Classification of syncope. What is syncopal syndrome in children and adults - causes, diagnosis and treatment methods

Syncope (syncope, fainting)- a symptom that manifests itself as a sudden, short-term loss of consciousness and is accompanied by a drop in muscle tone. Occurs as a result of transient hypoperfusion of the brain.

In patients with syncope, pallor of the skin, hyperhidrosis, lack of spontaneous activity, hypotension, cold extremities, weak pulse, and frequent shallow breathing are observed. The duration of syncope is usually about 20 seconds.

After fainting, the patient's condition usually recovers quickly and completely, but weakness and fatigue are noted. Elderly patients may experience retrograde amnesia.

Syncopal and pre-syncope conditions are recorded in 30% of people at least once.

It is important to diagnose the causes of syncope, as they can be life-threatening conditions (tachyarrhythmias, heart block).

• Epidemiology of syncope

  About 500 thousand new cases of syncope are registered annually in the world. Of these, approximately 15% - in children and adolescents under the age of 18 years. In 61-71% of cases in this population, reflex syncope is recorded; in 11-19% of cases - fainting due to cerebrovascular diseases; in 6% - syncope caused by cardiovascular pathology.

  The incidence of syncope in men aged 40-59 years is 16%; in women aged 40-59 years - 19%, in people over the age of 70 years - 23%.

  Approximately 30% of the population will experience at least one episode of syncope during their lifetime. Syncope recurs in 25% of cases.

• Classification of syncope

  Syncopal states are classified according to the pathophysiological mechanism. However, in 38-47% of patients, the cause of syncope cannot be established.

  • Neurogenic (reflex) syncope.
    • Vaso-vagal syncope:
      • Typical.
      • Atypical.
    • Syncope caused by hypersensitivity of the carotid sinus (situational syncope).

      Occurs at the sight of blood, during coughing, sneezing, swallowing, defecation, urination, after physical activity, eating, when playing wind instruments, during weightlifting.

    • Syncope that occurs with neuralgia of the trigeminal or glossopharyngeal nerves.
  • Orthostatic syncope.
    • Orthostatic syncope (caused by lack of autonomic regulation).
      • Orthostatic syncope in the syndrome of primary insufficiency of autonomic regulation (multiple system atrophy, Parkinson's disease with insufficiency of autonomic regulation).
      • Orthostatic syncope in the syndrome secondary insufficiency autonomic regulation (diabetic neuropathy, amyloid neuropathy).
      • Postload orthostatic syncope.
      • Postprandial (occurring after eating) orthostatic syncope.
    • Orthostatic syncope caused by ingestion medicines or alcohol.
    • Orthostatic syncope caused by hypovolemia (with Addison's disease, bleeding, diarrhea).
  • Cardiogenic syncope.

    In 18-20% of cases, the cause of syncope is cardiovascular (cardiovascular) pathology: rhythm and conduction disturbances, structural and morphological changes in the heart and blood vessels.

    • Arrhythmogenic syncope.
      • Sinus node dysfunction (including tachycardia/bradycardia syndrome).
      • Atrioventricular conduction disorders.
      • Paroxysmal supraventricular and ventricular tachycardias.
      • Idiopathic arrhythmias (long QT syndrome, Brugada syndrome).
      • Violations of the functioning of artificial pacemakers and implanted cardioverter-defibrillators.
      • Proarrhythmic effect of drugs.
    • Syncope caused by diseases of cardio-vascular system.
      • Diseases of the valves of the heart.
      • Acute myocardial infarction/ischemia.
      • Obstructive cardiomyopathy.
      • Atrial myxoma.
      • Acute dissection of an aortic aneurysm.
      • Pericarditis.
      • Thromboembolism pulmonary artery.
      • Arterial pulmonary hypertension.
  • Cerebrovascular syncope.

    Observed in subclavian "steal" syndrome, which is based on a sharp narrowing or blockage subclavian vein. With this syndrome, there are: dizziness, diplopia, dysarthria, syncope.

  There are also non-syncope conditions that are diagnosed as syncope.

  • Non-syncope states that occur with partial or total loss consciousness.
    • Metabolic disorders (caused by hypoglycemia, hypoxia, hyperventilation, hypercapnia).
    • Epilepsy.
    • Intoxication.
    • Vertebrobasilar transient ischemic attacks.
  • Non-syncope states that occur without loss of consciousness.
    • Cataplexy (short-term relaxation of the muscles, accompanied by a fall of the patient; usually occurs in connection with emotional experiences).
    • Psychogenic pseudosyncope.
    • Panic attacks.
    • Transient ischemic attacks of carotid origin.

      If the cause of transient ischemic attacks is blood flow disorders in the carotid arteries, then loss of consciousness is recorded when the perfusion of the reticular pharmacy of the brain is disturbed.

    • hysterical syndrome.

Diagnostics

• Goals of diagnosing syncope
  • Establish whether an attack of loss of consciousness is syncope.
  • As early as possible, identify a patient with a cardiovascular pathology leading to fainting.
  • Establish the cause of syncope.

• Diagnostic methods

  Diagnosis of syncopal conditions is carried out by invasive and non-invasive methods.

  non-invasive diagnostic methods studies are carried out on an outpatient basis. In the case of invasive examination methods, hospitalization is necessary.

  • Non-invasive methods for examining patients with syncope

• Tactics of examination of patients with syncope

  When examining patients with syncope, it is necessary to identify cardiovascular pathology as early as possible.

  In the absence of cardiovascular disease in a patient, it is important to establish other likely causes of syncope.

  • Patients who are suspected of having cardiogenic syncope (heart murmurs, signs of myocardial ischemia) are recommended to be examined to identify cardiovascular pathology. The survey should begin with the following activities:
    • Determination of cardiospecific biochemical markers in the blood.
    • Holter ECG monitoring.
    • Echocardiography.
    • Test with physical activity - according to indications.
    • Electrophysiological study - according to indications.
  • Examination of patients for the purpose of diagnosing neurogenic syncope is carried out in the presence of recurrent syncope, accompanied by pronounced emotional and motor reactions that occur during exercise; in a horizontal position of the body; in patients with an unfavorable family history (cases of sudden cardiac death in relatives under the age of 30 years). The examination of patients should begin with the following activities:
    • Tilt test.
    • Carotid sinus massage.
    • Holter ECG monitoring (performed upon receipt of negative results of the tilt test and massage of the carotid sinus).
  • Examination of patients with syncope, in the genesis of which metabolic disorders are assumed, should begin with laboratory diagnostic methods.
  • In patients who develop syncope when the head is turned to the side, the examination should begin with a massage of the carotid sinus.
  • If syncope occurs during or immediately after exercise, evaluation begins with an echocardiogram and an exercise stress test.
  • Patients with frequent, recurrent syncope, presenting a variety of somatic complaints, especially during stressful situations, need to consult a psychiatrist.
  • If after complete examination Since the mechanism of development of syncope has not been established, for the purpose of long-term outpatient monitoring of the heart rate, the use of an implantable ECG loop recorder is recommended.

• Differential diagnosis of syncope

  In young patients, syncope can be a symptom of manifestation of the syndromes of lengthening the QT interval, Brugada, Wolff-Parkinson-White, polymorphic ventricular tachycardia, arrhythmogenic right ventricular cardiomyopathy, myocarditis, pulmonary arterial hypertension.

  Need to diagnose life threatening pathological conditions in patients with syncope, accompanied by pronounced emotional and motor reactions, with syncope that occurs during physical activity, in a horizontal position of the body; in patients with an unfavorable family history (cases of sudden cardiac death in relatives under the age of 30 years).

  	Syncope	Adams-Morgagni-Stokes syndrome	convulsive attack
  body position	vertical		Vertical/horizontal
  Skin color	Pale	Paleness/cyanosis	Not changed
  Injuries	Rarely	Often	Often
  Duration of loss of consciousness	short	May vary in duration	Long
  Tonic-clonic limb movements	Sometimes	Sometimes	Often
  Tongue biting	Rarely	Rarely	Often
  Involuntary urination (defecation)		Rarely involuntary urination	Often involuntary bowel movements
  Condition after an attack		Rapid recovery of consciousness	After the attack, there is a slow recovery of consciousness; headache, weakness

It is usually classified and discussed along with syncope because it has the same causes.

Seizures may cause sudden loss of consciousness, but are not considered syncope. However, in patients with syncope, it is necessary to exclude the presence of a seizure syndrome, since the collection of 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 careful history taking, eyewitness accounts, or examination during the attack.

Pathophysiology of syncope

Most syncope is due to insufficiency cerebral circulation. In some cases, there may be normal blood flow, but a lack of other substrates (O2 Glucose or both).

Insufficiency of cerebral circulation

Most cases of cerebrovascular insufficiency are the result of a decrease in cardiac output (CO).

The decrease in CO may be due to:

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

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

Aremias result in syncope if the rhythm is too fast to adequately fill the ventricles (eg, greater than 150–180 bpm) or too slow to maintain normal output (eg, less than 30–35 bpm).

Venous return may be reduced by blood loss, increased intrathoracic pressure, increased vagal tone, and reduced sympathetic tone (eg, due to medication, carotid sinus pressure, or autonomic dysfunction). Syncope resulting from these mechanisms (with the exception of bleeding) is often referred to as vasovagal or neurocardiogenic and is usually benign.

Orthostatic hypotension, which is common cause syncope may result from the inability of normal compensatory mechanisms (eg, sinus tachycardia, vasoconstriction, or both) to support the temporary reduction in venous return that occurs with assuming an upright position.

Cerebrovascular disease rarely results in syncope, since most of them occur without involvement of the centrocephalic structures, which must be affected to cause loss of consciousness. However, ischemia in the area of ​​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 CNS needs O2 and glucose to function properly. From a practical point of view, the main cause is hypoglycemia, since hypoxia rarely develops in such a way as to cause a sudden loss of consciousness (except during flights or diving). Loss of consciousness due to hypoglycemia usually does not develop as suddenly as syncope or convulsions, since hypoglycemia is preceded by a number of symptoms (with the exception of patients taking β-blockers); however, the doctor may not know the circumstances of the development of the attack, if there were no witnesses.

Causes of syncope

Obstruction of the outflow or inflow tract:

Rhythm disturbances

Ventricular dysfunction:

Vasovagal (neurocardiogenic):

Orthostatic hypotension:

Cerebrovascular diseases:

Other reasons:

Some medications that can cause syncope include:

Syncope examination

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

Assessment of the state of organs and systems. The patient should be asked about the presence of pain or injury, episodes of dizziness or presyncope when standing up, and about attacks of palpitations or pain in chest during physical exertion. The patient should be asked about the symptoms, which may be manifestations of the underlying disease, incl. about availability liquid stool or blood in the stool, profuse menstrual bleeding(anemia); vomiting, diarrhea, or massive urination (dehydration or electrolyte disturbances); and risk factors for pulmonary embolism (recent surgical intervention or immobilization, presence of malignancy, history of coagulation disorder).

The anamnesis of other diseases should contain information about previous syncopal conditions, the presence of cardiovascular pathology, as well as a history of convulsions. The patient should be asked about the medications taken (especially antihypertensives, diuretics, vasodilators and arthiarrhythmics).

Physical examination

During a general examination, the mental status of the patient is assessed, incl. the presence of disorientation or hesitation, indicative of a postictal state, as well as signs of trauma (for example, bruising, swelling, tension, biting of the tongue).

During auscultation of the heart, attention should be paid to the presence of noise; the change in noise when performing a Valsalva test, 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 in the diagnosis of rhythm disturbances if ECG registration is not possible.

Some clinicians perform unilateral carotid sinus massage during ECG monitoring with the patient lying down to detect bradycardia or block and diagnose carotid sinus hypersensitivity.

On palpation of the abdomen, attention should be paid to the presence of muscle tension, and a rectal examination is performed to detect overt or hidden bleeding.

Full neurological examination to identify focal symptoms, which may indicate CNS damage as the cause of syncope (for example, convulsive disorders).

Signs that need more attention

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

• Syncope during exercise.
• Multiple episodes within a short period of time.
• Presence of a heart murmur or other signs of structural abnormality (such as chest pain).
• Elderly age.
• Significant injury during an episode of syncope.
• Family history of sudden death.

Interpretation of the received data

Although the causes of syncope are often benign, it is important to identify conditions that are life-threatening (eg, tachyarrhythmias, blocks) that cause sudden death. Clinical data suggest a cause in 40-50% of cases. You can summarize them as follows.

Benign causes often lead to syncope. Syncope preceded by physical or emotional exertion (eg, pain, fear) that occurs in an upright position, often with vagal precursors (eg, nausea, weakness, yawning, anxiety, blurred vision, sweating) are commonly referred to as vasovagal syncope. states.

Syncope, which usually occurs when moving to an upright position, indicates an orthostatic cause. Syncope that occurs with prolonged immobility is usually due to the deposition of blood in the venous bed.

Loss of consciousness that occurs suddenly, associated with muscle twitches or convulsions, incontinence or biting of the tongue, followed by postictal disorientation or somnolence, is indicative of convulsive syndromes.

The presence of signs that heightened attention, indicates a serious cause of syncope.

Syncope that occurs on the background of physical activity indicates obstruction of the outflow tract of the heart. These patients sometimes also present with 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 radiating to the carotid arteries, indicates aortic stenosis; systolic murmur that increases with Valsalva and decreases with squatting may be a sign of hypertrophic cardiomyopathy.

Syncope, which come and go 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 seizures increases and, accordingly, alertness increases. The presence of harbingers 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 a 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, a more thorough evaluation is required.

If you suspect a rhythm disorder, myocarditis or coronary heart disease, the patient needs to be hospitalized for examination.

ECG is performed for all patients. An ECG may reveal arrhythmias, conduction disturbances, myocardial hypertrophy, accessory pathways, OT interval prolongation, pacemaker failure, myocardial ischemia, or myocardial infarction. In the absence of clinical signs in elderly patients, it is advisable to determine the level of markers of myocardial damage to rule out a heart attack, as well as conduct ECG monitoring for at least 24 hours. syncope does not develop during monitoring. On the other hand, the presence of symptoms in the absence of rhythm disturbances rules out this cause of syncope. The use of recorders may be useful if syncope is preceded by precursors.

Laboratory studies are performed depending on the clinical situation; automatically posted standard laboratory examination usually not informative. However, all women of childbearing age should have a pregnancy test. If anemia is suspected, the hematocrit level is determined. Determination of electrolytes is carried out, if there are grounds. Serum troponin levels are assessed to rule out acute myocardial infarction.

Echocardiography is indicated in patients who experience syncope during exercise, if there is a heart murmur, or if a heart tumor is suspected (eg, in the presence of postural syncope).

It is advisable to perform a tilt test if, during the collection of anamnesis or physical examination, data are obtained for the vasodepressor or other reflex nature of syncope. This method is also used to assess stress-induced syncope.

Stress tests are performed when transient myocardial ischemia is suspected. Often used in patients with stress-induced symptoms.

An invasive electrophysiological study is performed if it was not possible to detect arrhythmia using non-invasive methods in patients with unexplained recurrent syncope; a negative result identifies a low-risk subgroup with a high likelihood of syncope remission. In other patients, the indications for an electrophysiological study are ambiguous. Exercise tests are less informative unless syncope is provoked by exercise.

EEG is indicated for suspected convulsive disorders.

Treatment of syncope

If syncope develops, the presence of a pulse should be determined immediately. In the absence of a pulse, cardiopulmonary resuscitation is performed. In the presence of heart contractions, atropine or transthoracic pacing is used to correct severe bradycardia. Isoproterenol may be used to maintain the heart rhythm until a temporary pacemaker is implanted.

Electrical cardioversion is fast and safe method with hemodynamic instability. In case of violation of venous return, it is necessary to give the patient a horizontal position with raised legs, and also to introduce him saline solutions. With tamponade, pericardiocentesis is indicated. Tension pneumothorax requires drainage of the pleural cavity. Adrenaline is administered parenterally for anaphylaxis.

Giving the patient a horizontal position with elevated legs, as a rule, leads to the resolution of syncope, after the exclusion of life-threatening conditions. If the patient moves quickly to a sitting position, syncope may recur; holding the patient in an upright position or transporting him in an upright position may increase the period of brain hypoperfusion and slow down 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 reduced skeletal muscle function due to insufficient physical activity, and sclerodegenerative changes in the sinoatrial node and conduction system as a result of heart disease.

In older patients, syncope often results from 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.

18.1. GENERAL PROVISIONS

Syncope (from the Greek. synkope - to weaken, exhaust, destroy), or fainting (little death), - the most common short-term paroxysmal disturbances of consciousness of non-epileptic origin, caused by insufficient blood flow in the vessels of the brain, its hypoxia or anoxia and diffuse disturbance 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 XIX century. Littre in the Dictionary of Medicine defined syncope as a sudden and short-term cessation or weakening of cardiac activity with interruption of breathing, impaired consciousness and voluntary movements.

Syncope can go through three subsequent stages: 1) the stage of precursors (pre-syncope, lipothymia); 2) the stage of culmination, or heat (actual syncope); 3) recovery period (post-syncope). The first stage may be preceded latency period (from 20 to 80 s), arising after the provoking situation.

Syncope can be triggered by emotional stress, orthostatic hypotension, being in a stuffy room, coughing fits, irritation of the carotid sinus, atrioventricular blockade, hypoglycemia, acute dyspepsia, profuse urination, etc. In patients with neuralgia of the IX nerve, syncope sometimes occurs when swallowing as a reaction to the resulting sharp pain. neurogenic syncope - one of the paroxysmal vegetative disorders, clearly demonstrating a decrease in the body's adaptive capabilities in providing various forms of its activity due to acute arterial hypotension and subsequent cerebral hypoxia. Arterial hypotension (AH) often predisposes to syncope. In the interictal period, patients with a history of syncope often complain of general weakness, increased fatigue, difficulty concentrating, diffuse headache (more often in the morning), signs of vegetative-vascular lability, migraine, cardialgia, elements of Raynaud's syndrome are possible.

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

"feeling bad" swoon(from the Greek leipe - loss, themos - thought, life): general weakness, accompanied by blanching of the face, a growing feeling of discomfort, lack of air, non-systemic dizziness, darkening of the eyes, ringing in the ears, nausea, hyperhidrosis; sometimes with yawning, palpitations, numbness of the lips, tongue, discomfort in the region of the heart, in the abdomen. Consciousness in the first moments of an attack may be narrowed, orientation - incomplete, while "the earth floats away from under your feet."

The loss of consciousness occurring 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 sharp - 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 stupefaction for a moment to a deep loss for 10 seconds or more. During the period of loss of consciousness, the patient's eyes are covered, the gaze is turned up, 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 threadlike, asystole is possible for 2-4 s, blood pressure is low (usually below 70/40 mm Hg), breathing is rare, shallow. If the loss of consciousness lasts more than 10 seconds, fascicular or myoclonic twitches are possible, as happens, in particular, with Shy-Drager syndrome.

The severity of the syncopal state is determined by the depth and duration of the disorder of consciousness. In severe cases, consciousness is disabled 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, biting of the tongue and involuntary urination.

During a syncopal state, the EEG usually shows signs of generalized cerebral hypoxia in the form of high-amplitude slow waves; ECG often bradycardia, sometimes arrhythmia, rarely asystole.

After the restoration of consciousness, patients may experience some general weakness, sometimes a feeling of heaviness in the head, a dull headache, discomfort in the region of the heart, in the abdomen. The horizontal position of the patient, fresh air, improved breathing conditions, the smell of ammonia, the introduction of cardiotonic drugs, caffeine contribute to the rapid recovery of consciousness. When leaving 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 move to a vertical position and to motor activity can provoke the development of repeated fainting. The normalization of the patient's condition after an attack depends on many factors, primarily on the severity of the condition that caused the paroxysmal condition.

Thus, in contrast to epileptic seizures in syncopal states, loss of consciousness is usually preceded by severe vegetative parasympathetic disorders, loss of consciousness and a decrease in muscle tone are not so acute, the patient, even when falling, usually does not get bruised. If an epileptic seizure can occur at any time, often quite unexpectedly for the patient, and does not depend on the position of the person’s body, then syncopal

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

About 30% of adults have had syncope at least once in their lives, most often at the age of 15-30 years. Fainting is noted in 1% of patients at the dentist's appointment, in 4-5% of donors during blood donation. Repeated syncopal states are detected in 6.8% of respondents (Akimov G.A. et al., 1978).

The polymorphism of the causes of syncope allows us to say that the syncope should be considered as a clinical phenomenon that may be due to various exogenous and endogenous factors, the nature of which may determine some of the nuances of the clinical manifestations of syncope, contributing to the recognition of its cause. At the same time, the possibility of achieving the same goal in the process of analyzing the anamnesis data, information about the state of the neurological and somatic status, and additional studies is undeniable.

18.2. CLASSIFICATION

The abundance of causes of syncope makes it difficult to classify them based on the etiological principle. 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; synocarotid syncope.

II. Cardiogenic type - decrease in cardiac output due to arrhythmia; attacks of Morgagni-Adams-Stokes, etc.; extensive myocardial infarction; aortic stenosis; myxoma of the left atrium; idiopathic hypertrophic subaortic stenosis; violation of inflow to the left half of the heart: a) pulmonary embolism; b) stenosis of the pulmonary artery; c) impaired venous return to the heart.

III. orthostatic type - orthostatic hypotension.

IV. cerebral type - transient ischemic attacks, vegetative-vascular reactions in migraine.

v. Decreased oxygen content 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 syncopal states are differentiated into three main groups: neurogenic syncope, somatogenic syncope, and extreme exposure syncope. Rarely occurring polyfactorial syncopal conditions are considered as an addition to these groups. Each of the groups is subdivided 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 emotional, associative, irritative, maladaptive and dyscirculatory.

18.3.1. Emotional syncope

The occurrence of emotiogenic syncope is associated with negative emotions, which may be due to sharp pain, the sight of blood, anxiety, fear, etc. Emotional syncope is possible in healthy person, but more often manifest 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 orientation of vascular reactions.

The cause of such syncope (fainting) can usually be traumatic factors that have an extraordinary personally significant content for this subject. Among them, unexpected news of tragic events, experiencing serious life failures, real or imagined threats to the lives of patients and their loved ones, medical manipulations(injections, punctures, blood sampling, tooth extraction, etc.), feelings or empathy in connection with the suffering of other people. Thus, following a syncope, a detailed history taking usually reveals the cause of the paroxysm, making it possible to understand its origin.

Emotional syncopal states usually develop after a distinct pre-syncope period (lipothymia), with autonomic parasympathetic disorders, a gradual decrease in muscle tone and a slow loss of consciousness being expressed. 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 (feeling of fear, shame), there is an increasing general weakness, dry mouth, an unpleasant feeling of tightness in the heart area , blanching of the face, decreased muscle tone, holding the breath, sometimes trembling of the eyelids, lips, limbs. The observed ischemic and hypoxic manifestations are confirmed by REG and EEG data, which have a diffuse character.

18.3.2. Associative syncope

Associative syncopal states are usually the result 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 during a second visit to the office of a dental surgeon.

18.3.3. Irritative syncope

Irritative syncopal states are the result 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 breakdown in the system of autoregulation of cerebral circulation, in particular, receptors in the carotid sinus zone, the vestibular apparatus, and parasympathetic structures. vagus nerve.

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

Carotid sinus syncope is provoked by irritation of the carotid sinus receptors. Excitation of these receptors on one or both sides, especially in the elderly, can cause reflex slowing of the heart rate (vagal type of response), less often - a drop in blood pressure without bradycardia (depressor type of response). Carotid sinus syncope occurs more often in men, especially when wearing a tight collar, tightly tied tie. Throwing the head back while shaving, following the flight of 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 compression of the throat and chest, lasting 15-25 seconds, from the onset of irritation of the carotid sinus are possible. receptor zone followed by loss of consciousness for 10 seconds or more, sometimes convulsions are possible.

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

I.V. Moldovanu (1991) notes that harbingers of carotid sinus syncope may be speech disorders, 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 disturbing consciousness. For the diagnosis of carotid syncope, it is proposed that the patient lying on his back be massaged or pressed on the area of ​​the carotid sinus alternately from one side and the other. 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, arising in connection with the re-irritation of the vestibular apparatus, the loss of consciousness is preceded by the so-called motion sickness symptom complex. It is characterized by a combination of sensory, vestibulosomatic and vestibulo-vegetative disorders. Sensory changes include systemic vertigo. Vestibulosomatic reactions are characterized by an imbalance associated with a change in the tone of the muscles of the trunk and limbs. In connection with pathological vestibulo-vegetative reflexes, there are violations of the functions of the cardiovascular system in the form of tachycardia or bradycardia, changes in blood pressure, blanching or hyperemia of the integument, as well as hyperhidrosis, rapid and shallow breathing, nausea, vomiting, general malaise. Some of these symptoms persist for quite a long time (within 30-40 minutes) even after the restoration of consciousness.

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

18.3.4. Maladaptive syncope

Disadaptive syncope occurs with an increase in motor or mental load, which requires appropriate additional metabolic, energy, vegetative support. Thus, they are caused by the insufficiency of the ergotropic functions of the nervous system, which occurs during temporary maladaptation of the body due to physical or mental overload and adverse environmental influences. An example of this variant of syncopal conditions are, in particular, orthostatic and hyperthermic syncope, as well as syncope that occurs under conditions of insufficient fresh air supply, during physical overload, etc.

Included in this group of disaptation syncope syncope 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 a violation of the reactivity of the 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. The fall in blood pressure, leading to a maladaptive syncope, in such cases may be the result of functional insufficiency of pre- or post-ganglionic sympathetic structures, ensuring the maintenance of blood pressure when the patient moves from a horizontal to a vertical position. Possible primary autonomic failure due to degenerative pathology (Shy-Drager syndrome), or idiopathic orthostatic hypotension. Secondary orthostatic hypotension may be due to autonomic polyneuropathy (due to alcoholism, diabetes mellitus, amyloidosis, etc.), taking excessive doses of certain medicines(antihypertensive drugs, tranquilizers), hypovolemia (with blood loss, increased diuresis, vomiting), prolonged bed rest.

18.3.5. Dyscirculatory syncopal conditions

Dyscirculatory syncope occurs due to regional cerebral ischemia, caused by angiospasm, impaired blood flow in main vessels heads, mainly in the vertebrobasilar system, by the phenomena of congestive hypoxia. Risk factors in this case may be neurocirculatory dystonia, atherosclerosis, hypertensive crises, vertebrobasilar insufficiency, various variants of cerebral stenosis. A common cause of acute regional ischemia of the brainstem are pathological changes in cervical region spine, anomalies of the craniovertebral articulation and vessels in the basin of the vertebral arteries.

Syncopal states are provoked by sudden movements of the head or its prolonged forced unusual position. An example of a dyscirculatory syncope would be shaving syndrome, or Unterharnscheidt's syndrome, in which fainting is provoked by sharp turns and tilting of the head, as well as Sistine Madonna Syndrome, arising from a prolonged unusual position of the head, for example, when examining the painting of temple structures.

With dyscirculatory syncope, the precursor stage is short; at this time, dizziness (possibly systemic) is rapidly increasing, occipital pain often appears. Sometimes the harbingers preceding the loss of consciousness are not captured 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. Differentiation of these paroxysms similar in clinical picture can be facilitated by the absence of seizure amnesia in syncope and the usual detection on the EEG in epilepsy of hypersynchronous neuronal discharges characteristic of it. In the case of circulatory

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

The causes of acute hypoxia of the brain, manifested by dyscirculatory syncope, may 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 in clinical picture there are clear manifestations chronic diseases internal organs, in particular, signs of cardiac decompensation (cyanosis, edema, tachycardia, arrhythmia), manifestations of peripheral vascular insufficiency, expressed allergic reactions possible anemia, blood diseases, diabetes, diseases of the liver, kidneys. In the classification of G.A. Akimova et al. (1987) revealed 5 main variants of syncope in this group.

Cardiogenic syncope are usually associated with a sudden decrease in cardiac output due to a sharp violation of 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. Their variant is the Morgagni-Adams-Stokes syndrome.

Morgagni-Adams-Stokes syndrome manifests itself as a syncope that occurs against the background of a complete atrioventricular blockade, caused by impaired conduction in the bundle of His and provoking ischemia of the brain, in particular, the reticular formation of its trunk. It is manifested by instantly onset general weakness with a sudden short-term loss of consciousness and a drop in muscle tone, while 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, sometimes a bilateral Babinsky symptom is detected. During an attack, it is usually not determined arterial pressure and heart sounds are often not audible. May be repeated several times a day. The syndrome was described by the Italian physician G. Morgagni (1682-1771) and the Irish physicians R. Adams (1791-1875) and W. Stokes (1804-1878).

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

belongs to the vasodepressor vasovagal syncope, due to autonomic imbalance with a predominance of parasympathetic reactions. Occurs with a drop in blood pressure and bradycardia; possible at any age, but more often observed in puberty, especially in girls, 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 the result of a small blood loss, starvation, anemia, prolonged bed rest. The prodromal period is characterized by nausea, discomfort in the epigastrium, yawning, hyperhidrosis, tachypnea, dilated pupils. During paroxysm, arterial hypotension, bradycardia, followed by tachycardia, are noted.

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

Hypoglycemic syncope associated with a drop in the concentration of glucose in the blood, may be the result of hyperinsulinemia of a functional or organic nature. They are characterized by the fact that against the background of a feeling of acute hunger, chronic alimentary insufficiency or insulin administration, a sharp weakness, a feeling of fatigue, a feeling of “emptyness in the head”, internal tremors develop, which may be accompanied by a tremor of the head and limbs, while marked hyperhidrosis, signs of autonomic dysfunction at first sympathetic-tonic, and then vagotonic character. Against this background, there is an oppression of consciousness from a slight stupor to a deep stupor. With prolonged hypoglycemia, motor excitation and productive psychopathological symptoms are possible. With absence emergency assistance patients fall into a coma.

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

18.5. SYNCOPAL CONDITIONS

FOR EXTREME EXPOSURE

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

Hypoxic syncope. Hypoxic syncope includes syncope that occurs due to exogenous hypoxia that occurs with a significant lack of oxygen in the inhaled air, for example, at a height (high-altitude fainting), in unventilated rooms.

A harbinger of such fainting is an irresistible desire for sleep, tachypnea, confusion, pallor of integumentary tissues, and sometimes muscle twitches. In hypoxic syncope, the face is pale with a grayish tint, the eyes are closed, the pupils are constricted, profuse, cold, sticky sweat, shallow, rare, arrhythmic breathing, the pulse is frequent, thready. Without help, high-altitude syncope can be fatal. After getting out of high-altitude syncope, in particular with the help of an oxygen mask, the victim experiences weakness, headache for some time; he usually does not remember about the passed syncope.

Hypovolemic syncope. Arise due to circulatory hypoxia due to unfavorable redistribution of blood when exposed to overload 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 g-forces in flight, central vision first deteriorates, a gray veil appears before the eyes, changing to black, complete disorientation occurs and loss of consciousness occurs, which occurs along with a sharp drop in muscle tone (gravitational syncope). Confusion and disorientation persist for some time after the cessation of the effects of acceleration.

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

Medical syncope. Syncope occurs as a result of the hypotensive or hypoglycemic side effects of certain drugs, may be the result of taking antipsychotic, ganglion blocking, antihypertensive, sugar-lowering drugs.

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

18.6. RARE POLYFACTORIAL

SYNCOPAL CONDITIONS

Among polyfactorial syncopal conditions in the classification of G.A. Akimova et al. (1987) presents the following.

Nicturic fainting. Occurs rarely, usually when getting out of bed at night and urinating or defecation; in most cases observed in men older than 50 years. 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 vagot-

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

Cough syncope, or bettolepsy. Cough syncope, or bettolepsy (from the Greek bettor - cough + lepsis - seizure, attack), occurs, as a rule, during the climax of a prolonged attack of coughing. It is usually observed in patients with chronic pulmonary heart disease. More often they are middle-aged men of picnic physique, 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, to venous congestion in the cranial cavity and hypoxia of the brain. Loss of consciousness during cough syncope usually occurs without precursors and does not depend on the patient's posture, it is also possible in the supine position. Impairment of 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, with swelling of the cervical veins, hyperhidrosis, sometimes accompanied by myoclonic reactions. The term "bettolepsy" was proposed in 1959 by a domestic neuropathologist

M.I. Kholodenko (1905-1979).

Patients with a history of syncope should undergo a somatic and neurological examination, 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 successfully. During fainting, the patient should be given a position that will ensure maximum blood flow to the head; best option- lay it down so that the legs are slightly higher than the head, while making sure that there is no sinking of the tongue and other obstacles to the free flow of air into Airways. Spraying can be positive cold water face and neck, the patient is given a sniff of ammonia. In case of an urge to vomit, the patient's head should be turned to the side, a towel should be placed. The patient should not attempt to administer medicine or water by mouth until he has recovered from unconsciousness.

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

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

Syncopal conditions due to respiratory failure can also occur with a lack of oxygen in the inhaled air (stuffy room, staying at a height, etc.), as well as with a decrease in the vital capacity of the lungs and with their hyperventilation.

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

With postural hypotension, patients should not rush when moving from a horizontal to a vertical position, sometimes with arterial hypotension, elastic stockings, taking tonic drugs (eleutherococcus, ginseng, etc.), psychostimulants such as meridil (centedrin), sydnocarb, acephene may be recommended . In chronic orthostatic hypotension, courses of corticosteroid treatment are sometimes appropriate. In case of heart rhythm disturbances, appropriate drug therapy is indicated, and if it is not effective enough, the installation of an electrocardiostimulator, a pacemaker. With reflex carotid sinus syncope, patients should not wear tight collars, sometimes the question of the advisability of surgical denervation of the carotid sinus should be discussed. In severe syncopal conditions during attacks, caffeine, ephedrine, cordiamine and other analeptic and adrenomimetic drugs can be parenterally administered.

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

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

A collapse must be distinguished from a syncopal state: although there is a vascular-regulatory disorder with it, however, loss of consciousness does not necessarily occur.

What is syncope and its neurological assessment

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

Syncope can occur at any age. Usually occurs in a sitting or standing position. Caused by acute stem or cerebral oxygen starvation.

Syncope must be distinguished from acute. 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 of the stages, its duration depends on the cause and mechanism of development of syncope.

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.

Manifested by weakness, blanching of the face (it can be replaced by redness), sweating, darkening of the eyes. If a person in this state has time to lie down or at least bow his head, then he does not come.

Under adverse conditions (impossibility to change the position of the body, continued exposure to provoking factors), general weakness increases, consciousness is disturbed. Duration - from seconds to ten minutes. The patient falls, but there is no significant physical damage, foam at the mouth or involuntary micturition are not observed. Pupils dilate, blood pressure drops.

The post-fainting 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 the pathophysiological principle. 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.

The following types of syncope are also distinguished:

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

There are also non-syncopal 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, psychogenic pseudosyncope, and 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 wall of the blood vessel;
• the level of systemic blood pressure;
• person's age.

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

1. Vasovagal syncope- syncope or vasodepressor states occur due to disorders of the autonomic regulation of blood vessels. Sympathetic tension nervous system rises, which increases blood pressure and heart rate. In the future, due to an increase in the 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 work of the vasomotor function. The development of orthostatic syncope is influenced by the intake of antihypertensive drugs, vasodilators, etc.
3. Due to a decrease in cardiac output, cardiogenic
4. With hypoglycemia, a decrease in the amount of oxygen in the blood develops cerebrovascular syncope. Elderly patients are also at risk due to the likelihood of developing.

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

Features of the clinical picture

Peculiarities clinical course different kind syncope are:

Diagnostic criteria

First of all, for the diagnosis of syncope, the collection of anamnesis is of great importance. It is extremely important for the doctor to find out in detail such circumstances: whether there were precursors, what character they had, what consciousness the person had before the attack, how quickly Clinical signs syncope, the nature of the fall of the patient directly during the attack, the color of his face, the presence of a pulse, the nature of the change in the pupils.

It is also important to indicate to the doctor the duration of the patient's being in a state of loss of consciousness, the presence of convulsions, involuntary urination and / or defecation, foam secreted from the mouth.

When examining patients, the following diagnostic procedures are carried out:

• measure blood pressure in a standing, sitting and lying position;
• conduct diagnostic tests with physical activity;
• do blood tests, urine tests (required!), with the determination of the amount of blood sugar, as well as hematocrit;
• do also electrocardiography,;
• if cardiac causes of syncope are suspected, an x-ray of the lungs, ultrasound of the lungs and heart is done;
• computer and is also shown.

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

Assistance Tactics and Strategy

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

First of all, when fainting, it is necessary to prevent a person from hitting. It must be laid and the legs placed as high as possible. Tight clothing should be unbuttoned and a sufficient supply of fresh air should be provided.

It is necessary to give ammonia to sniff, 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 severe fainting, Metazon is administered orally in a 1% solution or Ephedrine in a 5% solution. An attack of bradycardia, syncope, is stopped by the introduction of atropine sulfate. Antiarrhythmic drugs should be administered only for cardiac arrhythmias.

If a 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, to allow overheating. It is useful to drink plenty of water with the addition of table salt. It is necessary to avoid a sudden change in body position, especially from a horizontal to a vertical position.

Therapy between attacks is reduced to taking the recommended medications. Non-drug treatment reduced to the abolition of diuretics, dilators. With hypovolemia, correction of this condition is indicated.

What are the consequences?

In rare syncopal conditions, 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 domestic injuries, death from road traffic accidents. Patients with heart failure, ventricular arrhythmias, and pathological signs on the electrocardiogram are at risk of sudden cardiac death.

Preventive actions

First of all, the prevention of any syncope comes down to the elimination of any provoking factors. These are stressful conditions, heavy physical exertion, emotional states.

It is necessary to go in for sports (naturally, in reasonable measures), temper, establish a normal mode of work. In the morning, do not make excessively sudden movements in bed.

With frequent fainting and excessive excitability, it is necessary to drink soothing infusions with mint, St. John's wort, lemon balm.

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

Syncope is a short-term fainting, which is accompanied by a decrease in muscle tone. Problems arise from transient hypoperfusion. Among characteristic symptoms pallor, poor activity, low pressure are observed.

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 losing consciousness, the head hurts, the body weakens, drowsiness appears.
• Loss of consciousness with various accompanying symptoms often manifests itself in children, adolescents and girls, and is also characteristic of adult men.
• In older people, the few minutes preceding the loss of consciousness are eliminated from memory.

In a fainting state, the patient's muscle tissues are relaxed, the pulse becomes slower, respiratory movements decrease. Skin covering turns pale, there is no reaction to the influence of environmental factors. In rare situations, urine is not held back during syncope.

Causes of fainting

Brain tissues require a regular blood supply. About 13% of the blood flow is required for normal operation. Indicators change in stressful situations, during physical exertion. Given the average weight of the brain, people require 750 ml of blood per minute for its normal functioning. Fainting occurs when such an indicator is reduced. The blood flow continues.

• Organic cardiovascular diseases.

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

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

• Problems with respiratory system heart diseases.
• Poor vascular condition.
• Epilepsy.
• Poor heart rate.
• Prolonged overheating of the body.

• Enhanced pain syndrome.
• Loss of a large volume of blood.
• Intense psychological stress. In most instances, fright may be accompanied by fainting. This factor often causes the development of syncope in babies.
• Neuralgia of the glossopharyngeal nerves.
• A sharp drop in blood pressure.

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

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

Sometimes it is not possible to determine the cause of fainting. It should be borne in mind that syncope occurs in everyone at least once in a lifetime. Problems occur in people from 10 to 30 years old, 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 from the influence of environmental factors on people.
• Hyperventilation This type of loss of consciousness occurs in several forms. Hypocapnic is manifested in the form of capillary spasms.

• Vasodepressor due to inadequate ventilation and elevated temperature in a buiding.
• Sinocarotid caused by changes in heart rate.
• cough manifested with severe bouts of coughing, causing disorders of the respiratory system.
• Swallowing syncope due to problems with the vagus nerve.
• nicturic- a person loses consciousness after urinating or at night when trying to get up from a bed.
• hysterical.
• Unclear etiology.

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

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

The intensity of symptoms and the duration of all stages are due to several separate factors.

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

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

This state does not last more than 30 minutes. Lasts a maximum of 3 minutes. Seizures are often accompanied by convulsions.

In the process of recovery from syncope, the following symptoms appear:

• Constant fatigue, increased drowsiness.
• Uncertain coordination.
• BP drops.
• A little dizzy.
• The patient is thirsty.
• Sweat is intense.

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

It takes about 1 hour to fully recover.

Diagnostics

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

non-invasive way performed on an outpatient basis, involves taking an anamnesis, obtaining tests, examining the patient, laboratory work. Diagnostic procedures include ECG, exercise use, 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 provision stationary conditions, use in the presence of symptoms of cardiovascular disorders, confirmed by non-invasive methods. Syncope diagnostic methods include electrophysiological examinations, angiography, launching a catheter in the heart, and venticulography.

For the treatment of syncopal paroxysm, emergency care will be needed, a reduction in the likelihood of injury and death, and measures to prevent recurrent syncope. Hospitalization of patients is performed in such cases:

• Refinement of syncopal diagnosis.
• Suspicion of disorders of the cardiovascular system.
• Fainting during physical exertion.
• Sudden death of other family members.
• Syncope is preceded by an arrhythmia or problems with the heart.
• Fainting in lying position.

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

Between attacks, take medication, use a defibrillator. Therapy without drugs involves a change in lifestyle, the rejection of alcohol, diuretics, you can not change position abruptly, is in a hot room. You need to follow a diet, water balance, wear abdominal bandages, perform physical exercises for the press and for the legs.

Treatment with drugs involves the treatment of pathologies that cause loss of consciousness. Of the procedures, it is customary to carry out: implantation of a defibrillator, stimulation of the heart muscle, therapeutic measures against arrhythmias.

First aid

In order for a person to get out of a faint without the help of a doctor, you need to perform the following actions:

1. Take a horizontal position, place the patient on his side.
2. Take off the tie, stretch the collar, provide fresh air.
3. Sprinkle some cold water on your face.
4. Ammonia is brought to the nose.

The syncopal state is characterized by a rapid and steady loss of consciousness, the patient can be quickly returned to his senses if he is given first aid. There are such dangers during fainting:

• Getting fractures or bruises.

• The 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 in the process of involuntary swallowing.

post-syncope

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

Prevention

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

• It is recommended to wear looser clothes.
• Monitor blood glucose levels.
• Engage in the treatment of chronic and ongoing disorders.
• Try to slowly change the position from horizontal to vertical.
• Avoid depression.

This syncope is most common, a person can lose consciousness due to stress. There are situations when they faint without distinct provoking factors. Often, fainting appears during long trips in transport, waiting in line.

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

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

It occurs during a long stay in a standing position or during a sharp transition from a lying to an upright position. This is possible due to a sharp jump in pressure - from low to high. Such a diagnosis is made by doctors when there is low blood pressure, the heart rate changes.

Doctors do tests with a half-hour stay in an upright position. The pressure also decreases with time. For accurate diagnosis, the orthostatic position is compared with the vasodepressor position. At the first, there are no specific external factors, during the second bradycardia is diagnosed.

Syncocarotid syncope

It is provoked by the high sensitivity of the carotid sinus. As a result, the heart rate changes, vascular tone appears. Often, this fainting condition is diagnosed in patients who are over 30. Often people pass out after throwing their head back quickly. Sometimes fainting comes from 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.