Vasomotor syncope classification pathogenesis diagnosis treatment prevention. Causes of syncope in young people. Sinocarotid syncope can be of several types

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:

Reflex. These include vasovagal and situational fainting.
Orthostatic. They arise due to insufficient autonomic regulation, taking certain medications, drinking alcoholic beverages, and hypovolemia.
Cardiogenic. The cause of syncope in this case is cardiovascular pathology.
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:

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.
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.
Due to a decrease in cardiac output, they develop cardiogenic
With hypoglycemia, a decrease in the amount of oxygen in the blood, cerebrovascular syncopation. Elderly patients are also at risk due to the likelihood of developing .

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

Features of the clinical picture

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

Diagnostic criteria

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

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

When examining patients, the following diagnostic procedures are performed:

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

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

Tactics and strategy for providing assistance

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

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

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

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

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

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

What are the consequences?

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

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

Preventive actions

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

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

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

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

Syncope (fainting)- a condition in which a person loses consciousness and from which he emerges spontaneously within a few minutes, often without any outside help. Every year, fainting occurs in 0.6% of people on the planet. The cause of syncope can be various pathological changes, but in a significant number of cases the etiology of syncope remains unknown.

Differential diagnosis of true syncope must be carried out with a number of pathological conditions in which loss of consciousness is associated with psychogenic causes (psychogenic syncope), diseases of the central nervous system (epilepsy, convulsive syndrome), metabolic disorders (hypoxia, hypoglycemia) and various types of intoxications (endogenous and exogenous origin).

CLASSIFICATION OF SYNCOPAL CONDITIONS

According to the classification adopted by the European Society of Cardiology, syncope is divided into 5 main categories: neurotransmitter, orthostatic, associated with cardiac arrhythmia, associated with structural heart disease and cerebrovascular.

Neurotransmitter syncope is caused by reflex vasodilation and bradycardia due to systemic hypotension and/or hypoperfusion. This category includes classic vasovagal syncope, carotid sinus syndrome, and situational syncope. Vasovagal syncope is triggered by emotions, unpleasant sights or sounds, pain, orthostatic stress (standing for prolonged periods in crowded or hot places) and is usually associated with subsequent fatigue, weakness, nausea, and vomiting. Carotid sinus syndrome is associated with accidental mechanical manipulation of the carotid sinus, such as turning the head, shaving, or tight collaring. Situational syncope is associated with specific actions, such as coughing, urination, and defecation.

Orthostatic syncope

This condition occurs when upright posture results in hypotension and cerebral hypoperfusion without detectable bradycardia. This type of fainting is usually associated with prolonged standing under strain or prolonged standing in crowded or hot places. Orthostatic syncope occurs when the autonomic nervous system does not respond correctly to a change in posture, or when the patient has a reduced blood volume. Orthostatic hypotension can be caused by certain medications, neurogenic factors (multiple system atrophy, parkinsonism, and diabetic neuropathy), and non-neurogenic factors (decreased venous return and circulating blood volume, heart failure).

Cardiac arrhythmia can cause syncope because bradycardia and tachycardia lead to a decrease in cardiac output regardless of circulatory demand. Potential causes of syncope in this category include sinus node dysfunction, atrioventricular conduction disorders, supraventricular and ventricular paroxysmal tachycardia, Wolff-Parkinson-White syndrome, and certain hereditary pathologies such as long QT syndrome or Brugada syndrome.

Structural heart diseases, such as aortic stenosis, pulmonary hypertension, and cardiac myxomas, can cause syncope because the body's circulatory demands exceed the heart's ability to increase cardiac output.

Cerebrovascular syncope

Cerebrovascular syncope occurs as a result of decreased cerebral perfusion associated with cerebrovascular disease. Among such diseases are “steal” syndrome and vertebrobasilar insufficiency. Examination of these patients may reveal a carotid bruit and weak or absent brachial and radial pulses.

In this category, it is worth highlighting fainting from sunstroke separately. Exposure to high temperature in humans leads to dehydration and dilation of peripheral blood vessels. A decrease in vascular tone entails blood flow to the periphery and its outflow from the central nervous system. Elderly people and children are most susceptible to fainting from sunstroke. Immediately after fainting, the patient's skin may be cold and clammy; Transient hypotension with a weak pulse is often observed.

DIAGNOSTICS OF SYNCOPAL CONDITIONS

The initial clinical assessment of a patient following syncope includes a history and physical examination, which includes horizontal and vertical pressure measurements and an ECG. Biological fluids (blood, urine) must be examined. According to indications, echo-CG, CT scan of the brain is performed to exclude tumor processes, laboratory research is performed to exclude anemic syndrome and intoxication syndrome with narcotic, psychotropic drugs, poisons of plant or synthetic origin, products of alcohol metabolism and endogenous metabolites.

It is important to establish the medications the patient is taking to exclude those that may cause orthostatic syncope or syncope associated with arrhythmia.

A well-compiled medical history should include a thorough description of prodromal symptoms, provoking events, anamnesis of life and illness, family history (whether there were similar conditions in the family and what they were associated with in relatives), as well as a description of the syncope itself by witnesses.

Physical examination data, such as age, gender, body features, condition of organs and systems, auscultatory data of the cardiovascular system, pulse characteristics and blood pressure, characteristics of psychotype and vasomotor reactions, neurological symptoms (if any), endocrinological status should be recorded appropriately in the medical history to analyze the etiological causes of recurrent syncope.

EMERGENCY MEDICAL CARE FOR syncope

Neurotransmitter (reflex) fainting

It is important to inform patients that reflex syncope is usually not life-threatening, but injury may occur during syncope if appropriate measures are not taken. Patients should be told about the warning signs of neurotransmitter syncope and taught how to prevent it. These include avoiding dehydration (drinking enough fluids, eating moderately salty foods), compensatory movements during the prodrome (eg, lie down and raise your legs, squat, isometrically clench your hands, tense your arms, cross your legs), wearing rubber stockings, standing training. Standing training results in decreased neurovascular sensitivity to orthostatic stress. It is recommended to start with 3-5 minutes of standing twice a day, gradually increasing the standing time to 30-40 minutes twice a day. Some patients require medications that increase blood volume, beta blockers, and vasoconstrictors.

Orthostatic syncope

Treatment of orthostatic syncope involves educating patients on the factors leading to orthostatic syncope, non-drug and drug treatment of decreased circulating blood volume and impaired autonomic regulation. A non-pharmacologic approach involves slowly and carefully changing positions, staying hydrated, increasing intravascular volume, wearing rubber stockings, and exercise. In cases of severe episodes of fainting, medications that increase blood volume and vasoconstrictors may be prescribed.

Syncope associated with cardiac arrhythmia

Bradycardia is often the cause of arrhythmic syncope. In such cases, patients need a pacemaker. If the cause of arrhythmic syncope is tachycardia, then patients are prescribed antiarrhythmic therapy, radiofrequency catheter destruction, implantation of a pacemaker or cardioverter-defibrillator.

Syncope associated with structural heart disease

Patients with structural heart disease will need drug therapy, catheterization, or surgery.

Cerebrovascular syncope

Treatment of cerebrovascular syncope is limited to surgical or subcutaneous revascularization. Carotid endarterectomy is the best method for eliminating severe forms of carotid stenosis.

Fainting due to sunstroke

For fainting caused by sunstroke, no specific treatment is required. The patient should be placed in a horizontal position, placed in a cool place, and given oral and/or intravenous rehydration.

Usually classified and discussed together with syncope because it has the same causes.

Seizures can cause sudden loss of consciousness, but are not considered syncope. However, in patients with syncope, it is necessary to exclude the presence of a convulsive syndrome, since taking an anamnesis may be difficult or impossible, and some types of seizures do not lead to tonic-clonic contractions. Moreover, short-term (less than 5 seconds) convulsions can occur with true syncope.

Diagnosis depends on a careful history, eyewitness accounts, or examination during the attack.

Pathophysiology of syncope

Most syncope is caused by cerebrovascular insufficiency. In some cases, there may be normal blood flow, but a lack of other substrates (Glucose or both).

Cerebrovascular insufficiency

Most cases of cerebrovascular insufficiency are a consequence of decreased cardiac output (CO).

A decrease in CO may be due to:

Pathology of the heart with obstruction of the outflow tract.
Heart pathology with systolic dysfunction.
Heart pathology with diastolic dysfunction.
Rhythm disturbances (rhythm too fast or too slow).
Conditions leading to decreased venous return.

Outflow tract obstruction may be aggravated by exercise, vasodilation, and hypovolemia (especially in aortic stenosis and hypertrophic cardiomyopathy), which can lead to syncope.

Arimias lead to syncope if the rhythm is too fast to adequately fill the ventricles (eg, more than 150-180 beats/min) or too slow to maintain normal output (eg, less than 30-35 beats/min).

Venous return may be reduced by blood loss, increased intrathoracic pressure, increased vagal tone, and decreased sympathetic tone (eg, due to medications, carotid sinus pressure, or autonomic dysfunction). Syncope that occurs against the background of these mechanisms (with the exception of bleeding) is often called vasovagal or neurocardiogenic; they, as a rule, have a benign course.

Orthostatic hypotension, a common cause of syncope, may result from the failure of normal compensatory mechanisms (eg, sinus tachycardia, vasoconstriction, or both) to support the transient decrease in venous return that occurs with upright posture.

Cerebrovascular diseases rarely cause syncope because most do not involve the centrocephalic structures that must be affected to cause loss of consciousness. However, ischemia in the basilar artery due to transient ischemic attack or migraine can lead to syncope. In rare cases, vertebrobasilar insufficiency and syncope may occur when turning the head in patients with severe arthritis or spondylitis of the cervical vertebrae.

Lack of other substrates

The central nervous system requires O2 and glucose for normal functioning. From a practical point of view, the main cause is hypoglycemia, since hypoxia rarely develops in such a way as to cause sudden loss of consciousness (except in the case of flying or diving). Loss of consciousness due to hypoglycemia usually does not develop as suddenly as syncope or seizures, since hypoglycemia is preceded by a number of symptoms (except in patients taking beta-blockers); however, the doctor may not know the circumstances of the attack if there were no witnesses.

Causes of syncope

Obstruction of the outflow or inflow tract:

Causes	Possible signs	Diagnostic approach
Valvular heart defects: aortic or mitral stenosis, tetralogy of Fallot, pathology or thrombosis of an artificial valve		Echocardiography
Hypertrophic cardiomyopathy, restrictive cardiomyopathy, tamponade, myocardial rupture	Young or elderly patients. Syncope often occurs during exercise; recovery occurs quickly. Heart murmur	Echocardiography
Tumors or blood clots in the heart	Syncope can be positional. Usually echocardiography murmur (may be variable). The phenomenon of peripheral embolism	Echocardiography
Pulmonary embolism, amniotic fluid embolism, or rarely air embolism	Usually due to a large embolus, accompanied by shortness of breath, tachycardia or tachypnea. Common risk factors for pulmonary embolism	CT angiography or nuclear scan

Rhythm disorders

Causes	Possible signs	Diagnostic approach
Bradyarrhythmias	Syncope occurs in the absence of warning signs; recovery immediately after the return of consciousness. May occur regardless of body position. Bradyarrhythmias are more common in the elderly. Patients taking medications, especially antiarrhythmic or other cardiovascular drugs. Structural heart diseases
Tachyarrhythmias, both supraventricular and ventricular (eg, due to ischemia, heart failure, myocardial disease, medications, electrolyte disturbances, arrhythmogenic right ventricular dysplasia, long OT syndrome, Brugada syndrome, ventricular overexcitation syndrome)	Syncope occurs in the absence of warning signs; recovery immediately after the return of consciousness. May occur regardless of body position. Patients taking medications, especially antiarrhythmic or other cardiovascular drugs. Structural heart diseases	If the ECG is uninformative, it is advisable to perform Holter monitoring or use a recorder. Electrophysiological study if indicated. Determination of serum electrolyte levels in the presence of predisposing factors (eg, diuretic therapy, vomiting, diarrhea)

Ventricular dysfunction:

Vasovagal (neurocardiogenic):

Causes	Possible signs	Diagnostic approach
Increased intrathoracic pressure (eg, tension pneumothorax, cough, straining to urinate or defecate, Valsalva maneuver)	Precursors are characteristic (for example, dizziness, nausea, sweating); recovery occurs quickly, but not instantly. The presence of precipitating factors is usually obvious	Clinical assessment
Strong emotions (eg pain, fear, sight of blood)	Presence of warning signs (for example, dizziness, nausea, sweating). Recovery is fast, but not instantaneous (5-15 min). The presence of precipitating factors is usually obvious	Clinical assessment
Carotid sinus massage		Clinical assessment
Swallowing movement	Presence of warning signs (for example, dizziness, nausea, sweating). Recovery is fast, but not instantaneous (5-15 min). The presence of precipitating factors is usually obvious	Clinical assessment
Anaphylaxis	Taking medications, insect bites, history of allergies	Allergy tests

Orthostatic hypotension:

Causes	Possible signs	Diagnostic approach
Drugs	Symptoms develop within a few minutes after assuming an upright position. Decreased blood pressure when taking an upright position during examination	Clinical assessment Sometimes tilt test
Autonomic dysfunction
Deterioration caused by prolonged bed rest	Symptoms develop within a few minutes after assuming an upright position. Decreased blood pressure when taking an upright position during examination	Clinical assessment. Sometimes tilt test
Anemia	Chronic weakness, sometimes dark stools, heavy menstrual bleeding	Complete clinical blood test

Cerebrovascular diseases:

Other reasons:

Causes	Possible signs	Diagnostic approach
Prolonged standing	Anamnesis data; no other symptoms	Clinical assessment
Pregnancy	Healthy woman of childbearing age; absence of other symptoms. Usually early in pregnancy or in undiagnosed pregnancies	Pregnancy test
Hyperventilation	Typically tingling around the mouth or in the fingers before syncope. Usually in the context of emotional stress	Clinical assessment
Hypoglycemia	Impaired consciousness persists if adequate treatment is not carried out, the onset is rarely sudden, sweating, piloerection. Usually a history of diabetes or insulinoma	Finger prick blood to determine glucose levels Response to glucose administration
Psychiatric diseases	They are not true syncope (the patient may partially respond to examination or be inadequate during the attack). Normal examination findings. Often an indication of a history of psychiatric illness	Clinical assessment

Some medications that may cause syncope:

Examination of syncope

The examination should be carried out as soon as possible after the attack. The further away from syncope, the more difficult it is to make a diagnosis. Information obtained from witnesses is very important and should be obtained as early as possible.

Anamnesis

The history of the present illness should contain information about the events immediately preceding syncope, incl. what the patient was doing (for example, exercising, arguing, being in a situation that could provoke emotional stress), body position (for example, horizontal or vertical) and, if the patient was standing, it is necessary to find out how long. It should be noted that there are associated symptoms before or immediately after the event, incl. feeling like you are about to pass out, nausea, sweating, blurred or tunnel vision, tingling in your lips or fingertips, chest pain, or palpitations. It is necessary to establish the duration of the recovery period after syncope. If there are witnesses, you should ask them to describe the episode, paying special attention to the presence and duration of seizures.

Assessment of the condition of organs and systems. The patient should be asked about the presence of pain or injury, episodes of dizziness or near-syncope when standing, and episodes of palpitations or chest pain during exercise. The patient should be asked about symptoms that may be manifestations of the underlying disease, incl. the presence of loose stools or blood in the stool, heavy menstrual bleeding (anemia); vomiting, diarrhea, or massive urination (dehydration or electrolyte disturbances); as well as risk factors for pulmonary embolism (recent surgery or immobilization, presence of malignancy, history of coagulation disorders).

The history of other diseases should contain information about previous syncope, the presence of cardiovascular pathology, as well as a history of convulsive syndrome. The patient should be asked about the medications he is taking (especially antihypertensives, diuretics, vasodilators, and arthiarrhythmics).

Physical examination

During a general examination, the patient’s mental status is assessed, incl. presence of confusion or hesitancy suggestive of a postictal state, as well as signs of trauma (eg, bruising, swelling, tension, tongue biting).

When auscultating the heart, you need to pay attention to the presence of murmurs; The change in noise when performing the Valsalva maneuver, standing up or squatting is also important.

Careful assessment of a regular pulse of 73-1 along with palpation of the carotid arteries or auscultation of the heart can help diagnose arrhythmias if ECG recording is not possible.

Some physicians perform unilateral carotid sinus massage while monitoring ECGs with the patient in the supine position to detect bradycardia or block and diagnose carotid sinus hypersensitivity.

When palpating the abdomen, it is necessary to pay attention to the presence of muscle tension, and a rectal examination is carried out to identify obvious or hidden bleeding.

A complete neurological examination is performed to identify focal symptoms, which may indicate central nervous system damage as the cause of syncope (for example, seizure disorders).

Signs that require increased attention

A number of signs indicate serious illnesses as causes of syncope:

Syncope during exercise.
Multiple episodes over a short period of time.
Presence of a heart murmur or other signs of structural pathology (eg, chest pain).
Elderly age.
Significant injury during an episode of syncope.
Family history of sudden death.

Interpretation of the data obtained

Although the causes of syncope are often benign, it is important to identify diseases that pose a threat to life (eg, tachyarrhythmias, heart blocks) and cause sudden death. Clinical data allow us to suspect a cause in 40-50% of cases. We can summarize them as follows.

Benign causes often lead to syncope. Syncope, which is preceded by physical or emotional stress (eg, pain, fear), occurs in an upright position, and often has precursors mediated by vagal influences (eg, nausea, weakness, yawning, anxiety, blurred vision, sweating) is usually classified as vasovagal syncope. states.

Syncope, which usually occurs when moving to a vertical position, indicates an orthostatic cause. Syncope, which occurs during prolonged standing, is usually caused by the deposition of blood in the venous bed.

Loss of consciousness that occurs suddenly, associated with muscle twitching or spasms, incontinence or tongue biting, followed by postictal confusion or somnolence, indicate seizure syndromes.

The presence of signs that require increased attention indicates a serious cause of syncope.

Syncope that occurs during physical activity indicates obstruction of the outflow tract of the heart. These patients sometimes also have chest pain, palpitations, or both. Physical examination findings may help determine the cause. A rough murmur at the base of the heart, increasing at the end of systole and directed to the carotid arteries, indicates aortic stenosis; A systolic murmur that increases with the Valsalva maneuver and decreases with squats may be a sign of hypertrophic cardiomyopathy.

Syncope, which occurs and passes suddenly and spontaneously, is characteristic of cardiac causes, most often of rhythm disturbances. Since vasovagal and orthostatic mechanisms do not imply the development of syncope in the horizontal position, the occurrence of syncope in the supine position may also indicate arrhythmias.

If the patient is injured during syncope, the likelihood of a cardiac cause or seizure syndrome increases and, accordingly, alertness increases. The presence of warning signs of loss of consciousness that accompany benign vasovagal syncope somewhat reduces the risk of injury during an attack.

Instrumental examination

Instrumental examination is usually indicated for these patients.

Pulse oximetry.
Sometimes echocardiography.
Sometimes tilt test.
Blood tests only if clinically indicated.
In rare cases, a CNS examination is performed.

In general, if syncope results in injury or recurs, more thorough evaluation is required.

If rhythm disturbances, myocarditis or coronary heart disease are suspected, the patient requires hospitalization for examination.

An ECG is performed on all patients. An ECG may reveal rhythm disturbances, conduction disturbances, myocardial hypertrophy, accessory pathways, prolongation of the OT interval, pacemaker dysfunction, myocardial ischemia or myocardial infarction. In the absence of clinical signs, it is advisable for elderly patients to determine the level of markers of myocardial damage to exclude infarction, as well as conduct ECG monitoring for at least 24 hours. If arrhythmias are detected, it is necessary to identify their connection with disturbances of consciousness in order to accurately establish the cause of syncope, however, in most patients syncope does not develop during monitoring. On the other hand, the presence of symptoms in the absence of rhythm disturbances allows us to exclude this cause of syncope. The use of recorders may be useful if syncope is preceded by warning signs.

Laboratory tests are performed depending on the clinical situation; An automatically performed standard laboratory examination is usually uninformative. However, all women of childbearing age should take a pregnancy test. If anemia is suspected, the hematocrit level is determined. Determination of electrolytes is carried out if there is reason. Serum troponin levels are assessed to rule out acute myocardial infarction.

Echocardiography is indicated for patients in whom syncope occurs during exercise, in the presence of a heart murmur, or in cases of suspected cardiac tumors (for example, in the presence of postural syncope).

It is advisable to perform a tilt test if the history or physical examination reveals evidence of a vasodepressor or other reflex syncope. This method is also used to evaluate stress-induced syncope.

Stress tests are performed if transient myocardial ischemia is suspected. Often performed on patients with stress-induced symptoms.

Invasive electrophysiological testing is performed if arrhythmia cannot be detected using non-invasive methods in patients with unexplained recurrent syncope; a negative result identifies a low-risk subgroup with a high likelihood of remission of syncope. In other patients, the indications for electrophysiological studies are ambiguous. Stress tests are less informative unless syncope is provoked by physical activity.

An EEG is indicated if a seizure disorder is suspected.

Treatment of syncope

If syncope develops, the presence of a pulse must be immediately determined. If there is no pulse, cardiopulmonary resuscitation is performed. In the presence of heart contractions, atropine or transthoracic pacing is used to correct severe bradycardia. Isoproterenol can be used to maintain heart rhythm until a temporary pacemaker is implanted.

Electrical cardioversion is a fast and safe method for hemodynamic instability. If venous return is impaired, it is necessary to place the patient in a horizontal position with raised legs, and also administer saline solutions. Pericardiocentesis is indicated for tamponade. Tension pneumothorax requires drainage of the pleural cavity. For anaphylaxis, adrenaline is administered parenterally.

Placing the patient in a horizontal position with the legs elevated will usually resolve the syncope, once life-threatening conditions have been ruled out. If the patient quickly moves to a sitting position, syncope may occur again; Keeping the patient upright or transporting him in an upright position may prolong the period of cerebral hypoperfusion and delay recovery.

The nature of specific therapy depends on the cause and pathophysiological mechanisms.

Features in the elderly

A common cause of syncope in elderly patients is postural hypotension associated with the combined action of a number of factors. These factors include the presence of stiff, inelastic arteries, impaired venous return due to decreased skeletal muscle function due to lack of physical activity, and sclerodegenerative changes in the sinoatrial node and conduction system as a result of heart disease.

In older patients, syncope often occurs as a result of several causes at the same time. For example, taking multiple medications for heart disease and high blood pressure, combined with standing upright in a stuffy church during a long service, can lead to syncope.

Syncope is a short-term fainting, which is accompanied by a decrease in muscle tone. Problems arise from transient hypoperfusion. Characteristic symptoms include pallor, poor activity, and low blood pressure.

This condition refers to a syndrome characterized by a sudden and temporary loss of consciousness. This reduces the resistance of muscle tissue tone. After fainting, the disorder of consciousness can be restored.

Loss of consciousness lasting a maximum of 1 minute.
Absence of any neurological consequences.
After loss of consciousness, the head hurts, the body weakens, and drowsiness appears.
Loss of consciousness with various accompanying symptoms often occurs in children, adolescents and girls, and is also typical for adult men.
In older people, the few minutes preceding loss of consciousness are eliminated from memory.

In a fainting state, the patient’s muscle tissues are relaxed, the pulse becomes slower, and breathing movements decrease. The skin turns pale and there is no reaction to environmental factors. In rare situations, urine cannot be held in during syncope.

Causes of fainting

Brain tissue requires regular blood supply. It requires about 13% of blood flow to function properly. Indicators change in stressful situations and during physical activity. Based on the average weight of the brain, humans require 750 ml of blood per minute for normal brain function. Fainting occurs when this indicator decreases. The blood flow continues at the same time.

Organic cardiovascular diseases.

VSD. The disease is characterized by the fact that the body does not adapt well to changes in its environment.
Infectious lesions.
Ischemic attacks.

Increased activity of the vagus nerve.
Orthostatic collapse contributes to an intense change in body position when quickly rising from a lying or sitting position. It occurs due to indiscriminate use of certain types of medications that lower blood pressure. Sometimes orthostatic collapse occurs in healthy people.
Hyperventilation of the respiratory tract.
Vasovagal reflexes.
Dehydration.

Problems with the respiratory system, heart disease.
Poor condition of blood vessels.
Epilepsy.
Poor heart rhythm.
Prolonged overheating of the body.

Increased painful syndrome.
Loss of large volume of blood.
Intense psychological stress. In most examples, fear may be accompanied by fainting. This factor often causes the development of syncope in children.
Neuralgia of the glossopharyngeal nerves.
A sharp decrease in blood pressure.

Hysteria, mental problems.
Increased barometric pressure.
Low blood sugar. This component is considered the main source of energy for the brain.
State of hypoperfusion.

A decrease in cardiac output in a complex form of arrhythmia most often occurs with myocardial infarction.
Vascular dystonia.

Sometimes it is not possible to determine the cause of fainting. It must be taken into account that everyone experiences syncope at least once in their life. Problems occur in people between 10 and 30 years of age, and the frequency of fainting increases with age.

Classification

Neurogenic, caused by problems with nervous regulation.
Somatogenic– develops simultaneously with other organ damage, and not due to brain diseases.
Extreme arises due to the influence of environmental factors on people.
Hyperventilation– This type of loss of consciousness occurs in several forms. Hypocapnic symptoms manifest as spasms of capillaries.

Vasodepressor due to insufficiently ventilated rooms and elevated temperatures in the building.
Sinocarotid caused by changes in heart rate.
Cough manifest themselves with severe attacks of coughing, causing disorders of the respiratory system.
Swallowing syncope arise due to problems with the vagus nerve.
Nocturic– a person loses consciousness after urinating or at night when trying to get up from a bed.
Hysterical.
Unclear etiology.

Some of the above syncope conditions are classified into separate groups.

Signs of syncope develop in several successive stages: the prodromal stage (symptoms that precede fainting appear), the fainting state itself, and the body after syncope.

The intensity of symptoms and the duration of all stages is determined by several individual factors.

The prodromal stage lasts from a few seconds to 10 minutes and appears after exposure to provoking factors. At this time the following symptoms appear: dizziness, goosebumps before the eyes, vision becomes blurry, general weakness, ringing or noise in the ears, pale skin, alternating with slight redness, intense sweating, feeling of nausea, pupils dilate, lack of oxygen.

It must be borne in mind that if during this period the patient manages to take a horizontal position or tilt his head slightly, he will remain conscious. Otherwise, the symptoms will worsen and he will faint.

This state does not last more than 30 minutes. Lasts a maximum of 3 minutes. Often the attacks are accompanied by convulsions.

During the recovery process from syncope, the following symptoms appear:

Constant fatigue, increased sleepiness.
Uncertain coordination.
Blood pressure drops.
I feel a little dizzy.
The patient is thirsty.
Sweat is released intensely.

These symptoms are considered common to all categories of syncope; some have unique specifics. With vasovagal loss of consciousness, the following symptoms are observed: a person feels nauseous, stomach pain, muscle tissue weakens, skin turns pale, normal heart rate, thready pulse.

It takes approximately 1 hour until you feel completely restored.

Diagnostics

Various diagnostic techniques are used to determine the causes of syncope. They differ in the nature of their implementation.

Non-invasive method performed on an outpatient basis, involves taking a medical history, obtaining tests, examining the patient, and laboratory work. Diagnostic procedures include ECG, exercise, tilt test, carotid sinus massage, electroencephalography, x-ray. Doctors sometimes use or, an examination is carried out by a psychiatrist and an ophthalmologist.

Invasive methods require the provision of inpatient conditions, use in the presence of symptoms of cardiovascular disorders confirmed by non-invasive techniques. Methods for syncope diagnostics include electrophysiological examinations, angiography, insertion of a catheter into the heart, and venticulography.

To treat syncopal paroxysm, you will need emergency care, reducing the likelihood of injury and death, and measures to prevent recurrent fainting. Hospitalization of patients is carried out in the following cases:

Clarification of syncope diagnostics.
Suspicion of disorders of the cardiovascular system.
For fainting during physical activity.
Sudden death of other family members.
Syncope is preceded by arrhythmia or problems with the heart.
Fainting while lying down.

Therapy for syncope syndromes may differ depending on the stage of development of syncope and the techniques used. The patient can be brought back to consciousness using ammonia and cold water. If there is no effect, metazone, ephedrine are administered, indirect massage of the heart muscle is performed, and hyperventilation of the respiratory organs is performed.

Between attacks, take medications and use a defibrillator. Therapy without drugs involves changing your lifestyle, giving up alcohol, diuretics, you should not change your position suddenly, and stay in a hot room. You need to follow a diet, stay hydrated, wear abdominal bands, and do physical exercises for your abs and legs.

Drug treatment involves treatment of pathologies that cause loss of consciousness. The following procedures are usually carried out: implantation of a defibrillator, stimulation of the heart muscle, therapeutic measures against arrhythmia.

First aid

In order for a person to recover from a fainting state without the help of a doctor, you need to perform the following steps:

Take a horizontal position and place the patient on his side.
Remove the tie, stretch the collar, provide fresh air.
You need to splash some cold water on your face.
Ammonia is brought to the nose.

Syncope is characterized by a rapid and sustained loss of consciousness; the patient can be quickly brought back to consciousness if first aid is provided. The following dangers occur during fainting:

Getting fractures or bruises.

Development of hidden diseases.
Death due to poor heart function.
Fetal hypoxia occurs when syncope occurs in pregnant women.
The tongue sinks, blocking the access of oxygen during involuntary swallowing.

Post-syncope state

After the patient has lost consciousness and regained consciousness, a post-syncope state begins, which lasts up to several hours. If the patient has an increased tendency to lose consciousness, he may faint again.

Prevention

A suitable way to prevent fainting is to limit the effect of provoking factors:

It is recommended to wear looser clothes.
Monitor blood glucose levels.
Treat chronic and current disorders.
Try to slowly change position from horizontal to vertical.
Avoid depression.

This type of syncope occurs most often; a person may lose consciousness due to stress. There are situations when people faint without clear provoking factors. Fainting often occurs during long trips in public transport or while waiting in line.

Placing in a room where there is not enough oxygen provokes compensatory hyperventilation. This causes syncope in children and adults.

Fever, drinking alcohol, and frequent fatigue are the causes of loss of consciousness. During such attacks, there is no mobility of the patient, the pressure decreases, and disturbances in the functioning of the heart appear.

Occurs during a prolonged stay in a standing position or during a sudden transition from a lying to a vertical position. This is possible due to a sharp jump in pressure - from low to high. Doctors make this diagnosis when there is low blood pressure and heart rate changes.

Doctors do tests with a half-hour stay in an upright position. The pressure indicator also decreases over time. For accurate diagnosis, a comparison of the orthostatic position with the vasodepressor position is performed. During the first, no specific external factors are observed; during the second, bradycardia is diagnosed.

Synocarotid syncope

It is provoked by the high sensitivity of the sinocarotid sinus. As a result, the heart rate changes and vascular tone appears. Often, this fainting condition is diagnosed in patients who are over 30. People often lose consciousness after quickly throwing their head back. Sometimes fainting occurs due to a tight tie.

In syncope, fainting and loss of consciousness is accompanied by a decrease in muscle tone, problems in the functioning of the heart and lungs. People recover from this without certain neurological abnormalities. There are somatogenic or neurogenic 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. Litt 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 pass 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 of the groups 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 mellitus, amyloidosis, etc.), taking excessive doses of certain medications (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, and various types of cerebral vascular stenosis. A common cause of acute regional ischemia of the brainstem is pathological changes in the cervical 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 medications 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 fainting 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.

For severe bradycardia, parenteral administration of atropine is advisable, and for low blood pressure - ephedrine and 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 heart rhythm disturbances, 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.