Syncope clinical history. Syncope in cardiological practice

Syncope (syncope syndrome) is a short-term loss of consciousness, combined with impaired muscle tone and dysfunction of the cardiovascular and respiratory systems.

Recently, fainting has been considered as a paroxysmal disorder of consciousness. In this regard, it is preferable to use the term “syncopation” - it defines pathological changes in the body much more broadly.

Collapse must be distinguished from syncope: although there is a vascular-regulatory disorder with it, loss of consciousness does not necessarily occur.

What is syncope and its neurological assessment

As already mentioned, with syncope, a short-term loss of consciousness occurs. At the same time, it decreases and the functions of the cardiovascular and respiratory systems are disrupted.

Syncope can occur at any age. Usually occurs while sitting or standing. Caused by acute brainstem or cerebral oxygen starvation.

Syncope must be distinguished from an acute one. In the first case, spontaneous recovery of cerebral functions is observed without the manifestation of residual neurological disorders.

Neurologists distinguish between neurogenic and somatogenic syncope.

Stages of development - from fright to hitting the floor

Syncope develops in three stages:

• prodromal (precursor stage);
• immediate loss of consciousness;
• post-fainting state.

The severity of each stage and its duration depend on the cause and mechanism of development of syncopal syndrome.

The prodromal stage develops as a result of the action of a provoking factor. It can last from a few seconds to tens of hours. Arises from pain, fear, tension, stuffiness, etc.

It manifests itself as weakness, paleness of the face (this may be replaced by redness), sweating, darkening of the eyes. If a person in such a state manages to lie down or at least bow his head, then he will not attack.

Under unfavorable conditions (inability to change body position, continued exposure to provoking factors), general weakness increases, consciousness is impaired. Duration - from seconds to ten minutes. The patient falls, but significant physical damage does not occur, foam at the mouth or involuntary movements are not observed. The pupils dilate and blood pressure drops.

The post-syncope state is characterized by the preservation of the ability to navigate in time and space. However, lethargy and weakness persist.

Classification subtypes of syndromes

The classification of syncope is very complex. They are distinguished according to pathophysiological principles. It should be noted that in a significant number of cases the cause of syncope cannot be determined. In this case, they speak of idiopathic syncope syndrome.

The following types of syncope also differ:

1. Reflex. These include vasovagal and situational fainting.
2. Orthostatic. They arise due to insufficient autonomic regulation, taking certain medications, drinking alcoholic beverages, and hypovolemia.
3. Cardiogenic. The cause of syncope in this case is cardiovascular pathology.
4. Cerebrovascular. Occurs due to blockage of the subclavian vein by a thrombus.

There are also non-syncope pathologies, but they are diagnosed as syncope. Complete or partial loss of consciousness during a fall occurs due to hypoglycemia, poisoning,.

There are non-syncope states without loss of consciousness. These include short-term muscle relaxation due to emotional overload, pseudosyncope of a psychogenic nature, as well as hysterical syndromes.

Etiology and pathogenesis

The causes of syncope are reflex, orthostatic, cardiogenic and cerebrovascular. The following factors influence the development of syncope:

• tone of the blood vessel wall;
• systemic blood pressure level;
• person's age.

The pathogenesis of different types of syncope syndromes is as follows:

1. Vasovagal syncope-syncope or vasodepressor conditions occur due to disorders of the autonomic regulation of blood vessels. The tension of the sympathetic nervous system increases, causing blood pressure and heart rate to increase. Subsequently, due to increased tone of the vagus nerve, blood pressure drops.
2. Orthostatic syncope occurs most often in older people. They increasingly show a discrepancy between the volume of blood in the bloodstream and the stable functioning of vasomotor function. The development of orthostatic syncope is influenced by the use of antihypertensive drugs, vasodilators, etc.
3. Due to a decrease in cardiac output, they develop cardiogenic
4. With hypoglycemia, a decrease in the amount of oxygen in the blood, cerebrovascular syncopation. Elderly patients are also at risk due to the likelihood of developing .

Mental illness and age over 45 years increase the frequency of recurrent syncope.

Features of the clinical picture

Features of the clinical course of different types of syncope are as follows:

Diagnostic criteria

First of all, collecting an anamnesis is of great importance for diagnosing syncope. It is extremely important for the doctor to find out in detail the following circumstances: whether there were precursors, what kind of character they had, what kind of consciousness the person had before the attack, how quickly the clinical signs of syncope grew, the nature of the patient’s fall directly during the attack, the color of his face, the presence of a pulse, character changes in pupils.

It is also important to indicate to the doctor the length of time the patient has been in a state of loss of consciousness, the presence of convulsions, involuntary urination and/or defecation, and foam discharged from the mouth.

When examining patients, the following diagnostic procedures are performed:

• measure blood pressure while standing, sitting and lying down;
• carry out diagnostic tests with physical activity;
• do blood and urine tests (required!), determining the amount of blood sugar, as well as hematocrit;
• They also do electrocardiography;
• if cardiac causes of syncope are suspected, an X-ray of the lungs, an ultrasound of the lungs and heart are performed;
• computer and .

It is important to distinguish between syncope and. Characteristic differential signs of syncope:

Tactics and strategy for providing assistance

The choice of treatment tactics primarily depends on the cause of syncope. Its purpose is, first of all, to provide emergency care, prevent repeated episodes of loss of consciousness, and reduce negative emotional complications.

First of all, in case of fainting, it is necessary to prevent the person from hitting himself. He needs to be laid down and his legs placed as high as possible. Tight clothing should be loosened and sufficient fresh air should be provided.

You need to give ammonia to sniff and spray your face with water. It is necessary to monitor the person’s condition, and if he does not wake up within 10 minutes, call an ambulance.

In case of severe fainting, Metazon in a 1% solution or Ephedrine in a 5% solution are administered orally. An attack of bradycardia and fainting is stopped by the administration of Atropine sulfate. Antiarrhythmic drugs should be administered only for cardiac arrhythmias.

If the person comes to his senses, you need to calm him down and ask him to avoid the influence of predisposing factors. It is strictly forbidden to give alcohol or allow overheating. Drinking plenty of water with added table salt is beneficial. It is necessary to avoid sudden changes in body position, especially from a horizontal to a vertical position.

Therapy between attacks is limited to taking recommended medications. Non-drug treatment boils down to the abolition of diuretics and dilators. In case of hypovolemia, correction of this condition is indicated.

What are the consequences?

In rare cases of syncope, when they are not caused by cardiovascular causes, the prognosis is usually favorable. Also a favorable prognosis for neurogenic and orthostatic syncope.

Syncope is a common cause of household injuries and death from road traffic accidents. Patients with heart failure, ventricular arrhythmias, and abnormal electrocardiogram findings are at risk of sudden cardiac death.

Preventive actions

First of all, preventing any syncope comes down to eliminating any precipitating factors. These are stressful conditions, heavy physical activity, emotional states.

It is necessary to play sports (naturally, in reasonable measures), harden yourself, and establish a normal work schedule. In the morning, you should not make excessively sudden movements in bed.

If you experience frequent fainting and excessive excitability, you should drink soothing infusions with mint, St. John's wort, and lemon balm.

Any type of syncope requires increased attention, as sometimes its consequences can be very serious.

Despite the variety of phenomenological manifestations of paroxysms characterized by impaired consciousness, there are currently two main groups of paroxysmal disorders of consciousness: epileptic And non-epileptic. In the structure of the latter syncopal(fainting) states occupy a leading place.

In some patients, convulsive syncope is disguised as an epileptic seizure.. After an initial neurological examination, such patients are often prescribed treatment with antiepileptic drugs. Despite the therapy, 25% of patients with epilepsy experience syncope.

Recommendations of the American College of Cardiology/American Heart Association (ACC/AHA), European Heart Society (ESC) and others indicate that patients with syncope, presyncope, dizziness, or repeated unexplained palpitations should undergo mandatory electrocardiogram (ECG) monitoring. With the diagnostic capabilities of ECG monitors, it is possible to carry out long-term monitoring and diagnosis of transient or rare symptoms.

Classification of syncope

Considering the fact that syncope occurs in the clinical practice of internists of any profile, a unified approach to their classification is necessary.

Currently, the following conditions are distinguished:
1. Neurogenic syncope: psychogenic, irritative, maladaptive, discirculatory.
2. Somatogenic syncope: cardiogenic, vasodepressor, anemic, hypoglycemic, respiratory.
3. Syncope due to extreme exposures: hypoxic, hypovolemic, intoxicating, medicinal, hyperbaric.
4. Rare and multifactorial syncope: nocturic, cough.

In addition, considering fainting as a process unfolded over time, the severity of syncope is distinguished.
1. Presyncope:
I degree – weakness, nausea, spots before the eyes;
II degree – more pronounced symptoms described above with elements of impaired postural tone.
2. Syncope:
I degree – short-term loss of consciousness for a few seconds without pronounced post-seizure syndrome;
II degree – longer loss of consciousness and pronounced post-ictal manifestations.
The above classification emphasizes that syncopal paroxysm is a step-by-step process in which transitional states can be distinguished
Fainting clinic

Fainting is characterized by:
generalized muscle weakness
decreased postural tone, inability to stand upright
loss of consciousness

The term "weakness" means lack of strength with a feeling of impending loss of consciousness. At the beginning of fainting (!!!) the patient is always in an upright position, with the exception of an Adams-Stokes attack. Usually the patient has a premonition of impending fainting. At first he feels bad, then there is a feeling of movement or swaying of the floor and surrounding objects, the patient yawns, spots appear before the eyes, tinnitus, nausea, sometimes vomiting, and vision is weakened. If fainting develops slowly, the patient can prevent falling and injury by quickly taking a horizontal position. In this case, there may not be a complete loss of consciousness.

The depth and duration of unconsciousness varies
sometimes the patient is not completely disconnected from the outside world
a deep coma may develop with complete loss of consciousness and lack of response to external stimuli.

A person can remain in this state for several seconds or minutes, sometimes even for about half an hour. As a rule, the patient lies motionless, the skeletal muscles are relaxed, but immediately after loss of consciousness, clonic twitching of the muscles of the face and torso occurs. The functions of the pelvic organs are usually controlled, the pulse is weak, sometimes not palpable, blood pressure (BP) is low, breathing is almost imperceptible. As soon as the patient assumes a horizontal position, blood flows to the brain, the pulse becomes stronger, breathing becomes more frequent and deeper, complexion normalizes, and consciousness is restored. From this moment, the person begins to adequately perceive the surrounding situation, but feels severe physical weakness; too hasty an attempt to get up can lead to repeated fainting.
Headache, drowsiness, and confusion do not usually occur after fainting.

Fainting of vascular origin

Vascular syncope includes conditions that occur as a result of a drop in blood pressure or a decrease in venous return of blood to the heart:
vasovagal
sinocarotid
orthostatic
situational syncope.
psychogenic fainting as a result of exposure to psychoemotional factors is also distinguished

Patients describe fainting as a feeling of lightheadedness and dizziness. They turn pale, sweat appears, then the patients lose consciousness. It is believed that the pathogenetic basis of vasovagal fainting is excessive deposition of blood in the veins of the lower extremities and a violation of reflex effects on the heart. Other variants of vasovagal syncope have been described. With intense pain syndrome of visceral origin, irritation of the vagus nerve can contribute to a slowdown in cardiac activity and even cardiac arrest, for example, during an attack of hepatic colic, damage to the esophagus, mediastinum, bronchoscopy, pleural puncture and laparocentesis, severe systemic dizziness in labyrinthine and vestibular disorders, puncture of body cavities. Sometimes fainting occurs during a severe migraine attack.

Sinocarotid syncope

They are typical for middle-aged people and are associated with irritation of the sinocarotid node and the development of reflex bradycardia, which lead to fainting. It occurs when the head is suddenly thrown back or the neck is compressed by a tightly tied tie or shirt collar. The specificity of the situation is the key to the diagnosis, to confirm which a careful unilateral massage of the sinocarotid sinus should be performed in a horizontal position of the patient, preferably under ECG control to record bradycardia. This massage is informative from a diagnostic point of view in elderly patients, (!!!) but it should not be performed during an outpatient appointment if murmurs are heard over the carotid artery, indicating the presence of an atherosclerotic plaque, or if there is a history of ventricular tachycardia, recent transient ischemic circulatory disorder, stroke or MI.

Orthostatic syncope

The main difference between orthostatic fainting– they appear exclusively during the transition from a horizontal to a vertical position.
Orthostatic arterial hypotension causes syncope in an average of 4-12% of patients.

This type of fainting occurs in people with chronic insufficiency or periodic instability of vasomotor reactions. A decrease in blood pressure after assuming a vertical position occurs due to a violation of the vasoconstrictor reactivity of the vessels of the lower extremities, which are responsible for the resistance and capacity of the blood vessels.

Postural fainting develops in practically healthy people who, for unknown reasons, have defective postural reactions (which can be familial). In such people, a feeling of weakness occurs when bending sharply, their blood pressure decreases slightly, and then settles at an even lower level. Soon, compensatory reactions weaken sharply and blood pressure continues to fall rapidly.

This type of fainting is possible with primary failure of the autonomic nervous system, familial autonomic dysfunction.

At least three syndromes of orthostatic syncope have been described:

I. Acute or subacute autonomic dysfunction. With this disease, in practically healthy adults or children, partial or complete disruption of the parasympathetic and sympathetic systems occurs over the course of several days or weeks. Pupillary reactions disappear, tears, salivation and sweating stop, impotence, paresis of the bladder and intestines, and orthostatic hypotension are observed. Additional studies reveal increased protein content in the cerebrospinal fluid and degeneration of unmyelinated autonomic nerve fibers. It is believed that this disease is a variant of acute idiopathic polyneuritis, similar to Landry-Guillain-Barré syndrome.

II. Chronic insufficiency of postganglionic autonomic nerve fibers. This disease develops in middle-aged and older people, who gradually develop chronic orthostatic hypotension, sometimes in combination with impotence and dysfunction of the pelvic organs. After remaining in an upright position for 5-10 minutes, blood pressure decreases by at least 35 mmHg. Art., pulse pressure decreases, while pallor, nausea and increased pulse rate are not observed. Men get sick more often than women. The condition is relatively benign and appears to be irreversible.

III. Chronic failure of preganglionic autonomic nerve fibers. In this disease, orthostatic hypotension, along with periodic anhidrosis, impotence and dysfunction of the pelvic organs, is combined with lesions of the central nervous system.
These include:
1. Shy-Drager syndrome, characterized by tremor, extrapyramidal rigidity and amnesia;
2. Progressive cerebellar degeneration, some varieties of which are familial;
3. More variable extrapyramidal and cerebellar diseases(striato-nigral degeneration).

These syndromes lead to disability and often death within a few years.

Orthostatic hypotension occurs secondary to
autonomic nervous system disorders
age-related physiological changes
adrenal insufficiency
hypovolemia
taking certain medications (antihypertensives, tricyclic antidepressants, levodopa, antipsychotics, β-blockers), especially in elderly patients who have to take several medications at the same time
Insufficiency of the autonomic nervous system - damage to pre- and postganglionic autonomic fibers - most often occurs when the lateral columns of the spinal cord (syringomyelia) or peripheral nerves are involved in the pathological process (diabetic, alcoholic, amyloid polyneuropathy, Eydie syndrome, hypovitaminosis, etc.)
Orthostatic hypotension is considered one of the manifestations of Parkinson's disease,
multisystem brain atrophy
subclavian artery steal syndrome
But more often the causes of orthostatic hypotension are fasting, anemia, prolonged bed rest

Situational fainting

Situational syncope occurs when coughing, urinating, defecating, and swallowing. Fainting during urination or defecation is a condition that is usually observed in older people during or after urination, especially after a sudden change from a horizontal to a vertical position. It can be distinguished as a separate type of postural fainting.

It is assumed that the decrease in intravesicular pressure causes rapid vasodilation, which increases in the upright position. Bradycardia, caused by the activity of the vagus nerve, also plays a certain role. Fainting when coughing and swallowing is quite rare and develops only when exposed to a provoking factor specific to each form.

Psychogenic fainting
The psychogenic nature of fainting is identified in patients after conducting possible studies in the absence of signs of heart disease or neurological disorders.

This group of patients can be divided into two categories:
patients who have had their first episode of syncope (further evaluation can be discontinued), and
patients who continue to experience fainting (the patient’s mental state should be assessed). In almost 25% of such cases, a psychiatric examination can detect mental disorders combined with fainting states.

Often, in emotionally labile people, against the background of a psychotraumatic factor, they develop panic attacks, which are characterized by a sudden onset, palpitations, a feeling of heat, lack of air, then chest pain, trembling, a feeling of fear and doom. Following hyperventilation, paresthesia occurs. At such moments, patients subjectively feel a loss of consciousness or even the onset of death, but a loss of consciousness or a fall does not occur. Conversations with eyewitnesses of the attacks, a test with hyperventilation and the appearance of the above symptoms help the clinician make the correct diagnosis.

It should be separately described non-epileptic seizures, or pseudoseizures. They are more common in women aged about 20 years, whose family history usually includes references to relatives who suffered from epilepsy. Such patients had the opportunity to observe the development of epileptic seizures, imitate them, or themselves suffer from mental illness. Pseudo-seizures are varied and longer lasting than true epileptic seizures. They are characterized by poor coordination of movements, complex localization, occur in crowded places, and injuries are very rare. During a seizure, the patient may resist being examined by a doctor.

Neurological syncope

In addition to syncope of cardiac origin, syncope includes conditions with a sudden onset of short-term impairment of consciousness, which may be the result of transient anemia of the brain. A sufficient level of blood supply to the brain depends on a number of physiological conditions of the state of cardiac activity and vascular tone, the volume of circulating blood and its physicochemical composition.

There are three main factors that contribute to the deterioration of cerebral blood flow, disruption of brain nutrition and, ultimately, episodic blackouts.
1. Cardiac– weakening of the force of cardiac contractions of a neurogenic nature or due to acute functional failure of the heart muscle, valvular apparatus, or cardiac arrhythmia.
2. Vascular– a drop in vascular tone of the arterial or venous systems, accompanied by a significant decrease in blood pressure.
3. Homeostatic– changes in the qualitative composition of the blood, especially a decrease in the content of sugar, carbon dioxide, and oxygen.

When selecting patients for a neurological examination, it is necessary to carefully collect a neurological history (find out the presence of a history of seizures, prolonged loss of consciousness, diplopia, headache, ask about the condition after loss of consciousness) and conduct a targeted physical examination, identifying vascular murmurs and focal neurological symptoms.

The survey should also include
electroencephalography
computer and magnetic resonance imaging of the brain
transcranial Doppler ultrasound if a stenotic process is suspected (in people over 45 years of age, when murmurs are detected above the carotid artery, in people who have suffered transient ischemic attacks or stroke).

Fainting in the elderly

(!!!) When fainting occurs in elderly patients, first of all you need to think about the appearance of a complete transverse conduction block or tachyarrhythmia. When examining them, it is necessary to remember the complex nature of fainting states and the fact that such patients are often taking several medications at the same time.

In old age, the most common causes of syncope are:
orthostatic hypotension
neurological disorders
arrhythmias

If examination reveals orthostatic hypotension, special attention must be paid to the patient's intake. medicines, contributing to a decrease in blood pressure with the development of postural disorders. If the patient does not take such drugs, then the main attention should be paid studies of the cardiovascular and nervous systems. If during a neurological examination there are no pathological changes, but there are complaints about impaired urination, sweating, constipation, impotence, and the patient talks about the development of fainting only after abruptly getting out of bed or after sleep, then the development of chronic autonomic failure. In this case, the main danger for the patient is not the loss of consciousness itself, but the accompanying fall, since this often leads to fractures.

The patient should be advised not to get out of bed abruptly, to first sit down or make several movements with his legs while lying down, to use elastic bandages and bandages, to lay carpets in the bathroom and hallway, since these are the most common places for falls due to fainting in older people. It is advisable to take walks in the fresh air in places where there is no hard surface; you should not stand still for a long time.

If, during a neurological examination of the patient, signs of damage to the nervous system are revealed, a more thorough examination in a specialized hospital is necessary to clarify the cause of syncope and select an adequate treatment regimen.

Sudden disturbances of consciousness are one of the most important problems of clinical medicine, since they can be manifestations of various cerebral and somatic pathologies. One of the most common types of paroxysmal disorders of consciousness are syncope (fainting) states, which are attacks of short-term loss of consciousness and disturbances of postural tone with disorders of cardiovascular and respiratory activity and have a variety of pathogenetic mechanisms.

According to population studies, about 30% of adults had at least one fainting spell, syncope occurs in 4-6% of donors, in 1.1% of patients in dental clinics, during certain medical procedures (gastro-, esophageal-, broncho-, sigmoidoscopy), uncontrolled use of certain medications (vasoactive, antiarrhythmic, antihypertensive, etc.). However, most often the cause of fainting is various cerebral and somatic pathologies.

All of the above emphasizes the relevance and multidisciplinary nature of the problem and requires timely, correct syndromological and nosological diagnosis in order to select adequate methods of therapy. At the same time, there are significant difficulties in elucidating the causes of syncope, which is due not only to the episodic nature of fainting and their short duration, but also to the variety of causes and pathogenetic mechanisms of their development. Even with a thorough examination of patients in a hospital, in approximately half of the cases of syncope, their cause cannot be established, and only dynamic observation of the patient makes it possible to identify the main pathogenetic mechanisms of the development of fainting.

Classification

Considering the fact that syncope occurs in the clinical practice of internists of any profile, a unified approach to their classification is necessary.

Currently there are:

1. Neurogenic fainting: - psychogenic; - irritative; - maladaptive; - dyscirculatory.

2. Somatogenic syncope: - cardiogenic; - vasodepressor; - anemic; - hypoglycemic; - respiratory.

3. Syncopal states under extreme influences: - hypoxic; - hypovolemic; - intoxication; - medicinal; - hyperbaric.

4. Rare and multifactorial syncope: - nocturic; - cough.

In addition, considering fainting as a process unfolded over time, the severity of syncope is distinguished:

1. Presyncopal state: I degree - weakness, nausea, “spots” before the eyes; II degree - more pronounced symptoms described above with elements of impaired postural tone.

2. Syncope: I degree - short-term loss of consciousness for a few seconds without pronounced post-seizure syndrome; II degree - longer loss of consciousness and pronounced post-ictal manifestations.

Cases of nonsyncope (usually diagnosed as syncope)

1. Disorders with worsening or loss of consciousness:

Metabolic syndromes, including hypoglycemia, hypoxia, hyperventilation with hypocapnia;

Epilepsy; - intoxication;

Vertebrobasilar transient ischemic attacks.

2. Disorders similar to syncope without loss of consciousness:

Cataplexy;

Psychogenic syncope (somatic variants);

Panic attacks;

Transient ischemic attacks (TIA) of carotid origin;

Disturbances of consciousness, possibly secondary to metabolic effects on a cerebrovascular background;

Hysteria. Etiology and pathogenesis of syncope

The development of syncope is associated with an acute disturbance of cerebral metabolism as a result of deep hypoxia.

In most cases, syncope is primarily of neurogenic origin, but at the same time, it can be caused by somatic diseases. In a certain percentage of cases, fainting can also occur in practically healthy people under extreme conditions that exceed the limits of physiological adaptation capabilities. In this regard, it seems appropriate to distinguish syncope, characterized by a one-time development of fainting in extreme conditions that do not require therapeutic measures, and syncope, which occurs with a certain combination of cerebral disorders and pathology of internal organs. The latter is characterized by its development over time in terms of increasing frequency, severity, number of provoking factors, and the possibility of developing transitional states from fainting to epilepsy as a result of the formation of hypoxic encephalopathy.

Pathogenesis

The pathogenetic mechanisms of fainting are very diverse: insufficiency of blood supply to the brain due to disorders of systemic hemodynamics; local cerebral ischemia due to pathology of the main and cerebral vessels, reduction of cerebral metabolism caused by non-hemodynamic disorders (anemia, hypoglycemia, disorders of the gas and electrolyte composition of the blood, etc.). The leading factor in the pathogenesis of syncope is cerebral hypoxia. Of no small importance are reflex vasomotor disorders, as well as various visceral reflexes, especially the vagus nerve, the fundamental possibility of which is due to the presence of a large number of physiological connections between the gastrointestinal and cardiovascular systems.

When analyzing the pathogenesis of syncope, it is necessary to identify not only the mechanisms that cause fainting, but also predisposing factors. First of all, one should keep in mind hereditary predisposition. When studying the family history of relatives, one can identify cardiovascular pathology, vascular-vegetative disorders, and, less often, epilepsy and paraepileptic phenomena. According to our data, fainting occurs in 30% of relatives of patients suffering from syncope, and there is a tendency for them to appear earlier in children compared to parents and to occur in fathers and sons or mothers and daughters (less often in brothers and sisters).

The next important point predisposing to the occurrence of syncope is dysplastic development, which, according to our data, occurs in 63% of patients with fainting. The combination of 5-7 stigmas in them may indicate a high probability of nervous system dysplasia as a possible pathogenetic factor in the development of syncope. Most often, defects are identified such as irregular structure of the feet, narrow high palate, incorrect location and shape of teeth, deformations of the chest, discrepancy between the brain and facial skull, changes in the shape, size and location of the ears, heterochromia of the iris, etc.

Perinatal pathology, which occurs in 17% of patients, is of no small importance in the development of syncope. Most often, hypoxia or asphyxia of the fetus and newborn is observed as a result of various diseases of the mother during pregnancy and obstetric pathology. Often birth trauma is combined with clinical signs of dysembryogenesis, i.e. The nervous system of an abnormally developing fetus is more often affected. Fainting in such children develops at an earlier age compared to children without a history of birth trauma.

Thus, we can distinguish the following pathophysiological basis for the development of syncope: the initial inferiority of cerebral structures that provide hemodynamics adequate to various forms of activity, due to hereditary predisposition, dysplastic development and perinatal pathology; the formation of “syncope readiness” as a result of increasing dysfunction of stem structures against the background of repeated hypoxic conditions; development of a stable pathological state of the brain with a defect in systems that provide adequate general and cerebral blood flow. Clinical manifestations of syncope.

Clinic

Syncope, despite its short duration, is a process unfolding over time, in which successive stages can be distinguished: precursors (presyncope), peak (syncope itself) and recovery (postsyncope). The severity of clinical manifestations and the duration of each of these stages are very diverse and depend mainly on the pathogenetic mechanisms of developing syncope, which makes a thorough analysis of the symptoms at each stage of the development of syncope, as well as the factors provoking it, extremely important for differential diagnosis. Thus, most cardiogenic syncope occurs during exercise or immediately after its cessation.

Fainting with myxoma, globular thrombus in the left atrium and orthostatic hypotension develops during the transition from a horizontal to a vertical position. Vasodepressor syncope is observed during prolonged standing in a stuffy room. Hypoglycemic - with long breaks in food intake. Psychogenic - against the background of emotional influences that are significant for the patient, etc.

Immediately after the provoking situation, a presyncope (lipothymic) state develops, lasting from several seconds to several minutes. At this stage, severe general weakness, unsystematic dizziness, nausea, flickering of “spots”, “veils” before the eyes are observed, these symptoms quickly increase, there is a premonition of a possible loss of consciousness, noise or ringing in the ears. At this stage, patients have time to call for help, apply techniques to prevent loss of consciousness (sit or lie down, lower their head, go out into the air, take sweet tea, etc.). Against the background of clinical manifestations of the presyncope state that are common to all fainting, with individual syncope, it is possible to identify some of its features that are important for differential diagnosis.

Thus, with cardiogenic fainting, there may be pain and discomfort in the heart area, a feeling of lack of air, a feeling of “stopping”, “fading” of the heart. In patients with fainting-like epileptic paroxysms, before the development of loss of consciousness, a feeling of a “big head”, unmotivated fear, taste and auditory deceptions of perception, abdominal pain with the urge to defecate, etc. may occur. Development of intense pain syndrome in the epigastric region or behind the sternum in combination with a feeling of lack of air is noted when fainting when swallowing. A special cough is characteristic of bettolepsy (cough fainting). In syncope conditions caused by vertebrobasilar vascular insufficiency, in the precursor stage, increasing systemic dizziness, headache of occipital localization, nausea are detected, visual disturbances in the form of flickering scotomas, hemianopsia, etc. are possible.

Objectively

In the presyncope period, pallor of the skin, local or general hyperhidrosis, decreased blood pressure, pulse instability, respiratory arrhythmia are noted, coordination of movements is impaired, and muscle tone decreases. The paroxysm can end at this stage or move on to the next stage - the actual syncope state, in which all the described symptoms increase, patients slowly fall, trying to hold on to surrounding objects, and consciousness is impaired. The depth of loss of consciousness varies from slight stupefaction to deep disturbance lasting several minutes. During this period, there is a further decrease in blood pressure, weak pulse filling, shallow breathing, muscles are completely relaxed, pupils are dilated, their reaction to light is slow, tendon reflexes are preserved. With a deep loss of consciousness, short-term convulsions, often tonic, and involuntary urination may develop, which in itself is not a basis for diagnosing an epileptic seizure, but only indicates severe brain hypoxia.

The analysis of clinical manifestations in the post-syncope period is also important for differential diagnosis. As a rule, the restoration of consciousness occurs quickly and completely, patients immediately orient themselves in the environment and what happened, and remember the circumstances preceding the loss of consciousness. The duration of the post-syncope period ranges from several minutes to several hours. During this period of time, general weakness, non-systemic dizziness, dry mouth are noted, pale skin remains, hyperhidrosis, decreased blood pressure, and uncertainty of movements. In patients with cardiogenic syncope during the recovery period, unpleasant sensations in the heart area may persist; lethargy, drowsiness, and diffuse headache are observed after fainting that developed against the background of hypoglycemia. General cerebral and focal neurological symptoms (visual disorders, paresthesia, weakness in the limbs, vestibular disorders, etc.) can persist in the post-syncope period in patients with organic brain damage (brain tumors, cerebral vascular aneurysms, vertebrobasilar insufficiency, etc.).

Thus, a thorough study of the features of the development of syncope at different stages makes it possible to assume their triggering and implementing pathogenetic mechanisms. Methods for diagnosing and objectifying syncope

Diagnostic tasks

It includes two main points - determining whether the developed paroxysm belongs to syncope and its genesis.

Diagnosis of transient disorders of consciousness

In this case, the main task in the first stages is to establish whether fainting is one of the symptoms of urgent somatic pathology (myocardial infarction, pulmonary embolism, bleeding, etc.) or organic damage to the nervous system (brain tumors, cerebral vascular aneurysms, etc.), which can only be achieved with a comprehensive examination of the patient by a neurologist and therapist. The short duration of fainting and seeking medical help in the post-syncope or interictal period significantly complicates diagnosis and emphasizes the importance of a thorough study of anamnestic data not only about the structure of the paroxysm, but also hereditary factors, previous diseases, and medications used.

In this case, if possible, you should clarify with the patient and eyewitnesses the features of the presyncope period and fainting itself, as well as the clinical manifestations of the disease in the interictal period. Next, a thorough examination of the somatic and neurological status should be carried out, which will make it possible to determine a further plan for examining the patient to clarify the pathogenetic mechanisms and causes of syncope.

When examining a patient, it seems appropriate to study according to the following scheme:

I History:

1. The patient’s age at the time of the first fainting episodes.

2. Factors preceding the first syncopation.

3. Frequency, periodicity, stereotypicality and seriality of attacks.

4. Provoking factors: - pain; - long standing; - staying in a stuffy room; - change in head and body position; - exercise stress; - emotional stress; - long breaks in eating; - straining; - cough; - urination; - swallowing; - others (specify which ones).

5. Ways and techniques to prevent the development of loss of consciousness: - transition to a horizontal position; - change of head position; - intake of food, water; - Fresh air; - others (specify which ones).

6. Clinical manifestations in the presyncope period: - dizziness and its nature; - headache; - pain or discomfort in the chest; - abdominal pain; - palpitations, feeling of “stopping”, “fading” of the heart, interruptions; - feeling of lack of air; - ringing in the ears; - darkening before the eyes; - other symptoms (specify which ones); - duration of the presyncope period.

7. Clinical manifestations during fainting: - position of the patient; - skin color (pallor, cyanosis); - dry skin, hyperhidrosis; - rhythm and frequency of breathing; - filling, rhythm, pulse rate; - blood pressure level; - muscle condition (hypotonia, tonic, clonic convulsions); - tongue bite; - urination; - position of the eyeballs, condition of the pupils; - duration of loss of consciousness.

8. Clinical manifestations in the post-syncope period: - speed and nature of the return of consciousness; - attack amnesia; - drowsiness; - headache; - dizziness; - discomfort in the chest; - difficulty breathing; - palpitations, interruptions; - general weakness; - other manifestations (specify which ones); - duration of the post-syncope period.

9. The patient’s condition and manifestation of the disease outside of fainting.

10. Previous and concomitant diseases.

11. Previously used medications.

12. Paraepileptic phenomena in childhood and now (night headaches, fears, screams, sleep talking, sleepwalking, enuresis, febrile convulsions, paroxysms of speech disorders).

13. Hereditary factors (the presence of similar attacks of loss of consciousness in relatives, a family history of cardiovascular pathology, autonomic-vascular disorders, epilepsy, paraepileptic phenomena, etc.).

II. Study of somatic and neurological status:

1. External examination of the patient with an emphasis on constitutional features and signs of dysplastic development.

2. Palpation and auscultation of peripheral vessels.

3. Auscultation of the heart.

4. Measuring blood pressure on both arms in a horizontal and vertical position.

5. Study of neurological status with an emphasis on identifying microfocal symptoms.

6. Study of the state of the autonomic nervous system: - determination of autonomic tone according to A.M. Wein’s tables; - determination of autonomic reactivity (local and reflex dermographism, oculocardiac Aschner-Danyini reflex, temperature curves, orthoclinostatic test, etc.); - determination of vegetative support of activity using tests with physical and psycho-emotional stress.

III.Instrumental research methods, mandatory for all patients:

1. General blood and urine analysis.

2. Blood sugar during fainting, on an empty stomach, sugar curve with exercise.

3. ECG in the interictal period in dynamics, if possible during fainting.

4. X-ray examination of the heart, aorta, lungs.

IV. Additional examination of patients according to indications:

1. If cardiogenic syncope is suspected and in case of syncope of unknown origin: - X-ray examination of the heart with contrasting of the esophagus; - phonocardiography; - echocardiography; - ECG monitoring; - ECG test with physical activity (Master’s test, bicycle ergometry, etc.); - electrophysiological study of the heart according to a special program (in specialized departments);

2. If organic cerebral pathology is suspected and in case of syncope of unknown origin: - radiography of the skull and cervical spine, including with special placements; - examination of the fundus and visual fields; - electroencephalography; - evoked brain potentials, EEG monitor study (if epileptic genesis of paroxysms is suspected); - echoencephaloscopy and computed tomography (if space-occupying processes in the brain and intracranial hypertension are suspected); - Doppler ultrasound (if pathology of extra- and intracranial vessels is suspected).

Daily ECG monitoring in patients with episodes of syncope. Holter ECG monitoring is a mandatory method of examination in patients with syncope. Continuous Holter ECG monitoring with automatic activation of the device is indicated for patients who experience episodes of complete loss of consciousness and who are unable to independently attach or activate the “episodic recorder”. If syncope occurs weekly or monthly, or with even longer intervals between attacks, continuous ECG monitoring does not make sense.

More informative in these cases is event-based ECG monitoring with activation of the device by the patient and the possibility of further transmission of the ECG signal by telephone. “Loop” monitoring is carried out during short-term attacks, when it is problematic to have time to record a regular ECG after the onset of symptoms. The device for “loop” monitoring is most appropriate to use for infrequent, mild, but persistent symptoms that may be due to arrhythmia.

Tilt test

This is the most commonly used method in studying the mechanisms of autonomic dysregulation and the development of syncope. In its simplest form, the tilt test involves changing the patient's body position from horizontal to vertical. In this case, under the influence of gravitational forces, blood is deposited in the lower part of the body, the filling pressure of the right chambers of the heart decreases, which triggers a whole group of reflexes. Normally, this change in body position increases the sympathetic response with arteriolar vasoconstriction and increased myocardial contractility.

In patients with SCS, cardiovagal tone increases and arteriolar vasodilation occurs, which can lead to sudden systemic hypotension and cardiac arrest with an attack of loss of consciousness. Classification of positive responses to the tilt test: 1. Type 1 - mixed: heart rate decreases during syncope, but not below 40 beats/min. or decreases to less than 40 beats/min, but not more than 10 seconds, with or without a period of asystole of less than 3 seconds. Before the heart rate decreases, blood pressure decreases.2. Type 2A - cardioinhibitory without asystole: heart rate decreases to at least 40 beats/min for 10 seconds, but asystole does not occur for more than 3 seconds. Before the heart rate decreases, blood pressure decreases.3. Type 2B - cardioinhibitory with asystole: asystole occurs for more than 3 seconds. Blood pressure decreases simultaneously with a decrease in heart rate.4. Type 3 - vasodepressor: Heart rate does not decrease by less than 10% of heart rate during syncope.

As a result of a thorough somatic and neurological examination of the patient, a final diagnosis is formed, which includes not only the underlying disease, but also the clinical variant of syncope with its leading pathogenetic mechanisms, which guides the doctor towards the possibility of etiological and pathogenetic treatment in each specific case.

General characteristics of cardiogenic syncope

Syncope can develop with various cardiac pathologies (myocardial infarction, malformations, heart failure, cardiomyopathy, etc.), leading to disorders of systemic and cerebral hemodynamics and transient disorders of cerebral metabolism. The most common causes of these disorders are mechanical obstruction to blood flow (with aortic stenosis, cardiomyopathy, pulmonary hypertension, atrial myxoma, etc.) and heart rhythm disturbances, as well as their combination.

It should be borne in mind that fainting can be the first, and sometimes the only clinical manifestation of the disease, being, in particular, a “signal symptom” for heart rhythm disorders. In such cases, patients who have not previously been observed by internists are often sent to neurological hospitals with diagnoses of “condition after an unknown seizure”, “cerebral vascular crisis”, “dyscirculation in the vertebrobasilar system”, etc.

In young people in these cases, epilepsy is often diagnosed, and anticonvulsants are prescribed without a thorough cardiac examination, while paroxysmal disorders of consciousness are caused by heart rhythm disturbances. Taking into account the above data, it becomes obvious the need for a thorough examination of the cardiovascular system using all modern research methods, not only in patients with indications in the anamnesis of a possible cardinal pathology, but also in syncope and convulsive conditions of unknown origin. On the other hand, it has been shown that even with a thorough cardiological examination of patients, some of them do not find any cardiac pathology leading to heart rhythm disturbances.

This gives reason to say that arrhythmias can be caused not only by primary damage to the heart, but also by extracardiac factors (increased intracranial pressure, irritation of the vessels of the circle of Willis, damage to the hypothalamic and temporal regions, reticular formation, autonomic-vascular and neuroendocrine disorders, etc. ), which in turn dictates the need for a thorough neurological examination of patients with syncope as a result of heart rhythm disorders. ECG changes leading to syncope: - bifascicular block (a combination of blockade of any branches of the left leg - the anterosuperior and posteroinferior branches of the left bundle branch and blockade of the right bundle branch); - other anomalies of AV conduction (QRS duration 0.12 s or more); - AV block (Mobitz I) and other options; - asymptomatic sinus bradycardia (<50 ударов/мин) или синоатриальная блокада;- синдромы преэкзитации;- удлинение интервала QT;- блокада правой ножки пучка Гиса с элевацией сегмента ST - в отведениях V1 -V3 (синдром Бругада);- негативный зубец T в правых грудных отведениях, эпсилон волна и поздние потенциалы желудочков;- врожденная аритмогенная дисплазия правого желудочка; - Q-инфаркт миокарда.

Minimum protocol for electrophysiological studies to diagnose syncope:

1.Measurement of sinus node function recovery time (SVFSU) - the longest post-stimulation pause - independent of stimulation frequency. Corrected sinus node function recovery time (CRST) is the difference between the duration of the post-stimulation pause and the duration of the spontaneous cardiac cycle. Blockade of autonomic regulation is used if sinus node dysfunction is suspected (if the above indicators are not informative).

2. Evaluation of the His-Purkinje system includes measurement of the HV (conduction from the His bundle to the ventricular myocardium) interval at the beginning of the study and after pacing the atria with increasing frequency. If the results are questionable, pharmacological tests are recommended: ajmaline (1 mg kg IV), procainamide (10 mg per kg IV), or disopyramide (2 mg per kg IV).

3. Assessment of ventricular arrhythmia, its induction by programmed stimulation of the ventricles in two areas in the region of the right ventricle (apex and outflow tract), at two frequencies of the imposed rhythm: a) 100 or 120 beats per minute and b) 140 or 150 beats per minute with two extrastimuli ( a third extrastimulus can be applied additionally, which will increase sensitivity but reduce specificity).

4. Evaluation of supraventricular arrhythmia caused by any atrial stimulation protocols.

For the first time, syncope as a result of cardiac arrhythmia can occur at different age periods, depending on etiological factors. However, it should be noted their high frequency in childhood (with congenital heart defects, Jerville-Lange-Nielson and Romano-Ward syndrome, etc.) and in people of older age groups. The factors that provoke such fainting are physical or emotional stress; less often, they occur when standing for a long time in a stuffy room, under the influence of painful stimuli. As a rule, patients do not indicate techniques to prevent paroxysms; only in some cases can a transition to a horizontal position be effective. Fainting develops in different positions of the patient, often lying down, and is repeated when trying to get up after the first paroxysm in the absence of stabilization of the heart rhythm. When analyzing the stages of development of fainting, attention is drawn to a short presyncope period with unpleasant sensations or pain in the heart area, sensations of “stopping”, “freezing” of the heart or palpitations, unsystematic dizziness, severe general weakness, darkening before the eyes, ringing in the ears, a feeling of heat in the head , unpleasant sensations in the epigastric region.

In some patients, the presyncope period may be absent, resulting in a rapid fall and injury, which makes these paroxysms similar to epileptic seizures. During fainting, pallor of the skin is noted, often with acrocyanoea, sticky cold sweat, frequent shallow breathing with difficulty exhaling, bradycardia with a heart rate of 32-48 per minute, rhythm disturbances, less often - tachycardia up to 150-180 beats per minute, preceding the development asystole, blood pressure drops to 90/60 mm Hg, then becomes undetectable.

Most patients experience diffuse muscle hypotension during loss of consciousness, but with deep loss of consciousness, convulsions, involuntary urination, and tongue bite are possible, which also makes them similar to. epileptic seizures. The duration of loss of consciousness is usually 1-2 minutes, less often - up to 3 minutes, the severity of fainting is I-II, more severe attacks are less common. Unlike epileptic seizures, consciousness returns immediately and completely; there is no amnesia for seizures.

In the post-syncope period, lasting from 5 minutes to an hour, severe general weakness, diffuse headache, non-systemic dizziness, pain and discomfort in the heart are noted; in some cases, the post-syncope period may be absent. As a rule, all syncopes develop stereotypically; their seriality is often noted (3-4 in a row when trying to get up after the first paroxysm in the absence of stabilization of the heart rate). The frequency of syncope ranges from 1-2 per year to 1-2 per 2-3 months.

Thus, cardiogenic syncope occurs predominantly after physical or emotional stress and is characterized by the rapid development of signs of circulatory failure and a serial occurrence. Syncope in certain forms of cardiac pathology Fainting in patients with mitral valve prolapse (MVP) occurs in 4-6% of cases. Most often, their development is associated with transient heart rhythm disorders (ventricular extrasystole, paroxysmal tachycardia, etc.), which are detected at rest in 50% of patients, and during physical activity in 75% of cases. The clinical picture of syncope with MVP, as a rule, does not differ from that with cardiogenic syncope of other etiologies.

It should be borne in mind that fainting can be the first, and sometimes the only manifestation of prolapse, and also precede sudden death as a result of ventricular fibrillation. At the same time, they can be combined with other neurological manifestations of MVP: migraine headaches, vegetative-vascular disorders with a predominance of sympathoadrenal activity, transient ischemic attacks, mainly in the vertebrobasilar system, etc. When examining patients, multiple dysplastic stigmas, asthenic physique, rapid fatigue during physical and mental stress, decreased performance, pain in the heart, palpitations, interruptions, shortness of breath during physical activity. In some patients, you can listen to the systolic murmur at the apex, register changes on the ECG (sinus tachycardia, WPW syndrome, signs of myocardial changes in the posterior wall, etc.).

On neurological examination in patients, microfocal symptoms are detected, which are caused by the inferiority of congenital cerebral structures (taking into account the signs of dysembryogenetic development) and repeated hypoxic states of the brain.

Syncope in patients with long QT interval syndrome (LQT): congenital (Jervell-Lange-Nielsen and Romano-Ward syndrome) and acquired (hypokalemia, hypocalcemia, intoxication with digitalis, quinidine, phenothiazides, infectious-toxic conditions, myocardial hypoxia, etc. ) character are leading in the clinical picture of the disease. The uniqueness of paroxysms and the absence of heart rhythm disturbances in the interictal period often lead to overdiagnosis of epilepsy in these patients, especially in childhood; the frequency of erroneous diagnoses reaches 20%. Syncope in patients with congenital long QT interval syndrome develops already in early childhood. Attacks occur during physical and emotional stress, they are caused by the development of ventricular fibrillation, less often - ventricular tachycardia, and even less often - ventricular asystole, leading to insufficiency of cardiac output and severe cerebral hypoxia.

Clinical picture of fainting is similar to that for other arrhythmogenic syncope; tonic and clonic convulsions and involuntary urination are often observed. The frequency of paroxysms can vary: from once every few years to several times a day; with age, fainting can become more frequent. In addition to syncope, these patients may experience attacks without loss of consciousness with a sudden cessation of movements, chest pain (sometimes abdominal pain), cardiac arrhythmia, and dizziness. In addition, sudden death may develop as a result of severe heart rhythm disorders (asystole and ventricular fibrillation). Paroxysmal conditions in Jervell-Lange-Nielsen syndrome are combined with congenital deaf-muteness, but this is not observed in Romano-Ward syndrome. In both patients, hereditary transmission of the disease occurs, while a clear accumulation of severe forms in descending generations is not observed.

Syncope in hypertrophic cardiomyopathy is mainly caused by the presence of a mechanical obstruction to blood flow, while heart rhythm disturbances are additional factors in their development. Mostly, these faints develop in men 40-50 years old during physical exertion, accompanied by pain in the heart, a feeling of lack of air; during an attack, a decrease in blood pressure and a weak, slow pulse are recorded; cramps and involuntary urination are rare.

In the post-syncope period, discomfort in the heart area, general weakness, and amnesia of attacks may persist. Fainting recurs with a frequency of 1-2 per month to several times in life; an increase in the frequency of attacks is a prognostically unfavorable sign. It should be borne in mind that the use of drugs with a positive inotropic effect, vasodilators and diuretics in such patients can lead to an increase in the degree of dynamic obstruction and the appearance or frequency of attacks.

In addition to fainting, patients with hypertrophic cardiomyopathy may also experience other neurological disorders: migraine-like headaches, dizziness, transient cerebrovascular accidents, decreased memory, work ability, etc. In the interictal period, the ECG reveals signs of myocardial hypertrophy with the formation of left bundle branch block, X-ray examination reveals left ventricular hypertrophy, dilatation of the ascending aorta; the diagnosis is confirmed by echocardiography.

A rare cause of syncope is a myxoma or globular thrombus in the left atrium; fainting in these cases develops as a result of a mechanical obstruction to blood flow (atrioventricular orifice obstruction). A feature of syncope in such patients is their development when changing body position (when moving from a horizontal to a vertical position). During the attack, severe cyanosis and signs of cardiac arrest are observed. The diagnosis is confirmed by echocardiography.

Syncope during myocardial infarction develops as a result of cerebral hypoxia caused by hemodynamic disturbances and is observed in 13% of patients. As a rule, fainting occurs during myocardial infarction of the posterior wall, and there is often no pain syndrome, and ECG signs are recorded only on days 2-5 of the disease. Loss of consciousness may be the first symptom of a developing heart attack, precede the onset of cardiogenic shock, complicate its course and complicate diagnosis. In the clinical picture of syncope during myocardial infarction, some features can be noted: the development of fainting in any position of the patient, combination with signs of cardiogenic collapse (pale skin, sticky cold sweat, shortness of breath, decreased blood pressure, vomiting, oliguria), deep loss of consciousness, tendency to a serial occurrence when trying to get up after the first paroxysm.

Diagnosis is possible with a dynamic ECG study and identification of biochemical resorptive-necrotic syndrome.

Irritative syncope

They arise as a result of irritation and repercussion from the receptor zones of the vagus nerve with the formation of pathological viscero-visceral reflexes. This group includes syncope that develops with neuralgia of the glossopharyngeal nerve, hypersensitivity of the carotid sinus, swallowing, some forms of pathology of internal organs (achalasia cardia, esophagocardiospasm, damage to the biliary tract, duodenum, etc.), as well as during endoscopic studies.

Fainting in these cases develops only when exposed to a provoking factor specific to each form (swallowing, irritation of the carotid sinus, a special attack of pain, etc.) “they have a short (several seconds) presyncope period with pain, a feeling of lack of air. During loss of consciousness lasting for no more than 1 minute, pallor of the skin, sticky cold sweat, rare breathing, absence of pulse, diffuse muscle hypotension are noted.The postparoxysmal period, as a rule, is absent, and a clear stereotypicality of attacks is revealed.

Syncope with neuralgia of the glossopharyngeal nerve develops against the background of intense pain (burning, shooting pain in the root of the tongue, pharynx, upper pharynx, often in the ear); sometimes the pain is preceded by fainting, which makes their differential diagnosis difficult. During such a faint, an ECG can record bradycardia with asystole for several seconds.

With hypersensitivity of the carotid sinus, fainting develops as a result of its irritation and can be of three types: cardioinhibitory (cardiac arrest with a subsequent drop in blood pressure), vasodepressor (with a pronounced primary drop in blood pressure) and cerebral (rapid loss of consciousness without pronounced changes in pulse and blood pressure ).

Fainting when swallowing is provoked by eating and occurs against the background of chronic coronary heart disease with angina at rest or exertion in combination with pathology of the gastrointestinal tract (esophageal diverticulum, hiatal hernia, etc.). The ECG records signs of myocardial ischemia, and during syncope it is possible to detect cardiac arrhythmias. It is possible to identify the dependence of the frequency of fainting on the state of cardiac activity (an increase in the frequency of paroxysms with an increase in angina attacks and a deterioration in coronary blood flow). At the same time, fainting when swallowing has also been described in practically healthy people when drinking cold and carbonated drinks under conditions of overheating.

Vestibular syncope is observed in patients with Menier's disease or syndrome, labyrinthine injuries, and peripheral vestibulopathies. In the presyncope period, systemic dizziness and pronounced sideways staggering are noted. Often such fainting develops without an immediate cause; patients suddenly fall, often in the same direction, and receive bruises. There is often no post-syncope period. This makes these fainting episodes similar to epileptic seizures. The diagnostic criteria are the suddenness of the fall and a very short period of loss of consciousness, systemic dizziness in combination with impaired coordination, the absence of pronounced vegetative manifestations (weakness, darkening before the eyes, pronounced changes in blood pressure, pulse, etc.).

Fainting with esophagocardiospasm and achalasia cardia occurs when eating food while it passes through the esophagus, which is often accompanied by angina pain. At the same time, with a long-term illness, fainting can be provoked by emotional stress and various pain crises not related to the passage of food. When recording an ECG during an attack of loss of consciousness, various heart rhythm disturbances can also be detected.

Thus, to identify the leading pathogenetic mechanisms of irritative syncope, it is necessary to conduct a thorough somatic examination, primarily cardiological, as well as a study of the function of the gastrointestinal tract in combination with a neurological examination and EEG recording to identify dysfunction of the midline structures of the brain. Maladaptive syncope

The leading factor in the pathogenesis of this group of syncope is

There is insufficiency of the ergotropic function of the nervous system, which manifests itself under conditions of increasing loads (motor, orthostatic, thermal, etc.), as well as unfavorable environmental conditions. This group includes vasovagal syncope, as well as orthostatic and hyperthermic syncope. Vasovagal syncope is the most common type of short-term loss of consciousness and, according to various authors, accounts for from 28 to 93% of syncope.

The leading factor in the pathogenesis of these fainting spells is a sharp decrease in total peripheral resistance with dilatation of peripheral vessels. In most patients, the first fainting occurs during the period of intensive growth and puberty; in women, a connection between syncope and the menstrual cycle and pregnancy is sometimes revealed. Fainting develops under the influence of various provoking factors: * staying in a stuffy room; * prolonged standing, painful stimulation; * emotional reactions (type of blood, preparation for injections, dental treatment); * overwork and physical stress; * overheating in the sun, in the bath; * long breaks in eating, etc.

Some patients experience an increase in the number of provoking factors over time. To prevent syncope, patients try to sit or lie down, go out into the fresh air, eliminate the traumatic situation, painful stimuli, and take a few steps in place. Using such techniques, it is sometimes possible to interrupt the development of paroxysm at the lipothymia stage. Vasovagal syncope develops only in an upright position and has a clear stage pattern. In the presyncope period, lasting 1-3 minutes, there is darkness before the eyes, severe general weakness, ringing in the ears, a feeling of lightheadedness; patients manage to sit up and call for help before loss of consciousness develops. During fainting, patients turn pale, there is local or general hyperhidrosis, rare breathing, a drop in blood pressure, then the pulse becomes thread-like and disappears, and diffuse muscle hypotension is noted. The duration of loss of consciousness is 1-2 minutes. In the post-syncope period, a sharp general weakness is observed for 5-60 minutes, diffuse or localized headache in the frontotemporal regions, non-systemic dizziness, and dry mouth are possible.

Seriality in the development of attacks is rare, their frequency ranges from 1-2 per month to 2-3 per year. The greatest number of attacks occurs between 16 and 20 years of age. In the interictal period, patients exhibit permanent and paroxysmal vegetative disorders: * general weakness; * increased fatigue; * decreased performance; * unstable blood pressure; * poor tolerance of high and low temperatures; * increased chilliness; * prolonged low-grade fever; * metabolic and endocrine disorders (obesity, weight loss, late onset of menstruation, algodismenorrhea, hypo- or hyperfunction of the thyroid gland, etc.); * disturbances in the rhythms of sleep and wakefulness, difficulty falling asleep, shallow sleep with frequent awakenings, lack of a feeling of rest after a night's sleep * tendency to allergic reactions. Fainting in some patients can be combined with migraine headaches and sympathoadrenal crises.

In the majority of patients, the neurological status reveals microfocal symptoms: nystagmoid in the extreme abductions of the eyeballs, weakness of convergence, diffuse muscle hypotonia, tendon anisoreflexia, facial asymmetry, etc. In addition, in these patients, attention is drawn to the pronounced instability of autonomic reactions, vascular tone, the predominance of parasympathetic reactions in the study of autonomic position reflexes and the Aschner-Dagnini test. Various types of emotional disorders are also revealed in them (increased irritability, phobic manifestations, low mood, hysterical stigmas, etc.).

Criteria for diagnosing vasovagal syncope

The presence of clear provoking factors and conditions for the development of fainting

Staging

Signs of psychovegetative syndrome in the interictal period

Slow wave activity in the EEG during syncope.

Syncope in idiopathic orthostatic hypotension (Shy-Drager syndrome) is dominant in the clinical picture of the disease. Idiopathic orthostatic hypotension is a disease of the nervous system of unknown etiology, a progressive course, the manifestation of which is a drop in blood pressure in an upright position.

Fainting develops when the patient moves from a horizontal to a vertical position or during a prolonged stay in a vertical position. In mild cases, after standing up, patients experience a feeling of lightheadedness, blurred vision, a feeling of heat in the head, ringing in the ears, a premonition of a possible loss of consciousness, with pallor of the skin and a decrease in blood pressure; this state lasts for several seconds and is called lipothymia. In severe cases, following the lipothymic state, loss of consciousness of varying duration develops, during which there is marked pallor and dryness of the skin, a drop in blood pressure, sometimes to zero, a threadlike but stable pulse, dilated pupils, a sharp decrease in muscle tone, with deep loss of consciousness, possible urination and tonic convulsions.

When moving to a horizontal position, blood pressure gradually increases, consciousness returns, and severe general weakness and sometimes drowsiness are noted. In the interictal period, in the absence of gross focal neurological symptoms, the patient’s peculiar gait draws attention - a wide, fast step, the legs are slightly bent at the knee joints, the torso is tilted forward, the head is lowered.

In order to increase the venous return of blood to the heart, patients tense their leg muscles, cross them, and squat. In addition to lipotinic and syncope, patients often exhibit other symptoms of progressive autonomic failure: hypo- or anhidrosis, “fixed” pulse, nonspecific gastrointestinal symptoms (diarrhea, constipation, anorexia, feeling of a full stomach after eating, etc.), impotence and etc.

Criteria for differential diagnosis

Development of syncope during the transition from a horizontal to a vertical position

Drop in blood pressure during syncope at normal heart rate

Detection of postural hypotension in the interictal period (a drop in systolic pressure of at least 30 mm Hg when moving from a horizontal to a vertical position)

Positive orthostatic test (sharp drop in blood pressure when standing up in the absence of compensatory tachycardia)

Detection of a gradual decrease in blood pressure during a 30-minute standing test

No increase in the concentration of aldosterone and catecholamines and their excretion in urine upon rising.

Discirculatory fainting

Syncopal vertebral syndrome of Unterharnscheidt develops with osteochondrosis, deforming spondylosis and some other lesions of the cervical spine. Syncope is the leading condition in the clinical picture of the disease, occurs in people of various age groups, and is provoked by turns and hyperextension of the head. In the presyncope period, severe headaches, tinnitus, and photopsia are sometimes observed, then a sudden and complete loss of consciousness occurs with a decrease in blood pressure and pronounced muscle hypotension, which persists in the postsyncope period.

This syndrome is associated with primary irritation of the spinal nerve and secondary vascular disorders in the vertebrobasilar system, leading to acute ischemia of the reticular formation and chiasm of the pyramids. In some cases, the development of severe syncopal paroxysms is preceded by drop attacks without loss of consciousness, which is also associated with sudden ischemia of the brain stem, as well as with a special functional state of the reticular formation, which contributes to periodic disruptions in the regulation of muscle tone even with minor ischemia.

Diagnosis is based, in addition to a thorough analysis of the characteristics of fainting, on an X-ray examination of the spine, which reveals the phenomena of cervical osteochondrosis in the form of uncovertebral arthrosis, subluxation according to Kovach, etc. In some cases, there is a need for angiography, which detects kinks, compression of the arteries by osteophytes, anomalies of their development (pathological tortuosity), stenosis, etc.

Syncope with vascular insufficiency in the carotid arteries (most often as a result of occlusion of one of them) develops with compression of the neck, sometimes without an obvious reason, and is much less common than with circulatory insufficiency in the vertebrobasilar system. Most often, loss of consciousness occurs in an upright position of the patient, but can develop while sitting or lying down. The presyncope period is often absent, but non-systemic dizziness and general weakness may be noted.

During loss of consciousness, pale skin is noted, sometimes with acrocyanosis, shallow breathing, a rare pulse, blood pressure can either increase or decrease. There are no convulsions, urination, tongue biting, or bruises when falling, and no serial attacks are noted. In the post-syncope period, diffuse headache, severe general weakness develop, and focal neurological symptoms (paresis, disturbances in sensitivity, speech, etc.) may be detected.

Along with syncope, patients experience headaches, transient hemiparesis, hemianopsia, and hemihypersthesia. Diagnosis is facilitated in the presence of weakened pulsation of the carotid artery; when a healthy vessel is pressed, focal symptoms increase; occlusion of the carotid artery is confirmed by Doppler sonography.

Fainting with aneurysms of cerebral vessels is rare; it can occur with arterial aneurysms in the vertebrobasilar system and arteriovenous aneurysms. Loss of consciousness occurs as a result of disturbances in the circulation of liquor in giant aneurysms, as well as as a result of their tears or ruptures.

In the presence of giant aneurysms in the pre-hemorrhagic period, loss of consciousness with pronounced weakness of the leg muscles occurs with sudden changes in the position of the head and torso, patients fall, break, convulsions, urination, tongue biting, as a rule, do not occur during loss of consciousness, as well as in post-syncope period, it is possible to identify transient focal neurological symptoms (anisocoria, strabismus, facial asymmetry, anisoreflexia, pathological foot reflexes, etc.).

These attacks can be combined with episodes of falling as a result of severe muscle weakness without loss of consciousness. Syncope may develop prior to aneurysm rupture, followed by subarachnoid hemorrhage as a result of small, diapedetic hemorrhages through the aneurysm wall or wall tears accompanied by vasospasm. In these cases, short-term loss of consciousness occurs against the background of headache, accompanied by photophobia, vomiting, non-systemic dizziness, diplopia, blurred vision, and sometimes it is possible to detect stiffness of the neck muscles. More often, loss of consciousness occurs when aneurysms rupture with the development of subarachnoid hemorrhage, while in addition to pronounced general cerebral symptoms (headache, vomiting), meningeal syndrome and focal neurological symptoms are detected, depending on the location and type of aneurysm.

Diagnosis of syncope developing against the background of cerebral aneurysms is extremely difficult, especially in cases where fainting is rare and no other symptoms are noted in the interictal period. At the same time, the development of loss of consciousness due to headache in combination with meningeal syndrome should alert us to the possible presence of an aneurysm of cerebral vessels with a tear or rupture of its wall. Lumbar puncture and angiography are important for diagnosis.

Fainting due to Arnold-Chiari malformation

Arnold-Chiari malformation is characterized by displacement of areas of the cerebellum or brain stem into the spinal canal due to impaired development of the posterior cranial fossa. Syncope in this form of pathology can occur against the background of a detailed clinical picture of the disease, less often - at its debut. Fainting develops when the head position changes, straining, or physical exertion. Their peculiarity is the preservation of the number of heart contractions and blood pressure during loss of consciousness. The EEG can record a slowing of the rhythm during an attack.

The pathogenetic mechanisms of these paroxysms are disturbances in liquor outflow and compression of the midbrain, which causes dysfunction of the ascending activating systems of the reticular formation. In the interictal period, patients complain of occipital headaches, dizziness, nausea, and visual disturbances. The examination reveals signs of dysplastic development, focal neurological symptoms in the form of narrowing of visual fields, nystagmus, dysarthria, symmetrical increase in tendon and periosteal reflexes, impaired pain and temperature sensitivity, ataxia, etc.

To clarify the diagnosis, a thorough X-ray examination of the craniovertebral region using special installations and computed tomography are required.

Syncope in brain tumors

Most often, fainting occurs with space-occupying processes in the posterior cranial fossa and temporal lobes of the brain. The reason for their development is disturbances in liquor circulation. Attacks occur when changing the position of the head, standing up abruptly, or at the height of the headache, and severe respiratory and circulatory disorders are noted - severe bradycardia, a drop in blood pressure, and respiratory arrest. During an attack, focal neurological symptoms of varying severity are revealed (anisocoria, strabismus, gaze paresis, hemiparesis, anisoreflexia, pathological reflexes, etc.). In the post-syncope period, general cerebral and focal neurological symptoms may persist. In the interictal period, hypertensive headaches and symptoms of damage to the structures of the posterior cranial fossa are often observed.

With large-scale processes of the temporal lobe, fainting-like paroxysms may be the only clinical symptoms of the disease; sometimes in the structure of an attack it is possible to identify taste or olfactory deceptions of perception before or after its development. Diagnosis is not difficult in the presence of pronounced cerebral symptoms, loss of consciousness at the height of headache, and identification of focal neurological symptoms. Difficulties arise in cases where syncope is the only clinical symptom of the disease.

To clarify the genesis of paroxysmal conditions, it is necessary to carry out the entire complex of neurological and neurosurgical examination of the patient: examination of the fundus, visual fields, X-ray examination of the skull, echoencephalography, electroencephalography, computed tomography, etc.

Fainting-like form of epilepsy

Fainting-like paroxysms can be the debut of epilepsy, while their true genesis can only be established retrospectively, but with the addition of developed general convulsive paroxysms. The clinical relationship between fainting and epilepsy and the possibility of their combination in the same patient reflect the presence of a common pathogenetic factor, which is cerebral hypoxia. Mild degrees of hypoxia can be clinically manifested by simple fainting or contribute to the development of hypersynchronous discharge and epileptic seizure. In addition, fainting-like seizures can occur as an independent form of epilepsy, as a transition from true fainting to epileptic fainting, and also be part of the structure and be a component of temporal lobe epilepsy.

Fainting-like epileptic paroxysms first appear during critical age periods (4-5,12-15,16-18 years). Factors that provoke the first paroxysms can be lack of sleep, overwork, and alcohol intake. In the future, an increase in the number of provoking factors may be observed, and attacks develop both under the influence of factors characteristic of provoking vasovagal syncope (prolonged standing, staying in a stuffy room, painful stimulation, psycho-emotional reactions, etc.), and under the influence of factors typical for provocation epileptic seizures (taking small doses of alcohol, watching TV, lack of sleep). In addition, attention should be paid to the discrepancy between the severity of the developing paroxysm and the nature of the provoking effect.

Individual attacks can occur without the influence of provoking factors, and the same patient may have syncope that develops under the influence of provoking factors characteristic of vasovagal syncope, specific to the provocation of epileptic seizures, and also occurring spontaneously. As a rule, with fainting-like epileptic paroxysms, patients fail to develop techniques that prevent the development of loss of consciousness.

Unlike other types of fainting, fainting-like epileptic seizures can develop in any position of the patient. The presyncope period is usually short, similar to that of vasovagal syncope. At the same time, in the structure of the presyncope period there may be phenomena that can be regarded as an aura of an epileptic seizure (a feeling of a “big head”, unmotivated fear, auditory and taste deceptions of perception, abdominal pain with the urge to defecate, etc.). Individual attacks occur without a clear presyncope period.

Loss of consciousness occurs quickly, patients do not have time to sit up or call for help, fall, and receive various traumatic injuries. During loss of consciousness, pale skin, acrocyanosis, general hyperhidrosis, rapid breathing are noted, blood pressure can either increase or decrease, and tachycardia is detected. Sometimes during an attack, urination and tongue biting are noted. In the post-syncope period, headache, weakness, and drowsiness are possible. At the same time, there may be no post-syncope period. Sometimes amnesia of individual attacks is observed. In patients with fainting-like paroxysms, there is a tendency for them to occur serially (2-3 in a row). There are two possible types of disease progression before pathogenetic therapy is prescribed: a rapid increase in the frequency of attacks with the development of asthenic syndrome; addition to fainting-like paroxysms of other paroxysmal disorders of consciousness, including general seizures.

In the interictal period, most patients do not experience any other symptoms of the disease; some of them exhibit migraine headaches, decreased performance, fatigue, and moderate mnestic disturbances. A somatic examination does not reveal any pathology; in the neurological status, most patients have microfocal symptoms (nystagmoid in extreme abductions of the eyeballs, weakness of convergence, tendon anisoreflexia, impaired performance of coordination tests, etc.).

Important for diagnosis is the analysis of the family history of patients, where it is possible to identify epilepsy, paraepileptic phenomena, and fainting more often than in patients with syncope of other etiologies. To clarify the diagnosis, it is necessary to dynamically monitor the patient with repeated electroencephalography, which often reveals epileptic phenomena (sharp waves, peaks, spikes, acute-slow wave complexes, high-amplitude hypersynchronous alpha rhythm, etc.). At the same time, the absence of epileptic activity on the EEG, especially during a single study, does not exclude the epileptic nature of the paroxysm.

Under conditions of hyperventilation, the percentage of detection of pathological changes on the EEG increases; in some cases, functional tests reveal typical epileptic activity. Sometimes, to clarify the epileptic genesis of paroxysms, it is useful to prescribe anticonvulsants, leading to a reduction or cessation of attacks.

Thus, the criteria for diagnosing fainting-like epileptic paroxysms are the following symptom complex proposed by L.G. Erokhina and N.I. Levitskaya in 1974:

• discrepancy between the functional significance of the provoking factor and the severity of paroxysms;
• the possibility of serial attacks occurring at intervals of several minutes;
• the uniqueness of the post-attack period (sleep, headache, confusion);
• the presence of family-hereditary manifestations of epilepsy;
• the presence of isolated episodes in a series of fainting-like attacks, the epileptic nature of which cannot be doubted;
• identification of clear epileptic activity on the EEG in a patient with syncope;
• the appearance of epileptic activity during functional loads;
• positive effect of treatment with anticonvulsants.

Treatment of patients with syncope

Treatment of patients with syncope includes provision of emergency care at the time of fainting and complex therapy in the interictal period, taking into account the main pathogenetic mechanisms.

Therapeutic measures during fainting

First of all, it is necessary to carry out measures aimed at improving blood supply and oxygenation of the brain: eliminate provoking factors, transfer the patient to a horizontal position, provide access to fresh air, free from restrictive clothing, and perform a light body massage. For a reflex effect on the centers of breathing and cardiovascular regulation, inhalation of ammonia vapor and splashing the face with cold water are recommended.

In case of severe fainting and no effect from the measures taken, in cases of a pronounced drop in blood pressure, sympathicotonic agents are administered: 1% mesatone solution, 5% ephedrine solution; for bradycardia or cardiac arrest, a 0.1% solution of atropine sulfate and chest compressions are indicated; for cardiac arrhythmias, antiarrhythmic drugs are indicated. In case of severe and prolonged fainting with severe disturbances of cardiac activity and breathing, it is necessary to carry out the entire complex of resuscitation measures, ensuring urgent hospitalization of the patient.

Treatment of patients in the interictal period

It is difficult to recommend a single treatment regimen for patients in the interictal period, since the causes and pathogenetic mechanisms of development of various variants of syncope are very diverse. Prescription of treatment is possible only after a thorough examination of the patient and substantiation of the diagnosis not only of the underlying disease, but also clarification of the leading pathogenetic mechanisms of the development of fainting.

In the treatment of patients with syncope, one can distinguish undifferentiated therapy, which is indicated for patients with various types of fainting, and differentiated therapy, used to treat individual clinical forms. Undifferentiated therapy is aimed at reducing the degree of neurovascular excitability and reactivity, increasing autonomic and mental stability. To increase mental stability, various psychotropic drugs are used, prescribed depending on the leading psychopathological syndrome with individual selection of drugs and dosages and a duration of use of 2-3 months.

If anxiety is dominant, the use of seduxen, relanium, elenium, grandoxin, etc. is indicated. Taking antelepsin 1 mg 3-4 times a day for 1-1.5 months is very effective. Antidepressants (amitriptyline, azaphene, pyrazidol, etc.) are prescribed for latent and overt depressive states. For severe anxiety-hypochondriacal disorders, the use of antipsychotics (Sonapax, Frenolone, Eglonia) under the control of blood pressure is indicated.

To increase the overall tone of the body, it is necessary to adhere to a work-rest regime with mandatory physical activity (gymnastics, skiing, etc.). B vitamins, vasoactive drugs and nootropics are used as drug treatment. Correction of autonomic disorders is very important, which includes both special breathing exercises and medications.

Breathing exercises, used to increase vegetative stability, is aimed at teaching the patient to gradually switch on, and, if possible, switch to diaphragmatic breathing, forming a 1:2 ratio between the duration of inhalation and exhalation, slowing down and (or) deepening breathing. The complexes of therapeutic breathing exercises used to achieve these goals are outlined in special manuals.

For drug correction of autonomic disorders, vegetotropic drugs are used: a drug such as Belloid (bellaspon, bellataminal), small doses of beta blockers (anaprilin, obzidan), combined alpha and beta blockers (pirroxan). If sympathetic reactions predominate, sydnocarb, caffeine, ascorbic acid, and belladonna preparations are prescribed. It should be emphasized that in all cases treatment of background and concomitant diseases is necessary.

Differentiated therapy for patients with syncope is carried out depending on the leading factor in their pathogenesis. For cardiogenic syncope, medications are selected together with a cardiologist. Depending on the underlying disease, drugs are prescribed that improve coronary blood flow (for fainting as a result of angina or myocardial infarction); nitrates, calcium antagonists, papaverine, nosh-pa, etc.; cardiac glycosides (for heart failure); antiarrhythmic drugs (for heart rhythm disorders); in case of disturbances of atrioventricular conduction, drugs of the atropine group (atropine in drops, tablets, injections, belladonna tincture, etc.) and isopropylnorepinephrine (isadrin, alupent) are indicated. In some cases, anticonvulsants (diphenin, carbamazepine) can be used to treat cardiac arrhythmias, and the positive effect of these drugs can be observed in the absence of affect from the most common antiarrhythmic drugs.

For the treatment of patients with vasovagal syncope, the above undifferentiated therapy is usually used. At the same time, with an increasing frequency of syncope, the appearance of hypersynchronization of the alpha rhythm on the EEG and the absence of effect from the therapy, small doses of anticonvulsants should be included in the complex of treatment measures: phenobarbital 0.05-0.1 at night, seduxen 5 mg in the morning and during the day, finlepsin 200-600 mg per day, diphenin 0.1 1-2 times a day.

The principles of treating orthostatic hypotension are to limit the volume that can be occupied by blood when changing their horizontal to vertical position, and to increase the mass of blood that fills this volume. For this purpose, drugs that cause vasoconstriction (ephedrine, nialamide), dihydroergotamine are used. However, they must be used with great caution because... can lead to a significant increase in blood pressure. The beta blocker pindolol is also indicated.

To prevent peripheral vasodilation, obzidan is used; cerucal and indomethacin have the same effect. Drugs that retain salts (synthetic fluorinated corticosteroids), caffeine, yohimbine, and tyramine derivatives are administered. Patients are prescribed a diet rich in salt, swimming, tight leg bandaging, and in severe cases, special inflatable suits. In the treatment of patients with dyscirculatory syncope, the emphasis should be on improving cerebral circulation, oxygenation of the brain and increasing its resistance to oxygen deficiency.

For this purpose, vasoactive agents (nicotinic acid, trental, cavinton, complamin, stugeron, etc.), drugs that improve microcirculation and brain metabolism (cinnarizine, piracetam, aminalon, encephabol, aminophylline, B vitamins, nikoverine, etc.) are widely used. . It is necessary to treat the underlying disease (atherosclerosis, arterial hypertension, osteochondrosis of the cervical spine, etc.), which has led to dyscirculatory disorders.

Treatment of patients with fainting-like epileptic paroxysms is based on the general principles of treatment of epilepsy. Patients should undergo repeated courses of therapy, including moderate dehydration (furosemide), absorbable agents (lidaza), vitamin B6, and anticonvulsants are prescribed for continuous use.

Indications for the use of anticonvulsants

Resistance to vasoactive drugs

The presence of paroxysmal, including clearly epileptic activity on the EEG against the background of functional loads;

Progression in the structure of repeated paroxysms of signs more characteristic of epilepsy (post-ictal stupor, disorientation, sleep, retrograde amnesia, etc.);

High frequency of attacks and their tendency to occur serially.

Various are used for treatment anticonvulsants(phenobarbital, diphenin, finlepsin, etc.) with individual selection of doses depending on the frequency of attacks and changes in the EEG. Drugs that affect cerebral blood flow (Nikospan, Cavinton, Stugeron, etc.) are also indicated for patients with fainting-like epileptic paroxysms.

To treat carotid sinus syndrome, cholinergic and sympatholytic drugs are used, and sinus blockade is performed using electrophoresis with novocaine. In severe cases, radiotherapy is performed on the carotid sinus area and surgical treatment (sinus deprivation, periarterial detachment, etc.).

Differentiated treatment of fainting when swallowing is aimed primarily at eliminating pathology of the esophagus and correcting cardiac activity. Atropine drugs and vegetotropic agents are also used.

To treat syncope with neuralgia of the glossopharyngeal nerve, anticonvulsants (carbamazepine, sodium volproate, etc.), atropine-type drugs are used; in severe cases of intractable pain syndromes, surgical treatment is performed (nerve transection, etc.).

When using complex treatment of patients with syncope, in most cases it is possible to achieve a positive effect with a reduction in the number of attacks or their complete cessation.

Indications for implantation of a cardioverter-defibrillator for syncope

1. Registered syncope due to ventricular tachycardia or ventricular fibrillation with ineffectiveness of antiarrhythmic therapy or its proarrhythmic effect.

2. Undocumented syncope, likely due to ventricular tachycardia or ventricular fibrillation:

History of myocardial infarction and monomorphic ventricular tachycardia induced during EPI (hemodynamically significant), in the absence of other causes of syncope;

Unexplained syncope in patients with left ventricular systolic dysfunction, in the absence of other causes of syncope;

Long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular dysplasia, hypertrophic obstructive cardiomyopathy (family history of sudden death in the absence of other causes of syncope).

Syncope is nothing more than fainting, which is short-term and reversible. During loss of consciousness, the body undergoes some changes, namely, muscle tone and the functioning of the cardiovascular and respiratory systems are disrupted.

The main reason for the development of this condition is insufficient blood flow to the brain. However, there are a large number of predisposing factors, ranging from strong emotional stress to the course of any illness.

This disorder has characteristic symptoms, including severe dizziness, blurred vision, lack of air, sometimes convulsions and loss of consciousness. For this reason, an experienced specialist will not have problems making the correct diagnosis. All laboratory and instrumental diagnostic methods will be aimed at identifying the etiological factor.

Treatment tactics will differ depending on what was the source of the short-term disturbance of consciousness.

In the international classification of diseases, such an ailment has its own meaning - ICD 10 code - R55.

Etiology

The fundamental source of the development of syncope is a change in the tone of the blood vessels that supply the brain, which causes insufficient blood flow to this organ. But such a process can take shape against the backdrop of a large number of factors. Thus, attacks of loss of consciousness occur for the following reasons:

• – such a disease is characterized by the fact that the human body is unadapted to environmental changes, for example, to changes in temperature or atmospheric pressure;
• Orthostatic collapse is a condition that occurs due to a sudden change in body position, in particular when suddenly rising from a horizontal or sitting position. A provocateur for this can be the indiscriminate use of certain medications, namely to lower blood pressure. In rare cases, it occurs in a completely healthy person;
• intense emotional stress - in the vast majority of cases, severe fright is accompanied by fainting. It is this factor that most often serves as the source of the development of syncope in children;
• a sharp drop in blood pressure;
• low blood sugar - this substance is the main source of energy for the brain;
• a decrease in cardiac output, which occurs in cases of severe and, but often occurs with;
• severe human poisoning by chemical or toxic substances;
• reduced oxygen content in the air inhaled by a person;
• high barometric pressure;
• Availability ;
• strong ;
• a wide range of lesions of the respiratory system and pathologies of the cardiovascular system;
• prolonged overheating of the body;
• loss of a large amount of blood.

In some cases, it is not possible to determine the source of fainting.

It is worth noting that every second person encounters a similar condition at least once in their life. Clinicians note that syncope is often observed in people aged ten to thirty years, but the frequency of fainting increases with age.

Classification

Depending on what caused the syncope, it is divided into:

• neurogenic or vasovagal, associated with a disorder of nervous regulation;
• somatogenic – develops against the background of damage to other internal organs and systems, and not due to pathologies of the brain;
• extreme – characterized by the influence of extreme environmental conditions on a person;
• hyperventilation - this type of loss of consciousness has several forms. The first is hypocapnic, which is caused by spasm of cerebral vessels, the second is of a vasodepressor nature, which is formed as a result of a poorly ventilated room and high temperatures;
• sinocarotid - such fainting is associated with changes in heart rhythm;
• cough - based on the name, they appear during a severe cough, which can accompany a large number of diseases, in particular the respiratory system;
• swallowing – impaired consciousness is observed directly during the process of swallowing, which is caused by irritation of the fibers of the vagus nerve system;
• nocturic – loss of consciousness occurs during or after urination, and is also observed at night when trying to get out of bed;
• hysterical;
• unknown etiology.

Some of the above types of syncope have their own classification. For example, neurogenic fainting occurs:

• emotional;
• maladaptive;
• discirculatory.

Types of somatogenic syncope:

• anemic;
• hypoglycemic;
• respiratory;
• situational;
• cardiogenic syncope.

Extreme fainting conditions are divided into:

• hypoxic;
• hypovolemic;
• intoxication;
• hyperbaric;
• toxic;
• drug.

In cases of unclear nature of the development of syncope, the correct diagnosis can be made by excluding all etiological factors.

Symptoms

Clinical manifestations of fainting go through several stages of development:

• prodromal stage, at which signs warning of loss of consciousness are expressed;
• directly ;
• condition after syncope.

The intensity of manifestation and duration of each stage depends on several factors - the cause and pathogenesis of fainting.

The prodromal stage can last from several seconds to ten minutes and develops as a result of the influence of a provoking factor. During this period, the following symptoms may be observed:

• severe dizziness;
• the appearance of “goosebumps” before the eyes;
• blurred visual image;
• weakness;
• ringing or noise in the ears;
• pallor of the skin of the face, which is replaced by redness;
• increased sweating;
• nausea;
• dilated pupils;
• lack of air.

It should be noted that if during such a period of time a person manages to lie down or at least tilt his head, then loss of consciousness may not occur, otherwise the above symptoms will increase, which will end in fainting and falling.

The fainting itself often does not exceed thirty minutes, but in the vast majority of cases it lasts about three minutes. Sometimes the attack itself may be accompanied by a symptom such as seizures.

During the recovery period after syncope, the following symptoms are expressed:

• drowsiness and fatigue;
• decrease in blood pressure;
• uncertainty of movements;
• slight dizziness;
• dry mouth;
• profuse sweating.

It is noteworthy that almost all persons who have suffered a loss of consciousness clearly remember everything that happened to them before fainting.

The above clinical manifestations are considered common to all types of syncope, but some of them may have specific symptoms. When fainting of a vasovagal nature in the prodromal period, the symptoms are expressed in:

• nausea;
• severe pain in the abdominal area;
• muscle weakness;
• pallor;
• threadlike pulse, with normal heart rate.

After syncope, weakness comes first. From the moment the warning signs appear until complete recovery, a maximum of an hour passes.

Fainting states of a cardiogenic nature are distinguished by the fact that the warning symptoms are completely absent, and after loss of consciousness they are expressed:

• inability to determine pulse and heartbeat;
• pale or bluish skin.

When the first clinical manifestations appear, it is very important to provide first aid rules, including:

• ensuring a flow of fresh air into the room where the victim is located;
• try to catch a falling person to avoid injury;
• lay the patient so that the head is below the level of the whole body, and it is best to raise the lower limbs;
• splash your face with ice water;
• if possible, administer a glucose solution or give him something sweet to eat.

Diagnostics

The etiological factors of syncope can only be identified through laboratory and instrumental examinations. However, before prescribing them, the clinician must independently:

• clarify the patient’s complaints;
• study the medical history and become familiar with the patient’s life history - sometimes this can directly indicate the causes of fainting;
• conduct an objective examination.

The initial examination can be carried out by a therapist, neurologist or pediatrician (if the patient is a child). After this, consultation with specialists from other fields of medicine may be required.

Laboratory tests include:

• clinical blood and urine analysis;
• study of blood gas composition;
• blood biochemistry;
• glucose tolerance test.

However, diagnosis is based on instrumental examinations of the patient, including:

In establishing the correct diagnosis, a procedure such as a passive orthostatic test plays an important role.

Treatment

Therapy for syncope is individual and directly depends on the etiological factor. Often, the use of medications in the interictal period is sufficient. Thus, treatment for syncope will involve taking several of the following medications:

• nootropics – to improve brain nutrition;
• adaptogens – to normalize adaptation to environmental conditions;
• venotonics - to restore the tone of the veins;
• vagolytics;
• serotonin uptake inhibitors;
• sedatives;
• anticonvulsants;
• vitamin complexes.

In addition, therapy for such a disorder must necessarily include measures to eliminate causative or concomitant pathologies.

Complications

Syncope can lead to:

• injuries to the head or other parts of the body during a fall;
• decreased work activity and quality of life with frequent fainting;
• difficulties in teaching children, but only under the condition of frequent syncope.

Prevention

Among the preventive measures to prevent syncope are:

• healthy lifestyle;
• proper and balanced nutrition;
• moderate physical activity;
• timely detection and treatment of those ailments that can lead to fainting;
• avoiding nervous and emotional stress;
• Regularly undergoing a full medical examination.

Often the prognosis for syncope itself is favorable, but it is characterized by what disease or factor caused its occurrence.

Is everything in the article correct from a medical point of view?

Answer only if you have proven medical knowledge

Syncope is a pressing problem both in pediatrics and in medicine in general, since loss of consciousness can occur during the patient’s activity and lead to personal injury and death (fainting while swimming or driving a vehicle). Syncope can also result from a more serious (usually heart) condition with a risk of sudden death.

According to the 2017 ACC/AHA/HRS Guidelines for the Diagnosis and Management of Patients with Syncope (American Society of Cardiology Task Force Report), syncope is a symptom that manifests itself as a sudden temporary loss of consciousness and is associated with the need to maintain forward tone, with rapid and spontaneous recovery. The likely mechanism for this symptom is cerebral hypoperfusion.

Epidemiology

According to the European Society of Cardiology, the annual prevalence of syncope in the general population ranges from 18.1 to 39.7 ‰. During the first two decades of life, approximately 15% of individuals experience at least one episode of loss of consciousness, and in approximately 1% of all pediatric illnesses, syncope is the chief complaint.

Etiology and pathogenesis

From the pathogenetic point of development of syncope, three main groups of syncope are defined:

1. reflex fainting,
2. cardiogenic syncope,
3. syncope due to orthostatic hypotension.

The most common reflex fainting in children is of four types:

1. vasovagal;
2. situational;
3. sinocarotid;
4. atypical.

The mechanism of development of vasovagal syncope is considered to be the Bezold-Jarisch reflex. During orthostasis, blood is deposited in the veins of the lower extremities, pelvic cavity and abdominal cavity. A decrease in blood flow to the heart is manifested by a decrease in pressure in the left ventricle and, as a result, an increase in the strength and frequency of heart contractions (HR). This leads to increased afferent impulses from the mechanoreceptors of the left ventricle and the occurrence of the Bezold-Jarisch reflex, which is manifested by activation of the parasympathetic nervous system and is accompanied by hypotension and / or bradycardia. However, today there are a number of studies that have proven the possibility of vasovagal syncope in people with heart transplants.

Inappropriate hyperactivation of the parasympathetic division of the autonomic nervous system (ANS) during situational (during coughing, urination, defecation, etc.) and sinocarotid (irritation of the sinocarotid node) syncope also leads to bradycardia / hypotension, resulting in hypoperfusion of the central nervous system (CNS) ) and fainting.

Regardless of the type, cardiogenic syncope has one pathogenetic direction: a decrease in cardiac output and, as a consequence, general cerebral hypoperfusion. The causes of cardiogenic syncope are divided into three groups:

1. disturbances of heart rhythm and conduction (Arrhythmogenic syncope)
2. structural and functional abnormalities of the heart (congenital and acquired heart defects, cardiomyopathies, myocardial infarction, etc.);
3. other causes (pulmonary embolism, dissecting aortic aneurysm, etc.).

Arrhythmogenic syncope (11-14%) occupies a significant place in the structure of syncope. Table 1 shows the main causes of cardiogenic syncope as defined by the European Society of Cardiology.

Table 1. Main causes of cardiogenic syncope

Arrhythmogenic

Bradycardia:

• sinus node dysfunction (including bradycardia-tachycardia syndrome)
• AV conduction disorder
• malfunction of implanted devices

Tachycardia:

• supraventricular;
• ventricular (idiopathic, due to structural lesions of the heart, due to
• channelopathies)

For structural heart lesions

• valvular heart defects;
• acute myocardial infarction (very rare in children);
• cardiomyopathy;
• atrial myxoma;
• pericardial disease and cardiac tamponade

Other reasons:

• pulmonary embolism;
• dissecting aortic aneurysm

General scheme of the pathogenesis of fainting with orthostatic hypotension

With orthostasis, the force of gravity causes some of the blood to “flow” into the lower half of the body, concentrating in the vascular bed of the lower extremities, pelvic cavity and abdominal cavity. This would lead to a decrease in blood flow to the heart and a decrease in cardiac output, but the sympathetic nervous system, responding to orthostasis, increases vascular tone, in particular in the lower half of the body, reducing their capacity. But for a number of reasons (impaired functioning of the autonomic nervous system - autonomic dysfunctions), causing insufficiency of the vasoconstrictor function of the sympathetic nervous system during orthostasis, this may not happen. The result will be the occurrence of orthostatic hypotension with the manifestation of syncope.

Making a diagnosis of syncope

If there are complaints of fainting, first of all it is necessary to make sure whether there really was a loss of consciousness, since patients by “fainting” can mean dizziness, darkening of the eyes, weakness and other symptoms with preserved consciousness, called “presyncope”.

Once confirmation of syncope has been obtained, the second step in obtaining a history is to determine the presence of three characteristics of the condition:

1. sudden onset (to exclude gradual impairment of consciousness during intoxication, shock, hyperglycemia, etc.);
2. short duration (to differentiate from conditions with long-term impairment of consciousness, for example, comma);
3. complete spontaneous recovery.

The third step is to exclude conditions with transient syncope with pathogenetic mechanisms other than global CNS hypoperfusion. Thus, you should make sure that there is no traumatic brain injury (complaints, anamnesis, examination) as the cause of loss of consciousness.

Since injuries are common during syncope, it is necessary in the case of an injury associated with a fall to establish the sequence of events: the loss of consciousness occurred after a head injury or the loss of consciousness was primary. In the first case, loss of consciousness is a symptom of traumatic brain injury and is not a syncope.

During the survey and further examination of patients, special attention should be paid to the differentiation of syncope with an epileptic attack (differential diagnosis is given in Table 2. We consider it rational to conduct electroencephalography when examining all patients with syncope.

Of great importance for establishing the diagnosis of syncope and for the differential diagnosis of various types and similar conditions is further thorough questioning of:

• a certain case (there were precursors, what was the course of the loss of consciousness, what was it accompanied by)
• presence of such cases in the past (frequency of occurrence, similarity to this case, identification of the cause)
• the presence of concomitant diseases (heart disease, epilepsy, diabetes mellitus, thyroid disease, etc.).

A list of conditions similar to fainting is given in Table 3.

Table 3. Conditions Most Often Misdiagnosed as Syncope

Conditions with transient complete or partial loss of consciousness, but without general cerebral hypoperfusion:

• epilepsy
• metabolic disorders, including hypoglycemia, hypoxia, hyperventilation with hypocapnia
• intoxication
• vertebrobasilar transient ischemic attack

Conditions without loss of consciousness:

• cataplexy (short-term, paroxysmal loss of muscle tone, which leads to the patient falling, without loss of consciousness against the background of severe emotional shock)
• drop attacks (a sharp decrease in muscle tone followed by a fall of the patient as a result of transient ischemia of the brain stem)
• a fall
• psychogenic pseudozomlinnya
• transient ischemic attack of carotid origin

Differential diagnosis of various syncope conditions

According to the Framingham study, in the general population, cardiogenic syncope is the third most common, but the first in danger and poor prognosis. That is why the differential diagnosis of syncope should begin with the exclusion of cardiogenic syncope.

Important in identifying arrhythmogenic syncope is the study of the electrical activity of the heart. The “gold standard” for diagnosing arrhythmogenic syncope is the establishment of a temporal correlation between the onset of symptoms and the detection of rhythm and conduction disturbances. This significantly reduces the diagnostic capabilities of conventional electrocardiography (ECG). They come down to cases of arrhythmogenic syncope during an ECG or an ECG immediately after syncope until the disappearance of paroxysmal arrhythmias. Basically, based on the results of a routine ECG, this diagnosis can be suspected. According to the European Society of Cardiology, ECG signs, the presence of which can suggest cardiogenic syncope, are shown in Table 4. To these, you can add some medical history: the presence of identified cardiac disease; a family history of sudden death of unknown origin or channelopathies; the occurrence of syncope during physical activity or while lying down; sudden palpitations before loss of consciousness.

Table 4. ECG signs suggesting the arrhythmogenic nature of syncope

• Bifascicular block (left or right bundle branch block in combination with left anterior or posterior fascicular block)
• Other intraventricular conduction disorders (QRS complex duration > 0.12 s)
• Second degree block (Mobitz I)
• Asymptomatic sinus bradycardia (HR<50 уд. / Мин), синоатриальная блокада или синусовая пауза ≥ 3 с при отсутствии приема препаратов с отрицательным хронотропным действием
• Non-sustained ventricular tachycardia
• Wolff-Parkinson-White syndrome
• Long or shortened QT interval
• Early repolarization syndrome
• Brugada syndrome
• Negative T waves in the right precordial leads, epsilon waves and late ventricular potentials, on the basis of which the presence of arrhythmogenic right ventricular cardiomyopathy can be suspected
• Q-waves, on the basis of which one can suspect the presence of myocardial infarction

Note. HR - heart rate.

Holter monitoring of ECG data provides great opportunities for diagnosing arrhythmogenic syncope. On the one hand, long-term monitoring increases the likelihood of recording changes during a syncope; on the other hand, analysis of heart rate variability makes it possible to establish the state of the autonomic nervous system, which is important for diagnosing the preconditions for reflex syncope and fainting as a result of orthostatic hypotension. According to the recommendations of the European Society of Cardiology, Holter ECG monitoring is prescribed to patients with frequent syncope (once a week or more) for 24-48 hours, in some cases - up to 7 days. Diagnostic criteria for ECG monitoring are given in Table 5.

So, the place of ECG monitoring in determining the causes of syncope is primarily to identify arrhythmogenic syncope in patients with relatively frequent episodes of loss of consciousness and to identify the background for the development of reflex syncope and fainting caused by orthostatic hypotension. Holter monitoring can also help establish the diagnosis of psychogenic pseudozomlinia in patients with frequent symptoms without any ECG findings at the time of loss of consciousness.

Table 5. Diagnostic criteria for arrhythmogenic syncope during 24-hour ECG monitoring

• Monitoring ECG data is diagnostic when there is a correlation between syncope and arrhythmia (brady- or tachyarrhythmias)
• In the absence of such a correlation, ECG monitoring is diagnostic if periods of Mobitz II or AV block of the third degree, ventricular asystole ≥ 3 s are detected (exceptions may be in patients taking drugs with a negative chronotropic effect in professional athletes; during sleep) or sudden prolonged supraventricular or ventricular tachycardia. If there is no arrhythmia during syncope, this excludes its arrhythmogenic nature.
• Presyncope in the absence of significant arrhythmia on the electrocardiogram is not the basis for a final diagnosis
• Asymptomatic arrhythmias, other than those listed above, are not grounds for a final diagnosis
• Sinus bradycardia (in the absence of syncope) is not a basis for a definitive diagnosis

If syncope occurs during or immediately after physical activity, its cardiogenic nature should also be suspected. In this case, the patient needs to undergo a load treadmill test or bicycle ergometry. The diagnostic test is syncope during or immediately after the test with the simultaneous presence of pathological abnormalities on the ECG or severe hypotension. In addition, the occurrence of 2nd degree atrioventricular block (Mobitz II) or 3rd degree AV block during exercise is diagnostic even in the absence of syncope.

All patients with syncope should also undergo transthoracic echocardiography to exclude syncope associated with structural heart disease. This method itself confirms the cardiogenic origin of syncope in the case of severe aortic stenosis, cardiac tumors or blood clots leading to obstruction, pericardial tamponade, aortic dissection, and congenital anomalies of the coronary arteries.

Sinocarotid syncope can be suspected when fainting occurs against the background of situations with mechanical impact on the carotid sinus (squeezing the neck with a tight collar, shaving, tying a tie, etc.). Diagnostically, it is necessary to reproduce symptoms within 10 seconds after alternating right- and left-sided massage of the carotid sinus, first in a supine position and then in an upright position, with constant monitoring of heart rate and periodic measurement of blood pressure (BP). An episode of ventricular asystole that lasted 3 s and/or a decrease in systolic pressure to<50 мм рт. ст. являются признаками гиперчувствительности каротидного синуса.

Vasovagal syncope can be suspected already at the stage of interviewing the patient and his parents. R. Sheldon et al. (2006) proposed an algorithm for collecting anamnesis in adult patients.

* When using the algorithm in children, the answer to this question is always negative.

** This controversial question is intended to confirm the fact of the actual loss of consciousness; with a score ≥ -2, a diagnosis of vasovagal syncope can be made with a sensitivity of 89% and a specificity of 91%.

The Japanese Clinical Guideline on Juvenile Orthostatic Dysregulation (2009) also proposed anamnestic criteria for diagnosing syncope in orthostatic dysregulation (against the background of orthostatic hypotension and vasovagal nature) (Table 7).

Table 7. Anamnestic criteria for diagnosing syncope in orthostatic dysregulation

• ≥ 3 major criteria or
• 2 major and ≥ 1 minor criteria, or
• 1 major criterion and ≥ 3 minor criteria

Large criteria:

A. Tendency to feel dizzy while standing

B. Tendency to faint when standing, which in severe cases leads to falling

B. Nausea when taking a hot shower/bath or in unpleasant situations

D. Palpitations and/or shortness of breath after minor physical activity

D. Weakness, dizziness when getting out of bed

Minor criteria:

A. Paleness

B. Anorexia

B. Periodic attacks of abdominal colic

D. Fatigue

D. Frequent headaches

E. Motion sickness in transport

In the instrumental diagnosis of vasovagal syncope and orthostatic hypotension, the “gold standard” is the tilt test. For this study, a table is used that changes position from horizontal to vertical and allows the patient to be fixed to prevent injury in the event of fainting. The patient is transferred to a nearly vertical position and pulse and blood pressure are monitored. The most recognized are the Westminster and Italian protocols with drug stimulation.

Vasovagal syncope is characterized by normal primary adaptation of the cardiovascular system to orthostasis (heart rate increases by 5-30 beats/min and does not exceed 120 beats/min, no drop in blood pressure) followed by the development of hypotension and/or bradycardia/asystole, which is accompanied by syncope . Types of vasovagal syncope and criteria for their diagnosis according to the tilt test are given in Table 8.

Table 8. Diagnosis criteria for various types of vasovagal syncope (N. Nagornaya et al., 2009)

It is characterized by a normal primary reaction to orthostasis and long-term stable blood pressure and heart rate during orthostasis. During syncope, a sharp decrease in blood pressure precedes a moderate decrease in heart rate. Heart rate does not decrease to the value<40 уд. / Мин более чем на 10 с.

Cardioinhibitory type (type 2)

Type 2A. Normal initial reaction to orthostasis. First, a decrease in blood pressure occurs, then syncope occurs against the background of a drop in heart rate to<40 уд. / Мин более чем на 10 с и / или асистолии продолжительностью>3 s.

Type 2B. Normal initial reaction to orthostasis. The simultaneous occurrence of asystole and a drop in blood pressure during syncope.

Vasodepressor type (type 3)

It is characterized by a normal primary reaction to orthostasis, the occurrence of syncope against the background of a significant drop in blood pressure and a possible drop in heart rate by no more than 10% from the initial level.

Notes: BP—blood pressure; HR - heart rate.

Orthostatic hypotension is characterized by a lack of normal orthostatic adaptation immediately upon transition to the orthostatic position. That is, initially the patient's pressure cannot be maintained by vasoconstriction. This leads to gradually progressive hypotension, which may, but not necessarily, end in syncope. Many patients with orthostasis experience presyncope (dizziness, darkening of the eyes, weakness, etc.) without loss of consciousness. All disorders of adaptation of the cardiovascular system to orthostasis with the occurrence of presyncope or syncope are called the general term “orthostatic intolerance.” Orthostatic intolerance can be diagnosed using both a tilt test and a conventional clinoorthostatic test.

The types of orthostatic intolerance, according to tilt testing, include:

• Classic orthostatic hypotension is characterized by a drop in systolic blood pressure of 20 mmHg. Art. or more during the first three minutes of orthostasis, and diastolic blood pressure by 10 mm Hg. Art. and more; symptoms of orthostatic intolerance occur no earlier than the first 30 seconds, but no later than the end of the 3rd minute.
• Early orthostatic hypotension occurs more often in young people and is characterized by a drop in blood pressure of more than 40 mmHg. Art. immediately after the transition to orthostasis, restoration of AO and disappearance of symptoms during the first 30 s. It is early orthostatic hypotension that may explain dizziness and fainting in adolescents during a sudden transition to a vertical position.
• Postural orthostatic tachycardia syndrome - diagnosed in the absence of syncope, but an increase in heart rate during the transition to orthostasis by more than 30 beats. / Min (or up to a value of more than 120 beats / Min). In this case, blood pressure often decreases, and symptoms of orthostatic intolerance occur.
• Chronotropic insufficiency - occurs when it is impossible to compensatory increase in heart rate during the transition to orthostasis. In this case, heart rate increases by less than 5 beats. / min, blood pressure progressively decreases, symptoms of orthostatic intolerance occur.

The tilt test requires valuable equipment, specially trained personnel, and is not available in all, even specialized, institutions. That is why, for the diagnosis of juvenile orthostatic dysregulation, a test protocol with a clinoorthostatic test was developed, which is simple, widely available and at the same time allows to differentiate the main types of orthostatic intolerance.

Methodology for conducting an orthostatic test

Environment: the office should be quiet and comfortable for the child; the height of the couch must be set individually for each child; if the height is significant, a step is needed; the test is carried out in the morning (if carried out in the evening, false negative results are possible).

Equipment: blood pressure monitor, stethoscope, clamp, stopwatch, ECG monitor, resuscitation kit.

Test protocol:

1. The child rests for 10 minutes in a lying position. Place a cuff on the shoulder, install an ECG monitor, and fix the stethoscope on the arm above the brachial artery.
2. The researcher will measure and calculate the average heart rate and blood pressure three times after 10 minutes of rest.
3. The examiner should inflate the blood pressure cuff to the mean systolic blood pressure level and clamp the rubber tube with a clamp. If the instructions are followed, muffled Korotkoff sounds can be heard using a stethoscope.
4. The child actively stands up, and the researcher starts the stopwatch and listens to Korotkoff sounds using a stethoscope.
5. With orthostasis, Korotkoff sounds disappear (drop in blood pressure), but normally appear again after an average of 17 seconds (restoration of the original blood pressure level). When the researcher hears that the tones have resumed, he records the time on a stopwatch - the time of restoration of the initial blood pressure level.
6. The examiner removes the clamp and deflates the cuff.
7. The examiner measures blood pressure and pulse rate in the usual manner at 1, 3, 5, 7 and 10 minutes.

Types of orthostatic dysregulation that are diagnosed using the following orthostatic test:

• Early orthostatic hypotension (OH). Moderately severe early OH is characterized by a drop in mean blood pressure by ≥ 60% and a blood pressure recovery time of ≥ 20-25 s. Severe early OH is characterized by the presence of the above symptoms and a decrease in systolic blood pressure by ≥ 15% during the late orthostatic phase (3-7 minutes).
• Delayed orthostatic hypotension. Characterized by a decrease in systolic blood pressure by ≥ 15% during the late phase of orthostasis (3-7 minutes) without signs of early OH.
• Postural orthostatic tachycardia syndrome (POTS). Increase in heart rate by ≥ 35 beats. / Min or up to a value of more than 115 beats. / Min with / without hypotension.
• Reflex fainting/presyncope. Clinical manifestations of presyncope/syncope against the background of a sharp drop in blood pressure with/without bradycardia.

Patient management

Including emergency care for syncope and anti-relapse therapy for syncope.

Emergency care for syncope of reflex origin or against the background of orthostatic hypotension is provided as follows:

1. Provide the patient with a horizontal position with raised lower limbs (30°).
2. Make sure the airway is open, provide access to fresh air, and release the pressure of any clothing items (collar, belt).
3. Provide reflex influences (ammonia, splashing cold water in the face).
4. In case of severe fainting with significant hypotension, administration of a 1% mesatone solution subcutaneously is indicated (0.1 ml/year of life, but not more than 1 ml)
5. For severe bradycardia, a 0.1% atropine solution is administered subcutaneously (0.05 ml/kg, not more than 1 ml).

For cardiogenic syncope, care is provided in accordance with protocols for the treatment of relevant conditions.

According to the European Society of Cardiology, anti-relapse therapy for reflex syncope and syncope due to orthostatic hypotension contains the following points:

1. Informing the patient and his parents about the possible risk of injury during syncope.
2. If there are warning signs, train the patient to recognize them and prevent arterial hypotension, fainting and injuries (you should know the triggers and avoid them, take a sitting or lying position in advance, use counterpressure methods).
3. In cases of severe and frequent proven cardioinhibitory syncope, it is possible to consider implantation.

For orthostatic hypotension additionally:

• Increasing the volume of drinking to the “sports” level - 2-3 liters per day.
• Sleep with your head elevated 10° above the level of the bed.
• Conducting tilt training (daily: stand with your back to the wall, place your soles at a distance of 10-15 cm from the wall, and lean your back against it, stand in this position, starting from 5 minutes and gradually increasing the time using the training method to 30 minutes).
• Wear tight pants and stockings (to compress the veins of the lower extremities and reduce the deposition of blood in them when moving to a vertical position).

The recommendations for the diagnosis and treatment of syncope of the European Society of Cardiology (2009) indicate that the only drugs that have been proven to have a positive effect on the condition of patients with reflex syncope and orthostatic hypotension are fludrocortisone (mineralocorticoid, increases circulating blood volume) and midodrine (vasopressors) . These recommendations indicate that the preventive effect of beta-blockers has not been proven, and their use is not recommended in the presence of reflex syncope and syncope with orthostatic hypotension. For juvenile orthostatic dysregulation, prophylactic administration of propranolol is recommended at a dose of 10 mg once in the morning for children 7-12 years old and at a dose of 10 mg twice a day (early morning and evening) for adolescents.