In an adult, the normal heart rate is in the range of 65-80 beats per minute. A heart rate slower than 60 beats per minute is called bradycardia. There are many reasons leading to bradycardia, which only a doctor can determine in a person.

Regulation of the activity of the heart

In physiology, there is such a thing as automatism of the heart. This means that the heart contracts under the influence of impulses that arise directly in itself, primarily in the sinus node. These are special neuromuscular fibers located at the confluence of the vena cava into the right atrium. The sinus node produces a bioelectrical impulse that propagates further through the atria and reaches the atrioventricular node. This is how the heart muscle contracts. Neurohumoral factors also influence the excitability and conduction of the myocardium.

Bradycardia can develop in two cases. First of all, a decrease in the activity of the sinus node leads to a decrease in the activity of the sinus node, when it generates few electrical impulses. This bradycardia is called sinus . And there is such a situation when the sinus node is working normally, but the electrical impulse cannot fully pass through the conduction paths and the heartbeat slows down.

Causes of physiological bradycardia

Bradycardia is not always a sign of pathology, it can be physiological . So, athletes often have a low heart rate. This is the result of constant stress on the heart during long workouts. How to understand is bradycardia the norm or pathology? A person needs to perform active physical exercises. At healthy people physical activity leads to an intense increase in heart rate. In violation of the excitability and conduction of the heart, exercise is accompanied by only a slight increase in heart rate.

In addition, the heart rate also slows down when the body. This is a compensatory mechanism, due to which blood circulation slows down and blood is directed from the skin to the internal organs.

The activity of the sinus node is affected by the nervous system. The parasympathetic nervous system reduces the heartbeat, the sympathetic - increases. Thus, stimulation of the parasympathetic nervous system leads to a decrease in heart rate. This is a well-known medical phenomenon, which, by the way, many people experience in life. So, with pressure on the eyes, stimulation is carried out vagus nerve(main nerve of the parasympathetic nervous system). As a result of this, the heartbeat is briefly reduced by eight to ten beats per minute. The same effect can be achieved by pressing on the area of ​​the carotid sinus in the neck. Stimulation of the carotid sinus can occur when wearing a tight collar, tie.

Causes of pathological bradycardia

Bradycardia can develop under the influence of a variety of factors. The most common causes of pathological bradycardia are:

1. Increased tone of the parasympathetic system;
2. heart disease;
3. Acceptance of certain medicines(cardiac glycosides, as well as beta-blockers, calcium channel blockers);
4. (FOS, lead, nicotine).

Increased tone of the parasympathetic system

Parasympathetic innervation of the myocardium is carried out by the vagus nerve. When activated, the heart rate slows down. Exists pathological conditions, in which there is irritation of the vagus nerve (its fibers located in the internal organs, or nerve nuclei in the brain).

An increase in the tone of the parasympathetic nervous system is noted in such diseases:

• (against the background of traumatic brain injury, hemorrhagic stroke, cerebral edema);
• Neoplasms in the mediastinum;
• Cardiopsychoneurosis;
• Condition after surgery in the head, as well as neck, mediastinum.

As soon as the factor that stimulates the parasympathetic nervous system is eliminated in this case, the heartbeat returns to normal. This type of bradycardia is defined by physicians as neurogenic.

Heart disease

Heart diseases (cardiosclerosis, myocarditis) lead to the development of certain changes in the myocardium. In this case, the impulse from the sinus node passes much more slowly in the pathologically altered part of the conduction system, due to which the heartbeat slows down.

When a violation of the conduction of an electrical impulse is localized in the atrioventricular node, they speak of the development of an atrioventricular block (AV block).

Symptoms of bradycardia

A moderate decrease in heart rate does not affect a person’s condition in any way, he feels good and does his usual things. But with a further decrease in heart rate, blood circulation is disturbed. The organs are not adequately supplied with blood and suffer from a lack of oxygen. The brain is especially sensitive to hypoxia. Therefore, with bradycardia, it is precisely the symptoms of damage to the nervous system that come to the fore.

With attacks of bradycardia, a person experiences weakness. Pre-fainting states and are also characteristic. Skin pale. Shortness of breath often develops, usually on the background of physical exertion.

With a heart rate of less than 40 beats per minute, blood circulation is significantly impaired. With slow blood flow, the myocardium does not receive oxygen adequately. The result is chest pain. This is a kind of signal from the heart that it lacks oxygen.

Diagnostics

In order to identify the cause of bradycardia, it is necessary to undergo an examination. First of all, you should pass. This method is based on the study of the passage of a bioelectrical impulse in the heart. Yes, at sinus bradycardia(when the sinus node rarely generates an impulse), there is a decrease in heart rate while maintaining normal sinus rhythm.

The appearance of such signs on the electrocardiogram as an increase in the duration of the P-Q interval, as well as deformation of the ventricular QRS complex, its loss from the rhythm, more atrial contractions than the number of QRS complexes will indicate the presence of AV block in a person.

If bradycardia is observed intermittently, and in the form of seizures, it is indicated. This will provide data on the functioning of the heart for twenty-four hours.

To clarify the diagnosis, finding the cause of bradycardia, the doctor may prescribe the patient to undergo the following studies:

1. echocardiography;
2. Determination in blood content;
3. Analysis for toxins.

Treatment of bradycardia

Physiological bradycardia does not require any treatment, as does bradycardia that does not affect general well-being. Therapy of pathological bradycardia is started after finding out the cause. The principle of treatment is to act on the root cause, against which the heart rate returns to normal.

Medical therapy is to prescribe medications that increase heart rate. These are medicines such as:

• Isadrin;
• Atropine;
• Isoprenaline;
• Eufilin.

The use of these drugs has its own characteristics, and therefore they can only be prescribed by a doctor.

In the event of hemodynamic disturbances (weakness, fatigue, dizziness), the doctor may prescribe tonic medicines for the patient: ginseng tincture, caffeine. These drugs increase heart rate and increase arterial pressure.

When a person has severe bradycardia and, against this background, heart failure develops, they resort to implanting a pacemaker in the heart. This device independently generates electrical impulses. stable preset heartbeat contributes to the restoration of adequate hemodynamics.

Grigorova Valeria, medical commentator

Chapter 17

Antihypertensives are drugs that lower blood pressure. Most often they are used for arterial hypertension, i.e. with high blood pressure. Therefore, this group of substances is also called antihypertensive agents.

Arterial hypertension is a symptom of many diseases. Distinguish between primary arterial hypertension, or hypertension (essential hypertension), as well as secondary (symptomatic) hypertension, for example, arterial hypertension with glomerulonephritis and nephrotic syndrome (renal hypertension), with narrowing renal arteries(renovascular hypertension), pheochromocytoma, hyperaldosteronism, etc.

In all cases, seek to cure the underlying disease. But even if this fails, arterial hypertension should be eliminated, since arterial hypertension contributes to the development of atherosclerosis, angina pectoris, myocardial infarction, heart failure, visual impairment, and impaired renal function. A sharp increase in blood pressure - a hypertensive crisis can lead to bleeding in the brain (hemorrhagic stroke).

In different diseases, the causes of arterial hypertension are different. In the initial stage hypertension Arterial hypertension is associated with an increase in the tone of the sympathetic nervous system, which leads to an increase in cardiac output and narrowing of blood vessels. In this case, blood pressure is effectively reduced by substances that reduce the influence of the sympathetic nervous system (antihypertensive drugs). central action, adrenoblockers).

In kidney diseases, in the late stages of hypertension, an increase in blood pressure is associated with activation of the renin-angiotensin system. The resulting angiotensin II constricts blood vessels, stimulates sympathetic system, increases the release of aldosterone, which increases the reabsorption of Na + ions in the renal tubules and thus retains sodium in the body. Drugs that reduce the activity of the renin-angiotensin system should be prescribed.

In pheochromocytoma (a tumor of the adrenal medulla), the adrenaline and norepinephrine secreted by the tumor stimulate the heart, constrict the blood vessels. Pheochromocytoma is removed surgically, but before surgery, during surgery, or if surgery is not possible, lower blood pressure with wasp-blockers.

A frequent cause of arterial hypertension may be a delay in the body of sodium due to excessive consumption of table salt and insufficiency of natriuretic factors. Increased content Na + in the smooth muscles of blood vessels leads to vasoconstriction (the function of the Na + / Ca 2+ exchanger is disturbed: the entry of Na + and the exit of Ca 2+ decrease; the level of Ca 2+ in the cytoplasm of smooth muscles increases). As a result, blood pressure rises. Therefore, in arterial hypertension, diuretics are often used that can remove excess sodium from the body.

In arterial hypertension of any genesis, myotropic vasodilators have an antihypertensive effect.

It is believed that in patients with arterial hypertension, antihypertensive drugs should be used systematically, preventing an increase in blood pressure. For this, it is advisable to prescribe antihypertensive drugs long-acting. Most often, drugs are used that act 24 hours and can be administered once a day (atenolol, amlodipine, enalapril, losartan, moxonidine).

In practical medicine, among antihypertensive drugs, diuretics, β-blockers, calcium channel blockers, α-blockers, ACE inhibitors, and AT 1 receptor blockers are most often used.

To stop hypertensive crises, diazoxide, clonidine, azamethonium, labetalol, sodium nitroprusside, nitroglycerin are administered intravenously. In non-severe hypertensive crises, captopril and clonidine are prescribed sublingually.

Classification of antihypertensive drugs

I. Drugs that reduce the influence of the sympathetic nervous system (neurotropic antihypertensive drugs):

1) means of central action,

2) means blocking sympathetic innervation.

P. Myotropic vasodilators:

1) donors N0,

2) potassium channel activators,

3) drugs with an unknown mechanism of action.

III. Calcium channel blockers.

IV. Means that reduce the effects of the renin-angiotensin system:

1) drugs that disrupt the formation of angiotensin II (drugs that reduce renin secretion, ACE inhibitors, vasopeptidase inhibitors),

2) blockers of AT 1 receptors.

V. Diuretics.

Drugs that reduce the effects of the sympathetic nervous system

(neurotropic antihypertensive drugs)

The higher centers of the sympathetic nervous system are located in the hypothalamus. From here, excitation is transmitted to the center of the sympathetic nervous system, located in the rostroventrolateral region of the medulla oblongata (RVLM - rostro-ventrolateral medulla), traditionally called the vasomotor center. From this center, impulses are transmitted to the sympathetic centers of the spinal cord and further along the sympathetic innervation to the heart and blood vessels. Activation of this center leads to an increase in the frequency and strength of heart contractions (increase in cardiac output) and to an increase in the tone of blood vessels - blood pressure rises.

It is possible to reduce blood pressure by inhibiting the centers of the sympathetic nervous system or by blocking the sympathetic innervation. In accordance with this, neurotropic antihypertensive drugs are divided into central and peripheral agents.

TO centrally acting antihypertensives include clonidine, moxonidine, guanfacine, methyldopa.

Clonidine (clophelin, hemiton) - a 2 -adrenomimetic, stimulates a 2A -adrenergic receptors in the center of the baroreceptor reflex in the medulla oblongata (nuclei of the solitary tract). In this case, the centers of the vagus (nucleus ambiguus) and inhibitory neurons are excited, which have a depressing effect on the RVLM (vasomotor center). In addition, the inhibitory effect of clonidine on RVLM is due to the fact that clonidine stimulates I 1 -receptors (imidazoline receptors).

As a result, the inhibitory effect of the vagus on the heart increases and the stimulating effect of sympathetic innervation on the heart and blood vessels decreases. As a result, it decreases cardiac output and tone of blood vessels (arterial and venous) - blood pressure decreases.

In part, the hypotensive effect of clonidine is associated with the activation of presynaptic a 2 -adrenergic receptors at the ends of sympathetic adrenergic fibers - the release of norepinephrine decreases.

At higher doses, clonidine stimulates extrasynaptic a 2 B -adrenergic receptors of the smooth muscles of blood vessels (Fig. 45) and, with rapid intravenous administration, can cause short-term vasoconstriction and an increase in blood pressure (therefore, intravenous clonidine is administered slowly, over 5-7 minutes).

In connection with the activation of a 2 -adrenergic receptors of the central nervous system, clonidine has a pronounced sedative effect, potentiates the action of ethanol, and exhibits analgesic properties.

Clonidine is a highly active antihypertensive agent (therapeutic dose when administered orally 0.000075 g); acts for about 12 hours. However, with systematic use, it can cause a subjectively unpleasant sedative effect (absent-mindedness, inability to concentrate), depression, decreased tolerance to alcohol, bradycardia, dry eyes, xerostomia (dry mouth), constipation, impotence. With a sharp cessation of the drug, the development pronounced syndrome cancellation: after 18-25 hours, blood pressure rises, a hypertensive crisis is possible. β-Adrenergic blockers increase the clonidine withdrawal syndrome, so these drugs are not prescribed together.

Clonidine is mainly used to quickly lower blood pressure in hypertensive crises. In this case, clonidine is administered intravenously over 5-7 minutes; with rapid administration, an increase in blood pressure is possible due to stimulation of a 2 -adrenergic receptors of blood vessels.

Solutions of clonidine in the form eye drops used in the treatment of glaucoma (reduces the production of intraocular fluid).

Moxonidine(cint) stimulates imidazoline 1 1 receptors in the medulla oblongata and, to a lesser extent, a 2 adrenoreceptors. As a result, the activity of the vasomotor center decreases, cardiac output and the tone of blood vessels decrease - blood pressure decreases.

The drug is prescribed orally for the systematic treatment of arterial hypertension 1 time per day. Unlike clonidine, when using moxonidine, sedation, dry mouth, constipation, and withdrawal syndrome are less pronounced.

Guanfacine(Estulik) similarly to clonidine stimulates central a 2 -adrenergic receptors. Unlike clonidine, it does not affect 1 1 receptors. The duration of the hypotensive effect is about 24 hours. Assign inside for the systematic treatment of arterial hypertension. The withdrawal syndrome is less pronounced than that of clonidine.

Methyldopa(dopegit, aldomet) according to the chemical structure - a-methyl-DOPA. The drug is prescribed inside. In the body, methyldopa is converted to methylnorepinephrine, and then to methyladrenaline, which stimulate the a 2 -adrenergic receptors of the center of the baroreceptor reflex.

Metabolism of methyldopa

The hypotensive effect of the drug develops after 3-4 hours and lasts about 24 hours.

Side effects of methyldopa: dizziness, sedation, depression, nasal congestion, bradycardia, dry mouth, nausea, constipation, liver dysfunction, leukopenia, thrombocytopenia. In connection with the blocking effect of a-methyl-dopamine on dopaminergic transmission, the following are possible: parkinsonism, increased production of prolactin, galactorrhea, amenorrhea, impotence (prolactin inhibits the production of gonadotropic hormones). With a sharp discontinuation of the drug, the withdrawal syndrome manifests itself after 48 hours.

Drugs that block peripheral sympathetic innervation.

To reduce blood pressure, sympathetic innervation can be blocked at the level of: 1) sympathetic ganglia, 2) endings of postganglionic sympathetic (adrenergic) fibers, 3) adrenoreceptors of the heart and blood vessels. Accordingly, ganglioblockers, sympatholytics, adrenoblockers are used.

Ganglioblockers - hexamethonium benzosulfonate(benzo-hexonium), azamethonium(pentamine), trimetaphan(Arfonad) block the transmission of excitation in the sympathetic ganglia (block N N -xo-linoreceptors of ganglionic neurons), block N N -cholinergic receptors of the chromaffin cells of the adrenal medulla and reduce the release of adrenaline and norepinephrine. Thus, ganglion blockers reduce the stimulating effect of sympathetic innervation and catecholamines on the heart and blood vessels. There is a weakening of contractions of the heart and expansion of arterial and venous vessels- arterial and venous pressure decreases. At the same time, ganglion blockers block the parasympathetic ganglia; thus eliminate the inhibitory effect of the vagus nerves on the heart and usually cause tachycardia.

Ganglioblockers are of little use for systematic use due to side effects (severe orthostatic hypotension, disturbance of accommodation, dry mouth, tachycardia; bowel and bladder atony, sexual dysfunction are possible).

Hexamethonium and azamethonium act for 2.5-3 hours; administered intramuscularly or under the skin in hypertensive crises. Azamethonium is also administered slowly intravenously in 20 ml of isotonic sodium chloride solution at hypertensive crisis, swelling of the brain, lungs against the background of high blood pressure, with spasms of peripheral vessels, with intestinal, hepatic or renal colic.

Trimetafan acts 10-15 minutes; is administered in solutions intravenously by drip for controlled hypotension during surgical operations.

Sympatholytics- reserpine, guanethidine(octadin) reduce the release of norepinephrine from the endings of sympathetic fibers and thus reduce the stimulating effect of sympathetic innervation on the heart and blood vessels - arterial and venous pressure decreases. Reserpine reduces the content of norepinephrine, dopamine and serotonin in the central nervous system, as well as the content of adrenaline and norepinephrine in the adrenal glands. Guanethidine does not penetrate the blood-brain barrier and does not change the content of catecholamines in the adrenal glands.

Both drugs differ in the duration of action: after the systematic administration is stopped, the hypotensive effect can persist for up to 2 weeks. Guanethidine is much more effective than reserpine, but due to severe side effects, it is rarely used.

In connection with the selective blockade of sympathetic innervation, the influences of the parasympathetic nervous system predominate. Therefore, when using sympatholytics, the following are possible: bradycardia, increased secretion of HC1 (contraindicated in case of peptic ulcer), diarrhea. Guanethidine causes significant orthostatic hypotension (associated with a decrease in venous pressure); when using reserpine, orthostatic hypotension is not very pronounced. Reserpine reduces the level of monoamines in the central nervous system, can cause sedation, depression.

a -Ldrenoblockers reduce the ability to stimulate the effect of sympathetic innervation on blood vessels (arteries and veins). In connection with the expansion of blood vessels, arterial and venous pressure decreases; heart contractions reflexively increase.

a 1 - Adrenoblockers - prazosin(minipress), doxazosin, terazosin administered orally for the systematic treatment of arterial hypertension. Prazosin acts 10-12 hours, doxazosin and terazosin - 18-24 hours.

Side effects of a 1 -blockers: dizziness, nasal congestion, moderate orthostatic hypotension, tachycardia, frequent urination.

a 1 a 2 - Adrenoblocker phentolamine used for pheochromocytoma before surgery and during surgery to remove pheochromocytoma, as well as in cases where surgery is not possible.

β -Adrenoblockers- one of the most commonly used groups of antihypertensive drugs. With systematic use, they cause a persistent hypotensive effect, prevent sharp rises in blood pressure, practically do not cause orthostatic hypotension, and, in addition to hypotensive properties, have antianginal and antiarrhythmic properties.

β-blockers weaken and slow down the contractions of the heart - systolic blood pressure decreases. At the same time, β-blockers constrict blood vessels (block β 2 -adrenergic receptors). Therefore, with a single use of β-blockers, mean arterial pressure usually decreases slightly (in isolated systolic hypertension, blood pressure may decrease after a single use of β-blockers).

However, if p-blockers are used systematically, then after 1-2 weeks, vasoconstriction is replaced by their expansion - blood pressure decreases. Vasodilation is explained by the fact that with the systematic use of β-blockers, due to a decrease in cardiac output, the baroreceptor depressor reflex is restored, which is weakened in arterial hypertension. In addition, vasodilation is facilitated by a decrease in renin secretion by juxtaglomerular cells of the kidneys (block of β 1 -adrenergic receptors), as well as blockade of presynaptic β 2 -adrenergic receptors at the endings of adrenergic fibers and a decrease in the release of norepinephrine.

For the systematic treatment of arterial hypertension, long-acting β 1 -adrenergic blockers are more often used - atenolol(tenormin; lasts about 24 hours), betaxolol(valid up to 36 hours).

Side effects of β-blockers: bradycardia, heart failure, difficulty in atrioventricular conduction, decreased HDL level in blood plasma, increased tone of the bronchi and peripheral vessels (less pronounced in β 1 -blockers), increased action of hypoglycemic agents, reduced physical activity.

a 2 β -Adrenoblockers - labetalol(transat), carvedilol(dilatrend) reduce cardiac output (block of p-adrenergic receptors) and reduce the tone of peripheral vessels (block of a-adrenergic receptors). The drugs are used orally for the systematic treatment of arterial hypertension. Labetalol is also administered intravenously in hypertensive crises.

Carvedilol is also used in chronic heart failure.

On the basis of anatomical and functional data, the nervous system is usually divided into somatic, responsible for the connection of the body with the external environment, and vegetative, or plant, regulating the physiological processes of the internal environment of the body, ensuring its constancy and adequate response to exposure. external environment. The ANS is in charge of energy, trophic, adaptive and protective functions common to animal and plant organisms. In the aspect of evolutionary vegetology, it is a complex biosystem that provides conditions for maintaining the existence and development of an organism as an independent individual and adapting it to the environment.

The ANS innervates not only the internal organs, but also the sense organs and muscular system. The studies of L. A. Orbeli and his school, the doctrine of the adaptive-trophic role of the sympathetic nervous system, showed that the autonomic and somatic nervous systems are in constant interaction. In the body, they are so closely intertwined with each other that it is sometimes impossible to separate them. This can be seen in the example of the pupillary reaction to light. The perception and transmission of light stimulation is carried out by the somatic (optic) nerve, and the constriction of the pupil is due to autonomic, parasympathetic fibers oculomotor nerve. Through the optical-vegetative system, light exerts its direct effect through the eye on the autonomic centers of the hypothalamus and pituitary gland (i.e., one can speak not only of the visual, but also of the photovegetative function of the eye).

The anatomical difference in the structure of the autonomic nervous system is that the nerve fibers do not come from the spinal cord or the corresponding nucleus cranial nerve directly to the working body, as somatic, but are interrupted at the nodes sympathetic trunk and other nodes of the ANS, a diffuse reaction is created when one or more preganglionic fibers are irritated.

The reflex arcs of the sympathetic division of the ANS can be closed both in the spinal cord and in the nodes.

An important difference between the ANS and the somatic is the structure of the fibers. Autonomic nerve fibers are thinner than somatic, covered with a thin myelin sheath or do not have it at all (non-myelinated or non-myelinated fibers). Conduction of an impulse along such fibers occurs much more slowly than along somatic fibers: on average, 0.4-0.5 m/s along sympathetic and 10.0-20.0 m/s along parasympathetic ones. Several fibers can be surrounded by a single Schwann sheath, so excitation can be transmitted along them in a cable type, i.e., an excitation wave running along one fiber can be transmitted to fibers located in this moment at rest. As a result, diffuse excitation along many nerve fibers arrives at the final destination of the nerve impulse. Direct impulse transmission through direct contact of unmyelinated fibers is also allowed.

main biological function ANS - trophoenergetic is divided into histotropic, trophic - to maintain a certain structure of organs and tissues, and ergotropic - to deploy their optimal activity.

If the trophotropic function is aimed at maintaining the dynamic constancy of the internal environment of the body, then the ergotropic function is aimed at the vegetative-metabolic provision of various forms of adaptive purposeful behavior (mental and physical activity implementation of biological motivations - food, sexual, motivations of fear and aggression, adaptation to changing environmental conditions).

The VNS implements its functions mainly in the following ways: 1) regional change vascular tone; 2) adaptive-trophic action; 3) function control internal organs.

The ANS is divided into the sympathetic, predominantly mobilized during the implementation of the ergotropic function, and the parasympathetic, more aimed at maintaining homeostatic balance - the trophotropic function.

These two departments of the ANS, functioning mostly antagonistically, provide, as a rule, a double innervation of the body.

The parasympathetic division of the ANS is more ancient. It regulates the activities of the organs responsible for the standard properties of the internal environment. The sympathetic department develops later. It changes the standard conditions of the internal environment and organs in relation to the functions they perform. The sympathetic nervous system inhibits anabolic processes and activates catabolic ones, while the parasympathetic, on the contrary, stimulates anabolic and inhibits catabolic processes.

The sympathetic division of the ANS is widely represented in all organs. Therefore, the processes in various organs and systems of the body are also reflected in the sympathetic nervous system. Its function also depends on the central nervous system, the endocrine system, processes occurring on the periphery and in the visceral sphere, and therefore its tone is unstable, requires constant adaptive-compensatory reactions.

The parasympathetic division is more autonomous and is not as closely dependent on the central nervous and endocrine systems as the sympathetic division. Mention should be made of the functional predominance at a certain time of one or another section of the ANS, associated with the general biological exogenous rhythm, for example, the sympathetic one during the day, and the parasympathetic one at night. In general, the functioning of the ANS is characterized by periodicity, which is associated, in particular, with seasonal changes in nutrition, the amount of vitamins entering the body, as well as light irritation. A change in the functions of the organs innervated by the ANS can be obtained by irritating the nerve fibers of this system, as well as by the action of certain chemicals. Some of them (choline, acetylcholine, physostigmine) reproduce parasympathetic effects, others (norepinephrine, mezaton, adrenaline, ephedrine) - sympathetic. Substances of the first group are called parasympathomimetics, and substances of the second group are called sympathomimetics. In this regard, the parasympathetic ANS is also called cholinergic, and the sympathetic - adrenergic. Different substances affect different parts of the ANS.

In the implementation of the specific functions of the ANS, its synapses are of great importance.

The vegetative system is closely connected with the endocrine glands, on the one hand, it innervates the endocrine glands and regulates their activity, on the other hand, the hormones secreted by the endocrine glands have a regulatory effect on the tone of the ANS. Therefore, it is more correct to speak of a single neurohumoral regulation of the body. Adrenal medulla hormone (adrenaline) and hormone thyroid gland(thyroidin) stimulate the sympathetic ANS. The hormone of the pancreas (insulin), the hormones of the adrenal cortex, and the hormone of the thymus gland (during the growth of the organism) stimulate the parasympathetic division. The hormones of the pituitary and gonads have a stimulating effect on both parts of the ANS. The activity of the VNS also depends on the concentration of enzymes and vitamins in the blood and tissue fluids.

The hypothalamus is closely connected with the pituitary gland, the neurosecretory cells of which send neurosecretion to the posterior lobe of the pituitary gland. In general integration physiological processes carried out by the ANS, of particular importance are the constant and reciprocal relationships between the sympathetic and parasympathetic systems, the functions of interoreceptors, humoral vegetative reflexes and the interaction of the ANS with the endocrine system and somatic, especially with its higher department - the cerebral cortex.

The tone of the autonomic nervous system

Many centers of the autonomic nervous system are constantly in a state of activity, as a result of which the organs innervated by them receive excitatory or inhibitory impulses from them continuously. So, for example, transection of both vagus nerves on the dog's neck entails an increase in heart rate, since this eliminates the inhibitory effect constantly exerted on the heart by the nuclei of the vagus nerves, which are in a state of tonic activity. A unilateral transection of the sympathetic nerve on the neck of a rabbit causes dilation of the ear vessels on the side of the cut nerve, since the vessels lose their tonic influence. When the peripheral segment of the cut nerve is irritated at a rhythm of 1-2 pulses / s, the rhythm of heart contractions that occurred before the transection of the vagus nerves is restored, or the degree of narrowing of the ear vessels that was with the integrity of the sympathetic nerve.

The tone of the autonomic centers is provided and maintained by afferent nerve signals coming from the receptors of the internal organs and partly from the exteroreceptors, as well as as a result of the impact on the centers of various blood and cerebrospinal fluid factors.

The autonomic or autonomic nervous system is usually contrasted with the abnormal or cerebrospinal nervous system. The latter innervates mainly the sense organs and organs of movement, that is, the entire striated muscles; its innervation is strictly segmental, and the nerve fibers come from the nerve centers ( nerve cell) to the working body without interruption. The autonomic nervous system innervates mainly smooth muscles, glands and internal organs of the body (organs of blood circulation, respiration, gastrointestinal tract, liver, kidneys, etc.), non-segmental innervation and with obligatory interruptions. Thus, the main function of the cerebrospinal nervous system is to regulate the relationship between the body and the environment, while the main function of the autonomic nervous system is to regulate the relationships and processes within the body. But it goes without saying that both the cerebrospinal and autonomic nervous systems are only parts of a single whole - a single nervous system of the body. They are related to each other both morphologically and functionally. Therefore, all organs of our body have a double - vegetative and cerebrospinal innervation. In this way, with the indispensable participation of internal secretion, which is closely connected in turn with the autonomic nervous system, the unity and integrity of the whole organism is achieved.

The autonomic nervous system, like the cerebrospinal system, is divided into central and peripheral. The central autonomic nervous system consists of accumulations of ganglion cells and fibers - vegetative centers and nuclei laid down in various parts of the central cerebrospinal system - in the brain, mainly in the striatum (corpus striatum), in the interstitial, medulla oblongata and spinal cord.

Higher vegetative centers that regulate all major general functions vegetative life of the organism, such as: body temperature, metabolism, respiration, blood circulation, etc., are located in the floors of the brain located one under the other - in the subcortical nodes, interstitial and medulla oblongata.

The peripheral autonomic nervous system is divided into two divisions: the sympathetic division and the parasympathetic nervous system.

The sympathetic nervous system originates partly in the medulla oblongata, but mainly in the spinal cord - from CVIII to LIII-IV (thoracolumbar subdivision of the autonomic nervous system), and its fibers, after a break in the prevertebral nodes (border column), extend to all areas of the body, so that sympathetic innervation has, one might say, universal significance.

The parasympathetic nervous system originates in the midbrain and medulla oblongata - the cranial subsection (nn. oculomotorius, vagus and glossopharyngeus) and in the sacral part of the spinal cord - the sacral subsection (n. pelvicus) - A break in parasympathetic fibers occurs either in plexuses on the surface of organs, or in the ganglia within the organs.

Adrenaline has the same effect as stimulation of the sympathetic nervous system, and choline and its derivatives (acetylcholine) cause the action, analogous to action parasympathetic nervous system. Thus, we can talk about the adrenalinotropy of the sympathetic and holinotropy of the parasympathetic nervous system. The action of these two divisions of the autonomic nervous system is in many cases opposite, so they used to talk about their antagonism.

However, this antagonism is not a law. There is no complete antagonism either between the sympathetic and parasympathetic divisions of the autonomic nervous system (there are holinotropic fibers in the sympathetic nervous system, and adrenalinotropic fibers in the parasympathetic one), or between the autonomic nervous system as a whole and the animal nervous system. It is much more correct to speak not of antagonism, but of their synergy. The vegetative, actually sympathetic nervous system, having a universal distribution and innervating all organs and tissues of the body, including the sense organs and the central nervous system, is the regulator of their work, changes the conditions of this work, nutritional conditions, etc., and thus plays an adaptive (adaptive) ) and trophic role.

The transmission of nerve influence or irritation to organs and tissues, as well as from one fiber to another (from preganglionic to postganglionic) occurs through special chemicals, chemical mediators or mediators (sympathin for the sympathetic nervous system, choline or acetylcholine for the parasympathetic nervous system). This fact, as it were, throws a bridge between the nervous and endocrine systems and binds them together. Relations between the autonomic nervous system and the adrenal glands are especially close, the medulla of which develops from the rudiments of the sympathetic ganglia. In view of such a close functional connection between the endocrine and autonomic nervous systems, they are often and not without reason combined into a single endocrine-vegetative system.

Violations of autonomic innervation occur depending on different kind endo- or exogenous moments in the direction of increasing or decreasing the tone of the autonomic nervous system, the entire tzaddik or its individual parts. Accordingly, pictures of hyper- or hypoamphotonia, hyper- or hyposympathicotonia, galere- or hypovagotonia develop. The diversity of clinical manifestations of vegetative innervation disorders and the difficulty of their correct assessment are aggravated by the fact that the same nervous excitation, just as it is observed under the action of hormones, causes a different effect depending on the state of reactivity of the working organ and on the physicochemical conditions of its environment. .

Symptoms of diseases of the autonomic nervous system
Signs of disturbed autonomic innervation are dysfunction of the working organs. Naturally, they are very numerous and very diverse in their degree of expression.

The following symptoms from various organs, if there are no special reasons for their occurrence, indicate a more or less disturbed autonomic innervation in its respective departments. Constriction of the pupils and lacrimation, increased salivation and sweating (saliva and sweat are liquid), coldness and blueness of the hands and feet (vascular paresis), spasm of the esophagus, dyspeptic symptoms (belching, heartburn, nausea, vomiting), spasms (pain) of the stomach, hypersecretion, constipation or diarrhea, spasms of the gallbladder, bradycardia, extrasystole, arterial hypotension, reduced tone of the heart muscle, the impossibility of a deep breath and full exhalation, attacks such as bronchial asthma, dysuric phenomena, increased carbohydrate tolerance, eosinophilia - all these are symptoms of increased excitability or increased tone of the parasympathetic nervous system, symptoms of vagotonia. Expansion of the pupils and glare of the eyes, a decrease in lacrimation and sweating, tachycardia and often hypertension, easy patency of the esophagus, atony of the stomach, splashing noise in it, low acidity gastric contents, atony of the large intestine, flatulence, reduced tolerance to carbohydrates - these are the main symptoms of increased tone of the sympathetic nervous system, symptoms of sympathicotonia.

In patients in the clinic, these two series of symptoms are very rarely observed in isolation; usually we see a motley picture of symptoms in connection with the simultaneous strengthening or weakening of the excitability of both parts of the autonomic nervous system.

Diagnostics
The pathology of the autonomic nervous system forms a border area between internal medicine and neuropathology, and the method of studying the autonomic nervous system is described mainly in the course of neuropathology. Therefore, we will confine ourselves here to pointing out the most commonly used research methods. Of these, in this case, questioning, examination and palpation find their application.

When questioning the patient, in addition to establishing complaints and their nature, Special attention should be given to clarifying the functional state of organs and systems - the so-called additional questioning (according to the questioning scheme outlined above in the General Part).

Examination of the patient can easily determine the presence autonomic nervous symptoms on the part of the eyes, skin, motor sphere, etc .: the condition of the pupils, eye shine, protrusion of the eyeballs, dryness or moisture of the skin, changes in its pigmentation, color (acrocyanosis), trembling, etc.

Palpation method research is used to determine the pulse rate, temperature and moisture of the skin, and also, along with an examination, to establish a number of vegetative-nervous reflexes that occur spontaneously and are used for diagnostic purposes and part of those already described above. Of these, we can note here: 1) viscero-sensory reflex (pain in a certain Gedian zone with damage to internal organs); 2) viscero-motor reflex (tension of certain muscles - "muscular protection" under the same conditions); 3) pupillary reflex(dilated pupils in response to strong pain or their narrowing in response to light stimulation); 4) vasomotor reflex (redness or blanching of the skin with various kinds of affects); 5) sweat reflex (copious, liquid sweat of parasympathetic origin, scanty, thick and cold sweat- sympathetic origin).

Functional research methods. To assess the functional state of the autonomic nervous system, either vegetative-nervous reflexes, mainly cardiac and skin reflexes, artificially evoked according to the principle of a dosed load, or studies of the reaction of the autonomic nervous system to certain pharmacological substances are used.

The most common cardiac reflexes are as follows:

1) the respiratory-cardiac reflex of Hering (Hering), or the so-called respiratory arrhythmia: slowing down the pulse with a deep breath and increasing it with exhalation;

2) Dagnini-Aschner's eye-cardiac reflex (Dagnini-Aschner): slowing of the pulse with pressure on the eyeballs;

3) cervical-cardiac reflex Czermak (Czermak): slowing of the pulse with compression of the vagus nerve in the neck.

All these reflexes are associated with the tone of the vagus nerve, and a significant slowdown in the pulse under these conditions (for the Ashner and Chermak reflexes by more than 8-10 beats per minute) indicates an increase in the tone of the parasympathetic nervous system.

From artificially induced skin reflexes highest value have:

1) vasomotor skin reflex or dermographism (dermographismus) - response vasomotor reaction of the skin to mechanical irritation; There are white, red and edematous dermographism: white (vasospasm), red (vasodilation) or raised roller-like (edema) stripes;

2) pilomotor or hair-muscle reflex - the appearance of the so-called goose bumps in response to various stimuli, the main stimulus being cold, then mechanical irritation, emotional experiences, etc.; to evoke this reflex, they resort to quickly exposing the skin (lifting the shirt), to applying a wet cold towel or bubble with cold water, to spraying with ether, etc. A pronounced pilomotor reflex indicates an increased excitability of the sympathetic nervous system.

All the methods just given for studying the autonomic nervous system are distinguished by the uncertainty of the results obtained, which is explained by the great variability of the tone of the autonomic nervous system, even in physiological conditions Therefore, these research methods are important only in a number of other research data.

For pharmacological research requiring a strictly clinical setting, subcutaneous (or intravenous) injections of atropine, pilocarpine and epinephrine are used. Atropine in the amount of 0.001 under the skin, paralyzing the endings of the vagus nerve, causes dryness of the mucous membranes and skin, reddening of the latter, dilated pupils, increased heart rate. Pilocarpine (0.01 subcutaneously), stimulating the endings of the vagus nerve, causes salivation, nausea, vomiting, sweating, and a drop in blood pressure. Adrenaline (0.001 subcutaneously), stimulating the sympathetic nervous system, causes vasoconstriction (blanching, trembling), increased heart rate, and increased blood pressure.

This is the scheme of influence on the autonomic nervous system of these pharmacological substances. Depending on the result of the applied test, i.e., the greater or lesser severity of the described phenomena, the tone of the corresponding section of the autonomic nervous system is judged. So, a weak action of atropine will speak for an increased tone of the parasympathetic nervous system, a sharp action - for a reduced tone. On the contrary, a sharp effect from the injection of pilocarpine will indicate an increased tone, and a weak effect - a reduced tone of the parasympathetic system. Finally, a weak reaction to adrenaline indicates a reduced, and a strong one, about increased tone sympathetic system.

The main syndromes of vegetative-nervous disorders

I. Syndrome of increased excitability of the sympathetic nervous system - sympathicotonia. This cider is characterized by the following symptoms:

1) dilated pupils, eye gleam, wide open palpebral fissures;

2) dry skin, its pallor, slight appearance of "goosebumps";

3) tachycardia, increased blood pressure;

4) rapid, free breathing;

5) dry mouth, decrease in the secretory and motor ability of the stomach, as well as the intestines (atonic constipation);

6) a tendency to lose weight due to increased metabolism, as well as to hyperglycemia and glycosuria.

More or less pronounced sympathicotonia often accompanies feverish state, manic state, Graves' disease and etc.

II. Syndrome of increased excitability of the parasympathetic nervous system - parasympathicotonia or vagotonia. This syndrome includes the following symptoms:

1) constriction of the pupils, narrowing of the palpebral fissure;

2) cold, moist and cyanotic skin, increased sweating;

3) a tendency to bradycardia, respiratory arrhythmia, a tendency to extrasystoles, a decrease in blood pressure;

4) slow and constrained breathing, a tendency to night attacks of shortness of breath (suffocation) with difficulty exhaling;

5) salivation, a tendency to vomit, increased secretory (hypersecretion) and motor (cardio- and pylorospasm) functions of the stomach and intestines (spastic constipation);

6) a tendency to obesity due to a slowdown in metabolism; increased absorption of sugar.

Manifestations of vagotonic syndrome are frequent with depressive states, shock, bronchial asthma.

III. The syndrome of increased excitability of both parts of the autonomic nervous system - hyperamphotonia - is characterized by a sharp instability of the autonomic nervous tone and an excessive reaction to stimuli from various organs and systems, and the symptoms of sympathetic and vagotonia are very variable, pronounced and often replace each other.

IV. The syndrome of reduced excitability of both parts of the autonomic nervous system - hypoamphotonia - is characterized by weakness and lethargy of all kinds of reactions to stimuli. In severe cases of this syndrome, the following picture is observed: an increase in heart rate and respiration, cold sweat, a decrease in body temperature, hiccups, nausea, vomiting, a drop in blood pressure, i.e., a picture of shock.

Vegetative-vascular dystonia (VVD) is a very common disease that can disguise itself as many others, or may have minor clinical manifestations. According to statistics, about 80% of people have one or another VVD symptoms. One third of these people need medical attention.

What is the autonomic nervous system?

The autonomic nervous system (ANS) consists of two subsystems - sympathetic and parasympathetic, the joint and coordinated activity of which allows, on the one hand, to maintain the internal constancy of the body (homeostasis), and on the other hand, to adapt to changing conditions environment.The ANS governs autonomous (consciously uncontrolled) regulatory mechanisms, such as:

• vascular tone (blood pressure);
• heart rate;
• secretion of glands of external and internal secretion (sweating, salivation, secretion gastric juice, adrenaline and so on);
• regulation motor activity smooth muscles (intestinal motility, gallbladder, etc.).

Due to various stress factors, chronic sleep deprivation, neuroticism and other things, the sympathetic and parasympathetic systems can lose control and start working on their own. As a result, a polymorphic clinical picture of vegetative-vascular dystonia appears.

The action of the sympathetic nervous system is realized with the help of the sympathetic-adrenal system, the central link of which are catecholamines (adrenaline and norepinephrine). A sharp increase in their concentration (release from the adrenal medulla) leads to sympatho-adrenal crisis ("panic attack") : tachycardia, rise in blood pressure, fear, followed by exhaustion of the nervous system.

The parasympathetic nervous system is realized through parasympathetic nerve fibers, the main representative of which is nervus vagus(nervus vagus). The chemical substance that is released at the endings of this nerve is acetylcholine, which causes a decrease in blood pressure, heart rate, increases intestinal motility, constricts the pupils, increases sweating and salivation, and increases the activity of the glands of external and internal secretion. Excessive activation of the parasympathetic nervous system leads to vagoinsular crisis , which is manifested by fainting, "bear's disease", abdominal pain, the concentration of insulin in the blood increases, which leads to hypoglycemia (a decrease in blood sugar), which causes excessive sweating.

Depending on which component of the ANS prevails (sympathetic or parasympathetic), there are three main types of this disease:

1. hypotonic type- the action of the parasympathetic nervous system prevails;
2. hypertonic type- the action of the sympathetic nervous system prevails;
3. normotonic type- there is no predominance of one or another system, but there is their dysfunction.

Symptoms of vegetative-vascular dystonia

Symptoms from the cardiovascular system:

• increased heart rate (tachyarrhythmia);
• decreased heart rate (bradyarrhythmia);
• interruptions in the work of the heart, palpitations;
• pain in the region of the heart;
• increased vascular tone (hypertension);
• decreased vascular tone (hypertension);
• the inability to maintain the proper level of blood pressure if necessary, up to the development of fainting;
• due to spasm or vasodilation, both local and general blanching or redness of the skin are possible with a decrease or increase in temperature in this area, respectively.

From the respiratory system shortness of breath may occur.

Symptoms from the gastrointestinal tract:

• diarrhea, constipation;
• spastic pains;
• irritable bowel syndrome.

Symptoms from the central nervous system:

• apathy;
• hypochondria;
• depression;
• nervousness;
• weather sensitivity;
• changes in body temperature;
• headache;
• insomnia.

Treatment of vegetative-vascular dystonia

For the treatment of VVD, both drug and non-drug methods are used. Moreover, the latter should be given more attention. Among the non-drug methods of treatment, the following can be distinguished.

Compliance healthy lifestyle life. Everything should start with the normalization of the daily routine. In the morning you need to get up at 6-7 o'clock, and go to bed at 10-11 o'clock. Thus, sleep time should be about 8 hours. The human body is accustomed to a daytime lifestyle, and if the "day" hormones are released during the day, then the "night" hormones are released at night. For example, the hormone intermedin, which is responsible for maintaining youth, is secreted from the middle lobe of the pituitary gland from 00:00 to 03:00 at night and only if a person is sleeping. If he is awake at this time, then intermedin is not released or is not released into large quantities. Of course, this has an impact on health. And for the money that you are paid for night hours on duty, in fact, you are selling your youth.

Sleep conditions should also be optimal. The room where you sleep should be comfortable for you in terms of temperature, humidity, noise level, and so on. Mattresses, pillows, bed linen should also not cause inconvenience. It is optimal if they are orthopedic. If you suffer from snoring, then you should try to eliminate it, as it can cause the so-called Ondine's curse syndrome or sleep apnea syndrome. This is a condition when, due to snoring or other reasons, the sleeping person stops breathing. At the same time, he may not even wake up, but his phase of REM sleep is replaced by a phase of light sleep. And if this happens during the night quite often, then the person simply will not get enough sleep.

Can't at work long time engage in the same activity. During breaks, you should switch from mental to physical loads, and vice versa. Time spent at the computer should be kept to a minimum. The same goes for watching TV. You can’t sit in one position for a long time, you should periodically do gymnastics, stretch your joints and muscles, do gymnastics for the eyes.

At work (and in life), you need to try to be less nervous. If you're angry with someone and can't tell them, write what you think of them on paper. You can not give this paper to that person. Part of the accumulated aggression can be burned in gym. In this case, you can also use autogenic training, conversations with a psychotherapist, acquaintance with the relevant psychotherapeutic literature.

Avoiding alcohol and smoking is required. These habits reduce the body's reserve capacity and often lead to various ailments. Alcohol can help you wait out a stressful situation, like anesthesia during surgery. But in general, its use on life and health has an adverse effect. Drinking alcohol does not contribute to the fight against stressful problems, it only displaces them, postpones them for later. And then they return in even greater volume and, accordingly, more “anesthesia funds” are required. But, nevertheless, it is sometimes recommended to drink a glass (50 ml) of expensive high-quality vodka or a glass (250 ml) of good wine a day before meals. This will be useful for those who have the smell, look and taste of alcohol does not cause a violent chain reaction.

Smoking is no less harmful to the body, as it keeps it in a state of chronic hypoxia and toxemia (intoxication). Of course, this reduces the reserve capacity of the body. In addition, when smoking, cases of diseases of the respiratory system, from colds to cancer, become more frequent.

Physical culture. Morning exercises bring your body into tone for the whole day, especially if it is combined with hardening. She not only wakes you up from sleep, but is also ideal prophylactic from many diseases.

In addition to charging, you should sign up for some kind of sports section. The best options for this would be yoga, swimming, walking, hiking and the like. You should avoid such sports that can create an excessive load on the cardiovascular system (bodybuilding, sprinting), as well as in which it is necessary to make sudden movements with a large amplitude and lowering the head below the abdomen, due to the possibility of fainting.

Nutrition should be rational and balanced. In addition, to improve the conduction of nerve impulses and the work of the heart, you must always eat foods with high content magnesium and potassium. The food should be rich in vitamins and other useful substances. The diet should contribute to the normalization of body weight. With hypertension, it is better to drink soothing teas, with hypotension - stimulating.

Physiotherapy is also used in the treatment of VVD. These procedures may be as follows:

• treatment with laser radiation;
• magnetotherapy;
• electropheresis with various drugs on the neck area;
• baths, various showers.

Acupuncture and manual therapy. Depending on the various forms of VVD, the chiropractor selects one or another type of massage.

Spa treatment.

Drug treatment of vegetative-vascular dystonia

VVD treatment with the help of drugs produced in the case of sharp deterioration states of crisis.

So, with sympathoadrenal crisis, caused by an excess of catecholamines, treatment consists in prescribing drugs that block the action of adrenaline and norepinephrine - blockers(metoprolol, propranolol, atenolol).

Anxiolytics (tranquilizers) have a sedative, anti-anxiety effect. Their introduction stops the sympathoadrenal crisis. The main representatives of this group are phenazepam, diazepam.

In vagoinsular crisis, occurring due to an excess of acetylcholine, a drug is used that blocks its action - atropine. This is a 0.1% solution, which is injected subcutaneously in 1 ml. To maintain the desired level of blood pressure and heart function, a 1% solution is used. cordiamine. It is administered in an amount of 3 ml intramuscularly. For the same purpose, 1 ml of a 10% solution is injected subcutaneously. caffeine.

With severe bronchospasm, inhaled bronchodilators are used: atrovent, salbutomol, berotek, berodual. Intramuscular administration of a 5% solution of ephedrine in a volume of 1 ml may help.

Lack of glucose in the blood hypoglycemia) is eliminated intravenous administration. You can give 20 ml of 40% glucose as an intravenous bolus.

Vestibular disorders (dizziness, nausea, vomiting) docked intramuscular injection 2 ml 5% solution haloperidol.

If saved dizziness, then they are treated with cinnarizine and vinpocetine who take 1 tablet 3 times a day.

Treatment of vegetative-vascular dystonia in children

Treatment of VVD in children is fundamentally the same as in adults. Crises in children are less common, so the treatment will be to normalize your lifestyle, diet, your behavior, habits, and other things, as described above. Drug therapy is carried out in accordance with the age (body weight) of the child. Drugs approved in pediatric practice are used. As a rule, if the VVD appeared in childhood, the risk of VVD is greatly increased during adult life. Therefore, for such people, VSD prevention should be considered throughout life.

Vegetative-vascular dystonia - treatment with folk remedies.

Phytotherapy - treatment of vegetative-vascular dystonia with herbs. This treatment great attention should be given. There are many herbs that can both stimulate the activity of the body and soothe its excessive activation.

Treatment of hypertensive type of VVD

In the hypertensive type of VVD, herbs are used that have a calming, hypnotic effect on the body. These herbs are not an alternative medicines treatment, but only an essential addition to this treatment. They should be taken only with mild symptoms of the disease. Their reception is long, about 20-30 days. Moreover, they should be taken no more than the specified period, so that there are no side effects. It is better to use several types of herbs with the same effects, which are applied in turn.

Here are the main representatives of herbs with soothing and hypnotic effect: valerian, lemon balm, St. John's wort, motherwort, chamomile, hops, linden, mint, clover, dill, blackberry, wild strawberry and some others.

Valerian is one of best herbs this series, which also has no contraindications. It is best to use valerian tincture, which is taken in 15 ml (1 tablespoon) 2 times a day. This treatment lasts one week, then a break is made for 2 weeks.

Motherwort - can significantly reduce blood pressure, so it should be used with caution.

Mint and lemon balm - used in the form of teas, tinctures. Long-term use is not recommended as it may Negative influence on the reproductive system person.

Treatment of hypotonic type of VVD

In the hypotonic type of VVD, herbs are used that increase the tone of the body and, in particular, the cardiovascular system. These herbs include: ginseng, eleutherococcus, coffee, black and green tea.

Ginseng is an adaptogen. Tincture from its root is taken 20 drops 30 minutes before meals. It should be taken in the morning, to prevent insomnia. Ginseng not only stimulates the work of the nervous and cardiovascular systems, but also increases potency. Ginseng treatment should not be continued for too long, otherwise exhaustion may occur.

Eleutherococcus is also an adaptogen. It selectively stimulates the nervous system, improves the transmission of nerve impulses. Take it in the same way as ginseng: in the morning 30 minutes before meals, 30 drops. The course of treatment is 15-20 days.

Collection of herbs for the treatment of VVD

Make a mixture of the following herbs: swamp cudweed (30 gr.), woolly-flowered astragalus (40 gr.), field horsetail (40 gr.), sweet clover (40 gr.) Make a decoction from the mixture and take 15 - 30 ml (1- 2 tablespoons) for 1-2 months.

Video: VSD, panic attacks. Occurrence and treatment.