Fainting: causes, emergency care, prevention. Fainting: causes, emergency care, prevention Fainting pathogenesis classification clinic treatment

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In table Figure 1 presents a pathophysiological classification of the known primary causes of syncope. Some disorders may resemble fainting for two different reasons. In some cases, consciousness is indeed lost, but the mechanism of development of this process differs from cerebral hypoperfusion (for example, epilepsy, some metabolic disorders, including hypoxia and hypoglycemia, and intoxication). In other disorders, consciousness is lost only at first glance (for example, with psychogenic pseudosyncope, catalepsy and panic attacks). With psychogenic pseudosyncope, patients can feign disturbances of consciousness. This condition can be viewed in the context of factitious disorders, malingering, and conversion.

Finally, some patients, in order to obtain certain benefits, can spontaneously cause true fainting, attracting the attention of others. In table Table 2 lists the most common conditions misdiagnosed as fainting. Differential diagnosis is of great importance, because the doctor, as a rule, encounters patients with sudden loss consciousness (real or perceived), which may be caused by causes unrelated to decreased cerebral blood flow, such as stroke and/or conversion reaction.

Table 1

Classification of fainting

table 2

Conditions often misdiagnosed as fainting

The classification of syncope (see Table 1) covers a large group of diseases with a common origin, associated with different risk profiles. The pathophysiological mechanisms for reducing systemic blood pressure, the substrate for the occurrence of syncope, vary significantly. Systemic blood pressure is a derivative of cardiac output and total peripheral vascular resistance (TPVR), and their dysfunction can cause syncope. More often, a combination of both mechanisms is present in syncope, even if their relative contribution to the etiology varies considerably.

In Fig. Figure 1 presents the pathophysiological mechanisms underlying the classification of syncope: low central pressure, low peripheral resistance and low cardiac output. Low TPR may be a consequence of defective reflex activation in the following cardiac cycle and lead to vasodepressor or reflex syncope. Other reasons for low peripheral vascular resistance include functional and structural disorders associated with the effects of drugs, primary and secondary autonomic failure.

There are three known causes of low cardiac output:

• reflex causing bradycardia (cardioinhibitory type of reflex fainting);
• cardiac cause associated with arrhythmia, structural heart disease, or pulmonary embolism;
• insufficient venous return due to a decrease in circulating blood volume or blood deposition in the venous system.

Rice. 1. Pathophysiological classification of fainting

Please note that reflex fainting can be caused by a combination of causes. A decrease in blood flow below a critical level leads to loss of consciousness and loss of muscle tone, and a slowing of the rhythm on the electroencephalogram (EEG) is noted.

Continued hypoperfusion leads to flattening of the EEG. In children with parasympathetic asystole caused by pressure on the eyeballs, EEG flattening occurs only in the case of a minimum duration of asystole of 9 s. It lasts longer if asystole persists for a longer time. Tilt test data showed that a decrease in systolic blood pressure by 40-60 mm Hg. associated with fainting.

To maintain adequate blood pressure and cerebral blood flow, the integration of a number of control mechanisms is critical. Among them, the cardiochronotropic function of arterial baroreceptors is distinguished; contractility of the heart muscle; systemic vascular resistance modulating circulation; vasoconstriction associated with the activity of renin, angiotensin and vasopressin; regulation of the volume of circulating fluid by the kidneys; the ability for cerebrovascular self-regulation, which allows maintaining constant cerebral blood flow in a relatively wide range of blood pressure.

Michele Brignole, Jean-Jacques Blanc, Richard Sutton and Angel Moya

Fainting- “syncope” (Greek syncope - cutting off, shortening) - a sudden short loss of consciousness due to transient cerebral ischemia. It occurs reflexively. It is the mildest form of acute vascular insufficiency.

• 1) a drop in blood pressure due to a decrease in peripheral vascular resistance during systemic vasodilation (for example: psychogenic syncope due to hyperactivity of p. vasodilation, orthostatic hypotension).
• 2) heart rhythm disturbances (for example: Morgagni-Edams-Stokes syndrome).
• 3) a decrease in the content of 0 2 in the blood, i.e. hypoxemia.

Symptoms, course of fainting. There are:

• 1) fainting reaction (lipothymia) and
• 2) actual fainting.

Lipotymia is characterized by sudden mild fogging, dizziness, ringing in the ears, nausea, and cold hands and feet. Objectively, sharp pallor of the skin, slight cyanosis of the lips, dilated pupils, low pulse, and decreased blood pressure are noted. The paroxysm of lipothymia lasts several seconds.

Fainting itself begins with symptoms of lipothymia, followed by loss of consciousness. The patient slowly falls (settles). The pulse is small or not detectable at all. Blood pressure is sharply reduced. Breathing is shallow, tendon and skin reflexes are not evoked. The duration of loss of consciousness is 10-30 seconds. After fainting, general weakness, nausea, and discomfort persist for some time. abdominal cavity. The most common type of fainting:

a) vasovagal syncope- provoked by negative emotions and pain, stuffiness, prolonged standing, a sharp transition from a horizontal to a vertical position. Examination of patients in the interictal period often reveals astheno-neurotic syndrome, arterial hypotension, and pulse lability.

To comparatively rare cases of fainting relate.

b) bettolipsia- fainting occurs at the height of a prolonged cough in patients with chronic diseases lungs, apparently due to increased pressure in the chest cavity and difficulty in the outflow of blood from the cranial cavity.

c) nocturic fainting- are more often observed in men and are manifested by a sudden loss of consciousness and a fall after urination at night or in the morning; they arise due to cerebral ischemia caused by a rush of blood to the abdominal organs.

For vasovagal syncope, drug treatment is not required; it is necessary to lay the patient down and free him from restrictive clothing. For symptomatic fainting, the underlying disease is treated. The prognosis is favorable, however, the frequency of vasovagal syncope can rarely be reduced, because their development is usually associated with a constitutional tendency to parasympathetic (vagal) reactions.

D. A. Enikeev, Pathophysiology of extreme and terminal conditions. 1997

Temporary loss of consciousness caused by transient general hypoperfusion of the brain. The clinical picture of syncope consists of precursors (lack of air, “lightheadedness,” fog or “floaters” before the eyes, dizziness), a period of lack of consciousness and a recovery stage in which weakness, hypotension, and dizziness persist. Diagnosis of syncope is based on tilt test data, clinical and biochemical tests, ECG, EEG, USDG of extracranial vessels. For patients with fainting, differentiated therapy is usually used, aimed at eliminating the etiopathogenetic mechanisms of the development of paroxysms. In the absence of convincing data on the genesis of syncope, undifferentiated treatment is carried out.

General information

Fainting (syncope, syncope) was previously regarded as a transient loss of consciousness with loss of postural tone. Indeed, it is a disorder of muscle tone that leads to a person falling when fainting. However, many other conditions fit this definition: different kinds epileptic seizures, hypoglycemia, head injury, TIA, acute alcohol intoxication, etc. Therefore, in 2009, a different definition was adopted, interpreting syncope as a transient loss of consciousness caused by general cerebral hypoperfusion.

According to generalized data, up to 50% of people have fainted at least once during their lives. Typically, the first episode of syncope occurs between 10 and 30 years of age, with a peak at puberty. Population-based studies indicate that the incidence of syncope increases with age. In 35% of patients, repeated fainting occurs within three years after the first.

Global transient cerebral ischemia, which causes fainting, can have a variety of causes, both neurogenic and somatic. The variety of etiopathogenetic mechanisms of syncope and its episodic nature explains the significant difficulties that doctors encounter in diagnosing the causes and choosing treatment tactics for fainting. The above emphasizes the interdisciplinary relevance of this problem, requiring the participation of specialists in the field of neurology, cardiology, and traumatology.

Causes of fainting

Normally, blood flow through the cerebral arteries is estimated at 60-100 ml of blood per 100 g of brain matter per minute. Its sharp decrease to 20 ml per 100 g per minute causes fainting. Factors that cause a sudden decrease in the volume of blood entering the cerebral vessels can be: a decrease in cardiac output (with myocardial infarction, massive acute blood loss, severe arrhythmia, ventricular tachycardia, bradycardia, hypovolemia due to profuse diarrhea), narrowing of the lumen of the arteries supplying the brain (with atherosclerosis , occlusion of the carotid arteries, vascular spasm), vascular dilatation, rapid change in body position (so-called orthostatic collapse).

Changes in tone (dilatation or spasm) of the vessels supplying the brain are often neuroreflex in nature and are the leading cause of syncope. Such fainting can provoke a strong psycho-emotional experience, pain, irritation of the carotid sinus (during coughing, swallowing, sneezing) and the vagus nerve (during otoscopy, gastrocardial syndrome), an attack of acute cholecystitis or renal colic, trigeminal neuralgia, glossopharyngeal neuralgia, an attack of vegetative-vascular dystonia, overdose of certain pharmaceuticals, etc.

Another mechanism that provokes fainting is a decrease in blood oxygenation, i.e., a decrease in the oxygen content in the blood with normal blood volume. Syncope of this origin can be observed with blood diseases (iron deficiency anemia, sickle cell anemia), carbon monoxide poisoning, respiratory diseases (bronchial asthma, obstructive bronchitis). Fainting can also be caused by a decrease in CO2 in the blood, which is often observed with hyperventilation. According to some data, about 41% are due to fainting, the etiology of which cannot be determined.

Classification of fainting

Attempts to systematize the various types of fainting have led to the creation of several classifications. Most of them are based on the etiopathogenetic principle. The group of neurogenic fainting includes vasovagal conditions, which are based on sharp vasodilation, and irritative (carotid sinus syndrome, fainting with glossopharyngeal and trigeminal neuralgia). Orthostatic syncope includes fainting caused by autonomic failure, decreased blood volume, and drug-induced orthostatic hypotension. Cardiogenic type fainting occurs due to cardiovascular diseases: hypertrophic cardiomyopathy, pulmonary stenosis, aortic stenosis, pulmonary hypertension, atrial myxoma, myocardial infarction, valvular heart defects. Arrhythmogenic syncope is provoked by the presence of arrhythmia (AV block, tachycardia, SSSU), malfunction of the pacemaker, side effect antiarrhythmics. There is also cerebrovascular (dyscirculatory) syncope associated with pathology of the vessels supplying blood to cerebral structures. Fainting, the trigger factor of which could not be determined, is classified as atypical.

Clinical picture of fainting

The maximum duration of syncope does not exceed 30 minutes; in most cases, fainting lasts no more than 2-3 minutes. Despite this, during the course of fainting, 3 stages are clearly visible: the presyncope state (precursor period), the fainting itself, and the postsyncope state (recovery period). The clinical picture and duration of each stage are highly variable and depend on the pathogenetic mechanisms underlying fainting.

The presyncope period lasts several seconds or minutes. It is described by patients as a feeling of lightheadedness, severe weakness, dizziness, lack of air, blurred vision. Possible nausea, flashing dots before the eyes, ringing in the ears. If a person manages to sit down with his head down or lie down, then loss of consciousness may not occur. Otherwise, the increase in these manifestations ends in loss of consciousness and fall. With the slow development of fainting, the patient, falling, holds on to surrounding objects, which allows him to avoid injury. A rapidly developing syncope can lead to serious consequences: head injury, fracture, spinal injury, etc.

During the period of fainting itself, a loss of consciousness varying in depth is noted, accompanied by shallow breathing and complete muscle relaxation. When examining a patient during the period of fainting, mydriasis and a slow reaction of the pupils to light, weak filling of the pulse, and arterial hypotension are observed. Tendon reflexes are intact. A deep disturbance of consciousness during fainting with severe cerebral hypoxia can occur with the occurrence of short-term convulsions and involuntary urination. But such a single syncopal paroxysm is not a reason to diagnose epilepsy.

The post-syncope period of syncope usually lasts no more than a few minutes, but can last 1-2 hours. There is some weakness and uncertainty of movements, dizziness, low blood pressure and pallor persist. Possible dry mouth, hyperhidrosis. It is typical that patients remember well everything that happened before the moment of loss of consciousness. This feature makes it possible to exclude TBI, which is typically characterized by the presence of retrograde amnesia. The absence of neurological deficit and general cerebral symptoms makes it possible to differentiate syncope from stroke.

Clinic of selected types of fainting

Vasovagal syncope- the most common type of syncope. Its pathogenetic mechanism consists of sharp peripheral vasodilation. The trigger for an attack can be prolonged standing, staying in a stuffy place, overheating (in a bathhouse, on the beach), excessive emotional reaction, pain impulse, etc. Vasovagal syncope develops only in an upright state. If the patient manages to lie down or sit down, or leave a stuffy or hot room, then fainting may end in the presyncope stage. The vasovagal type of syncope is characterized by pronounced stages. The first stage lasts up to 3 minutes, during which patients manage to tell others that they “feel bad.” The stage of fainting itself lasts 1-2 minutes and is accompanied by hyperhidrosis, pallor, muscle hypotension, a drop in blood pressure with a thread-like pulse at a normal heart rate. In the post-syncope stage (from 5 minutes to 1 hour), weakness comes to the fore.

Cerebrovascular syncope often occurs with pathology of the spine in the cervical region (spondyloarthrosis, osteochondrosis, spondylosis). The pathognomonic trigger for this type of syncope is sudden turning of the head. The resulting compression of the vertebral artery leads to sudden cerebral ischemia, leading to loss of consciousness. At the presyncopal stage, photopsia, tinnitus, and sometimes intense cephalgia are possible. Fainting itself is characterized by a sharp weakening of postural tone, which persists in the postsyncopal stage.

Irritative fainting develops as a consequence of reflex bradycardia when the vagus nerve is irritated by impulses from its receptor zones. The appearance of such fainting can be observed with achalasia cardia, peptic ulcer of the 12th colon, hyperkinesia of the biliary tract and other diseases accompanied by the formation of abnormal viscero-visceral reflexes. Each type of irritative syncope has its own trigger, for example, a specific attack of pain, swallowing, gastroscopy. This type of syncope is characterized by a short, just a few seconds, period of warning signs. Consciousness turns off for 1-2 minutes. There is often no post-syncope period. As a rule, repeated stereotypic fainting is observed.

Cardio- and arrhythmogenic syncope observed in 13% of patients with myocardial infarction. In such cases, syncope is the first symptom and seriously complicates the diagnosis of the underlying pathology. Features are: occurrence regardless of the person’s position, the presence of symptoms of cardiogenic collapse, great depth loss of consciousness, repetition of syncopal paroxysm when the patient tries to get up after the first fainting. Syncope, included in the clinical picture of Morgagni–Edams–Stokes syndrome, is characterized by the absence of precursors, the inability to determine the pulse and heartbeat, pallor, reaching the point of cyanosis, and the beginning of the recovery of consciousness after the appearance of heart contractions.

Orthostatic syncope develops only during the transition from a horizontal position to a vertical position. It is observed in hypotensive patients, persons with autonomic dysfunction, elderly and debilitated patients. Typically, such patients indicate repeated cases of dizziness or “fogging” with a sudden change in body position. Often, orthostatic syncope is not a pathological condition and does not require additional treatment.

Diagnostics

A thorough and consistent interview of the patient, aimed at identifying the trigger that provoked fainting and analysis of the clinical features of syncope, allows the doctor to establish the type of fainting, adequately determine the need and direction of a diagnostic search for the pathology behind syncope. In this case, the first priority is to exclude urgent conditions that can manifest as fainting (PE, acute myocardial ischemia, bleeding, etc.). At the second stage, it is determined whether syncope is a manifestation organic disease brain (aneurysms of cerebral vessels, etc.). The initial examination of the patient is carried out by a therapist or pediatrician, neurologist. In the future, you may need to consult a cardiologist, epileptologist, endocrinologist, or MRI of the brain, MRA, duplex scanning or transcranial ultrasound, radiography of the spine in the cervical region.

In the diagnosis of syncope of unknown origin, the tilt test has found widespread use, making it possible to determine the mechanism of occurrence of syncope.

First aid for fainting

The primary goal is to create conditions that promote better oxygenation of the brain. To do this, the patient is given horizontal position, loosen the tie, unbutton the collar of the shirt, provide an influx of fresh air. Splashing in the patient's face cold water and bringing ammonia to the nose, they try to cause reflex stimulation of the vascular and respiratory centers. In case of severe syncope with a significant drop in blood pressure, if the above actions are not successful, the administration of sympathicotonic drugs (ephedrine, phenylephrine) is indicated. For arrhythmia, antiarrhythmics are recommended; for cardiac arrest, administration of atropine and chest compressions.

Treatment of patients with syncope

Therapeutic tactics in patients with syncope are divided into undifferentiated and differentiated treatment. An undifferentiated approach is common to all types of syncope and is especially relevant when the genesis of syncope is unknown. Its main directions are: reducing the threshold of neurovascular excitability, increasing the level of autonomic stability, achieving a state of mental balance. First-line drugs in the treatment of fainting are b-blockers (atenolol, metoprolol). If there are contraindications to the use of beta-blockers, ephedrine and theophylline are used. Second-line drugs include vagolytics (disopyramide, scopolamine). It is possible to prescribe vasoconstrictors (etafedrine, midodrine), serotonin uptake inhibitors (methylphenidate, sertraline). In combination treatment, various sedatives are used (valerian root extract, lemon mint and peppermint extract, ergotamine, ergotoxin, belladonna extract, phenobarbital), sometimes tranquilizers (oxazepam, medazepam, phenazepam).

Differentiated therapy for fainting is selected according to its type and clinical characteristics. Thus, the treatment of fainting in carotid sinus syndrome is based on the use of sympatho- and anticholinergic drugs. In severe cases, surgical denervation of the sinus is indicated. The main treatment for syncope associated with trigeminal or glossopharyngeal neuralgia is the use of anticonvulsants (carbamazepine). Vasovagal syncope is treated primarily as part of undifferentiated therapy.

Recurrent orthostatic syncope requires measures aimed at limiting the volume of blood deposited in the lower body when moving to an upright position. To achieve peripheral vasoconstriction, dihydroergotamine and α-adrenomimetics are prescribed, and propranolol is prescribed to block vasodilation of peripheral vessels. Patients with cardiogenic syncope are managed by a cardiologist. If necessary, the issue of implanting a cardioverter-defibrillator is resolved.

It should be noted that in all cases of syncope, treatment of patients necessarily includes therapy for concomitant and causative diseases.

An attack of short-term loss of consciousness caused by a temporary disruption of cerebral blood flow. cerebral consciousness. The diagnosis of SIMPLE syncope can be given to the victim only if the loss of consciousness occurred in an upright position, and its recovery occurred several tens of seconds (up to 5 minutes) after the body was in horizontal position.

1. Standing suddenly or standing for a long time, especially in the heat (orthostatic type of fainting). 2. Factors that activate vasovagal reflexes: pain, the sight of blood, fear, psycho-emotional overload, urination, defecation, cough (vasodepressor (vasovagal) type of fainting). 3. Compression of the carotid sinus area (fainting with carotid sinus hypersensitivity syndrome). 4. Autonomic neuropathy. 5. Uncontrolled use of antihypertensive, sedatives, antihistamines and other drugs.

Simple fainting is associated with a short-term decrease in venous vascular tone lower limbs and abdominal cavity, i.e. (bcc) becomes relatively small for the vascular bed and blood is deposited in the periphery. This causes a decrease in venous return and a drop in cardiac output and, as a consequence, a disruption of the blood supply to the brain occurs. The basis of the vasodepressor type of fainting (during defecation, urination) is a sharp increase in intrathoracic pressure during straining, which causes a decrease in venous inflow and a drop in cardiac output.

Fainting can occur suddenly or with warning signs. Precursors are the appearance of a feeling of weakness, dizziness, nausea, and darkening in the victim. Objectively, one can note pallor of the skin, beads of sweat on the face, bradycardia and hypotension, decreased muscle tone and weakened tendon reflexes, and sinus bradycardia. The rapid restoration of consciousness in a horizontal position confirms the correct diagnosis of syncope. With deep fainting, urinary incontinence is possible, but this syndrome is more common in epilepsy.

The patient should be placed or maintained in a horizontal position with the leg end raised, ensure free breathing: unfasten the collar, belt; splash your face with cold water, pat your cheeks; Inhaling stimulants (ammonia, vinegar) helps well; in case of prolonged fainting, the body should be rubbed and covered with warm heating pads; 1 ml of 10% caffeine solution is indicated subcutaneously; for severe hypotension and bradycardia subcutaneously 0.5-1 ml of 0.1% atropine sulfate solution.

IF THE LOSS OF CONSCIOUSNESS CONTINUES MORE THAN A FEW MINUTES, YOU SHOULD THINK ABOUT THE DEVELOPMENT OF A COMATOSE CONDITION Make sure there is breathing and a pulse in the carotid arteries; if they are absent, begin resuscitation measures, as in case of cardiac arrest. If there are convulsions, to avoid biting the tongue, place a suitable object (but not metal!) between the patient’s teeth; stop convulsive syndrome In case of injury, if there is external bleeding, stop it Look in your pockets or wallet for a medical card (epileptic, diabetic, etc.) or medications that can cause loss of consciousness Protect the patient from overheating or hypothermia If the cause of the coma still remains unclear, nonspecific testing should be performed symptomatic treatment, laboratory and instrumental express diagnostics.

Administer 4060 ml of 40% glucose solution intravenously. If the cause of the comatose state is hypoglycemic coma, the patient will regain consciousness. In all other cases, glucose will be absorbed as an energy product. Note. If the patient subsequently develops even a ketoacidotic coma, then the glucose administered in this amount will not cause harm. Normalize intracranial pressure if there are signs of increase. Buy seizures(diazepam) if available. Start fighting the infection if there are signs of bacterial meningitis or purulent otitis. Enter vitamin B (thiamine has cardiotrophic and neuroprotective effects). If there are signs of acute poisoning, select a specific antidote and begin antidote therapy. Protect your eyes. In patients who are in comatose, the eyelids are raised, there is no blinking, as a result of which the cornea dries out. To prevent this complication, it is necessary to periodically instill saline or albucide solution as the cornea dries.

Clear consciousness, its complete preservation, adequate reaction to the environment, complete orientation, wakefulness. Moderate stupor, moderate drowsiness, partial disorientation, delay in answering questions (repetition often required), slow execution of commands. Deep stupor, deep drowsiness, disorientation, almost complete sleepy state, limitation and difficulty in speech contact, monosyllabic answers to repeated questions, execution of only simple commands. Stupor (unconsciousness, deep sleep) almost complete absence of consciousness, preservation of purposeful, coordinated defensive movements, opening of the eyes to painful and sound stimuli, occasional monosyllabic answers to multiple repetitions of a question, immobility or automated stereotypical movements, loss of control over pelvic functions.

Moderate coma (I) inability to wake up, chaotic uncoordinated defensive movements to painful stimuli, lack of opening the eyes to stimuli and control of pelvic functions, mild respiratory disturbances and cardiovascular activities. Deep coma (II) inability to wake up, lack of protective movements, impaired muscle tone, inhibition of tendon reflexes, severe respiratory failure, cardiovascular decompensation. Transcendental (terminal) coma (III) agonal state, atony, areflexia, vital functions are supported by breathing apparatus and cardiovascular drugs.

Eye opening: absent to pain 2 to speech 3 Spontaneous 4 Response to a painful stimulus: no flexion reaction 2 extension reaction 3 Withdrawal 4 localization of irritation 5 command execution 6 Verbal response: no inarticulate sounds 2 incomprehensible words 3 confused speech 4 complete orientation 5 State assessment consciousness is carried out by total counting of points from each subgroup. 15 points correspond to a state of clear consciousness, 1314 stupor, 912 stupor, 4-8 coma, 3 points brain death.

1. Diseases not accompanied by focal neurological signs. The cellular composition of the cerebrospinal fluid is normal. Normal (CT) and (MRI). This group includes: intoxications (alcohol, barbiturates, opiates, anticonvulsants, benzolyazepines, tricyclic antidepressants, phenothiazines, ethylene glycol) metabolic disorders (hypoxia, diabetic acidosis, uremia, hepatic coma, hypoglycemia, adrenal insufficiency); heavy common infections(pneumonia, typhoid, malaria, sepsis); vascular collapse (shock) of any etiology and cardiac decompensation in old age; epilepsy; hypertensive encephalopathy and eclampsia; hyperthermia and hypothermia.

2. Diseases that cause irritation of the meninges with an admixture of blood or cytosis in the cerebrospinal fluid, usually without focal cerebral and brainstem signs. Diseases in this group include: subarachnoid bleeding due to aneurysm rupture; acute bacterial meningitis; some forms of viral encephalitis.

3. Diseases accompanied by focal brainstem or lateralized brain signs with or without changes in the cerebrospinal fluid. This group includes: cerebral hemorrhages; cerebral infarction due to thrombosis or embolism; brain abscesses and subdural empyemas; epidural and subdural hematomas; brain contusion; brain tumors.

The pathogenesis of coma of any etiology is based on damage to the central nervous system, and in most cases the prognosis of the coma itself depends on the degree of this damage. Loss of consciousness occurs as a result of a decrease in the spontaneous activity of the cortex and a number of subcortical formations, as well as a violation of the cortical-subcortical relationships. This is caused by either damage to the brain stem (especially the midbrain), or extensive functional or structural disorders in the cerebral hemispheres, or both in combination.

Under the influence of these factors, the supply of nutrients and oxygen to the brain is disrupted, the enzyme systems of nerve cells are damaged, which leads to energy starvation of the brain. The sensitivity of different parts of the brain to damaging influences varies. Complex young structures are more vulnerable, and less complex “ancient” formations are relatively resistant to the influence of harmful factors.

Skin: moist, dry, hyperemic, cyanotic, icteric Head and face: presence of injuries Eyes: conjunctiva (hemorrhage, jaundice); reaction of pupils to light; fundus (disc edema, hypertensive or diabetic retinopathy) Nose and ears: discharge of pus, blood; liquorrhea; acrocyanosis Tongue: dry; bite marks or scars Breath: smell of urine, acetone, alcohol Neck: stiff neck, pulsation of carotid arteries Rib cage: frequency, depth, rhythm of breathing Heart: rhythm disturbance (bradycardia); sources of cerebral embolism (mitral stenosis) Abdomen: enlarged liver, spleen or kidneys Arms: blood pressure, hemiplegia, injection marks Hands: frequency, rhythm and filling of the pulse, tremor Legs: hemiplegia, plantar reflexes Urine: incontinence or retention, protein, sugar , acetone

First of all, when examining a patient, TBI should be excluded. At the slightest suspicion, an X-ray examination of the skull should be done in 2 projections. Focal neurological symptoms suggest the presence of an acute cerebrovascular accident. Fresh tongue bites or old scars on the tongue are highly likely to indicate epilepsy. The presence of multiple traces of subcutaneous injections in typical places will indicate diabetes mellitus, and multiple traces of intravenous injections, often in the most unexpected places, suggests drug addiction. At the slightest suspicion of a hypoglycemic state, 4060 ml of 40% glucose solution should be urgently administered intravenously. If the patient subsequently develops even a ketoacidotic coma, his condition will not worsen from this, and with hypoglycemia this in a simple way treatment will save the life of the victim.

For a systematic approach to the issues of diagnosis and emergency care, all accidents with loss of consciousness are most conveniently considered according to the following types (Colin Ogilvie, 1981): Sudden and short-term loss of consciousness (simple fainting, transient narrowing or occlusion of the arteries supplying the brain) Sudden and short-term loss of consciousness (simple fainting, transient narrowing or occlusion of the arteries supplying the brain) prolonged loss of consciousness (acute cerebrovascular accident, hypoglycemia, epilepsy and hysteria) Prolonged loss of consciousness with a gradual onset. Loss of consciousness with unknown onset and duration.

1. SYNOPSIS is characterized by generalized muscle weakness, decreased postural tone, inability to stand upright and loss of consciousness. Emergency care: the patient should be placed or maintained in a horizontal position with the leg end raised; ensure free breathing: unfasten the collar, belt; splash your face with cold water, pat your cheeks; Inhaling stimulants (ammonia, vinegar) helps well; 2. COMA (from the Greek cat, deep sleep) complete loss of consciousness with a total loss of perception of the environment and oneself and with more or less pronounced neurological and autonomic disorders. The severity of coma depends on the duration of neurological and autonomic disorders. Comas of any etiology have common symptoms and are manifested by loss of consciousness, decrease or disappearance of sensitivity, reflexes, skeletal muscle tone and disorder of the autonomic functions of the body. Along with this, symptoms characteristic of the underlying disease are observed (focal neurological symptoms, jaundice, azotemia. To make a diagnosis, it is necessary to assess the state of consciousness using the Glasgow scale, find out etiological factor and general condition. Urgent hospitalization.

Short-term fainting is a loss of consciousness within 8-10 seconds, caused by a decrease in cerebral blood supply, a violation of the mental and sensory functions of the body. In parallel with this, the physiological tone of the muscles decreases, which often leads to a person falling. A characteristic feature fainting is a further relatively rapid return of the patient to consciousness.

Fainting is an attack of short-term loss of consciousness

A temporary decrease in cerebral blood supply, which causes fainting, is an excessive or, conversely, insufficient response of the body to physiological regulatory factors.
Acuteness of the current clinical picture fainting is determined by its etiology, pathogenesis, as well as the strength of the stimulus that is the source of reflexes that are directed to the vasomotor center. In addition, the state of the body depends on its individual reactivity (fainting most often occurs in people of a closed nature, somewhat less often in people with a labile nervous system). Loss of consciousness sometimes occurs when a person is hungry, exhausted, or weakened by illness.

The development of fainting can be accelerated by the patient's warm or tight clothing, as well as the appearance of pain that is superimposed on anxiety. Occurring against an unfavorable background (suppressed immunity, hunger, overwork, etc.), this condition can develop into hypovolemia (collapse). Manifestations such as general weakness, dizziness, speech disorders, convulsions, shock () or coma should not be confused with fainting.

The main causes of reactions that cause fainting are:

• emotional (fear of, taking blood, injecting with an injection needle during exercise without superficial anesthesia, etc.)
• reflex, caused by increased stimulation of receptors that are involved in the regulation of homeostasis: intoxication with anesthetics and vasoconstrictors, neurocardiogenic, vasopressor, excessive sensitivity of the carotid glomerulus, alcoholic and food poisoning, acute diseases (infectious), hunger, overwork, etc.
• cardiogenic in nature (obstructions to blood flow in the chambers of the heart, pulmonary stenosis, contractile insufficiency, acute myocardial infarction, cardiac tamponade, bradyarrhythmias, tachyarrhythmias)
• mental origin (panic disorders, conversion reaction, epilepsy, etc.)
• orthostatic hypotension (autonomic dysfunction, decreased circulating blood volume)
• situational (during coughing, sneezing, urination, defecation, instrumental procedures, etc.)
• medicinal origin (direct effect on the body; interaction of MAO drugs or phenothiazines with vasoconstrictors that are part of local anesthetics or lytic cocktails)
• polyetiological nature
• unknown origin

Fainting: causes

Typical forms of fainting caused by emotional reactions include the cases described above. Among the reasons that most often cause fainting, the main ones are:

• anxiety or fear of intervention
• long wait to be called to the surgeon's office
• deontological flaws of medical staff (tactless behavior, unkempt appearance, etc.)
• screams and moans coming from the office where the intervention is carried out
• untidy and stuffy office
• type of blood or cutting and piercing instruments (scalpel, syringe, etc.)
• instrumental manipulation

Clinical manifestations of syncope

Most often, the development of fainting begins with the following manifestations:

• sudden general weakness
• dizziness
• noise or ringing in the ears
• darkening of the eyes, blurred vision or temporary loss of vision
• nausea (sometimes turning into vomiting).

Objective symptoms of fainting include:

• constriction of the pupils
• pale skin, especially on the face
• increased sweating
• rapid, weak filling and tension pulse
• shallow breathing
• low blood and venous pressure
• decreased skeletal muscle tone
• cooling of extremities

The described symptoms in mild forms of this complication often cause dizziness with partial preservation of consciousness, but more often a loss of consciousness occurs with a complete loss of muscle tone.
Some patients may exhibit atypical forms of fainting, similar to those that occur during intoxication - clonic convulsions, increased movement eyeballs, muscle rigidity. Such symptoms indicate hypoxia, which is caused by a sharp decrease in blood pressure. Again, the most likely cause of syncope is a psychogenic factor.

In severe clinical cases (severe emotional stress, sharp pain etc.) possible disruption of blood circulation to vital organs (myocardial infarction, stroke, etc.).

First aid for fainting

When the first warning signs of fainting appear (general weakness, pallor, increased sweating, decreased skeletal muscle tone, etc.), you need to:

• stop all manipulations immediately
• make sure the airway is open
• determine the presence of breathing and pulse in the carotid arteries (if they are absent, begin resuscitation measures)
• If you have cramps, place a spacer between your teeth to avoid biting your tongue.
• put the victim on his back, ensuring a short-term elevated position of his legs (if fainting occurs in a dental chair, then the chair together with the patient should be given a horizontal position, while lowering the part for the head slightly lower). In modern dental settings, this position of the patient in a chair is called the “safety position”; it is instantly achieved by pressing a special key.
• remove warm or tight clothing, unbutton the collar of a shirt or blouse, loosen the belt (for women, a bra)
• provide access to fresh, cool air
• Sprinkle cold water on your face and chest
• pat the patient firmly on the cheeks with a hand or soaked in cold water with a towel.

If fainting is caused only by psycho-emotional stress and fear, then the measures listed are completely sufficient to bring a person to his senses. In cases where the above tips do not have an effect, then you should not waste precious time using vapors of ammonia, vinegar or other irritating chemicals, since in this situation they will also be ineffective. The only correct way out of this dangerous situation is the early start of pharmacotherapy.

Delay in medical measures when a patient faints is unacceptable. Failure to provide timely assistance may result in prolonged hypoxia, which threatens the development of changes in the brain.

Medicines for fainting

If the above measures do not help a patient who is in a state of fainting, the medical staff immediately begins pharmacotherapy.

To normalize blood pressure, the patient is given the following for hypertension:

After removing the victim from a state of fainting, he needs to be calmed down, wait until the pulse begins to fill rhythmically, increases blood pressure, restoration of skin color, satisfactory general condition. Further manipulations can be continued only when the patient’s condition does not cause the slightest concern.

Preventive treatment is not necessary, but the causes of cardiac origin must be eliminated!

Prolonged fainting

In case of loss of consciousness, which lasts several minutes, the doctor, in addition to the above measures, must immediately carry out the following actions:

• look in the patient's pockets or wallet for a medical card (diabetic, epileptic, etc.) or medications
• examine the patient (determine the color of the skin, the nature of the pulse, and if there are movements, their nature)
• in case of ongoing hemodynamic disorders, administer drugs that normalize blood pressure
• After regaining consciousness and normalizing the pulse and blood pressure, the patient must be reassured, given hot strong tea or coffee, and provided with rest.

If weakness, discomfort in the head, chest, abdomen, sweating and hypotension persist for an hour or longer, and repeated states of fainting occur each time for a longer duration, there is every reason to suspect the development of life-threatening conditions: internal bleeding, atrioventricular block , arrhythmia, hypoglycemic coma and the like.

In such cases, you should immediately call ambulance. Such patients must be urgently transported to a specialized department of the hospital, where it is necessary to conduct a thorough examination and begin treatment for the illness that led to loss of consciousness.

Reflexogenic syncope

Reflex reactions, as noted, include reflexogenic (vaso-vagal) and those caused by manipulation with increased sensitivity of the carotid glomerulus.
Reflexogenic fainting is one of the leading complications that occurs during dental treatment. Due to the action of the reflexogenic factor, the central regulation of vascular tone is disrupted, after which anemia of the cerebral vessels occurs and blood accumulates in the vessels of the abdominal cavity.
Reflexogenic fainting occurs in most cases in young people and, as a rule, when they are in an upright position. You can often find symptoms indicating excessive autonomic activity. nervous system: epigastric discomfort, nausea, pallor, sweating, blurred vision and a feeling of depersonalization.

Fainting due to hypersensitivity of the carotid glomerulus

Increased sensitivity of the carotid glomerulus is usually observed in older people, mainly men. Its occurrence is promoted diabetes, hypertension and atherosclerosis. There may also be local reasons: dense scars on the neck, or enlarged The lymph nodes, which are located next to the carotid glomerulus and put pressure on it. Rarely does it occur as a primary tumor.

Fainting due to hypersensitivity of the carotid glomerulus occurs in everyday life in an older person during careful shaving of an area at the angle of the lower jaw with an electric razor. Sometimes this condition is also observed in a summer person who wears a shirt with a tight collar and still tightens his tie tightly. This often happens when you suddenly turn your head.

Manifestations of hypersensitivity of the carotid glomerulus

Reflexes from the carotid glomerulus occupy an important place in the regulation of cardiac output and peripheral vascular tone. Normally, afferent impulses from the carotid glomerulus are transmitted through n. glossopharyngeus to the vasomotor and cardioinhibitory center of the brain stem.

The efferent part of the carotid glomerulus reflex contains vagus nerve fibers and cervical sympathetic fibers. Afferent impulses from the carotid glomerulus enter the brain with a frequency that depends both on the amount of pressure on the artery wall and on the rate of its changes. An increase in pressure causes an increase in the frequency of afferent stimulation of the vasomotor center. As a result, parasympathetic activity increases and sympathetic activity decreases, which causes systemic vasodilation and a decrease in heart rate.

Manifestations of hypersensitivity of the carotid glomerulus are ventricular asystole lasting more than 3 seconds and a decrease in systolic blood pressure by more than 50 mm. rt. Art. during a massage in the area of ​​this anatomical formation.

Forms of hypersensitivity
There are three variants of increased sensitivity of the carotid glomerulus:

• cardioinhibitory, which is accompanied by inhibition of both the sinus and atrioventricular nodes; this is the most common form, accounting for more than 70% of all cases; It can be prevented by intramuscular injection of atropine
• vasodepressor, which is characterized by profound hypotension due to peripheral vasodilation, but without significant bradycardia; this is a fairly rare form (10%), which, unlike the previous one, is not blocked by atropine, but by adrenaline
• mixed form, combining both cardioinhibitory and vasodepressor reactions; observed in 20-25% of cases.

Preventing fainting

Before the main measures aimed at preventing fainting in persons with hypersensitivity of the carotid glomerulus,
relate:

• a thorough history of syncope and careful analysis possible reasons their development
• mandatory measurement of heart rate and blood pressure before the start of the intervention and during its implementation; determination of these indicators is also required when palpating or massaging an area of ​​the carotid glomerulus for diagnostic purposes (5-10 seconds)

Prevention of possible irritation of the carotid glomerulus:

• in everyday life - avoid tight collars of shirts, ties, sudden movements of the head; when using an electric razor - switch to other shaving methods or grow a beard
• in the clinic - remove tight socks or a tie, loosen the collar of your shirt, and avoid unexpected head movements.

For diagnostic purposes possible reaction from the side of the carotid glomerulus, it is necessary to carefully palpate the area of ​​the carotid sinus.

Fainting during local anesthesia
Monitoring the patient's psycho-emotional state before the start of local anesthesia is an extremely important element of the safety of the intervention. Therefore, before injecting an anesthetic, the doctor must find out how the patient tolerates the injections. This approach often allows us to establish a cause-and-effect relationship.
Patients with increased functional lability in acute stressful situations react to a physical factor (pain, injection) by involuntary holding their breath; through this, the access of oxygen to the tissues decreases, which most often causes fainting. From the above we can come to the conclusion: the first prerequisite for the safety of anesthesia and intervention in this situation is to calm the patient and the mandatory implementation of preliminary anesthesia of the mucous membrane at the site of the planned injection.

Prevention of fainting caused solely by injection during local anesthesia is as follows: before the intervention, the doctor must explain to the patient the features of this manipulation, in particular, tell that after superficial anesthesia of the mucous membrane, the needle will be inserted at the height of inspiration (with a warning).

Therefore, the dentist informs the patient that the needle will advance only if he or she breathes continuously and evenly. This approach will allow the doctor not only to divert the patient’s attention, but also to prevent possible brain hypoxia and the development of fainting.

Differential diagnosis of reactions caused by local anesthesia
The majority of complications in dental practice are a consequence of the patient’s increased reflex reaction. Much less of them are caused by incorrect posture of the patient’s body (head, neck, torso), in particular its rapid change (orthostatic collapse). And very rarely conditions arise due to hypersensitivity to a particular drug or its overdose. However, whatever the reason for the body’s defensive reaction, the doctor must identify and eliminate it as quickly as possible.

Differentiating the causes of an acute general reaction to local anesthetic injections is generally quite simple. If the cause of the complication is an emotional reaction, then its symptoms appear instantly and, as a rule, do not last long. When the occurrence of a reaction is associated with hypersensitivity to the drug or its overdose, then a certain period of time is needed for the injected drug to enter the bloodstream. In such cases, complications begin later and last longer.

Prevention of common reactions of emotional etiology

Changes in the body caused by fear of surgery are often found even in mentally healthy patients. It is clear that with age, with a decrease in the compensatory capabilities and resistance of the body, and especially if patients have concomitant pathologies, general reactions become more pronounced.

Disorders of cardiac activity, as well as changes in indicators of the functional activity of the autonomic nervous system that occur during local anesthesia and during surgical interventions, usually have a psycho-emotional overtones. The intensity of these disorders depends on the state of the cardiovascular system and the mobility of the patient’s neuro-reflex activity.
Emotional changes that can disrupt metabolism, hemodynamics and breathing are also determined by the following factors:

• patient's age
• his physical condition
• severity of the main and concomitant diseases
• information about the nature of the surgical intervention (volume, duration, etc.)

All this, as a rule, not only excludes the possibility of safe and highly effective pain relief, but also threatens a number of various reactions or complications. They can be prevented with the help of appropriate preventive psychological and medicinal measures.

If psychological and medicinal preparation is not carried out, then under the influence of fear the patient may release a significant amount of adrenaline and norepinephrine, which will stimulate the hypothalamus. In such cases, to inhibit the mentioned processes, it is necessary to use a significantly larger dose of anesthetic (toxicity!) than would be the case after premedication. In addition, due to the patient’s anxiety, the possibility of developing various complications cannot be excluded (ineffectiveness of pain relief, soft tissue injury from sudden head movements, and even the development of threatening conditions in the body).

Basics of preventing emotional reactions

To prevent the development of emotional reactions in patients, in particular fainting, it is necessary:

• collect a thorough anamnesis regarding the patient’s experience of fear, pain, injection with an injection needle, and response to instrumental manipulations (without such data, starting local anesthesia or surgical intervention is contraindicated)
• carry out an objective examination of the patient’s psycho-emotional and physical condition
• prevent the patient from waiting for a long time to be called to the surgical room or operating room
• create a calm environment in the department, guaranteeing a tactful attitude of medical staff towards patients
• provide access to clean, fresh, preferably cool air into the office
• prevent the development of fear and negative emotions through psychotherapy and premedication with sedatives, in particular anxiolytic drugs
• free the patient from tight or warm clothing
• determine heart rate and blood pressure before any intervention
• begin anesthesia, in particular the introduction of an injection needle, only after first explaining to the patient some of the features of pain relief
• try to perform all manipulations painlessly, without harsh pressure on the tissue, and also avoiding statements that could cause fear or intensify a psycho-emotional reaction.

Prevention of the development of severe emotional reactions in persons who are scheduled surgical intervention under local anesthesia, is to create a favorable psycho-emotional background and conduct painless and safe treatment. All this, of course, is achieved thanks to the high professionalism of the doctor.

Carrying out local anesthesia during surgical procedures without a previous assessment of the patient’s psycho-emotional and physical condition, as well as if he has a negative attitude towards the doctor, is unacceptable. Only if these rules are followed, as well as with the use of appropriate psychological and medicinal preparation of the patient, can the doctor count on the safety of the intervention.

If a patient is diagnosed with certain concomitant ailments, including moderate and severe ones, the dentist must take all measures to ensure that the operation does not cause an exacerbation of the existing pathology, much less the development of a threatening condition. To do this, the doctor must obtain the opinion of an appropriate specialist (cardiologist, endocrinologist, psychiatrist, etc.) on the possibility of safely performing surgical procedures.

Coherence of actions and mutual understanding between the dentist and doctors of other specialties is the key to safe intervention and highly effective medical care.

Forms of fainting

Fainting due to orthostatic hypotension
Orthostatic hypotension is caused by a decrease in circulating blood volume or primary or secondary autonomic dysfunction. Normally, reflex tachycardia and vasoconstriction, which are a consequence of sympathetic stimulation, can compensate for the peripheral deposition of blood, a decrease in cardiac output, and a sharp decrease in blood pressure when the body position changes from horizontal to vertical. The loss of these compensatory mechanisms causes significant hypotension on rising, especially in the elderly.

Patients with orthostatic hypotension do not tolerate even minor fluctuations in blood pressure. In this situation, stress itself can cause them to faint. Pain is layered with fear, accelerating the development of this condition.

The main causes of fainting in patients with orthostatic hypotension include taking certain medications (antihypertensives, diuretics, MAO drugs, phenothiazines, ganglion blockers).
To avoid syncope due to orthostatic hypotension, the dentist performing dental surgery under local anesthesia must first check the patient's orthostatic response. To do this, he needs to monitor his heart rate and measure his blood pressure immediately and a few minutes after changing his body position to vertical!

A sudden decrease in systolic pressure by 10-25 mm Hg. below 90 mm Hg. Art. (or the magnitude that causes symptoms) after a few minutes of standing, the patient suspects that orthostatic hypotension may lead to syncope.

Prevention of syncope caused by orthostatic hypotension
To prevent the development of fainting caused by orthostatic hypotension, you need to:

• prevent the patient’s emotional and stressful conditions, in particular fear and pain
• If orthostatic hypotension is detected in a patient, it is imperative to preventively use medications that tone and normalize blood pressure
• ensure optimal (reclining and lying) position of the patient
• prevent rapid or sudden change of position of the patient from horizontal to vertical

Fainting caused by irritation of receptors that are involved in the regulation of homeostasis
The main causes of complications caused by excessive stimulation of receptors that are involved in the regulation of homeostasis include:

• intoxication with local anesthetics
• overdose
• injecting too quickly into highly vascularized areas
• erroneous injection of anesthetic into a vessel
• vasoconstrictor poisoning
• use of non-ampoule solution
• entry of most of the vasoconstrictor into the bloodstream
• reactions to taking certain medications (antihypertensives, diuretics, ganglion blockers, etc.)
• food and alcohol intoxication
• acute vicissitudes of diseases (severe pneumonia, infectious processes)
• anemia
• suppressed immunity, overwork, hunger, etc.
• exhaustion from a serious illness suffered by the patient

From the above data it is clear that there are many factors that can cause the above-mentioned fainting, and therefore make diagnosis difficult.

Drugs that cause fainting

As already noted, a thorough history taking and its critical assessment very often allow the doctor to prevent the occurrence of various general reactions at the patient. An important role in the prevention of dangerous conditions belongs to careful questioning of the patient about the medications he has taken or has been taking recently. This approach often helps determine the cause of fainting, which can be a consequence of many medications.

Medicines that can cause fainting:

Preventing drug-induced fainting
To prevent fainting caused by the action of medications, the doctor should not begin any manipulation without the following actions:

• carefully questioning the patient about the medications he is taking or has taken for the main or accompanying ailments (for example, in cases of using antidepressant drugs, anesthesia can be administered only two weeks after the end of the course drug treatment)
• mandatory preliminary determination of heart rate and blood pressure
• strict adherence to the rules that determine the possibility of developing pharmacological incompatibility

Frequent fainting

Fainting not associated with pathology of the cardiovascular system, as a rule, does not pose a threat to human life. Injuries during a fall can be dangerous, especially in older people. If the patient’s fainting condition is frequent and they recur regularly, then this is already a symptom, which deserves the attention of a doctor to carefully determine its cause.

The doctor must remember that repeated states of syncope of cardiogenic etiology can lead to fatal consequences. If a person with heart disease lost consciousness and then quickly came to his senses without consequences, this is already a bad sign. The next case can be fatal in its consequences (ventricular fibrillation).