Syncope is a temporary loss of consciousness caused by transient general hypoperfusion of the brain. Syncope clinic consists of precursors (lack of air, “nausea”, fog or “flies” in front of the eyes, dizziness), a period of unconsciousness and a recovery stage in which weakness, hypotension, dizziness persists. Diagnosis of syncopal conditions is based on tilt test data, clinical and biochemical analyses, ECG, EEG, ultrasound of extracranial vessels. In relation to patients with fainting, as a rule, differentiated therapy is 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
Syncope (syncopal state, syncope) was previously regarded as a transient loss of consciousness with loss of postural tone. Indeed, it is the disorder of muscle tone that leads to a person fainting. However, many other conditions fit this definition: various types of epiprimes, hypoglycemia, TBI, TIA, acute alcohol intoxication, etc. Therefore, in 2009, another definition was adopted, interpreting fainting 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 life. As a rule, the first episode of syncope occurs during the period of 10-30 years, with a peak at puberty. Population studies indicate that the frequency of syncopal states increases with age. In 35% of patients, repeated fainting occurs within three years after the first one.
Global transient cerebral ischemia, which causes syncope, 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 have in diagnosing the causes and choosing therapeutic tactics for syncope. The above highlights the interdisciplinary relevance of this problem, which requires the participation of specialists in the field of neurology, cardiology, traumatology.
Causes
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 causing a sudden decrease in the volume of blood entering the cerebral vessels may 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 feeding the brain (with atherosclerosis, occlusion of the carotid arteries, vascular spasm), dilation vessels, rapid change in body position (so-called orthostatic collapse).
The change in tone (dilation or spasm) of the vessels feeding the brain is often of a neuroreflective nature and is the leading cause of syncope. Such a fainting can provoke a strong psychoemotional experience, pain, irritation of the carotid sinus (with coughing, swallowing, sneezing) and the vagus nerve (with otoscopy, gastrocardial syndrome), an attack of acute cholecystitis or renal colic, trigeminal neuralgia, neuralgia of the lingopharyngeal nerve, an attack of vegetative-vascular dystonia, an overdose of some 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 BV. Syncope of this genesis can be observed in blood diseases (iron deficiency anemia, sickle cell anemia), carbon monoxide poisoning, respiratory diseases (bronchial asthma, obstructive bronchitis). A decrease in the CO2 content in the blood can also cause fainting, which is often observed with hyperventilation of the lungs. According to some reports, about 41% is due to fainting, the etiology of which cannot be established.
Classification
Attempts to systematize various types of syncope have led to the creation of several classifications. Most of them are based on the etiopathogenetic principle. The group of neurogenic syncope includes vasovagal conditions, which are based on a sharp vasodilation, and irritative (carotid sinus syndrome, syncope with lingopharyngeal and trigeminal neuralgia). Orthostatic syncope includes fainting due to vegetative insufficiency, a decrease in BV, and drug-induced orthostatic hypotension. Cardiogenic syncope occurs due to cardiovascular diseases: hypertrophic cardiomyopathy, pulmonary artery stenosis, aortic stenosis, pulmonary hypertension, atrial myxoma, myocardial infarction, valvular heart defects. Arrhythmogenic syncope is provoked by the presence of arrhythmia (AV block, tachycardia, SSS), malfunction of the pacemaker, side effect of antiarrhythmics. Cerebrovascular (dyscirculatory) syncope is also isolated, associated with the pathology of blood vessels supplying cerebral structures. Fainting, the trigger factor of which could not be established, is classified as atypical.
Syncope symptoms
The maximum duration of the syncopal state does not exceed 30 minutes, in most cases, fainting lasts no more than 2-3 minutes. Despite this, there are clearly 3 stages during fainting: the presyncopal state (the period of precursors), the actual fainting and the postsyncopal state (the recovery period). The clinic and duration of each stage are highly variable and depend on the pathogenetic mechanisms underlying syncope.
The presyncopal period lasts several seconds or minutes. It is described by patients as a feeling of nausea, sharp weakness, dizziness, lack of air, blurred vision. Nausea, flashing dots in front of the eyes, ringing in the ears is possible. If a person manages to sit down with his head down, or lie down, then loss of consciousness may not occur. Otherwise, the increase of these manifestations ends in loss of consciousness and fall. With the slow development of fainting, the patient, falling, is held by the surrounding objects, which allows him to avoid injury. A rapidly developing syncopal condition can lead to serious consequences: TBI, fracture, spinal injury, etc.
During the period of actual fainting, there is a loss of consciousness of varying depth, accompanied by shallow breathing, complete muscle relaxation. When examining the patient during the actual fainting period, mydriasis and a delayed reaction of the pupils to light, weak pulse filling, arterial hypotension are observed. Tendon reflexes are preserved. Deep disorder of consciousness in fainting with severe cerebral hypoxia may occur with the occurrence of short-term seizures and involuntary urination. But such a single syncopal paroxysm is not a reason for diagnosing epilepsy.
The post-syncopal period of syncope usually lasts no more than a few minutes, but it can last 1-2 hours. There is some weakness and uncertainty of movements, dizziness, low blood pressure and pallor remain. Possible dry mouth, hyperhidrosis. It is characteristic that patients remember well everything that happened before the moment of loss of consciousness. This feature makes it possible to exclude TBI, for which the presence of retrograde amnesia is typical. The absence of neurological deficit and general cerebral symptoms allows to differentiate syncope from ACVA.
Symptoms of certain types of fainting
Vasovagal syncope is the most common type of syncopal condition. Its pathogenetic mechanism consists in a sharp peripheral vasodilation. The trigger of an attack can be prolonged standing, staying in a stuffy place, overheating (in a bath, on the beach), excessive emotional reaction, pain impulse, etc. The vasovagal syncopal state develops only in an upright state. If the patient manages to lie down or sit down, get out of a stuffy or hot room, then fainting may end at the presyncopal stage. The vasovagal type of syncope is characterized by pronounced stages. The first stage lasts up to 3 minutes, during which patients have time to inform others that they are “ill”. The stage of actual fainting lasts 1-2 minutes, accompanied by hyperhidrosis, pallor, muscle hypotension, a drop in blood pressure with a threadlike pulse at normal heart rate. In the post-syncopal stage (from 5 minutes to 1 hour), weakness comes to the fore.
Cerebrovascular syncope often occurs with spinal pathology in the cervical region (spondyloarthrosis, osteochondrosis, spondylosis). The pathognomonic trigger of this type of fainting is a sharp turn of the head. The compression of the vertebral artery that occurs in this case leads to sudden cerebral ischemia, resulting in loss of consciousness. At the presyncopal stage, photopsias, tinnitus, and sometimes intense cephalgia are possible. Actually, fainting is characterized by a sharp weakening of postural tone, which persists in the postsyncopal stage.
Irritative syncope 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 of the cardia, peptic ulcer of the 12th intestine, hyperkinesia of the biliary tract, and other diseases accompanied by the formation of abnormal viscero-visceral reflexes. Each type of irritative fainting has its own trigger, for example, a specific pain attack, swallowing, gastroscopy. This type of syncopal state is characterized by a short, only a few seconds, period of precursors. Consciousness turns off for 1-2 minutes . The post-syncopal period is often absent. As a rule, repeated stereotypical fainting is noted.
Cardio- and arrhythmogenic syncope is 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. The features are: the occurrence regardless of the person’s position, the presence of symptoms of cardiogenic collapse, a large depth of loss of consciousness, repetition of syncopal paroxysm when the patient tries to get up after the first fainting. Syncopal conditions included in the clinic of the Morgagni–Edems–Stokes syndrome are characterized by the absence of precursors, the inability to determine the pulse and heartbeat, pallor reaching cyanosis, the beginning of the restoration 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 hypotonic patients, persons with autonomic dysfunction, elderly and debilitated patients. Usually, such patients indicate repeated cases of dizziness or “blurring” with a sharp change in body position. Often, orthostatic syncope is not a pathological condition and does not require additional treatment.
Diagnostics
A thorough and consistent survey of the patient, aimed at identifying the trigger that provoked the syncope and analyzing the features of the syncopal condition clinic, allows the doctor to determine the type of syncope, adequately determine the need and direction of the diagnostic search for the pathology behind the syncope. At the same time, the priority is to exclude urgent conditions that can manifest as fainting (PE, acute myocardial ischemia, bleeding, etc.). At the second stage, it is established whether syncope is a manifestation of an organic brain disease (cerebral vascular aneurysms, intracerebral tumors, 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, psychiatrist, etc. narrow specialists.
From laboratory methods in the diagnosis of the genesis of syncope, a general analysis of urine and blood, a study of the gas composition of blood, determination of blood sugar, glucose tolerance test, biochemical blood analysis help. The examination plan for patients with syncopal conditions usually includes: ECG, EEG, REG, Echo-EG, ultrasound of extracranial vessels. If the cardiogenic nature of syncope is suspected, an ultrasound of the heart, phonocardiography, daily ECG monitoring, and stress tests are additionally prescribed. If organic brain damage is assumed, then MSCT or MRI of the brain, MRA, duplex scanning or transcranial ultrasound, radiography of the spine in the cervical region are performed.
Tilt-test, which allows to determine the mechanism of syncope occurrence, has found wide application in the diagnosis of syncopal states of uncertain genesis.
First aid
The creation of conditions conducive to better oxygenation of the brain is paramount. To do this, the patient is given a horizontal position, the tie is loosened, the shirt collar is unbuttoned, and fresh air is provided. Splashing cold water into the patient’s face and bringing ammonia to the nose, they try to cause reflex excitation of the vascular and respiratory centers. In severe syncope with a significant drop in blood pressure, if the above actions have not been successful, the introduction of sympathicotonics (ephedrine, phenylephrine) is indicated. Antiarrhythmics are recommended for arrhythmia, atropine administration and indirect heart massage are recommended for cardiac arrest.
Syncope treatment
Therapeutic tactics in patients with syncope are divided into undifferentiated and differentiated treatment. The undifferentiated approach is common to all types of syncopal states and is especially relevant for the unidentified genesis of syncope. Its main directions are: lowering the threshold of neurovascular excitability, increasing the level of vegetative stability, achieving a state of mental balance. The 1st-line drugs in the treatment of syncope are b-blockers (atenolol, metoprolol). If there are contraindications to the appointment of b-blockers, ephedrine and theophylline are used. The drugs of the 2nd series include vagolytics (disopyramide, scopolamine). It is possible to prescribe vasoconstrictors (ethaphedrine, 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 of syncope is selected according to its type and clinical features. Thus, the therapy of syncope in carotid sinus syndrome is based on the use of sympatho- and cholinolytics. In severe cases, surgical denervation of the sinus is indicated. The main thing in the treatment of syncope associated with trigeminal or pharyngeal neuralgia is the use of anticonvulsants (carbamazepine). Vasovagal syncope is treated mainly within the framework of undifferentiated therapy.
Repetitive orthostatic syncope requires measures aimed at limiting the volume of blood deposited in the lower part of the body when moving to an upright position. To achieve peripheral vasoconstriction, dihydroergotamine and a-adrenomimetics are prescribed, propranolol is used to block vasodilation of peripheral vessels. Patients with cardiogenic syncope are supervised by a cardiologist. If necessary, the issue of implantation of a cardioverter-defibrillator is resolved.
It should be noted that in all cases of syncope, the treatment of patients necessarily includes therapy of concomitant and causal diseases.