Fainting is a sudden loss of consciousness of a non-epileptic nature due to a diffuse decrease in brain metabolism caused by a short-term decrease in cerebral blood flow. Nearly a third of people experience fainting at some time in their lives, but only in a small number of cases is fainting a manifestation of a serious, life-threatening illness.
The cause of fainting can be a variety of conditions, but it is possible to establish a specific cause in only half of the patients.
Vasodepressor (vasovagal) syncope is the most common type of syncope in adolescence and young adulthood. Provoking factors are not often emotional reactions (pain, fear, the sight of blood, etc.), being in a cramped stuffy room. A few seconds before the loss of consciousness, nausea or lightheadedness, profuse sweating, a feeling of warmth spreading through the body, and palpitations traditionally appear. After regaining consciousness, patients often complain of general weakness, nausea, discomfort in the abdominal cavity. With age, syncope often regresses.
Situational syncope occurs under certain conditions. Nicturic syncope traditionally develops in older men with nocturnal urination. In their origin, the orthostatic component, the expansion of skin vessels in a warm bed, but mainly the reflex activation of the vagus nerve and inhibition of the sympathetic system at the time of urination, is important.
In fainting associated with defecation, straining also plays an important role, causing an increase in intrathoracic pressure and a decrease in venous return. A similar mechanism underlies cough syncope that occurs in patients with chronic obstructive pulmonary disease with a paroxysm of prolonged cough.
Carotid sinus hyperresponsiveness is one of the common causes of syncope in older men with hypertension and carotid atherosclerosis. Fainting is provoked by wearing clothes with a tight collar or turning the head. The mechanism of syncope is associated with the activation of the vagus nerve.
Orthostatic hypotension is responsible for approximately 10% of syncope cases. It is caused by a violation of postural cardiovascular reflexes associated with damage to the trunk, spinal cord (above the upper thoracic region), sympathectomy, polyneuropathies involving autonomic fibers. Orthostatic hypotension is caused by antihypertensives, phenathiazines, tricyclic antidepressants, levodopa products, and dopamine agonists.
Heart disease is responsible for approximately 25% of syncope cases. This is the most dangerous variant of fainting, which should be excluded in the first place. Very often, fainting, especially in the elderly, appears due to a violation of the heart rhythm (syndrome of weakness of the sinus node, blockade of the conduction system of the heart, atrial or ventricular tachyarrhythmias). With complete atrioventricular blockade, a very rapid loss of consciousness occurs, the pulse is not palpable, with sick sinus syndrome, bradycardia is detected. Unlike other variants, cardiogenic syncope does not always appear in an upright position. Syncope that occurs against the background of ventricular tachy- or bradyarrhythmias is characterized by the absence of prodromal symptoms. Patients with vasodepressor syncope often complain of palpitations before fainting, than patients with tachyarrhythmia, especially ventricular. Unlike vasodepressor syncope, loss of consciousness in cardiogenic syncope is so sudden that the patient may be injured. Cardiogenic syncope can occur with heart defects, hypertrophic cardiomyopathy.
Neurological causes account for no more than 5% of syncope cases. Occasionally, the cause of fainting is vertebrobasilar insufficiency, loss of consciousness is traditionally accompanied by focal stem symptoms (double vision, dizziness, ataxia, nystagmus, dysarthria, facial numbness) or hemianopsia. With stenosing lesions of the vertebral arteries, syncope can be provoked by prolonged hyperextension of the head. An even rarer underlying cause of syncope is subclavian steal syndrome, caused by occlusion of one of the subclavian arteries proximal to the origin of the vertebral artery. Blood flow into the distal subclavian artery by retrograde blood flow through the vertebral artery on the same side and robs the basilar and opposite vertebral arteries, causing transient hemodynamic insufficiency throughout the vertebrobasilar basin. Unilateral carotid stenosis or occlusion does not traditionally cause syncope, but it is extremely rare for severe bilateral carotid stenosis to cause syncope, especially when systemic blood pressure decreases. A sudden increase in intracranial pressure due to acute hydrocephalus reduces cerebral blood flow in colloid cysts, tumors, and intracerebral hemorrhages.
Occasionally, fainting is associated with a lack of oxygen (with acute hypoxia, anemia, hemoglobinopathies, carbon monoxide poisoning), with hypoglycemia.
Fainting is often preceded by dizziness, veil before the eyes, blurred vision, general weakness, tinnitus, nausea, paresthesia in the distal extremities. On examination, pallor, profuse sweating, low blood pressure, weak rapid or slow (depending on the syncope mechanism) pulse are traditionally detected. There is no pause in breathing. Muscle tone is reduced. Not infrequently there are single short-term myoclonic twitches in the limbs (convulsive syncope). Urinary incontinence is not common. In most cases, fainting is associated with a certain position of the body: consciousness, as a rule, is lost in an upright position, but quickly, over several seconds, returns to a horizontal one, as soon as blood flow to the brain increases. But sometimes consciousness is restored more slowly, for several minutes. In contrast to an epileptic seizure, syncope develops more gradually and the fall traditionally occurs more slowly (the patient “sinks” rather than “falls” on the floor), so the person has time to protect himself from injury. After a faint, confusion is possible, but unlike an epileptic seizure, it is always short-lived.
Fainting usually lasts no longer than a few minutes. For the first time, fainting may be a manifestation of life-threatening diseases – severe cardiac arrhythmias, subarachnoid hemorrhage, gastrointestinal bleeding, pulmonary embolism, myocardial infarction, dissecting aortic aneurysm. Inspection during an attack (BP, heart rhythm) may be of diagnostic value. Orthostatic test and examination of the heart are important. During a neurological examination, it is important to pay attention to a focal lesion (stroke), signs of polyneuropathy, extrapyramidal disorders. Reproduction of symptoms is likely with hyperventilation or carotid sinus massage, but is consequently dangerous and should only be done in a state of readiness for resuscitation. A comprehensive examination should include electrocardiography.
With vasodepressor syncope in young people, there is often no need for special treatment. It is enough to relieve the patient of the fear of an attack, explaining in detail the nature of the disease to him, and increase salt intake. Sometimes beta-blockers also help – propranolol (anaprilin), bellataminal, ephedrine, disopyramide (ritmilen), blocking the activity of the vagus nerve, serotonin reuptake inhibitors (fluoxetine or sertraline), acting on central mechanisms.