Orthostatic (postural) hypotension is a sudden drop in blood pressure(most often more than 20/10 mm Hg) when the patient takes a vertical position. For a few seconds or longer, fainting, loss and confusion of consciousness, dizziness, blurred vision may occur. Some patients have serial syncope. Physical activity or a heavy meal can provoke such conditions. Most of the other manifestations are related to the underlying cause. Orthostatic hypotension is a manifestation of abnormal regulation of blood pressure due to various reasons rather than a single disease.
Orthostatic hypotension occurs in 20% of the elderly. It is more common in people with comorbidities, predominantly arterial hypertension, and in patients long time observing bed rest. Many falls are due to unrecognized orthostatic hypotension. Manifestations of hypotension are aggravated immediately after eating and stimulation vagus nerve(eg, after urination, defecation).
Postural orthostatic tachycardia syndrome (POTS), or the so-called spontaneous postural tachycardia, or chronic or idiopathic orthostatic reaction, is a syndrome of pronounced propensity to orthostatic reactions at a young age. Getting up is accompanied by the appearance of tachycardia and various other symptoms(such as weakness, dizziness, inability to exercise, 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 standing up quickly leads to the movement of a certain amount of blood (from 0.5 to 1 liter) into the veins 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 reduced 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 activation autonomic reflexes aimed at restoring blood pressure. The sympathetic nervous system increases heart rate and myocardial contractility. Then the tone of storage veins increases. At the same time, the inhibition of parasympathetic reactions leads to an increase in the heart rate. If the patient continues to stand, the activation of the renin-angiotensin-aldosterone system and the secretion of antidiuretic hormone (ADH) occur, resulting in the retention of sodium and water ions, an increase in circulating blood volume.
Causes of orthostatic hypotension
Mechanisms for maintaining homeostasis may not be able to cope with the restoration of blood pressure in the event of a violation of the afferent, central or efferent link of autonomic reflexes. This may occur when taking certain medicines, in the event that myocardial contractility or vascular resistance is depressed, with hypovolemia and dyshormonal conditions.
Causes of hypotension
Permanent arterial hypotension may be hereditary. So-called essential hypotension(primary hypotension) is the most common form of lowering blood pressure. Primary hypotension occurs mainly in young women with low body weight, more often in cases where there is a family predisposition. Currently, there is no clear explanation of the cause of persistent hypotension. One way or another, the predisposition to low blood pressure can pass from generation to generation. For example, hypotension is often seen in the same family in mother and daughter. If there are no complaints associated with low blood pressure, then essential hypotension will not harm the body. Moreover, hypotension can prevent the development of diseases associated with increased level blood pressure. Individuals with hypotension have a lower risk of developing sclerosis blood vessels(arteriosclerosis), as well as its consequences, such as coronary heart disease, myocardial infarction, stroke and arteritis obliterans.
Secondary hypotension is called a decrease in blood pressure due to a disease or the action of a drug.
Hypotension may be caused by:
- Hypofunction thyroid gland(hypothyroidism)
- Hypofunction of the adrenal cortex (Addison's disease)
- Hypofunction of the pituitary gland (failure of the anterior pituitary gland)
- Cardiac disorders (eg, heart failure, disorders heart rate, pericarditis)
- Prolonged bed rest
- Fluid deficiency (hypovolemia)
- Salt deficiency (hyponatremia)
Drugs that can cause hypotension include:
- Antiarrhythmic drugs (used to treat abnormal heart rhythms)
- Antihypertensive drugs (used to control high blood pressure)
- Diuretics (diuretics)
- Anti-ischemic drugs (used to treat coronary disease hearts; e.g. nitrates in spray form)
- Vasodilators (vasodilators)
Psychotropic drugs (used to treat 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. In orthostatic hypotension, the brain is not supplied with enough 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 Schellong test.
TO possible reasons development of orthostatic hypotension include:
- Secondary hypotension
- Autonomic nervous system disorders (eg, due to diabetes mellitus)
- Damage nerve cells in the brain (eg, due to some forms of Parkinson's disease, hydrocephalus, alcohol abuse)
- Post-thrombotic syndrome (which develops after deep vein thrombosis of the lower extremities)
- Varicose veins (varicose veins)
Causes
Diagnostics
- Analysis of the history of the disease and complaints - when (how long ago) dizziness, weakness, blurred vision appeared, what the patient associates the occurrence of these symptoms with, whether there was a long-term medication, bed rest, fluid loss.
- Life history and family history. When collecting anamnesis of life, attention is paid to the presence of similar symptoms in the early periods of life, symptoms of diseases that can cause orthostatic hypotension.
- Family history. They will find out if there were similar conditions (dizziness, blackouts in the eyes, pre-fainting and fainting when moving from a horizontal position to a vertical one), as well as cardiovascular diseases from close relatives.
- Inspection. Blood pressure is measured in the patient's supine position after 5 minutes of quiet lying, then after the patient has taken a standing position (at the first and third minutes). Detect heart murmurs. Also note the color skin, signs of dehydration, the veins of the legs are examined. Examination reveals diseases that can cause severe hypotension.
- General blood analysis.
Thanks to the study in patients with arterial hypotension, anemia can be detected (with bleeding, anemia).
Indicators such as creatinine (a substance formed in the muscles, entering the bloodstream and then excreted by the kidneys. Therefore, the level of creatinine in the blood serves as an indicator of kidney activity), urea (the end product of protein metabolism), cholesterol (a fat-like substance, a building block of cells) are determined. ; levels of potassium and sodium, which are electrolytes and affect the water-salt balance in the body.
To detect adrenal insufficiency, the level of cortisol (adrenal hormone) is determined to detect pathology (disorders) of the thyroid gland (hypothyroidism - a lack of thyroid hormones; hyperthyroidism - an excess of thyroid hormones).
Treatment of orthostatic hypotension
Treatment depends on the cause of the disease.
- Reception Cancellation medicines leading to the development of the disease.
- Light exercise, periodically sit down, it is recommended for patients who are forced to stay in bed for a long time.
- Increasing dietary salt intake. Edible salt contains sodium ( chemical element, which retains water in the body and, as a result, increases blood pressure). Salt intake is not recommended for elderly patients and patients with diseases of the cardiovascular system.
- Wearing elastic stockings if hypotension is due to expansion 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, resort to the appointment of drugs.
- Adaptogens - 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, digestion, excretion, reproduction, and metabolism organs)
- Adrenergic drugs of peripheral action (drugs that spasm (constrict) blood vessels to exclude sharp drop blood pressure during the transfer of body position from horizontal to vertical)
- Mineralocorticoids. The drugs of this group retain sodium ions in the blood, increase the spasm of peripheral vessels to prevent a sharp drop in blood pressure during the transfer of the body position from horizontal to vertical).
- Non-steroidal anti-inflammatory drugs. They have a spasmodic effect on peripheral vessels.
- Beta - blockers. Enhance the action 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 pressure) affect the tone of the autonomic nervous system, blood vessels .
Fainting as a clinical syndrome is characterized by muscle weakness, arterial hypotension and loss of consciousness. Immediately before fainting, the patient is always in an upright position. An exception is syncope due to atrioventricular blockade of the second and third degree (attacks of Adams-Stokes).
Orthostatic arterial hypotension is understood as a decrease in both systolic and diastolic blood pressure by at least 20 mm Hg. Art. when the body moves to a vertical position.
Postural arterial hypotension is a decrease in blood pressure due to a change in body position. Postural hypotension in late pregnancy occurs in the supine position, in which the uterus compresses the pelvic and abdominal veins.
As a result, the preload of the heart is reduced in such a way that arterial hypotension develops. With a left atrial myxoma and a pedunculated thrombus of the same localization, syncope and postural hypotension may occur in the sitting position, in which the mobile tumor and thrombus move and close the left atrioventricular orifice.
Regardless of the origin of orthostatic arterial hypotension, its clinical picture always the same:
Disorders of vision and speech, as well as dizziness when transferring the body to a vertical position, after which a coma may occur.
Pallor of the skin, tachycardia and increased sweating, which are especially pronounced in patients with sympathicotonic type of orthostatic arterial hypotension (see below).
Reversal of symptoms when the body returns to a horizontal position.
With the sympathicotonic type of orthostatic arterial hypotension, the minute volume of blood circulation drops to such an extent that, despite the compensatory enhanced adrenergic stimulation of capacitive and resistive vessels, blood pressure decreases abnormally (Table 3.6).
|
Pathological condition and disease that cause orthostatic hypotension |
The main link in the pathogenesis of orthostatic arterial hypothesia |
|
|
Due to a decrease in total venous return to the heart at the level of skeletal muscles, veins and heart |
Muscular atrophy |
|
|
Underdevelopment of voluntary muscles in young people |
Low strength and intensity of the mechanical effect of skeletal muscles on the veins as the reason for the decrease in the volumetric velocity of blood flow through the capacitive vessels |
|
|
Insufficiency of venous valves |
Decreased volumetric velocity of blood moving towards the heart |
|
|
Compression of the veins (in late pregnancy, etc.) |
Decreased volumetric velocity of blood moving towards the heart |
|
|
Cardiac tamponade, constrictive pericarditis, and right atrial globular thrombus |
Blockade of diastolic filling with blood of the right ventricle |
Table 3.6. Pathogenetic classification of sympathicotonic postural arterial hypotension
|
Type of sympathicotonic arterial hypotension |
Pathological conditions that cause orthostatic arterial hypotension |
|
|
Associated with decreased intravascular plasma and blood volumes |
Side effects of nitrates Angiomatosis |
Relative hypovolemia, that is, a discrepancy between the volume of circulating blood and the volume of capacitive vessels due to their dilation |
|
Blood loss Decrease in the volume of extracellular fluid due to vomiting, diarrhea, excessive diuresis Pathological capillary permeability (with sepsis, systemic inflammatory reaction, in the focus of skin lesions) Decreased total body sodium and extracellular fluid volume due to hypoaldosteronism |
hypovolemia |
|
|
Type of sympathicotonic arterial hypotension |
A pathological condition that causes orthostatic arterial hypotension |
The main link in the pathogenesis of orthostatic arterial hypotension |
|
Caused by a decrease in the pumping function of the heart |
Myocarditis Ischemic heart disease in angina pectoris of the third-fourth functional classes |
Low contractility |
|
Bradyarrhythmia in response to a change in body position |
Decreased cardiac output due to infrequent ejection of blood into the aorta by the left ventricle |
|
|
Tachyarrhythmia in response to a change in body position |
Decrease in minute volume of blood circulation due to a decrease in the total duration of diastolic filling of the left ventricle |
|
|
aortic stenosis Stenosis pulmonary artery |
Obstruction of blood flow at the level of the aorta and pulmonary artery |
Table 3.6. (continuation)
With the sympatholytic type of orthostatic arterial hypotension (Table 3.7), it is a consequence of blockade in any of the links reflex arc sympathetic reflexes aimed at preventing a decrease in blood pressure due to the transfer of the body to a vertical position. Most often, in patients with sympatholytic arterial hypotension, it occurs due to the side effects of drugs that block synaptic transmission in the sympathetic ganglia and excitation of alpha-one-adrenergic receptors, as well as affecting the release of norepinephrine from nerve endings.
Often, the insufficient effectiveness of sympathetic reflexes, which ensure the constancy of blood pressure, regardless of body position, is due to systemic typical pathological processes caused by prolonged physical inactivity (including in a horizontal position), starvation, etc. It should be noted that prolonged physical inactivity in a horizontal position predisposes to arterial hypotension of any origin.
The syndrome of idiopathic orthostatic arterial hypotension consists of orthostatic arterial hypotension, dry skin as a result of low sweating, abnormal stability of the heart rate, increased peripheral reflexes (an element of the denervation syndrome), dysregulation of urination (urinary incontinence) with normal cognitive functions. Some patients develop impotence. Especially often this syndrome is combined with parkinsonism. The morphopathogenesis of the syndrome in some patients is the degeneration of sympathetic nerves and ganglia. Consequences of low systemic adrenergic stimulation in this syndrome is low level activation of the renin-angiotensin-aldosterone mechanism and an abnormally reduced concentration of catecholamines in the circulating blood.
|
Pathological conditions and disease that cause arterial hypotension |
The main link in the pathogenesis of orthostatic arterial hypotension |
|
|
Caused by expansion of resistive vessels |
Vasculitis and amyloidosis, including as causes of denervation of resistance vessels. Expansion of resistive vessels due to side effects of nitroprusside and nitrates |
Fall in total peripheral vascular resistance |
|
Caused by blockade of the afferent link of sympathetic reflexes |
spinal atrophy ( chronic inflammation and progressive sclerosis of the posterior roots and pillars spinal cord, Duchenne disease) |
Interruption of centrifugal impulses to effectors of sympathetic reflexes |
|
Updated by blockade of sympathetic reflexes in the central link |
Shy-Drager syndrome (progressive encephalomyopathy affecting the autonomic nervous system with outward eye paresis, iris atrophy, emotional lability, anhidrosis, impotence, and tremor). Atherosclerosis of cerebral vessels (including as a cause of parkinsonism). Wernicke syndrome. Syringomyelia. Myelopathy. Side effects of neurotropic drugs (benzodiazepines, etc.) |
Lack of growth of adrenergic stimulation of resistive vessels and capacitive vessels in response to the transition of the body to a vertical position |
|
Type of sympathicolytic arterial hypotension |
Pathological condition and disease that cause orthostatic arterial hypotension |
The main link in the pathogenesis of orthostatic arterial hypotension |
Table 3.7. Sympathicolytic arterial hypotension
|
Caused by damage to the efferent link of sympathetic reflexes |
Chronic idiopathic orthostatic arterial hypotension (see below). Polyneuritis caused by diabetes mellitus, porphyria, etc. Myelopathy. Iatrogenia (sequelae of sympathectomy, side effect sympatholytic drugs). Insufficiency of secretion of hormones of the adrenal cortex. |
Deficiency of efferent conduction along sympathetic conductors Blockade of efferent sympathetic impulse conduction through ganglia and synapses. Low sensitivity of adrenergic receptors associated with adrenal insufficiency. |
Table 3.7. Sympathicolytic hypotension (continued)
Definition. Orthostatic [arterial] hypotension (hereinafter referred to as OH) is a pathological decrease in systolic blood pressure in a standing position [orthostasis]. According to various estimates, the prevalence of OH ranges from 5 to 20% (including depending on age). Often this condition remains undiagnosed. OH most often occurs in adulthood and old age (one of the reasons for this is the age-related decrease in the sensitivity of baroreceptors).
Classification. According to the time of occurrence after the transition to a standing position, early, classic and delayed (delayed) OH are distinguished. Early OH develops within the first 15 seconds after getting up and is characterized by a decrease in blood pressure by more than 40 mm Hg. immediately after going upright. Then, BP spontaneously and quickly normalizes, so hypotension and symptoms persist for a short time - less than 30 s (early OH - common cause symptoms of orthostatic insufficiency, indeed, many people are familiar with the feeling of "lightness in the head" and darkening in the eyes that occur immediately after standing up). Classical OH is characterized by a decrease in systolic blood pressure≥20 and diastolic blood pressure≥10 mm Hg. within 3 minutes after moving to a standing position. It develops in patients with pure autonomic insufficiency, hypovolemia and other forms of insufficiency of the autonomic system. Delayed (progressive, delayed) OH is characterized by a slow progressive decrease in systolic blood pressure between the 5th and 45th minutes after the transition to a vertical position. The time of occurrence of OH correlates with the degree of autonomic insufficiency. Often seen in older people. It is associated with age-related impairment of compensatory reflexes and myocardial thickening in elderly patients sensitive to reduced preload.
note! There is a syndrome of postural orthostatic tachycardia (POTS). Some patients, mostly young women, have orthostatic symptoms (but no syncope), which are associated with a sharp increase in heart rate (more than 30 per minute or more than 120 per minute) and BP instability. POTS is often associated with chronic fatigue syndrome. The mechanisms of its development have not been established.
According to the course, OH can be divided into acute and chronic. Acute develops over a relatively short period of time, often manifests as a symptomatic course and is a consequence of conditions such as myocardial ischemia, the start of a number of medications, sepsis, dehydration. Chronic OH develops gradually over a relatively long period of time and initial period often asymptomatic (see diagram).
The etiological classification of OH traditionally distinguishes neurogenic forms of OH, which are the result of diseases of both the central and peripheral autonomic nervous system (ANS), drug-induced OG and OG with reduced circulating blood volume(see "reasons for the development of OH").
Symptoms OH, as a rule, develop in response to a sudden change in body position (most often when moving from a supine position to a standing position, rarely developing while lying down), as well as when eating (postprandial arterial hypotension) and prolonged standing (symptoms may also be aggravated with exercise and with an increase in temperature environment). Symptoms of OH are a consequence of cerebral hypoperfusion and include general weakness, dizziness and fainting, blurred vision or darkening in the eyes, with severe manifestations - loss of consciousness (fainting, or syncope). Less commonly, OH can lead to angina or stroke. Patients may also complain of pain in the suboccipital region, along the back of the neck, in the area of the shoulder girdle. It must be remembered that in individuals with preserved mechanisms of cerebral circulation autoregulation, OH may be asymptomatic, but such patients still have a risk of falls and loss of consciousness. The severity of symptoms of OH can range from mild to extremely severe. Patients with severe OH sometimes cannot move from a horizontal to a vertical position without experiencing pre-syncope or losing consciousness. In rare cases, OH is associated with the development of cardiovascular and cerebrovascular complications, with the risk of congestive heart failure and paroxysmal atrial fibrillation, with an increased risk of falls and increased mortality in the elderly due to falls. In contrast, some patients with OAH may be asymptomatic. It should also be taken into account that many patients with OH, especially those with pre-existing autonomic failure, have systolic hypertension in the sitting or lying position.
note! "Orthostasis intolerance" refers to a set of symptoms (in various combinations), which occur in an upright position as a result of circulation disturbance. They include fainting, as well as (1) dizziness and lightheadedness, (2) weakness, fatigue, disorientation, (3) palpitations, sweating, (4) visual disturbances (including blurred vision, increased brightness, tunnel vision), (5) hearing loss (including hearing loss, crackling, and tinnitus), (6) pain in the neck (occiput, neck, and shoulder), lower back, or heart. The various clinical syndromes of orthostasis intolerance are listed in (these also include forms of reflex syncope triggered by orthostatic stress).
Neurogenic OH develops in the second half of life, with the exception of genetically determined diseases. It includes diseases of both the central and peripheral ANS and is characterized by a fixed pulse (pulse that does not increase when standing up), as well as arterial hypertension in the supine position. At the same time, OH is often, especially in diseases of the central ANS, accompanied by local autonomic insufficiency, manifested by dysfunction various bodies (Bladder, intestines and reproductive system). Clinical manifestations of local autonomic insufficiency include hypohidrosis, gastroparesis, impotence, urinary incontinence, diarrhea and constipation.
Pure (isolated) autonomic insufficiency (Bradbury-Eggleston syndrome). A degenerative disease of the autonomic nervous system that debuts in adulthood and is more common in men. It is characterized by an acute onset, a gradually progressive course, and responds well to treatment. OH is the core of the clinical picture. Sweating, salivation, urination and other disorders autonomic disorders possible, but not dominant. There are no motor impairments, rarely the condition progresses to Parkinson's disease or dementia with Lewy bodies. With this disease, the content of norepinephrine in blood plasma and urine is significantly reduced, sometimes up to 10% of the norm or lower (the independence of this nosological form is doubtful, it is probably identical to the Shy-Drager syndrome).
Multiple system atrophy (Shy-Dreijer syndrome). It is a sporadic progressive disease characterized by autonomic dysfunction, parkinsonism and ataxia in various combinations. Expressed autonomic dysfunction occurs on early stages disease and may be the only symptom, manifested by OH, impotence, impaired urination. Parkinson's syndrome and cerebellar signs usually occur in combination, but sometimes its individual manifestations can dominate. The average life expectancy of patients is significantly reduced and is 7-9 years.
Parkinson's disease. OH occurs in the later stages of the disease and not in all patients; it is often provoked by antiparkinsonian drugs. Very rarely, OH is as severe as in multiple system atrophy. Lewy dementia is important to recognize in patients with parkinsonism. In this disease, OH occurs in the early stages of the disease. Progressive dementia in these patients can be dramatic, often accompanied by visual hallucinations. Cognitive deficits precede or accompany parkinsonism.
Dopamine-β-hydroxylase deficiency is perhaps the only syndrome of primary autonomic insufficiency, the mechanism and specific treatment which is currently the most fully developed. Dopamine-β-hydroxylase is a key enzyme in the formation of norepinephrine. Main clinical manifestation diseases - OH, the symptoms of which begin to appear in childhood and adolescence. The literature describes clinical case successful treatment Droxidopa dopamine-β-hydroxylase deficiency in a 20-year-old patient. The time she was in an upright position before the start of treatment was 2 minutes, and as a result drug treatment and training, she was able to successfully participate in the marathon race.
Any pathological process that causes peripheral neuropathy involving thin fibers can lead to autonomic failure. The most common cause of secondary autonomic insufficiency is diabetes mellitus. Other diseases of this group include amyloidosis and lung cancer. Much less often, orthostatic hypotension is associated with peripheral neuropathies that occur with vitamin B12 deficiency, exposure to neurotoxins, infections (eg, acquired immunodeficiency syndrome), and porphyria.
It should be noted that the diagnostic approach to patients with identified OH should be based primarily on the identification of potentially treatable conditions that may cause or significantly exacerbate orthostatic hypotension. During the examination, the following parameters should be clarified:
a detailed list of medications used by the patient (both prescription and over-the-counter); some of them that can lead to OG;
a recent history of events that may cause a decrease in circulating blood volume (vomiting, diarrhea, restriction of fluid intake, fever);
a history of congestive heart failure, malignant neoplasms, diabetes, alcoholism;
the patient has parkinsonism, ataxia, polyneuropathy, or dysautonomia (for example, impaired pupillary reflex, constipation or erectile dysfunction).
You can get all the necessary information about the pathogenesis, diagnosis and treatment of OH from the following sources:
article "Orthostatic arterial hypotension in neurological diseases: concept, etiology, diagnostic and treatment algorithms" Yu.A. Seliverstov (magazine " Nervous diseases"No. 3, 2014) [read];
lecture “Orthostatic hypotension. View of a cardiologist "G.A. Golovina, Federal State Budgetary Institution of Health Care "Samara Medical Clinical Center" of the Federal Medical and Biological Agency, Tolyatti, Russia; D.V. Duplyakov, State Health Institution "Samara Regional Clinical Cardiological Dispensary", Samara, Russia (magazine " Arterial hypertension"No. 2, 2014) [read];
article "Syndrome of postural orthostatic tachycardia" D.V. Duplyakov, Samara Regional Clinical Cardiological Dispensary; O.V. Gorbachev, G.A. Golovina, FBUZ SMCC FMBA of Russia, Togliatti (journal "Bulletin of Arrhythmology" No. 66, 2011) [read];
Guidelines for the diagnosis and treatment of syncope (2009); Working group on the diagnosis and treatment of syncope of the European Society of Cardiology (ESC); journal "Rational pharmacotherapy in cardiology" No. 6 (1), 2010 [read];
article "Orthostatic hypotension as a modifiable risk factor for the development of cognitive impairment: a review of the literature" Ostroumova O.D., Shikh E.V., Rebrova E.V., Ryazanova A.Yu.; Federal State Autonomous Educational Institution of Higher Education “First Moscow State Medical University named after I.I. THEM. Sechenov, Ministry of Health of the Russian Federation, Moscow; Federal State Budgetary Educational Institution of Higher Education “Russian National Research Medical University named after N.N. N.I. Pirogov" Ministry of Health of the Russian Federation - OSB "Russian Gerontological scientific and clinical center", Moscow; Federal State Budgetary Educational Institution "Volgograd State Medical University" of the Ministry of Health of the Russian Federation, Volgograd (journal "Neurology, Neuropsychiatry, Psychosomatics" No. 1, 2019) [read].
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ORTHOSTATIC ARTERIAL HYPOTHEUS
Orthostatic arterial hypotension - this is any decrease in blood pressure that occurs in the patient when moving from the position /, / ! "lying" to the "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 can be assumed that the frequency in the general population may be from 0.5 to 1.5%. At the same time, the frequency of detecting OH significantly increases among hospital patients - 7-33%, among the elderly and senile it reaches 14-50%. Thus, OH is one of the most frequent 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 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.
At healthy people OG is usually transient in nature due to the inclusion of the most important regulatory mechanisms:
Excitation of the vasomotor center in the brainstem 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, the renin-angiotensin-aldosterone system is activated;
An increase in the secretion of vasopressin by the hypothalamus, which causes spasm of the arteries, arterioles, 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.
At pathological conditions the development of OH is due to various mechanisms: excessive deposition of blood in the venous bed, a decrease in BCC, a decrease in total peripheral vascular resistance. These mechanisms are expressed to varying degrees and are often combined in various forms OG. However, OG is primarily 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
for 4 groups: *
Primary diseases of the autonomic and / or central nervous system;
Secondary damage to the autonomic nervous system;
Diseases that cause OH in a relatively intact autonomic nervous system;
External factors inducing OH.
Etiopathogenetic forms of chronic orthostatic
hypotension
1. Orthostatic hypotension due to a primary CNS lesionand/or autonomic nervous system.
Idiopathic functional sympathicotonic OH
Bradbury-Eggleston syndrome (true autonomic failure)
Multiple system atrophy (Shy-Drager syndrome)
Syndrome of baroreflex insufficiency
Dopamine B-hydroxylase deficiency
Riley-Day syndrome (familial dysautonomy)
Vasovagal syncope
Parkinson's disease with dysfunction of the autonomic nervous system
Atherosclerosis of the arteries of the brain
2. Orthostatic hypotension due to secondary involvementautonomic nervous system
Diabetes »^ -« ""
Autoimmune diseases (Guillain-Barré syndrome, rheumatoid arthritis, SLE)
Infections (diphtheria, botulism, tetanus)
CNS diseases ( multiple sclerosis, Wernicke's 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 BCC (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 BCC (IHD with cardiac arrhythmias, 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, antihypertensive drugs central action, insulin, drugs, antiparkinsonian drugs)
Prolonged lying
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 of the mechanisms for the formation of GO is insufficiency of the autonomic nervous system. Patients with OH have insufficient activation of the sympathetic division 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 divisions does not increase sufficiently in orthostasis or even decreases, an inadequately 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 innormal, deposition of blood in the venous system of the lower extremities.
Patients with OH found reduced 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 absence of an increase in aldosterone secretion by the glomerular zone of the adrenal cortex does not provide a proper increase in BCC.
A number of vasoactive substances. An increase in the production of such vasodilating factors as adenosine, natriuretic peptide and insufficient production of endothelin-1, angiotensin-11 was established.
Clinical picture
All etiological forms of OH are manifested by a fairly similar clinical picture, the severity of which depends on the severity of the disease. All the symptoms of OH syndrome appear when moving from a horizontal position to a vertical or sitting position. Immediately after getting up, the patient experiences a fainting state (lipothymia), there is a feeling of lightheadedness, nausea, dizziness, darkening in the eyes, sweating, tinnitus, a feeling of "falling through", it seems to the patient that "the earth is floating away from under his feet", "the legs become wadded." 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-syncope state disappears, and the patient quickly adapts to the orthostatic position, with a more pronounced OH, fainting develops. During fainting, the patient has marked pallor, muscle hypotension, dilated pupils, sweating appears, the pulse is barely palpable, blood pressure drops significantly. With prolonged fainting (more than 10 seconds), the development of a convulsive syndrome, inhibition of tendon reflexes, and the appearance of more pronounced neurological symptoms are possible.
OH is often more pronounced in the morning, worse in warm (especially hot) weather, after a heavy meal (especially common in older people), physical activity.
In most patients, OH is accompanied by an increase in heart rate 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, reduced 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 shye-drager syndrome or multiple system atrophy. With this disease m
A rarer, inherited disease is riley-day syndrome,
which is characterized by a primary lesion of the autonomic nervous system and
along with OH, it is manifested by severe hyperhidrosis, salivation,
emotional lability, transient pustular skin rash,
impaired coordination of movements, decreased pain sensitivity,
violation of thermoregulation.
Clinical features of exertional angina with concomitant OH, ^
The developing activation of the sympathetic-adrenal system during the transition to a vertical position can serve as an independent triggering factor for an anginal attack in patients with angina pectoris of 2-4 functional classes. In this case, it becomes possible the development of seizures in connection with getting up(without physical activity). Often patients can walk a considerable distance, but when they get up they develop an attack. Usually in such situations there are significant fluctuations in physical toleranceload 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 capacity after meals.
Characteristic for OG is nitrate resistance, which, in general, is not characteristic of angina pectoris. Exacerbation of OH can sometimes be caused by calcium antagonists. Of particular note is the combination 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 exacerbate OH in patients who already have it, gives a weak antianginal effect. Perhaps the development of a paradoxical reaction - an increase in the severity of angina pectoris. The change in the clinical presentation of angina pectoris can be significant and cause difficulties in making a diagnosis.
The following clinical observation can serve as an illustration of such a situation:
Patient Sh., 72 years old, was hospitalized with complaints of burning chest pains that occur in the following situations:
20-25 minutes after breakfast, lasting for 30-60 minutes, decreasing in a horizontal position, nitroglycerin does not stop the pain;
At night when going to the toilet, short-term, passing on their own when laying down;
During the day, when climbing stairs 2 floors at an average pace,
short-term, passing at a stop.
More reliable results can be obtained with active orthostatic test with impedance cardiographic monitoring of central hemodynamic parameters. This method allows to evaluate with high accuracy changes in stroke and minute volume, peripheral resistance, filling pressure of the left ventricle, blood volume in main vessels chest during the orthostatic test. These indicators make it possible to fix signs of a pathological decrease in blood flow to the heart, even in the absence or indistinct reaction of blood pressure and heart rate. Current electrodes are placed on the patient's forehead, left leg, ring-shaped voltage electrodes are placed at the level of the 7th cervical vertebra and grounds xiphoid process. The patient after staying for 10-15 minutes in
in a sitting position with legs stretched forward, gets up and then stands, legs apart shoulder-width apart, for 15 minutes. Blood pressure is measured every minute, and central hemodynamic parameters are recorded automatically every 30 seconds during the entire test. Diagnostic criteria are the same as for an active orthostatic test, with additional criteria being a decrease in SV by 25% or more, a decrease in MOS by 25% or more, or an increase in baseline impedance by 15% or more compared with the average values obtained in this patient in lying position. Passive orthostatic tests(tilt tests) are carried out using a special device - a turntable. The electrodes of the rheograph are applied to the patient, he is fastened to the turntable and lies for 30 minutes in a horizontal position. Then the table is rotated into an inclined position (head up) at an angle of 60 degrees and is 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. and 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 directions are distinguished:
1.Non-drug therapy.
2. Pharmacological therapy.
3. Surgical treatment (implantation of a pacemaker).
^Combination therapy.
Non-drug therapy can play an independent role in leveling moderately severe symptoms OG. Patients may be advised to:
Compliance with the regime of physical activity;
Carefully selected exercises of therapeutic gymnastics;
Sleep with a raised head end or on an inclined plane up to 15 degrees;
Short-term rest (15-30 minutes) in a lying position or sitting with legs raised after breakfast;
Optimum ambient temperature in the room;
High content diet table salt and potassium;
Use of mechanical devices for external counter-pressure: wearing elastic stockings, using anti-gravity suits.
Older people are advised to change the posture slowly. Head-elevated sleep promotes sodium retention and reduces nocturnal diuresis. Patients should avoid prolonged standing. Food should be fractional and not plentiful.
Pharmacological therapy OG must be differentiated, its purpose requires knowledge of specific pathophysiological mechanisms its development. Currently, for the treatment of OH, drugs are used that, by their main pharmacological action can be divided into two groups:
1. Drugs that increase the volume of circulating blood.
2. Drugs with vasopressor or inhibitory vasodilationeffects.
With neurogenic OH, it is possible to maintain blood pressure at an adequate level with the help of adrenomimetics. It is preferable to use midodrine -selective A 1-agonist with less pronounced central and cardiotropic action. Concomitant Therapy is reduced to an increase in the volume of circulating plasma, first by increasing the intake of sodium, and then with the help of mineralocorticoids that 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 collapse (orthostatic hypotension) is a human condition in which a sharp transition of the body from a horizontal to a vertical position or prolonged standing causes a decrease in blood pressure as a result of insufficient blood flow to the brain or a delayed reaction of the heart to a change in body position. Orthostatic hypotension is accompanied by dizziness and darkening of the eyes, after which fainting may develop.
| ICD-10 | I95.1 |
|---|---|
| ICD-9 | 458.0 |
| DiseasesDB | 10470 |
| Medline Plus | 10470 |
| eMedicine | ped/2860 |
| MeSH | D007024 |
General information
The clinical picture of the collapse was described by various scientists long before the appearance of the term itself (for example, a complete picture of the infectious collapse in typhoid fever was presented by S.P. Botkin at a lecture in 1883).
The doctrine of collapse developed as ideas about circulatory insufficiency developed. In 1894, IP Pavlov drew attention to the dependence of collapse on a decrease in the volume of circulating blood, and noted that the development of collapse is not associated with weakness of the heart.
G. F. Lang, N. D. Strazhesko, I. R. Petrova, V. A. Negovsky and other scientists studied the causes and mechanisms of collapse development, but the generally accepted definition of collapse has not been developed to this day. Disagreement causes a distinction between the concepts of "collapse" and "shock". Scientists have not yet come to a consensus whether these phenomena are periods of the same pathological process, or independent states.
Forms
Depending on the causes of occurrence, orthostatic collapse is distinguished, caused by:
- primary neuropathies;
- secondary neuropathies;
- idiopathic factors (for unknown reasons);
- taking medications;
- infectious diseases;
- anemia;
- diseases of the cardiovascular system;
- blood loss;
- prolonged bed rest;
- disorders of the adrenal glands;
- violations of water and electrolyte balance, which lead to dehydration.
Depending on the severity of the condition, there are:
- mild I degree, which is manifested by rare pre-syncope states without loss of consciousness;
- moderate II degree, in which episodic fainting occurs after the body is transferred to a vertical position or as a result of prolonged standing in a fixed position;
- severe III degree, which is accompanied by frequent fainting, occurring even in a sitting and half-sitting position or as a result of short-term standing in an immobile position.
Depending on the duration of the periods during which episodes of orthostatic collapse occur, there are:
- subacute orthostatic hypotension, which lasts for several days or weeks and is associated in most cases with transient disorders the work of the autonomic nervous system due to medication, intoxication or infectious diseases;
- chronic orthostatic hypotension, which lasts more than a month and in most cases is caused by pathologies of the endocrine, nervous or cardiovascular systems;
- chronic progressive hypotension that lasts for years (observed with idiopathic orthostatic hypotension).
Reasons for development
The development of orthostatic hypotension is associated with sharp decline pressure, which is caused by insufficient supply of oxygen to the brain, a delay in the reaction of blood vessels and the heart at the moment the body moves from a horizontal to a vertical position.
The development of orthostatic collapse can be observed when:
- Primary neuropathies characterized by disorders normal operation peripheral nervous system as a result hereditary diseases. Orthostatic collapse can develop with Bradbury-Eggleston syndrome affecting the sympathetic nervous system, Shy-Drager syndrome (characterized by a lack of a factor in the blood that has a vasoconstrictive effect), Riley-Day syndrome, Parkinson's disease.
- Secondary neuropathies that develop as a result of autoimmune diseases, at diabetes, post-infectious polyneuropathy, amyloidosis, alcoholism, porphyria, paraneoplastic syndromes, dorsal tabes, beriberi, as well as after sympathectomy.
- Taking medicines. Orthostatic hypotension can be provoked by diuretics, calcium antagonists, nitrates, angiotensin inhibitors, dopaminergic drugs used in Parkinson's disease or hyperprolactinemia, some antidepressants, barbiturates, the herbal antitumor agent Vincristine, the antiarrhythmic agent Quinidine, etc.
- Severe varicose veins, pulmonary embolism, aortic stenosis.
- Myocardial infarction, severe cardiomyopathy, heart failure, constrictive pericarditis,.
- Bleeding.
- infectious diseases.
- Anemiah.
- Violations of the water and electrolyte balance, causing dehydration.
- Hormonally active tumor adrenal or extra-adrenal localization that secretes a large number of catecholamines (pheochromocytoma), (increased secretion of aldosterone by the adrenal cortex), adrenal insufficiency.
Orthostatic hypotension is also caused by prolonged bed rest, overeating, the use of products that reduce blood pressure (juice chokeberry etc.), redistribution of blood under the influence of acceleration forces (for pilots and cosmonauts), a tightly tightened corset or legs tightly tied with seat belts.
Pathogenesis
Orthostatic collapse is based on two main mechanisms of development:
- Decrease in the tone of arterioles and veins under the influence of physical, infectious, toxic and other factors that affect the wall of blood vessels, vascular receptors and the vasomotor center. If there is a lack of compensatory mechanisms, the resulting decrease in peripheral vascular resistance causes a pathological increase in the capacity of the vascular bed, a decrease in the volume of circulating blood with its deposition (accumulation) in some vascular areas, a decrease in venous flow to the heart, an increase in heart rate and a drop in blood pressure.
- A rapid decrease in the mass of circulating blood (massive blood loss that exceeds the compensatory capabilities of the body, etc.) causes a reflex spasm of small vessels, provoking an increased release of catecholamines into the blood and a subsequent increase in heart rate, which is insufficient to maintain normal level HELL. As a result of a decrease in the volume of circulating blood, the return of blood to the heart and cardiac output decrease, the microcirculation system is disturbed, blood accumulates in the capillaries and a drop in blood pressure occurs. Since the delivery of oxygen to the tissues is impaired, circulatory hypoxia develops, and acid-base balance shifts towards increased acidity (metabolic acidosis). Hypoxia and acidosis cause damage vascular wall and contribute to an increase in its permeability, as well as a loss of tone of precapillary sphincters while maintaining the tone of postcapillary sphincters. As a result, the rheological properties of blood are disturbed and conditions arise that promote the formation of microthrombi.
Symptoms
Orthostatic collapse in most cases proceeds in the same way, regardless of its origin - consciousness persists for a long time, but patients are outwardly indifferent to the environment (while they often complain of dizziness, blurred vision, a feeling of melancholy, etc.).
At the same time, a change in a horizontal position to a vertical one or a long stay in a standing position is accompanied by:
- sudden increasing general weakness;
- "fog" before the eyes;
- dizziness, which is accompanied by sensations of "loss of support", "falling through" and other similar forebodings of fainting;
- V individual cases heartbeat.
If orthostatic hypotension was caused by prolonged and immobile standing, then the symptoms are often added to:
- feeling of perspiration on the face;
- chilliness;
- nausea.
These symptoms are characteristic of mild orthostatic hypotension. In most cases, they are eliminated on their own when walking, stepping from heel to toe, or performing exercises related to muscle tension.
Moderate degree of orthostatic hypotension is accompanied by:
- increasing pallor;
- wet palms and cold sweat on the face and neck;
- cold extremities;
- loss of consciousness for a few seconds, in which involuntary urination may occur.
The pulse may be thready, while systolic and diastolic pressures decrease and increase. It is also possible to reduce systolic and increase diastolic pressure, accompanied by severe tachycardia.
With a mild and moderate degree of orthostatic collapse, the symptoms develop gradually, within a few seconds, so the patient has time to take some measures (sit down, lean on his arm, etc.).
Severe orthostatic hypotension is accompanied by:
- sudden and prolonged fainting, which can lead to injury from a fall;
- involuntary urination;
- convulsions.
Breathing in patients is superficial, the skin is pale, marbled,. Body temperature and tissue turgor are lowered.
Since episodes of orthostatic collapse in severe cases last for a long time, patients have a change in gait (sweeping steps, head low, knees bent).
Diagnostics
Diagnosis of orthostatic hypotension is based on:
- analysis of the anamnesis of the disease and family history;
- examination, including the measurement of blood pressure in the supine position and standing at 1 and 3 minutes after 5 minutes of lying at rest, auscultation of the heart, examination of the veins, etc.;
- general and biochemical analysis blood, allowing to detect anemia, violation of the water-salt balance, etc .;
- hormonal analysis, which allows you to determine the level of cortisol;
- Holter monitoring of cardiac activity;
- orthostatic test, which allows to identify the reaction of the cardiovascular system to a change in body position.
Methods for diagnosing orthostatic hypotension also include:
- ECG, which allows to identify concomitant pathology;
- consultationhelping to exclude other neurological diseases (this is especially important against the background of the development of convulsions during fainting);
- vagal tests that reveal the presence of an excessive influence of the autonomic nervous system on cardiovascular activity;
- Echocardiography, which helps to assess the condition of the heart valves, the size of the walls of the heart muscle and the cavity of the heart.
Treatment
First aid for orthostatic collapse includes:
- laying the patient in a horizontal position on a hard surface (legs raised);
- supply of fresh air;
- removal of restrictive clothing;
- splashing the face and chest with cold water;
- use of ammonia.
1-2 ml of cordiamine or 1 ml of a 10% caffeine solution are injected subcutaneously. Vasodilator drugs are contraindicated.
After the return of consciousness, the patient should be given warm tea or coffee with sugar.
Further therapy depends on the severity and nature of the disease causing orthostatic collapse.
Prevention
Prevention of orthostatic collapse is:
- choosing the right mode of physical activity;
- discontinuation of drugs that can cause hypotension;
- medical gymnastics;
- observance of the optimal temperature regime in the room;
- a diet that includes potassium-rich foods and an increased amount of salt;
- sleeping on a bed with a raised head end.
