home Audience 5 SSSU on ecg. Pacemaker. Symptoms will not leave the disease unnoticed

SSSU on ecg. Pacemaker. Symptoms will not leave the disease unnoticed

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Treatment Goals

Prevention of SCD due to bradyarrhythmia, elimination or alleviation of the clinical manifestations of the disease, as well as prevention of possible complications (thromboembolism, heart and coronary insufficiency).

Indications for hospitalization

Severe symptoms of the disease. So, in the case of fainting, frequent pre-syncope conditions, emergency hospitalization is indicated.
Planned pacemaker implantation.
The need to select antiarrhythmic therapy for bradycardia-tachycardia syndrome.

Non-drug treatment

Non-drug treatment of patients with coronary artery disease, hypertension, heart failure includes standard dietary recommendations, as well as psychotherapeutic intervention. In addition, drugs (if possible) that may have caused or exacerbated SSSS should be discontinued (eg, beta-blockers, calcium channel blockers, class I and III antiarrhythmics, digoxin).

Medical treatment

The options for medical treatment of SSS are limited. Therapy of the underlying disease that caused the development of SSSU (etiotropic treatment) is carried out according to the general rules. In emergency cases (severe sinus bradycardia, which worsens hemodynamics), 0.5-1 ml of a 0.1% solution of atropine is injected intravenously. If symptoms persist, a temporary pacemaker is established. In the event of an attack of Morgagni-Adams-Stokes, resuscitation is necessary.

With severe symptoms, to increase heart rate, Belloid can be prescribed (1 tablet 4-5 times a day), prolonged forms of theophylline (75-150 mg 2-3 times a day). However, when using these drugs, it is necessary to remember the danger of provoking heterotopic arrhythmias. Therapy of concomitant tachyarrhythmias should be carried out with great caution. Almost all modern antiarrhythmic drugs have an inhibitory effect on the function of the sinus node. This property is somewhat less pronounced in allapinin, a trial appointment of which in small doses (12.5 mg 3-4 times a day) is possible.

In patients with vagotonic dysfunction of the sinus node, in contrast to SSS caused by organic causes, conservative therapy is of primary importance. Treatment of vegetative dystonia is carried out according to general principles, including measures aimed at limiting parasympathetic effects on the heart (they do not recommend wearing clothes that squeeze the neck, they treat concomitant pathologies of the gastrointestinal tract), dosed physical activity, and rational psychotherapy. A positive effect in such patients gives clonazepam at a dose of 0.5-1 mg at night with a possible subsequent increase in dose to 1.5-2 mg in 2-3 doses. The drug allows you to correct psychovegetative disorders leading to the formation of vagotonic dysfunction of the sinus node, which is manifested by the elimination of not only fainting, weakness, dizziness, but also a decrease in the severity of bradycardia and other ECG signs. In patients with sleep apnea syndrome, with adequate treatment of this disease (CPAP therapy, surgical treatment), the disappearance or decrease in the manifestations of sinus node dysfunction is observed.

Surgery

The main method of treating organic SSSU is the implantation of a permanent pacemaker.

Indications for pacemaker implantation in SSSU are divided into classes.

Sinus node dysfunction with documented bradycardia or pauses accompanied by symptoms, including as a result of therapy that cannot be canceled or replaced.
Clinically manifest chronotropic incompetence.

Class IIa.

Sinus node dysfunction with heart rate less than 40 per minute and clinical symptoms in the absence of documentary evidence that the symptoms are due to bradycardia.
Syncope for unknown reasons, in combination with violations of the function of the sinus node identified during an electrophysiological study.

Class IIb.

Minimal symptomatology with a heart rate in the waking state of less than 40 per minute.

In patients with SSSU, it is preferable to use the pacemaker in AAI or (with concomitant AV conduction disorders) DDD, and in cases of symptomatic chronotropic insufficiency - AAIR or DDDR.

Approximate periods of incapacity for work

Approximate terms of disability are determined by the severity of the underlying disease. As a rule, in the absence of complications, the terms of hospitalization for pacemaker implantation rarely exceed 10-15 days. Patients cannot work in professions that threaten the safety of others.

Further management

Further management of patients with SSSU includes:

control of the ECS system, selection of stimulation parameters, determination of the time for replacing the ECS, carried out in specialized arrhythmological centers;
treatment of the underlying disease;
treatment of concomitant tachyarrhythmias.

Information for the patient

The patient is recommended to regularly undergo preventive control of the EKS system. If new symptoms occur or recurrence of previous symptoms (fainting, dizziness, shortness of breath on exertion), you should immediately consult a doctor.

Patients with SSS who have not been implanted with a pacemaker are prohibited from taking any antiarrhythmic drugs (especially β-blockers, verapamil, cardiac glycosides) without prior consultation with a cardiologist.

Daily monitoring of heart rate is necessary, and if aggravation of bradycardia is detected, immediate medical attention should be sought. Periodic ECG registration is shown (the frequency is determined by the attending physician), and, if necessary, Holter ECG monitoring.

Forecast

With timely implantation of the pacemaker, the prognosis for life and recovery is regarded as favorable. In 19-27% of patients with SSSU, a permanent form of AF is established within 2-8 years, which can be equated to self-healing from SSSU.

Tsaregorodtsev D.A.

The sinoatrial node is the main regulator of the heart rate. It is a collection of atypical heart cells that are automatic and capable of spreading impulses. The loss of the control function of the node leads to a violation of the heart rhythm.

Reasons for the formation of sinus node weakness

The sinoatrial node, located in the wall of the right atrium near the superior vena cava, is an accumulation of cells capable of spontaneous depolarization - the activation of electrical excitation. This means that under the influence of an impulse of the nervous system, these cardiomyocytes begin to transmit a signal of contraction along the muscle fibers. Repolarization is the return of the heart cell to its resting state.

On the electrocardiogram, depolarization is indicated by the P wave, and ventricular depolarization is indicated by the QRS complex. Repolarization of the ventricles responds to the ST-T complex.

The sinoatrial node (SA) is innervated by parasympathetic and sympathetic nerve fibers:

The parasympathetic system through the vagus nerve reduces the activity of the node, slows down the heartbeat.
Sympathetic - through the stellate ganglion causes an increase in rhythm (tachycardia), acts similarly to the release of catecholamines by the adrenal glands during exercise and stress.

Hyperactivity of parasympathetic stimulation leads to bradycardia, sinus node pauses, blockades. The automatism decreases, the heartbeat slows down. Sympathetic - increases spontaneous depolarization, increases SA automatism, accelerates the heartbeat. The cells are fed by the right coronary artery.

The epidemiology of sick sinus syndrome (SSS) is difficult to account for. Dysfunction manifests itself in patients 60–70 years of age and older. Occurs as a result of violations of automatism or conduction. Fibrosis of the sinus node cells is the most common cause of weakness.

The right vagus nerve innervates the sinoatrial node, its hyperactivity leads to bradycardia.
The left vagus nerve innervates the atrioventricular node, its stimulation leads to AV blockade.
The heart rate is affected by the work of internal organs that have similar innervation with the vagus nerve. Irritation of the pulmonary branches leads to a slowing of the heart rate, as does irritation in the larynx. Bradycardia syndrome can be caused by diseases of hollow organs (glomerulonephritis, hiatal hernia, obstructive jaundice) or develop as a complication of gallbladder removal surgery.
The main reasons for the activation of vagotonic reflexes are dysfunctions of the first vertebra, and the provocateur of the suppression of the parasympathetic system is a spasm of the muscles of the cervical region and the thoracic diaphragm.
Sick sinus syndrome develops against the background of fibrosis of the cells of the sinoatrial node.

Diseases and conditions that cause scarring or damage to the electrical system of the heart cause dysfunction. Scar tissue after surgery causes SSS in children, less often there is a genetic cause of the pathology. Dysfunction is provoked by calcium channel blockers or beta-blockers - drugs that are used for hypertension. In most cases, SA function is impaired due to age-related wear of the heart muscle and poor blood supply. In adolescence, the anomaly develops against the background of neurovegetative disorders due to active growth. This leads to a decrease in electrolyte imbalance, a change in the resting membrane potential and cell excitability.

Against the background of myocarditis, cardiomyodystrophy, a dangerous tachy-brady syndrome develops, when tachycardia suppresses sinus rhythm. Increased risk of systemic embolism.

Classification and symptoms

SSSU is an abnormal formation and distribution of sinus rhythm, which is often accompanied by similar abnormalities in the atria and in the conduction system of the heart. The rate of ventricular contractions decreases and long pauses occur at rest and during stress. In a mild form, sinus node weakness occurs without symptoms. With a more pronounced course, patients develop an irregular heartbeat and the blood supply to the organs is disturbed. The most common symptoms of sinus node weakness are:

Sinus node weakness is manifested by exacerbations that alternate with periods of normal myocardial function. The disease progresses, increasing the likelihood of developing atrial tachyarrhythmia. The course of the disease is difficult to predict, and treatment is often symptomatic. The arrhythmia syndrome develops due to the replacement of the sinus rhythm with an A-B rhythm. Conduction disturbance is associated with a progressive pathological process affecting the atria and other parts of the heart.

The classification of SA includes several manifestations:

Sinoatrial block is diagnosed when electrical impulses travel too slowly from the sinus node to other pacemakers, which slows the heart.
Stopping the sinus node is expressed in the appearance of missed heart beats.
Bradycardia-tachycardia syndrome is an alternation of sessions of abnormally fast and slow rhythms with long pauses (asystole) between beats. A synonym is Short's syndrome.
Sinus bradycardia is a slow heartbeat below 50 beats per minute.

Arrhythmic syndrome is a complication of the disorder, when atrial fibrillation completely replaces the slow rhythm.

Diagnostics

Dizziness, shortness of breath and fainting are symptoms of many diseases. But with sick sinus syndrome, they are observed against the background of an abnormal heartbeat.

When diagnosing pathology, the doctor conducts a physical examination and collects a medical history. As a rule, all the patient's complaints are reduced to a violation of the heart rhythm.

A number of tests are used to make a diagnosis:

The electrocardiogram shows patterns that are characteristic of the syndrome, such as a high heart rate, slow pulse, or long pauses in the heartbeat after an accelerated heart rate - asystole.
Holter monitoring involves carrying a portable device in your pocket that records heart activity for 24-72 hours for a deeper study of pathological factors.

Sick sinus syndrome on the ECG is manifested by signs:

atrial bradyarrhythmia;
atrial tachyarrhythmia;
tachyarrhythmias and bradyarrhythmias in the complex;
sinus bradycardia;
stop sinus node;
atrial fibrillation.

The severity of SSS in fibrillation is manifested by a slow rate of ventricular contraction without the introduction of drugs such as propranolol or foxglove.

Functional sinus bradycardia, increased vagal activity, gastrointestinal and neurological disorders, and other causes can provoke signs that resemble SA weakness syndrome. Dysfunction may occur in the postoperative period due to an increase in vagal tone during anesthesia and surgery.

The diagnostic test used - performing the Valsalva maneuver (inhalation followed by exhalation through pursed lips) - leads to an increase in heart rate. With weakness of the sinus node, such a reaction is not observed.

Sometimes a transesophageal electrophysiological study is performed if the ECG does not confirm the diagnosis. Two criteria are defined:

sinus node function recovery time - the interval between the last stimulus and the sinus P wave (the norm is 1,500–1,600 ms);
corrected sinus node recovery time - the difference between the positive period of sinus node function recovery and the spontaneous cardiac cycle during stimulation (normal - 525-600 ms).

These criteria are important for diagnosing asymptomatic disorders.

The development of SSSU in childhood is associated with myocardial inflammation or congenital heart disease. In 20% of cases in children from 3 to 20 years old, the pathology proceeds without symptoms, therefore it requires careful diagnosis. Dizziness, heart pain, headaches, and fainting are signs of impaired pacemaker function. The child's heart function is tested with an exercise stress test or atropine to differentiate sinus node weakness.

In adolescents, VSD is complicated by CVD associated with neurovegetative disorders and metabolic dysfunctions of cardiomyocytes. Main complaints: lack of air, weakness, unstable blood pressure. The syndrome becomes the basis for the issuance of a military ID in the "B" category of validity - it is limitedly suitable for the army.

Treatment of the syndrome

The only therapeutic approach is the correction of external causes. According to medical indications, a pacemaker is implanted.

Treatment of asymptomatic dysfunction is not required, even if an abnormal sinus node recovery time is present. If the patient is taking drugs that can provoke sinus bradyarrhythmias (beta-blockers, ACE inhibitors), they should be discontinued.

Urgent Care

Therapy includes intravenous atropine (0.04 mg per kg of body weight every 2-4 hours) in combination with isoproterenol (0.05-0.5 micrograms per kg per minute intravenously). Transvenous pacemakers are sometimes used if medical support fails.

Emergency care for loss of consciousness of three minutes or more includes chest compressions.

Conservative methods of therapy

People diagnosed with sinus syndrome and tachycardia do not benefit from drugs that slow the heart rate. There is a risk of sinoatrial blockade. After its occurrence, the question of the implantation of a pacemaker is raised.

With a mild form of dysfunction that occurs without symptoms, the patient is recommended to visit a cardiologist regularly in order to prevent complications in time. The only way to stop the progression of sinus node weakness is to treat the causes of its development. For prevention, you can visit an osteopath that eliminates the influence of the autonomic system.

If there are complaints, two options for conservative therapy are chosen:

Prescribing drugs. To begin with, the cardiologist will review the list of medications taken for a side effect in the form of tachyarrhythmia or bradycardia.
For tachycardia, drugs that slow the heartbeat are used - beta-blockers or calcium channel blockers. If tachycardia attacks are combined with bradycardia, the selection of drugs occurs under the supervision of Holter monitoring.

Additionally, anticoagulants are prescribed for the prevention of thrombosis in patients with atrial fibrillation - "Warfarin" or "Aspirin Cardio".

With bradyarrhythmia-achyarrhythmia, the heartbeat is controlled with Digoxin, Propranolol or Quinidine. With the help of a Holter, the effectiveness of therapy is monitored, preventing the development of congestive heart failure. Dizziness indicates drug intolerance. With frequent exacerbation of symptoms, a decision is made to install a pacemaker.

Folk remedies for the treatment of a serious disease are not provided. At home, you can take mint, lemon balm or valerian.

Surgery

A pacemaker is a small device implanted under the left pectoral muscle under the collarbone. It is positioned so that the electrode coming from the device is guided through the subclavian vein into the chambers of the heart. If electrical signals travel slowly through the sinus node, the pacemaker sends an electrical impulse to restore and maintain a normal heart rhythm. There are one-, two- and three-chamber pacemakers. The last cardioverters are considered the most physiological in terms of imitation of the function of the pacemaker.

It is known that our heart has rhythms, the violation of which significantly affects the entire cardiovascular system. These failures have different causes. For example, if the rhythm disturbance is caused by the cessation or weakening of the automatism function of the atriosinus node, sick sinus node syndrome (SSS) develops. This means that the impulse is not conducted into the atrium from the sinus node as it should. This manifests itself in the form of bradycardia, that is, a decrease in the heart rate, which is accompanied by ectopic arrhythmias. Patients who develop this syndrome may experience sudden cardiac arrest.

The sinus node itself consists of a complex of pacemaker cells, the main function of which is the function of automatism. To implement it, you need good sinoauricular conduction, that is, so that the impulses that are produced in the sinus node pass to the atria. The sinus node must function under different conditions, therefore, in order to always have a good heart rate, it is necessary to use different mechanisms, which includes both a change in the ratio of parasympathetic and sympathetic influences, and a change in the source of automatism, as well as other mechanisms.

Under certain pathological and physiological conditions, groups of cells become pacemakers that perform the function of a backup pacemaker, which has a less pronounced ability for automatism. This may lead to a slight change in the shape of the P teeth. Such conditions may be electrolyte volume disturbances, vagus nerve stimulation, and so on.

adductor system of the heart

In order for sinus node dysfunction to occur, a very low speed with which impulses propagate through the cells is also needed. Any, even a small deterioration in conductivity, which is due to organic damage to the myocardium or dysfunction of the nervous autonomic system, can lead to intranodal blockade of impulses. Phenomena such as necrosis, ischemia, and so on lead to the fact that the cells of the sinus node are replaced by connective tissue.

Causes

I would like to discuss in more detail the causes that lead to SSS, as well as the classification of this syndrome. There are two main groups of factors that can lead to sinus node dysfunction.

Conditions and diseases that cause changes in the structure of cells or changes in the contractile atrial myocardium surrounding the node. These defeats can be called internal theological factors. These lesions can be classified into several forms. For example, idiopathic infiltrative and degenerative diseases. The most common organic cause of the syndrome is sclerodegenerative isolated fibrosis of the sinus node. With age, the surrounding SA node of the myocardium is replaced by fibrous tissue. As fibrosis progresses, automatism decreases, as does sinoarterial conduction. It is possible that in some patients this condition is determined genetically.

IHD can also cause node weakness, and the cause can be both chronic ischemic heart disease, as well as acute myocardial infarction. Node dysfunction in this disease develops in an acute form with thrombosis, which affects the arteries that feed this node. In this regard, acute myocardial infarction, which has a lateral or lower localization, may be complicated by the cessation of node activity or severe bradycardia. Typically, these arrhythmias are temporary.

Cardiomyopathy is also a cause of SSSU. And this applies to different forms. For example, inflammatory nonspecific cardiomyopathies occur. The risk of developing SSS is especially high when cardiomyopathies are combined with pericarditis. Often, conduction disturbances disappear. It is also worth mentioning infiltrating cardiomyopathies. They develop with tumor diseases, hemochromatosis and amyloidosis. Other cardiomyopathies may also be the cause.

SSS can also develop due to arterial hypertension, hypothyroidism, surgical trauma, and disorders of the musculoskeletal system.

The second group is external factors that lead to dysfunction of the node when there are no morphological changes. Here, too, two groups can be distinguished. The first group is drugs that reduce the function of the node. These include beta-blockers excluding diltiazem and verapamil, cardiac glycosides, class 1C and 1A antiarrhythmic membrane-active drugs, and drugs that do not often reduce function, such as phenytoin, cimetidine, and so on.

The second group is autonomic dysfunction of the sinus node. It is associated with too strong activation of the vagus nerve, due to which the sinus rhythm becomes less frequent, and the refractory period of the node lengthens. Vagus nerve tone can increase physiologically, that is, with urination, coughing, defecation, swallowing, Valsalva maneuver, vomiting, nausea, and during sleep. An increase in tone can also be pathological. We are talking about diseases of the digestive tract, pharynx, genitourinary system and so on. Typically, this group of external factors occurs at a young age and is combined with significant neuroticism and mesenchial dysplasia syndrome. Sinus bradycardia of a persistent nature can be observed in trained athletes due to the fact that vagal tone strongly predominates. This phenomenon is not a sign of SSSU.

Symptoms

Sick sinus syndrome can express itself in a variety of ways. In some patients, the clinical course may not be expressed for a long time. Other people may experience obvious heart rhythm disturbances, which is accompanied by dizziness, headache, and Morgagni-Adams-Stokes attacks. Hemodynamics may be impaired due to a decrease in cardiac output and stroke volume. Cardiac asthma, coronary insufficiency and pulmonary edema may also develop.

In relation to the clinic, two groups of symptoms can be distinguished.

cerebral symptoms. If the rhythm is not strongly disturbed, irritability, fatigue, forgetfulness and emotional lability are observed. Elderly patients complain of a decrease in memory and intelligence. If the syndrome progresses and circulatory failure in the brain increases, the symptoms also begin to increase. There are fainting and conditions that precede them, that is, tinnitus, a feeling of sinking heart, severe weakness. The skin becomes pale, cold and sweaty. Arterial pressure drops sharply. Fainting can occur due to a sharp turn of the head, coughing, or a tight collar. Fainting usually resolves on its own, but if it persists, help is needed.

Explicit bradycardia can lead to dyscirculatory encephalopathy, which is characterized by more severe dizziness, instant memory lapses, irritability, insomnia, paresis, memory loss and swallowing of words.

cardiac symptoms. The patient begins to feel an irregular or slow pulse and retrosternal pain. This is joined by interruptions in cardiac work, weakness, shortness of breath, palpitations, the development of chronic heart failure. Progressing, cider begins to manifest itself more clearly, fibrillation or ventricular tachycardia begins to develop, which increase the likelihood of sudden death.

SSSU may present with other signs, such as oliguria, gastrointestinal disturbances, muscle weakness, and intermittent claudication. Sinus bradycardia manifests itself, which is especially noticeable at night, it persists even with physical exertion.

Features of the clinical manifestation allow us to divide the syndrome into some forms.

latent form. At the same time, there are no clinical manifestations, as well as manifestations on the ECG. Node dysfunction can be detected by electrophysiological examination. Employability for this period is not limited.
compensated form. She has two options. The bradysystolic variant has weak manifestations. There is weakness and dizziness. Employability may be limited on the professional side. The bradytachysystolic variant is complemented by paroxysmal arrhythmias.
decompensated form. There are the same two options. The bradysystolic variant is determined by persistent severe sinus bradycardia. At the same time, cerebral blood flow is disturbed, which manifests itself in dizziness, fainting and transient paresis. Heart failure also develops, which is caused by bradyarrhythmia. The bradytachysystolic variant is complemented by atrial flutter, fibrillation, and supraventricular tachycardia. In this case, the patient is unable to work.
Bradysystolic form of atrial fibrillation of a permanent nature. The development of this form is preceded by one of the above.

Diagnostics

First resort to non-invasive methods. If with their help it was not possible to confirm the diagnosis, but the suspicion of SSS remains, EFI is used. So, generally speaking, there are several diagnostic methods.

ECG. First, this study is carried out in twelve leads. If necessary, Holter monitoring is carried out, which lasts a day or two days. The patient should keep a diary that allows him to evaluate his complaints and changes on the ECG. To register rare events, loop recorders are used, which are recorded over several weeks and carried out on a closed tape. Recorders can also be used, which the patient turns on himself if complaints appear.

Study of the nervous autonomic system. This method is based on several methods. The first of these is carotid sinus massage. In this case, carotid sinus syndrome can be distinguished from SSSU. In the first case, asystole occurs for more than three seconds, and the pressure decreases by more than fifty millimeters. The essence of the massage is in dense pressure, which is carried out on one side of the carotid sinus for five seconds. If everything is normal, massage does not stop the sinus node, but it can slow down its rate and impair AV conduction.

The next method is a test on an orthostatic table. This is how vasovagal syncope can be diagnosed. If such a test provokes bradycardia, most likely this is due to disorders of the autonomic system, and the syndrome of weakness of the sinus node has nothing to do with it.

In order to accurately distinguish autonomic disorders from SSS, pharmacological tests are carried out. The bottom line is the introduction of atropine and propranolol, which can achieve complete pharmacological cardiac denervation. Using a special formula, the normal value of the patient's rhythm rate is calculated. If the actual frequency is lower than the calculated frequency, then SSAS may be present.

EFI. The function of the sinus node is usually evaluated by indirect indicators. Direct measurement of node activity is difficult to do. One metric is node recovery time. During this time, the activity of the node resumes after an atrial rapid pacemaker, which suppressed its function. Pathology is considered to be time exceeding 1400 ms. From the recovery time, you need to subtract the length of the RR interval before the pacemaker, which will allow you to get a corrected node recovery time. If the value is greater than 550 ms, then SSS is occurring.

Another indicator is the time of sinoarterial conduction. At the beginning, the atrial frequency is determined, after which extrastimuli are given. Then you need to determine the interval between the extrastimulus and the atrial spontaneous impulse that follows it.

Treatment

Treatment of sinus node weakness syndrome includes various measures, the volume of which depends on how conduction is disturbed, how acute the rhythm disturbance is, and so on. If SSSU manifests very little or does not appear at all, treatment is directed to the underlying disease. It is important to be seen by a cardiologist.

Treatment with drugs is carried out when the manifestations of brady- and tachyarrhythmias are moderate. Although it must be admitted that such treatment is not very effective.

Still, the main method of treating SSSU is continuous pacing. If the clinic begins to be pronounced, the VVFSU lengthens to five seconds and signs of chronic heart failure appear, a pacemaker is implanted, which generates impulses when the heart rate drops to critical levels.

Consequences

The course of the disease is usually progressive. Therefore, if there is no appropriate treatment, the symptoms will worsen. If there are organic heart diseases, the prognosis is even more unfavorable.

The combination of atrial tachyarrhythmias and sinus bradycardia is considered especially unfavorable. If there is a combination with sinus nodes, the situation is better. A more satisfactory prognosis is observed when there is isolated sinus bradycardia.

The main preventive measures are aimed at detecting the development of the disease in time and conducting appropriate treatment. Of course, it is best to lead a healthy lifestyle to minimize the risk of such heart problems.

ECG sick sinus syndrome has symptoms similar to those of or heart block against the background of which attacks of various arrhythmias develop. When making a diagnosis, they often write not the full name of the syndrome, but abbreviated - SSSU.

The syndrome, as usual, means a set of symptoms in which the sinus node is not able to adequately perform the functions of a pacemaker (pacemaker), up to their partial or complete loss.

As a result, arrhythmias develop. To get out of this situation, it is provided until the sinus node is fully restored to working capacity as the main source of automatism of the heart, that is, until the heart block is eliminated.

The force that causes the myocardium of the heart (heart muscle) to contract arises according to the principle of automation and is formed in the form of electrical impulses. These impulses are generated by special cells - atypical cardiomyocytes, which form several different clusters in the heart walls.

For reference. The leading and most important accumulation of cardiomyocytes is localized in the region of the right atrium and is called ““. In a healthy person, the impulses sent from this formation cause the heart muscle to contract and form a regular, or sinus, heart rhythm.

The sinoatrial node causes the muscle fibers of the heart to contract 60-80 times per minute.

The generation of impulses of the sinus node is tightly interconnected with the functioning of the autonomic nervous system. Its departments - sympathetic and parasympathetic - control the activity of internal organs.

In particular, the vagus nerve affects the heart's pulsation and its strength, slowing it down. Sympathy, on the contrary, causes an acceleration of the heart pulsation. In view of this, any deviations in the number of heart beats from normal values (tachycardia or bradycardia) can appear in patients with neurocirculatory dysfunction or with impaired functioning of the autonomic system. In the latter case, autonomic dysfunction of the sinus node (VDS) occurs.

Attention. At the moment when the myocardium of the heart is damaged, a disease is formed called sick sinus syndrome. It consists in reducing the number of heart beats, which negatively affects the oxygen supply of the brain and internal organs.

This disease can occur in people of all ages, but most often it affects elderly patients.

Causes of sinus node weakness

Causes of sinus node weakness in pediatric patients:

Amyloid degeneration with myocardial destruction - accumulation of amyloid glycoprotein in the muscle fibers of the heart;
Autoimmune destruction of the muscular membrane of the heart as a consequence of Liebman-Sachs disease, rheumatic fever, systemic scleroderma;
Inflammation of the heart muscle after a viral illness;
The toxic effect of a number of substances - drugs against arrhythmia, organophosphorus compounds, calcium channel blockers - in this situation, immediately after a person stops taking these drugs and detoxification treatment is carried out, all symptoms disappear.

For reference. These causes can similarly cause disease in the adult population.

In addition to them, there are other factors that provoke the formation of sick sinus syndrome in adult patients:

- becomes a factor in the failure of blood circulation in the area of localization of the sinus node;
Postponed heart attacks of the muscular membrane of the heart - scar formation near the pacemaker;
Hypofunction or hyperfunction of the thyroid gland;
Cancer tumors in the tissues of the heart;
Scleroderma, Limban-Sachs disease;
Sarcoidosis;
The accumulation of calcium salts or the replacement of sinus node cardiomyocytes with connective tissue cells is most often characteristic of elderly people;
Diabetes;
Cardiac injuries suffered on the organ of surgical intervention;
Prolonged hypertension;
The late period of the course of syphilis;
Deposition of potassium salts;
Overactivity of the vagus nerve;
Insufficient blood supply to the sinus node from the right coronary cardiac artery.

Symptoms of the disease

Symptoms in sick sinus syndrome vary and are directly dependent on the clinical course of the disease. Medics
there are several types:

Latent;
Compensated;
decompensated;
Bradisystolic, accompanied by atrial failure of the heart rhythm.

The latent type is characterized by the absence of manifestations and the normal result of electrocardiographic diagnosis. Sinus node weakness syndrome is detected after an electrophysiological study.

For reference. Patients with this type of disease do not feel a decrease in performance, and they do not require the installation of a pacemaker.

The compensated type of sinus node weakness syndrome manifests itself in two forms:

Bradysystolic;
Bradytachysystolic.

With bradysystolic form, patients complain of a weak condition, dizziness. There is limited work capacity. However, such patients do not receive a pacemaker.

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Atrial fibrillation and atrial fibrillation

The braditachysystolic form has the same symptoms, but at the same time, paroxysmal increases in the frequency of heart rhythms in its upper sections join it. Such patients need surgical treatment, and in addition - antiarrhythmic therapy.

The decompensated type of sinus node weakness syndrome has exactly the same division into subspecies as the previous type. With the bradysystolic form of this type of disease, there is a decrease in the number of heart beats, cerebral circulation failures, and cardiac insufficiency. Such patients have reduced performance, and they often require the implantation of an artificial pacemaker.

With the braditachysystolic form of the decompensated type, supraventricular acceleration of contractions, flutter and atrial fibrillation are added to all the symptoms. These people are characterized by a complete loss of working capacity. For treatment, only surgical implantation of a pacemaker is used.

The bradysystolic type with atrial fibrillation worries patients with an increase or decrease in the number of heart beats. In the first situation, the patient's ability to work has no restrictions, and implantation of a pacemaker is not required. The second case is characterized by impaired blood supply to the brain and heart failure, which is the reason for the implantation of a pacemaker.

For reference. The syndrome of weakness of the sinus node proceeds in an acute form or protracted. The acute type of the disease is formed as a complication of myocardial infarction. Repetitions of attacks of a syndrome are capable to progress strenuously.

It should be noted that the symptoms of SSS are very variable. In a number of patients, the disease proceeds completely without any symptoms, while in others it can provoke heart rhythm failures, MES attacks, and other clinical signs. The disease can provoke:

formation of acute left ventricular failure,
pulmonary edema,
angina pectoris,
sometimes myocardial infarction.

The symptomatology of sick sinus syndrome concerns, for the most part, the heart and brain. The patient usually complains of fatigue and irritability, memory impairment. In the future, with an increased development of the disease, the patient may develop presyncope conditions, hypotension and blanching of the skin.
If the patient develops a slow heart rate, memory impairment, dizziness, decreased muscle strength and sleep disturbances are possible.

From the side of the heart, the symptoms are completely different:

feeling your own pulse
pain in the chest area,
dyspnea,
rhythm failure is formed,
cardiac function is impaired.

Attention. With the progression of the syndrome of weakness of the sinus node, supraventricular tachycardia and inconsistent contraction of the muscle fibers of the heart are formed, which threatens the patient's life.

In addition, often symptoms of sick sinus syndrome are a decrease in the amount of urine excreted, intermittent claudication, impaired functioning of the digestive system, and muscle weakness.

Diagnostics

If there are suspicions of SSSU, the doctor sends the patient to the following examinations: