Fainting (loss of consciousness)

Syncope (syncope) - a short-term loss of consciousness caused by anemia of the brain and accompanied by a weakening of the cardiac and respiratory systems. The pathophysiological basis of its development is a short-term disruption of the blood supply to the brain.

A complete loss of consciousness does not always develop. Sometimes everything is limited to a sudden feeling of faintness, ringing or noise in the ears, uneven dizziness, the appearance of paresthesia, muscle weakness and clouding of consciousness, in connection with which the patient does not fall, but gradually settles.

Most attacks of short-term loss of consciousness are associated with syncope (syncope) or, more rarely, epilepsy. When you leave this state, satisfactory or well-being returns quickly enough.

[1], [2], [3], [4], [5], [6], [7], [8]

What causes syncope?

Causes of syncope are functional shifts and organic diseases. Fainting often occurs in persons with a labile nervous system when they are fatigued, the form of blood, fear, pain, being in a stuffy substitution, etc. Fainting can be a symptom of various physical illnesses (heart defects, bleeding, cardiac rhythm and conduction disorders, epilepsy, etc.).

Vazovagalny (simple) syncope - is due to an increase in the tone of the vagus nerve. The provoking factors are usually pain, fear, excitement, hypoxia (for example, when staying in a stuffy room). Loss of consciousness usually occurs in a standing position, rarely - sitting or lying down. Fainting does not occur during exercise, but can develop after a lot of physical stress. Before fainting, many often experience weakness, nausea, sweating, a feeling of heat or chills. With the development of fainting, the patient "settles down", looks pale. Consciousness is missing for no more than a minute.

As one of the variants of vasovagal syncope, fainting occurs when the Valsalva is taken (a test) with a closed vocal cicle.

Vasovagal syncope can also occur when pressing on the area of the carotid sinus.

With such a faint, it is first of all necessary to put the patient correctly - the head should be below the trunk. Simultaneously, a slight irritating therapy is performed, for example, rubbing the face with cold water, bringing ammonia to the nose.

Orthostatic syncope (as a manifestation of orthostatic arterial hypotension) occurs as a result of a disorder of vasomotor reflexes in the patient's rapid transition from a lying position to a standing position. The most common cause is the intake of various antihypertensive drugs, Orthostatic hypotension often develops in elderly patients, especially with prolonged observance of bed rest.

Cough fainting (with a fit of coughing) is sometimes observed in chronic bronchitis in full-blooded patients with obesity, smokers and alcohol abusers.

Cardiogenic syncope. The most common causes are arrhythmia, PE, myocardial infarction, as well as conditions accompanied by the cytoplasm of the left ventricular outflow tract (stenosis of the aortic aorta, hypertrophic cardiomyopathy). There is a rule: "Fainting that occurs during physical exertion is associated with the pathology of the heart."

Neurological fainting is observed with transient ischemic attacks, vertebrobasilar pool insufficiency, migraine. With vertebrobasilar insufficiency, often accompanied by dizziness or diplopia (double vision), the onset of fainting can provoke a turning or tilting of the head.

Loss of consciousness associated with epileptic seizures. Epileptic seizures are characterized by a sudden onset and development of seizures, and involuntary urination and biting of the tongue often occur.

A sudden fall can cause head damage. Sometimes loss of consciousness lasts a few seconds and is not accompanied by cramps.

Violation of consciousness in a fit of hysteria. Attacks of hysteria occur only in the presence of people. The limb movements are usually coordinated and often directed aggressively against others. Hysterical attacks are not accompanied by complete loss of consciousness, and such manifestations as incontinence of urine and feces, biting of the tongue are usually absent. Patients are often frightened, because they do not understand what is happening to them. A very characteristic for hysteria manifestation is the so-called hysterical lump (globus hystericus) in the throat: a sensation of spasm, rolling up to the throat of the ball, a ball that appears at the beginning of a hysterical fit.

The development of fainting in the elderly is facilitated by the following factors:

1. violation of the mechanisms of maintenance of arterial pressure (decrease in the frequency of cardiac contractions with changes in the position of the body, a violation of the ability of the kidneys to retain sodium, a decrease in baroreflex mechanisms);
2. shortness of breath and hyperventilation with heart failure (cerebral blood flow may be reduced to 40%); high prevalence of chronic obstructive pulmonary diseases and anemia, which reduce the saturation of blood with oxygen;
3. a sudden change in the tone of the vessels or the effectiveness of the heart: sudden violation of the heart rhythm, taking antihypertensive drugs, diseases with severe intoxication, urination and defecation, eating, changing the position of the tep. Based on the causes of development, syncope can be divided as follows:
   • cardiac (with aortic stenosis, ischemic heart disease, tachy- and bradyarrhythmias, blockades, weakness syndrome of the sinus node);
   • vasomotor (with orthostatic hypotension, carotid sinus syndrome, irritation of the endings of the vagus nerve, etc.);
   • cerebral (due to acute and chronic disturbance of cerebral circulation);
   • hypovopaemic (with insufficient intake or abundant loss of fluid by the body);
   • metabolic (with oxygen starvation of the brain due to severe hypoxemia or lack of energy due to hypoglycemia).

How does fainting develop?

The following pathological processes underlie various syncope states:

1. Imbalance between the volume of circulating blood and the capacity of the vascular bed due to the inadequacy of vasomotor mechanisms of a reflex nature (60-70% of cases of syncope). This mechanism develops vasopressor, orthostatic, sinocarotid, hypovolemic and cough collapse.
2. Diseases of the heart with insufficient cardiac output (heart defects, myxoma, free thrombus of the left atrium, arrhythmia, blockade of the conduction system, asystole). In 15-20% of cases, the onset of syncope is associated with manifestations of heart disease.
3. Neurological and mental diseases (stenosis of extracranial cerebral vessels, hypertensive encephalopathy, hysteria, epilepsy). Approximately 5-10% of syncope states are caused by these diseases.
4. Metabolic disorders (hypoglycemia, hyperventilation, etc.) - the remaining 5-10%.

People of elderly and senile age often meet:

1. orthostatic hypotension (a high risk of its development is indicated by a drop in systolic blood pressure of 20 mm or more mmHg with a sharp rise);
2. postprandial hypotension (a decrease in systolic blood pressure during the first hour after a meal due to increased blood flow in the gastrointestinal tract and an inadequate reaction to this sympathetic nervous system);
3. carotid sinus syndrome - a syncope that occurs when sharp turns or tilting the head.

How does syncope manifest?

Vasopressor syncope is caused by sudden pronounced dilatation of arterioles with a drop in effective cerebral blood flow and systemic arterial pressure in the absence of compensatory increase in stroke volume and heart rate. Reduction of the total peripheral resistance is due mainly to the dilatation of peripheral mainly muscular vessels. In most cases, simple vasopressor syncope develops in practically healthy people with a labile nervous system.

Also, syncope may be due to the lack of tonus of adrenergic innervation in organic lesions of the cardiovascular system.

Clinically, the vasopressor syncope manifests itself in the development of the unconscious state. Loss of consciousness does not come immediately. Usually there is a short prodromal period characterized by dizziness, ringing in the ears, darkening in the eyes, nausea, clouding of consciousness, etc. Pallor of the skin, increased sweating.

These symptoms are mainly associated with a violation of the balance of regulation of the autonomic nervous system, in particular with increased secretion of catecholamines and antidiuretic hormone.

In the prodromal period, the heart rate is not changed or a slight increase is observed. At the height of syncope, the pulse is weak, and blood pressure is reduced. The heart rate varies depending on the cause that caused fainting. As fainting develops, muscle weakness develops, the patient loses balance and consciousness. At the height of syncope, the muscle tone is sharply reduced and the reflexes are depressed. Breathing shallow and rapid. On the encephalogram, slow high-amplitude waves are recorded.

The duration of syncope is usually several tens of seconds. In the horizontal position, there is a rapid recovery of consciousness and an improvement in the general condition of the patient. Some time after fainting, general weakness, pale skin, increased sweating and nausea remain. Due to dilatation of peripheral vessels, the skin after fainting is usually warm.

If the duration of the unconscious state exceeds 20-30 seconds, then the development of convulsive syndrome is possible.

Orthostatic syncope is characterized by the development of the unconscious state as a result of a sharp transition of a person from the horizontal to the vertical position. Rarely, it is due to a prolonged stay of a person in an upright position. The immediate mechanism for the development of this type of acute vascular insufficiency is the deposition of blood in the vessels of the lower body and, as a consequence, a decrease in venous return to the heart.

Orthostatic syncope often develops after prolonged bed rest, against adrenergic, diuretic medications, and the like. Normally, the transition from horizontal to vertical position is accompanied by a small short-term decrease in blood pressure. After a few seconds, it is restored to the original level or even slightly exceeds it. Rapid recovery of blood pressure is normal due to compensatory vasoconstriction caused by activation of the mechanoreceptors of the aortic arch and carotid sinuses.

This adaptive mechanism does not work when the sympathetic part of the autonomic nervous system is affected, as well as by turning off the functions of its peripheral parts. Compensatory vasoconstriction does not develop, which leads to the accumulation of blood in the venous network of a large range of blood circulation, a decrease in venous return, a decrease in blood pressure and a violation of the blood supply to the brain.

The clinical picture in postural syncope is quite typical. Usually, loss of consciousness develops in the morning after getting out of bed.

In contrast to vasopressor syncope, it develops instantaneously, without a prodromal period and precursors. Bradycardia is not observed. Also, there are no signs of increased blood filling of the skin vessels. After the transition to the horizontal state, consciousness is quickly restored.

Sino-carotid syncope develops due to the increased sensitivity of the carotid sinus to mechanical irritations. Normally, the carotid sinus takes part in the regulation of heart rate and the level of systemic arterial pressure.

In the field of bifurcation of the common carotid artery there are numerous nerve endings that form the sinus nerve of Goering. Its fibers in the composition of the glossopharyngeal nerve go to the vasomotor center. When the mechanoreceptors of the carotid sinus stimulate, the vessels of the skin, muscles and abdominal organs expand, as well as the reduction in the heart rate.

The total volume of circulating blood does not decrease, but only redistributes from the arterial bed to the venous. In a healthy person, lowering blood pressure when irritating the carotid sinus is 10-40 mm Hg. Art. With increased sensitivity of the carotid sinus, even a slight irritation leads to a significant decrease in blood pressure and pronounced bradycardia. Often a short-term loss of consciousness develops. It is possible to develop a prolonged syncope with convulsive syndrome.

The diagnosis of sinocarotid syncope is made if a characteristic clinical picture is reproduced during mechanical stimulation of the carotid sinus.

Most often, the cause of the pathology of the carotid sinus is atherosclerotic occlusion of the carotid or vertebral artery, less often pathological processes in the area of the sinus (tumor, etc.).

Depending on the type of hemodynamic disorders, two main forms of sinocarotid syncope are distinguished: cardioinhibitory and depressor syncope. There is cardioinhibitory, which is manifested by pronounced bradycardia, complete atrioventricular blockage or short-term extrasystole. Depressor form is much less common, depends on the dilatation of peripheral vessels.

Fainting conditions of cardiac origin are most often due to coronary heart disease, heart defects, vessel stenoses, etc. A significant proportion of "cardiac" syncope consists of various types of heart rhythm and conduction disorders (Adams-Stokes-Morgagni syndrome).

It is generally believed that normal cerebral blood flow is maintained at a sufficient level with significant fluctuations in the heart rate (from 40 to 180 per minute). Concomitant cardiac pathology leads to a worsening of the tolerability of cardiac arrhythmias and the development of impaired consciousness. Associated with inadequate blood supply to the brain. Usually. At the same time there is a detailed symptomatology of heart disease (dyspnea, cyanosis, stenocardia, stagnation in the lungs, etc.).

The relationship between syncope states with cardiac rhythm disturbances and cardiac conduction is determined by electrocardiographic studies.

Loss of consciousness may be due to short-term attacks of fibrillation in the syndrome of delayed repolarization. With this syndrome, with an increase in the heart rate, the duration of the QT interval does not decrease. On the contrary, it becomes elongated. Outside the attack, the extended QT interval is the only manifestation of the disease.

Other causes of syncope. In addition to the described options for syncope, one should remember the possibility of mental disorders due to acute disorders of cerebral circulation, epilepsy, hypoglycemia, hyperventilation, acute hypovolemia, pulmonary hypertension, etc.

Emergency care in syncope

Fainting is not an independent nosological unit, it is a manifestation of a large group of functional disorders and organic diseases. Therefore, for the purpose of their relief, both symptomatic therapy and special treatment of the underlying disease are carried out. Patients with simple syncope (vasopressor, postural) usually do not need intensive care and hospitalization.

It is recommended to adhere to the following sequence of treatment activities:

1. Give the patient a prone position with raised legs.
2. Provide access to fresh air (open the window, unbutton the collar, loosen the tightening clothes).
3. Temperature irritation of body skin receptors (wiping or sprinkling with cold water).
4. Bring to the nose a cotton wool with ammonia.
5. In case of low effectiveness of these measures, subcutaneous administration of 1 ml of 10% caffeine solution and / or 2 ml of cordiamine is indicated.
6. In the presence of bradycardia, 0.3-1 ml of 0.1% atropine solution can be administered subcutaneously.

If these measures did not help and the patient did not recover, one should think about the presence of a serious disease. To exclude acute cardiac pathology, electrocardiography should be performed. If a suspected organic disease is present, the patient should be hospitalized for examination.

With transient asystole due to intracardiac blockades, weakness syndrome of the sinus node, the question of installing a permanent pacemaker should be addressed. If the cause of syncope is paroxysmal tachyarrhythmias, medication or electromotgulsive therapy is conducted according to general principles. If the cause of syncope is severe obstructive heart disease, stenosis of extracranial vessels or atrial thrombosis, then cardiosurgical intervention is indicated.

When caring for geriatric patients with a tendency to fainting, remember the following points:

• be sure to find out the conditions under which syncope occurs;
• syncope may be triggered by the following medications: antidepressants, phenothiazides (hypnotics), reserpine or clonidine (as well as other drugs with sympatholytic activity), diuretics, vasodilators (eg nitrates, alcohol);
• monitor the fragmentation of the patient's diet: in small portions 5-6 times a day;
• to determine the risk of fainting, you should monitor the level of blood pressure and pulse before and after meals (the high risk of postprandial hypotension is indicated by a decrease in systolic blood pressure by 10 or more mm Hg). And before and after (the first and third minutes) of getting up. In this case, the absence of changes in heart rate may be a sign of violation of baroreflex mechanisms, and an excessively high increase in heart rate - talk about loss of fluid;
• periodically (1-2 times a week) measure the water balance and, if necessary, increase the intake of table salt (if there is a violation of the ability of the kidneys to retain sodium);
• with carotid sinus syndrome carefully taken beta-blockers, calcium antagonists, digitalis preparations and methyldopa;
• orthostatic hypotension requires an elevated position of the head end of the bed, training the patient to the rules of gradual getting up and wearing elastic stockings;
• to prevent the occurrence of hemodynamic conditions of syncope, patients should avoid cases of abrupt increase in intra-abdominal pressure during straining - conduct timely prevention of constipation, effective treatment of prostate adenoma and cough;
• in rooms where people with pronounced signs of aging are, it is necessary to follow the regime of intensive ventilation, patients are recommended to perform breathing exercises that promote blood oxygenation. Treatment of patients with a high risk of developing syncope should be aimed at eliminating the causative disease and adapting to age-related changes.

[9], [10], [11], [12], [13], [14], [15]