Syncope (loss of consciousness)

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

Not always does a complete loss of consciousness develop. Sometimes everything is limited to a sudden feeling of nausea, ringing or noise in the ears, non-systemic dizziness, the appearance of paresthesia, muscle weakness and clouding of consciousness, due to which the patient does not fall, but gradually sinks.

Most episodes of short-term loss of consciousness are associated with fainting (syncope) or, less commonly, epilepsy. When recovering from this condition, satisfactory or good health returns fairly quickly.

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What causes fainting?

Fainting states may be caused by functional shifts and organic diseases. Fainting often occurs in people with a labile nervous system when they are tired, see blood, are afraid, in pain, are in a stuffy room, etc. Fainting may be a symptom of various somatic diseases (heart defects, bleeding, heart rhythm and conduction disorders, epilepsy, etc.).

Vasovagal (simple) fainting - caused by increased vagus nerve tone. 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 physical exertion, but can develop after great physical exertion. Before fainting, many often feel weakness, nausea, sweating, a feeling of heat or chills. As fainting develops, the patient "sinks", looks pale. Consciousness is absent for no more than a minute.

Fainting that occurs during the Valsalva maneuver (straining with the glottis closed) is considered one of the variants of vasovagal syncope.

Vasovagal syncope can also occur when pressure is applied to the carotid sinus area.

In case of such fainting, the patient should first be correctly positioned - the head should be lower than the body. At the same time, light irritant therapy is carried out, for example, wiping the face with cold water, holding ammonia to the nose.

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

Cough syncope (during a coughing fit) is sometimes observed in chronic bronchitis in obese, full-blooded patients who smoke and abuse alcohol.

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

Neurological fainting is observed in transient ischemic attacks, vertebrobasilar insufficiency, and migraine. In vertebrobasilar insufficiency, often accompanied by dizziness or diplopia (double vision), fainting can be provoked by turning or throwing back the head.

Loss of consciousness associated with epileptic seizures. An epileptic seizure is characterized by a sudden onset and progression of convulsions, often accompanied by involuntary urination and tongue biting.

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

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

The following factors contribute to the development of fainting in older people:

1. disruption of mechanisms for maintaining blood pressure (decrease in heart rate when changing body position, disruption of the kidneys' ability to conserve sodium, reduction of baroreflex mechanisms);
2. shortness of breath and hyperventilation in heart failure (cerebral blood flow can decrease by up to 40%); high prevalence of chronic obstructive pulmonary diseases and anemias that reduce blood oxygen saturation;
3. a sharp change in vascular tone or cardiac efficiency: sudden disturbance of heart rhythm, taking antihypertensive drugs, diseases with severe intoxication, urination and defecation, eating, change in body position. Based on the causes of development, fainting can be divided as follows:
   • cardiac (with aortic stenosis, coronary heart disease, tachy- and bradyarrhythmia, blockades, sick sinus syndrome);
   • vasomotor (with orthostatic hypotension, carotid sinus syndrome, irritation of the endings of the vagus nerve, etc.);
   • cerebral (due to acute and chronic cerebrovascular accident);
   • hypovolemic (with insufficient intake or excessive loss of fluid from the body);
   • metabolic (during oxygen starvation of the brain due to severe hypoxemia or due to a lack of energy substances due to hypoglycemia).

How does fainting develop?

The following pathological processes underlie various fainting states:

1. An imbalance between the volume of circulating blood and the capacity of the vascular bed due to the inadequacy of the vasomotor mechanisms of a reflex nature (60-70% of cases of fainting). Vasopressor, orthostatic, sinus-carotid, hypovolemic and cough collapse develops according to this mechanism.
2. Heart diseases with insufficient cardiac output (heart defects, myxoma, free thrombus of the left atrium, arrhythmia, conduction system block, asystole). In 15-20% of cases, the occurrence of fainting is associated with manifestations of heart diseases.
3. Neurological and mental diseases (stenosis of extracranial cerebral vessels, hypertensive encephalopathy, hysteria, epilepsy). Approximately 5-10% of fainting spells are caused by these diseases.
4. Metabolic disorders (hypoglycemia, hyperventilation, etc.) - the remaining 5-10%.

Elderly and old people are more likely to experience:

1. orthostatic hypotension (a high risk of its development is indicated by a drop in systolic blood pressure by 20 mm Hg or more when standing up abruptly);
2. postprandial hypotension (a decrease in systolic blood pressure during the first hour after eating due to increased blood flow in the gastrointestinal tract and an inadequate response to this by the sympathetic nervous system);
3. carotid sinus syndrome - fainting that occurs when turning sharply or throwing the head back.

How does fainting manifest itself?

Vasopressor syncope is caused by sudden marked dilation of arterioles with a fall in effective cerebral blood flow and systemic arterial pressure against the background of the absence of a compensatory increase in stroke volume and heart rate. The decrease in total peripheral resistance is caused mainly by dilation of peripheral, mainly muscular vessels. In most cases, simple vasopressor syncope develops in apparently healthy people with a labile nervous system.

Fainting can also be caused by insufficient adrenergic innervation tone in organic lesions of the cardiovascular system.

Clinically, vasopressor syncope is manifested by the development of an unconscious state. Loss of consciousness does not occur immediately. Usually, a short prodromal period is observed, which is characterized by dizziness, ringing in the ears, darkening of the eyes, nausea, clouding of consciousness, etc. Paleness of the skin and increased sweating are noted.

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

In the prodromal period, the heart rate is unchanged or slightly increased. At the height of fainting, the pulse is weak and blood pressure is reduced. The heart rate varies depending on the cause of the fainting. As the fainting condition develops, muscle weakness increases, the patient loses balance and consciousness. At the height of fainting, muscle tone is sharply reduced and reflexes are depressed. Breathing is shallow and rapid. Slow waves of high amplitude are recorded on the encephalogram.

The duration of fainting is usually several tens of seconds. In a horizontal position, consciousness is quickly restored and the patient's general condition improves. General weakness, pale skin, increased sweating and nausea persist for some time after fainting. Due to dilation 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 a convulsive syndrome is possible.

Orthostatic syncope is characterized by the development of an unconscious state as a result of a person's sudden transition from a horizontal to a vertical position. Less often, it is caused by a person staying in a vertical position for a long time. The immediate mechanism for the development of this type of acute vascular insufficiency is the deposition of blood in the vessels of the lower part of the body and, as a consequence, a decrease in venous return to the heart.

Orthostatic syncope often develops after prolonged bed rest, while taking adrenolytic, diuretic drugs, etc. Normally, the transition from a horizontal to a 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 restoration of blood pressure is normally associated with compensatory vasoconstriction caused by the activation of mechanoreceptors of the aortic arch and carotid sinuses.

This adaptive mechanism does not work when the sympathetic part of the autonomic nervous system is damaged, as well as when the functions of its peripheral parts are switched off. Compensatory vasoconstriction does not develop, which leads to accumulation of blood in the venous network of the systemic circulation, a decrease in venous return, a decrease in arterial pressure and a disruption of the blood supply to the brain.

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

Unlike vasopressor syncope, it develops instantly, without a prodromal period or precursors. Bradycardia is not observed. There are also no signs of increased blood filling of the skin vessels. After transition to a horizontal state, consciousness is quickly restored.

Carotid sinus syncope develops due to increased sensitivity of the carotid sinus to mechanical stimuli. Normally, the carotid sinus is involved in regulating heart rate and systemic arterial pressure.

In the area of the bifurcation of the common carotid artery there are numerous nerve endings that form the sinus nerve of Hering. Its fibers as part of the glossopharyngeal nerve go to the vasomotor center. When the mechanoreceptors of the carotid sinus are irritated, the vessels of the skin, muscles and abdominal organs dilate, and the heart rate slows.

The total volume of circulating blood does not decrease, but is only redistributed from the arterial bed to the venous bed. In a healthy person, the decrease in arterial pressure with irritation of the carotid sinus is 10-40 mm Hg. With increased sensitivity of the carotid sinus, even slight irritation leads to a significant decrease in arterial pressure and pronounced bradycardia. Short-term loss of consciousness often develops. The development of a prolonged fainting state with convulsive syndrome is possible.

The diagnosis of carotid sinus syncope is made if mechanical irritation of the carotid sinus produces a characteristic clinical picture.

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

Depending on the type of hemodynamic disorders, there are two main forms of carotid sinus syncope: cardioinhibitory and depressor. The cardioinhibitory form is more common, which is manifested by pronounced bradycardia, complete atrioventricular block, or short-term extrasystole. The depressor form is much less common and depends on the dilation of peripheral vessels.

Fainting states of cardiac origin are most often caused by ischemic heart disease, heart defects, vascular stenosis, etc. A significant proportion of "cardiac" fainting is caused by various types of cardiac rhythm and conduction disorders (Adams-Stokes-Morgagni syndrome).

It is generally accepted that cerebral blood flow is maintained at a sufficient level with significant fluctuations in heart rate (from 40 to 180 per minute). Associated cardiac pathology leads to deterioration in tolerance of cardiac arrhythmias and development of disturbances of consciousness associated with inadequate blood supply to the brain. As a rule, there is extensive symptomatology of heart disease (shortness of breath, cyanosis, angina, pulmonary congestion, etc.).

The connection between fainting spells and disturbances in heart rhythm and cardiac conduction is determined using electrocardiographic examination.

Loss of consciousness may be caused by short-term attacks of fibrillation in the syndrome of delayed repolarization. In this syndrome, with an increase in heart rate, there is no reduction in the duration of the QT interval. On the contrary, it becomes extended. Outside of an attack, the extended QT interval is the only manifestation of the disease.

Other causes of fainting. In addition to the described types of fainting, one should remember the possibility of impaired consciousness due to acute cerebrovascular accidents, epilepsy, hypoglycemia, hyperventilation, acute hypovolemia, pulmonary hypertension, etc.

First aid for fainting

Fainting is not an independent nosological entity, it is a manifestation of a large group of functional disorders and organic diseases. Therefore, in order to stop them, both symptomatic therapy and special treatment of the underlying disease are carried out. Patients with simple fainting (vasopressor, postural) usually do not need intensive care and hospitalization.

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

1. Place the patient in a lying position with legs raised.
2. Provide access to fresh air (open a window, unbutton your collar, loosen tight clothing).
3. Thermal irritation of the body's skin receptors (wiping or spraying with cold water).
4. Bring a cotton ball with ammonia to your nose.
5. If these measures are ineffective, subcutaneous administration of 1 ml of a 10% caffeine solution and/or 2 ml of cordiamine is indicated.
6. If bradycardia is present, 0.3-1 ml of 0.1% atropine solution can be administered subcutaneously.

If these measures do not help and the patient does not regain consciousness, one should think about the presence of a serious disease. To exclude acute cardiac pathology, one should perform an electrocardiogram. If an organic disease is suspected, the patient should be hospitalized for examination.

In case of transient asystole caused by intracardiac blockades, sick sinus syndrome, the issue of installing a permanent pacemaker should be resolved. If the cause of fainting is paroxysmal tachyarrhythmia, drug or electroimpulse therapy is carried out according to general principles. If the causes of fainting are severe obstructive heart diseases, stenosis of extracranial vessels or intraatrial thrombosis, then cardiac surgery is indicated.

When caring for geriatric patients with a tendency to faint, the following points should be kept in mind:

• It is essential to find out the conditions under which fainting occurs;
• Fainting can be caused by taking the following medications: antidepressants, phenothiazides (sleeping pills), reserpine or clonidine (as well as other drugs with sympatholytic activity), diuretics, vasodilators (for example, nitrates, alcohol);
• control the frequency of the patient’s meals: small portions 5-6 times a day;
• In order to determine the risk of fainting, blood pressure and pulse should be monitored before and after meals (a high risk of postprandial hypotension is indicated by a decrease in systolic blood pressure by 10 mm Hg or more), as well as before and after (in the first and third minutes) standing up. In this case, the absence of changes in heart rate may be a sign of a violation of baroreflex mechanisms, and an excessively high increase in heart rate may indicate fluid loss;
• periodically (1-2 times a week) measure water balance and, if necessary, increase the intake of table salt (if there is a violation of the kidneys' ability to retain sodium);
• in case of carotid sinus syndrome, beta-blockers, calcium antagonists, digitalis and methyldopa preparations are taken with caution;
• in case of orthostatic hypotension, it is necessary to elevate the head of the bed, teach the patient the rules of gradual standing up and wearing elastic stockings;
• to prevent the occurrence of hemodynamic conditions for fainting, patients need to avoid cases of a sharp increase in intra-abdominal pressure during straining - carry out timely prevention of constipation, effective treatment of prostate adenoma and cough;
• In rooms where there are people with pronounced signs of aging, it is necessary to maintain an intensive ventilation regime, patients are recommended to perform breathing exercises that promote blood oxygenation. Treatment of patients with a high risk of fainting should be aimed at eliminating the causative disease and adaptation to age-related changes.

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