by Elsa C. Raimondi

The term syncope derives from the latin "syncope" and this from the Greek "synkopé", and is equivalent to fainting, fainting, lipothymia.

For medicine, it is a frequently observed entity and must be conceived in terms of a relatively abrupt loss of consciousness, of short duration and of spontaneous recovery in the vast majority of cases.

Although various causes can be mentioned in their origin, in general terms they coincide in such a way that the final result is a transitory disturbance of the brain metabolism and more particularly of the activating reticular system. The neurons that make it up require the continuous supply, without breaks, of oxygen, glucose and electrolytes that reach them thanks to adequate cerebral blood flow. This, which in the normal adult is around 54 ml per gram of tissue per minute, is directly proportional to the perfusion pressure and inversely proportional to the vascular resistance. When some factor modifies that relationship and determines that the cerebral flow falls beyond what is allowed by a minimum threshold, clinical manifestations arise; among these is syncope, which is one of the most frequent pictures of medical practice. It can be experienced at any age and in different circumstances, and is referred to by those who suffer from it under various appreciations.

Syncope classification

It is performed considering the pathophysiology of the symptoms and is presented in Table 49-1.

Table 49-1. Pathophysiological classification of syncope.

  1. Cardiovascular (they are the most frequent and depend on insufficient brain irrigation)
    1. Reflexes
      1. Vasovagal or vasodepressant
      2. Carotid sinus
      3. Urination
    2. Due to insufficient vasoconstriction
      1. Orthostatic hypotension
      2. Due to autonomic nervous system affection: Shy-Drager syndrome
    3. Due to decreased cardiac venous return
      1. By "Valsalva effect"
      2. Cough syncope (also reflex)
    4. Due to decreased cardiac output
      1. Mechanical obstructions
        • Aortic stenosis
        • Pulmonary stenosis
        • Chronic pulmonary hypertension
      2. Acute heart failure
        • Myocardial infarction
        • Cardiac tamponade
        • Stokes-Adams crisis
        • Paroxysmal ventricular tachycardia
        • Episodic ventricular fibrillation
        • Sinus bradycardia
  2. Chemicals (due to changes in the composition of the blood)
    1. Hyperventilation syncope
    2. Syncope in hypoglycemia
    3. Syncope due to anemia
    4. Syncope due to hypoxia
  3. Cerebral (the cause lies in the same nervous system; they are, in general, infrequent)
    1. In valve intracranial hypertension
    2. In hypertensive encephalopathy
    3. In vertebral artery stenosis and "theft" syndrome
    4. In fleeting ischemic attacks

Common clinical characters of syncope

Although there may be some different nuances according to the original cause, syncope is manifested by a sign that is essential: loss of consciousness. Sudden by definition, however, in most cases (exceptions will be mentioned in the corresponding section), it requires 5 to 8 seconds to establish; During this brief period prior to fainting, the patient experiences some symptoms that alert him and correspond to feelings of epigastric discomfort, nausea, perspiration, muscle weakness, clouding of the mind or empty head, visual darkening, distancing from things and then falling and total loss of consciousness if the affected person does not take the necessary precautions. In general, all this happens while the individual is standing and can be aborted if he is immediately placed in a horizontal position. In the brief moments when he remains senseless, the subject is pale, sweaty, with a barely perceptible pulse and greatly decreased systolic blood pressure (below 50 mm Hg). Breathing is shallow, muscles remain relaxed, and there is no sphincter incontinence. Once the horizontal position is reached, either voluntarily or through unconsciousness, and in a few seconds, normal brain function is restored and the patient fully and completely recovers his senses. Occasionally, unconsciousness lasts for a few more seconds (up to 20 sec), in which case some seizure movements may appear. Breathing is shallow, muscles remain relaxed, and there is no sphincter incontinence. Once the horizontal position is reached, either voluntarily or through unconsciousness, and in a few seconds, normal brain function is restored and the patient fully and completely recovers his senses. Occasionally, unconsciousness lasts for a few more seconds (up to 20 sec), in which case some seizure movements may appear. Breathing is shallow, muscles remain relaxed, and there is no sphincter incontinence. Once the horizontal position is reached, either voluntarily or through unconsciousness, and in a few seconds, normal brain function is restored and the patient fully and completely recovers his senses. Occasionally, unconsciousness lasts for a few more seconds (up to 20 sec), in which case some seizure movements may appear.

Repetition of the condition in the same patient is quite frequent if the appropriate precautions are not taken and recovery always occurs, except in the instance of cardiac syncope that results in immediate death due to severe asystole.

When the clinical picture is incompletely presented, only with clouding of consciousness, attenuation of the senses and feeling of distance and muscle loosening, without reaching complete unconsciousness, it is often spoken of as frustrated syncope.

Due to its practical importance or for differential diagnosis with other entities, some types of syncope in particular will develop.

Vasovagal or vasodepressant syncope. It is the most common of blackouts and can be triggered by emotional stimuli such as fear, anxiety, witnessing accidents, seeing blood, etc., and in response to deep pain. It occurs while the subject is standing or eventually sitting and, after a few seconds in which he experiences a feeling of gastric discomfort, blurred vision, "lightness of the head", perspiration, etc., the patient falls unconscious for a few seconds and at those moments pale, sweaty, hypotensive, and bradycardic. Recovery is quick when horizontal and the compensatory mechanisms are put into action; if the patient is to be reinstated quickly in such circumstances, this recovery may be prevented and he may present some myoclonic movements, generally facial and finger movements.

After recovery, the sensorium regains its full lucidity.

This syncope takes place reflexively from influences emanating from higher levels (cerebral cortex and limbic structures especially) that produce a stimulation of the vasodepressor center, which brings about vagal stimulation and with them bradycardia and decreased peripheral vascular resistance, which causes, in turn, a deficient blood supply and consecutive cerebral hypoxia.

Carotid sinus syncope . Baroreceptors are stretch receptors located in blood vessels and in the heart. Those of the carotid sinus are located in a small dilation of the internal carotid artery, immediately above its origin. The impulses originated in them reach the vasodepressor and cardioinhibitory centers through the vagus and glossopharyngeal nerves and produce vasodilation with a drop in blood pressure and bradycardia.

Some subjects have hypersensitivity of the carotid sinus; they are generally older men, especially those with cardiovascular disease. In them, mechanical stimulation of the carotid sinus, either by massage in the area of ​​the carotid sinus, by compression of a tight shirt collar, or by rotation of the head, can give rise to reflex responses that can take the following modalities: a ) cardioinhibitory reflex, leading to bradycardia or transient asystole; b) vasodepressant reflex, manifested by arterial hypotension; and c) total baroreceptor reflex, sum of the above and resulting in bradycardia, hypotension and syncope. In the latter case, the onset is sudden, with a very short period of "empty head" sensation and subsequent fall, since it usually occurs while the subject is standing. The period of unconsciousness lasts a few seconds and sometimes lasts a few minutes, in which case there may be some myoclonic movements. Once recovered, the subject is fully lucid.

In some electroencephalography laboratories, and instead of performing carotid arteriography, compression of the region of the carotid artery where the corresponding sinus is located is usually done as a test of compensatory cerebral flow: if one of these arteries is semi-occluded, compression that is exerted on the opposite one can give rise to a syncope when annulling or diminishing to critical levels the blood flow towards both cerebral hemispheres. Therefore, carotid compression should be avoided in people who have hypersensitivity of the carotid sinus or in whom significant atheromatous lesions in the arterial system are suspected.

Urination syncope . It is an interesting picture that occurs in male subjects when they leave the bed at night to urinate. A commonly reported story is that they get up promptly to empty their bladder and, after doing so quickly, pass out, with a recovery that is immediate and complete. A predisposing factor is alcohol intake at night.

It is known that the bladder, when full, causes vasoconstriction and hypertension by a reflex mediated through the spinal cord and is normally counteracted by carotid sinus baroreceptors. When a distended bladder empties rapidly, that vasoconstriction ceases, and vasodilation and bradycardia occur; cerebral circulation decreases to critical levels and syncope appears. It also contributes to the latter occurring the vertical posture acquired moments before. These syncopes can be misinterpreted as transient epileptic or ischemic attacks.

Syncope due to primary orthostatic hypotension. In these cases, the autonomic nervous system, alone or in combination with other pathologies, presents alterations that translate into inappropriate functioning. Such is the situation in family dysautonomia and in Shy-Drager syndrome. The first is a familial vegetative dysfunction that is inherited with an autosomal recessive character and that manifests itself from an early age, especially in Jewish children. Extrapyramidal symptoms, muscle atrophy, fasciculations, bladder atony, and anhidrosis or hypohidrosis are found in Shy-Drager syndrome. Both pictures present as a common feature the drop in blood pressure when adopting the vertical position and as a result of poor vasoconstriction; in such circumstances the patient may have a brief feeling of fainting and fainting, and in these cases paleness is lacking,

Syncope due to secondary orthostatic hypotension . It is relatively frequent to listen to the story of subjects who faint when adopting the erect position, especially if inaction to get up has been rapid. The original causes can be multiple and varied diseases of the peripheral nerves that also involve the vegetative nerves (diabetic and amyloidosis neuropathies), syringomyelia, after sympathetic, due to drug action (hypotensive, especially diuretics, phenothiazines, tricyclic antidepressants , L-Dopa), in marked venous insufficiencies, in people with marked muscular flaccidity, in those who have been in bed for a long time, etc.

The common feature of all these causes is the stagnation of blood that occurs in the lower regions of the body and is not compensated by the vasoconstrictor mechanisms quickly enough to avoid the reduction of cardiac output due to decreased venous return. Blood pressure drops and, if it reaches critical levels, blurred vision, dizziness, weakness, paleness, sweating and subsequent fainting appear.

Syncope due to "Valsalva effect" . Fading can occur when an individual tries to breathe out against resistance. It usually happens as part of children's games in which, for example, they hyperventilate vigorously and then try to blow through the nose that they have previously covered; The same effect can be produced when making intense efforts with the glottis closed. The fading is short-lived and occurs with greatly increased intrathoracic pressure, which interferes with venous return to the heart and therefore cardiac output.

Cough syncope. In this type of fainting, the patient who suffers it is usually a male, chronic smoker. It often happens that, after a vigorous coughing fit, the subject feels slack and may lose consciousness for a few brief seconds. You can also have this type of syncope in a whooping cough fit. In all cases, it is due to a decrease in blood pressure and brain irrigation, and this as a consequence of: a) elevation of intrathoracic pressure and difficulty in venous return, with the consequent reduction in cardiac output; b) stimulation of carotid sinus baroreceptors; This occurs through increased pressure in the chest that is transmitted to the aorta and from there to the baroreceptors, which cause the aforementioned reflex regarding carotid sinus syncope.

Syncope due to decreased cardiac output.

The aforementioned causes due to: a) mechanical obstructions and b) acute heart failure are among the most serious because they involve a significant organic alteration, and some of them, in turn —for example, myocardial infarction— can lead to sudden death.

In some cases, a sum of factors is required to predispose to syncope, as occurs, for example, in aortic stenosis when an effort is made. In most cases of acute heart failure, the presence of an arrhythmia —with production of asystole of variable duration— leads to syncope, especially if the patient is standing and if there are arteriosclerotic alterations of the cerebral vessels or modifications in the composition of the blood. In the particular case of Stokes-Adams syndrome, in which there is an atrioventricular block, intermittent asystoles may occur, which can last 4-12 seconds, with the consequent drop in cardiac output and brain flow. In these instances, the patient becomes pale, his legs loosen and he passes out. There are no prodromal symptoms and the accesses attack the subject in any position and situation. If the asystole lasts more than 15 seconds, myoclonic jerks can be added, and even, if the period is longer, check for some post-sync neurological sequelae originating in focal lesions following arteriosclerotic vascular disorders.

Chemical syncope . They manifest under certain circumstances and when there is any modification or alteration in the relative composition of the blood. A direct oxygen and glucose deficit may result from this, as in cases of anemia or hypoglycemia, or through cerebral hypoflow due to hypocapnia.

Syncope due to hyperventilation is usually observed especially in women who present tachypnea as a consequence of an anxiety crisis or hysteria. As a result of this, hypocapnia, alkalosis and decreased brain flow occur. Many times, it is not possible to lose consciousness and the patients, on the other hand, report feelings of instability, blurred vision, dullness of the senses and perioral and finger paresthesias. There is no pallor and the position of the body does not influence the triggering of the picture.

Although some cases are mentioned, syncope in hypoglycemia is rare; it is more common to collect a history of either weakness and asthenia or, at the other extreme, coma.

When there is more or less significant anemia, an additional event that causes arterial hypotension (for example, ingestion of medications) or that diverts blood to other territories (the muscles, when exerting itself), can lead to fainting due to cerebral hypoflow. , which is corrected with the horizontal position.

Brain syncopes . They are infrequent and when they generally occur there are already other symptoms or signs of central nervous system dysfunction. They will not be discussed in detail; it is only relevant to mention that, when referring to the valve mechanism, reference is made to the effect that an intraventricular pedicle brain tumor produces with changes in the position of the head: in some circumstances the circulation of the cerebrospinal fluid can be interfered with with increased pressure intracranial, increased resistance to blood circulation and consecutive hypoflow.

When we speak of "theft" syndrome, we are referring to the mechanism by which blood is diverted to territories other than the original ones; it usually occurs in the face of an increase in the blood demand of these territories, usually as a consequence of some effort.

Fleeting ischemic attacks can cause transient symptoms of blurred vision, diplopia, paraesthesia, instability and dizzying sensation, and "dull senses," in patients predisposed to cerebral artery disease, which can sometimes lead to brief unconsciousness.

Those mentioned so far do not include all the causes capable of causing syncope; however, they are the most frequently observed or those of greatest practical importance for the clinical physician; the rarest cases are the property of the corresponding specialists.

Physicians dealing with patients with these problems should prepare a detailed medical history, especially in the elderly, without forgetting to ask about taking medications, and complement the evaluation with routine tests, an electrocardiogram and an electroencephalogram. .