Fainting is cardiogenic. Cardiogenic syncope, presyncope, dizziness are harbingers of sudden cardiac death

The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC)

Developed in collaboration with, European Heart Rhythm Association (EHRA), Heart Failure Association (HFA), and Heart Rhythm Society (HRS)

Endorsed by the following societies, European Society of Emergency Medicine (EuSEM), European Federation of Internal Medicine (EFIM), European Union Geriatric Medicine Society (EUGMS), American Geriatrics Society (AGS), European Neurological Society (ENS), European Federation of Autonomic Societies (EFAS), American Autonomic Society (AAS)

Guidelines for the diagnosis and treatment of syncope (version 2009)

Task Force on the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). Developed in collaboration with the European Heart Rhythm Association (EHRA), the Heart Failure Association (HFA) and the Heart Rhythm Society (HRS).

Abbreviations and acronyms

Preamble

Introduction

Part 1. Definitions, classification and pathophysiology, epidemiology, prognosis, impact on quality of life, economic issues

1.1 Definitions
1.2 Classification and pathophysiology 1.2.1 Placement of syncope within the broader framework of loss of consciousness (real or perceived)
1.2.2.1 Reflex syncope (neurotransmitter syncope)
1.2.2.2 Orthostatic hypotension and orthostatic intolerance syndrome
1.2.2.3 Cardiac (cardiovascular) syncope
1.3 Epidemiology
1.3.1 Proportion of syncope in the general population
1.3.2 From the general population to medical facilities
1.3.3 Prevalence of causes of syncope
1.4 Predictions
1.4.1 Risk of death and life-threatening events
1.4.2 Frequency of syncope and risk of injury
1.5 Impact on quality of life
1.6 Economic issues

Part 2. Initial assessments, diagnosis and risk stratification

2.1 Initial evaluation
2.1.1 Syncope diagnosis
2.1.2 Etiological diagnosis
2.1.3 Risk stratification
2.2 Diagnostic tests
2.2.1 Carotid sinus massage
2.2.2 Orthostatic test
2.2.2.1 Active lifting
2.2.2.2 Tilt testing
2.2.3 ECG monitoring (non-invasive and invasive)
2.2.3.1 Monitoring in hospital
2.2.3.2 Holter monitoring
2.2.3.3 Perspectives on external event recorders
2.2.3.4 Outdoor loop recorders
2.2.3.5 Implantable loop recorders
2.2.3.6 Remote telemetry (at home)
2.2.3.7 Classification of electrocardiographic recordings
2.2.3.8 ECG monitoring of syncope in the workplace
2.2.4 Electrophysiological studies
2.2.4.1 Suspected intermittent bradycardia
2.2.4.2 Syncope in patients with double bundle His block ( a high degree atrioventricular block)
2.2.4.3 Suspected tachycardia
2.2.5 ATP sample
2.2.6 Echocardiography and other imaging modalities
2.2.7 Stress testing
2.2.8 Cardiac catheterization
2.2.9 Psychiatric evaluation
2.2.10 Neurological assessment
2.2.10.1 Clinical condition
2.2.10.2 Neurological tests

Part 3. Treatment

3.1 Treatment of patients with reflex syncope and orthostatic intolerance
3.1.1 Reflex syncope
3.1.1.1 Therapy
3.1.1.2 Individual characteristics
3.1.2 Orthostatic hypotension and orthostatic intolerance
3.2 Arrhythmia as the main cause of syncope
3.2.1 Dysfunction sinus node
3.2.2 Atrioventricular conduction disorders
3.2.3 Paroxysmal supraventricular and ventricular tachycardias
3.2.4 Malfunctions of implanted devices
3.3 Fainting at organic lesions heart or circulatory system
3.4 Unexplained syncope in patients at high risk of sudden cardiac death
3.4.1 Ischemic and non-ischemic cardiomyopathies
3.4.2 Hypertrophic cardiomyopathy
3.4.3 Arrhythmogenic cardiomyopathy of the right ventricle
3.4.4 Patients with primary electrical heart disease

Part 4: Special Issues

4.1 Fainting in old age
4.2 Syncope in pediatric practice
4.3 Driving and fainting

Part 5. Organizational aspects

5.1 Management of syncope in general practice
5.2 Management of syncope in the emergency department
5.3 Uniform management of syncope (T-LOC)
5.3.1 Current model for unified management of syncope
5.3.2 Proposed model

Bibliography

Abbreviations and acronyms

• ANF ​​insufficiency of the autonomic nervous system
• ANS autonomic nervous system
• ARVC arrhythmogenic cardiomyopathy of the right ventricle
• ATP adenosine triphosphate
• AV atrioventricular
• AVID implantable antiarrhythmic device - defibrillator
• BBB bundle branch block
• BP blood pressure
• b.p.m. beats per minute
• CAD coronary heart disease
• CO Cardiac output
• CSH carotid sinus hypersensitivity
• CSM carotid sinus massage
• CSS carotid sinus syndrome
• CSNRT KVVFSU
• CT computed tomography
• DCM dilated cardiomyopathy
• ECG electrocardiogram
• ED emergency department
• EEG electroencephalogram
• EPS electrophysiological study
• ESC European Society of Cardiology
• FASS Fainting and Falls Service
• FDA Food and Drug Administration
• HF heart failure
• HOCM obstructive hypertrophic cardiomyopathy
• HR heart rate
• HV hiso-ventricular
• ICD Implantable Cardioverter Defibrillator
• ILR implantable loop recorder
• LBBB left bundle branch block
• LOC loss of consciousness
• LVEF left ventricular ejection fraction
• MRI magnetic resonance imaging
• OH orthostatic hypotension
• PCM "Physical Counter-Pressure" maneuver
• PDA personal digital assistant (handheld computer)
• POTS Postural Orthostatic Tachycardia Syndrome
• RBBB blockade right leg bundle of His
• SCD sudden cardiac death
• SNRT sinus node function recovery time
• SVR systemic vascular resistance (SVR)
• SVT supraventricular tachycardia
• TIA transient ischemic attack
• T-LOC transient loss of consciousness
• VT ventricular tachycardia
• VVS vasovagal syncope

Preamble

Guidelines and expert consensus documents summarize and evaluate all currently available evidence on a specific issue in order to assist physicians in choosing the optimal system of management strategies for a typical patient suffering from this condition, taking into account the impact on the final result, as well as risk/benefit ratios. specific diagnostic or therapeutic agents. Manuals cannot replace textbooks. The legal implications of the application of the guidelines have been discussed previously. A large number of guidelines and expert consensus documents have been issued in recent years by the European Society of Cardiology (ESC) and other societies and organizations.

Due to the impact on clinical practice, quality criteria for the development of guidelines were created in order to make all decisions transparent to the user. Documents can be found on the ESC website (http://www.escardio.org/guidelines). Guidelines and recommendations should assist physicians in clinical practice, however, the final decision on the treatment of a patient must be made by the patient's physician.

Note: *Use of ESC Class III is not recommended.

Table 2 Levels of evidence

Introduction

The first ESC guidelines for the management of syncope were published in 2001 and revised in 2004. In March 2008, the Practice Guidelines Committee decided that there was enough new evidence to develop new guidelines. There are two main aspects of this document that distinguish it from its predecessors. One is to identify the exact cause of syncope in order to provide an adequate and effective mechanism for specific treatment and determine the specific risk to the patient, which often depends on the underlying disease rather than syncope. The second aspect is to prepare a comprehensive document that is addressed not only to cardiologists, but to all physicians interested in this field. To achieve this goal, a large number of specialists from other specialties took part. A total of 76 specialists from various disciplines took part in this project.

The most significant changes are listed here:

• An updated classification of syncope within the broader framework of transient loss of consciousness (T-Loc).
• New data on epidemiology.
• A new diagnostic approach focused on risk stratification of sudden cardiac death (SCD) and CV events after initial assessment, including some recommendations for the treatment of patients with high-risk unexplained syncope.
• Emphasis on enhancing the role of a diagnostic strategy based on long-term monitoring, as opposed to the traditional strategy based on laboratory tests.
• Evidence-Based Treatment Update.

The literature on the evaluation and treatment of syncope is largely based on case series, cohort studies, or retrospective analyzes of existing data. The impact of these approaches on treatment outcomes and reduction in syncope recurrence is difficult to assess without the implementation of randomized and blinded trials.

We acknowledge that for some of the recommendations related to diagnostic and therapeutic processes, controlled trials have never been conducted. Consequently, some of these recommendations are based on small studies, clinical practice, expert consensus, and sometimes just common sense. In these cases, in accordance with the current recommendation format, level of evidence C is given.

Part 1. Definitions, classification.

Syncope is a transient loss of consciousness (T-LOC) caused by transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery.

Transient global cerebral hypoperfusion syncope differs from other loss of consciousness. Without this addition, the definition of syncope becomes broad enough to include disorders such as epileptic seizures and concussion.

The term T-LOC is specifically intended to cover all disorders characterized by self-recovering loss of consciousness (LOC), regardless of mechanism (Figure 1).

This definition minimizes conceptual and diagnostic confusion.

In the documents of the past, fainting was often not mentioned, or it was superfluous, for example, epileptic seizures and even a stroke were attributed to fainting. This confusion can still be found in the literature.

Sometimes syncope can have a prodromal period during which various symptoms (dizziness, nausea, sweating, weakness, visual disturbances) warn that fainting is imminent.

Often, however, LOC occurs "without warning". An accurate estimate of the duration of spontaneous episodes is rarely available.

The typical syncope is brief. Complete loss of consciousness during reflex syncope lasts no more than 20 seconds. However, in rare cases, fainting may last longer, even up to several minutes. In such cases, the differential diagnosis between syncope and other causes of loss of consciousness (LOC) can be difficult.

Recovery from syncope is usually accompanied by an almost immediate return to proper behavior and orientation. Retrograde amnesia, although considered unusual, may be more common than previously thought, particularly in older people. Sometimes the recovery period can be marked by severe weakness.

The adjective "pre-syncope" is used to refer to the symptoms and signs of what happens before fainting, and is synonymous with "warning" and "prodromal". The noun "pre-syncope" or "near-syncope" is often used to describe a state that resembles the onset of a syncope, but is not followed by loss of consciousness (LOC); doubts remain as to whether the mechanisms involved in these phenomena are the same as in syncope.

1.2 Classification and pathophysiology

1.2.1 Placing syncope within the broader framework of transient loss of consciousness (real or perceived)

The concept of Transient Loss of Consciousness (T-LOC) is shown in Figure 1.

Two decision trees separate T-LOC from other conditions: First, is there a loss of consciousness or not?

In case of loss of consciousness, are 4 signs present: Transient, Rapid onset, Brief attack, Spontaneous recovery?

With a positive answer, T-LOC is stated.

T-LOC is subdivided into traumatic and non-traumatic forms. The traumatic form of T-LOC is usually represented by concussion. Non-traumatic T-LOC is divided into syncope, epileptic seizures, psychogenic pseudosyncopes, and T-LOC from rare miscellaneous causes.

Psychogenic pseudosyncopes are discussed elsewhere in this document. Rare Miscellaneous disorders include, for example, cataplexy or those whose clinical presentation resembles T-LOC only in rare cases (eg, excessive daytime sleepiness).

Some disorders may resemble syncope in two ways: (Table 3).

Table 3 Conditions misdiagnosed as syncope

In some cases, there is indeed a loss of consciousness, but its mechanism is different than global cerebral hypoperfusion. Examples are epilepsy, certain metabolic disorders (including hypoxia and hypoglycemia), intoxication, and vertebrobasilar transient ischemic attack (TIA).

In other disorders, consciousness is only superficially lost, such as cataplexy, hypotonic attack, drop attack, psychogenic pseudosyncope, and carotid TIA. In these cases, the differential diagnosis from syncope is usually obvious, but can sometimes be difficult due to lack of history, misleading features, or confusion about the definition of syncope.

This differentiation is important to the clinician, who often encounters patients with sudden LOC (real or imaginary) that may be due to causes other than a decrease in global cerebral blood flow.

1.2.2 Classification and pathophysiology of syncope

Table 4 presents the pathophysiological classification of the main causes of syncope, highlighting the large groups of diseases associated with different risk profiles. Various pathophysiological processes can lead to a drop in systemic arterial pressure (BP) with a decrease in global cerebral blood flow, which is the main cause of syncope. A sudden cessation of cerebral blood flow for 6-8 seconds is enough to cause loss of consciousness. Experience with Tilt testing has shown that a decrease in systolic blood pressure of 60 mm or less leads to syncope. Systemic BP is determined by cardiac output (CO) and total peripheral vascular resistance, and the fall in BP can be determined by either one of the factors or a combination of them, although their relative contributions can vary significantly.

Table 4. Classification of syncope.

Figure 2 shows how pathophysiology underlies the classification.

Feasible translation and illustration in higher quality:

In the center of the figure - low blood pressure / global cerebral hypoperfusion, next - the left half-ring reflects low or insufficient peripheral resistance, the right half-ring - low cardiac output.

Low or insufficient peripheral resistance may be due to abnormal reflex activity (depicted in the next circle) causing vasodilation and bradycardia. Reflex syncope is due to vasodilation, due to slowing of cardiac activity, or mixed. They are reflected at the top of the outermost ring.

The cause of low or insufficient peripheral resistance may also be functional or structural disorders of the autonomic nervous system (ANS) with drug-induced, primary or secondary insufficiency of the autonomic nervous system (ANF). They are reflected in the lower left of the outer ring. In ANF, the vasomotor response fails to increase total peripheral vascular resistance.

When assuming an upright position, gravity combined with vasomotor weakness leads to a concentration of venous blood below the diaphragm, which leads to a decrease in venous return and, therefore, a transient decrease in cardiac output up to 3 times.

The first reason that reduces cardiac output is reflex bradycardia. The second group of reasons - arrhythmias and organic diseases heart and lungs, including pulmonary embolism and pulmonary hypertension.

Third, there is insufficient venous return due to hypovolemia or venous deposition.

The three final mechanisms, reflex, orthostatic, and cardiovascular, are shown outside the rings in Figure 2.

1.2.2.1 Reflex syncope (neurotransmitter syncope)

Reflex syncope traditionally refers to a heterogeneous group of conditions in which cardiovascular reflexes, which are normally necessary for controlling blood circulation, periodically become pathological. This leads to vasodilatation and/or bradycardia and thus to a decrease in blood pressure and global cerebral perfusion.

Reflex syncope is usually classified based on the efferent pathway most involved - sympathetic or parasympathetic.

The term "Vasodepressor type" is usually used in hypotension due to the predominance of vasodilating tone over vasoconstrictor.

The term "Cardioinhibitory type" is used when bradycardia or asystole predominates.

The term "Mixed type" is used if both mechanisms are present.

Reflex syncope can also be classified based on the triggering mechanism, i.e. afferent pathway(Table 4).

It should be recognized that this is a simplification, because in the context of specific situations, such as syncope during urination or defecation, many different mechanisms can operate simultaneously. Triggering situations vary significantly between individual patients. In most cases, efferent pathways are not highly dependent on the nature of the trigger (eg, urinary syncope and vasovagal syncope (VVS) can be either cardioinhibitory or vasodepressor syncope). Knowing the various triggers is clinically important, as their recognition can be a tool in the diagnosis of syncope:

• Vasovagal syncope (VVS), also known as "normal syncope", is triggered by emotion or orthostatic stress. As a rule, it is preceded by prodromal symptoms of autonomic activation (sweating, pallor, nausea).
• Situational syncope traditionally refers to syncope reflexively associated with some specific circumstance. Syncope can occur in young athletes after exercise, and among middle-aged and elderly people, it can manifest as an early manifestation of "autonomic nervous system insufficiency" (ANF) before becoming "typical orthostatic hypotension".
• Carotid sinus syncope deserves special mention. In its rare spontaneous form, it is caused by mechanical manipulation of the carotid sinuses. In a more frequent form, no mechanical trigger is found and the diagnosis is made by carotid sinus massage.
• term " Atypical form» is used to describe those situations in which reflex syncope occurs in undefined triggering situations and even in the apparent absence of triggers. The diagnosis in this case is based not so much on the history taking, but on the exclusion of other causes of syncope (absence of organic heart disease), and on the reproduction of symptoms on a tilt test.

The classic form of VVS usually begins at a young age as an isolated episode, which is different from other forms with atypical manifestation, onset in old age and often associated with cardiovascular and neurological disorders, possibly in the form of orthostatic or postprandial hypotension. In these latter forms, reflex syncope appears to be an expression of a pathological process, mainly related to the impaired ability of the autonomic nervous system to activate compensatory reflexes, so that there is a duplication of "autonomic nervous system insufficiency" (ANF).

Comparative data on orthostatic syncope are presented in Table 5.

1.2.2.2 Syndromes of orthostatic hypotension and orthostatic intolerance

In contrast to reflex syncope, in "autonomic failure" (ANF), efferent sympathetic activity is chronically impaired, resulting in insufficient vasoconstriction. In a standing position, blood pressure drops and fainting or pre-syncope occurs.

Orthostatic hypotension is defined as an abnormal decrease in systolic blood pressure when standing. Strictly speaking, from a pathophysiological point of view, there is no "overlap" between reflex syncope and ANF, but the clinical manifestations of these two conditions often overlap, sometimes the differential diagnosis is very difficult.

"Orthostatic intolerance" is defined as a symptom complex that occurs in vertical position due to circulatory disorders. Fainting is one of the symptoms, others are possible:

• dizziness, pre-fainting (II),
• weakness, fatigue, lethargy (III),
• palpitations, sweating (IV),
• visual disturbances (including blurred vision, increased brightness, tunnel vision) (V),
• hearing impairment (including crackling tinnitus) (VI),
• pain in the neck (occipital, paracervical and in the shoulder), in the lower back or pain in the heart.

Various clinical syndromes of orthostatic intolerance are shown in Table 5.

Also included among these forms are reflex syncope, in which orthostatic stress is the main trigger.

• "Classic" orthostatic hypotension is defined as a decrease in systolic blood pressure of at least 20 mm Hg. and diastolic blood pressure by at least 10 mm Hg. within 3 minutes of standing up (Fig. 3) described in patients with pure ANF, with hypovolemia, or with other forms of ANF.
• "Initial (early)" orthostatic hypotension is characterized by a decrease in blood pressure immediately after standing up by more than 40 mmHg, after which blood pressure spontaneously and quickly returns to normal, so the period of hypotension and clinical symptoms short, less than 30 s. (Fig. 3).
• "Late (progressive)" orthostatic hypotension is not uncommon in the elderly. This is due to age-related violations of compensatory reflexes, cardiac rigidity in old age, sensitive to a decrease in preload. This form is characterized by a slow gradual decrease in systolic blood pressure after standing up. The absence of bradycardia distinguishes orthostatic hypotension from reflex syncope. Bradycardia can sometimes occur later, but the pressure drop curve is less steep than at a young age (Fig. 4).
• Postural orthostatic tachycardia syndrome (POTS). Some patients, mostly young women with severe orthostatic intolerance (but not syncope), report a very marked increase in heart rate(When standing up, heart rate increases by more than 30 beats per minute or to more than 120, and the rhythm is unstable.) POTS is often found in the syndrome chronic fatigue. The pathophysiology of the process has yet to be determined.

Syncope (syncope syndrome,) is a short loss of consciousness, combined with a violation of 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;
• after fainting.

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. The tension of the sympathetic nervous system increases, which increases the pressure and speed of heart contractions. In the future, due to increased tone 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;
• perform 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, 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 is 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 transient loss of consciousness due to short-term general hypoperfusion of the brain.

The main signs of fainting are rapid development, short duration and independent spontaneous recovery of consciousness.

Epidemiology

Fainting is not uncommon in the general population. For the first time, fainting usually occurs at a certain age.

Vasovagal syncope occurs in approximately 1% of young children. The first fainting episode most often develops between the ages of 10 and 30; the maximum increase in cases of the disease is noted at the age of 15 years (in 47% of women and 31% in men).

The most commonly diagnosed reflex syncope, which began in adolescence and young age.

The next most common occurrence is syncope associated with cardiovascular disease.

Etiopathogenesis

The main role in the occurrence of fainting is assigned to a decrease in systemic arterial pressure, which leads to deterioration cerebral circulation.

For a complete loss of consciousness, a sudden cessation of cerebral blood flow for 6–8 seconds is sufficient; in addition, fainting develops with a decrease in systolic blood pressure to 60 mm Hg. Art. or below.

Systemic arterial pressure is formed by the values ​​of cardiac output and total peripheral vascular resistance. A decrease in one of the indicators can cause fainting, but, as a rule, both pathogenic factors of varying severity are observed.

A decrease in peripheral vascular resistance can lead to a violation of reflex activity and cause vasodilation and bradycardia, and as a result - vasodepressor, mixed or cardioinhibitory reflex syncope.

In addition, peripheral vascular resistance may change with structural or transient disorders of the autonomic nervous system (drug-provoked, primary, secondary autonomic failure).

With autonomic failure, sympathetic vasomotor fibers do not provide an increase in peripheral vascular resistance when moving to a standing position. Gravitational stress combined with vasomotor insufficiency leads to blood retention in the veins of the lower body, resulting in a decrease in venous return and, consequently, cardiac output.

The main causes of a transient decrease in cardiac output:

- reflex bradycardia, which is the cause of cardioinhibitory reflex syncope;

- all kinds of cardiovascular diseases (arrhythmias and organic diseases, pulmonary embolism, pulmonary hypertension);

- defective venous return associated with a decrease in the volume of circulating blood or blood retention in the veins.

Clinical picture

In some types of syncope, a prodromal period may develop, during which the patient is disturbed by dizziness, nausea, sweating, weakness, and blurred vision. Quite often, fainting develops without any previous manifestations.

It is not often possible to accurately determine the duration of spontaneous syncope. Classical syncope is characterized by a short duration. Complete loss of consciousness during reflex syncope lasts no more than 20 s. In exceptional cases, the duration of fainting can be several minutes. Such cases are difficult to differentiate with other causes of loss of consciousness.

Recovery of consciousness after fainting is usually accompanied by an almost immediate resumption of adequate behavior and orientation. Retrograde amnesia appears to be more common than previously thought, especially in older patients. In some cases, after fainting, fatigue persists for some time.

Reflex syncope (neurogenic)

Reflex syncope is a multifactorial group of conditions in which cardiovascular reflexes change for a short time, capable of controlling the response of the vascular system to various influences in the normal state. As a result, vasodilation and/or bradycardia occurs, and, as a result, a decrease in systemic arterial pressure and a decrease in cerebral perfusion.

Reflex syncope is most often divided depending on the primary lesion of sympathetic or parasympathetic efferent fibers.

The expression "vasopressor syncope" is used if the leading cause of the condition that has arisen is a decrease in systemic arterial pressure, which is due to an imbalance in vasoconstrictor tone in an upright position.

Cardioinhibitory Syncope refers to conditions that occur against the background of bradycardia or the inefficiency of heart contractions.

In addition, reflex syncope can be subdivided depending on the trigger, i.e. afferent pathways:

• Normal syncope (vasovagal) - the trigger is most often emotional or orthostatic stress. Before the development of this type of syncope, quite often there are prodromal symptoms indicating activation of the autonomic nervous system (sweating, blanching, nausea).

Most often, the condition occurs in young people in the form of separate episodes. In the older age group, syncope, as a rule, is combined with cardiovascular and / or neurological diseases and may be accompanied by orthostatic or postprandial hypotension.

• Situational syncope - occurs in a specific situation. In young athletes, it can develop after physical exertion. The situational cause of shock can be coughing or sneezing, irritation of the gastrointestinal tract (swallowing, defecation, abdominal pain, heavy eating), urination, other causes (laughing, playing wind instruments, lifting weights).
• Fainting provoked by mechanical irritation of the carotid sinus.
• “Atypical syncope”, the starting cause of which cannot be established (in the absence of cardiovascular diseases) or fainting develops when exposed to an atypical stimulus.

Orthostatic hypotension and orthostasis intolerance syndrome

Orthostatic hypotension is an abnormal decrease in systolic blood pressure when standing. The difference between reflex syncope and autonomic insufficiency is the development of chronic disorders of sympathetic efferent activity, which leads to a weakening of the vasoconstrictor response.

There are the following forms of orthostatic disorders:

• Typical orthostatic hypotension is characterized by a decrease in systolic pressure below 20 mm Hg. Art. and diastolic below 10 mm Hg. Art. within 3 minutes after moving to a standing position. It occurs in patients with isolated autonomic failure, hypovolemia and other forms of autonomic failure.
• Early orthostatic hypotension is characterized by a drop in blood pressure below 40 mm Hg. Art. immediately after the transition to a vertical position, after which blood pressure independently and quickly returns to normal, so hypotension and symptoms persist for a very short time (no more than 30 seconds).
• Delayed (progressive) orthostatic hypotension, as a rule, is observed in the elderly. It develops as an age-related violation of compensatory reflexes and myocardial sclerosis in patients sensitive to preload. In such patients, when moving to a vertical position, blood pressure slowly progressively decreases.
• The syndrome of postural orthostatic tachycardia is more typical for young women and is characterized by a significant increase in heart rate (more than 30 beats from the original) and instability of blood pressure without the development of syncope.

Cardiogenic syncope (cardiovascular)

The most common cause of cardiogenic syncope is arrhythmia, which can be accompanied by a critical decrease in cardiac output and cerebral blood flow, especially atrial fibrillation.

Sick sinus syndrome may be accompanied by episodes of asystole, a similar condition most often occurs with a sudden cessation of atrial tachyarrhythmia (brady-tachycardia syndrome).

Fainting may occur in severe forms of acquired atrioventricular block. Syncope develops as a result of a delay in the activity of additional pacemakers.

Fainting or pre-fainting often develops initially with an attack of paroxysmal tachycardia, after which vascular compensatory mechanisms are activated. Consciousness is usually restored before the attack stops. If circulation remains inadequate in combination with tachycardia, then consciousness may not be restored. In such a case, it is necessary to think not about fainting, but about cardiac arrest.

Fainting can be observed with polymorphic ventricular tachycardia of the pirouette type, especially in women - a similar arrhythmia develops during treatment with pharmaceuticals that lengthen the QT interval.

Cardiovascular disease can be accompanied by the development of fainting if the heart is not able to provide the necessary blood circulation to the brain.

The possibility of syncope is of particular concern in the presence of fixed or dynamic obstruction of blood flow from the left ventricle.

Therefore, syncope can have a multifactorial origin. Since the cause of fainting can be a disease of the heart and blood vessels, in such cases it is necessary to treat the underlying disease.

Diagnosis and differential diagnosis

The initial examination of the patient includes a thorough history taking, physical examinations, including blood pressure measurements in the supine and standing position, electrocardiography, and, if necessary, Holter monitoring (if the suspected cause is cardiac arrhythmias).

Diagnostic massage of the carotid sinus is carried out in patients over 40 years old, echocardiography is carried out to exclude cardiovascular diseases that can provoke fainting.

An orthostatic test is recommended in cases of fainting that occurs when the position of the body in space changes (when changing the lying position, to the standing position); tilt test, which makes it possible to reproduce the neurogenic reflex (the occurrence of fainting during prolonged standing) in a clinical setting.

Some psychotropic drugs can lead to orthostatic hypotension and prolongation of the QT interval.

Individual states with external manifestations are very similar to fainting, but not every episode, accompanied by loss of consciousness, develops due to a short-term decrease in the blood supply to the brain.

Syncope must be differentiated from epilepsy, various metabolic disorders (including hypoxia and hypoglycemia), intoxication, vertebrobasilar and/or carotid transient ischemic attack, psychogenic pseudosyncope, conversion reaction, post-traumatic loss of consciousness.

General principles of treatment

The main goal of treatment is to reduce mortality as much as possible, to prevent physical injuries and the recurrence of fainting.

For example, in patients with attacks of ventricular tachycardia, which is accompanied by syncope, the greatest threat is the occurrence of a fatal outcome, and in patients with reflex syncope, prevention of recurrence of syncope and mechanical damage is considered important.

The clarified cause of fainting is of decisive importance for the choice of methodology and further tactics of therapeutic measures.

A complete treatment of fainting should include the elimination of the cause of the decrease in blood circulation to the brain.

Treatment of reflex syncope and orthostatic hypotension primarily involves informing the patient about the benign course of the disease so that such conditions do not cause him excessive anxiety and fear.

The patient is advised, if possible, to avoid situations that can provoke him to faint (presence of a large number of people, loss of fluid). In addition, the patient must learn to independently identify the precursors of fainting and take measures to stop it (situate themselves horizontally, thereby preventing a fall, take a few sips of water, perform certain physical isometric exercises - clenching the hands into a fist, crossing lower extremities with muscle tension).

It is necessary with great care to take pharmaceuticals that reduce blood pressure, diuretics, alcohol.

The method of choice in the treatment of reflex syncope is considered predominantly non-pharmacological measures, which include isometric physical exercise(tension of muscle groups without movement). The isometric tension of the muscle groups of the upper or lower extremities allows you to increase blood pressure before the development of fainting and, thereby, prevent its occurrence.

You can reduce the likelihood of fainting that occurs when you change your body position with the help of daily orthostatic training - tilt training.

The use of various medical methods for the treatment of reflex syncope in the predominant number of episodes was ineffective.

With confirmed cardiogenic syncope, the main method of their elimination and prevention is the treatment of the underlying disease, which may be accompanied by a decrease in cardiac output or peripheral vascular resistance.

If the cause cannot be established or the identified cause cannot be eliminated, then therapeutic measures should be aimed at improving cerebral circulation.

Outcome and forecast

Fainting limits the active life position of patients, complicates their daily activities and the ability to self-service, provokes or aggravates depression, pain and discomfort.

To assess the danger and prognosis of syncope, it is necessary to consider the possibility of death and life-threatening complications, especially in cardiogenic syncope, and the likelihood of repeated syncope, the possibility of physical damage.

With various methods of risk stratification during the initial examination, the detection of pathological signs on the electrocardiogram, advanced age, or symptoms of heart disease, as a rule, indicate an unfavorable prognosis over the next 1–2 years.

Fainting [syncope] and collapse (R55)

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

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

American College of Cardiology/American Heart Association (ACC/AHA) guidelines, European Society heart (ESC) and others indicate that patients with syncope, presyncope, dizziness, or recurrent unexplained palpitations should be subject to mandatory electrocardiogram (ECG) monitoring. With the diagnostic capabilities of ECG monitors, it is possible to carry out long-term monitoring and diagnosis of transient or rare symptoms.

Classification of syncope

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

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

In addition, considering fainting as a process unfolded in time, the severity of syncopal conditions is distinguished.
1. Presyncope:
I degree - weakness, nausea, flies before the eyes;
II degree - more pronounced symptoms described above with elements of impaired postural tone.
2. Syncope:
I degree - short-term shutdown of consciousness for a few seconds without a pronounced post-seizure syndrome;
II degree - a longer loss of consciousness and pronounced post-seizure manifestations.
The above classification emphasizes that syncopal paroxysm is a phased process in which transitional states can be distinguished.
fainting clinic

Fainting is characterized by:
generalized muscle weakness
decreased postural tone, inability to stand upright
loss of consciousness

The term "weakness" means a lack of strength with a feeling of impending loss of consciousness. At the beginning of fainting (!!!) the patient is always in an upright position, except for the Adams-Stokes attack. Usually the patient has a presentiment of impending fainting. At first, he becomes ill, then there is a feeling of movement or swaying of the floor and surrounding objects, the patient yawns, flies appear before his eyes, tinnitus, nausea, sometimes vomiting, vision is weakened. With a slow onset of syncope, the patient can prevent falls and injury by quickly assuming a horizontal position. In this case, there may not be a complete loss of consciousness.

The depth and duration of the unconscious state are different
sometimes the patient is not completely disconnected from the outside world
a deep coma may develop with complete loss of consciousness and lack of response to external stimuli.

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

Fainting of vascular origin

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

Patients describe fainting as the appearance of a feeling of lightheadedness, dizziness. They turn pale, perspiration appears, then the patients lose consciousness. It is believed that the pathogenetic basis of vasovagal syncope is excessive deposition of blood in the veins of the lower extremities and a violation of reflex effects on the heart. Other variants of vasovagal syncope have also been described. With intense pain syndrome of visceral origin, irritation of the vagus nerve can contribute to a slowdown in cardiac activity and even cardiac arrest, for example, with an attack of hepatic colic, damage to the esophagus, mediastinum, bronchoscopy, pleural puncture and laparocentesis, severe systemic dizziness with labyrinthine and vestibular disorders, puncture of body cavities. Sometimes fainting develops with a severe migraine attack.

Sinocarotid syncope

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

Orthostatic syncope

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

This type of syncope occurs in individuals from chronic insufficiency or periodic instability of vasomotor reactions. A decrease in blood pressure after taking a vertical position occurs due to a violation of the vasoconstrictor reactivity of the vessels of the lower extremities, which are responsible for the resistance and capacity of the vessels.

Postural syncope develops in apparently healthy people who, for unknown reasons, have defective postural responses (which may be familial). In such people, a feeling of weakness occurs with sharp inclinations, their blood pressure drops slightly, and then sets at an even lower level. Soon, compensatory reactions weaken sharply and blood pressure continues to fall rapidly.

This type of syncope is possible with primary insufficiency of the autonomic nervous system, family autonomic dysfunctions.

At least three syndromes of orthostatic syncope have been described:

I. Acute or subacute autonomic dysfunction. With this disease, in practically healthy adults or children, a partial or complete disruption of the activity of the parasympathetic and sympathetic systems occurs within a few days or weeks. Pupillary reactions disappear, lacrimal, salivary and sweating stop, impotence, paresis are observed Bladder and intestines, orthostatic hypotension. Additional studies reveal an increased protein content in the cerebrospinal fluid, degeneration of unmyelinated autonomic nerve fibers. It is believed that this disease is a variant of acute idiopathic polyneuritis, similar to Landry-Guillain-Barré syndrome.

II. Chronic insufficiency of postganglionic autonomic nerve fibers. This disease develops in people of middle and older age, who gradually develop chronic orthostatic hypotension, sometimes in combination with impotence and dysfunction of the pelvic organs. After staying in an upright position for 5-10 minutes, blood pressure decreases by at least 35 mm Hg. Art., pulse pressure decreases, while pallor, nausea and increased pulse rate are not observed. Men get sick more often than women. The condition is relatively benign and apparently irreversible.

III. Chronic insufficiency of preganglionic autonomic nerve fibers. In this disease, orthostatic hypotension, along with recurrent anhidrosis, impotence, and dysfunction of the pelvic organs, is combined with lesions of the central nervous system.
These include:
1. Shy-Drager Syndrome characterized by tremor, extrapyramidal rigidity and amnesia;
2. Progressive cerebellar degeneration, some varieties of which are family;
3. More variable extrapyramidal and cerebellar diseases(striato-nigral degeneration).

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

Secondary orthostatic hypotension results from
disorders of the autonomic nervous system
age physiological changes
adrenal insufficiency
hypovolemia
taking some medicines(antihypertensive drugs, tricyclic antidepressants, levodopa drugs, antipsychotics, -blockers), especially in elderly patients who have to take several drugs at the same time
Insufficiency of the autonomic nervous system - damage to pre- and postganglionic autonomic fibers - most often occurs when the lateral columns of the spinal cord (syringomyelia) or peripheral nerves are involved in the pathological process (diabetic, alcoholic, amyloid polyneuropathy, Adie's syndrome, hypovitaminosis, etc.)
orthostatic hypotension is considered one of the manifestations of Parkinson's disease,
multisystem atrophy of the brain
subclavian artery steal syndrome
But more often the causes of orthostatic hypotension are starvation, anemia, prolonged bed rest.

Situational syncope

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

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

Syncope of a psychogenic nature
The psychogenic nature of syncope is detected in patients after possible studies in the absence of signs of heart disease or neurological disorders.

This group patients can be divided into two categories:
patients who have had a first episode of syncope (further examination may be discontinued), and
patients who continue to suffer from fainting (an assessment of the mental state of the patient should be carried out). In almost 25% of such cases, a psychiatric examination can detect mental disorders combined with fainting.

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

Separately, it is necessary to describe non-epileptic seizures, or pseudo-seizures. They are more common in women around the age of 20, in whose family history, as a rule, there are references to relatives who suffered from epilepsy. Such patients had the opportunity to observe the development of epileptic seizures, imitate them, or suffer themselves mental illness. Pseudo-seizures are varied and last longer than true ones. epileptic seizures. They are characterized by poor coordination of movements, complex localization, occur in crowded places, injuries are very rare. During a seizure, the patient may resist seeing a doctor.

Neurological syncope

In addition to syncope of cardiac origin, syncope includes conditions with a sudden onset of short-term impairment of consciousness, which may be the result of transient anemia of the brain. A sufficient level of blood supply to the brain depends on a number of physiological conditions of the state of cardiac activity and vascular tone, the volume of circulating blood and its physicochemical composition.

There are three main factors that contribute to the deterioration of cerebral blood flow, malnutrition of the brain and, ultimately, episodic blackouts.
1. Cardiac- weakening of the force of contractions of the heart of a neurogenic nature or due to acute functional insufficiency of the heart muscle, valvular apparatus, cardiac arrhythmias.
2. Vascular- a drop in vascular tone of the arterial or venous systems, accompanied by a significant decrease in blood pressure.
3. Homeostatic- a change in the qualitative composition of the blood, especially a decrease in the content of sugar, carbon dioxide, oxygen.

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

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

Fainting in the elderly

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

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

If the examination revealed orthostatic hypotension, it is necessary to pay special attention to the patient's admission medicines, contributing to a decrease in blood pressure with the development of postural disorders. If the patient does not take such drugs, then the main attention should be paid to studies of the cardiovascular and nervous systems. If at neurological examination No pathological changes, but there are complaints about impaired urination, sweating, constipation, impotence, and the patient talks about the development of fainting only after getting out of bed abruptly or after sleep, then they suggest the development chronic vegetative insufficiency. In this case, the main danger for the patient is not the loss of consciousness itself, but the accompanying fall, since this often leads to fractures.

The patient should be advised not to get out of bed abruptly, first sit down or make several movements with the legs lying down, use elastic bandages and bandages, lay carpets in the bathroom and corridor, as these are the most common places for falls due to fainting in the elderly. It is advisable to take walks in the fresh air in places where there is no hard surface, you should not stand still for a long time.

If, however, during a neurological examination of the patient, signs of damage to the nervous system are revealed, a more thorough examination in a specialized hospital is necessary to clarify the cause of syncope and select an adequate treatment regimen.

In healthy people slowing of the ventricular rate, but not less than 35-40 beats per minute, and its increase, but not more than 180 beats per minute, does not cause a decrease in cerebral blood flow, especially when a person is in a horizontal position. Changes in pulse rate that go beyond the above values ​​can cause cerebrovascular accident and disruption of brain activity. Resistance to changes in pulse rate decreases in a person who is in an upright position, with cerebrovascular diseases, anemia, lesions of the coronary vessels, myocardium, and heart valves.

Complete atrioventricular block. Syncope attacks in combination with this pathology are called the Morgagni-Adams-Stokes syndrome. Morgagni-Adams-Stokes attacks usually occur in the form of an instant attack of weakness. The patient suddenly loses consciousness, after asystole lasting for several seconds, he turns pale, loses consciousness, clonic convulsions may develop. With a longer period of asystole, the skin color turns from ash-gray to cyanotic, fixed pupils, urinary and fecal incontinence, bilateral Babinsky's symptom. In some patients, confusion and neurological symptoms may subsequently be observed for a long time due to cerebral ischemia, and a persistent impairment of mental activity may also develop, although focal neurological symptoms are rarely noted. Similar cardiac syncope can be repeated several times a day.

In patients with similar bouts of blockade may be permanent or transient. It is often preceded or later by conduction disturbances in one or two of the three bundles that normally activate the ventricles, as well as second-degree atrioventricular block (Mobitz II, bi- or trifascicular blocks). If there is a complete blockade and the pacemaker below the blockade does not function, fainting occurs. A brief episode of tachycardia or ventricular fibrillation can also lead to fainting. Repeated syncope with ventricular fibrillation is described, characterized by a prolongation of the Q-T interval (sometimes in combination with congenital deafness), this pathology may be familial or occur sporadically.

less often fainting occurs when the sinus rhythm of the heart is disturbed. Repeated episodes of tachyarrhythmias, including atrial flutter and paroxysmal atrial and ventricular tachycardias with intact atrioventricular conduction, can also dramatically reduce cardiac output and, as a result, cause syncope.

With another variety cardiac syncope heart block occurs reflexively due to excitation of the vagus nerve. Similar phenomena were observed in patients with esophageal diverticula, mediastinal tumors, lesions of the gallbladder, carotid sinus, glossopharyngeal neuralgia, irritation of the pleura or lung. However, with this pathology, reflex tachycardia is more often of the sinus-atrial type than of the atrioventricular type.
Features of the onset of an attack can help in diagnosing the causes that cause fainting.

When an attack develops within seconds, carotid sinus syncope, postural hypotension, acute atrioventricular block, asystole, or ventricular fibrillation are most likely to be suspected.
With the duration of the attack more than a few minutes but less than an hour, it is preferable to think of hypoglycemia or hyperventilation.

Syncope development during or immediately after exertion suggests aortic stenosis, idiopathic hypertrophic subaortic stenosis, marked bradycardia, or, in the elderly, postural hypotension. Sometimes syncope that occurs with stress is observed in patients with aortic valve insufficiency and gross occlusive lesions of the arteries of the brain.

In patients with asystole or fibrillation ventricular loss of consciousness occurs within a few seconds, then often there are short-term clonic muscle cramps.

In older people, suddenly, without visible causes of fainting makes one suspect a complete heart block, even when no changes are found on examination of the patient.
fainting that occur with convulsive activity, but without significant changes in hemodynamic parameters, are presumably epileptic.

In a patient with a feeling of weakness or fainting accompanied by bradycardia, neurogenic seizures should be distinguished from cardiogenic (Morgagni-Adams-Stokes). In such cases, the ECG is of decisive importance, but even in its absence, the clinical signs of the Morgagni-Adams-Stokes syndrome can be noted. They are characterized by a longer duration, a constantly slow heart rate, the presence of murmurs synchronous with atrial contractions and atrial contraction waves (A) during jugular vein pulsation, as well as a changing intensity of the first tone, despite a regular heart rhythm.
The problem of differential diagnosing the causes of fainting is still relevant.

First of all, you need to exclude or confirm such emergencies, in which the first fainting condition may become the leading symptom: massive internal bleeding, myocardial infarction (which can occur in a painless form), acute cardiac arrhythmias.
Repeated fainting require a different approach to identifying the causes leading to it.

Causes of repeated bouts of weakness and disturbances of consciousness can be the following:

I. Hemodynamic (decreased cerebral blood flow)
A. Inadequate mechanisms of vasoconstriction:
1. Vasovagal (vasodilating).
2. Postural hypotension.
3. Primary insufficiency of the autonomic nervous system.
4. Sympathectomy (pharmacological when taking such antihypertensive drugs as alpha-methyldopa and apressin, or surgical).
5. Diseases of the central and peripheral nervous system, including autonomic nerve fibers.
6. Carotid syncope. B. Hypovolemia:

1. Loss of blood due to gastrointestinal bleeding.
2. Addison's disease.

IN. Mechanical restriction of venous return:
1. Valsalva test.
2. Cough.
3. Urination.
4. Atrial myxoma, globular valvular thrombus. D. Decreased cardiac output:

1. Obstruction of the ejection of blood from the left ventricle: aortic stenosis, hypertrophic subaortic stenosis.
2. Obstruction of blood flow through the pulmonary artery: pulmonary artery stenosis, primary pulmonary hypertension, pulmonary embolism.
3. Extensive myocardial infarction with insufficiency of pumping function.
4. Cardiac tamponade.

D. Arrhythmias:
1. Bradyarrhythmias:
a) atrioventricular blockade (second and third degree) with Adams-Stokes attacks;
b) ventricular asystole;
c) sinus bradycardia, sinus-atrial blockade, cessation of activity of the sinus node, weakness syndrome of the sinus node;
d) carotid syncope;
e) neuralgia of the glossopharyngeal nerve.

2. Tachyarrhythmias:
a) periodic ventricular fibrillation in combination with bradyarrhythmias or without them;
b) ventricular tachycardia;
c) supraventricular tachycardia without atrioventricular block.

II. Other causes of weakness and periodic disturbances of consciousness

A. Changes in blood composition:
1. Hypoxia.
2. Anemia.
3. Decrease in CO2 concentration due to hyperventilation.
4. Hypoglycemia.

B. Cerebral disorders:
1. Cerebrovascular disorders:
a) circulatory failure in the pools of extracranial vessels (vertebrobasilar, carotid);
b) diffuse spasm of cerebral arterioles (hypertensive encephalopathy).

2. Emotional disorders.

In other cases, even at the present stage, the possibilities of clinical medicine do not allow establish the nature of fainting almost 26% of the time. Samples with dosed physical activity on a bicycle ergometer or treadmill are used; long passive orthostatic test. When conducting these tests, they distinguish:
Cardioinhibitory vasovagal syncope - development at the time of an attack of arterial hypotension (a decrease in systolic pressure below 80 mm Hg) and bradycardia with a heart rate of less than 40 beats / min.
Vasodepressor vasovagal syncope - arterial hypotension with changes in heart rate within 10% compared with the indicators observed during the development of syncope.
Vasovagal syncope of mixed type - arterial hypotension and bradycardia. At the same time, bradycardia in terms of values ​​could be absolute (less than 60 per minute) or relative compared to the heart rate before the attack.