Atrial fibrillation: symptoms and treatment. Atrial and ventricular fibrillation

Atrial flutter: causes, forms, diagnosis, treatment, prognosis

Atrial flutter (AF) is one of the supraventricular tachycardias, when the atria contract with very high speed- more than 200 times per minute, but the rhythm of contractions of the entire heart remains correct.

Atrial flutter is several times more common in men; patients are usually elderly people aged 60 years and older. The exact prevalence of this type of arrhythmia is difficult to determine due to its instability. AFL is often short-lived, so it can be difficult to document it on an ECG and in diagnosis.

Atrial flutter lasts from several seconds to several days (paroxysmal form), rarely more than a week. When short-term disturbance rhythm, the patient feels discomfort, which quickly passes or is replaced by it. In some patients, flutter and flicker are combined, periodically replacing each other.

The severity of symptoms depends on the speed of atrial contraction: the greater it is, the higher the likelihood of hemodynamic disorders. This arrhythmia is especially dangerous in patients with severe structural changes in the left ventricle, in the presence of chronic heart failure.

In most cases, with atrial flutter, the rhythm is restored on its own, but it happens that the disorder progresses, the heart cannot cope with its function, and the patient needs urgent health care. Antiarrhythmic drugs are not always effective desired effect, That's why TP is the case when it is advisable to resolve the issue of cardiac surgery.

Atrial flutter is a serious pathology, although not only many patients, but also doctors do not pay due attention to its episodes. The result is expansion of the heart chambers with progressive heart failure, thromboembolism, which can cost life, therefore, any attack of rhythm disturbance should not be ignored, and if it occurs, you should go to a cardiologist.

How and why does atrial flutter occur?

Atrial flutter is a variant of supraventricular tachycardia, that is, the focus of excitation appears in the atria, causing them to contract too frequently.

The heart rhythm during atrial flutter remains regular, unlike ( atrial fibrillation), when the atria contract rapidly and chaotically. More rare contractions of the ventricles are achieved by partial blockade of impulses to the ventricular myocardium.

The causes of atrial flutter are quite varied, but it is always based on organic damage to the cardiac tissue, that is, a change in the heart itself. anatomical structure organ. This can be associated with a higher frequency of pathology in older people, while in young people arrhythmias are more of a functional and dysmetabolic nature.

Among the diseases accompanied by TP are:

• Ischemic disease in the form of a diffuse, post-infarction scar or;
• Inflammatory processes in and;
• , especially with a strong one.

There are frequent cases of atrial flutter in patients with pulmonary pathology - chronic obstructive diseases (bronchitis, asthma, emphysema). The expansion of the right chambers of the heart due to increased pressure in the heart predisposes to this phenomenon. pulmonary artery against the background of sclerosis of the parenchyma and blood vessels of the lungs.

After cardiac surgery, the risk of this type of rhythm disturbance is high in the first week. It is diagnosed after correction birth defects, coronary artery bypass grafting.

Risk factors for TP consider diabetes mellitus, disorders electrolyte metabolism, excess hormonal function thyroid gland, various intoxications (medicines, alcohol).

As a rule, the cause of atrial flutter is clear, but it happens that the arrhythmia overtakes almost healthy person, Then we're talking about about the idiopathic form of TP. The role of a hereditary factor cannot be excluded.

The mechanism for the appearance of atrial flutter is based on repeated excitation of atrial fibers of the macro-re-entry type (the impulse seems to go in a circle, involving into contraction those fibers that have already contracted and should be relaxed at this moment). “Re-entry” of the impulse and excitation of cardiomyocytes is characteristic of structural damage (scar, necrosis, inflammation), when an obstacle is created to the normal propagation of the impulse along the fibers of the heart.

Having arisen in the atrium and causing repeated contraction of its fibers, the impulse still reaches the atrioventricular (AV) node, but since the latter cannot conduct such frequent impulses, at most half of the atrial impulses arise - at most - half of the atrial impulses reach the ventricles.

The rhythm remains regular, and the ratio of the number of contractions of the atria and ventricles is proportional depending on the number of impulses conducted to the ventricular myocardium (2:1, 3:1, etc.). If half the impulses reach the ventricles, the patient will have tachycardia up to 150 beats per minute.

atrial flutter moving from 5:1 to 4:1

It is very dangerous when all atrial impulses reach the ventricles, and the ratio of systoles of all parts of the heart becomes 1:1. In this case, the rhythm frequency reaches 250-300, hemodynamics are sharply disrupted, the patient loses consciousness and signs of acute heart failure appear.

AFL can spontaneously develop into atrial fibrillation, which is not characterized by a regular rhythm and a clear ratio of the number of ventricular to atrial contractions.

In cardiology, there are two types of atrial flutter:

typical and reverse typical TP

1. Typical
2. Atypical.

In a typical case In case of TP syndrome, the excitation wave travels through the right atrium, the systolic frequency reaches 340 per minute. In 90% of cases, contraction occurs around the tricuspid valve counterclockwise, in other patients it occurs clockwise.

At atypical form TP the wave of myocardial excitation does not pass in a typical circle, affecting the isthmus between the mouth of the vena cava and tricuspid valve, and along the right or left atrium, causing contractions up to 340-440 per minute. This form cannot be treated with transesophageal pacing.

Manifestations of atrial flutter

In the clinic it is customary to highlight:

• New atrial flutter;
• Paroxysmal form;
• Constant;
• Persistent.

At paroxysmal In this form, the duration of TP is no more than a week, the arrhythmia resolves spontaneously. persistent the course is characterized by a duration of disturbance of more than 7 days, and independent normalization of the rhythm is impossible. ABOUT constant form it is said when an attack of fluttering cannot be stopped or no treatment was carried out.

It is not the duration of AFL that is clinically important, but the frequency with which the atria contract: the higher it is, the more obvious the hemodynamic disturbance and complications are more likely. With frequent contractions, the atria do not have time to provide the ventricles with the required volume of blood, gradually expanding. With frequent episodes of atrial flutter or a permanent form of pathology, circulatory disorder occurs in both circles and dilated cardiomyopathy is possible.

In addition to insufficient cardiac output, the lack of blood going to the coronary arteries. With severe AFL, the lack of perfusion reaches 60% or more, and this is the likelihood of acute heart failure and heart attack.

Clinical signs of atrial flutter appear during paroxysmal arrhythmia. Among the complaints of patients, weakness and fatigue are possible, especially with physical exercise, discomfort in chest, rapid breathing.

In case of shortage coronary circulation symptoms appear, in patients with coronary heart disease the pain intensifies or is progressive. The lack of systemic blood flow contributes to hypotension, then dizziness, darkening of the eyes, and nausea are added to the symptoms. A high frequency of atrial contractions can provoke syncope and severe fainting.

Attacks of atrial flutter more often appear in hot weather, after physical exertion, strong emotional experiences. Alcohol intake, errors in diet, and intestinal disorders can also provoke paroxysms of atrial flutter.

When there are 2-4 atrial contractions per ventricular contraction, patients have relatively few complaints; this ratio of contractions is more easily tolerated than atrial fibrillation, because the rhythm is regular.

The danger of atrial flutter is its unpredictability: at any moment, the frequency of contractions can become very high, palpitations will appear, shortness of breath will increase, and symptoms of insufficient blood supply to the brain will develop - dizziness and fainting.

If the ratio of atrial to ventricular contractions is stable, the pulse will be rhythmic, but when this ratio fluctuates, the pulse will become irregular. A characteristic symptom there will also be pulsation of the veins of the neck, the frequency of which exceeds two or more times the pulse per peripheral vessels.

As a rule, TP appears in the form of short and infrequent paroxysms, but with a strong increase in contractions of the heart chambers, complications are possible - thromboembolism, pulmonary edema, acute heart failure, ventricular fibrillation and death.

Diagnosis and treatment of atrial flutter

In the diagnosis of atrial flutter, electrocardiography is of paramount importance. After examining the patient and determining the pulse, the diagnosis can only be speculative. When the ratio between contractions of the heart is stable, the pulse will be either more frequent or normal. If the conduction coefficient fluctuates, the rhythm will become abnormal, as with atrial fibrillation, but it is impossible to distinguish these two types of disorders by pulse. In the primary diagnosis, assessment of the pulsation of the neck veins, which exceeds the pulse by 2 or more times, helps.

ECG signs of atrial flutter consist of the appearance of so-called atrial F waves, but the ventricular complexes will be regular and unchanged. At daily monitoring The frequency and duration of paroxysms of TP, their relationship with exercise and sleep are recorded.

Video: lesson on ECG for non-sinus tachycardias

To clarify the anatomical changes in the heart, diagnose the defect and determine the location of organic damage, a test is carried out, during which the doctor specifies the size of the organ cavities, the contractility of the heart muscle, and the features of the valve apparatus.

Laboratory tests are used as additional diagnostic methods - determination of the level of thyroid hormones in order to exclude thyrotoxicosis, rheumatic tests for rheumatism or suspicion of it, determination of blood electrolytes.

Treatment of atrial flutter can be medication or cardiac surgery. The greatest difficulty is the resistance of TP to drug effects, unlike flicker, which can almost always be corrected with medication.

Drug therapy and first aid

Conservative treatment includes prescribing:

• (metoprolol);
• (verapamil, diltiazem);
• Antiarrhythmic drugs (amiodarone, flecainide, ibutilide);
• Potassium preparations;
• (digoxin);
• (warfarin, heparin).

Beta blockers, cardiac glycosides, calcium channel blockers are prescribed in parallel with antiarrhythmics in order to prevent improvement of conduction in the atrioventricular node, since there is a risk that all atrial impulses will reach the ventricles and provoke ventricular tachycardia. Verapamil is most commonly used to control ventricular rate.

If paroxysm of atrial flutter occurs against a background when conduction along the main pathways of the heart is impaired, all drugs from the above groups are strictly contraindicated, except for anticoagulants and antiarrhythmics.

Emergency care for paroxysm of atrial flutter, accompanied by angina pectoris, signs of cerebral ischemia, severe hypotension, and progression of heart failure consists of: emergency electrical cardioversion with low power current. In parallel, antiarrhythmics are administered to increase the effectiveness of electrical stimulation of the myocardium.

Drug therapy for an attack of flutter is prescribed if there is a risk of complications or poor tolerability of the attack, and amiodarone is injected into a vein. If amiodarone does not restore the rhythm within half an hour, cardiac glycosides (strophanthin, digoxin) are indicated. If there is no effect from the drugs, electrical cardiac stimulation is started.

Another treatment regimen is possible for an attack whose duration does not exceed two days. In this case, procainamide, propafenone, quinidine with verapamil, disopyramide, amiodarone, and electrical pulse therapy are used.

If appropriate, transesophageal or intraatrial myocardial stimulation is indicated to restore sinus rhythm. Exposure to ultrahigh frequency current is carried out for patients who have undergone heart surgery.

If atrial flutter lasts more than two days, then before starting treatment, anticoagulants (heparin) must be administered to prevent thromboembolic complications. For three weeks of anticoagulant therapy, beta blockers, cardiac glycosides, and antiarrhythmic drugs are prescribed in parallel.

Surgical treatment

RF ablation for AFL

If atrial flutter is persistent or has frequent relapses, the cardiologist may recommend a test that is effective in classic form AFL with circular circulation of the impulse through the right atrium. If atrial flutter is combined with sick sinus syndrome, then in addition to ablation of the conduction pathways in the atrium, the atrioventricular node is also exposed to the current, and subsequently, ensuring the correct heart rhythm.

Resistance of atrial flutter to drug treatment leads to increasingly frequent use radiofrequency ablation (RFA), which is especially effective in the typical form of pathology. The action of radio waves is directed to the isthmus between the mouth of the vena cava and the tricuspid valve, where the circulation of the electrical impulse most often occurs.

RFA can be performed both at the time of paroxysm and as planned during sinus rhythm. The indication for the procedure will be not only a prolonged attack or severe course TP, but also the situation when the patient agrees to it, because long-term use conservative methods may provoke new types of arrhythmias and is not economically feasible.

Absolute indications for RFA– lack of effect from antiarrhythmic drugs, their unsatisfactory tolerability, or the patient’s reluctance to take any medications for a long time.

A distinctive feature of TP is its resistance to drug treatment and a greater likelihood of recurrence of flutter attacks. This course of pathology greatly predisposes to intracardiac thrombus formation and the spread of blood clots throughout big circle, as a result - strokes, intestinal gangrene, infarctions of the kidneys and heart.

The prognosis for atrial flutter is always serious, but depends on the frequency of arrhythmia paroxysms and duration, as well as on the speed of atrial contraction. Even with a relatively favorable course of the disease, one cannot ignore it or refuse the proposed treatment, because no one can predict what strength and duration the attack will be, and, therefore, the risk of dangerous complications and death of the patient from acute failure There are always hearts in TP.

Video: atrial flutter, program “Live Healthy!”

Diseases of cardio-vascular system occupy a leading position compared to other pathologies. Many patients have atrial fibrillation or atrial flutter. They are the main representatives of the group of arrhythmias. When a person knows about their manifestations, he can independently seek help in time.

Myocardial fibrillation and atrial flutter have similar mechanisms of occurrence, but also a number of differences. The first term refers to a type of tachyarrhythmia of the supraventricular type. At this moment, heart contractions become chaotic, and the counting rate reaches 350-750 beats per minute. This feature excludes the possibility of rhythmic operation of the atria during atrial fibrillation.

Atrial fibrillation

Depending on the classification, fibrillation is divided into several forms. Development mechanisms may have some differences from each other. These include the following:

• provoked by a certain disease;
• resting atrial fibrillation, permanent form;
• hyperadrenergic;
• potassium deficiency;
• hemodynamic.

A permanent form of atrial fibrillation (or paroxysmal) becomes a manifestation of a number of diseases. In many patients, mitral stenosis, thyrotoxicosis or atherosclerosis is most often found. The circle of patients with arrhythmia due to a degenerative process in the myocardium of an alcoholic nature, diabetes mellitus and hormonal imbalance is expanding.

Paroxysmal arrhythmia occurs in patients in horizontal position. During sleep they often wake up from unpleasant symptoms. It can appear when the body turns sharply when a person is lying down. The mechanism of occurrence of such disorders is associated with pronounced reflex influences to the myocardium of the vagus nerve.

Under their influence, the conduction of nerve impulses in the atria slows down. For this reason, fibrillation begins with them. Described form of violations heart rate able to normalize on its own. This is explained by a decrease in the impact of the nerve on the muscle over time.

Hyperadrenergic paroxysms are more common than those described above. They appear in the morning and during physical and emotional stress. The last, chronic variant of arrhythmia is called hemodynamic.

It is classified as a congestive form of pathology, which is associated with the presence of an obstacle to normal myocardial contraction. Gradually the atria begin to expand. The leading reasons are:

• weakness of the left ventricular wall;
• narrowing of the lumen of the holes between the cavities in the heart;
• insufficiency of the valve apparatus function;
• reverse blood flow (regurgitation) into the atria;
• tumor-like formations in cavities;
• thrombus formation;
• chest injury.

In many cases, fibrillation becomes a manifestation of the disease. For this reason, before starting treatment, its origin must be established.

Flutter is characterized by heart contractions up to 350 per minute. This form is called supraventricular or “flutter” of the atrium myocardium. Tachyarrhythmia differs from that described above in the presence of the correct rhythm in most patients.

There are people with the characteristics of this disease. They have normal sinus contractions alternating with episodes of flutter. The rhythm is called permanent. This variant of heart pathology has the following etiology (causes):

• IHD ( ischemic disease hearts);
• defects of rheumatic origin;
• pericarditis;
• myocarditis;
• arterial hypertension;
• after surgery for defects or bypass surgery;
• emphysema.

Tachysystolic rhythm occurs in patients with diabetes mellitus, insufficient level of potassium in the blood, intoxication with drugs and alcohol. The basis of pathogenesis (development mechanism) is repeated repeated excitation in the myocardium. Paroxysm is explained by the circulation of such impulses a large number of once.

Provoking factors include episodes of flickering and extrasystoles. The frequency of contractions in the atria increases to 350 beats per minute.

Unlike them, the ventricles cannot do this. This is due to the lack of pacemaker capability for high throughput. For this reason, they contract no more than 150 per minute. The permanent form of atrial fibrillation is characterized by blocks, which explains such differences between the cavities of the heart.

Manifestations of atrial flutter

Atrial flutter and atrial fibrillation do not always occur under the influence of the same factors. Stress, physical activity, and sudden changes in weather can worsen your well-being. The typical symptoms are:

• pain in the heart or discomfort in this area;
• dizziness;
• weakness that does not disappear after rest;
• feeling of heartbeat;
• dyspnea;
• low blood pressure;
• sensation of interruptions in the heart area.

Transient disturbances can occur several times a year or more often, when the normosystolic rhythm gives way to flutter. IN at a young age they appear under the influence of provoking factors. Elderly people are bothered by signs of arrhythmia even at rest.

Asymptomatic course is considered the most dangerous. The patient is not worried about anything, which increases the risk of complications - stroke, myocardial infarction, blood clots and heart failure.

Diagnostics

Treatment of a permanent form of atrial fibrillation is carried out on the basis of data obtained after a comprehensive diagnosis. The exact cause is determined using clinical, laboratory and instrumental studies. The main sign that helps to suspect the disease is frequent and rhythmic pulsation in the veins of the neck.

It corresponds to the atrial contractions of the myocardium, but exceeds the frequency in the peripheral arteries. There is a noticeable difference between the data obtained during the examination. TO additional methods include the following:

• blood test for biochemistry;
• INR level (international normalized ratio);
• ECG (electrocardiography);
• daily ECG monitoring;
• samples;
• ultrasound examination of the heart (ultrasound);
• transesophageal echocardiography.

To establish a diagnosis, unlike other pathologies, several diagnostic methods from the list above are sufficient. In complex cases, a more detailed examination may be required.

Blood chemistry

The main indicator that is determined during paroxysmal rhythm is the level of lipids in the blood plasma. It is one of the predisposing factors of atherosclerosis. The following data is important:

• creatinine;
• liver enzymes - ALT, AST, LDH, CPK;
• electrolytes in blood plasma - magnesium, sodium and potassium.

They must be taken into account before prescribing treatment to the patient. If necessary, the study is repeated.

INR

For diagnostics this indicator very important. It reflects the state of the blood coagulation system. If there is a need to prescribe Warfarin, it must be done. During the treatment of atrial fibrillation or flutter, the INR level should be regularly monitored.

ECG (electrocardiography)

With atrial fibrillation or flutter, even in the absence of clinical disease, changes are detected on the electrocardiogram film. Instead of P waves, pyloric waves appear in leads I, III and avf. The wave frequency reaches 300 per minute. There are patients who have a permanent form of atrial fibrillation of an atypical nature. In this situation, such teeth on the film will be positive.

The study reveals an irregular rhythm, which is associated with a violation of the conduction of impulses through the atrioventricular node. The opposite situation also occurs when a norm form is observed. The pulse of such people is always within acceptable values.

In some cases, atrioventricular blockades are detected on the electrocardiogram film. There are several options for changes:

• 1st degree;
• 2nd degree (includes 2 more types);
• 3rd degree.

When the conduction of nerve impulses through the pacemaker slows down, the P-R interval lengthens. Such changes are typical for 1st degree blockade. It appears in patients with constant treatment with certain drugs, damage to the myocardial conduction system, or an increase in parasympathetic tone.

Degree 2 violations are divided into 2 types. First, the Mobitz type is characterized by an extended P-R interval. In some cases, impulse transmission to the ventricles does not occur. When examining the electrocardiogram film, prolapse is detected QRS complex.

Type 2 with sudden absence of the QRS complex is common. Extensions P-R interval not detected. With a 3rd degree block, there are no signs of nerve impulses being transmitted to the ventricles. The rhythm slows down to 50 beats per minute.

Daily ECG monitoring

This method for atrial fibrillation or flutter is considered one of the main instrumental ones. With its help, you can trace what changes occur during the work of the myocardium in different situations. During the day, tachysystoles, blockades and other disorders are detected.

The study is based on recording electrical activity during cardiac activity. All data is transferred to a portable device, which processes it into information in the form of a graphical curve. The electrocardiogram is saved on the device media.

For some patients, if there is flickering, an additional cuff is placed on the shoulder area. This allows you to control the level in dynamics blood pressure electronically.

Samples

Test with physical activity(treadmill test) or bicycle ergometry is indicated for the patient to determine disorders of the cardiovascular system. The duration of the study may vary. When unpleasant symptoms appear, it is stopped and the data obtained are evaluated.

Ultrasound examination of the heart (ultrasound)

Signs pathological changes in the heart is detected using ultrasound. The state of blood flow, pressure, valve apparatus, and the presence of blood clots are assessed.

Transesophageal echocardiography

A special sensor is inserted into the esophagus to obtain data. When the patient has a permanent form of atrial fibrillation, atrial flutter, treatment should take about 2 days. For this reason, the main recommendation is to undergo therapy until the normal rhythm is restored. Target instrumental research– detect blood clots and assess the condition of the left atrium.

Treatment of atrial flutter

The treatment of atrial fibrillation in older people and especially the chronic form is of great difficulty. Almost always corrected using medicines atrial flutter. After diagnosis, drug therapy is started.

Drug therapy

Treatment begins with an integrated approach; more than one remedy is included. Conservative therapy includes the following groups of drugs:

• beta blockers;
• cardiac glycosides;
• calcium ion blockers – “Verapamil”;
• potassium preparations;
• anticoagulants - Heparin, Warfarin;
• antiarrhythmic drugs - Ibutilide, Amiodarone.

Together with antiarrhythmic drugs, beta blockers, calcium channel blockers and glycosides are included in the regimen. This is done to prevent tachycardia in the ventricles. It can be triggered by an improvement in the conduction of nerve impulses in the pacemaker.

In the presence of congenital anomalies The listed funds are not used in young and older people. Normally, it is necessary to prescribe anticoagulants and drugs to eliminate arrhythmia. If there are no contraindications to traditional methods treatment, then you can take herbal remedies. Before this, the patient must obtain consent to receive them from his doctor.

First aid

At sudden appearance signs of flutter or fibrillation in combination with hypotension, cerebral ischemia, cardioversion is indicated. It is carried out electric shock slight tension. At the same time, antiarrhythmic drugs are injected into the vein. They increase the effectiveness of therapy.

If there is a risk of complications, then Amiodarone in the form of a solution is required. In the absence of dynamics, cardiac glycosides are needed. When sinus rhythm If all stages of the patient's management scheme are followed, the patient does not recover, electrical stimulation is indicated.

There are separate tactics for managing patients with attacks that last 2 days. When it continues to persist, Amiodarone, Cordarone, Verapamil, and Disopyramide are indicated. To restore sinus rhythm, transesophageal myocardial stimulation is prescribed. When the arrhythmia continues for more than 2 days, anticoagulants are administered before cardioversion.

Surgical treatment

In the absence of effectiveness drug therapy ablation is prescribed. Other indications are frequent relapses and a permanent variant of arrhythmia. The prognosis after treatment is favorable for the patient’s life.

A special approach is needed when identifying Frederick's syndrome. In history, it was first described in 1904. The disease is rare, but poses a great danger. It includes clinical and electrocardiographic changes complete blockade together with cardiac fibrillation (or atrial flutter).

Pathology differs not only in manifestations. Drug treatment does not give a positive answer. The only way out is to install an artificial pacemaker. It will generate a pulse of electricity when necessary.

Atrial and ventricular fibrillation are forms of disturbance of the conduction of excitation waves through the conduction system of the heart, characterized by changes in the rhythm and frequency of heart contractions. These are two fundamentally different diseases that have different clinical manifestations, treatment approaches, as well as prognosis for life and health.

Atrial fibrillation and flutter are characterized by the presence in the conduction system of the heart of pathological closed systems for conducting the excitation wave (re-entry mechanism). Circulating through the myocardium, the impulse causes multiple and asynchronous contractions of cardiomyocytes, which creates the basis for the clinical picture of arrhythmia.

Atrial flutter is characterized by relative preservation of the heart rhythm and more harmonious circles of pathological excitation. With atrial fibrillation (or fibrillation), the impulse moves almost chaotically, causing disorganized myocardial contractions.

Atrial fibrillation on ECG

The electrocardiographic picture of atrial fibrillation is characterized by the following features:

• Absence of P waves in all leads.
• Presence of f-waves of atrial fibrillation.
• Irregularity of heart rate, which is manifested by differences in R-R intervals.

The frequency of f-waves during atrial fibrillation ranges from 350-400 to 600-700.

Often, the ECG reveals other signs of myocardial damage, especially in older people.

Treatment of atrial fibrillation

Treatment for atrial fibrillation depends on the type of arrhythmia. Paroxysm of atrial fibrillation requires drug cardioversion or electrical pulse therapy, depending on the general condition of the patient.

With a permanent form of atrial fibrillation, heart rate control and prevention of thrombus formation are indicated. For this purpose, beta blockers, cardiac glycosides, antiplatelet agents, anticoagulants and other groups of drugs are used.

Ventricular fibrillation and flutter

Ventricular arrhythmias are life-threatening pathological conditions and require emergency medical attention. This is due high probability development of severe hemodynamic disturbances and asystole (cardiac arrest).

Ventricular fibrillation (or ventricular fibrillation) is characterized by frequent asynchronous contractions of cardiomyocytes due to multiple pathological circuits of excitation. IN in this case the heart cannot cope with its pumping function, and if cardioversion is not performed in time, the patient will die.

Ventricular fibrillation on ECG

The electrocardiographic picture of ventricular fibrillation is characterized by the following features:

• Absence of ventricular complexes (QRS).
• The presence of multiple irregular and disorganized waves of excitation through the ventricles.
• Increasing heart rate to 180 beats per minute and above.

The ECG of a patient with ventricular fibrillation, figuratively speaking, presents many chaotic sawtooth and wave-like patterns, the number of which corresponds to the number of leads recorded on the device.

Treatment of ventricular fibrillation

Without emergency cardioversion, a patient with ventricular fibrillation will die, so any person suspected of having this arrhythmia should receive immediate medical attention.

To relieve paroxysm of ventricular fibrillation, both medications and non-drug methods treatment. Electrocardioversion using a defibrillator is most effective. If this is impossible for one reason or another, it is indicated intravenous administration antiarrhythmic drugs. Further therapeutic tactics necessarily include a search for the causes of ventricular fibrillation.

If arising outside sinus node, in the wall of the atrium, with a high frequency, an impulse in the right or wrong rhythm effectively irritates the muscles of the atria, then it can carry out a flickering movement in the right or wrong rhythm or always in the wrong rhythm, a fluttering movement.

The mechanism of atrial fibrillation and flutter is an often disputed and still unclear issue. B. Kish sums up the theories known so far well. Engelmann, B. Kish, Scherf and others believe that the incorrect excitation circulating in the muscles of the atria comes from several centers. Supporters of Rothberger and Vinterberg suggest the existence of single-focal excitation, and in a center that can form impulses at a very high speed. Prinzmetal also subscribes to this view. Unfortunately, this theory in the same way has only evidence in experiments on animals, like Meyer’s views, which became widespread thanks to the teachings of Lewis. The most commonly stated opinion is that the cause of this phenomenon is excitation circulating in the musculature of the atria. According to this theory, the muscles of the atria are effectively excited by an impulse circulating around the opening of the vena cava, when it is carried out in a centrifugal direction. If the impulse is carried out all the time in the same circle, we speak of pure atrial flutter, and if the circular movement is incorrect, we speak of impure atrial flutter. When moving very quickly in a circular motion along the wrong path or multiple paths, atrial flutter occurs. These three phenomena occur independently of each other or interspersed. They sometimes last for a short time, sometimes with interruptions or continuously for years.

IN childhood atrial fibrillation and flutter are quite rare. In our material, out of almost 40,000 ECG recordings made from 16,000 new patients, we recorded this phenomenon in only 11 cases. Of these 11, one was an infant in whom we simultaneously observed supraventricular paroxysmal tachycardia during rhythmic atrial fibrillation. This case confirms the view known from the literature, according to which in infancy and childhood, a very well-functioning atrioventricular conduction system conducts all atrial impulses into the ventricles, and the atrial fibrillation that occurs from time to time manifests itself in the form of supraventricular paroxysmal tachycardia. In 10 children we observed, atrial fibrillation appeared under the same conditions and their course was identical. All patients were over 10 years old. We have been treating them for years for frequently recurring rheumatic fever and carditis. The impulse generation disorder manifests itself in the atrial musculature, which is partly a result of repeated inflammations, partly developed during this time combined mitral disease was overstretched. In our experience, this rhythm disorder in the underlying diseases mentioned is a very poor prognostic symptom. Despite a temporary improvement in their condition, these patients die very quickly.

From a clinical point of view, atrial fibrillation and atrial flutter have many similarities.

Atrial fibrillation. An impulse that occurs in the wrong place and is repeated with a high frequency does not cause normal P waves on the ECG, and with pure flicker we see rhythmic, generally identical waves of high frequency, and with impure flicker we see not quite rhythmic atrial waves of varying shapes. With atrial fibrillation, the frequency of atrial contractions is between 240-350/min.

If the atrial contraction waves in the limb leads are not clearly visible, then the recording should be repeated with thoracic electrodes or with a needle lead. Thoracic electrodes are placed on right side parasternally in the 4th intercostal space, and needle electrodes: one on the right side parasternally in the 2nd, and the other in the 4th intercostal space.

If the impulse circulating in the atrium encounters a good conduction system, then each individual impulse can be conducted effectively to the ventricles, and the ventricles respond to this by the frequency of atrial contractions with an accelerated rhythm. In atrial fibrillation, an anatomically and functionally perfect conduction system in infants would thus lead to supraventricular paroxysmal tachycardia. However, if the conduction system is not able to conduct every impulse and if the ventricles respond only to every second, third or fourth impulse, then in the case correct implementation we have rhythmic activity of the ventricles, imitating atrioventricular block in the ratio of 2: 1, 3: 1, 4: 1, etc. In case of improper conduction, the activity of the ventricles becomes arrhythmic, and in such cases atrial fibrillation is accompanied by complete arrhythmia. In a form that completely imitates atrioventricular block, the activity of the ventricles can be rhythmic. In this case, the independent activity of the ventricles is controlled by other, usually nodal, centers.

The effect of cardiac activity during atrial fibrillation and flutter is determined by the frequency of ventricular activity. On this basis we distinguish between fast and slow types. With the fast type, the heart rate is higher than 90-100/min, and with the slow type, it is lower. Type knowledge has great importance from a treatment point of view.

With an unaffected conduction system on the electrocardiogram, the shape of the ventricular complex is normal, but with anatomical or functional blockade it is deformed. With prolonged ventricular activity of high frequency at first, the correct ventricular complexes may later become deformed.

Atrial flutter. With atrial flutter, the impulse circulating in the atria travels along the wrong path or paths in the wrong rhythm with a very high frequency (over 350/min). As a sign of abnormal atrial activity on the electrocardiogram, atrial waves appear in an irregular rhythm, have an irregular shape, and can often only be recognized in a thoracic lead. The rhythm of ventricular activity is also incorrect, i.e., complete arrhythmia always occurs. If the ventricular rhythm in such cases is correct, this is because with complete atrioventricular block the ventricles usually act in a nodal rhythm (pseudonorrhythm).

Complete arrhythmia accompanying atrial flutter can be of a frequent or rare type, depending on the frequency of ventricular activity. With the rare type, cardiac activity for a long time is accompanied by a good mechanical effect, while with the common type, an imbalance in the blood circulation very soon occurs. In the latter case, individual contractions of the arrhythmic ventricles due to insufficient filling are not accompanied by the proper mechanical effect and often do not cause a pulse wave at all. In other cases, they form such an incomplete pulse wave that the pulse cannot be felt in the peripheral vessels. Auscultation of the heart reveals more frequent cardiac activity than corresponds to the pulse counted in the peripheral vessels (pulse deficit). However, if with improvement of the condition the frequency of ventricular activity decreases, then the gradual or sudden cessation of the pulse deficit indicates the disappearance of ineffective contractions. Thus, one of the signs successful treatment is a decrease or complete disappearance of the pulse deficit.

On the electrocardiogram, along with flutter waves, ventricular complexes are often distorted. The deformity is caused either by a functional blockade of the intraventricular conduction system, or the assessment of the recording is complicated by the merging of the already pathological T wave or ST segment with the flutter waves.

From clinical symptoms subjective ones are also typical. Ventricular arrhythmia, accompanied by atrial fibrillation or flutter, is often perceived by children as a very unpleasant and scary phenomenon. After a long existence, patients get used to abnormal cardiac activity, and in such cases there are no longer any subjective complaints. If normal cardiac activity is restored, patients immediately report that their heart beats as before. Thoracic pulsation is frequent and irregular. In the case of rhythmic activity of the ventricles, heart sounds and murmurs are rhythmic, and the sounds of old defects are clearly audible. The only exception is presystolic murmur with mitral stenosis. By feeling the pulse on the radial artery, we can determine whether the activity of the ventricles is rhythmic or arrhythmic (pay attention to the possibility of pseudonormorhythmia). In the case of complete arrhythmia - by comparing the number of heart contractions and the number of pulse beats on the radial artery - it is necessary to establish the pulse deficit and its degree. When measuring blood pressure it is necessary to listen at separate pressure levels for a long time, because with a pulse deficit due to missing pulse waves it is possible to obtain lower values ​​than corresponds to the true position. At x-ray examination The rhythm of cardiac activity and the unevenness of individual cycles are clearly visible.

The prognosis for this disorder in childhood, as opposed to in adults, is poor. Atrial fibrillation or flutter, which occurs in connection with rheumatic carditis, is a symptom of such a difficult situation that it leads to death in a short time. In such cases, optimism is not justified, even if normal rhythm is restored for a more or less long period.

Treatment of atrial fibrillation and flutter determined partly by the underlying disease, partly by the type of flickering or fluttering. In case of flickering or fluttering of a rare type, heart failure should be treated with strophanthin. The highest dose appropriate for the child's age should be injected twice a day, unless active myocardial inflammation forces the dose to be reduced. In the latter case, you should rather give small doses 2-3 times a day. Otherwise, you should adhere to the principles used in the treatment of carditis. For flickering or fluttering of the frequent type, we try, using large doses of digitalis, to reduce the frequency of ventricular contractions to the most appropriate level from the point of view of mechanical work. The limit to which the heart rate can be reduced is the normal rate corresponding to the patient’s age. At this level, the pulse deficit usually disappears. Treatment is then continued with small doses of digitalis over a long period of time.

Initial high dose: 2 mg/kg weight of foxglove leaf powder. As a total dose, it should be divided into parts and given for three days. After the pulse deficit has decreased or disappeared, 1/3 of the daily dose calculated in this way should be given, if necessary, for many weeks. For example, a child weighing 30 kg receives 60 mg of digitalis leaf powder over 3 days or a dose of crystalline glucoside corresponding to this amount, i.e., 20 mg per day for three days. If the appropriate result is achieved, treatment continues with doses of 5-8 mg.

Only after restoring the balance of blood circulation can you try to stop increased excitability atrial muscles with quinidine. Such treatment poses some danger, because in severe decompensation, blood clots that form in the dilated and improperly contracting atrial muscles can, with a sudden normalization of atrial activity, break away from their bases and cause distant embolisms.

Before starting treatment with quinidine, a sensitivity test must be performed, and if increased sensitivity is not detected, then only then can therapy begin. The evening before the start of the course of treatment, the child should be given 10-15 mg, depending on his age, and if vomiting, diarrhea, symptoms hypersensitivity do not appear, then you can start treatment with full doses. The first daily dose is 30-60 mg, depending on age, distributed at regular intervals throughout the day. In subsequent days, the dose is increased by 10-20 mg per day until the effect occurs. If the heart rate returns to normal, then quinidine is given for a few more days. Quinidine should never be used under non-stationary conditions for more than 6 days.

In case of possible phenomena from the brain, injections of camphor substitutes are made: tetracor, cardiazol, corediol and, possibly, adrenaline (1% solution of 0.2-0.3 ml intramuscularly). For syncope, if the patient has not received digitalis immediately before, a small (0.15 mg) dose of strophanthin in a glucose solution is given intravenously.

Atrial fibrillation: More than 400 pulses per minute occur.

Etiology. 1. Possibly associated with the circular movement of excitation. 2. Due to the occurrence of a large number of foci of excitation. 3. There is continuous excitation of the atria ( various groups muscle fibers).

The atria practically do not contract, but impulses are born and some of them pass through the atrioventricular node (part of the impulses reaches the ventricles, according to the limited capacity of the atrioventricular node). Impulses to the ventricles arrive randomly, the rhythm of the ventricles is completely incorrect. Hence the name - "delirium cordis". Nowadays the term “atrial fibrillation”, proposed by G.F. Lang, is also used.

There are two forms of atrial fibrillation: 1. Tachysystolic form (more than 90 per minute), 2. Bradysystolic form (less than 60 per minute).

The norosystolic form occupies an intermediate position. Patients with atrial fibrillation have various manifestations heart failure.

Clinic. The pulse is arrhythmic with waves of different filling, the presence of a pulse deficit (the heart works “idle”), different intervals and different volumes of heart sounds during auscultation.

ECG signs: no P wave before the ventricular complex (no complete excitation of the atria); different R-R intervals; the presence of P-like oscillations (small waves and uneven contours).

Atrial flutter:

Associated with a violation of the functional homogeneity of the atria. there is a continuous movement of impulses along vicious circle. 240-450 impulses are born, but the throughput of the atrioventricular node is lower, so the ventricles are excited much less frequently than the atria. There are two forms: 1. With the correct ventricular rhythm. 2. With irregular ventricular rhythm. It happens more often and clinically resembles atrial fibrillation. The final diagnosis is possible only by ECG: a large number of P waves, they are arranged in a saw-shaped palisade or between them - deformed or non-deformed QRS complexes; F waves are especially well represented in standard III and right chest leads.

Like atrial fibrillation, it can occur in tachy-, normo- and bradysystolic forms. The most common form is the tachysystolic form, which occasionally spontaneously transforms into the normo- and bradysystolic forms.

Treatment of atrial fibrillation and flutter:

The goal of therapy is to establish the correct rhythm.

QUINIDINE. Effective in 60% of cases with the correct treatment tactics. Start with 0.2-0.4 and gradually increase the dose to 2.4 -3.0 grams per day. NOVOCAINAMIDE 0.25 3 times a day. Electropulse therapy is effective in 80-90% of cases.

It is advisable to transform the tachysystolic form into a more prognostically favorable bradysystolic form.

Preparation for electropulse therapy: 1. Minimize the manifestations of heart failure. In this case, it is necessary to use drugs that are quickly eliminated from the body and do not accumulate.

2. With arrhythmias, due to unequal contraction of the atria, their dilatation occurs and the formation of blood clots is possible, which, with improved blood flow, can break off and lead to thromboembolic complications. For the purpose of prevention, introduce indirect anticoagulants within 2 weeks.

3. It is necessary to correct the concentration of potassium in the body; a polarizing mixture is introduced within 2 weeks.

4. 1-2 days before EIT is given antiarrhythmic drugs that will be used for treatment in the future (quinidine no more than 1 gram, beta blockers no more than 40 mg). If the patient is over 70 years old, then with the normo- and bradysystolic form of atrial fibrillation it is not necessary to achieve restoration of sinus rhythm.

Complications of electropulse therapy: Acute heart failure, which can occur after EIT; Thromboembolic complications; Sinus rhythm may disappear.

At the time of shock application, it is necessary to clamp the carotid arteries to reduce the risk of thromboembolic complications.

Addition to 22

TREATMENT OF BLOCKES:

A. If a blockade is detected, especially in an elderly person, hospitalization is required, especially with Morgagni-Edams-Stokes syndrome and its equivalents.

B. It is important to establish both the nature of the blockade and the nature of the underlying pathological process.

In case of acute nature of the disorder.

1. Administer drugs that reduce vagal influences (anticholinergics): ATROPINE 0.1% 1.0 intravenously; PLATIFILLINE 0.2% 1.0 subcutaneously or if intravenously, then per 500 ml of 5% glucose;

2. Strengthen the sympathetic effect on the conduction system: NORADRENALINE 0.2% 1.0 intravenously on glucose; EPHEDRINE 5% 1.0 intramuscular, subcutaneous, intravenous; ALUPENT 0.05% 0.5-1.0 intramuscularly or intravenously; IZADRIN 0.1% 1.0

3. Glucocorticoids: HYDROCORTISONE 200 mg per day. Relieves inflammation and swelling. Reduces the potassium content in the area where the impulse is carried out along the damaged area. Potentiates sympathetic reactions. It is reintroduced after a few hours.

4. Reduce potassium levels: LASIX 1% 2.0 intravenously.

5. If the above measures are ineffective or there is a complete block or Mobitz II in combination with a block of the left Hiss bundle branch, then it is necessary to introduce a temporary pacemaker (using a catheter probe, an electrode is inserted into the right ventricle). If a patient has an anterior myocardial infarction, an anterior block may develop - this is also an indication for transferring the patient to cardiac stimulation. If the course of the disease is complicated by Morgagni-Adams-Stokes syndrome, then immediate medical attention is needed - apply several punches to the sternum with your fist (mechanical start of the heart), indirect massage heart (60 beats per minute) with artificial respiration(14 times per 1 minute). It is advisable to connect an ECG machine to determine the nature of the cardiac dysfunction. If on ECG fibrillation ventricles - defibrillation is necessary. If it is ineffective, intracardiac adrenaline or norepinephrine and repeated electric shock (sometimes up to 10 or more shocks are necessary).

In case of chronic blockade, treatment of the underlying disease is important. Thus, in case of intoxication with drugs, their abolition is necessary; in case of inflammatory diseases, special treatment is also necessary.

1. Anticholinergics, most often in tablets and powders: PLATIFILLINE 0.005 3 times a day, 0.2% 1.0 ml; DRY BELLADONNA EXTRACT, powders 0.02 3 times a day.

2. Sympathomimetics: EPHEDRINE 0.025 3 times a day; ALUPENT 0.05% 1.0 intramuscular; IZADRIN 0.005 sublingually.

3. Saluretics: HYPOTHIAZIDE, tablets of 0.025 and 0.1, apply according to the scheme. Reduces potassium content and thereby improves conductivity.

4. Glucocorticoids in the event that there is an inflammatory process (myocarditis), but if the main pathological process is chronic ischemic heart disease, there is no need to prescribe.

5. Electrical stimulation - an artificial heterotopic pacemaker is created. Indications for electrical stimulation: All blockades occurring with Morgagni-Adams-Stokes syndrome; Circulatory failure, heart failure due to blockade; Heart rate less than 40 per minute; Severe sick sinus syndrome (severe paroxysms, not just bradycardia).

There are different types of stimulation - external, internal, permanent, temporary, etc.

Two types of stimulators: 1. Rase-Make - a permanent pacemaker that works independently of the heart’s own rhythm.

2. Decampier - physiologically more beneficial, since it gives impulses only if the R-R interval becomes greater than the given specific time interval.