Test for orthostatic hypotension. Orthostatic hypotension - what is it? Terminology, types and causes of orthostatic hypotension

Orthostatic hypotension (postural orthostatic hypotension, orthostatic collapse) is a syndrome that is expressed in a sharp change in systolic and diastolic pressure. It should be noted that this syndrome manifests itself at the moment when a person abruptly changes position from horizontal to vertical.

Orthostatic arterial hypotension is a consequence of dysfunction of the vestibular apparatus and never occurs as an independent disease. Therefore, it is not advisable to carry out only symptomatic treatment in this case.

To determine the causes of the appearance of such a syndrome, it is necessary to carry out a comprehensive diagnosis: physical examination, laboratory and instrumental research methods. Based on the diagnostic results, further tactics of therapeutic measures are determined.

It is quite difficult to make an unambiguous forecast in this case, since everything will depend on the underlying factor. However, the sooner treatment is started, the greater the chances of a full recovery. It should be noted that if you have such a syndrome in your personal history, it is necessary to register with a cardiologist, as well as systematically undergo a medical examination.

Etiology

The following etiological factors can provoke orthostatic collapse:

• diseases of the cardiovascular system, including chronic ones;
• disruption of the adrenal cortex;
• hormonal disorders;
• diseases of the nervous system;
• and diseases in the clinical picture of which there is this pathological process;
• diabetic;
• vascular pathologies, especially in chronic form;
• changes in hormonal levels during pregnancy;
• massive blood loss, including internal blood loss;
• postthrombotic syndrome;
• the body as a result of extensive poisoning with heavy metals, poisons and other substances;
• unbalanced diet, strict diets that are not justified from a medical point of view;
• chronic, constant nervous tension;
• long-term bed rest;
• alcohol abuse on a regular basis.

In addition, orthostatic hypotension can develop while taking certain medications and even traditional medicine. In some cases, this syndrome occurs against the background of spinal injuries.

If it is not possible to determine the provoking causes of such a syndrome, a diagnosis of “idiopathic orthostatic hypotension” is made.

Classification

Orthostatic hypotension is divided into the following subtypes, depending on the etiological factor:

• medicinal – caused by excessive use of medications or taking medications that are not suitable for the patient;
• subacute – develops due to a decrease in blood circulation against the background of intoxication of the body, dehydration and massive blood loss;
• acute - the etiology is the same as described above, but the clinical picture is more pronounced;
• Shy-Drager syndrome – pressure drops are caused by hormonal imbalances and diseases of the nervous system;
• idiopathic – the cause of the disorder has not been established.

Determination of the root cause factor is carried out only through diagnostic measures. The clinical picture can be supplemented by specific symptoms, but it is impossible to make an accurate diagnosis based on symptoms alone; therefore, self-medication is unacceptable.

Symptoms

Most often, symptoms appear in the morning, when a person just gets up. The duration and frequency of the attack will depend on the underlying disease. Also, a sharp drop in pressure can occur if a person quickly changes body position - gets up after sitting in one place for a long time.

The general clinical picture includes the following signs:

• dizziness - it is noteworthy that it does not go away even if the person sits down or lies down;
• noise, ringing in the ears;
• feeling of heaviness in the head;
• increasing weakness, malaise;
• darkening of the eyes;
• cold hands and feet, cold sweating;
• pale skin;
• cramps in the limbs;
• nausea and vomiting;
• pre-fainting state.

In addition, the clinical picture may be supplemented by such signs as:

• symptoms;
• heartache;
• shortness of breath, shallow breathing;
• loss of consciousness.

It should also be noted that the general clinical picture can be supplemented by specific symptoms that will be characteristic of the pathological process that provoked this syndrome.

The following symptoms may appear:

• disturbance of orientation in space, problem with coordination of movement;
• sudden mood swings, apathetic mood;
• loss of appetite, weight loss;
• general deterioration of health;
• exacerbation of chronic diseases, if any;
• headaches of a chronic nature, which lead to a decrease in a person’s performance and worsen the quality of his life.

Similar symptoms can occur with a fairly large number of cardiovascular diseases. Therefore, it is strongly recommended not to take any drugs at your own discretion: such actions can lead to extremely negative consequences, some of which may be irreversible.

Diagnostics

Treatment of orthostatic collapse is carried out only by complex methods, but to determine treatment tactics it is necessary to conduct a comprehensive examination and establish the root cause.

Diagnostics is carried out in two stages.

First of all, the doctor conducts a physical examination of the patient, during which:

• conducts a survey of the patient, which will give a complete picture of the current clinical picture;
• collects personal and family history;
• studies medical history.

The next stage will be the implementation of laboratory and instrumental research methods:

• general and biochemical blood test;
• general urine analysis;
• determination of hormone levels in the blood;
• echocardiography;
• Holter monitoring;
• orthostatic tests.

Orthostatic tests are:

• active load - the patient lies for several minutes, after which he must suddenly change his body position;
• passive load – carried out on a special simulator.

Based on the results of diagnostic measures, it will be determined what exactly caused the appearance of such a syndrome, and what therapeutic measures should be taken to eliminate it.

Treatment

As mentioned above, treatment for orthostatic hypotension involves only comprehensive treatment - drug therapy, diet, physiotherapeutic procedures and general recommendations.

The pharmacological part of therapy is based on the following drugs:

• adaptogens;
• beta blockers;
• non-steroidal anti-inflammatory drugs;
• mineralocorticoids;
• muscle relaxants;
• antidepressants (Venlafaxine is most often prescribed).
• adrenomimetics.

In some cases, the patient needs a diet, but the specific dietary table is determined on an individual basis.

Traditional medicine is not excluded, however, they should be considered only as additional, and can only be used in consultation with the attending physician.

The prognosis, if treatment is carried out promptly and correctly, can be favorable, but it is also necessary to take into account the nature of the course of the underlying factor. Therefore, at the first symptoms, you should consult a doctor: timely initiation of therapy significantly increases the chances of a full recovery.

Regarding prevention, only general recommendations can be made:

• lead a healthy lifestyle;
• Healthy food;
• take medications only on the recommendation of a doctor;
• include moderate physical activity in your regimen.

People who have a history of cardiovascular disease should undergo a systematic medical examination.

Postural or orthostatic hypotension is a short-term disturbance in blood pressure that occurs when changing body position. Orthostatic hypotension occurs when the body suddenly moves from a horizontal to a vertical position. At this moment, blood pressure drops sharply, by an average of 20 mmHg, which is accompanied by sudden weakness and dizziness.

Postural hypotension is a consequence of disruption of the autonomic nervous system. A feature of the disease is a sudden drop in pressure only when changing body position.

Orthostatic arterial hypotension occurs only with orthostasis, that is, when the body position is transferred to a vertical position. A characteristic sign of this disorder is a sudden deterioration in health when suddenly rising from bed. In particularly severe cases, symptoms of orthostatic arterial hypotension appear when suddenly rising from a chair after prolonged sitting at a table.

Today, orthostatic hypotension is considered the most common disorder accompanied by a decrease in blood pressure. People of all age groups experience discomfort due to a sharp drop in blood pressure. Quite often, the first signs and symptoms of orthostatic hypotension appear in adolescence. This is usually accompanied by autonomic dysfunction of the nervous system, that is, disruption of the regulation of nervous processes responsible for normalizing vascular tone, ensuring heart rate and respiration.

The discomfort usually does not last long. Orthostatic collapse passes quickly, the duration of the attack of lightheadedness is from a few seconds to a couple of minutes. Nevertheless, such a disorder greatly complicates the patient’s life and therefore requires complex treatment. Orthostatic hypotension is a neurological rather than a cardiac disorder, but in some cases it may indicate serious circulatory disorders, heart failure or ischemia.

Symptoms of the disorder

Symptoms of orthostatic hypotension are caused by three factors:

• disruption of oxygen transport to the heart and brain;
• slow reaction of the heart when changing body position;
• a decrease in pressure by 20 mmHg. and more at the moment of transition to a vertical position.

These factors cause the general malaise that appears at this moment. Orthostatic hypotension is characterized by sudden dizziness. A person may experience dark vision, weakness and tinnitus. Confusion and disorientation appear, and in severe cases, fainting may develop. Many patients complain of a feeling of blood pulsating in the ears and discomfort in the chest. This is due to the delayed reaction of the heart to changes in blood circulation.

With a strong decrease in pressure when standing up suddenly, a person’s legs can weaken, which leads to loss of support and a fall. Despite the frightening symptoms, such symptoms do not last long. It is enough to return to the starting position for the discomfort to go away in a few seconds.

Reasons for the development of the disorder

Dizziness causes a sharp decrease in blood flow to the brain

Quite often it is not possible to determine the causes of orthostatic hypotension. This disorder is associated with a decrease in circulating blood volume at the time of change in body position. As a result, blood flow to the heart decreases. In response to this, special receptors located in the heart and cervical artery react, which increase the heart rate. Due to a sudden change in heart rate and vascular tone, symptoms of orthostatic hypotension appear.

In itself, such a reaction of the body does not cause concern, as it is explained by human physiology. A change in blood circulation due to a sudden change in body position is an absolutely normal reaction. However, a slow response of baroreceptors to a decrease in the volume of blood that flows to the heart indicates a disruption in the functioning of the autonomic nervous system.

Thus, the main cause of orthostatic hypotension is a neurological disorder known as vegetative-vascular or neurocirculatory dystonia. The remaining causes of the development of the disorder can be divided into two groups - permanent factors, or chronic pathologies that provoke a decrease in pressure, and short-term factors.

Constant factors include:

• diseases of the nervous system;
• diabetes;
• hypothyroidism and other endocrine disorders;
• heart diseases.

In addition to VSD, orthostatic hypotension can be provoked by Parkinson's disease, amyloidosis, and senile dementia. Orthostatic hypotension in young people is often caused by vegetative disorders; in old people, it is caused by severe diseases of the nervous system and senile dementia. This is explained by the fact that the primary manifestations of VSD are observed in adolescence due to the rapid maturation of the body and changes in hormonal levels, which increases the load on the nervous system. As a result, the autonomic nervous system simply cannot cope with its functions, so periodic changes in blood pressure, heart rate, and breathing problems occur.

Damage to nerve fibers is common in diabetes. This leads to disruption of the conduction of nerve impulses that regulate vascular tone. Blood pressure disorders are also observed with hypofunction of the thyroid gland.

Another cause of orthostatic hypotension is myocardial dysfunction. Chronic heart failure, arrhythmia, bradycardia disrupt the normal functioning of the mechanisms that normalize blood circulation when changing body position. The result is short-term discomfort in orthostasis. Orthostatic hypotension can also occur after myocardial infarction.

Short-term factors that provoke a decrease in pressure when changing body position:

• dehydration;
• taking certain groups of drugs;
• eating;
• long-term bed rest;
• hot climate.

When dehydrated, blood circulation is impaired. This leads to a decrease in pressure in orthostasis. Orthostatic hypotension can also occur at high temperatures. Due to increased sweating, the body loses water, vascular tone and blood circulation are disrupted, so sudden movements may be accompanied by a decrease in blood pressure.

Lack of fluid in the body can lead to short-term dizziness

Quite often, a heavy lunch provokes a drop in blood pressure. This phenomenon is usually encountered by older people who, after eating, prefer to rest a little in bed. A sudden rise is accompanied by short-term malaise due to a decrease in pressure.

If you stay in bed for a long time, for example, in case of a serious illness or rehabilitation after surgery, orthostatic hypotension will be observed at first. This is explained by general weakness and changes in vascular tone. In most cases, such a disorder does not require treatment; the symptoms of hypotension in orthostasis disappear as the body recovers.

Some medications cause orthostatic hypotension during administration. A decrease in blood pressure can be observed during long-term therapy with antidepressants, tranquilizers, and drugs that reduce muscle and vascular tone. A decrease in blood pressure occurs while taking diuretics. Men may experience orthostatic hypotension as a side effect of taking medications that affect potency. Moreover, this side effect is reported for almost all drugs used in the treatment of erectile dysfunction.

Most often, drug-induced orthostatic hypotension is observed in hypertensive patients. Tablets to lower blood pressure require compliance with the rules of administration and the correct dosage. Inadequate treatment of hypertension can lead to short-term decreases in blood pressure, including when changing body position.

Hypotension caused by the action of such factors most often goes away on its own, after the cause of its development is eliminated. It is enough to stop taking medications, follow a diet or normalize your drinking regime to get rid of the disorder.

If at a young age the cause of orthostatic hypotension lies in autonomic disorders, in the elderly it accompanies more serious illnesses

Types of orthostatic hypotension

Due to development, there are several types of disorders:

• Shy-Drager syndrome;
• idiopathic hypotension;
• drug-induced orthostatic hypotension;
• hypovolemia.

Shy-Drager syndrome is characterized by impaired production of norepinephrine. Under the influence of this hormone, vascular tone increases and pressure increases. As a result of its deficiency, the body cannot adequately respond to changes in blood circulation when changing body position, which leads to symptoms of low blood pressure.

Idiopathic orthostatic hypotension is a form of the disease in which it is impossible to identify the causes of impaired blood circulation and low blood pressure.

Drug-induced orthostatic hypotension is a decrease in vascular tone due to long-term therapy with diuretics, antidepressants, muscle relaxants, or medications for hypertension.

Hypovolemia is a decrease in the volume of blood circulating in the body. This pathology can be caused by significant blood loss, disruption of the adrenal glands, and dehydration. Patients with diabetes mellitus often encounter this disorder.

Separately, orthostatic hypotension of a neurological nature is distinguished. According to statistics, more than half of patients with low blood pressure experience this form of the disease. In this case, autonomic disorders of the nervous system are noted, caused by a deficiency of B vitamins, amyloidosis, neurocirculatory dystonia and other pathological conditions.

Orthostatic hypotension according to ICD-10 is designated I95.1. Neurogenic orthostatic hypotension caused by the syndrome of impaired adrenaline production is designated in ICD-10 as G23.8. It should be noted that this disease is a rare disease. Quite often, orthostatic hypotension is part of the symptom complex of neurocirculatory dystonia, which is designated G90 in the International Classification of Diseases (ICD).

Diagnostics

To confirm the diagnosis, you must first consult with a therapist. The doctor will collect anamnesis, analyze the patient’s complaints, and conduct a physical examination.

Be sure to ask questions about all medications the patient is taking. Often, the sudden development of orthostatic hypotension is associated with the start of taking a new drug to treat another pathology.

Pressure measurement is required. In this case, measurements are first taken in a lying position, and then in a sitting position. A sharp drop in pressure of more than 20 mmHg. is the basis for the assumption of orthostatic hypotension.

After the initial examination, the doctor will order the following examinations:

• general and biochemical blood test;
• blood test for hormone levels;
• examination of cardiac activity;
• orthostatic tests;
• ECG and EchoCG.

A consultation with a neurologist and vagal tests are required. This examination allows us to identify the connection between disruption of the autonomic nervous system in response to changes in cardiac activity.

An important part of diagnosis is orthostatic tests. This method allows you to determine the reaction of the cardiovascular system to sudden changes in body position. Typically, an orthostatic test is performed on a special rotating platform.

Types of orthostatic tests

Possible risks

Orthostatic hypotension can cause fainting. This is the most common complication of a sudden drop in blood pressure. In this case, there is a risk of developing deep fainting, accompanied by a convulsive seizure.

Feeling faint when standing up can cause sudden loss of support and a fall. This causes injury and is especially dangerous for older patients.

In severe cases, cerebral hypoxia develops. This complication entails the development of neurological disorders. In old age, orthostatic hypotension increases the risk of developing senile dementia due to impaired blood supply to the brain.

The most dangerous complication is a cerebral stroke.

Treatment principle

For orthostatic hypotension, treatment depends on the type of disorder. If the disorder is caused by temporary factors, the patient must:

• do light gymnastics;
• Healthy food;
• increase salt intake;
• review the list of medications taken.

First of all, you should replace all medications that cause a drop in blood pressure. To do this, you definitely need to consult a doctor. To eliminate hypotension, the patient needs gymnastics. The main exercises consist of slow squats followed by returning to a vertical position. Such exercises are a workout for the cardiovascular system and allow you to restore the speed of the heart's reaction to changes in body position.

If the disorder is caused by dehydration, it is necessary to increase salt intake and maintain a drinking regime. It is also recommended to avoid heavy foods.

If the disease is caused by other pathologies, only the attending physician can tell how to treat hypotension and orthostatic hypotension. First of all, a comprehensive examination and treatment of the pathology that led to the pressure disorder is necessary. To correct the body’s inadequate response to changes in body position, the following is used:

• medications to normalize the activity of the autonomic nervous system (adaptogens);
• drugs to increase vascular tone;
• medications that prevent sodium from being washed out of the body.

A diet is required. It is necessary to consume more citrus fruits, fresh fruits and vegetables, as they have a tonic effect. Green tea is recommended for patients. When your blood pressure drops, you can drink coffee and strong black tea.

Preventing the development of the disease comes down to being attentive to your own health. Any chronic diseases should be under control. Stress that weakens the nervous system should be avoided. It is necessary to eat properly and maintain a drinking regime. An excellent preventive measure would be sports and regular walks in the fresh air.

Orthostatic hypotension - This is any decrease in blood pressure that occurs in a patient when moving from the position /,/! “lying” to a “standing” position, accompanied by the appearance of clinical symptoms associated with a decrease in blood supply to the brain.

Prevalence

The true prevalence of orthostatic hypotension (OH) has not been established. Based on preliminary data, it is estimated that the incidence in the general population may be between 0.5 and 1.5%. At the same time, the frequency of detection of OH increases significantly among hospital patients - 7-33%; among elderly and senile people it reaches 14-50%. Thus, OH is one of the most common syndromes in the practice of therapists and cardiologists.

Etiology

In a healthy person, when standing up, diastolic blood pressure does not change or decreases slightly, and systolic blood pressure decreases, but not by more than 10 mm Hg. This is explained by the fact that in a vertical state, blood is retained in the veins located below the level of the heart (primarily in the veins of the lower extremities), and blood is deposited in them. As a result, the return of blood to the heart decreases and, consequently, cardiac output and blood supply to the aorta decrease.

In healthy people, OH is usually transient due to the activation of the most important regulatory mechanisms:

Excitation of the vasomotor center in the brain stem with the transmission of impulses through the efferent sympathetic nerves innervating the heart, peripheral vessels, kidneys, adrenal glands, while constriction of arterioles and venules occurs, heart rate increases, the content of plasma catecholamines increases, the renin-angiotensin-aldosterone system is activated;

Increased secretion of vasopressin by the hypothalamus, which causes spasm of arteries, arterioles, and increases peripheral resistance;

Decreased secretion of natriuretic peptide, which leads to a decrease in its vasodilating effect.

The causes of OH are varied; it is observed in a number of diseases, and often turns out to be the first or leading syndrome of a number of diseases and conditions, which include occult bleeding, chronic infections, polyneuropathy, etc.

In pathological conditions, the development of OH is caused by various mechanisms: excessive deposition of blood in the venous bed, a decrease in blood volume, a decrease in total peripheral vascular resistance. These mechanisms are expressed to varying degrees and are often combined in various forms of OH. However, first of all, the OG is determined the state of the autonomic nervous system and the degree of its involvement in the pathological process.

In this regard, all causes of orthostatic arterial hypotension are divided into
into 4 groups: *

Primary diseases of the autonomic and/or central nervous system;

Secondary damage to the autonomic nervous system;

Diseases that cause OH with a relatively intact autonomic nervous system;

External factors inducing OH.

Etiopathogenetic forms of chronic orthostatic

hypotension

1. Orthostatic hypotension caused by primary damage to the central nervous systemand/or the autonomic nervous system.

Idiopathic functional sympathicotonic OH

Bradbury-Eggleston syndrome (true autonomic failure)

Multiple system atrophy (Shy-Drager syndrome)

Baroreflex insufficiency syndrome

Dopamine B-hydroxylase deficiency

Riley-Day syndrome (familial dysautonomia)

Vasovagal syncope

Parkinson's disease with autonomic nervous system dysfunction

Atherosclerosis of the cerebral arteries

2. Orthostatic hypotension due to secondary involvementautonomic nervous system

Diabetes mellitus »^ -« " "

Autoimmune diseases (Guillain-Barré syndrome, rheumatoid arthritis, SLE)

Infections (diphtheria, botulism, tetanus)

Diseases of the central nervous system (multiple sclerosis, Wernicke encephalopathy, vascular lesions and tumors of the hypothalamus and midbrain with the development of secondary adrenal insufficiency, parkinsonism)

Arterial hypertension

Amyloidosis

Alcoholism

Chronic renal failure

3. Orthostatic hypotension with relatively intact autonomicnervous system

OH with reduced blood volume (loss of blood volume, anemia, vascular insufficiency, profuse vomiting, diarrhea, sepsis, hemodialysis, diabetes insipidus, pregnancy)

OH against the background of somatic diseases without a decrease in blood volume (coronary heart disease with heart rhythm disturbances, pheochromocytoma with predominant secretion of adrenaline by the tumor, atrial myxoma, malnutrition, cachexia, hypokalemia, adrenal insufficiency, mitral valve prolapse)

4. Orthostatic hypotension induced by external factors Iatrogenic OH (use of diuretics, A-blockers, ACE inhibitors, antidepressants, tranquilizers, barbiturates, calcium antagonists, centrally acting antihypertensive drugs, insulin, narcotics, antiparkinsonian drugs)

Prolonged lying down

Weightlessness

Hemodialysis

Intoxication with salts of heavy metals

Pathogenesis

The mechanisms of development of OH have their own characteristics in each etiopathogenetic group. However, there are general patterns that are the same for all groups.

The most important mechanism for the formation of OG is failure of the autonomic nervous system. In patients with OH, there is insufficient activation of the sympathetic part of the autonomic nervous system, low levels of catecholamines in the blood, as a result of which the total peripheral vascular resistance of the arterial and venous parts increases in orthostasis insufficiently or even decreases, an inappropriately low increase in heart rate is observed, and blood pressure decreases when standing up.

The second most important mechanism for the development of OG is significantly more than inNormally, blood is deposited in the venous system of the lower extremities.

In patients with OH it was found decreased levels of renin in the blood, which is explained by a decrease in adrenergic stimulation of renin production in the kidneys; at the same time, the level of aldosterone in the blood remains normal, which has not yet been explained. Perhaps the lack of an increase in aldosterone secretion by the zona glomerulosa of the adrenal cortex does not provide a proper increase in BCC.

A number of people take part in the development of OG vasoactive substances. An increase in the production of vasodilating factors such as adenosine and natriuretic peptide and insufficient production of endothelin-1 and angiotensin-11 have been established.

Clinical picture

All etiological forms of OH manifest themselves with a fairly uniform clinical picture, the severity of which depends on the severity of the disease. All symptoms of OH syndrome appear when moving from a horizontal position to a vertical or sitting one. Immediately after getting up, the patient experiences a pre-fainting state (lipothymia), a feeling of lightheadedness, nausea, dizziness, darkening of the eyes, sweating, tinnitus, a feeling of “sinking” appears, the patient feels as if “the earth is floating away from under his feet”, “his legs become stiff.” cotton wool." The duration of lipothymia is 3-5 s. The appearance of these sensations frightens the patient, and he tries to lie down again. In mild cases, the pre-fainting state passes, and the patient quickly adapts to the orthostatic position; with more severe OH, fainting develops. During fainting, the patient experiences severe pallor, muscle hypotension, dilated pupils, sweating appears, the pulse is barely palpable, and blood pressure drops significantly. With prolonged fainting (more than 10 seconds), the development of convulsive syndrome, inhibition of tendon reflexes, and the appearance of more pronounced neurological symptoms are possible.

OH is often more pronounced in the morning, intensifying in warm (especially hot) weather, after a heavy meal (especially common in older people), and physical activity.

In most patients, OH is accompanied by an increase in pulse when moving to a vertical position, which is due to reflex activation of the sympathetic nervous system.

The first group of OH caused by primary lesions of the autonomic > nervous system includes Bradbury-Eggleston syndrome, which is characterized by the clinical picture of OH, as well as other manifestations of autonomic dysfunction:

constipation, nocturia, sexual weakness, decreased sweating. The etiology of this disease is unknown, and its morphological substrate is degenerative processes in the neurons of the lateral horns of the spinal cord and sympathetic ganglia.

Another pathology with pronounced symptoms of OH is Shy-Drager syndrome or multiple system atrophy. With this disease m

A rarer, hereditary disease is Riley-Day syndrome,

The developing activation of the sympathetic-adrenal system during the transition to a vertical position can serve as an independent trigger factor for an anginal attack in patients with exertional angina of functional classes 2-4. In this case it becomes possible development of seizures due to standing up(without physical activity). Often patients can walk a significant distance, but when standing up they develop a seizure. Typically in such situations there are significant fluctuations in physical toleranceloads during the day. Usually, exercise tolerance is minimal in the morning and night hours and increases significantly in the evening. There may be significant decreased exercise tolerance after eating.

Characteristic of OG is nitrate resistance, which, in general, is not typical for angina pectoris. Calcium antagonists can sometimes cause OH to worsen. Particularly noteworthy are combinations of nitrates with calcium antagonists, which can cause pronounced vasodilation, and the use of which relatively often leads to the development of OH. As a rule, the use of drugs that aggravate OH in patients who already have it gives a weak antianginal effect. A paradoxical reaction may develop - increased severity of angina pectoris. Changes in the clinical picture of exertional angina can be significant and cause difficulties in making a diagnosis.

The following clinical observation can serve as an illustration of this situation:

Patient Sh., 72 years old, was hospitalized with complaints of burning chest pain that occurs in the following situations:

20-25 minutes after breakfast, continuing for 30-60 minutes, decreasing in a horizontal position, nitroglycerin does not relieve pain;

At night, when going to the toilet, short-term, passing on its own when lying down;

During the day, when climbing stairs 2 floors at an average pace,

short-term, passing when stopping.

More reliable results can be obtained using active orthostatic test with impedance-cardiographic monitoring of central hemodynamics. This method allows highly accurate assessment of changes in stroke and minute volume, peripheral resistance, left ventricular filling pressure, and blood volume in the great vessels of the chest during an orthostatic test. These indicators make it possible to record signs of a pathological decrease in blood flow to the heart, even in the absence or unclear response of blood pressure and heart rate. Current electrodes are applied to the patient's forehead, left leg, ring-shaped voltage electrodes are placed at the level of the 7th cervical vertebra and the base of the xiphoid process. The patient after staying for 10-15 minutes in

in a sitting position with legs extended forward, stands and then stands with feet shoulder-width apart for 15 minutes. Blood pressure is measured every minute, and central hemodynamic parameters are recorded automatically every 30 seconds throughout the test. Diagnostic criteria are the same as for an active orthostatic test; additional criteria are a decrease in SV by 25% or more, a decrease in MVR by 25% or more, or an increase in baseline impedance by 15% or more compared to the average values ​​​​obtained from this patient in lying position. Passive orthostatic tests (tilt tests) are carried out using a special device - a turntable. The rheograph electrodes are applied to the patient, he is fastened to the turntable and lies for 30 minutes in a horizontal position. The table is then rotated to an inclined position (head up) at an angle of 60 degrees and remains in this position for 45 minutes, after which the table returns to its original position. Registration of blood pressure and rhythm is carried out in all three phases of the study. Criteria for a positive test: decrease in blood pressure by 20 mm Hg. or more and diastolic by 10 mm Hg. and in the presence of cerebral ischemia or tachycardia, as well as neurogenic syncope that occurred during the test.

Treatment

In the treatment of patients with OH, the following areas are distinguished:

1.Non-drug therapy.

2. Pharmacological therapy.

3. Surgical treatment (implantation of an electrical pacemaker).

^Combination therapy.

Non-drug therapy may play an independent role in leveling moderately severe symptoms of OH. The following measures may be recommended for patients:

Compliance with physical activity;

Carefully selected therapeutic exercises;

Sleeping with the head end elevated or on an inclined plane up to 15 degrees;

Short rest (15-30 minutes) in a lying position or sitting with legs raised after breakfast;

Optimum ambient temperature in the room;

Diet with a high content of table salt and potassium;

Use of mechanical devices for external counterpressure: wearing elastic stockings, using anti-gravity suits.

Elderly people are advised to change positions slowly. Sleeping with your head elevated promotes sodium retention and reduces nocturnal diuresis. Patients should avoid prolonged standing. Meals should be small and not plentiful.

Pharmacological therapy OH must be differentiated; its purpose requires knowledge of the specific pathophysiological mechanisms of its development. Currently, drugs are used to treat OH, which, according to their main pharmacological action, can be divided into two groups:

1. Drugs that increase the volume of circulating blood.

2. Drugs with vasopressor or vasodilation inhibitory propertieseffects.

With neurogenic hypertension, blood pressure can be maintained at an adequate level with the help of adrenergic agonists. Preferred use midodrina -selective A 1-adrenergic agonist with a less pronounced central and cardiotropic effect. Concomitant therapy is reduced to increasing the volume of circulating plasma, first by increasing sodium intake, and then with the help of mineralcorticoids, which inhibit their release. Commonly used fludrocortisone, which also enhances peripheral vasoconstriction. There are reports that propranolol enhances the positive effects of sodium and mineralcorticoid therapy.

Orthostatic hypotension is an important clinical syndrome that occurs in many neurological and somatic diseases. With orthostatic hypotension, the neurologist is primarily faced with the 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 while standing. 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 position 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 fainting state. This condition, called lipothymia, is manifested by a feeling of lightheadedness, dizziness, and a premonition of loss of consciousness. The patient, as a rule, complains of general weakness, darkening of the eyes, sweating, noise in the ears and head, discomfort in the epigastric region, sometimes a feeling of “sinking”, “the ground floating from under the feet”, “emptiness in the head” and so on. Pallor of the skin, sometimes with a waxy tint, and short-term postural instability are noted. The duration of lipothymia is 3-4 s.

In more severe cases, the listed symptoms become more pronounced, and mild psychosensory disorders may appear. Orthostatic hemodynamic disturbances in mild cases are limited to manifestations of the lipotimic state; in more severe cases, fainting develops after the stage of lipothymia. The duration of the unconscious state depends on the cause that caused it. With neurogenic, reflex fainting, it is about 10 s. In severe cases (for example, with Shy-Drager syndrome), it can last tens of seconds. Severe orthostatic circulatory disorders can lead to death. During the unconscious state, diffuse muscle hypotonia, dilated pupils, and the eyeballs are retracted upward are noted; due to retraction of the tongue, mechanical asphyxia is possible; The pulse is thready, blood pressure drops.

With a longer duration of unconsciousness (more than 10 s), convulsions may occur (so-called convulsive syncope). Convulsions are predominantly tonic in nature, their intensity can reach opisthotonus, and are accompanied by clenching of fists. The pupils are sharply dilated, tendon reflexes are depressed, hypersalivation may be observed, and in severe and deep fainting - loss of urine, rarely stool, and in extremely rare cases, tongue biting may occur. Clonic convulsions are observed rarely, usually in the form of isolated individual twitches, never becoming generalized. After regaining consciousness, patients complain of general weakness, sweating, headache or heaviness in the head, and 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 Shay-Drager syndrome, the time interval from the moment the patient moves from a horizontal to a vertical position until the development of fainting 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 occur even while sitting. In less severe 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 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 the preconditions for ischemic damage to internal organs and the brain. This explains the 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 legs slightly bent at the knees, bending the torso low forward and lowering the head (skater's pose). To extend the time spent in an upright position, patients often tense their leg muscles, cross them, etc. in order to increase venous return of blood to the heart.

Causes and pathogenesis of orthostatic hypotension

Normally, when moving from a horizontal to a vertical position, gravitational movements of blood develop with the 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 the pathology of the central mechanisms of regulation of orthostatic reactions and disorders of the executive links of the cardiovascular system (defects and other heart 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 providing sufficient cardiac output;
2. heart rhythm disturbances that do 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 case of orthostatic circulatory disorders associated with autonomic nerve pathology, one of the following pathological mechanisms is more 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 blood vessels that ensure stability of blood pressure in the aorta;
3. disruption of regional mechanisms of redistribution of reduced blood circulation volume.

A known pathogenetic role may also be played by insufficient increase in heart rate in response to orthostatics (for example, a fixed heart rate 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 is reduced, due to which the latter can develop even with a short-term decrease in blood pressure.

Idiopathic orthostatic hypotension, first described by S. strongradbury and C. Egglestone in 1925, is based on progressive autonomic failure, associated in this case with damage to 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 slow down the heart rate. Sympathetic denervation is accompanied by the development of hypersensitivity of alpha-blockers 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 brain structures related to the segmental and stem autonomic (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 commonly cerebellar syndrome, amyotrophy, myoclonus and other optional symptoms). Currently, Shy-Drager syndrome, together with olivo-ponto-cerebellar and strionigral 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 more and more 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 making a differential diagnosis with a wide range of syndromes and diseases accompanied by paroxysmal disorders of consciousness. The most pressing task is to distinguish 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 the differential diagnosis, since convulsions can appear 15-20 s after a 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 to prolonged standing (queuing, 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 a horizontal position of the body and never occurs during sleep (at the same time, they are possible when getting out of bed at night). Orthostatic hypotension can be easily detected on a rotary table (passive change of body position). After the patient has been in a horizontal position for several minutes, he is turned to a vertical position. Over a short period of time, blood pressure drops and heart rate does not rise enough (or does not rise 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 mmHg. Art. when moving from a horizontal to a vertical position.

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

To exclude the epileptic nature of paroxysm, a thorough EEG study is necessary. At the same time, the detection of nonspecific changes in the EEG in the interictal period or a decrease in the threshold of convulsive readiness are not sufficient grounds for the diagnosis of epilepsy. Only the presence of classic epileptic phenomena on the EEG at the time of the attack (for example, the peak-wave complex) allows epilepsy to be diagnosed. Preliminary night sleep deprivation or a polygraphic sleep study can help identify the latter. It must also be remembered that epilepsy can occur with non-convulsive epileptic paroxysms. A hyperventilation test can provoke both simple (neurogenic) fainting 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 slowdown of the pulse by more than 10-12 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 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 be accompanied (or not 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 clinical manifestations. Symptoms are more pronounced in the morning, as well as after meals. Worsening 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-Barre syndrome, chronic renal failure, porphyria, bronchial carcinoma, leprosy and other diseases.

A deficiency of adrenergic effects 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 (ganglionic blockers, antihypertensive drugs, dopaminomimetics such as Nakoma, 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 systolic murmur and “cat purring” (easier heard in a standing position or in the "a la yours")

Sympathectomy can lead to insufficient venous return and, as a result, to orthostatic circulatory disorders. The same mechanism for the development of orthostatic hypotension occurs when using ganglion blockers, some tranquilizers, antidepressants and antiadrenergic agents. Certain conditions associated with decreased blood volume (anemia, acute blood loss, hypoproteinemia and low plasma volume, dehydration) predispose to fainting. In patients with suspected or existing blood volume deficiency, unusual tachycardia while sitting up in bed is of important diagnostic value. The likelihood of orthostatic hypotension and syncope due to blood loss depends on the amount of blood lost and the speed of this loss, on the patient's fear 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 removed within 6 to 13 minutes. Much more often, syncope is the result of pain or fear of blood loss. A more rare cause of syncope is mechanical obstruction of venous return in pregnant women, when a distended uterus can compress the inferior vena cava when the patient is lying down. Correcting 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 an autonomic response can come from different organs, the afferent innervation of which is vagal, trigeminal, glossopharyngeal or spinal. Syncope due to an increased vagal reflex can develop from pressure on the eyeballs, esophageal dilatation (for example, from swallowing a soda drink), a distended rectum, or a distended vagina. The common factor here is probably visceral pain. Atropine is an effective means of preventing the consequences of increased vagal reflexes.

, , , , , , [If neurogenic fainting can be successfully treated with the help of psychotropic, vegetotropic and restorative 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 cautiously (eg, ephedrine), but some patients find relief from combining these drugs with MAO inhibitors (eg, nialamide at regular dosage) or dihydroergotamine. The beta-blocker pindolol (Wisken), which has a beneficial effect on the heart muscle, is indicated. Obzidan is also used (to prevent peripheral vasodilation). Nerucal and indomethacin have the same property. A salt-rich diet is indicated. Drugs that retain salt (synthetic fluorinated corticosteroids), caffeine, yohimbine, and tyramine derivatives are administered. A positive result of implantation of a pacemaker that sets the heart rate to 100 per minute is described. They also use tight bandaging of the lower extremities, pelvic girdle and abdomen, and special inflatable suits. Swimming has a good effect. It is necessary to recommend 4 full meals a day. Some types of orthostatic hypotension (for example, caused by dopaminomimetics) are successfully prevented abroad using a peripheral dopamine receptor blocker - domperidone. There are also reports of a beneficial effect of a combination of mineralocorticoids (DOXA), sympathomimetics, L-dopa and monoamine oxidase inhibitors. A person with orthostatic hypotension is recommended to sleep with his head slightly elevated (5-20 degrees), which helps reduce hypertension in the supine position, as well as nocturnal diuresis. Since a significant increase in neurological symptoms in patients with Shy-Drager syndrome while smoking has been repeatedly described, such patients should be strongly advised to stop smoking.

Orthostatic (postural) hypotension is a sharp drop in blood pressure (most often more than 20/10 mmHg) when the patient assumes an upright position. Fainting, loss and confusion, dizziness, and blurred vision may occur within a few seconds or over a longer period. Some patients experience serial syncope. Physical activity or large meals can trigger such conditions. Most other manifestations are related to the underlying cause. Orthostatic hypotension is a manifestation of abnormal regulation of blood pressure due to various reasons, and not a separate disease.

Orthostatic hypotension occurs in 20% of older people. More often, it may be present in people with concomitant diseases, mainly arterial hypertension, and in patients who have been on bed rest for a long time. Many falls occur due to unrecognized orthostatic hypotension. Manifestations of hypotension are aggravated immediately after eating and stimulation of the vagus nerve (for example, after urination, defecation).

Postural orthostatic tachycardia syndrome (POTS), or so-called spontaneous postural tachycardia, or chronic or idiopathic orthostatic reaction, is a syndrome of pronounced tendency to orthostatic reactions at a young age. Standing up is accompanied by the appearance of tachycardia and various other symptoms(such as weakness, dizziness, inability to perform physical activity, clouding of consciousness), while blood pressure decreases by a very small amount or does not change. The cause of the syndrome is unknown.

Pathophysiology of orthostatic hypotension

Normally, gravitational stress due to rapid standing up leads to the movement of a certain volume of blood (from 0.5 to 1 l) into the veins of the lower extremities and torso. The subsequent transient decrease in venous return reduces cardiac output and hence blood pressure. The first manifestations may be signs of decreased blood supply to the brain. At the same time, a decrease in blood pressure does not always lead to brain hypoperfusion.

Baroreceptors of the aortic arch and carotid zone respond to arterial hypotension by activating autonomic reflexes aimed at restoring blood pressure. The sympathetic nervous system increases heart rate and myocardial contractility. Then the tone of the storage veins increases. At the same time, an increase in heart rate is caused by inhibition of parasympathetic reactions. If the patient continues to stand, activation of the renin-angiotensin-aldosterone system and secretion of antidiuretic hormone (ADH) occur, resulting in the retention of sodium and water ions and an increase in circulating blood volume.

Causes of orthostatic hypotension

The mechanisms for maintaining homeostasis may not be able to cope with the restoration of blood pressure in the event of disruption of the afferent, central or efferent link of autonomic reflexes. This can occur when taking certain medications, if myocardial contractility or vascular resistance are suppressed, with hypovolemia and dyshormonal conditions.

Causes of hypotension

Persistent arterial hypotension may be hereditary. So-called essential hypotension(primary hypotension) is the most common form of low blood pressure. Primary hypotension occurs mainly in young women with low body weight, more often in cases where there is a family predisposition. There is currently no clear explanation for the cause of persistent hypotension. One way or another, a predisposition to low blood pressure can pass from generation to generation. For example, hypotension is often observed in the same family in both mother and daughter. If there are no complaints associated with low blood pressure, then essential hypotension will not cause harm to the body. Moreover, hypotension can prevent the development of diseases associated with high blood pressure. People with hypotension have a lower risk of developing sclerosis of the blood vessels (arteriosclerosis), as well as its consequences, such as coronary heart disease, myocardial infarction, stroke and arteritis obliterans.

Secondary hypotension called a decrease in blood pressure due to a disease or drug.

The following diseases can cause the development of hypotension:

• Underfunction of the thyroid gland (hypothyroidism)
• Hypofunction of the adrenal cortex (Addison's disease)
• Hypofunction of the pituitary gland (insufficiency of the anterior lobe of the pituitary gland)
• Cardiac pathology (eg, heart failure, cardiac arrhythmias, pericarditis)
• Prolonged bed rest
• Fluid deficiency (hypovolemia)
• Salt deficiency (hyponatremia)

Drugs that can cause hypotension include:

• Antiarrhythmic drugs (intended to combat irregular heart rhythms)
• Antihypertensive drugs (used to treat high blood pressure)
• Diuretics (diuretics)
• Anti-ischemic drugs (used to treat coronary heart disease; eg, nitrate spray)
• Vasodilators (vasodilators)

Psychotropic medications (intended to combat depression, anxiety, insomnia)

Orthostatic hypotension(orthostasis = vertical position of the body) develops as a result of the fact that blood rushes into the vessels of the lower half of the body after a person quickly sits down or stands up. With orthostatic hypotension, the brain is supplied with insufficient blood for a short period of time. As a result, a person may feel dizzy. In the worst case, loss of consciousness occurs. Orthostatic episodes often accompany secondary hypotension. In most cases, the cause of circulatory disorders can be determined using the Shellong test.

Possible causes of orthostatic hypotension include:

• Secondary hypotension
• Autonomic nervous system dysfunction (eg, due to diabetes mellitus)
• Damage to nerve cells in the brain (eg, due to some forms of Parkinson's disease, hydrocephalus, alcohol abuse)
• Postthrombotic syndrome (which develops after deep vein thrombosis of the lower extremities)
• Varicose veins (varicose veins)

Causes

Diagnostics

• Analysis of the medical history and complaints - when (how long ago) dizziness, weakness, blurred vision appeared, what the patient associates with the occurrence of these symptoms, whether there was a long-term use of medications, bed rest, fluid loss.
• Life history and family history. When collecting a life history, attention is paid to the presence of similar symptoms in early periods of life, symptoms of diseases that can cause orthostatic hypotension.
• Family history. Find out whether there were similar conditions (dizziness, darkening of the eyes, pre-syncope and fainting when moving from a horizontal to a vertical position), as well as cardiovascular diseases in close relatives.
• Inspection. Blood pressure is measured with the patient lying down after 5 minutes of quiet lying, then after the patient assumes a standing position (in the first and third minutes). Detect heart murmurs. In addition, the color of the skin, signs of dehydration are noted, and the veins of the legs are examined. Examination can identify diseases that can cause severe hypotension.
• General blood analysis.

Thanks to the study, anemia can be detected in patients with arterial hypotension (with bleeding, anemia).

Treatment of orthostatic hypotension

Treatment depends on the cause of the disease.

• Stop taking medications that lead to the development of the disease.
• Light physical exercise, sitting down periodically, is recommended for patients who are forced to remain on bed rest for a long time.
• Increasing salt intake from food. Table salt contains sodium (a chemical element that retains water in the body and, as a result, increases blood pressure). Salt consumption is not recommended for elderly patients and patients with cardiovascular diseases.
• Wearing elastic stockings if hypotension is associated with dilation of the leg muscles.
• Slow and gradual getting out of bed is recommended, especially for elderly patients and pregnant women.

If the disease is chronic, they resort to prescribing medications.

• Adaptogens are agents that stimulate the central nervous system and the activity of the sympathetic division of the autonomic nervous system (part of the nervous system that regulates the activity of the circulatory, respiratory, digestive, excretory, reproductive, and metabolic organs)
• Adrenergic drugs of peripheral action (drugs that spasm (constrict) blood vessels to prevent a sharp drop in blood pressure during the transfer of body position from horizontal to vertical)
• Mineralocorticoids. Drugs of this group retain sodium ions in the blood, increase spasm of peripheral vessels to prevent a sharp drop in blood pressure during the transfer of body position from horizontal to vertical).
• Non-steroidal anti-inflammatory drugs. They have a spasmodic effect on peripheral vessels.
• Beta-adrenergic blockers. They enhance the effect of mineralocorticoids (hormones of the adrenal cortex that affect the water-salt balance and, accordingly, the level of blood pressure in the body) and sodium (a chemical element that retains water in the body and, as a result, increases blood pressure) affect the tone of the autonomic nervous system, blood vessels .