Syncope syndrome. Syncope

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

IN Lately fainting is considered a paroxysmal disorder of consciousness. In this regard, it is preferable to use the term “syncopation” - it defines much more broadly pathological changes in organism.

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

What is syncope and its neurological assessment

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

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

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

Neurologists distinguish between neurogenic and somatogenic syncope.

Stages of development - from fright to hitting the floor

Syncope develops in three stages:

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

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

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

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

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

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

Classification subtypes of syndromes

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

The following types of syncope also differ:

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

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

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

Etiology and pathogenesis

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

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

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

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

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

Features of the clinical picture

Peculiarities clinical course different types of syncope are:

Diagnostic criteria

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

It is also important to indicate to the doctor how long the patient has been in a state of loss of consciousness, the presence of convulsions, involuntary urination and/or defecation, foam 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 a sufficient supply of fresh air.

You need to give it a sniff ammonia, 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 horizontal position to vertical.

Therapy between attacks is limited to taking recommended medications. Non-drug treatment comes 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. In patients with heart failure, ventricular arrhythmias, pathological signs electrocardiogram shows a 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 is nothing more than fainting, which is short-term and reversible. During loss of consciousness, the body undergoes some changes, namely, muscle tone and the functioning of the cardiovascular and respiratory systems are disrupted.

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

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

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

In the international classification of diseases, such a disease has eigenvalue– ICD 10 code – R55.

Etiology

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

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

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

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

Classification

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

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

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

• emotional;
• maladaptive;
• discirculatory.

Types of somatogenic syncope:

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

Extreme fainting conditions are divided into:

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

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

Symptoms

Clinical manifestations fainting go through several stages of development:

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

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

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

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

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

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

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

• drowsiness and fatigue;
• decrease in blood pressure;
• uncertainty of movements;
• slight dizziness;
• dryness in oral cavity;
• copious discharge sweat.

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

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

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

After syncope, weakness comes first. From the moment the harbingers appear until full recovery It takes an hour at most.

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

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

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

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

Diagnostics

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

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

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

Laboratory tests include:

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

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

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

Treatment

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

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

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

Complications

Syncope can lead to:

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

Prevention

Among the preventive measures to prevent syncope are:

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

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

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

Answer only if you have proven medical knowledge

Cardiogenic syncopeCardiogenic syncope occur with cardiac arrhythmias, conduction block, myocardial infarction.

Cardiogenic syncope can pose not only an indirect (injury from a fall), but also a direct threat to life.

It is especially likely sudden death in patients with repeated fainting with frequent or group ventricular extrasystole, episodes of asystole lasting more than 2 seconds, or with congestive heart failure.

Mechanism- a decrease in cardiac output caused by a pathological increase (usually more than 180 per minute) or decrease (less than 35–40 per minute) of the rhythm.
Provoking factors - rapid change in heart rhythm.
Predisposing factors - organic heart disease and old age reduce tolerance to rhythm disturbances.
Prodromal symptoms - often absent.
Effect of body position
Recovery - rapid recovery of consciousness if brain damage has not occurred.

Fainting with aortic stenosis and hypertrophic cardiomyopathy

Mechanism- a decrease in peripheral vascular resistance in the absence of a compensatory increase in cardiac output.

Provoking factors - exercise stress.
Predisposing factors - cardiac dysfunction.

Prodromal symptoms - often absent.
Effect of body position - fainting occurs during or after physical activity.

Recovery - usually rapid recovery of consciousness.

Mechanism- sudden arrhythmia or decreased cardiac output.

Provoking factors - different.
Predisposing factors - ischemic disease hearts.

Prodromal symptoms - often absent.
Effect of body position - Fainting can occur in any position of the body.

Recovery

Mechanism- sudden hypoxia or decreased cardiac output.

Provoking factors - different.
Predisposing factors - deep vein thrombosis.

Prodromal symptoms - often absent.
Effect of body position - Fainting can occur in any position of the body.

Recovery - duration recovery period varies.

18.1. GENERAL PROVISIONS

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

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

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

Syncope can be provoked by emotional stress, orthostatic hypotension, staying in a stuffy room, coughing fits, irritation 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 leaving unconsciousness the patient is well oriented in place and time; sometimes anxious, frightened, usually remembers pre-syncope sensations, notes general weakness, while attempting to quickly transition into 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 it difficult to classify them based on 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; 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) embolism pulmonary artery; b) pulmonary artery stenosis; c) impaired venous return to the heart.

III. Orthostatic type - orthostatic hypotension.

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

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

VI. Psychogenic type - hysteria, hyperventilation syndrome.

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

18.3. NEUROGENIC (PSYCHOGENIC) SYNCOPAL CONDITIONS

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

18.3.1. Emotional syncope

The occurrence of emotiogenic syncope is associated with negative emotions, which can be caused by severe pain, the sight of blood, anxiety, fear, etc. Emotionogenic fainting is possible in a healthy person, but more often occurs against the background of neurosis or neurosis-like conditions with hyperreactivity 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. With personally significant stressful situation(threat, insult, resentment, accident, etc.) first, general tension appears, and in the case of an asthenic nature of the emotional reaction (feelings of fear, shame), increasing general weakness, dry mouth, an unpleasant feeling of tightness in the heart area, 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 sharp decline 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, various options stenosis of cerebral vessels. A common cause of acute regional ischemia of the brainstem is pathological changes in cervical spine spine, anomalies of the craniovertebral joint and vessels in the vertebral artery basin.

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

With dyscirculatory fainting, the precursor stage is short; at this time, dizziness (possibly systemic) quickly increases, and occipital pain often appears. Sometimes the warning signs that precede loss of consciousness are not detected at all. A feature of such fainting is the very rapid a sharp decline 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 in clinical picture there are pronounced manifestations chronic diseases 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, 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, sometimes detected bilateral symptom Babinsky. 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 epigastrium, yawning, hyperhidrosis, tachypnea, dilated pupils. During paroxysm, arterial hypotension and bradycardia are observed, followed by tachycardia.

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

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

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

18.5. SYNCOPAL CONDITIONS

UNDER EXTREME EXPOSURES

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

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

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

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

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

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

Hyperbaric syncope. Fainting is possible in cases sharp increase pressure in the airways during hyperbarotherapy in the case of creating excessively high pressure 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 fast emptying 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, to 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. To the necessary additional research 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 it so that the legs are slightly higher than the head, while making sure that there is no sticking of the tongue or other obstacles to the free flow of air into the Airways. Spraying can have a positive effect cold water face and neck, the patient is given ammonia to smell. 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 autonomic lability in young people and the presence of psychogenic associative, as well as psychogenic dyscirculatory syncope, systematically necessary physiotherapy, hardening procedures, restorative drugs. 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.

Authors): Roberto A.Santilli Med.Vet., PhD, D.E.C.V.I.M.-C.A. (Cardiology)
Organization(s): Clinica veterinaria Malpensa-Samarate-Varese-Italy Ospedale Veterinario I Portoni Rossi – Zola Predosa - Bologna – Italy Cornell University- cardiology department_New York – USA
Magazine: №3 - 2017

IVCS MATERIALS

translation from English by Maria Nazarova

Introduction

Transient loss of consciousness (TLOC) is a short-term loss of consciousness with sudden onset, short duration and spontaneous fast recovery. The main forms of TLOC are: traumatic loss of consciousness, or concussion, and non-traumatic loss of consciousness, which in turn is divided into: syncope, epileptic seizure And various groups rare disorders such as catalepsy.

Syncope is loss of consciousness due to global cerebral hypoperfusion due to a drop in systemic blood pressure due to a sharp decrease in vascular resistance or a drop in heart rate.

The typical syncope is short. Complete loss of consciousness in cases of reflex syncope lasts no more than 20 seconds. However, fainting rarely lasts longer, up to several minutes. In such cases, differentiating the diagnosis between syncope and other causes of loss of consciousness may be difficult. Recovery from syncope is usually accompanied by an immediate return to normal behavior and orientation. Fatigue may sometimes be noticeable during the recovery period. Presyncope is a term used to identify the precursor to fainting, but this stage is not accompanied by loss of consciousness. A sudden cessation of blood flow to the brain for a short period of just 6–8 seconds is enough to cause complete loss of consciousness. Systemic blood pressure is determined by cardiac output and total peripheral vascular resistance, and a fall in either of these parameters causes syncope, but a combination of a fall in both can also occur—with to varying degrees the severity of each component.

Low or inadequate peripheral vascular resistance may result from an inadequate reflex response, which leads to vasodilation and bradycardia and is referred to as vasodepressor, mixed, or cardioinhibitory reflex syncope. Other reasons for inadequate peripheral resistance vessels are functional and structural damage to the autonomic nervous system, such as dysautonomia (due to, for example, drug therapy). In the case of disturbances in the functioning of the autonomic nervous system, the sympathetic vasomotor pathways are unable to provide an increase in total peripheral vascular resistance (TPVR) in response to a change in body position (from lying to standing). Gravity stress, in combination with vasomotor insufficiency, leads to the deposition of blood in the veins abdominal cavity and pelvic limbs, causing a sharp decrease in preload (venous return) and, as a consequence, cardiac output. The causes of a transient decrease in cardiac output are: reflex bradycardia, known as the cardioinhibitory type of reflex syncope, cardiovascular diseases(arrhythmias, structural diseases, pulmonary embolism and pulmonary hypertension), inadequate venous return due to emptying of the veins or deposition of blood in the veins. According to the underlying mechanism, fainting is divided into: reflex, orthostatic and cardiogenic.

Reflex fainting

Reflex syncope traditionally refers to a heterogeneous group of conditions in which cardiovascular reflexes that normally control circulation become intermittently inappropriate in response and act as triggers, causing vasodilation and/or bradycardia, thereby leading to a drop in blood pressure and global cerebral hypoperfusion . Reflex syncope is usually classified based on the efferent pathways most involved, i.e., sympathetic or parasympathetic. The term "vasodepressor" type usually means that hypotension predominates due to loss of vasoconstrictor tone during standing. The “cardioinhibitory” type is used when bradycardia or asystole predominate, the “mixed” type is used when both mechanisms (*vasodepressor and cardioinhibitory) are present. Vasovagal syncope is caused by pain, emotional or orthostatic stress. There are usually previous symptoms of activation of the autonomic nervous system (pallor, nausea). Situational fainting traditionally refers to reflexive, associated with certain circumstances (coughing, urination, defecation, vomiting, pain, physical activity). Syncope due to carotid sinus stimulation is a rare, sudden disorder caused by mechanical manipulation of the carotid sinus.

Orthostatic syncope

In contrast to reflex syncope, in dysautonomia, sympathetic efferent activity is impaired and there is a deficit in vasoconstriction. When standing, the pressure drops and fainting or near-syncope occurs. Orthostatic hypotension is defined as an abnormal decrease in systolic blood pressure when the body changes position to standing. Orthostatic intolerance can cause fainting, but also dizziness, lightheadedness, weakness, fatigue and lethargy.

Classically, orthostatic hypotension is characterized by a decrease in systolic pressure by more than 20 mmHg. Art. and diastolic - more than 10 mm Hg. Art. within 3 minutes after taking a standing position.

Orthostatic hypotension may be caused by structural damage to the autonomic nervous system, medications that cause autonomic failure, and inadequate venous return due to decreased blood volume or pooling of blood in the veins.

Cardiogenic syncope

Structural diseases of the cardiovascular system (valvular disease, ischemia, hypertrophic cardiomyopathy, cardiac neoplasms, pericardial disease and tamponade), pulmonary embolism or pulmonary hypertension can cause syncope, and they are associated with the fact that the body's needs cannot be met by the impaired ability of the heart increase your emissions. The basis for syncope is inadequate blood flow resulting from mechanical obstruction.

However, in some cases, syncope not only results from decreased cardiac output, but may also be caused in part by an inappropriate reflex response or orthostatic hypotension.

Arrhythmias are the most common reason cardiogenic syncope. They cause hemodynamic disturbances, which lead to a critical decrease in cardiac output and blood flow in the brain. Fainting often depends on a number of associated factors, which include heart rate, type of arrhythmia (supraventricular or ventricular), left ventricular function, body position, and adequacy of vascular compensation. The last factor includes the reflex response from baroreceptors, as well as the response to orthostatic hypotension due to arrhythmia.

Sick sinus syndrome, atrial inactivity, and severe degrees of atrioventricular block (high-grade 2nd degree AV block or 3rd degree AV block) are most often associated with syncope.

Arrhythmogenic syncope

Arrhythmias are the most common cardiogenic causes of syncope. They lead to hemodynamic disturbances that can cause a critical decrease in cardiac output and blood flow to the brain. However, fainting often requires a combination of various factors such as heart rate, type of arrhythmia (supraventricular or ventricular), left ventricular function, body position, adequacy of the vascular response. The latter involves reflexes controlled by baroreceptors and the response to orthostatic hypertension caused by arrhythmia.

Sick sinus syndrome, atrial inactivity and the most severe forms of AV block (high grade 2 or grade 3) are most often associated with the occurrence of syncope.

The hemodynamic contribution of arrhythmias depends on various factors, including: changes in atrial and ventricular rates, duration of rhythm changes, ventricular functional status, concomitant drug therapy, peripheral vasomotor function, and concomitant systemic diseases.

Changes in the frequency of ventricular contractions are one of the factors of hemodynamic disturbances in dogs with arrhythmias. Marked increases in ventricular rate (185–230 beats/min) during atrial stimulation lead to a fall in cardiac output, while changes in systemic blood pressure and coronary blood flow occur with high frequency. Inadequate ventricular diastolic filling is a likely cause of decreased cardiac output. The reduction in ventricular rate causes a fall in cardiac output and a subsequent fall in systemic blood pressure, despite an increase in stroke volume in response to increased preload. In such cases, systolic blood pressure is usually preserved, but prolonged diastolic pauses are associated with low diastolic blood pressure.

The long course of tachycardia of both supraventricular and ventricular origin leads to hemodynamic changes, the result of which most often is heart failure, weakness or cardiogenic shock. Fainting is less common in the absence of concomitant dysautonomia or systolic dysfunction. Continuous tachycardia provokes the development of cardiomyopathy, which is called arrhythmia-induced cardiomyopathy, and occurs as a result of increased myocardial oxygen demand, increased myocyte-capillary distance, decreased AMP c production, and abnormal concentrations of sarcoplasmic and myofibrillar calcium ATPase.

Also, chronic bradycardia associated with high-grade AV block or sick sinus syndrome can cause syncope, fatigue, weakness, and heart failure. Reflex syncope can be caused by a vasovagal or situational reflex, which was accompanied by cardiac inhibition, which, in turn, is characterized by the presence of sinus node arrest, blockade of the impulse exit from the sinus node, 2nd degree high grade AV block or 3rd degree AV block.

The hemodynamic effects of arrhythmias are potentiated by the presence of systolic dysfunction. In such cases, the contribution of the atria is decisive for cardiac output, and very often a high ventricular rate, particularly when ventricular tachycardia, may lead to symptoms of syncope or cardiogenic shock. The consequences of ventricular activation are also important, especially when systolic function is impaired, because if healthy heart ventricular depolarizations themselves lead to minor changes in cardiac output.

Anxiety, loss of peripheral vasomotor function, concomitant drug therapy, circulating catecholamine levels, increased blood viscosity or redistribution, neurogenic reflexes, and systemic disease may also contribute to hemodynamics in dogs with arrhythmias that would otherwise be stable if the arrhythmia were present alone.

Diagnosis of arrhythmias and reflex fainting

Holter monitoring and event monitors are important diagnostic tools for determining the cause of transient loss of consciousness caused by arrhythmia or neurogenic bradycardia. Currently available in practice are ECG monitoring (Holter) for 24–48 hours, or event monitors that allow recording for 7 days. However, because most patients do not become symptomatic during the monitoring period, the true value of Holter in identifying the causes of syncope may be small. Holter monitoring may be more informative if symptoms are very frequent. If one or more episodes of transient loss of consciousness occur per day, this increases the likelihood of obtaining information and correlating symptoms with ECG changes. Among dogs, almost ¼ of cases of syncope occurred during 24-hour ECG recording, which was associated with diagnosis in 42% of cases. Arrhythmia as the cause of fainting was found in 30% of them, and in 20% these were tachyarrhythmias and in 10% bradyarrhythmias. In 38% of patients, as a result of Holter monitoring, treatment tactics changed. Event monitors, designed for 7 days of study, are also external recording devices in which the recording loop is designed in such a way that the previous ECG tape is constantly recorded and deleted. When the device is activated by the owner, usually during a fainting episode, the ECG is stored and can be sent for analysis. Such an event monitor (R-test) has great diagnostic value in cats and dogs (a diagnosis can be made in 84.4% of cases), and according to this monitoring, on average, arrhythmia or reflex syncope was detected in 34.7% of patients. These event monitors are usually smaller and lighter than Holter, making them more convenient for diagnosing patients. small dogs and cats. Implantable loop recorders (ILRs) are placed subcutaneously under local anesthesia and have a battery life of 36 months. Such devices have long-term memory that stores ECG data retrospectively, and storage occurs when the device is activated by the owner when fainting is detected, or automatically if parameters have been set characterizing the arrhythmia that needs to be recognized. Such devices are successfully used in the diagnosis of fainting (informative in 56.5–66% of cases). Disadvantages are: the need for small surgical procedure, the fact that it is sometimes impossible to differentiate between supraventricular and ventricular arrhythmias, the presence of errors associated with differences in algorithms for diagnosing arrhythmias in humans and animals, as well as the cost of the device.

Treatment options

All true bradyarrhythmias can be treated by implantation of a permanent pacemaker.

Reflex syncope with a significant cardiac inhibitory component can be partially controlled with a pacemaker, but because the accompanying vasodepressor component cannot be fully appreciated, complete resolution of symptoms is rarely achieved.

Ventricular and supraventricular arrhythmias can be controlled with antiarrhythmic drugs, monitored by Holter monitoring, or treated with catheter ablation.