulants

Assign:

Acenocoumarol
Acetylsalicylic acid
Warfarin
Phenylin
under the control of the INR
Anticoagulants should be used for
at least 3 weeks before cardioversion and not
less than 4 weeks after

Prospects for antithrombotic therapy in AF

Comparative evaluation of standard
warfarin therapy and pharmacotherapy
other drugs (including combined
the use of acetylsalicylic acid and
clopidogrel)
Introduced into practice synthetic
direct active site inhibitor
thrombin ximelagatran.

Ventricular tachycardia

3 or wider in a row
complexes deformed by the BNPG type,
Heart rate 120-200 per min. The only reliable
atrioventricular dissociation is a sign of VT.
Stable monomorphic (classical) VT
refers to life-threatening arrhythmias and
requires urgent therapy:
Emergency electrical cardioversion
in the absence of hemodynamic disturbances
it is possible to use antiarrhythmic drugs IА,
IС, II and III classes:

Amiodarone
Aymalin
Bretilla tonsilat
Lidocaine
Procainamide
Sotalol
With the ineffectiveness of pharmacotherapy
electrical cardioversion shown

Prevention of VT recurrence

BB (atenolol, bisoprolol, metoprolol,
pindolol, propranolol, timolol)
amiodarone

Atrial flutter and fibrillation

With TJ and VF, a stop is noted
blood circulation with loss of consciousness,
lack of pulse, breathing, expansion
pupils with no reaction to light
Immediate start required
resuscitation measures, including
indirect heart massage, artificial
ventilation of the lungs, defibrillation.

WOLF-PARKINSON-WHITE syndrome
(WPW) -Premature Syndrome
excitation of the ventricles is a combination
electrocardiographic phenomenon
premature excitement of one
from the ventricles (shortening the PQ interval,
expansion of the ventricular complex for
delta wave count) and occurrence
paroxysmal SVT, flickering and
atrial flutter

The syndrome is based on impulse conduction
along additional conducting paths (beam
Kent)
In the absence of paroxysms, treatment is not
required
Antiarrhythmic therapy:
BB, calcium antagonists (verapamil, diltiazem)
An alternative to pharmacotherapy is
catheter destruction of the accessory pathway.
Verapamil, digoxin, and apparently adenosine
phosphate is contraindicated in AF in patients with
WPW syndrome, because these drugs can
improve conduction along the additional path