FAINTING

FALL (syn: syncope) - 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. Fainting occurs in one or another period of life in almost a third of people, but only a small number of cases of syncope is a manifestation of a serious disease that threatens life.

Fainting is often preceded by dizziness , a veil before the eyes, blurred vision, general weakness, tinnitus, nausea , paresthesia in the distal parts of the limbs. When examined, usually show pallor, profuse sweating, low blood pressure, weak rapidity or slow (depending on the mechanism of syncope) pulse . No breathing stops. Muscle tone is reduced. Often there are single short-term myoclonic twitchings in the extremities (convulsive syncope). Urinary incontinence is rare. In most cases, syncope is associated with a particular position of the body: consciousness, as a rule, is lost in the vertical position, but quickly, within a few seconds, returns to horizontal as soon as the blood flow to the brain increases. But sometimes the consciousness recovers more slowly, within a few minutes. Unlike the epileptic fit, syncope develops more gradually and the fall usually occurs more slowly (the patient "settles down" rather than "falls" on the floor), so a person manages to protect himself from damage. After fainting, confusion is possible, but unlike epileptic seizures, it is always short-lived.

The cause of syncope can be a variety of conditions, but to establish a specific cause is possible only in half of patients.

Vaso-depressor (vasovagal) syncope is the most frequent variant of syncope in adolescence and young age. Provoking factors are often emotional reactions (pain, fear, type of blood, etc.), stay in a close stuffy room. A few seconds before the loss of consciousness, usually there is nausea or lightheadedness, profuse sweating, a feeling of warmth, spilling over the body, palpitations. After the restoration of consciousness, patients often complain of general weakness, nausea, discomfort in the abdominal cavity. With age, fainting often regress.

Situational fainting occurs in certain conditions. Nictic syncope usually develops in older men with nocturnal urination. In their origin, the orthostatic component, the expansion of the cutaneous vessels in the warm bed, but mainly the reflex activation of the vagus nerve and the inhibition of the sympathetic system at the time of urination, are important.

In fainting associated with defecation, an important role is played by straining, which causes an increase in intrathoracic pressure and a decrease in venous return. A similar mechanism underlies the cough fainting that occurs in patients with chronic obstructive pulmonary diseases in the course of paroxysm of prolonged cough.

Hypersensitivity of the carotid sinus is one of the common causes of syncope in elderly men with arterial hypertension and atherosclerosis of the carotid arteries. Fainting provoke wearing a tight collar or turning the head. The mechanism of syncope is associated with the activation of the vagus nerve.

Orthostatic hypotension is the cause of approximately 10% of cases of syncope. It is caused by violation of postural cardiovascular reflexes associated with damage to the trunk, spinal cord (above the upper thoracic department), sympathectomy, polyneuropathies involving vegetative fibers. Orthostatic hypotension is caused by hypotensive drugs, phenatiazines, tricyclic antidepressants, levodopa preparations and dopamine agonists.

Heart diseases cause about 25% of cases of syncope. This is the most dangerous variant of fainting, which should be ruled out first. Very often fainting, especially in elderly individuals, occurs due to a violation of the heart rhythm (syndrome of sinus node weakness, blockade of the conduction system of the heart, atrial or ventricular tachyarrhythmias). With complete atrioventricular blockade, there is a very rapid loss of consciousness, the pulse is not probed, the syndrome of weakness of the sinus node reveals bradycardia . Unlike other options, cardiogenic syncope does not always occur in an upright position. For syncope arising on the background of ventricular tachy- or bradyarrhythmias, there is a lack of prodromal symptoms. At the heartbeat before fainting, patients with vasodepressor syncope complain more often than patients with tachyarrhythmia, especially ventricular fainting. In contrast to vasodepressor loss of consciousness in cardiogenic syncope is so sudden that the patient can get injured. Cardiogenic syncope may occur with heart defects, hypertrophic cardiomyopathy.

Neurological causes account for no more than 5% of cases of syncope. Occasionally, the cause of syncope is vertebrobasilar insufficiency, loss of consciousness is usually accompanied by focal stem symptoms (double vision, dizziness, ataxia, nystagmus, dysarthria, numbness of the face) or hemianopsia. With stenosing lesions of vertebral arteries, syncope can be triggered by prolonged overexpansion of the head. An even more rare cause of syncope is the syndrome of subclavian stealing, caused by the occlusion of one of the subclavian arteries proximal to the vertebral artery spasm. The blood flow to the distal part of the subclavian artery by the retrograde blood flow along the vertebral artery on the same side and steals the basilar and opposite vertebral arteries, causing transient hemodynamic insufficiency throughout the vertebrobasilar basin. Unilateral stenosis or occlusion of the carotid artery usually does not cause fainting, but extremely rarely a bilateral bilateral stenosis of the carotid arteries can cause syncope, especially against a background of lowering systemic blood pressure. 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.

The diagnosis . Fainting usually lasts no longer than a few minutes. For the first time, syncope may be a manifestation of life-threatening diseases - severe cardiac arrhythmias, subarachnoid hemorrhage, gastrointestinal bleeding, pulmonary artery embolism, myocardial infarction, exfoliating aortic aneurysm. Examination during an attack (BP, heart rhythm) can have diagnostic value. An orthostatic test and examination of the heart are important. When neurological examination is important to pay attention to focal damage (stroke), signs of polyneuropathy , extrapyramidal disorders. Reproduction of symptoms is possible with the help of hyperventilation or massage of the carotid sinus, but the latter is dangerous and should be done only in a state of readiness for resuscitation. A comprehensive examination should include electrocardiography.

Treatment . When vasodepressor syncope in young people often there is no need for special treatment. It is enough to relieve the patient of fear of an attack, explaining in detail the nature of the disease, and to increase salt intake. Sometimes beta blockers, such as propranolol (anaprilin), bellataminal, ephedrine, disopyramide (rhythmelene), blocking vagus nerve activity, serotonin reuptake inhibitors (fluoxetine or sertraline) acting on the central mechanisms also help.

The prognosis is usually good, if there is no serious heart disease.