Pacemaker. Causes of sick sinus syndrome, symptoms and signs on the ecg, treatment and prognosis. Etiology and pathogenesis

Parenteral nutrition is one of the types of therapeutic food intake, in which the patient's body is saturated with energy resources, essential proteins, vitamins and trace elements, supplied by introducing special infusion solutions into a vein. With such nutrition, all nutrients immediately enter the bloodstream, bypassing the gastrointestinal tract. Parenteral nutrition is a mandatory component of the complex treatment of a patient who has lost the ability to eat in the usual way.

The concept of parenteral nutrition

This is maintaining a constant acid-base balance in the blood, that is, homeostasis. Through intravenous administration, all the necessary nutrients are supplied to the patient's body.

This nutrition is very important for diseases of the digestive system that need resuscitation, as well as in the postoperative period.

After surgery, there is an increased breakdown of proteins due to:

• high need of the body for energy;
• protein loss through drains and wound surface;
• lack of proper nutrition, since the patient cannot eat a balanced diet after surgery;
• production of hormones of the adrenal cortex, as a response to injury.

With parenteral nutrition, all components are delivered to the body in the right quantities, and their assimilation occurs instantly.

For complex therapy to be successful, nutrient solutions must be administered in a timely and continuous manner until the end of the restoration of impaired functions. They must also be adequate in their composition, the ratio of components, energy value and the volume of fluid injected.

According to the type of introduction of nutrient solutions into the vascular bed, parenteral nutrition can be:

• auxiliary - addition to the natural way;
• mixed - the main nutrients are introduced;
• complete - all the needs of the body are replenished, including electrolytes and water.

Such nutrition can be carried out for a long period of time, and according to the method of its introduction, it is classified as follows:

• intravenous - through veins that have a good blood flow;
• intra-aortic - solutions are injected through the umbilical vein;
• intraosseous - bones with good venous outflow are used.

Indications and contraindications

Indications for total parenteral nutrition are most often violations of the functionality of the large or small intestine, their obstruction or obstruction of the higher located sections of the gastrointestinal tract.

Important! Parenteral nutrition is prescribed on the assumption that adverse circumstances will persist for more than a week.

Special indications:

1. Indomitable vomiting - with chemotherapy, with severe toxicosis in the first half of pregnancy, with severe pancreatitis in acute form.
2. Severe diarrhea - with a stool volume of more than 500 ml. It can be observed with sprue or sprue-like conditions, acute inflammatory process in the intestine, with short bowel syndrome, with radiation enteritis.
3. Severe inflammatory process in the mucous membranes of the esophagus.
4. Paralytic ileus - with extensive surgical interventions in the abdominal cavity, with serious injuries.
5. Intestinal obstruction - with adhesions, oncology, pseudo-obstruction, infectious diseases.
6. Resting colon syndrome - intestinal fistulas, Korn's disease, anastomotic leaks.
7. The preoperative period is exclusively for severe malnutrition.

Peripheral parenteral nutrition is indicated for a period of not more than 10 days, it is prescribed in the case when the main part of the nutritional needs can be met by the enteral method. It is mainly prescribed for a lack of proteins.

Intradialysis parenteral nutrition is prescribed only for patients on chronic hemodialysis. At the end of the last century, such nutrition was prescribed only according to strict indications.

As for contraindications to parenteral nutrition, they are as follows:

• acute bleeding;
• hypoxemia;
• dehydration or hyperhydration;
• acute renal or hepatic failure;
• significant violations of osmolarity, ionic balance and CBS.

With caution, this type of food is prescribed for diseases of the liver, kidneys, heart, lungs.

Applied solutions

The main drugs for parenteral nutrition are:

• protein hydrolysates, amino acid solutions;
• solutions of carbohydrates;
• fat emulsions;
• electrolytes;
• vitamins.

In order for these substances to be absorbed qualitatively, anabolic steroid hormones are included in the scheme.

Protein deficiency is a very undesirable phenomenon, so it is necessary to minimize the possibility of its development. If this could not be prevented, it is urgent to restore the nitrogen balance. This can be achieved by introducing amino acid mixtures and protein hydrolysates into the parenteral diet.

The most common synthetic amino acids are:

• Moriamin S-2;
• Alvezin;
• Vamin;
• Freamin;
• Polyamine;
• Azonutril.

Fat emulsions are introduced during parenteral nutrition because they are high-calorie and energy preparations, in addition, they contain linoleic, linolenic and arachidonic acids.

Carbohydrate solutions are used due to the fact that they represent the most accessible source of energy.

The water requirement for parenteral nutrition is calculated from the amount of excretion.

Electrolytes are important components of total parenteral nutrition. Potassium, phosphorus and magnesium are needed to optimize nitrogen in the body, sodium and chlorine are needed for acid-base balance and osmolarity, calcium prevents demineralization of bone tissue.

To fill the need for electrolytes, the following media are introduced:

• Trisol;
• Laktsol;
• Acesol;
• isotonic sodium chloride solution.

Parenteral nutrition for cancer patients

In oncology, the pathological focus begins to compete for nutrition with normal cellular elements, so oncological cells grow faster than healthy ones. As a consequence, normal cells must be maintained by reserves, such as adipose tissue. However, these reserves can also feed the cancer focus, as a result of which the cancer simply simply eats its carrier.

Most often, cancer patients are able to eat on their own, but over time, they refuse to eat normally, and a number of problems arise:

• dehydration;
• significant loss of body weight;
• salt deposition in the kidneys and bladder.

It has also been proven that most anticancer drugs, pain and depression increase energy and protein deficiency in cancer patients. According to modern concepts, the tumor process occurs in violation of metabolism, and is characterized by the following phenomena:

• reduced glucose tolerance;
• tendency to hyperglycemia with the development of hypoglycemia;
• decrease in glycogen stores in muscles and liver;
• depletion of fat reserves;
• muscle dystrophy;
• immunosuppression.

Such complications can be prevented with the help of Kabiven. This is a plastic bag that contains nutrients. The input is carried out intravenously.

Reference! The agent must be administered for 8-10 hours, if necessary, vitamins and albumin infusions can be additionally injected into the bag with the drug.

The disadvantage of Kabiven is its high cost. But there are similar

epati. For example:

• Aminoven;
• Aminosteril;
• Aminoplasmal.

The disadvantage of these drugs is that they contain only protein, which means that carbohydrates and glucose will have to be administered separately.

To restore amino acids in the body of a cancer patient, the following solutions are most often used:

• Infezol 40;
• Vamin 14;
• Aminosol-800;
• Polyamine;
• Neonutrin.

The indications for total parenteral nutrition in oncology are as follows:

• severely malnourished patients after surgery;
• patients who have complications after surgery;
• patients who had complications during conservative treatment.

Routine total parenteral nutrition is not indicated for cancer patients.

Parenteral nutrition for children

In childhood, parenteral nutrition may be prescribed for:

• severe gastroenteritis;
• necrotic enterocolitis;
• idiopathic diarrhea;
• after operations on the intestines;
• impossibility of enteral nutrition.

As in an adult, parenteral nutrition in a child can be complete, partial and supplementary. Nutrition is carried out by introducing the necessary solutions into a vein, and can last from several days to several years.

Since any veins are used to administer solutions, catheterization of large vessels is performed in childhood.

As for preparations for administration, protein solutions are used, the best of which is TSOLIPC for children. Glucose is used as an energy substrate, but fructose, xylitol, sorbitol, invert sugar, diols can also be used.

Possible Complications

Complications may be associated with the installation of a catheter in the central vein:

• puncture;
• pneumothorax;
• air embolism;
• hemorrhagic complications;
• insertion of a catheter outside a vein;
• improper placement of the catheter;
• disruption in heart rate.

Late complications:

• thrombosis, thromboembolism;
• hemorrhagic;
• infectious;
• mechanical - air embolism, vein perforation.

Metabolic Complications:

• water and electrolyte disturbances;
• hyperglycemia;
• hypertriglyceridemia;
• high nitrogen levels;
• excess levels of aminotransferase.

Complications can be avoided by observing the technique and methodology for installing a catheter for parenteral nutrition, as well as with the correct calculation of the diet.

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In this article, you will learn: what is sick sinus syndrome (SSS for short), and why is it so dangerous. Symptoms, what methods to confirm the diagnosis, what methods of treatment exist, and how effective they are.

Article publication date: 01/14/2017

Date of article update: 05/25/2019

With sick sinus syndrome, the main plexus of cells responsible for independent regular contractions of the heart (this is the sinus node) is unable to produce normal excitatory impulses and conduct them throughout the myocardium.

As a result, the heart contracts much less frequently than it should (less than 40-50 times / min), and arrhythmias may occur due to the appearance of additional impulses from less active foci that can generate excitation.

Normal sinus rhythm
The intervals of too rare a pulse are marked with arrows.

Such a change in cardiac activity the more disrupts the condition of patients, the less often the heart contracts: from the complete absence of symptoms and mild general weakness to loss of consciousness and threat.

Specialized treatment of sick sinus syndrome (abbreviated SSSU) is carried out by cardiologists-arrhythmologists and cardiac surgeons. The success of modern methods of treatment suggests that the disease can be either completely curable if its cause is eliminated, or it is possible to restore and maintain a normal heart rhythm.

The root of the problem is a “lazy” heart

Heart contraction is a spontaneous involuntary process that is possible due to the automatic activity of special myocardial cells. Their largest accumulation in the form of a focus about 1.5 × 0.4 cm in size is called the sinus node. It is located in the upper part of the heart, at the junction of the superior and inferior vena cava, which empty into the right atrium.

Some of the cells in this cluster regularly generate electrical discharges (impulses) at a frequency of 60–90/min, while others conduct them to the atrial myocardium. The strength of the impulses from the sinus node is so great that they pass through the entire myocardium (heart muscle), causing a consistent contraction of each section. Therefore, it is called the main pacemaker.

Sick sinus syndrome (SSS) is a pathological condition in which the main pacemaker of the heart, the sinus node, becomes weak. It cannot generate excitatory impulses with normal frequency and strength. They either occur rarely (less than 40–50/min), or are so weak that they are not carried out to other parts of the myocardium. As a result:

• heart contractions become rare and irregular (less than 40/min);
• other clusters of cells with automatism are activated, which gives rise to various rhythm disturbances (arrhythmias);
• blood circulation is disturbed throughout the body, primarily in the brain, myocardium and other vital organs.

In sinus node syndrome, the heart beats sluggishly and lazily, as if every beat is the last.

Different variants of the disease - different levels of danger

In practice, it is important to divide SSSU into subtypes depending on the degree of impairment and severity of manifestations. This makes it possible for all specialists to understand the problem in the same way and to choose the right treatment for a particular patient.

The table shows the main types of disease, depending on the danger they threaten.

A special kind of sick sinus syndrome is the bradysystolic variant of atrial fibrillation. Therefore, all patients with atrial fibrillation who have a total heart rate of less than 50-60/min should be examined for CVD.

Causes and risk factors

All the reasons why the sinus node loses its activity can be divided into two large groups:

1. Primary causes

Primary - direct damage to only the sinus node or the heart as a whole (cardiac pathology):

• Ischemic disease (myocardial infarction, diffuse cardiosclerosis, angina pectoris).
• Hypertensive and hypertrophic cardiomyopathy.
• Myocarditis.
• Congenital and acquired heart defects.
• Trauma and heart surgery.
• Autoimmune and degenerative systemic connective tissue diseases (vasculitis, lupus, rheumatoid arthritis).
• Idiopathic (causeless) weakness of the sinus node.

2. Secondary causes

These are external influences and internal changes in the body that disrupt normal cardiac activity:

• Endocrine disorders (decreased hormonal activity of the thyroid gland (hypothyroidism) and adrenal glands (hypocorticism)).
• General emaciation and dystrophy.
• Senile restructuring of the body.
• Tertiary form of syphilis.
• Electrolyte disorders (elevated levels of potassium and calcium).
• Overdose or individual reaction to drugs that slow down the rhythm (cardiac glycosides, beta-blockers, amiodarone, verapamil, clonidine).
• Violations of the autonomic regulation of the automatism of the sinus node (reflex vagal disorders): a state of deep sleep, severe coughing and vomiting, tumors of the pharynx of the neck and chest, irritating the vagus nerve, systematic sports, severe cardiac forms of age, increased intracranial pressure.
• Intoxication with external toxic compounds or internal toxins (hepatic-renal failure, sepsis, cancer intoxication).

The main category of people who develop sick sinus syndrome (risk group) are older patients with heart pathology (after 60–65 years) – 70–80%. The remaining 20-30% are children and adolescents, as well as people over 30 years old (the older the age, the more common the disease). But, depending on the cause, pathology can occur at any age, equally often in both women and men.

Symptoms will not leave the disease unnoticed

The general clinical picture for all forms of SSS is represented by three syndromes:

1. Cardiac - cardiac manifestations;
2. Cerebral - brain disorders;
3. Astheno-vegetative - common symptoms.

Description of the main manifestations of these syndromes is given in the table.

Possible manifestations of sick sinus syndrome:

• Chronic course with a constant slowing of the rhythm (50-59 / min) and periodic deterioration during physical exertion (when walking, working) or in sleep: a person suddenly feels severe weakness, shortness of breath, dizziness, the pulse slows down even more (40-50 / min) and heartbeat, interruptions may appear (atrial fibrillation, paroxysmal tachycardia,).
• Against the background of a normal rhythm (60-90 beats / min), sudden attacks of loss of consciousness, severe bradycardia (pulse within 30-40 / min), and a decrease in pressure occur. This variant of the disease is called the Morgagni-Adams-Stokes syndrome.
• Sudden at rest and during exercise without a previous slowing of the rhythm - retrosternal pain, severe shortness of breath, wheezing in the lungs, bradycardia (pulse 40-55), arrhythmia is possible.
• Latent asymptomatic course - there are no symptoms, bradycardia is determined only periodically, mainly during sleep.

SSS with a pronounced slowing of the rhythm (less than 35/min) and arrhythmias threatens with cardiac arrest, acute myocardial infarction, stroke, and pulmonary edema.

Diagnosis: Detect and detail the problem

The main manifestation, on the basis of which the syndrome of weakness of the sinus node is diagnosed, is severe bradycardia (slow heart rate less than 40-50 beats / min). 75% of people with these rhythm disturbances are diagnosed with SSSU. For an accurate diagnosis of the disease are carried out:

• test with a load (veloergometry - riding an exercise bike or squats);
• test with Atropine (administration of a drug that speeds up heartbeats).

Sick sinus syndrome is considered confirmed if, after testing, the heart does not respond with an acceleration of contractions of more than 90 / min.

1. Transesophageal electrical stimulation of the heart is a targeted stimulation of the myocardium by weak electrical currents through the esophagus. In this case, a tachycardia of about 110 beats / min should normally occur. If this does not happen, or after the restoration of a normal rhythm, the pause between beats on the ECG exceeds 1.5 seconds, the diagnosis of SSS is considered confirmed.
2. Additional studies to clarify possible cardiac pathology: echocardiography (ultrasound), cardiac tomography, blood tests for calcium and potassium levels.

The right treatment

Treatment of sick sinus syndrome is represented by two directions:

1. Elimination of the cause - a disease that was complicated by SSSU.
2. Restoration of a normal rhythm - support of the sinus node or its artificial replacement.

Both goals of treatment are achievable, which allows you to fully recover or restore normal cardiac activity, eliminating possible threats. These issues are dealt with by cardiologists-arrhythmologists and cardiac surgeons.

If the cause of SSSU is established, patients undergo the necessary set of therapeutic measures depending on the primary disease (medications, diet, sparing regimen, surgical treatment).

Possibilities of medical rhythm restoration

The possibilities of drug therapy for sick sinus syndrome are small. The drugs used have a weak effect and only in mild forms of pathology. It can be:

• Eufillin in injectable form (injections);
• Theophylline (short-acting tablets);
• Teotard (long-acting tablets);
• Atropine (injections that are administered only for the purpose of providing an ambulance).

With SSSU, accompanied by atrial fibrillation, or other rhythm disturbances (Amiodarone, Bisoprolol) are used with caution, as they will slow down the heartbeat even more. In patients in whom the disease may be associated with an overdose of these drugs, they are completely canceled.

pacing

The main treatment for SSSU is artificial pacing. For this, a special device is implanted (introduced) under the skin of the patient -. Older samples constantly emit electrical impulses that replace the insufficiency of the sinus node. Modern devices work offline, controlling the heart rate. If it is normal, the pacemaker maintains standby mode. As soon as the rhythm slows down below the required numbers, it begins to generate regular impulses, replacing the function of the pacemaker until it restores functional activity.

The main indications for a pacemaker:

• Loss of consciousness on the background of bradycardia (Morgagni-Adams-Stokes syndrome).
• Frequent or severe disorders of cerebral and coronary circulation (severe dizziness, pain in the heart, shortness of breath at rest).
• The combination of SSSU with a pronounced increase or decrease in pressure and any arrhythmias.
• Decreased heart rate less than 40/min.

Forecast: how the patient's life will turn out

The main pattern that applies to all patients with CVD is that refusal to treat results in rapid progression of the disease and severe consequences, especially if the cause is associated with heart pathology.

If the treatment is carried out in the right amount, improvement or recovery without implantation of a pacemaker is possible only with isolated bradycardia, not accompanied by arrhythmias and circulatory disorders (in 50-60% of patients). In all other cases, no one will be able to avoid pacing.

More than 90% of patients who have been implanted with a stimulator note the normalization of their condition and live in their usual mode. Their life expectancy cannot be predicted: from several weeks to tens of years, depending on the general condition and existing diseases. The overall annual mortality in sinus node syndrome is 5% and is mainly associated with sudden cardiac arrest.

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 planned to fully restore the performance of the sinus node as the main source of automatism of the heart, that is, until the heart blockade 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 effects 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.

Read also related

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:

• Electrocardiographic study - able to detect a disease caused by blocking impulses on the way from the sinus node to the atrium; if the syndrome of weakness of the sinus node is caused by blockade of the first degree on the ECG, signs are sometimes not detected;
• Holter monitoring an electrocardiographic study and blood pressure gives more information, but pathology is also not recorded in all cases, especially when the patient has short-term attacks of increased heart rate, followed by bradycardia;
• Removal of an electrocardiogram after a small work load, in particular, after exercising on a treadmill or riding an exercise bike. In this situation, an assessment of physiological tachycardia is made. With the syndrome of weakness of the sinus node, it is absent or mild;
• Endocardial electrophysiological diagnostics. With this research method, microelectrodes are introduced through the vessels into the heart, causing the heart to contract. There is an increase in the number of heartbeats, and if there are pauses longer than three seconds, indicating delays in the transmission of impulses, suggest sinus node weakness syndrome;
• Transesophageal EFI is a similar diagnostic method, its meaning is to introduce a stimulator into the esophagus in the area where the right atrium is closest to the organ;
• Pharmacological tests - the introduction of special medications that limit the effect of the autonomic nervous system on the functions of the sinus node. The received heart rate is a true indicator of the work of the sinus node;
• Tilt test. In order to carry out this diagnosis, the patient is placed on a special bed, where his body is located at an angle of sixty degrees for half an hour. During this period of time, an electrocardiographic study is performed and blood pressure is measured. With this research method, it becomes clear whether syncopal conditions are associated with impaired work of the sinus node of the heart;
• Echocardiographic study of the heart. The structure of the heart is studied, the presence of any modifications of its structures is checked - increased wall thickness, increased chamber sizes, etc .;
• A blood test for hormones, which allows you to identify malfunctions in the endocrine system;
• A general blood test, a venous blood test and a general urinalysis - in this way, the possible causes that provoked the syndrome of weakness of the sinus node are revealed.

For citation: Yalymov A.A., Zadionchenko V.S., Shekhyan G.G., Shchikota A.M., Timofeeva N.Yu., Snetkova A.A. Diagnosis and treatment of sick sinus syndrome // RMJ. 2012. No. 25. S. 1309

Sinus node weakness syndrome , its inability to normally perform the function of a pacemaker of the heart and (or) ensure regular conduction of automatic impulses to the atria. SSSU should include a strictly defined range of arrhythmias and blockades that are directly related to the SA node. These include:

1. Persistent pronounced sinus bradycardia.
2. The minimum heart rate during the day determined by daily ECG monitoring< 40 уд./мин., а ее рост во время физической нагрузки не превышает 90 уд./мин.
3. Bradysystolic form of atrial fibrillation.
4. Migration of the atrial pacemaker.
5. Stopping the sinus node and replacing it with other ectopic rhythms.
6. Sinoauricular blockade.
7. Pauses >2.5 s resulting from sinus node arrest, SA blockade, or rare replacement rhythms.
8. Tachy-brady syndrome, alternating periods of tachycardia and bradycardia.
9. Rarely - attacks of ventricular tachycardia and / or ventricular fibrillation.
10. Slow and unstable recovery of sinus node function after extrasystoles, paroxysms of tachycardia and fibrillation, as well as at the moment of cessation of stimulation during electrophysiological examination of the heart (post-tachycardial pause, which does not normally exceed 1.5 s, can reach 4–5 s with SSSU).
11. Inadequate slowing of the rhythm when using even small doses of β-blockers. Preservation of bradycardia with the introduction of atropine and the exercise test.
History reference
For the first time SA-blockade was described by J. Mackenzie in 1902 during an influenza epidemic. In 1909, E. Laslet observed a Morgagni-Adams-Stokes (MAC) attack in a 40-year-old woman, in whom pauses in heart contractions reached 2–5 s; the atria stopped along with the ventricles, which, as the author emphasized, distinguished this phenomenon from a complete atrioventricular (AV) blockade. D. Short (1954) drew attention to the alternation of sinus bradycardia with atrial fibrillation (MP) in some patients. He called it "bradycardia-tachycardia alternation syndrome" (Short's syndrome). The study of sinus dysfunction was facilitated by clinical studies by V. Lown (1967), who noted an unstable recovery of automatism of the SA node in a number of patients who underwent electrical defibrillation. V. Lown defined this condition as sick sinus syndrome (SSS) - sick sinus syndrome (SSS). A year later, M. Ferrer (1968) extended this term to a group of bradyarrhythmias caused by a weakening of the functions of the SA node and accompanied by appropriate clinical symptoms.
Sinus node anatomy
The sinus node (sinoauricular node, Keys-Flak node, pacemaker of the first order) is a bundle of specific cardiac muscle tissue, the length of which reaches 10–20 mm and the width is 3–5 mm. It is located subepicardially in the wall of the right atrium between the orifices of the vena cava. There are two types of sinus node cells - the pacemaker (P-cells) and conduction (T-cells). P-cells (pacemaker) generate electrical impulses, and T-cells perform a predominantly conductive function. The sinus node is the normal pacemaker of the heart - the pacemaker of the first order, it generates 60-90 impulses per minute, and the heart rhythm recorded on the ECG is called sinus.
The blood supply to the sinus node is carried out by the SA-artery, in 60% of cases this artery departs from the right coronary artery, and in 40% from the left. The sinus node is innervated by the sympathetic and parasympathetic nervous systems.
Prevalence of SSS
The prevalence of sinus node dysfunction in the general population is unknown. According to the incomplete information available, in cardiac patients it is approximately 3:5000. Signs of sinus node disease are observed in 6.3–24% of patients, and therefore these patients underwent implantation of a pacemaker. It is believed that dysfunction of the sinus node is equally common in men and women. With age, the incidence of SSS increases.
Etiology of SSSU
The cases of primary SSSU include dysfunction caused by organic lesions of the SA zone with:
a) cardiac pathology - ischemic heart disease, hypertension, cardiomyopathy, heart defects, myocarditis, surgical operations and heart transplantation;
b) idiopathic degenerative and infiltrative diseases;
c) hypothyroidism, degeneration of the musculoskeletal system, senile amyloidosis, sarcoidosis, scleroderma heart, malignant tumors of the heart, in the stage of tertiary syphilis, etc.
Ischemia caused by stenosis of the artery supplying the sinus node and SA zone, inflammation and infiltration, hemorrhage, dystrophy, local necrosis, interstitial fibrosis and sclerosis cause the development of functional cells of the sinoatrial node of the connective tissue in place.
Secondary SSSU is caused by external (exogenous) factors affecting the sinus node. Exogenous factors include hyperkalemia, hypercalcemia, treatment with drugs that reduce the automatism of the sinus node (β-blockers, sotalol, amiodarone, verapamil, diltiazem, procainamide, cardiac glycosides, dopegit, reserpine, etc.).
Especially among the external factors, autonomic dysfunction of the sinus node (VDS) is distinguished. VASU is often observed in connection with hyperactivation of the vagus nerve (reflex or long-term), causing a decrease in sinus rhythm and lengthening of the refractoriness of the sinus node.
The vagus nerve tone can increase during various physiological processes: during sleep, during urination, defecation, coughing, swallowing, nausea and vomiting, during the Valsalva test. Pathological activation of the vagus nerve can be associated with diseases of the pharynx, genitourinary and digestive tracts, which have abundant innervation, as well as with hypothermia, hyperkalemia, sepsis, and increased intracranial pressure.
WDSU is more often observed in adolescents and young people due to significant neuroticism. A persistent sinus bradycardia rhythm can also be observed in trained athletes due to the pronounced predominance of vagal tone, however, such bradycardia is not a sign of SSSU, because. the increase in heart rate occurs adequately to the load. At the same time, athletes can develop true SSSU in combination with other rhythm disturbances caused by myocardial dystrophy.
SSSU classification
There is no single classification of SSSU. Depending on the nature of the lesion, true (organic), regulatory (vagal), medicinal (toxic) and idiopathic SSSU are distinguished.
According to the features of the clinical manifestation, the following forms of SSSU and variants of their course are distinguished:
1. Latent form - the absence of clinical and ECG manifestations; sinus node dysfunction is determined by electrophysiological examination. There are no work restrictions; implantation of a pacemaker (EX) is not indicated.
2. Compensated form: there are no clinical changes, there are changes on the ECG:
a) bradysystolic variant - mild clinical manifestations, complaints of dizziness and weakness. There may be an occupational disability; pacemaker implantation is not indicated;
b) brady/tachysystolic variant - paroxysmal tachyarrhythmias are added to the symptoms of the bradysystolic variant. Implantation of the pacemaker is indicated in cases of decompensated SSSU under the influence of antiarrhythmic therapy.
3. Decompensated form: there are clinical and ECG manifestations of the disease.
a) bradysystolic variant - persistent sinus bradycardia is determined, it is manifested by a violation of cerebral blood flow (dizziness, fainting, transient paresis), heart failure caused by bradyarrhythmia. Significant disability; indications for implantation are asystole and sinus node function recovery time (VVFSU) of more than 3 s;
b) brady / tachysystolic variant (Short's syndrome) - paroxysmal tachyarrhythmias (supraventricular tachycardia, atrial fibrillation and flutter) are added to the symptoms of the bradysystolic variant of the decompensated form. Patients are completely disabled; Indications for pacemaker implantation are the same as for the bradysystolic variant.
4. Permanent bradysystolic form of atrial fibrillation (against the background of previously diagnosed SSSU):
a) tachysystolic variant - disability; there are no indications for pacemaker implantation;
b) bradysystolic variant - disability; indications for pacemaker implantation are cerebral symptoms and heart failure. The development of the bradysystolic form of atrial fibrillation may be preceded by any of the forms of sinus node dysfunction (Table 1).
Depending on the registration of signs of SSSU during Holter ECG monitoring, latent (signs of SSSU are not detected), intermittent (signs of SSSU are detected with a decrease in sympathetic and an increase in parasympathetic tone, for example, at night) and a manifesting course (signs of SSSU are detected at each daily ECG) – monitoring).
SSSU can be acute or chronic, with relapses. Acute SSSU is often observed in myocardial infarction. The recurrent course of SSSU may be stable or slowly progressive.
According to etiological factors, primary and secondary forms of SSS are distinguished: the primary is caused by organic lesions of the sinus-atrial zone, the secondary is caused by a violation of its autonomic regulation.
Clinical manifestations of SSSU
The clinical manifestation of SSSU may be different. In the early stages, the course of the disease may be asymptomatic even if there are pauses of more than 4 seconds. As the disease progresses, patients report symptoms associated with bradycardia. The most common complaints include a feeling of dizziness and severe weakness, up to fainting (MAS syndrome), retrosternal pain due to myocardial hypoperfusion, and shortness of breath caused by a limitation of the chronotropic reserve. In some cases, chronic heart failure develops. Fainting of a cardiac nature (MAS syndrome) is characterized by the absence of aura, convulsions (with the exception of cases of prolonged asystole).
Patients with mild symptoms may complain of fatigue, irritability, emotional lability, and forgetfulness. In elderly patients, there may be a decrease in memory and intelligence. As the disease progresses and further circulatory disorders, cerebral symptoms become more pronounced.
Possible cooling and blanching of the skin with a sharp drop in blood pressure, cold sweat. Fainting can be provoked by coughing, a sharp turn of the head, wearing a tight collar. Fainting ends on its own, but with a protracted nature, resuscitation may be required.
The progression of bradycardia may be accompanied by symptoms of dyscirculatory encephalopathy (appearance or intensification of dizziness, instant memory lapses, paresis, "swallowing" words, irritability, insomnia, memory loss).
The appearance of escape rhythms can be felt as a heartbeat and interruptions in the work of the heart. Due to hypoperfusion of internal organs, oliguria, acute ulcers of the gastrointestinal tract may develop, symptoms of intermittent claudication and muscle weakness may increase.
ECG diagnostics of SSSU
With dysfunctions of the SA node, electrocardiographic signs of sinus dysfunctions can be recorded long before the onset of clinical symptoms.
1. Sinus bradycardia - slowing of the sinus rhythm with a heart rate of less than 60 in 1 min. due to reduced automatism of the sinus node. In SSSU, sinus bradycardia is persistent, prolonged, refractory to exercise and atropine administration (Fig. 1).
2. Bradysystolic form of atrial fibrillation (MA, atrial fibrillation, atrial fibrillation, absolute arrhythmia, atrial fibrillation, vorhofflimmern, arrhythmia perpetua, delirium cordis, arrhythmia completa) - chaotic, fast and irregular, uncoordinated fibrillations of individual fibers of the atrial muscle as a result of ectopic atrial impulses with a frequency of 350 to 750 per minute, causing a complete disorder of ventricular contractions. In the bradysystolic form of MA, the number of ventricular contractions is less than 60 per minute. (Fig. 2).
3. Migration of the pacemaker through the atria (wandering rhythm, sliding rhythm, migrating rhythm, migration of the pacemaker, wandering pacemaker). There are several variants of wandering (wandering) rhythm:
a) wandering rhythm in the sinus node. The P wave is sinus in origin (positive in leads II, III, AVF), but its shape changes with different heartbeats. The PR interval remains relatively constant. There is always a pronounced sinus arrhythmia;
b) wandering rhythm in the atria. The P wave is positive in leads II, III, AVF, its shape and size change with different heartbeats. Along with this, the duration of the PR interval changes;
c) wandering rhythm between the sinus and AV nodes. This is the most common variant of the wandering rhythm. With it, the heart contracts under the influence of impulses that periodically change their place, gradually moving from the sinus node, through the atrial muscles to the AV junction, and again returning to the sinus node. ECG criteria for pacemaker migration through the atria are three or more different P waves in a series of cardiac cycles, a change in the duration of the PR interval. The QRS complex does not change (Fig. 3 and 4).
4. Passive ectopic rhythms. Reduced activity of the sinus node or complete blockade of sinus impulses due to functional or organic damage to the sinus node cause the activation of automatic centers of the II order (cells of atrial pacemakers, AV connection), III order (His system) and IV order (Purkinje fibers, ventricular muscles ).
Automatic centers of the second order cause unchanged ventricular complexes (supraventricular type), while centers III and IV of the order generate dilated and deformed ventricular complexes (ventricular, idioventricular type). The following rhythm disturbances have a replacing character: atrial, nodal, migration of the pacemaker through the atria, ventricular (idioventricular rhythm), jumping contractions.
4.1. Atrial rhythm (slow atrial rhythm) - a very slow ectopic rhythm with foci of impulse generation in the atria (Table 2):
a) right atrial ectopic rhythm - the rhythm of an ectopic focus located in the right atrium. On the ECG, a negative P' wave is recorded in leads V1–V6, II, III, aVF. PQ interval of normal duration, QRST complex unchanged;
b) rhythm of the coronary sinus (rhythm of the coronary sinus) - impulses to excite the heart come from cells located in the lower part of the right atrium and the coronary sinus vein. The impulse propagates through the atria in a retrograde manner from bottom to top. This leads to the registration of negative P' waves in II, III, aVF leads. The P wave aVR is positive. In leads V1-V6, the P' wave is positive or biphasic. The PQ interval is shortened and is usually less than 0.12 s. The QRST complex is not changed. The rhythm of the coronary sinus may differ from the right atrial ectopic rhythm only by shortening the PQ interval;
c) left atrial ectopic rhythm - impulses to excite the heart come from the left atrium. At the same time, a negative P' wave is recorded on the ECG in II, III, aVF, V3–V6 leads. It is also possible the appearance of negative P' waves in I, aVL; the P' wave in aVR is positive. A characteristic sign of a left atrial rhythm is the P' wave in lead V1 with an initial rounded domed part, followed by a pointed peak - “shield and sword” (“dome and steeple”, “bow and arrow”). The P' wave precedes the QRS complex with a normal PR interval of 0.12–0.2 s. The atrial rate is 60–100 per minute, rarely below 60 (45–59) per minute. or above 100 (101-120) per min. The rhythm is correct, the QRS complex is not changed (Fig. 5);
d) lower atrial ectopic rhythm - the rhythm of an ectopic focus located in the lower parts of the right or left atrium. This leads to the registration of negative P' waves in II, III, aVF leads and a positive P' wave in aVR. The PQ interval is shortened (Fig. 6).
4.2. Nodal rhythm (AV-rhythm replacing AV junctional rhythm) - heart rhythm under the action of impulses from the AV-connection with a frequency of 40-60 per minute. There are two main types of AV rhythm:
a) junctional rhythm with simultaneous excitation of the atria and ventricles (nodal rhythm without a P' wave, junctional rhythm with AV dissociation without a P' wave): an unchanged or slightly deformed QRST complex is recorded on the ECG, there is no P wave (Fig. 7);
b) nodal rhythm with excitation of the ventricles at different times, and then the atria (nodal rhythm with a retrograde P wave, an isolated form of AV rhythm): an unchanged QRST complex is recorded on the ECG, followed by a negative P wave (Fig. 8).
4.3. Idioventricular (ventricular) rhythm (intrinsic ventricular rhythm, ventricular automatism, intraventricular rhythm) - ventricular contraction impulses occur in the ventricles themselves. ECG criteria: widened and deformed QRS complex (greater than 0.12 s), rhythm with heart rate less than 40 (20-30) per minute. The terminal idioventricular rhythm is very slow and unstable. The rhythm is more often correct, but may be irregular in the presence of several ectopic foci in the ventricles or a single lesion with varying degrees of impulse generation or exit block. If atrial rhythm is present (sinus rhythm, atrial fibrillation/flutter, ectopic atrial rhythm), then it is independent of ventricular rhythm (AV dissociation) (Fig. 9).
5. Sinoauricular blockade (blockade of the exit from the SA node, dissociatio sino-atriale, SA-block) - a violation of the formation and / or conduction of an impulse from the sinus node to the atria. SA blockade occurs in 0.16-2.4% of people, mainly in people over 50-60 years old, more often in women than in men.
5.1. Sinoauricular blockade of the first degree is manifested by the slow formation of impulses in the sinus node or their slow conduction to the atria. A conventional ECG is uninformative, diagnosed by electrical stimulation of the atria or by recording the potentials of the sinus node and based on changes in the conduction time in the sinoauricular node.
5.2. Sinoauricular blockade of the II degree is manifested by partial conduction of impulses from the sinus node, which leads to loss of atrial and ventricular contractions. There are two types of sinoauricular block II degree:
Sinoauricular block II degree type I (with periodicals of Samoilov-Wenckebach):
a) progressive shortening of RR intervals (Samoilov-Wenckebach periodical), followed by a long pause in RR;
b) the greatest distance PP - during a pause at the moment of loss of contraction of the heart;
c) this distance is not equal to two normal RR intervals and is less than them in duration;
d) the first RR interval after the pause is longer than the last RR interval before the pause (Fig. 10).
Sinoauricular block II degree II type:
a) asystole - the absence of electrical activity of the heart (the P wave and the QRST complex are absent), the contraction of the atria and ventricles drops out;
b) pause (asystole) is a multiple of one normal RR (PP) interval or equal to two normal RR (PP) periods of the main rhythm (Fig. 11).
Far-reaching sinoauricular block II degree type II. By analogy with AV blockade, prolonged SA blockade 4:1, 5:1, etc. should be called advanced SA-block II degree type II. In some cases, the pause (isoelectric line) is interrupted by escape complexes (rhythms) from the atrial centers of automatism or, more often, from the AV junction area.
Sometimes delayed sinus impulses meet (coincide) with AV escape impulses. On the ECG, rare P waves are located in close proximity to the escape QRS complexes. These P waves are not routed to the ventricles. The emerging AV dissociation can be complete or incomplete with ventricular seizures. One of the variants of incomplete AV dissociation, when each escape complex is followed by the capture of the ventricles with a sinus impulse, is called escape-capture-bigemini (bigeminy of the "escape-capture" type).
5.3. Sinoauricular blockade of the III degree (complete sinoauricular blockade) is characterized by the absence of excitation of the atria and ventricles from the sinus node. Asystole occurs and continues until the automatic center of the II, III or IV order begins to act (Fig. 12).
6. Stopping the sinus node (failure of the sinus node, sinus arrest, sinus pause, sinus-inertio) - periodic loss of the ability to generate impulses by the sinus node. This leads to loss of excitation and contraction of the atria and ventricles. There is a long pause on the ECG, during which the P and QRST waves are not recorded and the isoline is recorded. The pause when stopping the sinus node is not a multiple of one RR (PP) interval (Fig. 13).
7. Atrial arrest (atrial asystole, atrial standstill, partial asystole) - the absence of atrial excitation, which is observed during one or (more often) more cardiac cycles. Atrial asystole can be combined with ventricular asystole, in such cases there is a complete asystole of the heart. However, during atrial asystole, pacemakers of the II, III, IV order usually begin to function, which cause excitation of the ventricles (Fig. 14). There are three main options for atrial arrest:
a) atrial arrest along with failure (stop) of the SA node: P waves are absent, as are the electrograms of the SA node; a slow replacement rhythm is recorded from the AV connection or from the idioventricular centers. A similar phenomenon can be encountered with severe quinidine and digitalis intoxication (Fig. 14);
b) the absence of electrical and mechanical activity (stop) of the atria while maintaining the automatism of the SA node, which continues to control the excitation of the AV node and ventricles. This pattern is observed with severe hyperkalemia (> 9-10 mm / l), when the correct rhythm appears with widened QRS complexes without P waves. This phenomenon is called sinoventricular conduction;
c) preservation of the automatism of the SA node and the electrical activity of the atria (P waves) in the absence of their contractions. The syndrome of electromechanical dissociation (uncoupling) in the atria can sometimes be observed in patients with dilated auricles after their electrical defibrillation.
Permanent arrest, or paralysis, of the atria is rare. There are reports in the literature about atrial paralysis in cardiac amyloidosis, widespread atrial fibrosis, fibroelastosis, fat infiltration, vacuolar degeneration, neuromuscular dystrophies, and in the terminal period of heart disease.
8. Bradycardia/tachycardia syndrome (tachy/brady syndrome).
With this variant, there is an alternation of a rare sinus or replacement supraventricular rhythm with attacks of tachysystole (Fig. 15).
Clinical evaluation of function
sinus node
SSSU should be considered as a probable diagnosis in patients with the symptoms described above. The most complex electrophysiological studies should be performed only when the diagnosis of sinus node dysfunction is in some doubt.
Valsalva test. The simplest vagal tests with holding the breath on a deep breath (including the Valsalva test), carried out in isolation or in combination with straining, sometimes reveal sinus pauses exceeding 2.5–3.0 s, which must be differentiated from pauses caused by disorders AV conduction.
Identification of such pauses indicates an increased sensitivity of the sinus node to vagal influences, which can occur both with VDSU and SSSU. If such pauses are accompanied by clinical symptoms, an in-depth examination of the patient is required to determine the tactics of treatment.
Carotid sinus massage. The carotid sinus is a small formation of the autonomic nervous system, located at the beginning of the internal carotid artery above the bifurcation of the common carotid artery. Carotid sinus receptors are associated with the vagus nerve. The carotid sinus reflex under physiological conditions causes bradycardia and hypotension due to irritation of the vagus nerve and vascular regulatory center in the medulla oblongata. With hypersensitive (hypersensitive) carotid sinus, pressure on it can cause sinus pauses exceeding 2.5–3.0 s, accompanied by a short-term disorder of consciousness. Before the massage of the carotid zones, such patients are shown an assessment of the state of blood flow in the carotid and vertebral arteries, tk. massage of arteries with pronounced atherosclerotic changes can lead to sad consequences (sharp bradycardia up to loss of consciousness and asystole!).
It is important to emphasize that the carotid sinus syndrome can, on the one hand, develop against the background of the normal function of the sinus node, and on the other hand, it does not exclude the presence of SSSU.
Tilt test. Tilt-test (passive orthostatic test) is considered today as the "gold standard" in the examination of patients with syncope of unknown etiology.
Load testing (veloergometry, treadmill test). Load testing allows you to evaluate the ability of the sinus node to speed up the rhythm in accordance with the internal physiological chronotropic stimulus.
Holter monitoring. Ambulatory Holter monitoring, when performed during normal daily activities, appears to be a more valuable physiological measure of sinus node function than exercise testing. The alternating appearance of bradyarrhythmias and tachyarrhythmias in patients with SSSS is often not detected on a conventional electrocardiogram at rest.
The study of the function of the sinus node by the method of CHPES. An indicator of the automatic activity of the sinus node is the duration of the sinus pause from the moment of termination of stimulation (the last artifact of the electrical stimulus) to the beginning of the first independent P wave. This period of time is called the recovery time of the sinus node function (VVFSU). Normally, the duration of this period does not exceed 1500–1600 ms. In addition to VVFSU, another indicator is calculated - the corrected recovery time of the sinus node function (KVVFSU), which takes into account the duration of the VVFSU indicator in relation to the initial frequency of the sinus rhythm.
Treatment of SSSU
At the beginning of SSSU therapy, all drugs that can contribute to conduction disturbance are canceled. In the presence of tachy-brady syndrome, tactics can be more flexible: with a combination of moderate sinus bradycardia, which is not yet an indication for the installation of a permanent pacemaker, and frequent brady-dependent paroxysms of atrial fibrillation, in some cases, a trial appointment of allapinin in a small dose (1/2 tab. 3–4 rubles/day) followed by obligatory control during Holter monitoring.
However, over time, the progression of conduction disorders may require discontinuation of drugs, followed by the installation of a pacemaker. While maintaining bradycardia, the simultaneous use of Belloid 1 tab. 4 rubles / day or teopeka 0.3 g 1/4 tab. 2-3 rubles / day
It is necessary to exclude hyperkalemia or hypothyroidism, in which the patient may be erroneously referred to the installation of a permanent pacemaker. If SSS is suspected, sinus node-suppressing drugs should be withheld until Holter monitoring and specific tests have been performed. The appointment of β-blockers, calcium antagonists (verapamil, diltiazem), sotalol, amiodarone, cardiac glycosides is impractical.
In cases of acute development of SSSU, etiotropic treatment is carried out first of all. If its inflammatory genesis is suspected, the administration of prednisolone 90-120 mg IV or 20-30 mg / day is indicated. inside. In acute myocardial infarction, anti-ischemic drugs (nitrates), antiplatelet agents (acetylsalicylic acid, clopidogrel), anticoagulants (heparin, low molecular weight heparins), cytoprotectors (trimetazidine) are prescribed.
Emergency therapy proper SSSU carried out depending on its severity. In cases of asystole, MAS attacks, resuscitation is necessary. Severe sinus bradycardia, worsening hemodynamics and / or provoking tachyarrhythmias, requires the appointment of atropine 0.5-1.0 ml of a 0.1% solution s / c up to 4-6 times / day, infusion of dopamine, dobutamine or aminophylline under the control of a heart monitor . A temporary endocardial pacemaker may be placed prophylactically.
Absolute indications for pacemaker implantation:
1. History of MAS attacks (at least once).
2. Severe bradycardia (less than 40 per minute) and / or pauses for more than 3 s.
3. VVFSU more than 3500 ms, KVVFSU - more than 2300 ms.
4. The presence of dizziness caused by bradycardia, presyncopal conditions, coronary insufficiency, congestive heart failure, high systolic arterial hypertension - regardless of heart rate.
5. SSS with rhythm disturbances requiring the appointment of antiarrhythmic drugs, which is impossible in conditions of impaired conduction.
Currently, it is patients with SSSU that make up the vast majority of patients with permanent pacemakers. It should be noted that this method, while improving the quality of life, sometimes significantly, usually does not allow to increase its duration, which is determined by the nature and severity of concomitant organic heart disease, mainly myocardial dysfunction. When choosing a method of pacing, one should strive to ensure not only an adequate ventricular rate, but also the preservation of atrial systole.