Orthostatic hypotension

Orthostatic hypotension is an important clinical syndrome that occurs in many neurological and somatic diseases. With orthostatic hypotension, the neurologist faces primarily problems with falls and fainting.

The clinical manifestations of this syndrome are based on orthostatic hemodynamic disorders in the form of postural hypotension and fainting in standing position. The main symptom of orthostatic hypotension is a sharp decrease and sometimes a drop to zero blood pressure in patients with a transition from a horizontal position to a sedentary or vertical. There may be a different severity of clinical manifestations. In mild cases, soon after taking a vertical position (rising), the patient begins to feel signs of a pre-stupor condition. This condition, called lipotomy, is manifested by a feeling of faintness, dizziness, a premonition of loss of consciousness. The patient, as a rule, complains of general weakness, darkening in the eyes, sweating, tinnitus and head, unpleasant sensations in the epigastric region, sometimes a feeling of "failure", "floating of the soil from under the feet," "emptiness in the head" etc. Pale skin, sometimes with a waxy shade, short-term postural instability are noted. The duration of lipotymia is 3-4 seconds.

In more severe cases, these symptoms become more pronounced, possibly the emergence of a rough psychosensory disorder. Orthostatic disorders of hemodynamics in mild cases are limited to manifestations of the lipotymic state, in more pronounced cases, fainting develops after the stage of lipotymia. The duration of the unconscious state depends on the cause that caused it. With neurogenic, reflex syncopes, it is about 10 seconds. In severe cases (for example, with the Shay-Drageer syndrome), it can last dozens of seconds. Coarse orthostatic circulatory disorders can lead to death. During the unconscious state, diffuse muscular hypotension, dilated pupils, and eyeballs are pointed upward; as a result of tongue twisting, mechanical asphyxiation is possible; pulse is threadlike, blood pressure drops.

With a longer duration of the unconscious state (more than 10 s), seizures may occur (so-called convulsive syncope). Seizures are predominantly tonic, intensity can reach opisthotonus, accompanied by compression of the fists. Pupils sharply dilated, tendon reflexes are depressed, hypersalivation can occur, severe and deep fainting - urine leakage, rarely feces, in very rare cases, bite of the tongue may occur. Clonic convulsions are rare, usually in the form of isolated individual twitchings that never take a generalized character. After the return of consciousness, patients complain of general weakness, sweating, headache or heaviness in the head, sometimes there is drowsiness. The severity of these phenomena depends on the depth and duration of the postural attack.

To assess the severity of orthostatic circulatory disorders, in addition to accounting for clinical manifestations, it is convenient to use two indicators: the level of systolic blood pressure and the rate of onset of syncope (or lipotymia) after taking the vertical position of the body. In practice, a simpler and more reliable method is the second (in connection with individual differences in the critical value of blood pressure, in which fainting may develop). So, with the Shay-Drageer syndrome, the time interval from the moment of patient's transition from the horizontal position to the vertical position to the development of syncope can be reduced to several minutes or even up to 1 minute or less. This indicator is always adequately understood by the patient and quite accurately characterizes the severity of orthostatic circulatory disturbances. In dynamics, it also reflects the rate of progression of the disease. In severe cases, fainting can develop even when sitting. In less pronounced cases of orthostatic circulatory disorders, a 30-minute standing test can be used (for example, with neurogenic syncope).

Idiopathic orthostatic hypotension is a disease of the nervous system of unknown etiology, the leading manifestation of which is the orthostatic fall in arterial pressure. The course of idiopathic orthostatic hypotension (or Shay-Drageer syndrome) is steadily progressing, the forecast is unfavorable.

Orthostatic circulatory disorders in the Shay-Drageer syndrome create the prerequisites for ischemic damage to internal organs and the brain. This explains the anoxic spasms during orthostatic fainting. It is also known that acute disorders of cerebral circulation of ischemic nature are a frequent cause of death in the Shay-Drageer syndrome.

Orthostatic changes in hemodynamics cause patients to adjust the posture or gait to these disorders: in the absence of cerebellar and sensitive ataxia, patients often move wide, directed slightly to the side with a quick step on slightly knees bent at the knees, lowering their torso forward and lowering their head (skater's posture). To prolong the time in the vertical position, patients often strain the muscles of their legs, cross them, and so on. With the aim of increasing the venous return of blood to the heart.

[1], [2], [3], [4], [5], [6], [7]

The causes and pathogenesis of orthostatic hypotension

Normally, when moving from a horizontal position to a vertical one, gravitational movements of blood develop with simultaneous automatic inclusion of compensatory reactions of the cardiovascular system aimed at maintaining adequate blood circulation of the brain. In the case of insufficient compensatory reactions in response to orthostasis, orthostatic circulatory disturbances develop.

The development of orthostatic disorders of blood circulation can be caused both by the pathology of the central mechanisms of regulation of orthostatic reactions, and by violations of the executive links of the cardiovascular system (vices and other heart diseases).

In any case, the immediate cause of loss of consciousness is ischemic anoxia. It can be based on the following mechanisms:

1. inconsistency of myocardium supply with sufficient cardiac output;
2. violation of the heart rate, which does not provide adequate cerebral perfusion (fibrillation, severe bradycardia or arrhythmia);
3. decrease in blood pressure due to active peripheral vasodilation, resulting in an insufficient blood flow to the brain.

When orthostatic circulatory disorders associated with pathology of the autonomic nerve, one of the following pathological mechanisms is more often observed:

1. decrease in venous return of blood to the heart, leading to a decrease in the volume of blood circulation;
2. violation of the compensatory tonic reaction of the vessels, ensuring the stability of blood pressure in the aorta;
3. violation of regional mechanisms of redistribution of reduced circulatory volume.

A known pathogenetic role may also be played by insufficient increase in heart rate in response to orthostatics (for example, a fixed heart rhythm in the Shay-Drageer syndrome or bradycardia in the Adams-Stokes-Morgagni syndrome).

Arterial hypertension increases the risk of cerebral ischemia with a rapid decrease in blood pressure (the threshold for ischemia decreases, whereby the latter can develop even with a short-term decrease in blood pressure.

At the heart of idiopathic orthostatic hypotension, first described by S. Strongradbury, C. Egglestone in 1925, is progressing vegetative failure, associated in this case with the lesion of preganglionic neurons of the lateral horns of the spinal cord. Idiopathic orthostatic hypotension and Shay-Drageer syndrome are considered by some authors as variants of a single pathology; both terms are often used as synonyms.

The development of orthostatic circulatory disturbances is associated with a deficit of adrenergic effects on the cardiovascular system. The decrease in the tone of sympathetic innervation is also manifested by the hypofunction of the sweat glands (up to the development of anhidrosis). It is known that the loss of consciousness in these patients differs from other faints by the presence of hypo-and anhidrosis and the absence of a vagal reaction slowing the rhythm of the heart. Sympathetic denervation is accompanied by the development of hypersensitivity of alpha-adrenoblockers of blood vessels to noradrenaline. In this regard, even a slow intravenous injection of norepinephrine by such a patient is fraught with the development of severe hypertensive reactions.

The etiology of idiopathic orthostatic hypotension and Shay-Drageer syndrome is unknown. Morphological substrates are degenerative changes in brain structures related to segmental and stem vegetative (adrenergic) and motor systems (black substance, pale sphere, spinal cord side horns, vegetative ganglia, etc.). Depending on the prevalence of the pathological process in the brain, concomitant neurologic syndromes (parkinsonism, less often cerebellar syndrome, amyotrophies, myoclonia and other facultative symptoms) may develop. Currently, the Shay-Drageer syndrome, together with olive-ponto-cerebellar and streonigral degeneration, suggest including in the group of presenile progressive multi-system degeneration (atrophy) of the brain (multiple system atrophy). The latter term is gradually gaining increasing popularity in foreign literature.

Diagnosis of orthostatic hypotension

If orthostatic circulatory disturbances occur with attacks of loss of consciousness, the neurologist faces the task of conducting a differential diagnosis with a wide range of syndromes and diseases accompanied by paroxysmal disorders of consciousness. The most urgent is the task of distinguishing between paroxysmal disturbances of consciousness (and paroxysmal states in general) of epileptic and non-epileptic nature. The presence of convulsions in the picture of paroxysm does not facilitate a differential diagnosis, since convulsions can appear 15-20 seconds after the decrease in effective cerebral blood flow, regardless of its pathogenetic mechanism. Decisive in the diagnosis of orthostatic circulatory disorders is the establishment of the orthostatic factor in their genesis. Intolerance of long standing (queues, waiting for transport, etc.), abrupt rising, gradual development of an attack with signs of lipotymia, pronounced arterial hypotension with pallor, impaired pulse - all these moments are typical for syncope and are easily detected in an anamnesis.

Fainting is very rare in the horizontal position of the body and never comes in a dream (at the same time they are possible when getting out of bed at night). Orthostatic hypotension can be easily detected on the pontic table (passive change of body position). After the patient was in a horizontal position for several minutes, it is turned into a vertical position. Within a short time the arterial pressure drops, and the heart rate rises insufficiently (or does not increase at all), and the patient can faint. The results of diagnostic orthostatic samples are always recommended to be compared with other clinical data.

Postural hypotension is considered established with a systolic blood pressure drop of at least 30 mm Hg. Art. When moving from horizontal to vertical position.

To clarify the nature of syncope, a cardiac examination is necessary to exclude the cardiogenic nature of syncope; A definite diagnostic value is provided by the Atttner test, as well as such techniques as compression of the carotid sinus, Valsalva test, 30-minute standing with periodic measurement of blood pressure and heart rate.

To exclude the epileptic nature of paroxysm, a thorough EEG study is necessary. In this case, the detection of nonspecific changes in the EEG in the interictal period or the reduction in the threshold of convulsive readiness are not sufficient grounds for the diagnosis of epilepsy. Only the presence of classical epileptic phenomena on the EEG at the time of the attack (for example, the peak-wave complex) allows to diagnose epilepsy. The detection of the latter can be helped by a preliminary deprivation of a night's sleep or a polygraph study of sleep. It must also be remembered that epilepsy can occur with non-convulsive epileptic paroxysms. A test with hyperventilation can trigger both simple (neurogenic) syncope and epileptic seizure. The Valsalva trial is most informative in patients with syncope arising from urination, defecation, bettolepsy (cough syndrome, sometimes with convulsions) and other conditions, accompanied by a brief increase in intrathoracic pressure.

Slowing the pulse more than 10-12 per 1 minute with the Dagnini-Ashner test indicates an increased reactivity of the vagus nerve (most often in patients with neurogenic syncope).

Massage of the carotid sinus helps to identify the hypersensitivity of the carotid sinus (GKS syndrome). In such patients, a history of poor tolerance of tight collars and ties is revealed. Compression of the area of the carotid sinus by the hand of a doctor in such persons can provoke lipotomy or fainting with a decrease in blood pressure and other vegetative manifestations.

Idiopathic orthostatic hypotension, as mentioned above, may or may not be accompanied by a specific neurological symptomatology (Parkinsonism, Shay-Drageer Syndrome). In any case, it is a generalized lesion of the sympathetic nervous system. At the same time, orthostatic circulatory disorders occupy a central place in clinical manifestations. Symptoms are more pronounced in the morning hours, as well as after eating. Deterioration occurs in hot weather and after physical exertion, as well as in all situations that cause undesirable redistribution of blood volume.

Orthostatic hypotension is the main sign of primary peripheral autonomic failure. Secondarily, it can be observed in amyloidosis, alcoholism, diabetes, Guillain-Barre syndrome, chronic renal failure, porphyria, bronchial carcinoma, leprosy and other diseases.

Deficiency of adrenergic influences and, consequently, clinical manifestations of orthostatic hypotension are possible in the picture of Addison's disease, in some cases, the use of pharmacological agents (ganglion blockers, hypotensive drugs, dopaminomimetics such as nachoma, madopara, parlodel, etc.).

Orthostatic disorders of blood circulation also occur with organic pathology of the heart and blood vessels. Thus, syncope can be a frequent manifestation of a complicated aortic current with aortic stenosis, ventricular arrhythmia, tachycardia, fibrillation, etc. Almost every patient with significant aortic stenosis has systolic murmur and "cat-purring" (easier to listen in standing or in position "A la yours").

Sympathectomy can lead to inadequate venous return and, as a consequence, to orthostatic circulatory disorders. The same mechanism of development of orthostatic hypotension occurs with the use of ganglion blockers, some tranquilizers, antidepressants and anti-adrenergic agents. Predispose to fainting some conditions associated with a decrease in blood volume (anemia, acute blood loss, hypoproteinemia and low plasma volume, dehydration). In patients with a presumed or present deficiency in blood volume, an important diagnostic value is an unusual tachycardia while sitting in bed. The likelihood of orthostatic hypotension and syncope in the loss of blood depends on the amount of blood lost and the speed of this loss, from the patient's fright and the state of the cardiovascular system. In professional donors who have no fear of venipuncture and blood loss, syncope only develops if 15 to 20% of the volume is recovered within 6 to 13 minutes. Much more often, syncope is the result of pain or fear of losing blood. A more rare cause of syncope is a mechanical obstruction of venous return in pregnant women, when the stretched uterus can squeeze the lower vena cava with the patient lying down. Pose correction usually allows you to eliminate the symptom. Syncope is described with bradycardia due to the enhancement of the vagal reflex. In this case, there is a cardiac arrest and loss of consciousness in the absence of any heart disease. It is suggested that stimuli capable of inducing such a vegetative response can come from different organs, the afferent innervation of which is vagal, trigeminal, glossopharyngeal or spinal. Syncope due to an intensified vagal reflex can develop with pressure on the eyeballs, esophagic dilatation (for example, when swallowing a soda drink), an elongated rectum or an elongated vagina. The common factor here is probably visceral pain. Atropine is an effective means of preventing the effects of enhanced vagal reflexes.

[8], [9], [10], [11], [12], [13], [14], [15]

Treatment of orthostatic hypotension

If neurogenic syncope can successfully be treated with psychotropic, vegetotrophic and restorative drugs (tranquilizers, antidepressants, anticholinergics, ergot preparations, stimulants, antihistamines, etc.). Then treatment of idiopathic orthostatic hypotension is always quite difficult for the doctor task.

In the treatment of orthostatic hypotension, there are two principles. One is to limit the volume that can be occupied by blood when taking the vertical position, the other is to increase the blood mass that fills this volume. As a rule, complex treatment is used. There are shown drugs that can increase the endogenous activity of the sympathetic nervous system and cause vasoconstriction (alpha-adrenomimetics). Their use, however, is associated with a risk of arterial hypertension and other complications. Such drugs are prescribed cautiously (for example, ephedrine), while some patients are relieved from the combination of these drugs with MAO inhibitors (eg, nialamide in the usual dosage) or dihydroergotamine. The beta-blocker pindolol (vine) is shown, which favorably affects the cardiac muscle. Use and obzidan (to prevent peripheral vasodilation). The same property is possessed by Nerukal and Indomethacin. A rich diet is shown. Introduce drugs that inhibit salt (synthetic fluorine-containing corticosteroids), caffeine, yohimbine, tyramine derivatives. A positive result of an implantation of a pacemaker giving a heart rate of 100 in 1 min is described. They also use a tight bandaging of the lower extremities, the pelvic girdle and abdomen, special inflatable suits. A good effect is swimming. It is necessary to recommend a full 4-meals a day. Some types of orthostatic hypotension (for example, caused by dopaminomimetics) abroad are successfully prevented with the help of a blocker of peripheral dopamine receptors - domperidone. There are also reports of a beneficial effect of a combination of mineralocorticoids (DOXA), sympathomimetics, L-dofa, and monoamine oxidase inhibitors. Freestyle with orthostatic hypotension is recommended to sleep with a slightly raised head (5-20 degrees), which helps to reduce hypertension in the prone position, as well as night diuresis. Since the reliable increase of neurological symptoms in patients with Shay-Drageer syndrome during smoking has been repeatedly described during smoking, such patients should be strongly advised to stop smoking.