Causes of syncope. Algorithm for diagnosis and treatment of syncope in neurological practice

In modern medical practice, the word “fainting” has not been used for a long time. The outdated name has been replaced by a new term - syncope. Attacks of sudden and persistent loss of consciousness for a short or long period of time occur periodically in adults and children. Syncope of any origin is dangerous for elderly people, as they lead to severe traumatic brain injuries and femoral neck fractures.

What is syncope?

Syncope is a syndrome characterized by a sudden short-term loss of consciousness, accompanied by a loss of resistance muscle tone. After fainting, the disorder of consciousness is quickly and completely restored. So, syncope (ICD code 10) is:

• Loss of consciousness lasting no more than a minute;
• There are no neurological disorders after syncope;
• After an attack, headache, weakness, and drowsiness may occur;
• Loss of consciousness of various etiologies is more often observed in children, women and adolescents, but can also occur in healthy men;
• Older people often forget the few minutes that precede a syncope attack.

During fainting, the patient has no tension in the muscles, the pulse slows down, and breathing movements decrease. A person’s skin becomes pale, he does not react in any way to external stimuli. In rare cases, involuntary urination may occur during syncope.

Causes of fainting

The human brain needs intensive blood supply to its tissues. For normal functioning, it requires 13% of the total blood flow. Against the background of stress, fasting or physical activity, these numbers change. Considering the average weight of the brain (1500 g), a person needs 750 ml of blood per minute. A reduction in the indicator leads to pre-fainting states. But the blood flow does not stop on its own. There are reasons for this:

• organic cardiovascular diseases;
• transient ischemic attacks;
• increased activity of the vagus nerve;
• decrease in blood glucose;
• pathological vasovagal reflex;
• dehydration or poisoning;
• heart rhythm disturbances;
• neuralgia of the glossopharyngeal nerve;
• mental disorders, hysteria;
• cerebral hypoperfusion;
• vegetative-vascular dystonia (VSD);
• infectious diseases;
• traumatic brain injuries;
• pulmonary hyperventilation syndrome;
• for pericarditis and epilepsy;
• congenital cardiogenic conditions;
• unknown genesis.

Classification of syncope

According to the classification adopted by the European Society of Cardiology, syncope syndrome is divided into 5 types.

1. Reflex (neurotransmitter) fainting. Syncope is caused by bradycardia and peripheral vasodilation due to hypoperfusion or hypotension. Situational fainting is provoked by unpleasant sounds, pain, emotions, coughing, a sharp turn of the head, or a tight collar.
2. Orthostatic collapse. Syncope occurs when standing for a long time in hot, crowded places or under load. There is an incorrect reaction of the nervous system to a change in posture (a sharp transition to a horizontal position). This type of fainting can be caused by problems with the heart, taking certain medications, multiple system atrophy, or Parkinson's disease.
3. Cardiac arrhythmia. Tachycardia, asystole and sinus bradycardia lead to decreased cardiac output. Potential causes of syncope include hereditary pathologies, ventricular or supraventricular paroxysmal tachycardia, and decreased atrioventricular conduction.
4. Structural heart diseases. These are systolic pulmonary hypertension, aortic stenosis, cardiac myxomas. The likelihood of syncope increases when the body's circulatory needs far exceed the organ's ability to increase cardiac output.
5. Cerebrovascular syncope. It occurs as a result of low perfusion of the brain, which is associated with cerebrovascular pathologies. Among these diseases are vertebrobasilar insufficiency and steal syndrome. Examination of patients sometimes reveals the absence of radial and brachial pulses and a murmur over the carotid artery.

Syncopal drowning

When talking about death in water, syncope drowning is placed in a separate category. After numerous studies, it was determined that some of the victims exhibit the following symptoms:

• There is almost no fluid in the respiratory tract;
• Death occurs even before entering the water;
• After removing a person from the water, a pale skin color is observed, and not the usual blueness;
• Resuscitation can be successful after 6 minutes;
• The majority of victims are children and women.

Syncopal drowning develops as a result of sudden entry into cold water or from hitting it. Sometimes the pathology is associated with nervous regulation, and the cause of death is often indicated as epilepsy, hypoglycemia, stroke or heart attack. The condition is called gentle, since the victim does not experience asphyxia and does not agonize. A drowned person has a very high chance of being resuscitated.

Diagnostics

A history of syncopal paroxysm (attack) is characterized by arrhythmic breathing, weak pulse, low blood pressure, and dilated pupils. Therefore, differential diagnosis is carried out simultaneously in cardiology and neurology. Particular attention is paid to clinical signs, since with a single fainting the diagnosis is difficult. If secondary or frequent falls and loss of orientation are observed, then the periodicity and frequency of manifestations of syncopal episodes is clarified, data is collected on the age when loss of consciousness began and on the events that preceded them.

Returning from syncope is important. The doctor is interested in previous illnesses, taking medications, and assessing vital functions (breathing, consciousness). Then the state of the autonomic nervous system and neurological status are examined, the patient is sent for general examinations: x-ray of the heart and lungs, ECG, urine and blood tests. If the cause of the development of syncope is not identified, then additional diagnostics are prescribed by other methods:

1. monitor ECG;
2. phonocardiography;
3. radiography of the skull;
4. carotid sinus massage for 10 seconds;
5. examination by an ophthalmologist;
6. electroencephalography;

First aid for syncope

People should be aware that competent emergency care for fainting may not always be provided. To avoid injury, you need to be able to recognize in advance the mechanisms of syncope: squeaking in the ears, flies flashing before the eyes, nausea, dizziness, profuse sweating, a feeling of general weakness. If such changes in health status are recorded, follow a number of simple steps:

• Lie on a flat surface, raise your legs 40-50 degrees;
• Loosen tight clothing and allow air flow;
• Massage the dimple on the upper lip and temple area;
• Inhale the ammonia vapor.

If a person has already lost consciousness, then those around him perform the following actions:

1. Lay the victim on his back so that his head and torso are at the same level. Turn your head to the side so that your tongue does not interfere with the breathing process.
2. Open doors or windows to allow oxygen to flow. Ask to free up space around the patient, unfasten the buttons of clothing.
3. To activate the vasomotor and respiratory centers, irritation of skin receptors is necessary. To do this, rub the person’s ears, splash his face with cold water, and pat his cheeks.

Treatment

Treatment of syncope in medicine is carried out using specific drugs. In case of syncope associated with severe hypotension, 1 ml of metazone (1%) or 2 ml of cordiamine is injected intramuscularly. Sometimes therapy may include subcutaneous injection of 1 ml of caffeine (10%). Further treatment options for the patient depend on the causes of the disease. Therapy for syncope is aimed at preventive measures that reduce neurovascular excitability and increase the stability of the mental and autonomic systems.

To regulate mental conditions, the doctor prescribes psychotropic medications, the course of treatment of which is at least 2 months. Antelepsin, Grandoxin, and Seduxen tablets help eliminate anxiety. A person should carefully monitor the general condition of his body. Regularly spend time in the fresh air, use moderate physical activity, ensure proper rest, monitor your work schedule, and monitor the level of systemic blood pressure.

To correct autonomic disorders, breathing exercises, taking B vitamins, vasoactive drugs, and nootropics are indicated. If syncope is caused by cardiac pathological processes, then drugs that improve coronary blood flow are prescribed: atropine, cardiac glycosides. Depending on the cause of loss of consciousness, anticonvulsant medications may be used. Hospitalization after syncope is reserved for patients who:

• repeated attacks;
• there is a disturbance in cardiac activity before fainting;
• poor family history;
• fainting occurs when lying down;
• injured after syncope;
• acute neurological symptoms;
• the presence of myocardial ischemia;
• the attack is caused by an arrhythmia.

Many paroxysmal disorders of consciousness in their clinical manifestations resemble epileptic seizures, which is important for making a differential diagnosis. According to the results of various authors, approximately 20–25% of patients diagnosed with epilepsy do not suffer from it at all, but receive incorrect treatment.

The differential diagnosis of paroxysmal nonepileptic disorders is extremely broad and includes syncope, panic attacks, pseudoepileptic seizures, transient ischemic attacks, sleep disorders, migraine, hypoglycemic conditions, etc. The most common of these are syncope and pseudoepileptic seizures.

Syncope is a common clinical syndrome that occurs at least once in a lifetime in half of the population, accounting for almost 3% of emergency room visits and 6% of hospital admissions. Syncopation is clinical manifestation temporary cessation of brain perfusion, in which there is a sudden transient loss of consciousness and postural tone with its spontaneous recovery without the development of neurological deficit. The causes of syncope include a range of physiological and pathological conditions.

Syncope of a reflex nature. It is currently accepted that the development of reflex syncope is caused by excessive afferent impulses arising from arterial or visceral mechanoreceptors. One of the important mechanisms for the development of such conditions is the Bezold-Jarisch inhibitory reflex, which develops with the activation of subendocardial mechano- and chemoreceptors located in the infero-posterior wall of the left ventricle. The mechanism of the Bezold-Jarisch reflex seems to be as follows: the resulting difficulty in venous outflow in a standing position leads to increased impulses from the structures of the sympathetic nervous system, which entails vigorous contraction of the left ventricle, excitation of intracardiac mechanoreceptors, an increase in the activity of parasympathetic influences with bradycardia and vasodilation. In this case, the activity of the sympathetic nerves, including those providing vasoconstriction, suddenly stops. This reflex, with predominant stimulation of cardiac chemoreceptors, also occurs during myocardial ischemia or infarction, or during coronary angiography.

Vasovagal syncope. The main pathogenetic mechanism of vasovagal (vasodepressor, neurocardiogenic) syncope is the Bezold-Jarisch reflex. Vasodilation as one of the components of this syncope was first described by John Hunter in 1773 in a patient undergoing phlebectomy. Another component of syncope (depression of heart rate caused by the vagus) was described in 1889 by Foster, who believed that severe bradycardia reduces cerebral blood flow to inadequate levels to maintain consciousness. Lewis (1932) in his studies observed the relationship between bradycardia and vasodilation, on the basis of which he proposed the term “vasovagal syncope.”

The clinical picture of vasovagal syncope is often preceded by prodromal symptoms: a feeling of heat in the body, increased sweating, nausea, dizziness and general weakness. The duration of this period ranges from 5 s to 4 min (average 1.5 min). Just before the loss of consciousness, patients note palpitations, blurred outlines of objects, and “darkening” in the eyes. With the development of syncope, tachycardia gives way to bradycardia (up to 50 beats per minute or less), a drop in blood pressure occurs (systolic - up to 70–50 mm Hg, diastolic - up to 30 mm Hg), pale skin, cold sweat are observed . The postural tone, which ensures the maintenance of the posture, gradually decreases until it is completely lost, as a result of which the patient slowly falls, as if settling. With mild syncope, consciousness is lost for a few seconds, with deep syncope - for several minutes. At this time, patients do not make contact and do not react to external stimuli. A neurological examination reveals mydriasis, low pupillary reactions to light, diffuse muscle hypotonia, and the absence of focal neurological symptoms. A deep syncope may be accompanied by short-term hypoxic tonic convulsions (less often two or three clonic twitches), involuntary urination and defecation. During a fall, up to 38% of patients receive some kind of injury (traumatic brain injury, body bruises, abrasions or other injuries). After the return of consciousness, patients correctly orient themselves in their own personality, place and time, remember the events and subjective sensations preceding the loss of consciousness. The period of recovery can last from 23 minutes to 8 hours (on average an hour and a half). At this time, more than 90% of patients feel weak and general weakness. Sweating and a feeling of heat in the body after syncope are observed in only half of the patients.

Diagnosis is based on medical history and additional research methods. Vasovagal syncope develops most often in patients under the age of 54 years, more often in women. It usually does not develop while lying down. Patients may have several episodes of syncope per year. In the precursor stage, there are subjective sensations and signs indicating an increase in parasympathetic tone: dizziness, increased sweating, a feeling of heat in the body, nausea. Loss of consciousness occurs slowly, unlike other syncope and epilepsy, in which the patient loses consciousness within seconds.

Among additional research methods highest value passive and active orthostatic tests are used in diagnosis, although the latter is less informative. If the patient develops signs of syncope (feeling of lightheadedness, dizziness, hypotension, bradycardia), the test is considered positive, and the patient should be quickly returned to a horizontal position, in which blood pressure is restored to the original level. If only subjective manifestations occur without concomitant bradycardia and hypotension, then a vasovagal cause of syncope can most likely be excluded (for vasovagal syncope, these signs are mandatory). The sensitivity of the test can be increased by intravenous drip administration of isoproterenol (isadrin) at an average dose of 2 mcg/min. The maximum rate of drug administration is 4 mcg/min.

Characteristic changes in the spectral analysis of heart rhythm during orthotest are observed. In patients with reflex syncope, it is usually determined in the supine position high degree tension in the functioning of both the sympathetic and parasympathetic nervous systems, with the former predominant. High activity of the sympathetic nervous system is indicated by a significant increase in the amplitude of slow waves and the appearance of additional peaks in this range (0.01-0.1 Hz). With the development of syncope (in a standing position), there is a sharp suppression of sympathetic influences - slow rhythms almost completely disappear, against the background of which the increased tone of the parasympathetic nervous system remains (a peak of respiratory waves is noted around 0.3 Hz with an amplitude of 120 conventional units, which is approximately twice the background level).

In the ortho position, there is an almost complete disappearance of respiratory waves (controlled by the vagus nerve) and an increase in the amplitude of slow waves, which indicates an increase in sympathetic activity.

During loss of consciousness, the electroencephalogram shows signs of brain hypoxia in the form of high-amplitude slow waves in all leads. With transcranial Doppler ultrasound during fainting, a significant decrease in linear blood flow velocities is noted, diastolic - to zero. During the interictal period, no changes in cerebral blood flow are detected.

Syncope caused by hypersensitivity of the carotid (carotid) sinus. The carotid sinus contains baro- and chemoreceptors, as a result of which it plays an important role in the reflex regulation of heart rate, blood pressure and peripheral vascular tone. Patients with carotid sinus hypersensitivity have an altered reflex to stimulation of its baroreceptors, which leads to a temporary decrease in cerebral perfusion, which is manifested by dizziness or syncope.

The clinical picture is very similar to that of vasovagal syncope. An attack can be caused by wearing a tight collar, a tie, or head movements (bending backwards, turning to the sides), but in most patients the cause of the attack cannot be accurately determined. The pre-syncope period and the typical post-syncope state may be absent in some patients.

Carotid sinus hypersensitivity usually occurs in older people, more often in men. Predisposing factors are atherosclerosis, hypertension, diabetes and tumor formations in the neck area, compressing the sinocarotid zone (enlarged lymph nodes, neck tumors, cancer metastases of another location). A sinocarotid test is used as a diagnostic test. If during its implementation there is asystole for more than 3 s, a decrease in systolic blood pressure by more than 50 mm Hg. Art. without developing fainting or by 30 mm Hg. Art. with its simultaneous development, then such patients can be diagnosed with carotid sinus hypersensitivity.

Situational syncopation. Syncope can occur in a variety of situations that contribute to decreased venous return to the heart and increased vagal activity. The central and efferent pathways of the reflex arcs of these syncope states are very similar to the Bezold–Jarisch reflex, but have varying degrees severity of cardioinhibitory and vasodepressor effects. The afferent pathways of reflexes can be multiple and different depending on the site of stimulation. Syncope when coughing (bettolepsy) is observed during a coughing attack, usually in patients with diseases of the respiratory system (chronic bronchitis, whooping cough, bronchial asthma, emphysema, acute pneumonia). When coughing, there is an increase in intrathoracic pressure, irritation of the vagus nerve receptors located in the respiratory organs, impaired ventilation of the lungs during a prolonged cough and a drop in blood oxygen saturation. Syncope can occur during various medical procedures (injections, dental extractions, pleural and abdominal punctures, etc.) due to both the actual unpleasant sensation (pain) and the patient’s impression. Syncope during swallowing is associated with increased activity of the vagus nerve and (or) increased sensitivity of cerebral mechanisms and the cardiovascular system to vagal influences. These conditions usually occur in people with diseases of the esophagus (diverticulum, esophageal stenosis), larynx, mediastinum, and hiatal hernias. Fainting when urinating occurs more often in older men during or immediately after urination.

Syncope with orthostatic hypotension. Orthostatic hypotension is a decrease in blood pressure in a person that occurs when moving from a lying position to a standing position and causes symptoms, in particular due to a decrease in blood supply to the brain. There are two mechanisms for the development of orthostatic hypotension: dysfunction of the segmental and suprasegmental parts of the autonomic nervous system and a decrease in intravascular volume. A decrease in circulating blood volume may be associated with blood loss, vomiting, diarrhea, and excessive enuresis. With autonomic failure, there is no adequate hemodynamic response to changes in body position, which is manifested by orthostatic hypotension. In its pathogenesis, the leading role is played by disturbances in the release of norepinephrine by efferent sympathetic fibers, adrenaline by the adrenal glands, and renin by the kidneys; as a result, despite the changed body position, there is no peripheral vasoconstriction and increased vascular resistance, an increase in stroke volume and heart rate. The causes of orthostatic hypotension and nosological forms of diseases, where it is the leading syndrome, are discussed in Chapter. 30 “Autonomic disorders.”

Syncope when exposed to extreme factors. It is necessary to especially highlight syncope that occurs in healthy people against the background of exposure to extreme factors that exceed individual physiological adaptation capabilities. These include hypoxic (lack of oxygen in the inhaled air, for example, in a closed chamber, on mountain altitude), hypovolemic (redistribution of blood “head - legs” with a decrease in blood volume in the vessels of the brain when tested in a centrifuge), intoxication, medication, hyperbaric (with an excess of oxygen under pressure, in pressure chambers). The pathogenesis of fainting conditions caused by all these reasons is based on vegetative-vascular paroxysm. Nevertheless, syncope states, identified in 1989 by O. A. Stykan as a separate group, which develop when the human body is exposed to extreme environmental factors, are important in purely practical terms, especially when it comes to problems of ergonomics and labor physiology.

Cardiogenic syncope. Maintaining constant blood pressure requires an optimal balance between cardiac output and total peripheral resistance. The decrease in total peripheral resistance is normally compensated by an increase in cardiac output.

Organic heart diseases. In patients with organic heart disease (aortic stenosis, obstructive hypertrophic cardiomyopathy, dilated idiopathic cardiomyopathy), cardiac output does not adequately increase in response to a decrease in total peripheral resistance, and the result is a marked decrease in blood pressure. Severe hypotension and syncope are a feature of virtually all forms of heart disease in which cardiac output is relatively fixed and does not increase in response to exercise.

Syncope, which occurs during physical stress, is most typical for severe aortic stenosis and other diseases in which there is a mechanical obstruction to the ejection of blood from the ventricles. With high resistance to blood flow from the left ventricle, there is hemodynamic instability, which is manifested by increased ventricular contractility, decreased chamber size, and decreased afterload. In the pathogenesis of syncope, a significant role may be played by a decrease in total peripheral resistance due to weakening of reflexes from the carotid and aortic baroreceptors.

In patients with congenital heart defects, in which blood is shunted from the right ventricle to the left, or there is a mechanical obstruction to the blood flow, or both (for example, with tetralogy of Fallot), the mechanism for the development of fainting states is similar to that described above. Significant obstruction in the prosthetic valve may also cause occasional syncope. Systemic hypotension and syncope may be a dangerous manifestation of pulmonary embolism or severe primary pulmonary hypertension. Both conditions lead to significant obstruction of blood flow from the right ventricle and reduced filling of the left chambers of the heart.

Cardiac ischemia. In patients with coronary heart disease, fainting can occur as a result of many factors. Their most common cause is heart rhythm disturbances (tachy- and bradyarrhythmias). In patients with reduced left ventricular function, as well as with primary myocardial infarction, paroxysmal ventricular tachycardia as a possible cause of syncope should be considered first. Disorders of the conduction system of the heart (sinus node, atrioventricular node, atrioventricular bundle (His bundle) and its subendocardial branches (Purkinje fibers)) can be observed in acute and chronic myocardial ischemia.

Fainting during exercise in patients with coronary artery disease should alert the clinician as a possible sign of severe myocardial ischemia or severe left ventricular failure, in which cardiac output does not adequately increase in response to exercise. Reflex and vasovagal syncope can occur during acute myocardial ischemia or after reperfusion of the ischemic site. In this case, activation of mechano- and chemoreceptors occurs in the infero-posterior part of the left ventricle, which leads to the development of the Bezold-Jarisch inhibitory reflex.

Arrhythmias. Syncope can occur with heart rhythm disorders - bradycardia or tachycardia. When arrhythmia occurs, cardiac output, and therefore cerebral perfusion, is markedly reduced, which can lead to the development of syncope. The degree of bradycardia or tachycardia is one of the factors that determines the severity of cerebral symptoms.

Syncope due to arrhythmia most often occurs after the age of 50 years, mainly in men. Bradyarrhythmias are characterized by a short, less than 5 s, presyncope period. With ventricular tachycardia it is longer - from 30 s to 2 min. Patients may experience interruptions in their heart function. The attack develops both in a standing and lying position. During the period of loss of consciousness, cyanosis of the skin is observed. After regaining consciousness, patients usually feel well, in contrast to reflex syncope, where the symptoms of poor health are significantly pronounced.

Patients with organic heart disease have a history of rheumatism, coronary artery disease, heart failure or other heart diseases. Suspecting cardiac causes of syncope is helped by its connection with physical activity, pain in the heart or chest, characteristic of an attack of angina, the presence of fading, interruptions in the work of the heart before loss of consciousness. Electrocardiography and Holter monitoring help establish the diagnosis. Sick sinus syndrome as a cause of syncope is established when Holter monitoring records a sinus pause lasting more than 3 seconds or sinus bradycardia less than 40 beats per minute associated with loss of consciousness. Possible reasons supraventricular tachycardia are established using non-invasive and invasive electrocardiographic studies. They may be the presence of additional conduction pathways, a decrease in atrioventricular delay time, atrial fibrillation, etc. Supraventricular tachycardia and sick sinus syndrome are unlikely causes of syncope if they are not directly related to loss of consciousness. Atrioventricular block can cause syncope when asystole occurs lasting 5-10 seconds or more with a sudden decrease in heart rate to 20 per minute or less. Echocardiography helps determine organic changes in the heart.

Cerebrovascular syncope (steal syndromes). “Steal” syndromes are a group of clinical syndromes caused by unfavorable redistribution of blood between organs and tissues through collaterals, which leads to the occurrence or worsening of their ischemia.

The subclavian “steal” syndrome is the most studied and is a symptom complex caused by compensatory retrograde blood flow in the vertebral or internal mammary artery due to occlusion of the proximal subclavian artery. The most common etiological factors are atherosclerosis and Takayasu's disease. In 1934, Naffziger described the syndrome of the anterior scalene muscle (scalenus syndrome), which occurs with cervical osteochondrosis, accessory cervical rib and other pathological processes accompanied by a reflex increase in the tone of the anterior scalene muscle. In this case, conditions arise for compression of the subclavian artery and the vertebral artery extending from it in the space between the clavicle and the first rib. With steal syndrome, the attack is often preceded by physical work involving stress on the upper limbs. Intense physical work with the hand significantly impoverishes hemoperfusion in the vertebral arteries and can lead to the development of syncope.

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. Occur due to insufficient autonomic regulation, taking certain medications, using alcoholic drinks, as well as 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 different types syncope are:

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 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 common cause domestic injuries, deaths from road 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.

The term “syncope” refers to fainting (short loss of consciousness), it is described in the international association: ICD 10 code - R55. During fainting, there is a decrease in muscle tone, disruption of the cardiovascular and respiratory systems.

Syncope can occur at any age, young or old. There are usually no consequences in such cases; all functions are restored. There can be many reasons for fainting. To get rid of this unpleasant phenomenon, you need to determine the root cause.

Fainting involves a brief loss of consciousness. This state lasts no more than a minute. It can occur in anyone, at any age, but more often women and children suffer from fainting. It is not always possible to reliably determine the cause of fainting. In about 4 out of 10 patients, the cause of syncope remains unknown.

Syncope (ICD 10) is not a separate disease. Rather, it is a manifestation of some ailment that needs to be determined. The reasons can be quite serious. To get rid of constant fainting, you need to correctly identify and eliminate their cause.

Causes of fainting	Provoking factors
Heat and stuffiness	Thermal or sunstroke when the patient is in the sun for a long time. In a stuffy room, there is a lack of oxygen, which also provokes syncope.
Heart diseases	Many heart diseases lead to fainting. For example, if the valves are weak and do not cope with their work, blood circulation in the tissues worsens, and oxygen starvation of all organs, including the brain, begins.
Physical exercise	Excessive physical activity causes shortness of breath and tachycardia. You need to get used to them gradually, otherwise you cannot avoid a syncope attack.
Arterial pressure	Pressure changes are noticeable to the body. A person may feel headache, weakness, dizziness. Fainting with hypertension and hypotension is not uncommon.
Oxygen starvation	Lack of oxygen and impaired lung function often lead to loss of consciousness. In these cases, before fainting, there will be shortness of breath, a feeling of lack of air, and there may also be fear and panic.
Stress	Too strong emotions can cause a jump in blood pressure and lead to fainting. Most often these are negative emotions: rage, fear.
Hunger	Strict diets and prolonged lack of food can lead to hungry fainting.

Immediately before losing consciousness, a person may experience weakness, dizziness, nausea, and spots appear before the eyes. In most cases, this condition appears in a sitting or standing position. If you lie down at the moment of fainting, loss of consciousness will not occur.

Classification of fainting

Fainting may vary in duration, causes, and symptoms. But as a rule, foaming at the mouth and involuntary urination are absent.

Depending on the cause, fainting can be divided into two large groups:

1. The first group includes neurogenic syncope, which is associated with a decrease in vascular tone due to factors caused by the external environment.
2. The second group includes fainting associated with diseases of the cardiovascular system. The second group is divided into two subgroups: syncope due to rhythm disturbances, syncope due to decreased cardiac output.

In this classification, the neurogenic group of fainting includes:

Types of fainting	Features of syncope
Vasodepressor	They occur when there is discomfort or fear at the sight of blood, stuffiness, pain, or stress. Vasodepressor syncope can occur with unexpected and unpleasant news. Such fainting is safe and does not require treatment, since it is the body’s reaction to an external stimulus.
Orthostatic	Such fainting occurs when a person suddenly changes body position. The cause of fainting in this case is a violation of autonomic neuroregulation. Typically, signs appear before syncope occurs. The patient complains of severe fatigue, even in the morning after a long sleep, migraines, and dizziness.
Vestibular	These fainting spells are associated with improper functioning of the vestibular apparatus. Such fainting can occur when traveling on a sea vessel or while riding on a swing. Vestibular syncope occurs more often in children. This type of fainting appears unexpectedly and does not last long.
Situational	These syncope occur with prolonged and painful coughing, prolonged diarrhea, and prolonged physical exertion, especially forceful exercise. To stop the occurrence of such fainting, it is enough to avoid situations that cause them.

There is another classification related to the principle of the occurrence of syncope. She divides fainting states into 4 groups:

• reflex
• cardiogenic
• orthostatic
• cerebrovascular

This classification is approved by the European Society of Cardiology.

Features of vasovagal syncope

The most common type of fainting is vasovagal. They arise due to a nonspecific reaction of the nervous system to an external stimulus. If a person experiences too strong an emotion, a short-term loss of consciousness occurs due to a sharp decrease in blood pressure and heart rate.

Immediately before fainting, the patient may feel nausea, noise in the ears and dark spots before the eyes, and the skin turns pale. It is worth clarifying that you can only faint while in an upright position. If the patient is lying down, there will be no loss of consciousness.

The following factors can lead to vasovagal syncope:

1. Powerful emotions. Positive emotions, such as joy, can also trigger fainting, but less often. Negative emotions, for example, strong uncontrollable fear, mental pain and resentment, often lead to loss of consciousness.
2. Physical pain. Fainting does not necessarily require severe pain, such as from a fracture. Sometimes the unpleasant sensations from the blood sampling procedure are enough for the patient to lose consciousness.
3. Physical exercise. These can be light loads, such as climbing stairs, or active ones. But usually they are associated with cardio loads and sudden stopping.
4. Lack of air. Fainting can be caused by a tight tie or collar, as well as staying in a stuffy room. In all these cases, a person experiences a lack of fresh air and oxygen starvation.

Vasovagal syncope is rarely prolonged. They last from a few seconds to a minute and go away on their own even without help. There are usually no complications or consequences.

Orthostatic syncope and its symptoms

Orthostatic syncope is different from vasovagal syncope. Its essence lies in the fact that the cardiovascular system does not respond in a timely manner to changes in body position. Fainting occurs because insufficient blood flows to the brain, and blood pressure decreases.

You can learn more about the causes of fainting from the video:

Such fainting can be either short-term or long-lasting. Prolonged fainting may be accompanied by convulsions, heavy sweating and urination. During a pre-fainting state, weakness, headache appear, and the picture in the eyes blurs.

Clinical picture of cerebrovascular syncope

Cerebrovascular syncope occurs due to blockage of the subclavian vein by a thrombus. These types of syncope are also called transient ischemic attacks. Such conditions are not often encountered; usually this type of fainting occurs in older people after 60 years of age.

Most often, cerebrovascular syncope is not dangerous, but it is associated with impaired blood circulation in the brain, so medical attention and a full examination are advisable.

This condition is based on narrowing or blockage of the subclavian vein. The characteristic first signs are a feeling of dizziness, sudden speech disturbances (dysarthria), followed by fainting (syncope).

Cardiovascular and arrhythmogenic syncope

Cardiogenic and arrhythmogenic syncope are associated with various diseases of the heart and blood vessels. Despite the fact that problems with rhythm and heart function often worsen with age, the largest number of cardiogenic syncope was recorded in 15-year-old adolescents.

Cardiogenic syncope accounts for about 5% of all recorded syncope attacks. They are especially dangerous. While all other syncope is fatal only 3% of the time, cardiogenic syncope increases this percentage to 24%. Heart pathologies can be very serious, so you need to be relatively attentive to all their manifestations.

Cardiogenic syncope can be caused by dysfunction of the valve apparatus, embolism, etc. Cardiogenic syncope has its own characteristics and characteristic signs:

• The onset and presyncope are not the same as those of a vasovagal attack. Fainting can occur in any position, even without visible provocateurs.
• If ordinary fainting in stressful situations lasts a minute, then with cardiogenic causes the attack can last quite a long time.
• Before losing consciousness, a person feels increased heartbeat and shortness of breath. It is also possible that seizures may occur.
• At first, the skin turns pale, as with any fainting spell, but then a sharp reddening of the skin is observed.
• Blue patches of skin may appear near the nose and ears and in the chest area.

It is worth remembering that in the case when the attack lasts a long time, the person does not regain consciousness, he begins to have convulsions, it is necessary to urgently call an ambulance and hospitalize the patient.

Cardiogenic syncope can occur if the patient has a pacemaker installed, but it does not work well.

Diagnosis of syncope

In terms of diagnosis, anamnesis plays an important role. The patient must accurately and in detail describe what he felt before losing consciousness, what he remembered last, what the signs were, what, in his opinion, provoked the fainting, and whether he has any chronic diseases.

If relatives or friends were nearby at that moment, they can say exactly how long the fainting lasted, which is also important for assessing the patient’s condition.

For diagnostic purposes, the doctor may prescribe a blood test, check the functioning of internal organs, determine blood sugar and cholesterol levels, ultrasound, and chest x-ray. All these examination methods will help to accurately determine the cause of the attacks.

First aid for fainting

If you witness a fainting state, you should provide first aid to the patient:

1. It is advisable to catch the person before he falls. It is very important to prevent him from hitting himself, especially his head.
2. The patient must be carefully placed on a flat surface, preferably hard. It is best to place him on his back without a pillow so that his head is slightly thrown back.
3. Your feet should be slightly higher than your head to improve blood flow to the brain. For this reason, it is better to place a pillow or cushion under your feet (ankles).
4. The patient needs to provide an influx of fresh air: open a window or window, unbutton his collar, loosen his tie or remove his scarf. If it's hot outside, it's better to turn on the air conditioning indoors.
5. If it is not possible to create an influx of cool air, you can simply wave a fan or folder and take the patient into the shade.
6. It is better to bring a person to consciousness carefully. Don't shake it sharply. For him to wake up, it is enough to talk to him, lightly pat his cheeks, and sprinkle him with cool water.
7. A good way to return the patient to consciousness is ammonia. They dab a cotton swab with it and bring it to the patient’s nose.

In case of any fainting condition, it is better to call a doctor. In some cases, you shouldn't hesitate.

You can learn more about how to properly provide assistance in case of fainting from the video:

Indications for hospitalization

As a rule, there is no need to hospitalize the patient; he is simply revived. It is necessary to take the patient to the hospital if he has foam at the corners of his mouth, convulsions, blood from the nose, he does not come to his senses for a long time, his pulse and breathing slow down.

Hospitalization is not required if the patient experiences vasovagal or situational syncope.

Mandatory indications for hospitalization are chest pain, swollen neck veins, heart rhythm disturbances detected by an electrocardiogram.

Drug treatment

Fainting in itself cannot be called a disease. To choose the right treatment, you need to know the root cause. If fainting is associated with fear or stress, no treatment is required at all. It is enough to bring the person to his senses, calm him down, and give him some water to drink.

Fainting conditions associated with blood pressure and heart function are of great danger. Surgical intervention is required only in rare cases, for example, to remove a blood clot from a vessel, install or change a pacemaker, or normalize the functioning of the valve apparatus.

Drug therapy for syncope may include:

Drug groups	Action	Name of drugs
Sedatives	Sometimes the cause of frequent fainting is emotional stress, constant neurosis and emotional instability. In this case, herbal sedatives may be prescribed.	Persen, Novopassit, Motherwort Forte
Antiarrhythmic drugs	They help avoid arrhythmogenic fainting, arrhythmia, and normalize heart function.	Ritmonorm, Sotalex, Cordaron
Nootropics	These drugs normalize brain nutrition and improve blood supply to brain tissue. Since it is oxygen starvation of brain tissue that often leads to fainting, nootropics can help.	Piracetam, Phenotropil

Surgical intervention

Surgical intervention after fainting is rarely required - the indication for it is usually heart pathologies. The patient is indicated for urgent surgery for diseases of the heart valves, tamponade of the heart and aorta, and other causes of obstructed blood flow.

Also, an indication for surgery is a cerebrovascular accident (stroke). Very little time is allotted for removing a blood clot; only emergency intervention can prevent the death of brain cells and loss of vital functions.

Treatment prognosis and possible complications

The prognosis for fainting itself is usually favorable. Syncope does not take a toll on the body. After a person regains consciousness, all brain functions are restored. Sometimes, in old age, a person may forget a couple of minutes before fainting.

The prognosis worsens with serious cardiac pathologies.

There are almost no complications after fainting. The only danger is injury. A person during syncope can hit his head hard or get into an accident if he loses consciousness while driving. Frequent fainting interferes with life and work, but in itself they are not dangerous. If a person often experiences fainting conditions, he learns to control them: take a horizontal position in time, avoid provoking factors.

18.1. GENERAL PROVISIONS

Syncope (from the Greek syncope - to weaken, exhaust, destroy), or fainting (little death), - the most common short-term paroxysmal disturbances of consciousness of non-epileptic origin, caused by insufficiency of blood flow in the vessels of the brain, its hypoxia or anoxia and diffuse disruption of metabolic processes in it. V.A. Karlov (1999) includes syncope in the group of anoxic seizures.

The term "syncope" appeared in French literature from the 14th century. In the middle of the 19th century. Littre in his Dictionary of Medicine defined syncope as a sudden and short-term cessation or weakening of cardiac activity with interruption of breathing, disturbance of consciousness and voluntary movements.

Syncope can go through three subsequent stages: 1) the stage of precursors (presyncope, lipothymia); 2) the stage of culmination, or height (actually syncope); 3) recovery period (post-syncope state). The first stage may be preceded by latent period (from 20 to 80 s), arising after a provoking situation.

Syncope can be provoked by emotional stress, orthostatic hypotension, staying in a stuffy room, coughing fits, irritation of the carotid sinus, atrioventricular block, hypoglycemia, acute dyspepsia, excessive urination, etc. In patients with neuralgia of the IX nerve, syncope sometimes occurs when swallowing as a reaction to the acute pain that occurs. Neurogenic syncope - one of the paroxysmal autonomic disorders, clearly demonstrating a decrease in the adaptive capabilities of the body in providing various forms of its activity due to acute arterial hypotension and subsequent cerebral hypoxia. Arterial hypotension (HTN) often predisposes to syncope. In the interictal period, patients with a history of syncope often have complaints of general weakness, increased fatigue, difficulty concentrating, diffuse headache (usually in the morning), signs of autonomic-vascular lability, migraine, cardialgia, and possible elements of Raynaud's syndrome.

The stage of precursors of syncope lasts from several seconds to 2 minutes. During this period, pre-fainting symptoms appear

"feeling unwell" - swoon(from the Greek leipe - loss, themos - thought, life): general weakness, accompanied by paleness of the face, an increasing feeling of discomfort, lack of air, non-systemic dizziness, darkening of the eyes, ringing in the ears, nausea, hyperhidrosis; sometimes there is yawning, a feeling of heartbeat, numbness of the lips, tongue, discomfort in the heart area, in the stomach. Consciousness in the first moments of an attack may be narrowed, orientation may be incomplete, and “the ground floats away from under your feet.”

The loss of consciousness that occurs against this background is accompanied by a pronounced decrease in muscle tone, which leads to a fall of the patient, which, however, is usually not sudden - the patient, who is in a standing or sitting position, gradually “settles”, and therefore traumatic injuries rarely occur during syncope. Disorder of consciousness during fainting varies from slight stupor for a moment to deep loss for 10 seconds or more. During the period of loss of consciousness, the patient’s eyes are closed, the gaze is turned upward, the pupils are dilated, their reaction to light is sluggish, sometimes nystagmus appears, tendon and skin reflexes are preserved or depressed, the pulse is rare (40-60 beats/min), weak filling, sometimes thread-like, asystole is possible for 2-4 s, blood pressure is low (usually below 70/40 mm Hg), breathing is rare and shallow. If the loss of consciousness lasts more than 10 s, fascicular or myoclonic jerks are possible, as happens, in particular, with Shy-Drager syndrome.

The severity of syncope is determined by the depth and duration of the disorder of consciousness. In severe cases, consciousness is turned off for more than 1 minute, sometimes up to 2 minutes (Bogolepov N.K. et al., 1976). Severe fainting, along with muscle twitching, is sometimes (very rarely) accompanied by convulsions, hypersalivation, tongue biting and involuntary urination.

During syncope, the EEG usually shows signs of generalized cerebral hypoxia in the form of high-amplitude slow waves; The ECG usually shows bradycardia, sometimes arrhythmia, less often asystole.

After regaining consciousness, patients may experience some general weakness, sometimes a feeling of heaviness in the head, a dull headache, discomfort in the heart area, in the abdomen. The rapid restoration of consciousness is facilitated by the horizontal position of the patient, fresh air, improved breathing conditions, the smell of ammonia, the introduction of cardiotonic drugs, caffeine. When emerging from an unconscious state, the patient is well oriented in place and time; sometimes anxious, frightened, usually remembers pre-syncope sensations, notes general weakness, while an attempt to quickly transition to a vertical position and physical activity can provoke the development of repeated fainting. Normalization of the patient’s condition after an attack depends on many factors, primarily on the severity of the paroxysmal state.

Thus, in contrast to epileptic seizures, in syncope, loss of consciousness is usually preceded by pronounced autonomic parasympathetic disorders, loss of consciousness and decrease in muscle tone do not occur so acutely, and the patient, as a rule, does not receive bruises even if he falls. If an epileptic seizure can occur at any time, often completely unexpectedly for the patient, and does not depend on the position of the person’s body, then syncope

This condition, with rare exceptions, has precursors in the form of increasing vegetative-vascular disorders and usually does not develop while the patient is in a horizontal position. In addition, when fainting, convulsive twitching, dysfunction of the pelvic organs, and tongue biting, characteristic of epileptic seizures, occur extremely rarely. If at the end of an epileptic seizure the patient is usually inclined to sleep, then after fainting only some general weakness is noted, but the patient is oriented and can continue the actions performed before the syncope. The EEG during syncopal paroxysms usually shows slow waves, but there are no signs characteristic of epilepsy. The ECG may show changes that clarify the pathogenesis of cardiogenic syncope. REG often reveals signs of low vascular tone and venous stagnation, characteristic of arterial hypotension predisposing to syncope.

About 30% of adults have had syncope at least once in their lives, most often between the ages of 15 and 30. Fainting occurs in 1% of patients at a dentist appointment, and in 4-5% of donors during blood donation. Repeated syncope is detected in 6.8% of respondents (Akimov G.A. et al., 1978).

The polymorphism of the causes of syncope allows us to say that syncope should be considered as a clinical phenomenon that can be caused by various exogenous and endogenous factors, the nature of which may determine some of the nuances of the clinical manifestations of syncope, facilitating the recognition of its cause. At the same time, there is no doubt that it is possible to achieve the same goal in the process of analyzing anamnesis data, information about the state of neurological and somatic status, and additional studies.

18.2. CLASSIFICATION

The abundance of causes of syncope makes their classification, based on the etiological principle, difficult. However, such a classification is possible.

In accordance with the classification of syncope (Adams R., Victor M., 1995), the following types are distinguished.

I. Neurogenic type - vasodepressor, vasovagal syncope; sinocarotid syncope.

II. Cardiogenic type - decreased cardiac output due to arrhythmia; Morgagni-Adams-Stokes attacks and others; extensive myocardial infarction; aortic stenosis; left atrial myxoma; idiopathic hypertrophic subaortic stenosis; disturbance of inflow to the left half of the heart: a) pulmonary embolism; b) pulmonary artery stenosis; c) impaired venous return to the heart.

III. Orthostatic type - orthostatic hypotension.

IV. Cerebral type - transient ischemic attacks, autonomic-vascular reactions during migraine.

V. Decreased oxygen levels in the blood - hypoxia, anemia.

VI. Psychogenic type - hysteria, hyperventilation syndrome.

In 1987, a more detailed classification of syncope was published. Its authors G.A. Akimov, L.G. Erokhin and O.A. Stykan all syncope states are differentiated into three main groups: neurogenic syncope, somatogenic syncope and syncope due to extreme exposure. As an addition to these groups, rare multifactorial syncope is considered. Each group is divided into several variants of syncope, the total number of which reaches 16.

18.3. NEUROGENIC (PSYCHOGENIC) SYNCOPAL CONDITIONS

Neurogenic syncope according to the classification of G.A. Akimova et al. (1987) can be emotiogenic, associative, irritative, maladaptive and discirculatory.

18.3.1. Emotional syncope

The occurrence of emotiogenic syncope is associated with negative emotions, which can be caused by severe pain, the sight of blood, anxiety, fear, etc. Emotionogenic fainting is possible in a healthy person, but more often occurs against the background of neurosis or neurosis-like states with hyperreactivity of the emotional sphere and vegetative-vascular dystonia with a predominance of the parasympathetic direction of vascular reactions.

The cause of such syncope (fainting) can usually be psychotraumatic factors that have extremely personally significant content for a given subject. These may include unexpected news of tragic events, experiences of serious everyday failures, real or imagined threats to the lives of patients and their loved ones, medical procedures (injections, punctures, blood sampling, tooth extraction, etc.), experiences or empathy in connection with suffering other people. Thus, a detailed history taking following syncope usually reveals the cause of the paroxysm and allows us to understand its origin.

Emotional syncope usually develops after a distinct pre-syncope period (lipothymia), with parasympathetic autonomic disorders, a gradual decrease in muscle tone and a slow impairment of consciousness. In a personally significant stressful situation (threat, insult, resentment, accident, etc.), general tension first appears, and in the case of an asthenic nature of the emotional reaction (feelings of fear, shame), increasing general weakness, dry mouth, and an unpleasant feeling of tightness in the heart area occur. , paleness of the face, decreased muscle tone, holding your breath, sometimes trembling of the eyelids, lips, and limbs. The ischemic and hypoxic manifestations observed in this case are confirmed by REG and EEG data, which are diffuse in nature.

18.3.2. Associated syncope

Associative syncope is usually a consequence of pathological conditioned reflexes that arise in connection with memories of an experienced emotional situation, which can be provoked, in particular, by a similar situation. For example, fainting when visiting the dental surgeon's office again.

18.3.3. Irritative syncope

Irritative syncope is a consequence of pathological unconditioned vegetative-vascular reflexes. The main risk factor in this case is the hypersensitivity of such reflexogenic zones, the overexcitation of which leads to a disorder of the autoregulation system of cerebral circulation, in particular the receptors of the sinocarotid zone, the vestibular apparatus, and the parasympathetic structures of the vagus nerve.

A variant of irritative syncope is sinocarotid syncope - a consequence of irritation of overly sensitive receptors of the sinocarotid zone. Normally, the carotid sinus receptors respond to stretching, pressure and give rise to sensory impulses that then pass along Hering’s nerve (a branch of the glossopharyngeal nerve) to the medulla oblongata.

Sinocarotid syncope is provoked by irritation of the carotid sinus receptors. Stimulation of these receptors on one or both sides, especially in older people, can cause reflex slowing of heart rate (vagal type of response), less often - a drop in blood pressure without bradycardia (depressor type of response). Sinocarotid syncope occurs more often in men, especially when wearing a tight collar or a tightly tied tie. Throwing the head back while shaving, watching an airplane, etc. can also provoke carotid syncope. Loss of consciousness is usually preceded by manifestations of lipothymia, during which shortness of breath, a feeling of constriction of the throat and chest, lasting 15-25 s, are possible from the onset of irritation of the sinocarotid receptor zone, followed by loss of consciousness for 10 s or more, and sometimes convulsions are possible.

During sinocarotid syncope, a cardioinhibitory effect is characteristic. It is manifested by a decrease in heart rate to 40-30 per minute, and sometimes short-term (2-4 s) asystole. Blackout, along with bradycardia, is preceded by vasodilation, dizziness, and decreased muscle tone. The REG shows signs of a decrease in pulse blood filling, evenly expressed in the anterior sections of the internal carotid arteries. Changes in bioelectrical activity appear in the form of typical slow waves characteristic of hypoxia, detected in all EEG leads. According to O.N. Stykana (1997), in 32% of cases, irritation of the sinocarotid region does not lead to a cardioinhibitory effect, and in such cases syncope occurs against the background of tachycardia and a peripheral vasodepressor effect.

I.V. Moldovanu (1991) notes that Precursors of sinocarotid syncope may include speech disturbances, in this case, he considers the paroxysm as cerebral (central) carotid syncope. He also notes that in cases of hypersensitivity of the carotid sinus, severe weakness is possible

and even loss of postural tone without disturbance of consciousness. To diagnose sinocarotid syncope, it is proposed to massage or apply pressure to the carotid sinus area alternately on one side and the other with the patient lying on his back. The diagnosis is confirmed by the occurrence of asystole for more than 3 s (with the carotid inhibitory variant) or a decrease in systolic blood pressure by more than 50 mm Hg. and the simultaneous development of fainting (vasodepressor variant).

In irritative syncope that occurs due to overstimulation of the vestibular apparatus, loss of consciousness is preceded by the so-called symptom complex of motion sickness. It is characterized by a combination of sensory, vestibulosomatic and vestibulo-vegetative disorders. Sensory changes include systemic dizziness. Vestibulosomatic reactions are characterized by imbalance associated with changes in the tone of the muscles of the trunk and limbs. In connection with pathological vestibulo-vegetative reflexes, dysfunctions of the cardiovascular system are observed in the form of tachycardia or bradycardia, changes in blood pressure, pallor or hyperemia of the integument, as well as hyperhidrosis, rapid and shallow breathing, nausea, vomiting, and general malaise. Some of these symptoms persist for quite a long time (within 30-40 minutes) even after the restoration of consciousness.

The group of irritative fainting may also include syncope when swallowing. Usually these paroxysms are associated with the vasovagal reflex, caused by overexcitation of sensory receptors of the vagus nerve. Irritative syncope is also possible in diseases of the esophagus, larynx, mediastinum, as well as some diagnostic procedures: esophagogastroscopy, bronchoscopy, intubation, combined pathology of the digestive tract and heart (angina pectoris, consequences of myocardial infarction). Irritative syncope often occurs in patients with diverticula or stenosis of the esophagus, hiatal hernia, spasm and achalasia of the cardia of the stomach. A similar pathogenesis is possible with irritative fainting, provoked by attacks of neuralgia of the glossopharyngeal nerve. The clinical picture of syncope in such cases has the character of vasodepressor syncope, but blood pressure does not decrease, but there is short-term asystole. Prevention of syncope as a result of the patient taking medications from the group of M-anticholinergics (atropine, etc.) may be of diagnostic importance.

18.3.4. Maladaptive syncope

Maladaptive syncope occurs with an increase in motor or mental load, requiring appropriate additional metabolic, energetic, and autonomic support. They are thus caused by insufficiency of ergotropic functions of the nervous system, which occurs during temporary maladaptation of the body due to physical or mental overload and unfavorable influences of the external environment. An example of this type of syncope is, in particular, orthostatic and hyperthermic fainting, as well as fainting that occurs in conditions of insufficient fresh air, during physical overload, etc.

Included in this group of disaptational syncope states Fainting with postural hypotension occurs in individuals with chronic vascular insufficiency or a periodic increase in vasomotor reactions. It is a consequence of cerebral ischemia due to a sharp decrease in blood pressure when moving from a horizontal to a vertical position or during prolonged standing due to impaired reactivity of vasoconstrictors of the lower extremities, which leads to a sharp increase in capacity and a decrease in vascular tone and can cause manifestations of orthostatic hypotension. A drop in blood pressure, leading to a maladaptive syncope, in such cases may be a consequence of functional failure of pre- or postganglionic sympathetic structures, ensuring the maintenance of blood pressure when the patient moves from a horizontal to a vertical position. Primary autonomic failure due to degenerative pathology (Shay-Drager syndrome) or idiopathic orthostatic hypotension are possible. Secondary orthostatic hypotension can be caused by autonomic polyneuropathy (due to alcoholism, diabetes, amyloidosis, etc.), taking excessive doses of certain medicines(hypotensive drugs, tranquilizers), hypovolemia (with blood loss, increased diuresis, vomiting), prolonged bed rest.

18.3.5. Dyscirculatory syncope

Dyscirculatory syncope occurs due to regional cerebral ischemia, caused by vasospasm, impaired blood flow in the main vessels of the head, mainly in the vertebrobasilar system, and phenomena of stagnant hypoxia. Risk factors for this may include neurocirculatory dystonia, atherosclerosis, hypertensive crises, vertebrobasilar insufficiency, various options stenosis of cerebral vessels. A common cause of acute regional ischemia of the brainstem is pathological changes in cervical spine spine, anomalies of the craniovertebral joint and vessels in the vertebral artery basin.

Syncope is provoked by sudden movements of the head or its prolonged forced unusual position. An example of dyscirculatory syncope could be shaving syndrome, or Unterharnscheidt syndrome, in which fainting is provoked by sudden turns and throwing back of the head, as well as Sistine Madonna syndrome, occurring during a prolonged unusual position of the head, for example, when looking at the paintings of temple buildings.

With dyscirculatory fainting, the precursor stage is short; at this time, dizziness (possibly systemic) quickly increases, and occipital pain often appears. Sometimes the warning signs that precede loss of consciousness are not detected at all. A feature of such fainting is a very rapid, sharp decrease in muscle tone, and in connection with this, the suddenness of the patient’s fall and loss of consciousness, which resembles the clinical picture of an atonic epileptic seizure. The differentiation of these paroxysms that are similar in clinical picture can be facilitated by the absence of seizure amnesia during syncope and the usual detection on the EEG of epilepsy of hypersynchronous neuronal discharges characteristic of it. In the case of discirculatory

Fainting on the EEG can reveal high-amplitude slow waves, predominantly in the delta range, characteristic of regional brain hypoxia, usually localized in the posterior parts of the brain, often in the occipital-parietal leads. On REG, in patients with dyscirculatory syncope due to vertebrobasilar insufficiency, when turning, bending or throwing back the head, the pulse blood supply usually clearly decreases, especially clearly expressed in the occipital-mastoid and occipital-parietal leads. After the head returns to its normal position, pulse blood flow is restored within 3-5 s.

The causes of acute cerebral hypoxia, manifested by discirculatory syncope, can be diseases accompanied by stenosis of the branches of the aortic arch, in particular Takayasu's disease, subclavian steal syndrome.

18.4. SOMATOGENIC SYNCOPAL CONDITIONS

Somatogenic syncope is a consequence of somatic pathology, periodically leading to severe disorders of general cerebral hemodynamics and metabolism. Often, with somatogenic syncope, the clinical picture contains pronounced manifestations of chronic diseases of internal organs, in particular signs of cardiac decompensation (cyanosis, edema, tachycardia, arrhythmia), manifestations of peripheral vascular insufficiency, severe allergic reactions, possible anemia, blood diseases, diabetes mellitus, liver and kidney diseases. In the classification of G.A. Akimova et al. (1987) identified 5 main variants of syncope in this group.

Cardiogenic syncope usually associated with a sudden decrease in cardiac blood output due to a sharp disturbance in the rhythm of the heart and a weakening of myocardial contractility. The cause of fainting may be manifestations of paroxysmal arrhythmia and heart block, myocarditis, myocardial dystrophy, ischemic disease, heart defects, mitral valve prolapse, acute myocardial infarction, especially combined with cardiogenic shock, aortic stenosis, cardiac tamponade, atrial myxoma, etc. Cardiogenic syncope can be life-threatening. A variant of this is Morgagni-Adams-Stokes syndrome.

Morgagni-Adams-Stokes syndrome manifests itself as a syncope that occurs against the background of complete atrioventricular block, caused by impaired conduction along the His bundle and provoking cerebral ischemia, in particular the reticular formation of its trunk. It manifests itself as an immediate general weakness with a sudden short-term loss of consciousness and a drop in muscle tone, and in some cases convulsions are possible. With prolonged asystole, the skin becomes pale, cyanotic, the pupils are motionless, breathing is stertorous, urinary and fecal incontinence is possible, and sometimes a bilateral Babinski sign is detected. During an attack, blood pressure is usually not determined and heart sounds are often not heard. May be repeated several times a day. The syndrome was described by the Italian physician G. Morgagni (1682-1771) and the Irish doctors R. Adams (1791-1875) and W. Stokes (1804-1878).

Vasodepressor syncope occur with a sharp drop in the tone of peripheral vessels, primarily veins. They usually appear against the background of hypotensive crises, collaptoid reactions during infections, intoxications, allergies, and usually occur when the patient is in an upright position.

Refers to vasodepressor vasovagal syncope, caused by autonomic imbalance with a predominance of parasympathetic reactions. Occurs when blood pressure drops and bradycardia; is possible at any age, but is more often observed during puberty, especially in girls and young women. Such fainting occurs as a result of a violation of hemodynamic mechanisms: a significant decrease in vascular resistance, which is not compensated by an increase in cardiac output. May be a consequence of slight blood loss, fasting, anemia, or prolonged bed rest. The prodromal period is characterized by nausea, unpleasant sensations in the epigastrium, yawning, hyperhidrosis, tachypnea, and dilated pupils. During paroxysm, arterial hypotension and bradycardia are observed, followed by tachycardia.

Anemic syncope arise with anemia and associated hemic hypoxia due to a critical decrease in the number of red blood cells and the hemoglobin content in them. They are usually observed in diseases of the blood (in particular, hypochromic anemia) and hematopoietic organs. Manifested by repeated fainting with short-term depression of consciousness.

Hypoglycemic syncope associated with a drop in blood glucose concentration, may be a consequence of hyperinsulinemia of a functional or organic nature. Characterized by the fact that, against the background of a feeling of acute hunger, chronic nutritional deficiency or insulin administration, severe weakness, a feeling of fatigue, a feeling of “emptiness in the head”, internal tremors develop, which may be accompanied by tremors of the head and limbs, while pronounced hyperhidrosis and signs of autonomic dysfunction are noted first of a sympathetic-tonic, and then of a vagotonic nature. Against this background, depression of consciousness occurs from mild stupor to deep stupor. With prolonged hypoglycemia, motor agitation and productive psychopathological symptoms are possible. In the absence of emergency help, patients fall into a coma.

Respiratory syncope occur against the background of specific and nonspecific lung diseases with obstruction of the airways. This group also includes fainting that occurs with tachypnea and excessive ventilation of the lungs, accompanied by dizziness, increasing cyanosis and decreased muscle tone.

18.5. SYNCOPAL CONDITIONS

UNDER EXTREME EXPOSURES

In this group of syncope states G.A. Akimov et al. (1987) included fainting spells, provoked by extreme factors: hypoxic, hypovolemic (massive blood loss), hyperbaric, intoxicating, medicinal (after taking drugs that cause an excessive decrease in blood pressure, hypoglycemia, etc.).

Hypoxic syncope. Hypoxic syncope conditions include fainting resulting from exogenous hypoxia, which occurs when there is a significant lack of oxygen in the inhaled air, for example, at altitude (high-altitude fainting), in unventilated rooms.

The harbinger of such fainting is an irresistible desire to sleep, tachypnea, confusion, pallor of the integumentary tissue, and sometimes muscle twitching. In hypoxic fainting, the face is pale with a grayish tint, the eyes are closed, the pupils are constricted, there is profuse, cold, sticky sweat, breathing is shallow, rare, arrhythmic, the pulse is rapid and thready. Without help, high-altitude syncope can result in death. After recovery from high-altitude fainting, in particular with the help of an oxygen mask, the victim experiences weakness and headache for some time; He usually does not remember the fainting spell he suffered.

Hypovolemic syncope. arise due to circulatory hypoxia caused by unfavorable redistribution of blood under the influence of overloads during high-speed flights, centrifuge tests, decompression of the lower half of the body, as well as massive blood loss, a sharp decrease in the amount of blood in the vessels of the brain. With massive overloads in flight, central vision first deteriorates, a gray veil appears before the eyes, followed by a black veil, complete disorientation occurs and loss of consciousness occurs, which occurs along with a sharp drop in muscle tone (gravitational fainting). Confusion and disorientation persist for some time after the effects of acceleration cease.

Intoxication syncope. Fainting may occur provoked by poisoning household, industrial and other poisons that cause neurotoxic, narcotic, hypoxic effects.

Drug-induced syncope. Syncope occurs as a result of hypotensive or hypoglycemic side effects of certain drugs, may be a consequence of taking antipsychotic, ganglion-blocking, antihypertensive, or hypoglycemic drugs.

Hyperbaric syncope. Fainting is possible in cases of a sharp increase in pressure in the airways during hyperbarotherapy if excessively high pressure is created in the chamber, which is characterized by the development of a symptom complex due to a pronounced cardioinhibitory effect, which is clinically manifested by pronounced bradycardia, up to asystole, and a rapid drop in systolic pressure.

18.6. RARELY ENCOUNTERED POLYFACTORY

SYNCOPAL CONDITIONS

Among multifactorial syncope conditions in the classification of G.A. Akimova et al. (1987) are presented as follows.

Nocturic syncope. Occurs rarely, usually when getting out of bed at night and urinating or defecating; in most cases it is observed in men over 50 years of age. A consequence of the orthostatic reaction and insufficiency of adaptive-compensatory capabilities during a rapid transition from a horizontal to a vertical position against the background of the predominance of vagoto-

nic reactions provoked by rapid emptying of the bladder or intestines, leading to a sharp change in intra-abdominal pressure.

Cough syncope, or bettolepsy. Cough fainting, or bettolepsy (from the Greek bettor - cough + lepsis - grasping, attack), occurs, as a rule, during the culmination of a protracted coughing attack. It is usually observed in patients with chronic pulmonary heart failure. Most often these are middle-aged men with a picnic build and heavy smokers. Attacks of bettolepsy are provoked by a prolonged cough, leading to an increase in intrathoracic and intra-abdominal pressure with impaired ventilation of the lungs and insufficient blood flow to the heart, venous stagnation in the cranial cavity and brain hypoxia. Loss of consciousness during cough syncope usually occurs without warning and does not depend on the patient’s posture; it is also possible in a lying position. Impaired consciousness usually lasts within 2-10 seconds, but sometimes lasts up to 2-3 minutes, usually combined with cyanosis of the face, neck, upper body, swelling of the jugular veins, hyperhidrosis, and sometimes accompanied by myoclonic reactions. The term “bettolepsy” was proposed in 1959 by a domestic neurologist

M.I. Kholodenko (1905-1979).

Patients with a history of fainting need to undergo somatic and neurological examinations, and information about the state of general and cerebral hemodynamics, the respiratory system, and blood composition is especially important. Necessary additional studies include ECG, REG, ultrasound, or duplex scanning.

18.7. TREATMENT AND PREVENTION

In most cases, syncope ends safely. During fainting, the patient should be placed in a position that will ensure maximum blood flow to the head; The best option is to lay him down so that his legs are slightly higher than his head, while making sure that there is no sticking of the tongue or other obstacles to the free flow of air into the respiratory tract. Spraying the face and neck with cold water can have a positive effect, and the patient is given ammonia to sniff. If there is a urge to vomit, the patient's head should be turned to the side and a towel should be placed. The patient should not attempt to administer medicine or water by mouth until he or she recovers from unconsciousness.

With severe bradycardia, parenteral administration of atropine is advisable, and with low blood pressure- ephedrine, caffeine. After the emergence of consciousness, the patient can get up only after he feels the restoration of muscle strength, and it must be borne in mind that when he moves from a horizontal to a vertical position, an orthostatic reaction is possible, which can provoke a recurrence of syncope.

It should be borne in mind that the cause of fainting may be a serious physical illness, in particular heart block, myocardial infarction, or blood diseases. Therefore, it is important to take measures to clarify the nature of the process that caused the occurrence of fainting, and then carry out appropriate treatment, as well as determine the most rational measures for the prevention of fainting in the future.

Syncope due to respiratory failure can also occur when there is a deficiency of oxygen in the inhaled air (stuffy room, staying at altitude, etc.), as well as when the vital capacity of the lungs decreases and when they are hyperventilated.

In cases of vegetative lability in young people and the presence of psychogenic associative, as well as psychogenic dyscirculatory syncope, physical therapy, hardening procedures, and restorative drugs are systematically necessary. It is advisable to avoid situations that provoke fainting. Taking sedatives, tranquilizers, beta-blockers (oxprenolol, pindolol), anticholinergics, antiarrhythmic drugs (disopyramide, procainamide, etc.), serotonin reuptake inhibitors (fluoxetine, fluvoxamine) may be useful.

With postural hypotension, patients should not rush when moving from a horizontal to a vertical position; sometimes with arterial hypotension, elastic stockings, taking tonic medications (eleutherococcus, ginseng, etc.), psychostimulants such as Meridil (Centedrine), Sidnocarb, Acephen may be recommended . For chronic orthostatic hypotension, courses of treatment with corticosteroids are sometimes appropriate. In case of cardiac arrhythmias, appropriate drug therapy is indicated, and if its effectiveness is insufficient, installation of an electrical pacemaker or pacemaker is indicated. With reflex sinocarotid syncope, patients should not wear tight collars; sometimes the advisability of surgical denervation of the carotid sinus should be discussed. In severe syncope during attacks, caffeine, ephedrine, cordiamine and other analeptic and adrenomimetic drugs can be administered parenterally.