Orthostatic hypotension

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

The clinical manifestations of this syndrome are based on orthostatic hemodynamic disorders in the form of postural hypotension and fainting in a standing position. The main symptom of orthostatic hypotension is a sharp decrease, and sometimes a drop to zero, in blood pressure in patients when moving from a horizontal to a sitting or vertical position. Clinical manifestations may vary in severity. In mild cases, soon after assuming a vertical position (standing up), the patient begins to feel signs of a pre-syncope state. This condition, called lipothymia, is manifested by a feeling of nausea, dizziness, and a premonition of loss of consciousness. The patient, as a rule, complains of general weakness, darkening in the eyes, sweating, tinnitus and noise in the head, unpleasant sensations in the epigastric region, sometimes a feeling of "falling through", "the ground slipping away from under the feet", "emptiness in the head", etc. The skin is pale, sometimes with a waxy tint, and there is short-term postural instability. The duration of lipothymia is 3-4 sec.

In more severe cases, the listed symptoms become more pronounced, and mild psychosensory disorders may occur. Orthostatic hemodynamic disorders in mild cases are limited to manifestations of the lipothymic state; in more severe cases, fainting develops following the lipothymic stage. The duration of the unconscious state depends on the cause that caused it. In neurogenic, reflex fainting, it is about 10 seconds. In severe cases (for example, in Shy-Drager syndrome), it can last tens of seconds. Severe orthostatic circulatory disorders can lead to death. During the unconscious state, diffuse muscle hypotension, dilated pupils, eyeballs are diverted upward are observed; mechanical asphyxia is possible due to the tongue falling back; the pulse is threadlike, arterial pressure drops.

With a longer duration of unconsciousness (more than 10 sec), convulsions may occur (the so-called convulsive syncope). Convulsions are predominantly tonic in nature, can reach opisthotonus in intensity, and are accompanied by clenching of the fists. The pupils are sharply dilated, tendon reflexes are depressed, hypersalivation may be observed, with severe and deep fainting - loss of urine, rarely feces, in extremely rare cases, biting of the tongue may occur. Clonic convulsions are rare, usually in the form of isolated individual twitching, never becoming generalized. After regaining consciousness, patients complain of general weakness, sweating, headache or heaviness in the head, sometimes drowsiness is noted. 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 taking into account clinical manifestations, it is convenient to use two indicators: the level of systolic blood pressure and the rate of onset of fainting (or lipothymia) after assuming a vertical body position. In practice, the second method is simpler and more reliable (due to individual differences in the critical value of blood pressure at which fainting may develop). Thus, with Shy-Drager syndrome, the time interval from the moment the patient moves from a horizontal to a vertical position until fainting develops can be reduced to several minutes or even to 1 minute or less. This indicator is always adequately understood by the patient and quite accurately characterizes the severity of orthostatic circulatory disorders. In dynamics, it also reflects the rate of progression of the disease. In severe cases, fainting can develop even in a sitting position. In less pronounced cases of orthostatic circulatory disorders, a 30-minute standing test can be used (for example, with neurogenic fainting).

Idiopathic orthostatic hypotension is a disease of the nervous system of unknown etiology, the leading manifestation of which is an orthostatic drop in blood pressure. The course of idiopathic orthostatic hypotension (or Shy-Drager syndrome) is steadily progressive, the prognosis is unfavorable.

Orthostatic circulatory disorders in Shy-Drager syndrome create preconditions for ischemic damage to internal organs and the brain. This explains anoxic convulsions during orthostatic syncope. It is also known that acute ischemic cerebrovascular accidents are a common cause of death in Shy-Drager syndrome.

Orthostatic changes in hemodynamics force patients to adapt their posture or gait to these disturbances: in the absence of cerebellar and sensory ataxia, patients often move with a wide, slightly to the side, quick step on slightly bent knees, with the body bent forward and the head down (skater's pose). To prolong the time spent in an upright position, patients often tense the leg muscles, cross them, etc., in order to increase the venous return of blood to the heart.

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

Causes and pathogenesis of orthostatic hypotension

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

The development of orthostatic circulatory disorders can be caused by both pathology of the central mechanisms regulating orthostatic reactions and disorders of the executive links of the cardiovascular system (heart defects and other diseases).

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

1. inadequacy of the myocardium to provide sufficient cardiac output;
2. disturbance of the heart rhythm that does not provide adequate cerebral perfusion (fibrillation, severe bradycardia or arrhythmia);
3. decreased blood pressure due to active peripheral vasodilation, leading to insufficient blood flow to the brain.

In orthostatic circulatory disorders associated with autonomic nervous system pathology, one of the following pathological mechanisms is most often observed:

1. decreased venous return of blood to the heart, leading to a decrease in circulatory volume;
2. violation of the compensatory tonic reaction of the vessels, ensuring stability of blood pressure in the aorta;
3. disruption of regional mechanisms for 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, fixed heart rhythm in Shy-Drager syndrome or bradycardia in Adams-Stokes-Morgagni syndrome).

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

The basis of idiopathic orthostatic hypotension, first described by S. Strongradbury, C. Egglestone in 1925, is progressive autonomic failure, associated in this case with damage to the preganglionic neurons of the lateral horns of the spinal cord. Idiopathic orthostatic hypotension and Shy-Drager syndrome are considered by some authors as variants of a single pathology; both terms are often used as synonyms.

The development of orthostatic circulatory disorders is associated with a deficiency of adrenergic effects on the cardiovascular system. A decrease in the tone of sympathetic innervation is also manifested by hypofunction of the sweat glands (up to the development of anhidrosis). It is known that attacks of loss of consciousness in these patients differ from other fainting spells by the presence of hypo- and anhidrosis and the absence of a vagal reaction to slowing down the heart rate. Sympathetic denervation is accompanied by the development of hypersensitivity of alpha-adrenoblockers of blood vessels to norepinephrine. In this regard, even slow intravenous administration of norepinephrine to such patients is fraught with the development of severe hypertensive reactions.

The etiology of idiopathic orthostatic hypotension and Shy-Drager syndrome is unknown. The morphological substrate is degenerative changes in the brain structures related to the segmental and brainstem vegetative (adrenergic) and motor systems (substantia nigra, globus pallidus, lateral horns of the spinal cord, autonomic ganglia, etc.). Depending on the prevalence of the pathological process in the brain, concomitant neurological syndromes may develop (parkinsonism, less often cerebellar syndrome, amyotrophy, myoclonus and other optional symptoms). Currently, Shy-Drager syndrome, along with olivo-ponto-cerebellar and striatonigral degeneration, is proposed to be included in the group of presenile progressive multisystem degenerations (atrophies) of the brain (multiple system atrophy). The latter term is gradually gaining popularity in foreign literature.

Diagnosis of orthostatic hypotension

If orthostatic circulatory disorders occur with attacks of loss of consciousness, then 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 task is to differentiate paroxysmal disorders of consciousness (and paroxysmal conditions in general) of epileptic and non-epileptic nature. The presence of seizures in the picture of a paroxysm does not facilitate differential diagnosis, since seizures can appear 15-20 seconds after a decrease in effective cerebral blood flow, regardless of its pathogenetic mechanism. The decisive factor in the diagnosis of orthostatic circulatory disorders is the establishment of the orthostatic factor in their genesis. Intolerance of prolonged standing (queues, waiting for transport, etc.), sudden standing up, gradual development of an attack with signs of lipothymia, severe arterial hypotension with pallor, weakened pulse - all these moments are typical for fainting and are easily identified in the anamnesis.

Fainting is very rare in the horizontal position of the body and never occurs during sleep (however, it is possible when getting out of bed at night). Orthostatic hypotension can be easily detected on a turntable (passive change of body position). After the patient has been in a horizontal position for several minutes, he is turned to a vertical position. Within a short time, the blood pressure drops, and the heart rate does not increase sufficiently (or does not increase at all), and the patient may faint. It is always recommended to compare the results of diagnostic orthostatic tests with other clinical data.

Postural hypotension is considered established when systolic blood pressure drops by at least 30 mm Hg when moving from a horizontal to a vertical position.

To clarify the nature of the faint, a cardiological examination is necessary to exclude the cardiogenic nature of syncope; the Attner test, as well as such techniques as compression of the carotid sinus, the Valsalva test, and 30-minute standing tests with periodic measurement of blood pressure and heart rate, have a certain diagnostic value.

A thorough EEG examination is necessary to exclude the epileptic nature of the paroxysm. However, detection of non-specific changes in the EEG in the interictal period or a decrease in the seizure threshold are not sufficient grounds for diagnosing epilepsy. Only the presence of classic epileptic phenomena on the EEG at the time of the seizure (for example, the peak-wave complex) allows diagnosing epilepsy. The latter can be identified by preliminary sleep deprivation or a polygraphic sleep study. It is also necessary to remember that epilepsy can occur with non-convulsive epileptic paroxysms. A hyperventilation test can provoke both a simple (neurogenic) faint and an epileptic seizure. The Valsalva test is most informative in patients with fainting that occurs during urination, defecation, bettolepsy (cough fainting, sometimes accompanied by convulsions) and other conditions accompanied by a short-term increase in intrathoracic pressure.

A decrease in pulse rate by more than 10-12 beats per minute during the Danini-Aschner test indicates increased reactivity of the vagus nerve (most often in patients with neurogenic syncope).

Carotid sinus massage helps to identify carotid sinus hypersensitivity (GCS syndrome). Such patients have a history of poor tolerance to tight collars and ties. Compression of the carotid sinus area by the doctor's hand in such individuals can provoke lipothymia 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 certain neurological symptoms (Parkinsonism, Shy-Drager syndrome). In any case, we are talking about a generalized lesion of the sympathetic nervous system. In this case, orthostatic circulatory disorders occupy a central place in the 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 symptom of primary peripheral autonomic failure. Secondarily, it can be observed in amyloidosis, alcoholism, diabetes mellitus, Guillain-Barré 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 of the use of pharmacological agents (ganglion blockers, antihypertensive drugs, dopamine mimetics such as nacom, madopar, parlodel, etc.).

Orthostatic circulatory disorders also occur with organic pathology of the heart and blood vessels. Thus, syncope can be a frequent manifestation of obstructed aortic flow with aortic stenosis, ventricular arrhythmia, tachycardia, fibrillation, etc. Almost every patient with significant aortic stenosis has a systolic murmur and a "cat purr" (easier to hear in a standing position or in a "your" position).

Sympathectomy may result in insufficient venous return and, as a consequence, in orthostatic circulatory disorders. The same mechanism of development of orthostatic hypotension occurs with the use of ganglionic blockers, some tranquilizers, antidepressants and antiadrenergic agents. Some conditions associated with a decrease in blood volume (anemia, acute blood loss, hypoproteinemia and low plasma volume, dehydration) predispose to syncope. In patients with suspected or actual blood volume deficit, unusual tachycardia while sitting up in bed is of great diagnostic value. The likelihood of orthostatic hypotension and syncope with blood loss depends on the amount of blood lost and the speed of this loss, on the patient's fright and the state of the cardiovascular system. In professional donors who have no fear of venipuncture and blood loss, syncope develops only if 15 to 20% of the volume is extracted within 6 to 13 minutes. Much more often, syncope is the result of pain or fear of blood loss. A rarer cause of syncope is mechanical obstruction of venous return in pregnant women, when the distended uterus can compress the inferior vena cava when the patient is lying down. Correction of the posture usually eliminates the symptom. Syncope has been described with bradycardia due to an increase in the vagal reflex. In this case, cardiac arrest and loss of consciousness occur in the absence of any heart disease. It is assumed that stimuli capable of causing such a vegetative response can come from different organs, the afferent innervation of which can be vagal, trigeminal, glossopharyngeal or spinal. Syncope due to exaggerated vagal reflexes may occur with pressure on the eyeballs, esophageal dilation (e.g., swallowing a soda), a distended rectum, or a distended vagina. Visceral pain is probably a common factor. Atropine is effective in preventing the effects of exaggerated vagal reflexes.

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

Treatment of orthostatic hypotension

If neurogenic syncope can be successfully treated with psychotropic, vegetotropic and general tonic drugs (tranquilizers, antidepressants, anticholinergics, ergot preparations, stimulants, antihistamines, etc.), then the treatment of idiopathic orthostatic hypotension is always a rather difficult task for the doctor.

There are two principles in the treatment of orthostatic hypotension. One is to limit the volume that can be occupied by blood when taking a vertical position, the other is to increase the mass of blood that fills this volume. As a rule, complex treatment is used. Drugs that can increase the endogenous activity of the sympathetic nervous system and cause vasoconstriction (alpha-adrenergic agonists) are indicated. Their use, however, is associated with the risk of arterial hypertension and other complications. Such drugs are prescribed with caution (for example, ephedrine), while some patients get relief from a combination of these drugs with MAO inhibitors (for example, nialamide in a normal dose) or dihydroergotamine. The beta-blocker pindolol (visken) is indicated, which has a beneficial effect on the heart muscle. Obzidan is also used (to prevent peripheral vasodilation). Nerucal and indomethacin have the same property. A salt-rich diet is indicated. Salt-retaining drugs (synthetic fluorinated corticosteroids), caffeine, yohimbine, and tyramine derivatives are administered. A positive result has been described from implanting a pacemaker that sets the heart rate to 100 beats per minute. Tight bandaging of the lower extremities, pelvic girdle, and abdomen, and special inflatable suits are also used. Swimming has a good effect. It is necessary to recommend a full 4-meal diet. Some types of orthostatic hypotension (for example, caused by dopamine mimetics) are successfully prevented abroad using a peripheral dopamine receptor blocker, domperidone. There are also reports of a favorable effect of a combination of mineralocorticoids (DOXA), sympathomimetics, L-dopa, and monoamine oxidase inhibitors. A patient with orthostatic hypotension is recommended to sleep with his head slightly elevated (by 5-20 degrees), which helps to reduce hypertension in the supine position, as well as nocturnal diuresis. Since a reliable increase in neurological symptoms in patients with Shy-Drager syndrome during smoking has been repeatedly described, such patients should be strongly advised to stop smoking.