Differential diagnosis of atrial fibrillation. Differential diagnosis and treatment of heart rhythm and conduction disorders

Cardiac cough is a much discussed and rather conventional term in the clinic of heart disease. It is used by both doctors and patients to indicate a manifestation that signals diseases of the cardiovascular system.

The primary concept - cough in heart disease - implied 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, the transudate (liquid) in which causes a protective mechanism - cough.

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

Provoking factors

The causes of cardiac cough are diseases that disrupt and exhaust the functioning of the heart to the stage of decompensation and the development of heart failure. The main ones:

• cardiac ischemia;
• cardiosclerosis after a heart attack;
• cardiomyopathy;
• myocarditis;
• arterial hypertension;
• arrhythmias;
• damage and congenital heart valve defects (especially the mitral valve);
• heart defects, most often acquired.

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

Characteristics and symptoms

Symptoms of cardiac cough appear in certain conditions and are directly dependent on physical activity. In the initial stage of the disease, the cough becomes more intense with muscle exertion, with the progression of the pathological process - with any physical stress.

The distinctive signs of cardiac cough from other types of cough are illustrated by the question “cardiac cough - what is it?”:

1. Causes discomfort and pain in the heart and chest area during coughing.
2. It is inevitably accompanied by a strong heartbeat in most cases.
3. As a rule, it is dry, without phlegm, in contrast to bronchial cough and in smokers. Appearance bloody discharge indicates an acute course or an advanced form of heart failure (impaired functioning of the left ventricle).
4. Patients experience hoarse and ineffective breathing, which is manifested by shortness of breath, a feeling of lack of oxygen and cyanosis. First, this condition occurs under significant loads, followed by minimal physical activity (climbing stairs, accelerating steps) or significant monologue during conversation.
5. Loss of consciousness (fainting) and possible swelling of the neck veins reveal poor circulation and an increase in chest pressure.

Cough in heart failure has special characteristics. With left ventricular damage, it is loud, exhausting, predominantly dry and irritable, occurs mainly in the evening and interferes with sleep. The patient's position 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 develops.

This set of signs will help distinguish it from a cough of another nature and refer you for consultation to a cardiologist.

Treatment

Basic principles and methods of therapy include:

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

Treatment for cardiac cough involves a combination optimal mode work and rest, diet according to the underlying disease, healthy lifestyle and purpose medications. To reduce pressure on the pulmonary circulation, diuretics and vasodilators are used. If necessary, antitussive and expectorant medications are used. 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 during 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 in full courses during the recovery stage and for the purpose of prevention.

Thus, the answer to the question “how to treat cardiac cough?” serves as 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. Application of funds traditional medicine possible with the permission of the attending physician.

As a result, “is there a cardiac cough?” we can say that it not only exists, but its presence is a signal to immediately seek medical advice without self-medicating.

Symptoms and treatment of paroxysmal atrial fibrillation

The heart works constantly, without stopping. The strong muscular walls of the heart sections - the atria and ventricles - help it pump blood. During contractions of muscle tissue, the heart contracts and pushes the blood flow.

• Atrial fibrillation - concept
• Classification of the disease
• Causes of atrial fibrillation
• Clinical picture of the pathology
• Diagnosis of atrial fibrillation
• Emergency assistance for an arrhythmia attack
• Treatment of atrial fibrillation
• Conservative treatment
• Electropulse therapy
• Surgery
• Traditional methods of therapy
• Complications of the disease
• Prevention measures
• Prognosis for atrial fibrillation

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

When the AV node receives too many impulses, a person experiences irregular heartbeat and is diagnosed with paroxysmal atrial fibrillation.

Atrial fibrillation - concept

PMA - paroxysmal atrial fibrillation (synonymous with atrial fibrillation, or AF) - is a type of arrhythmia, a widespread disorder 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 chambers of the heart contract at a high frequency and irregularly, and the attack can last from a couple of minutes to several days.

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

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

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

The risk of sudden death with atrial fibrillation increases by 2 times compared to a healthy person. The lethal outcome is caused by severe hemodynamic and thromboembolic complications. A person with AF is exempt from military service.

Classification of the disease

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

1. Fluttering with a contraction frequency of up to 200 beats.
2. Flickering with a contraction frequency of 200 beats.

Since the ventricles begin to contract more intensely against the background of arrhythmia, the classification takes into account the following forms of the disease:

1. Tachysystolic (tachyform) - the ventricles contract more than 90 times per minute.
2. Bradysystolic - the rate is less than 60 times per minute.
3. Normosystolic - the contraction rate is between 60 and 90.

Another classification divides arrhythmia into the following forms:

• ventricular, with severe disturbances of heart rhythms, clearly expressed by ECG;
• atrial, with changes in His bundle conductivity;
• mixed, with a combination of the two indicated forms.

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

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

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

According to the signs, AF is divided into classes:

1. The first is that there is no clinical picture.
2. Second, the quality of life does not suffer, but there are mild signs of illness.
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 determined. In other cases, drug addiction and alcoholism, hereditary predisposition and genetic diseases can disrupt the functioning of the heart in a patient under 30 years of age.

In older people, ischemic heart disease (CHD) is considered the main cause of atrial fibrillation.

The etiology of paroxysms of atrial fibrillation may 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 hypertension;
• obstructive apnea syndrome;
• previous ischemic stroke, heart attack;
• amyloidosis;
• myxoma and sarcoma of the heart;
• hemochromatosis;
• serious types of anemia;
• low potassium levels in the body;
• lung cancer, emphysema, pneumonia, pulmonary embolism;
• severe poisoning;
• electric shock;
• SVC syndrome (Wolf-Parkinson-White syndrome).

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

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

The pathogenesis of paroxysmal contractions of the heart is associated with a combination of the appearance of multiple waves and focal changes. Several rhythm centers 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 manner, transmitting impulses to the ventricles.

Clinical picture of the pathology

Symptoms in mild forms of heart damage may be completely absent. Episodes of atrial fibrillation may occur without obvious manifestations, or a person may notice slight discomfort in the chest. The symptoms are not the same in each specific case of arrhythmia attacks.

The clinical picture of cardiac arrhythmia can be highly variable and include the following components:

• chest pain;
• hypotension (pressure drop);
• feeling of rapid heartbeat;
• general weakness, dizziness;
• feeling of shortness of breath and lack of air;
• cold hands and feet;
• the appearance of cold sweat;
• chills, trembling;
• faintness, loss of consciousness;
• increased urination;
• arrhythmia (irregularity) of the pulse in the arm, neck;
• panic, fear, feeling of imminent death;
• pale skin, blue 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 type of AF development is the most severe and can be fatal.

Diagnosis of atrial fibrillation

If a patient is admitted to the hospital with an acute attack of arrhythmia, the examination is carried out in the hospital. Pre-hospital diagnostics are 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 years. According to the ECG, signs of atrial fibrillation with attacks of paroxysms are the absence of the P wave in all leads, which is replaced by chaotic waves of tachysystoles f. R-R intervals unequal in duration.

If the patient indicates characteristic symptoms in the anamnesis, but there are no obvious changes in the ECG, Holter monitoring is performed. An exercise ECG can help identify AF.

Organic causes of atrial fibrillation are identified after an ultrasound of the heart. Transesophageal ultrasound is indicated for suspected cardiac thrombus but is rarely performed.

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

Emergency assistance for an arrhythmia attack

If an attack of cardiac arrhythmia develops, the task of the patient and his relatives is to consult a doctor as soon as possible, no later than 48 hours. After 2 days, there is a high risk of blood clots appearing inside the heart and the development of heart attack and stroke.

Algorithm for providing emergency care at home:

1. Lay the person on the bed, sofa, floor.
2. Open the window and provide air access.
3. Advise the patient to take a deep breath, then puff out his cheeks with his mouth closed and nose pinched. 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 abdominals.
4. Have the person take Warfarin or another previously prescribed anticoagulant to reduce the risk of blood clots.

At the same time, you should call the emergency team. To stop arrhythmia paroxysm, the doctor urgently administers a cardiac glycoside (Korglikon, Strophanthin) or a Novocainomide solution, a Lidocaine solution on glucose (intravenously).

Treatment of atrial fibrillation

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

For mild forms, treatment can be done on an outpatient basis. Indications for hospitalization are:

• first episode of fibrillation to occur;
• 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 the 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 anyone diagnosed with a paroxysmal form of arrhythmia, the doctor is required to write a prescription for anticoagulants and antiplatelet agents.

If a person is under 60 years of age and there is no organic damage to 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 a short period of time.

To restore the rhythm it is prescribed health care(cardioversion), which can be pharmacological or instrumental.

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

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

If a heart rate control strategy is chosen without eliminating arrhythmia, then these drugs are not prescribed, but are replaced with beta-blockers (Carvedilol, Metoprolol, Betaloc), calcium channel blockers (Lerkamen, Amlodipine).

Electropulse therapy

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

Cardioversion can be done on an emergency or elective basis. If the procedure is planned, the person should take Warfarin for a month before and after it. Before emergency cardioversion, the patient is urgently administered Heparin.

Surgery

In case of a recurrent form of the disease and the ineffectiveness of other methods, an operation - radiofrequency catheter ablation - is indicated. This is a minimally invasive intervention.

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

Traditional methods of therapy

Paroxysmal forms of arrhythmia are very life-threatening, so their treatment should only be done under the supervision of a doctor. Folk remedies can only serve as auxiliary measures to maintain and strengthen the heart muscle.

For this purpose, it is recommended to take infusions of hawthorn and rose hips, it is useful to eat lemons with honey, and 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 leave the atria in full, so it stagnates. When a thrombus embolizes, it can cause an ischemic stroke.

Prevention measures

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

• give up a lot of coffee and energy drinks;
• do not abuse alcohol, do not smoke;
• Do not take medications containing pseudoephedrine without a doctor’s prescription;
• Healthy food;
• 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 disease or other disease that caused the arrhythmia. With AF, the risk of stroke is 1.5% before age 60, 25% after age 80.

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

For the differential diagnosis of supraventricular tachyarrhythmias, the scheme proposed by A.S. is convenient. Smetnev and N.M. Shevchenko.

Differential diagnosis of supraventricular tachyarrhythmias

The complete irregularity of the rhythm of ventricular contraction, the absence of P waves and the presence of flicker waves make it possible to diagnose atrial fibrillation. In the presence of second degree atrioventricular block during tachyarrhythmia, a judgment is made about atrial tachyarrhythmia. The diagnosis is determined by the shape and frequency of the atrial complexes - atrial flutter or atrial tachycardia.

With atrial flutter the number of contractions of the ventricles is about 150 per 1 minute, the number of contractions of the atria is 300 per 1 minute. This is the most common form of 2:1 flutter.

At atrial paroxysmal tachycardia the frequency of contraction of the atria is less than 300, and that of the ventricles is more than 150.

In the absence of second degree atrioventricular block and the impossibility of causing it without interrupting the attack, a conclusion is made about atrioventricular tachycardia. If there is alternation of ventricular complexes, the most likely diagnosis is atrioventricular tachycardia involving additional conduction pathways. When P waves are not visible or negative before the QRS complex, atrioventricular nodal tachycardia is diagnosed, and if they are detected behind the QRS complexes in the S-T interval region, a diagnosis of atrioventricular tachycardia involving additional atrioventricular conduction pathways is made.

At paroxysmal tachycardia with wide QRS complexes, the differential diagnosis is made with:

• supraventricular atrial tachycardia with functional intraventricular block (with aberrant conduction);
• supraventricular paroxysmal tachycardia with previous disturbance of intraventricular conduction;
• supraventricular paroxysmal tachycardia WPW syndrome (antidromic type);
• ventricular tachycardia.

For supraventricular tachycardia with functional intraventricular block, the width of the QRS complexes is 0.12 s in the presence of the P wave.

Supraventricular paroxysmal tachycardia in WPW syndrome characterized by the presence of a delta wave.

Doctor of Medical Sciences, Prof. H.A.Manak

"Differential diagnosis of supraventricular arrhythmias" and other articles from the section

Differential diagnosis atrial fibrillation sometimes you have to carry out sinus tachycardia, supraventricular form of paroxysmal tachycardia, atrial flutter and ventricular paroxysmal tachycardia. It should be taken into account that in the ventricular form of paroxysmal tachycardia, the QRS complex is always widened by more than 0.12 s and deformed. However, if atrial fibrillation is associated with a preexisting bundle branch block or aberrant ventricular conduction, the shape of the QRS complex is of little help in the differential diagnosis.

If a positive P wave is recorded before each QRS complex, this indicates the supraventricular nature of the tachycardia (sinus or atrial paroxysmal) and allows us to reject both ventricular paroxysmal tachycardia and atrial fibrillation. The differential diagnosis should take into account the nature of the rhythm. The rhythm of ventricular tachycardia may be somewhat irregular. In such cases, the differential diagnosis with atrial fibrillation and aberrant complexes or with concomitant branch block is especially difficult when high frequency heartbeats.

Large-wave atrial fibrillation must be differentiated from atrial flutter. With small-wave fibrillation, signs of electrical activity of the atria on the ECG may not be detected, which, with a tendency to bradycardia, may resemble an escape rhythm from the atrioventricular junction. Distinctive signs of atrial fibrillation in this case are the variability of the RR interval, as well as the detection of flicker f waves when recording an enhanced ECG or transesophageal ECG.

The differential diagnosis of atrial fibrillation with individual aberrant QRS complexes and ventricular extrasystole accompanying atrial fibrillation may present certain difficulties. The following evidence supports aberrant intraventricular conduction of impulses:

1) the appearance of aberrance in a short cardiac cycle, which is preceded by a long cardiac cycle (Ashman phenomenon);

2) blockade of the right bundle branch (often, but not necessarily);

3) absence of a compensatory pause;

4) absence of aberration in short cardiac cycles without a previous pause;

5) disappearance of aberrance with minimal changes in the duration of the cardiac cycle.

Even greater problems arise in the differential diagnosis of atrial fibrillation with wide QRS complexes due to the “old” concomitant bundle branch block or Wolff-Parkinson-White syndrome and ventricular tachycardia, especially with a rapid ventricular rhythm when fluctuations in the RR interval are minimal. It should be taken into account that ventricular tachycardia, as a rule, is accompanied by hemodynamic disturbances and, characterized by instability, quite quickly turns into ventricular fibrillation. In contrast, the relative stability of hemodynamics with relatively long-term persistence of tachyarrhythmia is more typical for atrial fibrillation. The diagnosis can be clarified only by recording an intracardiac ECG.

Based on the above and taking into account the following: the patient’s complaints about fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of ​​a compressive nature at night (relieved by nitroglycerin), shortness of breath with insignificant physical activity, memory loss, periodic headaches, dizziness, weakness; history data - considers himself sick for 2 weeks, when complaints appeared about fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of ​​a compressive nature (relieved by nitroglycerin), shortness of breath with physical activity, periodic headaches, dizziness, weakness, observed in the student. rarely sees a therapist, does not take medications regularly (dibazol, adelfan), has been suffering from hypertension for about 5-7 years, heart rhythm disturbances, according to the patient, appeared about a year ago, the patient’s mother suffered from hypertension and had arrhythmia; objective examination data - expansion of the boundaries of relative dullness to the left, increased apex impulse, blood pressure 150/95 mmHg, arrhythmic pulse, pulse deficit; further clinical and laboratory examination, which revealed Echography of the heart:ECG: X-ray signs of stagnation in the ICC; the following diagnosis can be made:

Basic

clinical diagnosis:

Basic: Arterial hypertension Stage III, degree 3, risk 4. Coronary heart disease. Heart rhythm disturbances, permanent form of atrial fibrillation (normosystole)

Complications: CHF IIA FCIII.

Related: Peptic ulcer stomach.

Rationale clinical diagnosis:

Based on the patient's complaints of: fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of ​​a compressive nature at night (relieved by nitroglycerin), shortness of breath with slight physical exertion, decreased memory , periodic headaches, dizziness, weakness; history data - considers himself sick for 2 weeks, when complaints appeared about fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of ​​a compressive nature (relieved by nitroglycerin), shortness of breath with physical activity, periodic headaches, dizziness, weakness, observed in the student. rarely sees a therapist, does not take medications regularly (dibazol, adelfan), has been suffering from hypertension for about 5-7 years, heart rhythm disturbances, according to the patient, appeared about a year ago, the patient’s mother suffered from hypertension and had arrhythmia; objective examination data - expansion of the boundaries of relative dullness to the left, increased apex impulse, blood pressure 150/95 mmHg, arrhythmic pulse, pulse deficit; further clinical and laboratory examination, which revealed Echography of the heart: Conclusion: Left ventricular systolic dysfunction. ECG: EOS is not rejected. Atrial fibrillation. Heart rate = 55-90 beats/min. Hypertrophy of the left ventricular myocardium with secondary disorders of repolarization processes. Chest X-ray: X-ray signs of stagnation in the ICC; data from the performed differential diagnosis; The following diagnosis can be made:

Basic: Arterial hypertension stage III, degree 3, risk 4.

Cardiac ischemia. Heart rhythm disturbances, constant form of atrial fibrillation (normosystole because heart rate is 60-90).

Stage III is characterized by a pronounced clinical picture. Signs found in the patient indicating stage III of hypertension: complaints of increased fatigue; Blood pressure is constantly elevated (at a level of about 150/90 with an increase to 210/120 mmHg; hypertension decreases under the influence of drug treatment; physical examination reveals signs of left ventricular hypertrophy; ECG shows signs of left ventricular hypertrophy and rhythm disturbances ( atrial fibrillation).

Stage 3 (severe) is assigned in accordance with the blood pressure level = 210 mm Hg. Art.

Risk 4, because there is a blood pressure>180/110 mm Hg. Art. and the presence of risk factors (genetic predisposition, excess body weight) and ACS (CHF).

Complications: CHF IIA FCIII.

CHF IIA FCIII can be diagnosed based on: characteristic symptoms and complaints - shortness of breath with slight physical exertion, fatigue, palpitations; physical examination data - wheezing and hard breathing, cardiomegaly (damage to the 1st (lesser) circulation - IIA); objective examination data - ECG, EchoCG, chest X-ray, 6-minute test data (200m - FCIII).

EPICRISIS

Zharovnya Vasilina Semenovna, 63 years old, was treated in City Hospital No. 4 from November 7, 2012 to November 17. 2012. She was admitted urgently to the emergency room with a diagnosis of acute bilateral lower lobe congestive pneumonia. After clinical, laboratory and instrumental studies, the following diagnosis was made:

Basic: Arterial hypertension stage III, degree 3, risk 4. Coronary heart disease. Heart rhythm disturbances, permanent form of atrial fibrillation (normosystole).

Complications: CHF IIA FCIII.

Related: Stomach ulcer.

This diagnosis based on:

Complaints:

for fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, heart palpitations, interruptions, pain in the heart area of ​​a compressive nature at night (self-limiting), shortness of breath with slight physical exertion, decreased memory, recurrent headaches, dizziness, weakness

History of present illness:

considers himself sick for 2 years, when there were complaints of fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of ​​a compressive nature (self-limiting), shortness of breath on exercise, periodic headaches, dizziness, weakness, medications taken independently (dibazol, adelfan), heart rhythm disturbances, according to the patient, appeared about a year ago, the patient’s mother suffered from hypertension and had arrhythmia.

Objective data:

expansion of the boundaries of relative dullness to the left, increased apical impulse, blood pressure 150/95 mmHg, arrhythmic pulse, pulse deficiency, subcutaneous tissue is overdeveloped.

Results of laboratory and instrumental research:

General blood analysis:

Blood chemistry:

General urine analysis:

color light yellow

acidic reaction

specific gravity 1024

transparency transparent

no protein

ketone bodies no

glucose no

Epithelial cells

Flat 3-4 in sight;

3 leukocytes in field of view

No red blood cells

Mucus neg.

Blood test for coagulogram:

Blood test for RW: negative.
Blood test for HbsAg and HCV: negative.
Blood test for HIV: negative.

Echography of the heart:

Conclusion: Left ventricular systolic dysfunction.

ECG:
EOS is not rejected. Atrial fibrillation. Heart rate = 55-90 beats/min. Hypertrophy of the left ventricular myocardium with secondary disorders of repolarization processes.

Chest X-ray:

X-ray signs of stagnation in the ICC.

Kidney ultrasound:
The kidneys are not enlarged, their topography is not changed, the parenchyma is of a homogeneous structure, of average echogenicity, up to 17 mm wide, without ecstasy and stones, up to 10 mm wide.

Doppler ultrasound of renal vessels:

An angiorenoscintigram performed with the patient in an upright position showed an image of both kidneys located at a typical level. The vertical size of the image of both kidneys is normal, the contours of the kidney image are clear.

The flow of radiopharmaceuticals into the arterial bed of both kidneys is within normal limits. The volume of renal perfusion on both sides and the rate of renal perfusion on both sides were within normal limits. The filtration and excretory capacity of both kidneys is within normal limits. Blood purification from RF is timely.

Result of analysis for metanephrine and normetanephrine in urine:

50 mcg/day - metanephrine; (normal)

40 mcg/day - normetanephrine (normal)

(in daily urine [mcg/day] - metanephrine<350, норметанеферин <600)

TSH study:

TSH – 2 Med/l (normal 1-4 Med/l);

ARS test:

25 units (20-40 normal) – within normal limits.

6 minute test results:

Parameters of physical activity and oxygen consumption in patients with CHF

The patient walks 200 meters, which indicates FC III CHF.

Conducted differential diagnosis.

She was discharged in satisfactory condition for outpatient treatment with a general practitioner at her place of residence.

Drug therapy was carried out:

1.Selective beta blockers block beta1 receptors of the heart, reduce the secretion of renin, increase the synthesis of vasodilating prostaglandins, increase the secretion of atrial natriuretic factor.

Rp.: Bisoprololi 1.5

D.t.d. No. 20 in tab.

S. One tablet 2 times a day

2.Diuretics inhibit the reabsorption of sodium ions in the cortical part of the loop of Henley, reduce arterial tone and reduce total peripheral vascular resistance.

Rp.: Sol. Furosimidi - 4.0 ml
D.t. d. №5 in amp..

S. intravenous injection for diuretic purposes.

Rp.: Veroshpironi 0.5

D.t.d. No. 20 in tab.

3.ACE inhibitors block the conversion of angiotensin 1 to angiotensin 2, which leads to a weakening of the vasoconstrictor effect and inhibition of aldosterone secretion.

Rp.: Tab. Enalaprili 0.01

S. 1 tablet 2 times a day, morning and evening.

4. Cardiac glycosides- in small doses. In case of atrial fibrillation, they remain a “first-line” treatment, and in case of sinus rhythm and ischemic etiology of CHF, the use requires caution and control.
Rp.: Digoxini 0.125
D.t. d. No. 10 in amp.
S. Inject intravenously the contents of 1 ampoule in 200 ml of physiological solution once a day at 18.00.
5. Polarizing mixture has a beneficial effect, including on rhythm stability, both indirectly by improving the metabolism of affected tissues and by increasing the content of intracellular potassium, since myocardial hypoxia causes the release of potassium from the cell into the extracellular space.
Insulin enhances the utilization of glucose and promotes the entry of potassium into the cell. Even without additional glucose, insulin ensures the accumulation of potassium in the cell. This should normalize polarization processes in the myocardial fibers and thus create a favorable basis for rhythm stabilization. It is also prescribed during diuretic therapy to replenish the loss of magnesium and potassium.

Rp.: Sol.Glu 5% - 200.0

Sol.Actropidi 4ED
D.t. d. No. 5 in amp.

6. For the prevention of thrombosis, thromboembolism and to improve hemorheology.

Clopidogrel 75 mg 1 tab. 1 time a day.

Treatment:

Bisoprolol 1.5 mg One tablet 2 times a day

Hypothiazide 12.5 1 tab once a day

Differential diagnosis of atrial fibrillation is presented as a result of laboratory tests, based on the clinical picture of the disease and some mathematical techniques.

Arrhythmia symptoms and diagnosis

Diagnosis of atrial fibrillation is based on electrocardiography data.

On the electrocardiogram, when flickering, instead of one distinct tooth, small multiple teeth are visible. 3-5-8 or more atrial waves fall on one gastric complex. Sometimes the cardiogram shows only a slight undulation. The ventricular teeth are in the wrong order, although they are normal, both in shape and direction. The venous pulse in atrial fibrillation is characterized by the disappearance of the wave and the same irregularity in the alternation of ventricular waves.

Diagnosis of arrhythmia is that usually with flickering the pulse is rapid, but it can also be slow (tachysystolic and bradysystolic forms).

Sometimes when the pulse is slow, its irregularity is smoothed out, and the pulse seems rhythmic; in such cases, it is easy to diagnose flicker on the electrocardiogram.

The significance of atrial fibrillation for clinical research is great. This type of rhythm disorder, occurring with serious anatomical changes in the heart, should accordingly influence the assessment of the patient’s position. Sometimes patients with atrial fibrillation last for many years and yet people continue to be able to work. But more often, the appearance of atrial fibrillation indicates that the heart disease is becoming severe.

Your doctor may detect abnormal heart rhythms during a physical examination by feeling your pulse. Symptoms of arrhythmia can be: irregular heartbeat, a feeling that the heart is running very quickly, dizziness, shortness of breath, chest discomfort, a feeling of extreme fatigue.

All these signs make it possible to make a correct diagnosis of the disease and prescribe effective treatment.

Differential diagnosis includes an ECG, Holter monitor, echocardiogram, cardiac catheterization, electrophysiological examination, and a stress test, which records the electrical activity of the heart. The diagnosis is determined by a cardiologist based on the examinations performed. A cardiologist may perform further diagnostic procedures to determine the cause and determine the correct treatment.

3) type of atrial excitation;

4) shape and duration of ventricular complexes;

5) connection between atrial excitation and ventricular excitation;

6) what arrhythmias are characterized by the signs identified on the ECG.

The rhythm frequency can be normal (60-90 per 1 min), less SCH in 1 minute or more than 90 in 1 minute.

Regularity of rhythm. The rhythm can be regular, irregular (chaotic), regular with occasional disturbances.

The regularity of the rhythm may be periodically disrupted:

Gradual or spasmodic decrease and increase in frequency;

Delay or absence of next complexes;

The presence of a second rhythm.

Atrial excitation is reflected on the ECG by sinus P waves, ectopic P' waves (constant or changing shape), and atrial flutter (F) or fibrillation (f) waves.

The shape of the ventricular complexes in one ECG lead can be constant or variable, change due to the initial or final parts of the QRS complex, and have an appearance characteristic of a blockade of a particular bundle branch or its branch. The duration of the ventricular complex is either normal (up to 0.1 s inclusive), or increased moderately (0.11-0.13 s) or significantly (0.14 s and more).

The connection between the excitation of the atria and ventricles may be constant, variable or absent:

P waves are recorded before each QRS complex at constant P-Q intervals of 0.12-0.20 (0.21) s;

P waves are detected before each QRS complex with constant P-Q intervals exceeding 0.20-0.21 s;

After the P waves, the QRS complex is not always determined, and the P-Q intervals are constant or change;

P waves are fixed before each QRS complex with a constant P-Q interval of less than OD 2 s;

P waves are recorded before the QRS complex, on it, after it at a constant distance;

There is no connection between atrial waves or waves and ventricular excitation.

Analysis of the ECG in the specified sequence allows us to identify existing disturbances in heart rhythm and conduction or, at a minimum, outline the range of arrhythmias for differential diagnosis.

Recognition of arrhythmias is helped by extended ECG recording in one lead. To assess atrial excitation, special leads are used (S 5. but Lewis et al. recording the esophageal ECG lead is even more informative).

To record lead Ss, the electrode for the right hand (red) is installed on the manubrium of the sternum, the electrode for the left hand (yellow) is installed in the fifth intercostal space at the left edge of the sternum, the lead switch is switched to I.

To record Lewis ECG, the electrode for the left hand (yellow) is fixed in the area of ​​the apex beat, the electrode

for the right hand (red) - to the right of the sternum at the level of the second-fourth intercostal space, the lead switch is switched to I.

To record a transesophageal lead, use an electrode for endocardial or transesophageal pacemaker, which is connected to the chest electrode of the electrocardiograph, and the lead switch is set to V. The electrode is inserted into the esophagus through the nasal passage or mouth, recording the ECG, and is gradually removed until the most visual representation of the atrial and ventricular electrical activity (the duration of the atrial complexes is less than the duration of the ventricular complexes), the ECG is recorded at the moment of holding the breath.

On a transesophageal ECG, the electrical activity of the atria is not determined only in its absence (sinus node arrest, idioventricular rhythm) or in the case of a rhythm from the AV junction with simultaneous excitation of the atria and ventricles. In the first half of the R-R interval, the atrial complex can be recorded either with tachycardia from the area of ​​the AV junction (R-P' interval is usually less than 0.1 s), or with tachycardia that has developed against the background of WPW syndrome (R-P' interval is usually greater than OD with ). In the second half of the R-R interval, P' waves are detected in atrial tachycardia.

At the end of this chapter, we provide tables on the differential diagnosis of the most common paroxysmal tachycardias and tachyarrhythmias (Table 3.2-3.6).

Grishkin Yu.N. Differential diagnosis of arrhythmias. ECG atlas DJVU

St. Petersburg Folio, 2000. - 480 p. ill. – ISBN06-Х.

Diagnosis of arrhythmias and blockades is carried out almost exclusively according to electrocardiography, and in complex cases - using transesophageal and endocardial electrograms. This manual presents 250 electrocardiograms recorded in patients with cardiac rhythm and conduction disorders, covering most types of arrhythmias. Almost all of them were recorded synchronously with intracardiac electrograms - the atria, the His bundle, and less often - with transesophageal electrocardiograms. Since most practicing doctors do not encounter such records in their daily activities, the beginning of the book provides basic information that allows you to navigate them more freely. A 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 basic electrocardiographic (and electrophysiological) characteristics of arrhythmias and blockades are given, then electrocardiograms are given, after which detailed comments are given for each of these electrocardiograms. The ECG number and the comment number are the same. All ECGs were recorded at a speed of 50 mm/s; each electrocardiogram shows the interval values ​​in fractions of a second and in milliseconds (ms). Each ECG has a scale bar that allows you, if desired, to measure any interval yourself.

Disorders of sinus node automaticity.

Rigid sinus rhythm.

Manifestations of automaticity of latent pacemakers.

Escaped (replacement) complexes and rhythms.

Atrial escape complexes and rhythms.

Escape complexes and rhythms from the AV junction.

Idioventricular (ventricular) replacement complexes and rhythms.

Accelerated slipping complexes and rhythms.

Migration of the supraventricular pacemaker.

Electrocardiograms from No. 1.1 to No. 1.16.

Comments on ECG from No. 1.1 to No. 1.16.

Extrasystoles from the AV connection.

Electrocardiograms from No. 2.1 to No. 2.39.

Comments on ECG from No. 2.1 to No. 2.39.

Supraventricular (supraventricular) tachycardia

Sinus reciprocal tachycardia.

Atrial reciprocal tachycardia.

Focal atrial tachycardia.

Chaotic (multifocal) atrial tachycardia.

Atrioventricular tachycardia (A B junction tachycardia).

Reciprocal AV nodal tachycardias.

Reciprocal AV tachycardia in ventricular preexcitation syndrome.

Non-paroxysmal tachycardia from the AV junction.

Focal paroxysmal and chronic tachycardias from the AV junction.

Electrocardiograms from No. 3.1 to No. 3.90.

Comments on ECG from No. 3.1 to No. 3.90.

Electrocardiograms from No. 4.1 to No. 4.33.

Comments on ECG No. 4.1 to No. 4.33.

Atrial fibrillation and flutter

Differential diagnosis of supraventricular arrhythmias

For the differential diagnosis of supraventricular tachyarrhythmias, the scheme proposed by A.S. is convenient. Smetnev and N.M. Shevchenko.

Differential diagnosis of supraventricular tachyarrhythmias

The complete irregularity of the ventricular contraction rhythm, the absence of P waves and the presence of flicker waves make it possible to diagnose atrial fibrillation. In the presence of second degree atrioventricular block during tachyarrhythmia, a judgment is made about atrial tachyarrhythmia. The diagnosis is determined by the shape and frequency of the atrial complexes - atrial flutter or atrial tachycardia.

With atrial flutter, the number of contractions of the ventricles is about 150 per 1 minute, and the number of contractions of the atria is about 150 per minute. This is the most common form of 2:1 flutter.

With atrial paroxysmal tachycardia, the frequency of contraction of the atria is less than 300, and the frequency of the ventricles is more than 150.

In the absence of second degree atrioventricular block and the impossibility of causing it without interrupting the attack, a conclusion is made about atrioventricular tachycardia. If there is alternation of ventricular complexes, the most likely diagnosis is atrioventricular tachycardia involving additional conduction pathways. When P waves are not visible or negative before the QRS complex, atrioventricular nodal tachycardia is diagnosed, and if they are detected behind the QRS complexes in the S-T interval region, a diagnosis of atrioventricular tachycardia involving additional atrioventricular conduction pathways is made.

For paroxysmal tachycardia with wide QRS complexes, the differential diagnosis is made with:

• supraventricular atrial tachycardia with functional intraventricular block (with aberrant conduction);
• supraventricular paroxysmal tachycardia with previous disturbance of intraventricular conduction;
• supraventricular paroxysmal tachycardia WPW syndrome (antidromic type);
• ventricular tachycardia.

In case of supraventricular tachycardia with functional intraventricular block, the width of the QRS complexes is 0.12 s in the presence of the P wave.

Supraventricular paroxysmal tachycardia in WPW syndrome is characterized by the presence of a delta wave.

“Differential diagnosis of supraventricular arrhythmias” and other articles from the Arrhythmias section

1.4. Atrial fibrillation and flutter

Atrial flutter (AFL) and atrial fibrillation (AF) are supraventricular tachyarrhythmias characterized by the highest atrial rate. The occurrence of AFL and AF is based on similar etiological factors and pathogenetic mechanisms, and therefore these arrhythmias often transform into one another. The term “atrial fibrillation-flutter”, which appears in clinical practice, is inappropriate. When AF and AFL are combined, both forms of arrhythmia must be indicated separately in the diagnosis.

1.4.1. Atrial flutter 1.4.1.1. Epidemiology, etiology, risk factors

Atrial flutter (AFL) is diagnosed in approximately 7-10% of cases of all supraventricular tachyarrhythmias. In men it is found approximately 4-5 times more often than in women. With age, the incidence of atrial flutter increases. Most patients with TP have one or another disease of the cardiovascular system. TP practically does not occur in relatively healthy people. Etiological risk factors for atrial flutter are described in the section “Atrial tachycardia”.

Anterograde conduction along the Kent point (AV=80 ms), retrograde along the AV connection (VA= 270 ms).

Retrograde P waves in lead II are shown by arrows.

1.4.1.2. Definition and classification

Atrial flutter (AFL) refers to atrial tachycardia caused by the circulation of an excitation wave along a topographically extensive contour (the so-called “macro-reentry”), usually around large anatomical structures in the right or left atrium. Depending on the topography of macro-reentry arrhythmias, there are two main types of AFL:

Typical or “isthmus-dependent” AFL,

In a typical AFL, the impulse circulates around the tricuspid valve (Fig. 13). A characteristic feature of this type of AFL is the obligatory repeated passage of the excitation wave along the so-called “cavotricuspid isthmus” (CTI) - the area of ​​the right atrium between the place where the inferior vena cava enters it and the fibrous ring of the tricuspid valve, which is the basis for calling a typical AFL “isthmus-dependent” . Depending on the direction of impulse movement, a typical TP is divided into two options:

- “common” variant - typical TP with the direction of movement of impulses around the tricuspid valve counterclockwise (when viewed from the right ventricle) (see Fig. 13-A);

With a “rare” version of a typical TP, the excitation wave propagates in the direction opposite to that with a “frequent”

Rice. 13. Circulation patterns of excitation in the right atrium with typical atrial flutter

ostomy" version - i.e. clockwise (see Fig. 13-B).

Atypical or “isthmus-independent” AFL includes all other types of atrial macro-re-entry that do not include the cavotricuspid isthmus region in the excitation re-entry circuit. Examples of atypical AFL include the circulation of electrical impulses around the mitral valve, pulmonary veins, and scars in the atria.

Due to the high frequency of atrial impulse, which, as a rule, exceeds the level of the “Wenckebach point” of the AV node, AFL almost always occurs with second-degree AV block and a certain, often changing frequency of atrioventricular conduction. With a constant multiplicity of AV conduction, they speak of the correct form of the atrial fibrillation (Fig. 14), with a non-constant multiplicity - of an irregular form of the atrial fibrillation (Fig. 15).

Depending on the frequency of the ventricular rhythm, there are:

Normosystolic variant of TP (average frequency in the range from 60 to 100 per minute),

Bradysystolic variant of AFL (rate less than 60 per minute) and

Tachysystolic variants of TP (rate more than 100 per minute).

The occurrence of AFL is a consequence of a disruption in the processes of conducting electrical excitation through the myocardium of the right or left atrium, caused by various pathological processes, which creates the possibility of stable

A. A common option is “counterclockwise”,

B. Rare “clockwise” option.

Designations: SVC - superior vena cava, IVC - inferior vena cava, RA - right atrium,

TC – tricuspid valve, CTI – cavotricuspid isthmus, MK – mitral valve, LA – left atrium.

how the electrical impulse circulates along a large excitation re-entry loop (macro-reentry). The critical components of the macro-reentry circuit of AF are the presence of an extended anatomical barrier around which circulation of impulses is possible, as well as zones of slow conduction in one or several sections of this chain, allowing the front of the excitation wave to slow down and not encounter the refractory section of the atria following the tail part re-entry waves.

1.4.1.4. Diagnostics, differential diagnosis

On the ECG, atrial flutter is a regular high-amplitude atrial rhythm with a high frequency (usually from 250 to 400 per minute) and the absence of a clear isoelectric line between the atrial complexes (F waves) in at least one ECG lead.

The leading electrocardiographic sign of a typical AFL is the “sawtooth” atrial “F” waves with the greatest amplitude in leads II, III and aVF, as well as the absence of an isoline between them in these or other ECG leads. It is important to note that with the frequent variant of impulse circulation around the tricuspid valve - in the “counterclockwise” direction, the F waves in leads II, IIIavF are negative (Fig. 15), with the rare variant of impulse circulation in the “clockwise” direction - they positive in the same ECG leads (Fig. 14).

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Rice. 14. Correct form of atrial flutter (AF) with atrial impulse rate (F waves) of 280 per minute and conduction to the ventricles 2:1. Typical isthmus-dependent AFL (rare “clockwise” variant)

Atypical AFL is usually wavy,

cardioversion. Cardioversion is also used routinely

less often - saw-tooth atrial activity, distinguishing

order if attempts at medication are ineffective

I differ in its ECG morphology from a typical AFL (Fig. 16). B

restoration of heart rhythm. In the latter case, it is recommended

In some cases of atypical AFL, discrete F waves may

the use of synchronized biphasic dis-

generally absent on a standard ECG, for accurate

series with a power of Joules, with the inefficiency of which

Gnostics type TP requires transesophageal or

Instead, higher power discharges are used.

If the episode of TP lasts more than 48 hours, the recovery

Spontaneous paroxysms of atrial flutter are initiated by atrial

the establishment of sinus rhythm requires prevention of development

extrasystoles, and during EPI they can be in-

tia of “normalizing” thromboembolic complications.

induced and terminated by electrical stimuli.

The preventive approaches used for this purpose are

Atrial flutter may be paroxysmal

are logical for those used for atrial fibrillation and dis-

(paroxysmal), continuously recurrent and chronic

ical current. Clinical manifestations of flutter are pre-

In order to reduce the frequency of the ventricular rhythm during tachycardia,

heart rate depend on the frequency of the ventricular rhythm and the severity of the

In the metropolitan version of TP, β-blockers are used,

new cardiac pathology and similar to those described above

digoxin and their combination, as well as verapamil, which are

for atrial tachycardias.

in acute situations they are used intravenously, as well as orally,

When the duration of LT is more than 48 hours, patients have increased

for the purpose of long-term control of operating frequency

the likelihood of thrombus formation in the atria is reduced

heart (doses of drugs are indicated in Tables 1 and 3).

(primarily in the left atrial appendage), which creates a threat

The method of choice in the treatment of patients with repeated pas-

cause of the development of thromboembolic complications. In the presence of

rhoxysms of typical TP and with persistent typical

two or more concomitant risk factors for thromboembolism

TP is catheter ablation of the cavo-tricuspi-

according to the CHADS2-VASC2 scale, these patients are indicated for long-term

distant isthmus. This intervention makes it possible to achieve

(lifelong) therapy with indirect anticoagulants. Question

to radically eliminate arrhythmia in the overwhelming majority

methods for preventing thromboembolic complications in patients

most (more than 90%) patients with typical flutter

patients with AFL and AF are presented in detail below.

atria. However, approximately 15-20% of patients

tov after successful ablation of the cavo-tricuspid isthmus

other supraventricular tachyarrhythmias occur, most often

To stop attacks of TP, intravenous

– paroxysmal atrial fibrillation (AF). Basic

administration of procainamide, propafenone, sotalol and amioda-

mi factors predisposing to the occurrence of AF in

rona (doses and schedules of drug administration are indicated in Table 3),

these patients have a long history of persistent

as well as transesophageal atrial stimulation. IN

general AFL, the presence of severe atrial dilatation and/or

cases when TP is accompanied by severe impairments

mitral regurgitation. For atypical TP, effectiveness

hemodynamic problems (arterial hypotension, acute coro-

catheter ablation is lower than with typical LT and is

heart failure or heart failure), the method of choice for

about 70%. In addition, the intervention is associated

cessation of arrhythmia is an electrical emergency

but with a relatively high risk of complications (up to 4.5%).

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Rice. 15. Irregular form of atrial flutter (AF) with an atrial impulse frequency (F waves) of 250 per minute and a multiplicity of conduction to the ventricles from 2:1 to 6:1. Typical isthmus-dependent AFL (often “counterclockwise” variant)

Rice. 16. Atypical atrial flutter, irregular shape with atrial impulse rate FF=300 per minute and conduction to the ventricles 2:1 and 3:1

Designations: TPEG – transesophageal electrogram, A – atrial oscillations, V – ventricular oscillations.

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An alternative to catheter ablation in this case is regular long-term use of class I antiarrhythmic drugs (propafenone, etacizine or allapinin, see Table 1). In order to prevent possible relapses of AFL with a high frequency of conduction to the ventricles, it is recommended to combine class I antiarrhythmic drugs with beta-blockers or verapamil (see Table 1). Prescription of class I drugs is contraindicated in patients with signs of structural heart damage, including in the presence of heart failure, with a decrease in the ejection fraction of the left ventricle to 40% or less, as well as with myocardial hypertrophy (the thickness of the walls of the left ventricle is 1.5 cm or more). Echo-CG data). Class III drugs (sotalol, dronedarone and amiodarone, see Table 1) are less effective in preventing recurrent episodes of AFL, but they can be prescribed in patients with structural heart disease, but in the presence of heart failure and/or a decrease in left ventricular ejection fraction to 40% or less, only amiodarone is allowed.

In the absence or low severity of clinical symptoms and hemodynamic disorders, treatment of patients with AFL may be limited to the prescription of drugs that control the ventricular rate (β-blockers, cardiac glycosides, verapamil, see Table 1). Beta-blockers (preferably long-acting cardioselective ones) are the basis of such treatment. They are most often used for these purposes in the form of monotherapy and in combination with cardiac glycosides, including in heart failure. The use of calcium antagonists for these purposes is permissible only if there are strict contraindications to the use of β-blockers, and the use of cardiac glycosides as monotherapy (without β-blockers) is possible only in elderly patients with an extremely low level of motor activity. The combination of non-dihydropyridine calcium antagonists and β-blockers is undesirable, as it can lead to a dangerous mutual potentiation of negative chronotropic and inotropic effects. The individual choice of doses of these drugs should be focused on target heart rate values: in the complete absence of symptoms - no higher than 110 per minute at rest; in the presence of symptoms - no higher than 80 per minute at rest and no higher than 110 per minute during physical activity. Individual monitoring of the effectiveness and safety of such treatment (there is a risk of developing clinically significant bradycardia, especially at night) should be carried out using Holter ECG monitoring. In patients with a high level of physical activity (mainly young patients), the effectiveness of the prescribed therapy should be assessed using exercise tests on a bicycle ergometer or treadmill.

1.4.1.6. Prevention, rehabilitation, clinical observation

Preventive and rehabilitation measures, as well as approaches to follow-up of patients with AFL, are similar to those described in the section on atrial tachycardias.

1.4.2. Atrial fibrillation 1.4.2.1. Epidemiology, etiology

Atrial fibrillation (AF) is the most common

This form of tachyarrhythmia occurs in 2% of cases in the general population. The likelihood of developing AF increases significantly with age. AF is detected in 3.8% of people over 60 years of age and in 9% of people over 80 years of age.

There are AF associated with damage to the heart valves (usually rheumatic mitral valve stenosis or mitral valve prosthesis, less often - damage to the tricuspid valve), and not associated with valvular pathology.

In the absence of valvular damage, the main causes of AF are: hypertension, ischemic heart disease, primary myocardial diseases, congenital heart defects, hyperthyroidism, pheochromocytoma, diabetes mellitus, alcohol abuse, excess body weight, sleep apnea, hypokalemia, Wolff-Parkinson-White syndrome, as well as genetic predisposition. In 30% of cases, a thorough clinical and instrumental examination fails to identify any cardiac or non-cardiac factors in the development of AF.

1.4.2.2. Definition and classification

Atrial fibrillation is a supraventricular tachyarrhythmia characterized by chaotic high-frequency atrial electrical activity (usually 300 to 700 per minute) and an irregular ventricular rhythm (in the absence of complete AV block).

In AF, just like in AFL, the frequency of the ventricular rhythm during wakefulness is distinguished:

Normosystolic variant (frequency in the range from 60 to 100 per minute (see Fig. 17-A);

Tachysystolic variant (frequency more than 100 per minute (see Fig. 17-B);

Bradysystolic variant (frequency less than 60 per minute)

Depending on the level of physical activity, the degree of emotional stress, as well as under the influence of medications and a number of other factors affecting the functional characteristics of the AV node, reversible transitions from one variant of AF to another are usually observed.

Based on the nature of the course and duration of arrhythmia, 5 types of AF are distinguished: newly diagnosed, paroxysmal, persistent, long-term persistent and permanent or chronic.

Any newly diagnosed episode of AF, regardless of the duration and severity of symptoms, is considered newly diagnosed AF.

Paroxysmal AF is a recurrent (2 or more episodes) AF that can stop on its own before 7 days have passed from the onset of the attack. Paroxysmal AF also includes AF that is terminated using medication or electrical cardioversion.

within 48 hours from the onset of arrhythmia. Persistent is primarily or repeatedly

incomplete AF lasting more than 7 days, not capable of spontaneous termination and requiring special measures (usually electrical cardioversion) to eliminate it.

Long-term persistent AF is called AF lasting more than a year if a decision is made to restore sinus rhythm using cardioversion or radical interventional (catheter ablation) and/or surgical treatment.

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Rice. 17. Atrial fibrillation

A. – normosystolic variant, B. – tachysystolic variant.

AF lasting more than 7 days is called persistent or chronic if attempts to eliminate it are ineffective or are not undertaken for one reason or another. The latter implies refusal to perform cardioversion, as well as any attempts at radical interventional and/or surgical treatment of arrhythmia.

Usually the establishment of a permanent form is preceded by a period of recurrence of paroxysms. In the same patient with a long history of AF at different stages of the disease, different types of arrhythmia may be observed, as well as their combinations. In such cases, the diagnosis indicates only the form of AF that was the reason for this hospitalization or intervention.

1.4.2.3. Pathogenetic mechanisms of AF

For the occurrence of stable AF, the presence of three components is necessary: ​​1) triggering, so-called. trigger factors of arrhythmia, 2) an arrhythmogenic substrate of arrhythmia, which ensures independent maintenance of AF, as well as 3) individual modulating influences that increase the susceptibility of an arrhythmogenic substrate to trigger factors of AF.

In the vast majority of cases (95%), the trigger factor for AF is pathological high-frequency electrical activity at the mouths of the pulmonary veins, which is reflected on the ECG as frequent early atrial extrasystole (of the “P to T” type, see Fig. 18) and/or atrial jogging tachycardia (both monofocal and chaotic).

More rare trigger factors for AF are extrasystoles from the vena cava, as well as atrial extrasystoles. The electrophysiological mechanisms of focal activity of the pulmonary and vena cava are trigger activity and re-entry of excitation in the muscle structures lining the places where they enter the atria. When performing EFI

an attack of AF can be caused by electrical stimulation of the atria. The arrhythmogenic substrate of AF is a structurally and functionally altered (remodeled) atrial myocardium, which ensures stable independent maintenance of AF. Remodeling is understood as a set of pathological processes that occur in the atria in response to the occurrence of AF and/or as a result of the action of known etiological factors of AF. Remodeling begins with a disruption of the ionic cellular mechanisms of impulse formation and ends with the structural and functional degradation of the atrial myocardium and atriomegaly. The main structural changes in the atrial myocardium that predispose to the occurrence of AF substrate are fibrosis, inflammation, apoptosis and hypertrophy of cardiomyocytes. Functional disorders in the atrial myocardium include the occurrence of heterogeneity in the speed of impulses in different directions, as well as dispersion of repolarization processes in the atrial myocardium. The progression of AF and resistance of arrhythmia to drug and interventional treatment, as a rule, is determined by the severity of atrial remodeling processes. Currently, two alternative electrophysiological hypotheses of independent

AF maintenance:

1) the presence of one or more high-frequency rotors in the atria or pulmonary veins with a constantly changing nature of impulse conduction to the surrounding atrial myocardium;

2) circulation of multiple micro-reentry waves in the atria along an uncertain, random path.

The most common modulating influence that contributes to the activation of the “dormant” arrhythmogenic substrate of AF in response to the action of a trigger factor is an imbalance

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Rice. 18. The occurrence of an attack of atrial fibrillation due to frequent ectopic activity from the mouth of the left superior pulmonary vein

Designations: LVPV – electrogram from the mouth of the left superior pulmonary vein; A – atrial oscillations.

Index 1 indicates electrical signals of sinus origin, index 2 indicates electrical signals of ectopia from the PVLV.

autonomic influences on the atrial myocardium. Depending on the nature of the violations of the autonomic regulation of the heart, the so-called are distinguished. “vagal” form of AF (arrhythmia occurs mainly during sleep or after overeating, with sudden bending or turning of the body, as well as any other factors that enhance parasympathetic influences on the heart), as well as the so-called. “hyperadrenergic” form of arrhythmia (AF occurs mainly during physical activity, stress, sudden fear and other conditions accompanied by an increase in sympathetic influences on the heart). Disorders of electrolyte metabolism (hypokalemia), transient myocardial ischemia and the proarrhythmic effect of drugs can also act as a modulating effect.

1.4.2.4. Diagnosis, differential diagnosis, clinical manifestations, prognosis

The diagnosis of AF is made on the basis of an ECG. Often, to confirm the diagnosis of paroxysmal AF, long-term ECG monitoring (from 24 hours to 7 days), the use of portable ECG recorders with the ability to transmit ECG by telephone, as well as implantable loop ECG recorders are required. Programmed atrial stimulation under EPI conditions to confirm the diagnosis of AF is not performed due to the low sensitivity and specificity of the method in relation to the reproducibility of clinically significant AF.

Characteristic ECG signs of AF are: the absence of P waves, the presence of multi-amplitude, polymorphic ff waves, transforming into one another without a clear isoline between them, as well as absolute chaoticity and irregularity of the ventricular rhythm (Fig. 17). The last sign is not recorded in cases of a combination of AF and third-degree AV block (with the so-called Frederick phenomenon).

Typical symptoms of AF are: increased, as

For example, irregular heartbeat, irregular heartbeat, shortness of breath, increased fatigue, poor exercise tolerance and sweating. AF accounts for a third of all hospitalizations for cardiac arrhythmias. The main reasons for hospitalization for AF are acute coronary syndrome, heart failure, thromboembolic complications and the need for urgent relief of AF. AF is associated with a twofold increase in the risk of death, primarily cardiac death, regardless of the presence of other risk factors. The most dangerous complications of AF are thromboembolic, including ischemic cardioembolic stroke (the occurrence of AF in patients without heart valve damage increases the risk of stroke by 5 times, and in the presence of valvular disease - by 17 times), thromboembolism of the vessels of the extremities and infarction of internal organs. In addition, AF can cause cognitive dysfunction, including vascular dementia. In patients with AF, the quality of life deteriorates, tolerance to physical activity decreases, and left ventricular dysfunction often appears and/or progresses with the development of heart failure. In approximately a quarter of cases, arrhythmia may be asymptomatic and detected incidentally during a medical examination.

Treatment of patients with AF is carried out with the aim of reducing the severity of AF symptoms, improving hemodynamic parameters, preventing possible complications of AF and improving the prognosis of these patients.

Targeting heart rhythm suggests two possible treatment strategies for patients with AF:

1) control of the ventricular rate against the background of persistent AF, the so-called. “rate control,” which involves abstaining from antiarrhythmic treatment;

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2) restoration (if necessary) and maintenance of sinus rhythm, the so-called. “control of heart rhythm” by means of medicinal and/or non-medicinal antiarrhythmic treatment. Carrying out antiarrhythmic treatment does not eliminate the need for “rate control”, since there is always a possibility of relapse of AF, which should not occur with an excessively high ventricular rhythm.

The choice of treatment strategy for AF is determined individually, depending on the nature of the arrhythmia, the severity of clinical manifestations, the presence of concomitant diseases, tolerability of various groups of drugs and with mandatory consideration of the opinion of the attending physician and the patient’s preferences.

Monitoring heart rate and cardiac rhythm during emergency care

In AF that occurs with severe symptoms, acute hemodynamic disturbances and/or coronary insufficiency, the elimination of these clinical manifestations in a significant proportion of cases can be achieved by intravenous or oral use of β-blockers or non-hydropyridine calcium antagonists (see Tables 1 and 3). If these measures are ineffective, emergency restoration of sinus rhythm (cardioversion) may be necessary. The therapeutic strategy for most of these patients is “heart rate control.” In these cases, cessation of AF and restoration of sinus rhythm can be achieved by intravenous use of antiarrhythmic drugs: procainamide, propafenone, amiodarone (for arrhythmia duration up to 48 hours), vernakalant (for arrhythmia duration up to 7 days), as well as nibentan and niferidil (for arrhythmia duration more than 7 days), see table. 3. This treatment method is called drug cardioversion. If intravenous administration of drugs is not possible, drug cardioversion can be carried out using oral administration of propafenone (300 mg orally, if the arrhythmia persists after 2 hours, an additional mg of the drug is taken). The first attempt to use this method of relief is permissible only in a hospital setting under ECG monitoring. If the effectiveness and (most importantly) safety of such a relief regimen is confirmed, it can be recommended to the patient for independent use on an outpatient basis if relapses occur.

If drug cardioversion is ineffective or impossible, emergency electrical cardioversion is used in acute cases, which is also used to restore sinus rhythm in patients with persistent AF (planned electrical cardioversion). With any method of cardioversion, it is necessary to comply with the requirements for the prevention of normalization thromboembolism (see below).

Long-term monitoring of heart rate and heart rhythm

Long-term drug control of ventricular rate is a fundamental treatment strategy for patients with AF and/or AFL and an equivalent alternative to long-term antiarrhythmic treatment for patients with various types of AF (see below). The equivalence of the “rate control” and “rhythm control” strategies in the treatment of patients with AF is determined by the absence of differences in the frequency

development of disease outcomes (progression of heart failure, re-hospitalizations, deaths from cardiovascular and other causes). Moreover, control of the ventricular rate should be ensured in all patients with AF receiving antiarrhythmic treatment, since there is always the possibility of relapse of AF, which should not occur with an excessively high ventricular rate.

The tactics of “ventricular rate control” using β-blockers, cardiac glycosides, non-dihydropyridine calcium antagonists (see Table 1) are more preferable in patients with asymptomatic or oligosymptomatic AF, with the ineffectiveness of previous attempts at preventive antiarrhythmic treatment (see below) and severe organic heart damage. Almost without exception, this treatment tactic is used for chronic AF.

Beta-blockers (preferably long-acting cardioselective ones) are the basis of such treatment. They are most often used for these purposes in the form of monotherapy and in combination with cardiac glycosides, including in heart failure. The use of calcium antagonists for these purposes is permissible only if there are strict contraindications to the use of β-blockers, and the use of cardiac glycosides as monotherapy (without β-blockers) is possible only in elderly patients with an extremely low level of motor activity. The combination of non-hydropyridine calcium antagonists and β-blockers is undesirable, as it can lead to a dangerous mutual potentiation of their negative chronotropic and inotropic effects. The individual choice of doses of these drugs should be focused on target heart rate values: in the complete absence of symptoms - no higher than 110 per minute at rest; in the presence of symptoms - no higher than 80 per minute at rest and no higher than 110 per minute during physical activity. Individual monitoring of the effectiveness and safety of such treatment (there is a risk of developing clinically significant bradycardia, especially at night) should be carried out using Holter ECG monitoring. In patients with a high level of physical activity (mainly young patients), the effectiveness of the prescribed therapy should be assessed using exercise tests on a bicycle ergometer or treadmill.

If the use of drugs that control the heart rate (including combinations of several drugs) is ineffective, they resort to catheter ablation of the AV node with simultaneous implantation of an artificial heart pacemaker. This type of intervention provides highly effective control of ventricular rhythm in patients with AF. However, being a palliative intervention after which the patient becomes permanently pacemaker dependent, AV node ablation should not be considered as an equivalent alternative to drug rhythm control. This method of treatment can be used only in cases where, if drug frequency control is ineffective, drug and non-drug (see below) antiarrhythmic treatment is ineffective or impossible. Selecting an implantable device after AV node ablation (pacer, biventricular pacemaker, or implantable cardioverter defibrillator)

Atrial fibrillation

Atrial fibrillation

Definition and classification

Classification of atrial fibrillation according to electrocardiographic and frequency characteristics

• atrial fibrillation bradysystolic form (atrial fibrillation bradysystolic, a.fibrillaris bradysystolica; synonym atrial fibrillation) - atrial fibrillation occurring with a normal or reduced heart rate (less than 60 ventricular contractions per minute) and the absence of pulse deficit.
• Atrial fibrillation tachysystolic (Atrial fibrillation tachysystolic a.fibrillaris tachysystolica; synonym tachyarrhythmia atrial fibrillation) - atrial fibrillation, characterized by increased heart rate (more than 100 per minute at rest) and accompanied by a pulse deficit.
• Normosystolic atrial fibrillation (Atrial fibrillation eurhythmic a.fibrillaris eurhythmica) - in which the frequency of ventricular contractions is within normal limits for a healthy person (per 1 minute).

Classification of atrial fibrillation according to the nature of f waves

• Large-wave atrial fibrillation (large-wave atrial fibrillation) - characterized by the presence on the ECG of relatively large and rare (per 1 minute) atrial fibrillation waves; usually observed with heart defects with atrial overload.
• Small-wave atrial fibrillation (small-wave atrial fibrillation) - characterized by the presence on the ECG of relatively small and frequent (per 1 minute) waves of atrial fibrillation; usually observed in cardiosclerosis.

Classification of AF according to the duration of arrhythmia existence

• Newly diagnosed atrial fibrillation is atrial fibrillation that appears for the first time, regardless of the duration of the arrhythmia or the presence and severity of symptoms associated with AF or its complications.
• The paroxysmal form of atrial fibrillation is a recurrent and self-terminating arrhythmia. Many patients have frequent symptomatic paroxysms of AF, usually lasting 48 hours or less, but less than 7 days. In clinical trials, AF is defined as an episode lasting longer than 30 seconds.
• Persistent atrial fibrillation lasts more than 7 days (by expert agreement) or is treated with cardioversion (medical or electrical). The term "persistent AF" also implies a desire to restore and maintain sinus rhythm. Long-term persistent forms of AF may continue for more than 12 months, but are designated as persistent rather than permanent if restoration of sinus rhythm is expected.
• Persistent atrial fibrillation exists for a long time and is determined by adherence to a rate control strategy, that is, the presence of AF is “accepted.” Interventions to restore rhythm (eg, antiarrhythmic drugs, cardioversion, catheter ablation, or surgery) are not used in patients with persistent AF.

Usually the establishment of a permanent form is preceded by a period of recurrence of paroxysms. The same patient with a long history of atrial fibrillation at different stages of the disease may experience different types of arrhythmia, as well as their combinations. In such cases, the diagnosis indicates only the form of AF that was the reason for this hospitalization or intervention.

EHRA classification according to the severity of clinical manifestations (EHRA scale)

• EHRA I No symptoms
• EHRA II Mild symptoms, patient's normal daily activities are not affected
• EHRA III Severe symptoms, patient's usual daily activities are impaired
• EHRA IV Disabling symptoms, patient's usual daily activities stopped

Pathogenetic mechanisms of atrial fibrillation

In the vast majority of cases (95%), the trigger factor for AF is pathological high-frequency electrical activity at the mouths of the pulmonary veins, which is reflected on the ECG as frequent early atrial extrasystole (of the “P to T” type, see Fig. 2) and/or atrial jogging tachycardia (both monofocal and chaotic).

More rare trigger factors for atrial fibrillation are extrasystoles from the vena cava, as well as atrial extrasystoles. The electrophysiological mechanisms of focal activity of the pulmonary and vena cava are trigger activity and re-entry of excitation in the muscle structures lining the places where they enter the atria. During EPI, an attack of AF can be caused by electrical stimulation of the atria.

The arrhythmogenic substrate of AF is a structurally and functionally altered (remodeled) atrial myocardium, which ensures stable independent maintenance of AF. Remodeling is understood as a set of pathological processes that occur in the atria in response to the occurrence of AF and/or as a result of the action of known etiological factors of AF. Remodeling begins with a disruption of the ionic cellular mechanisms of impulse formation and ends with the structural and functional degradation of the atrial myocardium and atriomegaly. The main structural changes in the atrial myocardium that predispose to the occurrence of AF substrate are fibrosis, inflammation, apoptosis and hypertrophy of cardiomyocytes. Functional disorders in the atrial myocardium include the occurrence of heterogeneity in the speed of impulses in different directions, as well as dispersion of repolarization processes in the atrial myocardium. The progression of AF and resistance of arrhythmia to drug and interventional treatment, as a rule, is determined by the severity of atrial remodeling processes. Currently, two alternative electrophysiological hypotheses for the independent maintenance of AF are being considered:

1. the presence of one or more high-frequency rotors in the atria or pulmonary veins with a constantly changing nature of impulse conduction to the surrounding atrial myocardium;
2. circulation of multiple micro-reentry waves in the atria along an uncertain, random path.

The most common modulating influence that promotes the activation of the “sleeping” arrhythmogenic substrate of AF in response to the action of a trigger factor is an imbalance of autonomic influences on the atrial myocardium. Depending on the nature of the violations of the autonomic regulation of the heart, the so-called are distinguished. “vagal” form of AF (arrhythmia occurs mainly during sleep or after overeating, with sudden bending or turning of the body, as well as any other factors that enhance parasympathetic influences on the heart), as well as the so-called. “hyperadrenergic” form of arrhythmia (AF occurs mainly during physical activity, stress, sudden fear and other conditions accompanied by an increase in sympathetic influences on the heart). Disorders of electrolyte metabolism (hypokalemia), transient myocardial ischemia and the proarrhythmic effect of drugs can also act as a modulating effect.

Diagnosis, differential diagnosis, clinical manifestations, prognosis

Typical symptoms of AF are: increased, usually irregular heartbeat, irregular heartbeat, shortness of breath, increased fatigue, poor exercise tolerance and sweating. AF accounts for a third of all hospitalizations for cardiac arrhythmias. The main reasons for hospitalization for AF are acute coronary syndrome, heart failure, thromboembolic complications and the need for urgent relief of AF. AF is associated with a twofold increase in the risk of death, primarily cardiac death, regardless of the presence of other risk factors. The most dangerous complications of AF are thromboembolic, including ischemic cardioembolic stroke (the occurrence of AF in patients without heart valve damage increases the risk of stroke by 5 times, and in the presence of valvular disease - by 17 times), thromboembolism of the vessels of the extremities and infarction of internal organs. In addition, AF can cause cognitive dysfunction, including vascular dementia. In patients with AF, the quality of life deteriorates, tolerance to physical activity decreases, and left ventricular dysfunction often appears and/or progresses with the development of heart failure. In approximately a quarter of cases, arrhythmia may be asymptomatic and detected incidentally during a medical examination.

Diagnosis and differential diagnosis of atrial fibrillation

It is not difficult to recognize atrial fibrillation (AF) by auscultation of the heart. Changes in the electrocardiogram (ECG) are very demonstrative.

In atrial fibrillation, all R-R intervals have different durations, coinciding only by chance, and the QRS complexes have different amplitudes (electrical alternans). The P wave is absent. The diastolic segment is saturated with frequent irregular f waves, reflecting chaotic excitation (undulation) of individual muscle bundles of the atria. They are best seen in leads V1 and V2.

With atrial flutter in leads III and aVF, the diastolic interval has a characteristic “sawtooth” pattern. In leads V1 and V2, the following atrial waves f with high frequency are clearly differentiated and counted. With an irregular form of flutter, as with fibrillation, ventricular activation is chaotic. With the correct form, the R-R intervals are the same, and each QRS complex is preceded by a constant number of atrial waves - two, three, etc. (correct flutter form is 2:1, 3:1, etc.).

In cases of 1:1 or 2:1 flutter, which are accompanied by a particularly high ventricular rate (activation), identification of f waves can be difficult and the electrocardiogram (ECG) resembles that of supraventricular paroxysmal tachycardia. For the purpose of differential diagnosis, one of the methods of reflex stimulation of the vagus is used, trying, by slowing down conduction, to change the ratio of atrial and ventricular activation to 3:1 or 4:1 and thereby facilitate the identification of f waves, and, consequently, clarify the shape of the arrhythmia.

Since the most common causes of atrial fibrillation (AF) are mitral stenosis, cardiosclerosis and thyrotoxicosis, the differential diagnosis is primarily made between these conditions.

Only by reasonably rejecting the above, as well as other pathologies of the myocardium and valvular apparatus (mitral valve prolapse, obvious Wolff-Parkinson-White syndrome, cardiomyopathy, etc.), can we dwell on the idiopathic form of atrial fibrillation (AF) of vegetative dystonic origin and further clarify the what type of paroxysms are we talking about - predominantly “vagal” or “adrenergic” (stress-dependent or catecholamine-dependent).