Syncope causes. Syncope (syncope, fainting)

Fainting(syncope) is called an attack of short-term loss of consciousness with a violation of postural tone and a quick, complete, independent restoration of a normal state. Main signs of any syncope are the suddenness of development, short duration and reversibility. Sometimes presyncopal (presyncope, lipothymic) states are also distinguished - there is no complete loss of consciousness with the persisting paroxysmal state.

From a practical point of view, it makes sense to distinguish 3 main groups syncope: neurogenic (neuromediated), cardiac, angiogenic. It is also important to differentiate fainting from other conditions with a short loss of consciousness (hypoglycemia, epileptic and hysterical seizures).

Characteristics of syncope

Neurogenic (neuromediated) syncope- syncope, in the pathogenesis of which the leading role is given to reflex effects on the cardiovascular system:

* Emotional syncope (normal, or vasovagal);

* Fainting in carotid sinus syndrome;

* Gastrointestinal stimulation (fainting when swallowing, defecation);

* Fainting when urinating;

* Glossopharyngeal syncope;

* Stimulation of the respiratory tract;

* Increased intrathoracic pressure (playing wind instruments, lifting weights, straining);

* Fainting with a prolonged cough (bettolepsy), with sneezing.

Neurogenic syncope often develops in a standing position, especially in a stuffy room. Provoking factors can be pain, emotional stress.

Neurocardiogenic syncope can develop in three ways: cardioinhibitory (the leading sign is bradycardia, episodes of asystole), vasodepressor (hypotension without bradycardia) or mixed. Their occurrence is preceded by a presyncope (presyncope): pallor and moisture of the skin, weakness, headache, dizziness, blurred vision, discomfort in the epigastric region, nausea. During syncope, confusion or loss of consciousness is noted against the background of a decrease in blood pressure and (or) bradycardia. The post-fainting state is characterized by a rapid recovery of consciousness, hyperemia and moisture of the skin.

The pathogenesis of neuromediated syncope remains unclear. Modern concepts suggest that afferent impulses from various peripheral receptors (for example, mechanoreceptors, chemoreceptors) of numerous organs and systems, as well as input impulses from the overlying parts of the CNS, collide in the vasomotor centers spinal cord, which leads to the emergence of efferent neural signals that cause bradycardia and peripheral vasodilation.

In vasovagal syncope, cardiopulmonary mechanoreceptors, although the main source of neural afferent signals required to trigger syncope in susceptible subjects, also require various precipitating factors (eg, anxiety, pain, exercise).

In carotid sinus syndrome (CSS), the main source of afferent neural activity is presumably carotid baroreceptors. The diagnosis of SCS is based on the appearance during the massage of the carotid sinus or an asystolic pause lasting at least 3 seconds, or a vasodepressor response with a decrease in blood pressure by more than 50 mm Hg. from the original. Quite often, with SCS, a transient atrioventricular block develops.

Cardiogenic syncope.

Arrhythmic syncope develops suddenly without presyncope.

* tachyarrhythmias (ventricular paroxysms, less often - over ventricular tachycardia).

* bradyarrhythmias (atrioventricular or sinoatrial blockade, sick sinus syndrome, sinoatrial node arrest, frequent blocked extrasystoles);

Tachyarrhythmias as the causes of syncopal conditions often develop in congenital (Romano-Ward syndrome - primary cardioneuropathy) and acquired (due to past myocardial diseases, electrolyte disorders, drug exposure) forms of long QT syndrome, WPW syndrome, atrioventricular dissociation and other conditions.

The syncope itself can be relatively prolonged, accompanied by severe tachycardia or bradycardia, a decrease in blood pressure, cyanosis. The post-fainting state is characterized by cyanosis, a feeling of interruptions in the work of the heart, and weakness.

Obstructive syncope develops in the presence of mechanical obstacles to filling the heart with blood or cardiac output (i.e., with violations of cardiac hemodynamics).

With aortic stenosis, syncope occurs during exercise, often against the background of shortness of breath and anginal pain due to a decrease in blood pressure; another cause of fainting may be ventricular tachycardia. Repeated syncope in patients of this category is an unfavorable prognostic sign and one of the indications for surgical correction of heart disease.

The same applies to patients with idiopathic hypertrophic subaortic stenosis or pulmonary stenosis.

With a spherical thrombus of the left atrium, fainting develops at the moment when the patient stands up or sits down. Before the onset of fainting, shortness of breath and finely spotted cyanosis appear, especially pronounced on the skin of the upper half of the body.

With atrial myxoma, syncope develops only in an upright position against the background of shortness of breath, cyanosis, and tachycardia.

Obstructive cardiogenic syncope can be caused by primary pulmonary hypertension or pulmonary embolism, less often by dissecting aortic aneurysm, cardiac tamponade, and malfunction of valve prostheses.

In the syndrome of connective tissue dysplasia of the heart with severe disorders of intracardiac hemodynamics, syncope is often the only clinical manifestation of the disease.

Syncopal conditions with little physical work, sometimes with a change in body position, can develop with coronarogenic changes in the myocardium: postinfarction cardiosclerosis with pronounced zones of hypokinesia, postinfarction aneurysms (due to a significant decrease in the effective work of the heart).

Vascular syncope.

Orthostatic syncope occurs when the patient quickly moves from a horizontal to a vertical position. There is no pre-syncope in orthostatic syncope. Syncope is short-term and proceeds without vegetative reactions, the skin is dry, of normal color, tachycardia or bradycardia does not develop. After fainting, short-term weakness may persist.

Cerebrovascular syncope is caused by damage to the cerebral or other arteries that affect the blood supply to the brain (carotid, vertebral, subclavian) arteries and develop when their tone changes, blood pressure decreases, compression, steal syndrome, short-term embolism.

Such syncope usually develops without warning and is relatively prolonged. Headaches, pain in the neck, transient neurological symptoms (paresis, short-term speech and vision disorders) are characteristic of the post-fainting state.

The development of fainting due to compression of the vertebral arteries may be indicated by the occurrence of a syncopal state with a sharp tilting of the head, the so-called "Sistine Chapel syndrome". A similar situation may be due to carotid sinus syndrome.

When blood flow is disturbed carotid artery short-term amaurosis on the side of the lesion and (or) hemiparesis on the opposite side may be noted.

Stenosis of the subclavian artery (proximal to the origin of the vertebral artery) is evidenced by the development of syncope when working with the affected hand, resulting in the development of the "steal" syndrome. In these cases, one can detect a significant difference in the filling of the pulse and the magnitude of blood pressure on a healthy and affected arm.

Against the background of cerebral atherosclerosis with stenotic lesions of the arteries of the brain, even a transient decrease in heart rate can cause additional deterioration of cerebral blood flow and lead to loss of consciousness. Repeatedly repeated bouts of loss of consciousness can lead to changes in the central nervous system with organic brain damage, manifested by focal symptoms.

The mechanisms of cerebral circulation disorders in atherosclerotic lesions of the brachiocephalic arteries include:

* local slowing of blood flow due to stenosis or pathological tortuosity of the extracranial segment of the artery;

* increased turbulence of blood flow, resulting in the formation of microaggregates, emboli, thrown into the intracranial arteries;

* arterio-arterial embolism with ulceration of atherosclerotic plaques of extracranial parts of cerebral arteries.

The similarity of the clinical picture of sick sinus syndrome (SSS) and damage to the branches of the aortic arch can cause difficulties in establishing the leading cause of syncope, which prevents the choice of the correct treatment tactics.

The clinical picture in patients with transient cerebrovascular accident is characterized by complaints of occipital headache, dizziness, often with ringing and tinnitus. The most frequently disturbed gait and static in the form of staggering when walking, there are visual disturbances - veil, double vision, episodes of loss of consciousness.

In the clinical manifestations of sinus dysfunction, dizziness, short-term “blackouts” or confusion, blackouts, staggering, fainting, as well as constant weakness and fatigue are of primary importance.

Approximately a quarter of elderly patients with SSSU have hemodynamically significant atherosclerotic lesions of the brachiocephalic arteries. In CVD-related bradycardia, interpretation of extracranial cerebral artery Doppler data can be difficult. Additional research methods in these patients are transcranial dopplerography, scintigraphy and computed tomography of the brain.

Other common causes of loss of consciousness are hypoglycemic conditions, epileptic and hysterical seizures.

Hypoglycemic states develop in diabetic patients receiving insulin. They are preceded by the introduction of insulin, insufficient food intake, agitation, hunger, increasing weakness. A characteristic symptom is severe sweating. Impairment of consciousness develops against the background of normal heart rate and normal blood pressure. After withdrawal from the hypoglycemic state, stupor persists. If a hypoglycemic condition is suspected, attention should be paid to the presence of traces of injections.

Epileptic seizures usually begin at a young age after an infection, traumatic brain injury, or chronic alcoholism. Seizures occur without visible reasons, in some patients, loss of consciousness is preceded by visual, auditory, gustatory, olfactory or sensitive auras, while the unusual sensations distinguish it from pre-syncope states.

Grand mal seizures usually begin with tonic convulsions that progress to clonic. Characterized by biting the tongue, involuntary urination, prolonged stupor after an attack, reminiscent of sleep, headache, fatigue. Pallor of the skin and arterial hypotension are uncharacteristic.

Small epileptic seizures often develop suddenly, occur with a short-term loss of consciousness, while in some cases muscle tone can be preserved and patients “freeze” for a few seconds, a sharp decrease is less often observed. muscle tone and falling sick.

The longer the patient suffers from epilepsy and the more often seizures occur, the more significant are the characteristic personality changes (irritability, viscosity, excessive accuracy). Important in the diagnosis of epilepsy are the results of additional research methods: electroencephalography (registration of specific changes in the electrical activity of the brain), computed tomography of the brain (volumetric formations, gross liquorodynamic disorders, pronounced atrophic processes - as sources of epileptogenic activity).

Hysterical seizures develop in patients with a demonstrative style of thinking from their youth. Seizures occur for obvious reasons, always in public, and of relatively long duration. Patients fall smoothly, gently, so there are practically no injuries. During a seizure, the color of the skin and mucous membranes does not change, the pupils respond well to light (the eyelids are compressed!), There is no bradycardia or arterial hypotension, biting of the lips (but not the tongue!), Moans, artsy postures, chaotic movements (but not tonic or clonic convulsions!). Sometimes it is possible to interrupt the seizure by holding the patient's mouth and nose for a short time.

Examination program for the differential diagnosis of syncope:

1. Anamnesis of life, information about previous diseases, injuries taken medicines Oh;

2. Complaints in the interictal period;

3. Data on how long and how often syncope occurs;

4. Factors provoking fainting;

5. Features of syncope:

* the presence, manifestations and duration of pre-syncope;

* symptoms during fainting (color and moisture skin, frequency and nature of respiration and pulse, convulsive syndrome);

* duration of fainting;

* the presence, manifestations and duration of the post-fainting state.

6. Physical examination with an emphasis on the detection of cardiovascular diseases (heart size, cardiac and vascular murmurs, blood pressure, pulse frequency and regularity, difference in pulse filling on both sides of the radial and carotid arteries, signs of heart failure, etc.) .

7. ECG analysis (if possible, evaluation of previous ECGs).

8. Examination by a neurologist.

9. If there are indications - laboratory research methods (hemoglobin, erythrocytes, hematocrit, blood glucose, etc.).

10. Depending on the identified features - conducting tests:

* active orthostatic test according to Tulesius;

* Valsalva tests;

* Carotid sinus massage.

11. Psychiatric consultation.

12. Special tests, daily monitoring of ECG, blood pressure, echocardiography, EFI.

Depending on the characteristics of the anamnesis or data from objective research methods, appropriate changes are made to the program.

Despite the variety of phenomenological manifestations of paroxysms characterized by impaired consciousness, two main groups of paroxysmal disorders of consciousness are currently distinguished - epileptic and non-epileptic. In the structure of the last syncope(fainting) states occupy a leading place.

In some patients, convulsive syncope masquerades as epileptic seizures.. After an initial neurological examination, such patients are often prescribed treatment with antiepileptic drugs. Despite ongoing therapy, 25% of patients with epilepsy have 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 recurrent unexplained palpitations should be subject to 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

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

The following states are currently distinguished:
1. neurogenic syncope: psychogenic, irritative, maladaptive, dyscirculatory.
2. Somatogenic syncope: cardiogenic, vasodepressor, anemic, hypoglycemic, respiratory.
3. Syncopal conditions during extreme exposure: hypoxic, hypovolemic, intoxication, drug, hyperbaric.
4. Rare and multifactorial syncope: nocturic, cough.

In addition, considering fainting as a process unfolded in time, the severity of syncopal conditions is distinguished.
1. Presyncope:
I degree - weakness, nausea, flies before the eyes;
II degree - more pronounced symptoms described above with elements of impaired postural tone.
2. Syncope:
I degree - short-term shutdown of consciousness for a few seconds without a pronounced post-seizure syndrome;
II degree - a longer loss of consciousness and pronounced post-seizure manifestations.
The above classification emphasizes that syncopal paroxysm is a phased 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 a lack of strength with a feeling of impending loss of consciousness. At the beginning of fainting (!!!) the patient is always in an upright position, except for the Adams-Stokes attack. Usually the patient has a presentiment of impending fainting. At first, he becomes ill, then there is a feeling of movement or swaying of the floor and surrounding objects, the patient yawns, flies appear before his eyes, tinnitus, nausea, sometimes vomiting, vision is weakened. With a slow onset of syncope, the patient can prevent falls and injury by quickly assuming a horizontal position. In this case total loss consciousness may not exist.

The depth and duration of the unconscious state are different
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 be in this state for several seconds or minutes, sometimes even about half an hour. As a rule, the patient lies motionless, skeletal muscles are relaxed, however, immediately after loss of consciousness, clonic twitches of the muscles of the face and trunk occur. The functions of the pelvic organs are usually controlled, the pulse is weak, sometimes not palpable, blood pressure (BP) is lowered, 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 deep, the complexion normalizes, consciousness is restored. From this moment on, a person begins to adequately perceive the environment, but feels a sharp physical weakness, too hasty an attempt to get up can lead to repeated fainting.
Headache, drowsiness, and confusion usually do not occur after fainting.

Fainting of vascular origin

Vascular syncope includes conditions resulting from a drop in blood pressure or a decrease in venous return of blood to the heart:
vasovagal
sinocarotid
orthostatic
situational syncope.
psychogenic syncope is also distinguished as a result of the influence of psycho-emotional factors

Patients describe fainting as the appearance of a feeling of lightheadedness, dizziness. They turn pale, perspiration appears, then the patients lose consciousness. It is believed that the pathogenetic basis of vasovagal syncope is excessive deposition of blood in the veins. lower extremities and disturbance of reflex influences on the heart. Other variants of vasovagal syncope have also been described. With intense pain syndrome of visceral origin, irritation vagus nerve can contribute to a slowdown in cardiac activity and even cardiac arrest, for example, with 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 develops with a severe migraine attack.

Sinocarotid syncope

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

Orthostatic syncope

The main difference between orthostatic syncope- their appearance only when moving from a horizontal to a vertical position.
Orthostatic arterial hypotension is the cause of syncope in an average of 4-12% of patients.

This type of syncope occurs in individuals With chronic insufficiency or periodic instability of vasomotor reactions. A decrease in blood pressure after taking 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 vessels.

Postural syncope develops in almost healthy people who, for unknown reasons, have defective postural responses (which may be familial). In such people, a feeling of weakness occurs with sharp inclinations, their blood pressure drops slightly, and then sets 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 insufficiency of the autonomic nervous system, family vegetative dysfunctions.

At least three syndromes of orthostatic syncope have been described:

I. Acute or subacute autonomic dysfunction. In this disease, in apparently healthy adults or in children, partial or complete breakdown activities of the parasympathetic and sympathetic systems. Pupillary reactions disappear, lacrimal, salivary and sweating stop, impotence, paresis are observed Bladder and intestines, orthostatic hypotension. Additional studies reveal an increased protein content in the cerebrospinal fluid, 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 people of middle and older age, who gradually develop chronic orthostatic hypotension, sometimes in combination with impotence and dysfunction of the pelvic organs. After staying in an upright position for 5-10 minutes, blood pressure decreases by at least 35 mm Hg. 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 apparently irreversible.

III. Chronic insufficiency of preganglionic autonomic nerve fibers. In this disease, orthostatic hypotension, along with recurrent 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 family;
3. More variable extrapyramidal and cerebellar diseases(striato-nigral degeneration).

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

Secondary orthostatic hypotension results from
disorders of the autonomic nervous system
age-related physiological changes
adrenal insufficiency
hypovolemia
taking certain drugs (hypotensive drugs, tricyclic antidepressants, levodopa drugs, neuroleptics, -blockers), especially in elderly patients who have to take several drugs 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 are involved in the pathological process (syringomyelia) or peripheral nerves(diabetic, alcoholic, amyloid polyneuropathy, Adie's syndrome, hypovitaminosis, etc.)
orthostatic hypotension is considered one of the manifestations parkinson's disease,
multisystem atrophy of the brain
subclavian artery steal syndrome
But more often the causes of orthostatic hypotension are starvation, anemia, prolonged bed rest.

Situational syncope

Situational syncope occurs with coughing, urinating, defecation, and swallowing. Fainting during urination or defecation is a condition commonly seen in older people during or after urination, especially after a sudden transition from a horizontal to an upright position. It can be distinguished as a separate type of postural syncope.

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

Syncope of a psychogenic nature
The psychogenic nature of syncope is detected in patients after 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 a first episode of syncope (further examination may be discontinued), and
patients who continue to worry about fainting (an assessment of the mental state of the patient should be carried out). In almost 25% of such cases, a psychiatric examination can detect mental disorders associated with fainting.

Often, emotionally labile people develop against the background of the action of a psychotraumatic factor. panic attacks, which are characterized by a sudden onset, palpitations, a feeling of heat, lack of air, then pain in chest, trembling, feeling of fear and doom. Hyperventilation is followed by paresthesias. At such moments, patients subjectively feel a loss of consciousness or even the onset of death, but there is no loss of consciousness or a fall. Conversation with eyewitnesses of seizures, the test with hyperventilation and the appearance of the above symptoms help the clinician to correctly diagnose.

Separately, it is necessary to describe non-epileptic seizures, or pseudo-seizures. They are more common in women around the age of 20, in whose family history, as a rule, there are references to relatives who suffered from epilepsy. Such patients had the opportunity to observe the development of epileptic seizures, imitate them, or suffer from mental illness themselves. Pseudo-seizures are varied and last longer than true epileptic seizures. They are characterized by poor coordination of movements, complex localization, occur in crowded places, injuries are very rare. During a seizure, the patient may resist seeing 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 contributing to the deterioration of cerebral blood flow, malnutrition of the brain and, ultimately, episodic blackouts.
1. Cardiac- weakening of the force of contractions of the heart of a neurogenic nature or due to acute functional insufficiency of the heart muscle, valvular apparatus, cardiac arrhythmias.
2. Vascular- a drop in vascular tone of the arterial or venous systems, accompanied by a significant decrease in blood pressure.
3. Homeostatic- a change in the qualitative composition of the blood, especially a decrease in the content of sugar, carbon dioxide, oxygen.

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

The survey should also include
electroencephalography
computed and magnetic resonance imaging of the brain
transcranial dopplerography in case of suspected presence of a stenosing process (in people over 45 years of age, in case of detection of noise over the carotid artery, in persons who have had transient ischemic attacks or stroke).

Fainting in the elderly

(!!!) With the development of syncope in elderly patients, first of all, you need to think about the appearance of a complete transverse blockade of conduction or tachyarrhythmia. When examining them, it is necessary to remember the complex nature of syncope and the fact that such patients often take several medications at the same time. medicines.

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

If the examination reveals orthostatic hypotension, it is necessary to Special attention for patient admission 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 to studies of the cardiovascular and nervous systems. If, during a neurological examination, there are no pathological changes, but there are complaints of impaired urination, sweating, constipation, impotence, and the patient talks about the development of fainting only after getting out of bed abruptly or after sleep, then the development chronic vegetative insufficiency. 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, first sit down or make several movements with the legs lying down, use elastic bandages and bandages, lay carpets in the bathroom and corridor, as this is the most frequent places falls due to syncope in the elderly. 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.

Fainting, also known as syncope or syncope in the language of official medicine, is a short-term disturbance of consciousness, usually leading to a fall.

The word "syncope" is of Greek origin ( syn- with, together; koptein- cut off, cut off), later this word migrated to the Latin language - syncopa from which it came into musical terminology (syncope). However, in clinical medicine to denote pathological conditions it is customary to use terms that are etymologically related to the Greek language, so the word “syncope” is still more correct.

In some cases, the development of fainting is preceded by a variety of symptoms, which is called lipothymia (weakness, sweating, headache, dizziness, visual disturbances, tinnitus, a premonition of an imminent fall), but more often syncope develops suddenly, sometimes against the background of "complete well-being".

At the same time, the presence of precursors of fainting is not similar to the aura that accompanies epileptic seizures. The harbingers of fainting are more "earthly" in nature and are never expressed in the form of bizarre sensations: the smell of roses, auditory hallucinations, etc.

Sometimes patients with habitual fainting, when lipothymia appears, may have time to sit or lie down, inflict painful irritations on themselves (pinch themselves or bite their lip), trying to avoid loss of consciousness. Often this succeeds.

The duration of loss of consciousness during fainting, as a rule, is 15-30 seconds, less often it drags on for up to several minutes. Protracted syncope can cause significant difficulties when trying to distinguish them from other diseases that may be accompanied by disorders of consciousness.

Not every time it is possible to distinguish an epileptic seizure from a faint. With prolonged fainting, as with a seizure, twitching of the muscles of the trunk and face may be noted. The only thing is that patients with fainting never arch into an arc - they do not have what is called generalized convulsions (simultaneous convulsive contraction of many muscles).

Causes of syncope

The cause of fainting is a sudden decrease in blood flow to the brain. With a sharp decrease in cerebral blood flow, six seconds may already be enough for the consciousness to turn off.

There may be several reasons behind this incident:

• reflex decrease in arterial tone or disruption of the heart, accompanied by a decrease in the amount of blood expelled from it;
• heart rhythm disturbances (sharp bradycardia or tachycardia, short-term episodes of cardiac arrest);
• changes in the heart, as a result of which there are disorders of blood flow inside the heart chambers (malformations).

The likely causes of fainting vary with age, in older people, first of all, disorders in the vessels that feed the brain (narrowing of these vessels caused by atherosclerosis) should be suspected, or various diseases hearts.

For young patients, fainting is more typical, developing as if in the absence of changes in the heart and blood vessels - most often these are fainting, which are based on impaired functioning of the nervous system or mental disorders.

In about one-third of all cases, the cause of fainting is never found, despite the ongoing examination.

One of the mechanisms for the development of fainting is the so-called orthostatic mechanism, a kind of human retribution for walking upright. The principle of orthostatic disorders is the insufficient supply of blood to the brain due to the victory of gravity and the accumulation of blood in the lower parts of the body. This occurs either due to insufficient vascular tone, or with a decrease in the volume of blood in the bloodstream.

Repeated fainting in a standing position can occur in people who have been suffering from diabetes mellitus for a long time, since this disrupts the innervation of blood vessels (autonomous diabetic neuropathy), with Parkinson's disease, with adrenal insufficiency (the amount of hormones responsible for maintaining blood pressure decreases).

A decrease in circulating blood volume can be caused by both bleeding and a decrease in the volume of the liquid part of the blood (for example, severe sweating in the heat, recurrent diarrhea, profuse vomiting).

In pregnant women, due to the inconsistency of the amount of blood with the needs of the "doubled" body, a tendency to fainting is also manifested.

Orthostatic reactions can provoke alcohol consumed in excessive doses, and some drugs. About drugs that can cause a short-term loss of consciousness, it should be said separately.

First of all, these are drugs that reduce blood pressure: drugs taken to dilate blood vessels and diuretics. When prescribing them, the doctor warns that the pressure may decrease excessively, so you should not walk for a long time after taking the medicine for the first time in your life or simply stand for a long time.

The most common are reactions to drugs based on nitroglycerin, so they should always be taken with great care.

Separately, I would like to warn: nitroglycerin is a drug intended for the treatment of angina pectoris. It is by no means a universal remedy for the treatment of all cases; in patients, at the time of fainting, sometimes there is a feeling of pressure in the region of the heart, stabbing pain and other discomfort in the chest.

Nitroglycerin, hastily thrust under the tongue, will only aggravate an already unpleasant situation. Therefore, in most cases of syncope, it should not be given, and if the need for this medicine is not in doubt, then at least an approximate estimate of the level of blood pressure is required. At low pressure, the presence of which can be suspected by such signs as a pulse of weak filling, cold and moist skin, nitroglycerin is contraindicated.

Drugs used to treat erectile dysfunction in men (sildenafil, vardenafil and tadalafil) can also contribute to the development of orthostatic reactions. The danger of their simultaneous administration with nitroglycerin is especially pointed out - the combined use of these drugs can very sharply reduce the level of blood pressure in the vessels due to a sharp expansion of the latter.

Another mechanism is involved in the basis neuroreflex syncope, the appearance of which is associated with irritation of certain reflexogenic zones. The triggered reflex causes a decrease in heart rate and vasodilation, which ultimately leads to a decrease in blood flow in the brain.

Receptors of the nervous system, the irritation of which can lead to fainting, are scattered throughout the body. Ear irritation with a funnel at an ENT doctor's appointment is one of the typical reasons fainting in medical institutions.

On the neck, near the corner mandible, in the place where the common carotid artery bifurcates, there are carotid sinus glomeruli, the irritation of which can cause loss of consciousness. This trouble primarily concerns men with a short neck, to whom the conservative dress code prescribes a tight buttoning of collars, accompanied by a tightening of the tie.

Men can also suffer from irritation of this area with a razor. At one time, even the "barber's symptom" stood out. Oddly enough, but heavy jewelry (massive earrings or chains) can also provoke fainting, pressing or sometimes simply touching an overly active reflexogenic zone.

An increase in chest pressure that occurs when coughing, sneezing, or straining causes fainting in people with overly sensitive receptors in the lungs. Associated with this is the dizziness that sometimes occurs when breaststroke swimming.

Reflex impulses from the intestines, resulting from banal flatulence, causing even a short-term disorder of consciousness, makes one think of a serious catastrophe abdominal cavity. The same can be said about the reflexes from the bladder when it is overdistended due to urinary retention (associated with illness or even arbitrary).

FROM bladder associated with such an unpleasant faint as a faint that occurs in men at the time of urination. Anatomically, the urethra in a man is several times longer than in a woman, the resistance to urine flow is again higher, and the reasons for increasing this resistance are more often (prostate adenoma, for example). And then, having experienced several losses of consciousness, a man has to adapt to the situation that has arisen (for example, to urinate while sitting).

Syncopal states that develop against the background of erotic stimulation or against the background of orgasm look quite “romantic”. Alas, they are not associated with an emotional outburst, but with the activation of the reflexogenic areas of the genital organs.

In addition to vasodilation and a decrease in cardiac output, the cause of loss of consciousness can also be cardiac arrhythmias. Of all situations, these are the most dangerous for the patient, as they represent the greatest risk to life.

The fact is that some rhythm disorders that do not initially lead to cardiac arrest can, after a few seconds or minutes, cause a potentially fatal disorder when the fibers of the heart “twitch” in different directions without carrying out any coordinated activity and without “chasing away” blood through the vessels. This disorder is called "fibrillation".

It follows that any cardiac arrhythmias that cause impaired consciousness should be considered very seriously and be the reason for hospitalization in a hospital for the purpose of both in-depth examination and the choice of treatment or even surgery.

Diseases of the heart and lungs that cause transient disorders of consciousness are a rather heterogeneous group of diseases. These can be heart valve lesions, in which there is a violation of intracardiac blood flow, and pulmonary disorders, when an obstruction to normal blood flow occurs already in the pulmonary circulation.

Finally, damage to the blood vessels that directly feed the brain can also lead to fainting. The cause of fainting is both internal barriers to blood flow (large atherosclerotic plaques, for example), and compression of a large vessel by something from the outside.

According to current ideas, not all short-term disorders of consciousness are usually classified as syncope. Non-syncopal is the nature of loss of consciousness during an epileptic seizure, heat or sunstroke, hyperventilation disorder (acute panic attack, accompanied by deep and rapid breathing).

Separately, such a disease as syncope migraine stands out. Being similar to migraine in its main manifestation - headache, it has one fundamental difference. If a classic migraine attack is also resolved classically - with severe nausea and vomiting, which brings immediate relief, then with syncope migraine, the apotheosis of the attack is not vomiting, but fainting. Waking up, the patient realizes that the headache has disappeared somewhere or almost disappeared.

Such, for example, a rare diagnosis as myxoma (a tumor growing into the lumen of the heart on a thin stalk), may be suspected if syncope develops when turning from side to side. This happens because a tumor “dangling” freely enough in the lumen of the chambers of the heart, under certain positions, can block the blood flow through the heart valve.

When syncope occurs stereotypically during defecation, urination, coughing, or swallowing, one speaks of situational syncope.

The situation when syncope is associated with tilting the head back (as if the patient wanted to look at the ceiling or at the stars) has a beautiful name "Sistine Chapel syndrome" and can be associated with both vascular pathology, and with hyperstimulation of the carotid sinus zones.

Syncopal conditions that occur during physical exertion suggest the presence of stenosis of the outflow tract of the left ventricle.

Establishing the cause of syncope can be greatly helped by the correct collection of complaints and medical history. The key points to be assessed are:

• establishing the posture in which syncope developed (standing, lying, sitting).

• clarification of the nature of the actions that led to syncope (standing, walking, turning the neck, physical exertion, defecation, urination, coughing, sneezing, swallowing).

• previous events (overeating, emotional reactions, etc.)

• detection of precursors of syncope (headache, dizziness, "aura", weakness, visual disturbances, etc.). Separately, you should find out the presence of symptoms such as nausea or vomiting before losing consciousness. Their absence makes one think about the possibility of developing cardiac arrhythmias.

• clarification of the circumstances of the syncopal episode itself - the duration, the nature of the fall (backwards, "sliding" or slow kneeling), the color of the skin, the presence or absence of convulsions and biting the tongue, the presence of respiratory disorders.

• characteristics of resolution of syncope - the presence of lethargy or confusion, involuntary urination or defecation, discoloration of the skin, nausea and vomiting, palpitations.

• anamnestic factors - a family history of sudden death, heart disease, syncope; a history of heart disease, lung disease, metabolic disorders (primarily diabetes and pathology of the adrenal glands); taking medications; data on previous syncope and examination results (if any).

In all cases of fainting, it may be necessary to make an electrocardiogram (if not immediately, then later). The fact is that a number of diseases that can cause heart rhythm disturbance, leading to loss of consciousness, are detected precisely with an ECG. In the worst case, loss of consciousness may be the debut of myocardial infarction, the diagnosis of which is also made on the basis of a cardiogram.

To confirm the orthostatic origin of syncope, an elementary test can be performed when measuring blood pressure. The first measurement is taken after a five-minute stay of the patient in the supine position. The patient then stands up and measurements are taken at one and three minutes.

In cases where the decrease in systolic pressure is more than 20 mm Hg. Art. (or below 90 mm Hg. Art.) is fixed in the first or third minutes, the sample should be considered positive. If the pressure reduction indicators do not reach the indicated values, but by the third minute the pressure continues to decrease, measurements should be continued every two minutes, either until the indicators stabilize or until critical numbers are reached. Naturally, this test should be carried out by a doctor.

Even if the usual test with the measurement of pressure did not give a result, suspicions of the orthostatic origin of syncope may still remain. For the final decision of a dubious issue, a “tilt test” is performed (from English, to tilt- tilt).

The patient is placed on the table and attached to this table so that when the table is tilted, it remains in a kind of "crucified" position. The table tilts, as if the patient is "put" on his feet, while determining changes in blood pressure during the transfer to a vertical position. A rapid decrease in blood pressure (and in rare cases, the development of pre-syncope) confirms the diagnosis of orthostatic syncope.

Blood pressure measurement should be taken on both arms. If the difference exceeds 10 mm Hg. Art., you can suspect the presence of aortoarteritis, subclavian artery syndrome or dissection of the aneurysm in the aortic arch, i.e. diseases, each of which can lead to uneven blood flow in the brain system, and each of which requires medical intervention.

Normally, in any person, the difference in pressure can reach 5-10% on two hands, but if these differences have become larger, increased or appeared for the first time in life, it makes sense to consult a doctor.

Treatment

Vasovagal syncope and other manifestations of the neuroreflex syndrome require only general measures - the patient should be placed in a place as cool as possible, with open access to fresh air, unfasten tight clothing or squeezing accessories (belt, collar, corset, bra, tie), give the legs an elevated position .

Turning the head to one side to prevent retraction of the tongue is allowed only if there is no damage to the subclavian, carotid and vertebral arteries.

The application of painful stimuli (slaps, for example), as a rule, is not required - the patient soon regains consciousness on his own. In protracted cases, a cotton wool with ammonia brought to the nose, or simply tickling the mucous membrane of the nasal passages, can accelerate the return of consciousness. The last two effects lead to the activation of the vasomotor and respiratory centers.

In a situation where previous profuse sweating led to the development of fainting, you should simply replenish the volume of fluid - give plenty of fluids. A universal remedy for post-fainting weakness is tea - a liquid plus caffeine, which maintains vascular tone and cardiac output, plus sugar, which is necessary taking into account possible hypoglycemia (low blood glucose).

Most syncope does not require specific drug therapy. Young patients prone to orthostatic reactions may be recommended to increase the amount of salty foods, and drugs that support vascular tone are occasionally prescribed.

Hospitalization

Patients with "habitual" or "situational" syncope, previously examined, who do not cause concern for further prognosis, are not required to be admitted to the hospital.

Patients are subject to hospitalization in order to clarify the diagnosis:

• with suspected heart disease, including with changes in the ECG;
• the development of syncope during exercise;
• family history of sudden death;
• sensations of arrhythmia or interruptions in the work of the heart immediately before syncope;
• recurrent syncope;
• development of syncope in the supine position.

Patients are subject to hospitalization for the purpose of treatment:

• with rhythm and conduction disturbances that led to the development of syncope;
• syncope, probably due to myocardial ischemia;
• secondary syncopal conditions in diseases of the heart and lungs;
• the presence of acute neurological symptoms;
• violations in the work of a permanent pacemaker;
• injuries resulting from a fall during syncope.

The content of the article

One fainting is an accident, and the second is a pattern. Her name is syncope. We talk about the causes of frequent fainting.

Syncope in numbers

The Latin word "syncope" means "chopping". So called sudden fainting, short-term loss of consciousness. The syncopal period lasts from 6 seconds to a couple of minutes, ending with a severe “turning on” to reality and muscle weakness.

Statistics say: every third adult has experienced syncope. The treatment of sudden fainting is a big medical problem. Often, it is possible to find out the root cause of the blackout only after a thorough clinical examination.

Causes of syncope

When on the tonometer "90 to 60"

Hypotension is a disease of people under 30. A typical portrait of a hypotensive patient: thinness, obsessive fears and thoughts, passive lifestyle, weather dependence. On the background asthenic syndrome often "sprouts" vegetovascular dystonia(VSD) according to the hypotonic type.

THIS VARIANT OF VVD TAKES THE FIRST PLACE AMONG THE NON-PATHOLOGICAL PROCESSES THAT CAUSE FAINS.

In addition to syncope, with hypotonic VSD, the following are observed:

• Constant fatigue;
• Insomnia;
• Poor adaptation to temperature changes;
• Pale skin;
• respiratory disorders and intermittent shortness of breath.

How to prepare for fainting?

Before a faint, there is a presyncope, or a pre-fainting, when a person feels - now he is falling asleep. Have time to sit down or warn others, avoid injury when falling.

Alarming factors:

• Cold sweat;
• Strange visual phenomena (fog, black flies before eyes);
• Dizziness;
• Noise in ears;
• Nausea;
• Unmotivated panic;
• Feeling of soaring.

What should hypotensive patients do?

Raise blood pressure– good protection against hypotonic shutdowns:

• Consume caffeine;
• Drink warm drinks;
• Walk more, run more;
• Breathe scientifically: Alternate short breaths and long exhalations for 1-2 minutes.

Now you know what syncope is, where it comes from and how to treat it. Lose consciousness from nerves, tachycardia, hypertension, lack of oxygen - pay attention to the drops of Cardiovalen.

The drug tones the blood vessels,

The prevalence of syncope is so great that it would be unforgivable to bypass this topic in this edition.

Definition. Fainting, or syncope, is a syndrome characterized by a brief and relatively sudden loss of consciousness, usually accompanied by loss of muscle tone and a fall. After a syncope, consciousness spontaneously, completely and usually quickly recovers.
Retrograde amnesia is usually not characteristic.
Sometimes in recovery period fatigue, weakness may be noted.
Pre-syncope is a situation in which patients feel on the verge of losing consciousness.

Clinical signs pre-syncope (eg, dizziness) are not always specific, usually they are similar to symptoms preceding complete syncope.

Pathophysiology of syncope. The main mechanism of syncope is short-term general hypoperfusion of the brain. Some forms of syncope may be preceded by cerebral symptoms (eg, dizziness, nausea, sweating, weakness, visual disturbances) warning of imminent loss of consciousness. Factors leading to syncope vary from patient to patient, but some general principles worthy of mention.
For a complete loss of consciousness, as a rule, it is enough to stop cerebral blood flow for 6-8 seconds or reduce the supply of oxygen to the brain by at least 20%.

Classification.
Causes of fainting:
1. Neurogenic syncope (due to reflexes that cause vasodilation and / or bradycarlia): vasovagal syncope (simple syncope); syncope with carotid sinus hypersensitivity syndrome; postprandial hypotension; situational syncope (at the sight of blood; when coughing, sneezing; when stimulating the digestive tract - swallowing, defecation, visceral pain; during or after urination; during or after exercise; in other situations, for example, when playing wind instruments, weight lifting); neuralgia of the trigeminal or glossopharyngeal nerve.

2. Orthostatic syncope (the result of the inability of the autonomic nervous system to maintain vasoconstriction mechanisms, which leads to orthostatic hypotension, especially with hypovolemia).

3. Hypovolemia: bleeding, diarrhea, Addison's disease; drug orthostatic hypotension (diuretics, antihypertensive drugs).
4. Arrhythmic syncope (the cause is a decrease in cardiac output, which in this case often does not meet the needs of blood circulation): violation of the automatism of the sinus node (SSS, regulatory dysfunction of the sinus node); violation of atrioventricular conduction; paroxysmal supraventricular and ventricular tachycardias; hereditary syndromes (eg, long QT syndrome, Brugada syndrome); malfunction of the implanted device (pacemaker, cardioverter-defibrillator); drug-induced arrhythmias.

5. Fainting in cardiovascular pathology (circulation demands exceed the capacity of the heart): valvular heart disease; acute myocardial infarction/CHD; obstructive cardiomyopathy; atrial myxoma; acute aortic dissection; pericardial disease/cardiac tamponade, pulmonary embolism/pulmonary hypertension.

6. Fainting in idiopathic arterial hypotension (due to initially low systemic blood pressure): cerebrovascular syncope (fainting due to short-term ischemia of the brain stem, occurring without focal neurological symptoms); atherosclerosis of the vertebral arteries in combination with cervical osteochondrosis; subclavian-spinal steal syndromes (may cause syncope when a blood vessel must simultaneously nourish both upper limb, and part of the brain); pathological tortuosity of brachiocephalic vessels; anomalies in the structure of the cranio-cervical junction (for example, the Sistine Chapel syndrome).
The prevalence of fainting.
Risk stratification.

The Framingham Study over a 26-year follow-up period found that at least one syncopal episode occurred in approximately 3% of men and 3.5% of women.
In some population groups, syncope is noted in 15-25% of cases.
In the elderly, the incidence of syncope is at least 6% per year, with a prevalence of up to 10%. Approximately 35% of patients recur during three years of follow-up, with 82% of recurrent episodes occurring in the first two years.
Patients with recurrent syncope have a limited functional status, similar to patients with other chronic diseases.
Mortality in patients with cardiogenic syncope during the year was significantly higher (18-33%) than in patients with non-cardiac causes (0-12%) or syncope of unknown etiology (6%).

Diagnostics. Survey tactics. Examination of a patient with syncopal syndrome should begin with a thorough history taking and physical examination, including measurement of blood pressure in orthostasis. A 12-lead ECG is required.

During the initial examination, three key questions should be answered: Is unconsciousness a syncope? Does the patient have heart disease? Do you have a history clinical features that can be used to suggest a diagnosis?

Differentiation of true syncope from other "non-syncopal" conditions is generally the first diagnostic step and influences the subsequent examination tactics.
The initial examination may lead to a definite or suspected diagnosis, or to no result.

In this case, they resort to: the term "fainting of unclear etiology."
If during the initial examination there is a suspicion of an organic heart lesion or ECG changes are detected, a cardiological examination is recommended for this group of patients, including echocardiography, a stress test and measures aimed at detecting arrhythmias - Holter monitoring or electrophysiological examination.

If such an examination does not give results, in cases of repeated or severe syncope, the diagnosis adopted for neurogenic and orthostatic syndromes is recommended. It includes a carotid sinus massage and a tilt test.
Massage of the carotid sinuses is recommended for patients over 40 years of age with syncope, the etiology of which remains unclear.
During the massage, continuous monitoring of the ECG and blood pressure is mandatory. The duration of the massage is from 5 to 10 s.
Massage should be performed both with the patient lying on his back and in a vertical position.
In the elderly, a more delicate effect is preliminarily carried out - pressing the carotid artery at the same time.
The result is considered positive if syncopal symptoms are reproduced during or immediately after the massage as a result of asystole for more than 3 s and / or a drop in systolic blood pressure by 50 mm Hg. Art. and more.
In this case, in the absence of another competing diagnosis, the etiology of syncope can be considered established.

Tilt test. After a five-minute rest in a horizontal position, the patient is placed for 45 minutes on a table with an angle of inclination from 60 to 70 degrees. The moment of the end of the test is the provocation of pre-syncope or the expiration of the scheduled tilt time of the table.
The test is considered positive if it was possible to provoke pre-syncope symptoms.

Evaluation of the results of the tilt test:
Type 1. Mixed. During fainting, the heart rate decreases, but it is at least 40 beats per minute, or it slows down to less than 40 beats per minute, but this lasts no more than 10 seconds. The fall in blood pressure precedes the fall in heart rate.

Type 2A. Cardioinhibition without asystole. The heart rate decreases to less than 40 bpm, which lasts more than 10 s, but there is no asystole for more than 3 s. The decrease in blood pressure outpaces the decrease in heart rate.

Type 2B. Cardioinhibition with asystole. Asystole lasts more than 3 seconds. The decrease in blood pressure coincides with the decrease in heart rate or ahead of it.

Type 3. Vasodepression. During syncope, the heart rate does not decrease by more than 10% of the original.
Exception 1. Chronotropic insufficiency. In orthostasis, the increase in heart rate is less than 10% of the original.
Exception 2. Excessive increase in heart rate. In orthostasis, heart rate increases by more than 130 bpm.

Tilt testing is not indicated for assessing the effectiveness of treatment; with single syncope without traumatization and high risk of consequences; with clear clinical vasovagal symptoms, allowing the diagnosis, when confirmation of a neurogenic mechanism would not change the tactics of management. Monitoring of the electrocardiogram.

Holter monitoring is indicated in patients with both established and undiagnosed heart disease and syncopal episodes if a high probability of detecting an arrhythmia causing syncope is suspected. ECG monitoring is diagnostically significant if the association of syncope with brady- or tachyarrhythmias is proven. ECG monitoring excludes an arrhythmic cause if syncope occurs against the background of sinus rhythm.

In the absence of syncopal episodes with repeated Holter monitoring and the preservation of the idea of ​​the arrhythmic nature of syncope, an additional examination is recommended (use of long-term ECG monitoring systems, electrophysiological examination). A transfusion water electrophysiological study is indicated for the detection of supraventricular tachycardia with a high heart rate in patients with a "syncope" history of palpitations, or with changes in the electrocardiogram, and / or heart disease, or in the case of sudden death in relatives; to assess the function of the sinus node and AV conduction in patients with syncope, probably associated with bradyarrhythmia.

An invasive electrophysiological study is indicated for suspected arrhythmic syncope, if transesophageal pacing does not initiate supraventricular tachycardia, syncope is suspected to be associated with ventricular tachycardia, or transient high-degree AV block is suspected in patients with bifascicular block.

A negative EPS result cannot completely rule out an arrhythmic cause of syncope; if an arrhythmia is still likely, further investigation is recommended. On the other hand, positive result EPS, depending on the clinical context, may not necessarily be interpreted as a cause of syncope.

Syncopal episodes that occur during exercise require a special test.
Test with physical activity is positive if syncope is reproduced during or immediately after it, and electrocardiographic and hemodynamic changes are recorded.
The exercise test is positive if, during exercise, even in the absence of syncope, second-degree Mobitz II or complete transverse block develops.

Treatment.
The main goals of treating a patient with syncope can be interpreted broadly: from preventing recurrence of syncope to reducing the risk of death.
Treatment should be based on the etiology of the disease, the risk of death, the risk of physical or emotional injury from recurrent syncope, the profession of the patient, the effectiveness, safety, and possible side effects of therapy.

Patients with single reflex syncope without a high risk of traumatizing themselves and others do not need treatment.
In the case of cardioinhibitory syncope, the appointment of b-blockers is contraindicated, as they can aggravate bradycardia.

For the treatment of patients with orthostatic hypotension, the main diagnosis is important. Some provisions of therapy, despite the pathogenetic differences in orthostatic and neurogenic syndromes are common.
This applies, for example, to the refusal of provoking agents (diuretics, vasodilators, alcohol); exclusion of provocative and trigger moments (sudden rising and prolonged standing, as well as lying down during the daytime, high temperature environment, straining, hyperventilation, significant stress, etc.); correction of the causative disease in primary and secondary autonomic insufficiency, hypovolemia; increased salt and fluid intake (up to 2-2.5 liters per day).

In case of ineffectiveness of non-drug methods as additional measure pharmacotherapy may be indicated.
For orthostatic syncope, the appointment of fludrocortisone (0.1-0.2 mg per day) is recommended; sleeping with the head end of the bed raised; use of abdominal bandages and / or elastic tights; use of portable seats; frequent use small amounts of food; the use of techniques such as crossing legs and squatting; special exercises for the legs and abdominals; administration of midodrine.

In syncope associated with SSS and / or impaired atrioventricular conduction, when there is evidence of a connection between bradyarrhythmia and syncope, pacing is indicated.
For paroxysmal supraventricular tachycardia leading to syncope, catheter ablation is performed.
In case of syncope due to ventricular tachycardia, antiarrhythmic therapy is recommended (preferably a class III antiarrhythmic agent, especially amiodarone).

In some forms of tachycardia (the location of the focus of arrhythmia in the outflow tract of the right ventricle), the method of choice is catheter ablation. Implantation of a cardioverter-defibrillator is indicated for syncope as a result of documented ventricular tachycardia or ventricular fibrillation without the possibility of correction of causes (for example, drug-dependent).

The next indication for implantation may be undocumented syncope, probably due to ventricular tachycardia or fibrillation from a previous myocardial infarction and induced sustained monomorphic ventricular tachycardia with serious hemodynamic consequences, and the absence of any competing diagnosis as a cause of syncope.

Treatment of other forms syncope should be directed to a specific causative disease or its consequences.

In a hospital setting, cardiac arrhythmias should be treated as the cause of fainting; fainting due to myocardial ischemia, due to cardiovascular pathology; with stroke or focal neurological symptoms; with a cardioinhibitory type of neurogenic syncope for the planned implantation of a pacemaker.