Vasovagal syncope is episodes of short–term loss of consciousness caused by reflex vasodilation and slowing of the heart rate as a result of increased excitability of the vagus nerve. Syncope is usually preceded by prodromal signs (dizziness, rapid heartbeat, pallor), weakness is present during the recovery period. Fainting is accompanied by falls, prone to relapse. Diagnostic measures include clinical examination, orthostatic tests, ECG monitoring. Treatment is carried out by non-drug, pharmacological, invasive methods.
ICD 10
R55 Fainting [syncope] and collapse
General information
Vasovagal (simple, vasomotor, vasodepressor) fainting is quite common in the population – they are diagnosed in 25% of the population. At least one episode of syncopal condition in the anamnesis is noted by 42% of women and 32% of men who have reached the age of 60. Children suffer relatively rarely, and the frequency of pathology increases significantly in adolescents. Most cases are registered before the age of 40, reflex syncope is extremely rare in the elderly. Vasovagal type fainting is more typical for women. According to some studies, African Americans may have a lower risk of developing pathology compared to representatives of the Caucasian race.
Causes
Syncopal state has a reflex genesis, due to the effect on the body of various external stimuli that trigger pathological vegetative reactions. As the most frequent type of neurogenic syncope, the vasovagal variant usually occurs in situations of severe psychoemotional stress. Fainting is provoked by sharp pain or its expectation (during dental treatment, injections, diagnostic procedures), other fears. A similar reaction occurs at the sight of blood – when it is taken for analysis, donation, medical students on operations.
In addition to the influence of emotional factors, the development of vasovagal syncope is preceded by orthostatic load. Prolonged standing or sitting, especially in crowded stuffy rooms and during fasting (“church fainting”), becomes a significant trigger of pathology. The predisposing factors are dehydration (intense physical activity, vomiting, menstrual blood loss), fatigue, lack of sleep. The occurrence of syncope is facilitated by an increase in the ambient temperature (in a sauna, hot tub), alcohol intake, antihypertensive drugs.
Vasovagal syncope develops against the background of an individual predisposition to a certain type of vegetative reactions. The role of hereditary factors is confirmed by various works, including the study of mono- and dizygotic twins. Describing recurrent syncope in patients and their relatives, the authors indicate a positive family history in 19-90% of cases. For vasovagal syncope, complex inheritance involving many genes is assumed, the influence of which is superimposed on environmental factors, but significant mutations have not yet been identified.
Pathogenesis
The exact mechanism of vasovagal syncope is not completely clear. Presumably, they occur due to reflex changes in vascular tone and/ or heart rate. Excessive deposition of blood in the system of the lower extremities, abdomen and pelvis leads to a sudden decrease in preload. Compensatory sympathetic stimulation increases the strength of myocardial contractions and provokes irritation of the mechanoreceptors of the ventricular wall, triggering the Bezold-Yarish cardioinhibitory reflex with increased vagal influence.
Caused by a lack of sympathetic tone, peripheral vasodilation and bradycardia provoke temporary hypotension, which is accompanied by a decrease in cerebral blood flow and loss of consciousness. Other putative mechanisms of vasomotor syncope include the influence of biological mediators and hormones – serotonin, vasopressin, endorphin, adrenaline. Patients with recurrent syncope have various phenotypic variants of catecholamine regulation of vascular tone.
Some researchers consider simple fainting not a pathology, but a useful reaction to strong stressful influences aimed at weakening potentially dangerous sympathetic stimulation. The slowing of the heart rate caused by the vasovagal reflex reduces the oxygen consumption of the myocardium in life-threatening conditions. Therefore, vasomotor syncope is proposed to be considered as an evolutionarily formed defense mechanism, which in humans, due to its upright posture and brain volume, takes a more pronounced form.
Classification
Simple syncopations are part of the structure of neurocardiogenic syncope. Taking into account the etiology, they are divided into two variants – typical (emotional, orthostatic) and atypical. The latter are characterized by the absence of triggers and prodromal phenomena, therefore they are sometimes called “malignant”. According to hemodynamic parameters, vasomotor syncope is classified as follows:
- Mixed (type 1). The heart rate decreases by more than 10% of the initial one, reaching 40 beats / min or less (but no longer than 10 seconds) without asystole or with cardiac arrest for up to 3 seconds. Bradycardia is preceded by a drop in blood pressure.
- Cardioinhibitory (type 2). The minimum heart rate remains below 40 beats per minute for more than 10 seconds. There is no asystole (type 2A) or it lasts more than 3 seconds (type 2B). In the second case, hypotension occurs simultaneously with a decrease in heart rate.
- Vasodepressors (type 3). Loss of consciousness is accompanied by arterial hypotension without pronounced bradycardia. The drop in heart rate is less than 1/10 of the maximum indicator.
Symptoms
Activation of the autonomic nervous system and hypoperfusion of brain tissues are usually accompanied by presyncopal phenomena. Prodromal symptoms are experienced by two-thirds of people with vasovagal episodes. They are represented by dizziness, noise in the ears, flashing “flies” in front of the eyes. Patients turn pale, note palpitations, nausea, a feeling of anxiety. The symptoms preceding the syncopal episode are short-lived (on average about 2.5 minutes), pass quickly in a horizontal position.
Patients often do not remember the very moment of loss of consciousness and falling. Amnesia is characteristic of 20% of young and 50% of elderly people. During fainting, focal neurological symptoms may occur that do not develop into a permanent deficit. Syncopal condition is usually short-term (30-60 seconds), characterized by arterial hypotension, thready pulse, bradycardia. With prolonged cerebral hypoperfusion, myoclonic seizures may occur.
Each case of vasovagal syncope has an individual set of predisposing factors and clinical signs. Up to a third of cases are accompanied by atypical manifestations with an absent or very short prodromal period. A sudden syncopal episode can last longer than usual – up to 4-5 minutes. The recovery period is characterized by severe fatigue lasting up to several hours. Headache, dizziness, dry mouth are possible. After the attack, the skin is warm and moist.
Vasovagal syncope is especially susceptible to adolescents and young people of high stature with an asthenic physique, poorly developed musculature. Upon detailed examination, they reveal other signs of autonomic dysfunction, anxiety disorders. Many clinical manifestations correspond to the syndromes of postural orthostatic tachycardia, chronic fatigue. Patients with reflex syncope may suffer from functional diseases of the gastrointestinal tract, neurocirculatory dystonia, Raynaud’s phenomenon and migraine.
Complications
Fainting at altitude, when working with moving mechanisms, near water or fire creates a risk of serious injury up to a fatal outcome. The probability of damage increases in old age, especially with concomitant diseases. Syncopal states in representatives of certain professions (drivers, machinists, pilots) pose a danger not only to the patients themselves, but also to others. Special attention should be paid to atypical cases with sudden prolonged loss of consciousness, often recurrent syncope with asystolic pauses.
Diagnostics
In the diagnosis of vasovagal syncope, great importance is given to a clinical examination with an analysis of complaints and anamnestic information. Important criteria include predisposing situations, prodromal phenomena, features of the recovery period, physical signs. When diagnostic difficulties arise, the following methods are used to confirm reflex vasomotor reactions:
- Active orthostatic Tulesis test. The patient’s blood pressure is measured first in the supine position, and then standing (5 and 10 minutes each). The diagnostic criteria for a positive test are the development of syncope, a decrease in systolic pressure by 30 mm Hg from the baseline level, accompanied by clinical symptoms.
- A test with passive orthostasis (tilt test). It is recognized as the “gold standard” for the diagnosis of vasovagal syncope. Tilt test is carried out by passively transferring the patient from a horizontal position to a vertical position with the table tilted by 60-80 ° with continuous monitoring of pulse, blood pressure, ECG. To identify a tendency to bradycardia, pharmacological provocative tests (with isadrin, nitroglycerin, clomipramine) can be performed.
- Long-term ECG monitoring. Round-the-clock ECG monitoring is used to verify the cardioinhibitory mechanism of transient loss of consciousness. The implantable loop cardioregistrator is considered to be the most effective, which makes it possible to identify the identity of the rhythmographic features of the initial and subsequent syncopal episodes.
Differential diagnosis is carried out with orthostatic syncope, carotid sinus syndrome. To exclude cardiac causes, a standard ECG, echocardiography, and a physical exercise test are used. With convulsions and prolonged unconscious episodes, it is recommended to undergo a neurophysiological examination. Vasovagal syncope should be distinguished from non–syncopal conditions – carotid TIA, epileptic seizures, drop attacks and other pathologies manifested by loss of consciousness and postural tone.
Treatment
Conservative therapy
Rare vasovagal syncope does not need specific treatment. Frequent fainting episodes with a high risk of adverse events and comorbidity require complex therapy, which involves influencing the known pathogenetic aspects of the vasovagal reflex in order to prevent relapses of fainting and related injuries. The main role is given to the following conservative methods:
- Educational work. Patients are informed about the causes of fainting, its benign nature and possible risks, emphasizing the importance of eliminating provoking situations. They are trained to recognize presyncopal signs in order to take preventive measures in time.
- Optimization of the diet. Studies have proven the positive effect of increasing the daily intake of liquid (up to 2-2.5 liters), table salt (up to 10 g). Dietary recommendations are aimed at increasing the content of extracellular sodium, BCC and venous return.
- Physical counter-maneuvers. Counteraction measures taken in the prodromal period help to stop the impending fainting: crossing the legs with muscle tension, pulling the clasped hands to the sides, squeezing the hand expander. The timely transition to a horizontal position, the use of compression knitwear allows you to prevent a syncopal state.
- Tilt training. Regular orthostatic training significantly reduces the symptoms of vasomotor syncope. The frequency of relapses can be reduced by performing exercises with inclined positioning at home, but passive orthostasis under the supervision of a doctor is recognized as a more effective strategy.
- Pharmacotherapy. In the treatment of vasovagal syncope, some alpha-adrenomimetics (midodrine), serotonin reuptake inhibitors (paroxetine), mineralocorticoids (fludrocortisone) demonstrated the best results. An important aspect of preventing relapses, especially in the elderly, is the abolition of antihypertensive drugs.
Nonspecific drug correction involves the appointment of B vitamins, nootropics, vasoactive agents. As methods of vegetative stabilization, patients are recommended to regularly exercise with moderate loads, take a contrast shower, and swim. It is possible to increase stress resistance by conducting cognitive behavioral psychotherapy, auto-training, respiratory gymnastics.
Surgical treatment
If conservative therapy of cardioinhibitory syncope is ineffective, electrocardiostimulation can be performed. Pacemaker therapy is recommended for older patients with frequently recurrent syncope, accompanied by pronounced prodromal phenomena, asystole, and an increased risk of injury. Studies have shown that after implantation of a pacemaker, the number of relapses over the next two years is halved.
Experimental treatment
Taking into account the risk of recurrent vasovagal syncope, the possibilities of existing therapy are quite limited, which necessitates the search for new methods. As a promising alternative, it is proposed to use endocardial catheter ablation of the ganglion plexuses of the left atrium, which can prevent recurrence of refractory syncope in the long term. For timely relief of symptoms, an implantable drug pump can be used, activated by the patient when harbingers appear.
Prognosis and prevention
Rare vasovagal syncope has a benign course, sudden and frequently recurring episodes can have a negative impact on the quality of life, limiting physical activity and career choice. In elderly patients, taking into account the high risk of injury and comorbidity, the prognosis is more serious. Primary prevention consists in eliminating known triggers, maintaining a healthy lifestyle, and increasing emotional stability. It is possible to prevent relapses with active timely therapeutic correction.