Drugs that reduce the influence of the sympathetic nervous system. unknown universe

Content

Parts of the autonomic system are the sympathetic and parasympathetic nervous systems, the latter having a direct impact and being closely related to the work of the heart muscle, the frequency of myocardial contraction. It is localized partially in the brain and spinal cord. The parasympathetic system provides relaxation and recovery of the body after physical, emotional stress, but cannot exist separately from the sympathetic department.

What is the parasympathetic nervous system

The department is responsible for the functionality of the organism without its participation. For example, parasympathetic fibers provide respiratory function, regulate the heartbeat, dilate blood vessels, control the natural process of digestion and protective functions, and provide other important mechanisms. The parasympathetic system is necessary for a person to relax the body after exercise. With its participation, muscle tone decreases, the pulse returns to normal, the pupil and vascular walls narrow. This happens without human intervention - arbitrarily, at the level of reflexes

The main centers of this autonomous structure are the brain and spinal cord, where nerve fibers are concentrated, providing the fastest possible transmission of impulses for the operation of internal organs and systems. With their help, you can control blood pressure, vascular permeability, cardiac activity, internal secretion of individual glands. Each nerve impulse is responsible for a certain part of the body, which, when excited, begins to react.

It all depends on the localization of the characteristic plexuses: if the nerve fibers are in the pelvic area, they are responsible for physical activity, and in the digestive system organs - for the secretion of gastric juice, intestinal motility. The structure of the autonomic nervous system has the following constructive sections with unique functions for the whole organism. This:

• pituitary;
• hypothalamus;
• nervus vagus;
• epiphysis

This is how the main elements of the parasympathetic centers are designated, and the following are considered additional structures:

• nerve nuclei of the occipital zone;
• sacral nuclei;
• cardiac plexuses to provide myocardial shocks;
• hypogastric plexus;
• lumbar, celiac and thoracic nerve plexuses.

Sympathetic and parasympathetic nervous system

Comparing the two departments, the main difference is obvious. The sympathetic department is responsible for activity, reacts in moments of stress, emotional arousal. As for the parasympathetic nervous system, it "connects" in the stage of physical and emotional relaxation. Another difference is the mediators that carry out the transition of nerve impulses in synapses: in sympathetic nerve endings it is norepinephrine, in parasympathetic nerve endings it is acetylcholine.

Features of interaction between departments

The parasympathetic division of the autonomic nervous system is responsible for the smooth operation of the cardiovascular, genitourinary and digestive systems, while parasympathetic innervation of the liver, thyroid gland, kidneys, and pancreas takes place. The functions are different, but the impact on the organic resource is complex. If the sympathetic department provides excitation of the internal organs, then the parasympathetic department helps to restore the general condition of the body. If there is an imbalance of the two systems, the patient needs treatment.

Where are the centers of the parasympathetic nervous system located?

The sympathetic nervous system is structurally represented by the sympathetic trunk in two rows of nodes on both sides of the spine. Externally, the structure is represented by a chain of nerve lumps. If we touch on the element of so-called relaxation, the parasympathetic part of the autonomic nervous system is localized in the spinal cord and brain. So, from the central sections of the brain, the impulses that arise in the nuclei go as part of the cranial nerves, from the sacral sections - as part of the pelvic splanchnic nerves, reach the organs of the small pelvis.

Functions of the parasympathetic nervous system

Parasympathetic nerves are responsible for the body's natural recovery, normal myocardial contraction, muscle tone, and productive smooth muscle relaxation. Parasympathetic fibers differ in local action, but in the end they act together - plexuses. With a local lesion of one of the centers, the autonomic nervous system as a whole suffers. The effect on the body is complex, and doctors distinguish the following useful functions:

• relaxation of the oculomotor nerve, pupil constriction;
• normalization of blood circulation, systemic blood flow;
• restoration of habitual breathing, narrowing of the bronchi;
• lowering blood pressure;
• control of an important indicator of blood glucose;
• reduction in heart rate;
• slowing down the passage of nerve impulses;
• decrease in eye pressure;
• regulation of the glands of the digestive system.

In addition, the parasympathetic system helps the vessels of the brain and genital organs to expand, and the smooth muscles to tone up. With its help, a natural cleansing of the body occurs due to such phenomena as sneezing, coughing, vomiting, going to the toilet. In addition, if symptoms of arterial hypertension begin to appear, it is important to understand that the above-described nervous system is responsible for cardiac activity. If one of the structures - sympathetic or parasympathetic - fails, it is necessary to take measures, since they are closely related.

Diseases

Before using certain medications, doing research, it is important to correctly diagnose diseases associated with impaired functioning of the parasympathetic structure of the brain and spinal cord. A health problem manifests itself spontaneously, it can affect internal organs, affect habitual reflexes. The following violations of the body of any age may be the basis:

1. Cyclic paralysis. The disease is provoked by cyclic spasms, severe damage to the oculomotor nerve. The disease occurs in patients of different ages, accompanied by degeneration of the nerves.
2. Syndrome of the oculomotor nerve. In such a difficult situation, the pupil can expand without exposure to a stream of light, which is preceded by damage to the afferent section of the pupillary reflex arc.
3. Block nerve syndrome. A characteristic ailment is manifested in the patient by a slight strabismus, imperceptible to the average layman, while the eyeball is directed inward or upward.
4. Injured abducens nerves. In the pathological process, strabismus, double vision, pronounced Fauville's syndrome are simultaneously combined in one clinical picture. Pathology affects not only the eyes, but also the facial nerves.
5. Trigeminal nerve syndrome. Among the main causes of pathology, doctors distinguish an increased activity of pathogenic infections, a violation of systemic blood flow, damage to the cortical-nuclear pathways, malignant tumors, and traumatic brain injury.
6. Syndrome of the facial nerve. There is an obvious distortion of the face, when a person arbitrarily has to smile, while experiencing pain. More often it is a complication of the disease.

Under the vegetative (from the Latin. vegetare - to grow) activity of the body is understood the work of internal organs, which provides energy and other components necessary for existence to all organs and tissues. At the end of the 19th century, the French physiologist Claude Bernard (Bernard C.) came to the conclusion that "the constancy of the internal environment of the body is the key to its free and independent life." As he noted back in 1878, the internal environment of the body is subject to strict control, keeping its parameters within certain limits. In 1929, the American physiologist Walter Cannon (Cannon W.) proposed to designate the relative constancy of the internal environment of the body and some physiological functions by the term homeostasis (Greek homoios - equal and stasis - state). There are two mechanisms for maintaining homeostasis: nervous and endocrine. This chapter will deal with the first of these.

11.1. autonomic nervous system

The autonomic nervous system innervates the smooth muscles of the internal organs, the heart and exocrine glands (digestive, sweat, etc.). Sometimes this part of the nervous system is called visceral (from Latin viscera - insides) and very often - autonomous. The last definition emphasizes an important feature of autonomic regulation: it occurs only reflexively, i.e., it is not recognized and does not submit to voluntary control, thereby fundamentally differing from the somatic nervous system that innervates skeletal muscles. In the English-language literature, the term autonomic nervous system is usually used, in the domestic literature it is often called the autonomic nervous system.

At the very end of the 19th century, the British physiologist John Langley (Langley J.) subdivided the autonomic nervous system into three sections: sympathetic, parasympathetic and enteral. This classification remains generally accepted at the present time (although in the domestic literature, the enteric region, consisting of neurons of the intermuscular and submucosal plexuses of the gastrointestinal tract, is quite often called metasympathetic). This chapter deals with the first two divisions of the autonomic nervous system. Cannon drew attention to their different functions: the sympathetic controls the reactions of fight or flight (in the English rhyming version: fight or flight), and the parasympathetic is necessary for rest and digestion of food (rest and digest). The Swiss physiologist Walter Hess (Hess W.) suggested calling the sympathetic department ergotropic, i.e., contributing to the mobilization of energy, intense activity, and the parasympathetic - trophotropic, i.e. regulating tissue nutrition, recovery processes.

11.2. Peripheral division of the autonomic nervous system

First of all, it should be noted that the peripheral part of the autonomic nervous system is exclusively efferent; it serves only to conduct excitation to effectors. If in the somatic nervous system only one neuron (motoneuron) is needed for this, then in the autonomic nervous system two neurons are used, connecting through a synapse in a special autonomic ganglion (Fig. 11.1).

The bodies of preganglionic neurons are located in the brainstem and spinal cord, and their axons go to the ganglia, where the bodies of postganglionic neurons are located. The working organs are innervated by axons of postganglionic neurons.

The sympathetic and parasympathetic divisions of the autonomic nervous system differ primarily in the location of the preganglionic neurons. The bodies of sympathetic neurons are located in the lateral horns of the thoracic and lumbar (two or three upper segments) sections. The preganglionic neurons of the parasympathetic division are, firstly, in the brainstem, from where the axons of these neurons emerge as part of four cranial nerves: oculomotor (III), facial (VII), glossopharyngeal (IX) and vagus (X). Second, parasympathetic preganglionic neurons are found in the sacral spinal cord (Fig. 11.2).

Sympathetic ganglia are usually divided into two types: paravertebral and prevertebral. Paravertebral ganglia form the so-called. sympathetic trunks, consisting of nodes connected by longitudinal fibers, which are located on both sides of the spine, extending from the base of the skull to the sacrum. In the sympathetic trunk, most axons of preganglionic neurons transmit excitation to postganglionic neurons. A smaller part of the preganglionic axons passes through the sympathetic trunk to the prevertebral ganglia: cervical, stellate, celiac, superior and inferior mesenteric - in these unpaired formations, as well as in the sympathetic trunk, there are sympathetic postganglionic neurons. In addition, part of the sympathetic preganglionic fibers innervates the adrenal medulla. The axons of preganglionic neurons are thin and, despite the fact that many of them are covered with a myelin sheath, the speed of excitation conduction along them is much less than along the axons of motor neurons.

In the ganglia, the fibers of the preganglionic axons branch and form synapses with the dendrites of many postganglionic neurons (a phenomenon of divergence), which, as a rule, are multipolar and have an average of about a dozen dendrites. There are on average about 100 postganglionic neurons per preganglionic sympathetic neuron. At the same time, in the sympathetic ganglia, the convergence of many preganglionic neurons to the same postganglionic neurons is also observed. Due to this, the summation of excitation occurs, which means that the reliability of signal transmission increases. Most of the sympathetic ganglia are located quite far from the innervated organs, and therefore the postganglionic neurons have rather long axons that are devoid of myelin coverage.

In the parasympathetic division, preganglionic neurons have long fibers, some of which are myelinated: they end near the innervated organs or in the organs themselves, where the parasympathetic ganglia are located. Therefore, in postganglionic neurons, the axons are short. The ratio of pre- and postganglionic neurons in the parasympathetic ganglia differs from the sympathetic ones: it is only 1: 2 here. Most internal organs have both sympathetic and parasympathetic innervation, an important exception to this rule is the smooth muscles of the blood vessels, which are regulated only by the sympathetic department. And only the arteries of the genital organs have a double innervation: both sympathetic and parasympathetic.

11.3. Autonomic nerve tone

Many autonomic neurons exhibit background spontaneous activity, i.e., the ability to spontaneously generate action potentials under resting conditions. This means that the organs innervated by them, in the absence of any irritation from the external or internal environment, still receive excitation, usually at a frequency of 0.1 to 4 impulses per second. This low frequency stimulation appears to maintain a constant slight contraction (tone) of the smooth muscles.

After cutting or pharmacological blockade of certain autonomic nerves, the innervated organs are deprived of their tonic influence and such a loss is immediately detected. Thus, for example, after unilateral transection of the sympathetic nerve that controls the vessels of the rabbit's ear, a sharp expansion of these vessels is detected, and after transection or blockade of the vagus nerves in the experimental animal, heart contractions become more frequent. Removing the blockade restores the normal heart rate. After cutting the nerves, the heart rate and vascular tone can be restored if the peripheral segments are artificially irritated with an electric current, choosing its parameters so that they are close to the natural rhythm of the impulse.

As a result of various influences on the vegetative centers (which is yet to be considered in this chapter), their tone may change. So, for example, if 2 impulses per second pass through the sympathetic nerves that control the smooth muscles of the arteries, then the width of the arteries is typical for a state of rest, and then normal blood pressure is recorded. If the tone of the sympathetic nerves increases and the frequency of nerve impulses entering the arteries increases, for example, up to 4-6 per second, then the smooth muscles of the vessels will contract more strongly, the lumen of the vessels will decrease, and blood pressure will increase. And vice versa: with a decrease in sympathetic tone, the frequency of impulses entering the arteries becomes less than usual, which leads to vasodilation and a decrease in blood pressure.

The tone of the autonomic nerves is extremely important in the regulation of the activity of internal organs. It is maintained due to the flow of afferent signals to the centers, the action of various components of cerebrospinal fluid and blood on them, as well as the coordinating influence of a number of brain structures, primarily the hypothalamus.

11.4. Afferent link of autonomic reflexes

Vegetative reactions can be observed upon stimulation of almost any receptive area, but most often they occur in connection with shifts in various parameters of the internal environment and activation of interoreceptors. For example, activation of mechanoreceptors located in the walls of hollow internal organs (blood vessels, digestive tract, bladder, etc.) occurs when pressure or volume changes in these organs. Excitation of the chemoreceptors of the aorta and carotid arteries occurs due to an increase in the arterial blood pressure of carbon dioxide or the concentration of hydrogen ions, as well as a decrease in oxygen tension. Osmoreceptors are activated depending on the concentration of salts in the blood or in the cerebrospinal fluid, glucoreceptors - depending on the concentration of glucose - any change in the parameters of the internal environment causes irritation of the corresponding receptors and a reflex reaction aimed at maintaining homeostasis. There are also pain receptors in the internal organs, which can be excited with a strong stretching or contraction of the walls of these organs, with their oxygen starvation, with inflammation.

Interoreceptors can belong to one of two types of sensory neurons. First, they can be sensitive endings of neurons in the spinal ganglia, and then excitation from the receptors is conducted, as usual, to the spinal cord and then, with the help of intercalary cells, to the corresponding sympathetic and parasympathetic neurons. Switching of excitation from sensitive to intercalary, and then efferent neurons often occurs in certain segments of the spinal cord. With a segmental organization, the activity of the internal organs is controlled by autonomic neurons located in the same segments of the spinal cord, which receive afferent information from these organs.

Secondly, the propagation of signals from interoreceptors can be carried out along sensory fibers that are part of the autonomic nerves themselves. So, for example, most of the fibers that form the vagus, glossopharyngeal, and celiac nerves do not belong to vegetative, but to sensory neurons, whose bodies are located in the corresponding ganglia.

11.5. The nature of sympathetic and parasympathetic influence on the activity of internal organs

Most organs have dual, i.e., sympathetic and parasympathetic innervation. The tone of each of these sections of the autonomic nervous system can be balanced by the influence of another section, but in certain situations, increased activity is detected, the predominance of one of them, and then the true nature of the influence of this section appears. Such an isolated action can also be found in experiments with cutting or pharmacological blockade of sympathetic or parasympathetic nerves. After such an intervention, the activity of the working organs changes under the influence of the department of the autonomic nervous system that has retained its connection with it. Another way of experimental study is to alternately stimulate the sympathetic and parasympathetic nerves with specially selected parameters of the electric current - this simulates an increase in sympathetic or parasympathetic tone.

The influence of the two divisions of the autonomic nervous system on the controlled organs is most often opposite in direction of shifts, which even gives reason to speak of the antagonistic nature of the relationship between the sympathetic and parasympathetic divisions. So, for example, when the sympathetic nerves that control the work of the heart are activated, the frequency and strength of its contractions increase, the excitability of the cells of the conduction system of the heart increases, and with an increase in the tone of the vagus nerves, opposite shifts are recorded: the frequency and strength of heart contractions decrease, the excitability of the elements of the conduction system decreases . Other examples of the opposite influence of sympathetic and parasympathetic nerves can be seen in table 11.1

Despite the fact that the influence of the sympathetic and parasympathetic divisions on many organs is opposite, they act as synergists, that is, friendly. With an increase in the tone of one of these departments, the tone of the other decreases synchronously: this means that physiological shifts of any direction are due to coordinated changes in the activity of both departments.

11.6. Transmission of excitation in the synapses of the autonomic nervous system

In the vegetative ganglia of both the sympathetic and parasympathetic divisions, the mediator is the same substance - acetylcholine (Fig. 11.3). The same mediator serves as a chemical mediator for the transmission of excitation from parasympathetic postganglionic neurons to the working organs. The main mediator of sympathetic postganglionic neurons is norepinephrine.

Although the same mediator is used in the autonomic ganglia and in the transmission of excitation from parasympathetic postganglionic neurons to the working organs, the cholinergic receptors interacting with it are not the same. In the autonomic ganglia, nicotine-sensitive or H-cholinergic receptors interact with the mediator. If in the experiment the cells of the autonomic ganglia are moistened with a 0.5% solution of nicotine, then they cease to conduct excitation. The introduction of a nicotine solution into the blood of experimental animals leads to the same result and thus creates a high concentration of this substance. In a small concentration, nicotine acts like acetylcholine, that is, it excites this type of cholinergic receptors. Such receptors are associated with ionotropic channels, and when they are excited, sodium channels of the postsynaptic membrane open.

Cholinergic receptors located in the working organs and interacting with acetylcholine of postganglionic neurons belong to a different type: they do not respond to nicotine, but they can be excited by a small amount of another alkaloid - muscarine or blocked by a high concentration of the same substance. Muscarin-sensitive or M-cholinergic receptors provide metabotropic control, which involves secondary messengers, and mediator-induced reactions develop more slowly and last longer than with ionotropic control.

The mediator of sympathetic postganglionic neurons, norepinephrine, can be bound by two types of metabotropic adrenoreceptors: a- or b, the ratio of which in different organs is not the same, which determines various physiological reactions to the action of norepinephrine. For example, b-adrenergic receptors predominate in the smooth muscles of the bronchi: the action of the mediator on them is accompanied by muscle relaxation, which leads to the expansion of the bronchi. In the smooth muscles of the arteries of the internal organs and skin, there are more a-adrenergic receptors, and here the muscles contract under the action of norepinephrine, which leads to a narrowing of these vessels. The secretion of sweat glands is controlled by special, cholinergic sympathetic neurons, the mediator of which is acetylcholine. There is also evidence that skeletal muscle arteries also innervate sympathetic cholinergic neurons. According to another point of view, skeletal muscle arteries are controlled by adrenergic neurons, and norepinephrine acts on them through a-adrenergic receptors. And the fact that during muscular work, which is always accompanied by an increase in sympathetic activity, the skeletal muscle arteries expand, is explained by the action of the adrenal medulla hormone adrenaline on β-adrenergic receptors.

With sympathetic activation, adrenaline is released in large quantities from the adrenal medulla (attention should be paid to the innervation of the adrenal medulla by sympathetic preganglionic neurons), and also interacts with adrenoreceptors. This enhances the sympathetic response, since the blood brings adrenaline to those cells near which there are no endings of sympathetic neurons. Norepinephrine and epinephrine stimulate the breakdown of glycogen in the liver and lipids in adipose tissue, acting there on b-adrenergic receptors. In the heart muscle, b-receptors are much more sensitive to norepinephrine than to adrenaline, while in the vessels and bronchi they are more easily activated by adrenaline. These differences formed the basis for the division of b-receptors into two types: b1 (in the heart) and b2 (in other organs).

Mediators of the autonomic nervous system can act not only on the postsynaptic, but also on the presynaptic membrane, where there are also corresponding receptors. Presynaptic receptors are used to regulate the amount of neurotransmitter released. For example, with an increased concentration of norepinephrine in the synaptic cleft, it acts on presynaptic a-receptors, which leads to a decrease in its further release from the presynaptic ending (negative feedback). If the concentration of the mediator in the synaptic cleft becomes low, the b-receptors of the presynaptic membrane interact with it, and this leads to an increase in the release of norepinephrine (positive feedback).

According to the same principle, i.e. with the participation of presynaptic receptors, the regulation of the release of acetylcholine is carried out. If the endings of sympathetic and parasympathetic postganglionic neurons are close to each other, then reciprocal influence of their mediators is possible. For example, the presynaptic endings of cholinergic neurons contain a-adrenergic receptors and, if norepinephrine acts on them, the release of acetylcholine will decrease. In the same way, acetylcholine can reduce the release of norepinephrine if it joins the M-cholinergic receptors of the adrenergic neuron. Thus, the sympathetic and parasympathetic divisions compete even at the level of postganglionic neurons.

A lot of drugs act on the transmission of excitation in the autonomic ganglia (ganglioblockers, a-blockers, b-blockers, etc.) and therefore are widely used in medical practice to correct various kinds of autonomic regulation disorders.

11.7. Centers of autonomic regulation of the spinal cord and trunk

Many preganglionic and postganglionic neurons are able to fire independently of each other. For example, some sympathetic neurons control sweating, while others control skin blood flow, some parasympathetic neurons increase the secretion of the salivary glands, and others increase the secretion of the glandular cells of the stomach. There are methods for detecting the activity of postganglionic neurons that make it possible to distinguish vasoconstrictor neurons of the skin from cholinergic neurons that control skeletal muscle vessels or from neurons that act on hairy muscles of the skin.

The topographically organized input of afferent fibers from different receptive areas to certain segments of the spinal cord or different areas of the brainstem excites intercalary neurons, and they transmit excitation to preganglionic autonomic neurons, thus closing the reflex arc. Along with this, the autonomic nervous system is characterized by integrative activity, which is especially pronounced in the sympathetic department. Under certain circumstances, for example, when experiencing emotions, the activity of the entire sympathetic department can increase, and, accordingly, the activity of parasympathetic neurons decreases. In addition, the activity of autonomic neurons is consistent with the activity of motor neurons, on which the work of skeletal muscles depends, but their supply with the glucose and oxygen necessary for work is carried out under the control of the autonomic nervous system. The participation of vegetative neurons in integrative activity is provided by the vegetative centers of the spinal cord and trunk.

In the thoracic and lumbar regions of the spinal cord are the bodies of sympathetic preganglionic neurons, which form the intermediate-lateral, intercalary and small central autonomic nuclei. Sympathetic neurons that control the sweat glands, blood vessels of the skin, and skeletal muscles are located lateral to the neurons that regulate the activity of internal organs. By the same principle, parasympathetic neurons are located in the sacral spinal cord: laterally - innervating the bladder, medially - the large intestine. After separation of the spinal cord from the brain, vegetative neurons are able to discharge rhythmically: for example, sympathetic neurons of twelve segments of the spinal cord, united by intraspinal pathways, can, to a certain extent, reflexively regulate the tone of blood vessels. However, in spinal animals the number of discharged sympathetic neurons and the frequency of discharges are less than in intact animals. This means that the spinal cord neurons that control vascular tone are stimulated not only by the afferent input, but also by the centers of the brain.

The brain stem contains the vasomotor and respiratory centers, which rhythmically activate the sympathetic nuclei of the spinal cord. Afferent information from baro- and chemoreceptors continuously enters the trunk, and in accordance with its nature, autonomic centers determine changes in the tone of not only sympathetic, but also parasympathetic nerves that control, for example, the work of the heart. This is a reflex regulation, in which the motor neurons of the respiratory muscles are also involved - they are rhythmically activated by the respiratory center.

In the reticular formation of the brain stem, where the vegetative centers are located, several mediator systems are used that control the most important homeostatic indicators and are in complex relationships with each other. Here, some groups of neurons can stimulate the activity of others, inhibit the activity of others, and simultaneously experience the influence of both of them on themselves. Along with the centers for regulating blood circulation and respiration, there are neurons here that coordinate many digestive reflexes: salivation and swallowing, secretion of gastric juice, gastric motility; a protective gag reflex can be mentioned separately. Different centers constantly coordinate their activities with each other: for example, when swallowing, the entrance to the respiratory tract reflexively closes and, thanks to this, inhalation is prevented. The activity of the stem centers subjugates the activity of the autonomic neurons of the spinal cord.

11. 8. The role of the hypothalamus in the regulation of autonomic functions

The hypothalamus accounts for less than 1% of the brain volume, but it plays a decisive role in the regulation of autonomic functions. This is due to several factors. First, the hypothalamus promptly receives information from interoreceptors, the signals from which come to it through the brainstem. Secondly, information comes here from the surface of the body and from a number of specialized sensory systems (visual, olfactory, auditory). Thirdly, some neurons of the hypothalamus have their own osmo-, thermo- and glucoreceptors (such receptors are called central). They can respond to shifts in osmotic pressure, temperature, and glucose levels in CSF and blood. In this regard, it should be recalled that in the hypothalamus, in comparison with the rest of the brain, the properties of the blood-brain barrier are manifested to a lesser extent. Fourth, the hypothalamus has bilateral connections with the limbic system of the brain, the reticular formation, and the cerebral cortex, which allows it to coordinate autonomic functions with certain behavior, for example, with the experience of emotions. Fifthly, the hypothalamus forms projections on the vegetative centers of the trunk and spinal cord, which allows it to directly control the activity of these centers. Sixth, the hypothalamus controls the most important mechanisms of endocrine regulation (See Chapter 12).

The most important switching for autonomic regulation is carried out by the neurons of the nuclei of the hypothalamus (Fig. 11.4), in different classifications they number from 16 to 48. hypothalamus in experimental animals and found different combinations of vegetative and behavioral responses.

When the posterior region of the hypothalamus and the gray matter adjacent to the water supply were stimulated, the blood pressure in the experimental animals increased, the heart rate increased, breathing quickened and deepened, the pupils dilated, and the hair rose, the back curved in a hump and the teeth bared, i.e., vegetative changes spoke about the activation of the sympathetic department, and the behavior was affective-defensive. Irritation of the rostral parts of the hypothalamus and the preoptic region evoked feeding behavior in the same animals: they began to eat, even if they were full of food, while salivation increased and motility of the stomach and intestines increased, while the heart rate and breathing decreased, and muscle blood flow also became smaller. , which is quite typical for an increase in parasympathetic tone. With a light hand of Hess, one region of the hypothalamus began to be called ergotropic, and the other - trophotropic; they are separated from each other by some 2-3 mm.

From these and many other studies, the idea gradually emerged that the activation of different areas of the hypothalamus triggers an already prepared complex of behavioral and autonomic reactions, which means that the role of the hypothalamus is to evaluate the information coming to it from different sources and, based on it, choose one or another option that combines behavior with a certain activity of both parts of the autonomic nervous system. The very same behavior can be considered in this situation as an activity aimed at preventing possible shifts in the internal environment. It should be noted that not only the deviations of homeostasis that have already occurred, but also any event potentially threatening homeostasis can activate the necessary activity of the hypothalamus. So, for example, in the event of a sudden threat, vegetative changes in a person (an increase in the heart rate, an increase in blood pressure, etc.) occur faster than he takes to flight, i.e. such shifts already take into account the nature of subsequent muscle activity.

The direct control of the tone of the autonomic centers, and hence the output activity of the autonomic nervous system, is carried out by the hypothalamus with the help of efferent connections with three most important areas (Fig. 11.5):

1). The nucleus of the solitary tract in the upper part of the medulla oblongata, which is the main recipient of sensory information from the internal organs. It interacts with the nucleus of the vagus nerve and other parasympathetic neurons and is involved in the control of temperature, circulation, and respiration. 2). Rostral ventral region of the medulla oblongata, which is crucial in increasing the overall output activity of the sympathetic division. This activity is manifested in an increase in blood pressure, an increase in the heart rate, secretion of sweat glands, dilation of the pupils and contraction of the muscles that raise the hair. 3). Autonomic neurons of the spinal cord, which can be directly influenced by the hypothalamus.

11.9. Vegetative mechanisms of blood circulation regulation

In a closed network of blood vessels and the heart (Fig. 11.6), blood is constantly moving, the volume of which averages 69 ml/kg of body weight in adult men and 65 ml/kg of body weight in women (i.e. with a body weight of 70 kg, it will be 4830 ml and 4550 ml, respectively). At rest, from 1/3 to 1/2 of this volume does not circulate through the vessels, but is located in the blood depots: capillaries and veins of the abdominal cavity, liver, spleen, lungs, and subcutaneous vessels.

During physical work, emotional reactions, stress, this blood passes from the depot into the general circulation. The movement of blood is provided by rhythmic contractions of the ventricles of the heart, each of which expels approximately 70 ml of blood into the aorta (left ventricle) and pulmonary artery (right ventricle), and with heavy physical exertion in well-trained people, this indicator (it is called systolic or stroke volume) can increase up to 180 ml. The heart of an adult is reduced at rest approximately 75 times per minute, which means that during this time over 5 liters of blood (75x70 = 5250 ml) must pass through it - this indicator is called the minute volume of blood circulation. With each contraction of the left ventricle, the pressure in the aorta, and then in the arteries, rises to 100-140 mm Hg. Art. (systolic pressure), and by the beginning of the next contraction it drops to 60-90 mm (diastolic pressure). In the pulmonary artery, these figures are less: systolic - 15-30 mm, diastolic - 2-7 mm - this is due to the fact that the so-called. the pulmonary circulation, starting from the right ventricle and delivering blood to the lungs, is shorter than the large one, and therefore has less resistance to blood flow and does not require high pressure. Thus, the main indicators of the function of blood circulation are the frequency and strength of heart contractions (the systolic volume depends on it), systolic and diastolic pressure, which are determined by the volume of fluid in a closed circulatory system, the minute volume of blood flow and the resistance of vessels to this blood flow. The resistance of the vessels changes due to the contractions of their smooth muscles: the narrower the lumen of the vessel becomes, the greater the resistance to blood flow it provides.

The constancy of the volume of fluid in the body is regulated by hormones (See Chapter 12), but what part of the blood will be in the depot, and what will circulate through the vessels, what resistance the vessels will provide to the blood flow - depends on the control of the vessels by the sympathetic department. The work of the heart, and hence the magnitude of blood pressure, primarily systolic, is controlled by both sympathetic and vagus nerves (although endocrine mechanisms and local self-regulation also play an important role here). The mechanism for monitoring changes in the most important parameters of the circulatory system is quite simple, it comes down to continuous recording by baroreceptors of the degree of stretching of the aortic arch and the place where the common carotid arteries are divided into external and internal (this area is called the carotid sinus). This is sufficient, since the stretching of these vessels reflects the work of the heart, and vascular resistance, and blood volume.

The more the aorta and carotid arteries are stretched, the more often nerve impulses propagate from baroceptors along the sensitive fibers of the glossopharyngeal and vagus nerves to the corresponding nuclei of the medulla oblongata. This leads to two consequences: an increase in the influence of the vagus nerve on the heart and a decrease in the sympathetic effect on the heart and blood vessels. As a result, the work of the heart decreases (the minute volume decreases) and the tone of the vessels that resist blood flow decreases, and this leads to a decrease in the stretching of the aorta and carotid arteries and a corresponding decrease in impulses from baroreceptors. If it begins to decrease, then there will be an increase in sympathetic activity and a decrease in the tone of the vagus nerves, and as a result, the proper value of the most important parameters of blood circulation will be restored again.

The continuous movement of blood is necessary, first of all, in order to deliver oxygen from the lungs to the working cells, and carry away the carbon dioxide formed in the cells to the lungs, where it is excreted from the body. The content of these gases in the arterial blood is maintained at a constant level, which reflects the values ​​of their partial pressure (from Latin pars - part, that is, partial of the whole atmospheric pressure): oxygen - 100 mm Hg. Art., carbon dioxide - about 40 mm Hg. Art. If the tissues begin to work more intensively, they will begin to take more oxygen from the blood and release more carbon dioxide into it, which will lead to a decrease in the oxygen content and an increase in carbon dioxide in the arterial blood, respectively. These shifts are picked up by chemoreceptors located in the same vascular regions as baroreceptors, i.e., in the aorta and forks in the carotid arteries that feed the brain. The arrival of more frequent signals from chemoreceptors to the medulla oblongata will lead to the activation of the sympathetic department and a decrease in the tone of the vagus nerves: as a result, the work of the heart will increase, the tone of the vessels will increase and, under high pressure, the blood will circulate faster between the lungs and tissues. At the same time, the increased frequency of impulses from the vascular chemoreceptors will lead to an increase and deepening of breathing, and the rapidly circulating blood will become faster saturated with oxygen and freed from excess carbon dioxide: as a result, the blood gas composition will normalize.

Thus, the baroreceptors and chemoreceptors of the aorta and carotid arteries immediately respond to shifts in hemodynamic parameters (manifested by an increase or decrease in the stretching of the walls of these vessels), as well as to changes in blood saturation with oxygen and carbon dioxide. The vegetative centers that received information from them change the tone of the sympathetic and parasympathetic divisions in such a way that their influence on the working organs leads to the normalization of parameters that have deviated from homeostatic constants.

Of course, this is only a part of a complex system of regulation of blood circulation, in which, along with nervous ones, there are also humoral and local mechanisms of regulation. For example, any particularly intensively working organ consumes more oxygen and forms more under-oxidized metabolic products, which themselves are able to expand the vessels that supply the organ with blood. As a result, he begins to take more from the general blood flow than he took before, and therefore, in the central vessels, due to the decreasing volume of blood, the pressure decreases and it becomes necessary to regulate this shift already with the help of nervous and humoral mechanisms.

During physical work, the circulatory system must adapt to muscle contractions, and to increased oxygen consumption, and to the accumulation of metabolic products, and to the changing activity of other organs. With various behavioral reactions, during the experience of emotions, complex changes occur in the body, which are reflected in the constancy of the internal environment: in such cases, the whole complex of such changes that activate different areas of the brain will certainly affect the activity of hypothalamus neurons, and it already coordinates the mechanisms of autonomic regulation with muscle work , emotional state or behavioral reactions.

11.10. The main links in the regulation of breathing

With calm breathing, about 300-500 cubic meters enter the lungs during inhalation. cm of air and the same volume of air when exhaled goes into the atmosphere - this is the so-called. respiratory volume. After a quiet breath, you can additionally inhale 1.5-2 liters of air - this is the inspiratory reserve volume, and after a normal exhalation, you can expel another 1-1.5 liters of air from the lungs - this is the expiratory reserve volume. The sum of respiratory and reserve volumes is the so-called. lung capacity, which is usually measured with a spirometer. Adults breathe on average 14-16 times per minute, ventilating 5-8 liters of air through the lungs during this time - this is the minute volume of breathing. With an increase in the depth of breathing due to reserve volumes and a simultaneous increase in the frequency of respiratory movements, it is possible to increase the minute ventilation of the lungs several times (on average, up to 90 liters per minute, and trained people can double this figure).

Air enters the alveoli of the lungs - air cells densely braided with a network of blood capillaries that carry venous blood: it is poorly saturated with oxygen and excess with carbon dioxide (Fig. 11.7).

Very thin walls of the alveoli and capillaries do not interfere with gas exchange: along the partial pressure gradient, oxygen from the alveolar air passes into the venous blood, and carbon dioxide diffuses into the alveoli. As a result, arterial blood flows from the alveoli with a partial pressure of oxygen in it of about 100 mm Hg. Art., and carbon dioxide - no more than 40 mm Hg. Art.. Ventilation of the lungs constantly updates the composition of the alveolar air, and continuous blood flow and diffusion of gases through the pulmonary membrane allow you to constantly turn venous blood into arterial.

Inhalation occurs due to contractions of the respiratory muscles: external intercostal and diaphragm, which are controlled by motor neurons of the cervical (diaphragm) and thoracic spinal cord (intercostal muscles). These neurons are activated by pathways descending from the respiratory center of the brainstem. The respiratory center is formed by several groups of neurons in the medulla oblongata and the pons, one of them (the dorsal inspiratory group) is spontaneously activated at rest 14-16 times per minute, and this excitation is conducted to the motor neurons of the respiratory muscles. In the lungs themselves, in the pleura covering them and in the airways, there are sensitive nerve endings that are excited when the lungs are stretched and air moves through the airways during inspiration. Signals from these receptors are sent to the respiratory center, which, based on them, regulates the duration and depth of inspiration.

With a lack of oxygen in the air (for example, in the rarefied air of mountain peaks) and during physical work, oxygen saturation of the blood decreases. During physical work, at the same time, the content of carbon dioxide in the arterial blood increases, since the lungs, working in the usual mode, do not have time to purify the blood from it to the required condition. Chemoreceptors of the aorta and carotid arteries respond to the shift in the gas composition of arterial blood, signals from which are sent to the respiratory center. This leads to a change in the nature of breathing: inhalation occurs more often and becomes deeper due to reserve volumes, exhalation, usually passive, becomes forced under such circumstances (the ventral group of neurons of the respiratory center is activated and the internal intercostal muscles begin to act). As a result, the minute volume of respiration increases and greater ventilation of the lungs with a simultaneously increased blood flow through them allows you to restore the gas composition of the blood to the homeostatic standard. Immediately after intense physical work, a person has shortness of breath and a rapid pulse, which stop when the oxygen debt is paid off.

The activity rhythm of the neurons of the respiratory center also adapts to the rhythmic activity of the respiratory and other skeletal muscles, from whose proprioceptors it continuously receives information. The coordination of the respiratory rhythm with other homeostatic mechanisms is carried out by the hypothalamus, which, interacting with the limbic system and the cortex, changes the breathing pattern during emotional reactions. The cerebral cortex can have a direct effect on the function of breathing, adapting it to talking or singing. Only the direct influence of the cortex makes it possible to arbitrarily change the nature of breathing, deliberately delay it, slow it down, or speed it up, but all this is possible only to a limited extent. So, for example, arbitrary holding of breath in most people does not exceed a minute, after which it involuntarily resumes due to excessive accumulation of carbon dioxide in the blood and a simultaneous decrease in oxygen in it.

Summary

The constancy of the internal environment of the organism is the guarantor of its free activity. The rapid recovery of displaced homeostatic constants is carried out by the autonomic nervous system. It is also able to prevent possible shifts in homeostasis associated with changes in the external environment. Two departments of the autonomic nervous system simultaneously control the activity of most internal organs, exerting an opposite effect on them. An increase in the tone of sympathetic centers is manifested by ergotropic reactions, and an increase in parasympathetic tone is manifested by trophotropic ones. The activity of the vegetative centers is coordinated by the hypothalamus, it coordinates their activity with the work of the muscles, emotional reactions and behavior. The hypothalamus interacts with the limbic system of the brain, the reticular formation and the cerebral cortex. Vegetative mechanisms of regulation play a major role in the implementation of the vital functions of blood circulation and respiration.

Questions for self-control

165. In what part of the spinal cord are the bodies of parasympathetic neurons located?

A. Sheyny; B. Thoracic; B. Upper segments of the lumbar; D. Lower segments of the lumbar; D. Sacred.

166. What cranial nerves do not contain fibers of parasympathetic neurons?

A. Trinity; B. Oculomotor; B. Facial; G. Wandering; D. Glossopharyngeal.

167. Which ganglia of the sympathetic department should be classified as paravertebral?

A. Sympathetic trunk; B. Neck; B. Starry; G. Chrevny; B. Inferior mesenteric.

168. Which of the following effectors mainly receives only sympathetic innervation?

A. Bronchi; B. Stomach; B. Intestine; D. Blood vessels; D. Bladder.

169. Which of the following reflects an increase in the tone of the parasympathetic division?

A. Pupil dilation; B. Bronchial dilatation; B. Increased heart rate; D. Increased secretion of the digestive glands; D. Increased secretion of sweat glands.

170. Which of the following is characteristic of an increase in the tone of the sympathetic department?

A. Increased secretion of bronchial glands; B. Increased motility of the stomach; B. Increased secretion of the lacrimal glands; D. Contraction of the muscles of the bladder; D. Increased breakdown of carbohydrates in cells.

171. The activity of what endocrine gland is controlled by sympathetic preganglionic neurons?

A. Adrenal cortex; B. Adrenal medulla; B. Pancreas; G. Thyroid gland; D. Parathyroid glands.

172. What neurotransmitter is used to transmit excitation in the sympathetic vegetative ganglia?

A. Adrenaline; B. Norepinephrine; B. Acetylcholine; G. Dopamine; D. Serotonin.

173. With what mediator do parasympathetic postganglionic neurons usually act on effectors?

A. Acetylcholine; B. Adrenaline; B. Norepinephrine; G. Serotonin; D. Substance R.

174. Which of the following characterizes H-cholinergic receptors?

A. Belong to the postsynaptic membrane of the working organs regulated by the parasympathetic division; B. Ionotropic; B. Activated by muscarine; G. Relate only to the parasympathetic department; D. They are located only on the presynaptic membrane.

175. What receptors must bind to the mediator in order for the increased breakdown of carbohydrates to begin in the effector cell?

A. a-adrenergic receptors; B. b-adrenergic receptors; B. N-cholinergic receptors; G. M-cholinergic receptors; D. Ionotropic receptors.

176. What brain structure coordinates vegetative functions and behavior?

A. spinal cord; B. medulla oblongata; B. Midbrain; G. Hypothalamus; D. The cerebral cortex.

177. What homeostatic shift will have a direct effect on the central receptors of the hypothalamus?

A. Increased blood pressure; B. Increase in blood temperature; B. Increase in blood volume; G. Increase in partial pressure of oxygen in arterial blood; D. Decreased blood pressure.

178. What is the value of the minute volume of blood circulation, if the stroke volume is 65 ml, and the heart rate is 78 per minute?

A. 4820 ml; B. 4960 ml; B. 5070 ml; D. 5140 ml; D. 5360 ml.

179. Where are the baroreceptors located that supply information to the vegetative centers of the medulla oblongata, which regulate the work of the heart and blood pressure?

A. Heart; B. Aorta and carotid arteries; B. Large veins; G. Small arteries; D. Hypothalamus.

180. In a lying position, a person reflexively decreases the frequency of contractions of the heart and blood pressure. Activation of what receptors causes these changes?

A. Intrafusal muscle receptors; B. Golgi tendon receptors; B. Vestibular receptors; D. Mechanoreceptors of the aortic arch and carotid arteries; D. Intracardiac mechanoreceptors.

181. What event is most likely to occur as a result of an increase in the tension of carbon dioxide in the blood?

A. Reducing the frequency of breathing; B. Reducing the depth of breathing; B. Decreased heart rate; D. Decrease in the strength of contractions of the heart; D. Increased blood pressure.

182. What is the vital capacity of the lungs if the tidal volume is 400 ml, the inspiratory reserve volume is 1500 ml, and the expiratory reserve volume is 2 liters?

A. 1900 ml; B. 2400 ml; B. 3.5 l; D. 3900 ml; E. It is impossible to determine the vital capacity of the lungs from the available data.

183. What can happen as a result of short-term voluntary hyperventilation of the lungs (frequent and deep breathing)?

A. Increased tone of the vagus nerves; B. Increased tone of sympathetic nerves; B. Increased impulses from vascular chemoreceptors; D. Increased impulses from vascular baroreceptors; D. Increased systolic pressure.

184. What is meant by the tone of the autonomic nerves?

A. Their ability to be excited by the action of a stimulus; B. Ability to conduct excitation; B. Presence of spontaneous background activity; D. Increasing the frequency of conducted signals; E. Any change in the frequency of transmitted signals.

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. There are primary arterial hypertension, or hypertension (essential hypertension), as well as secondary (symptomatic) hypertension, for example, arterial hypertension in glomerulonephritis and nephrotic syndrome (renal hypertension), with narrowing of the 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 of 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 (hypotensive agents of 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 the 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. The pheochromocytoma is removed surgically, but before the operation, during the operation or, if the operation is not possible, lower the blood pressure with the help of oc-blockers.

A frequent cause of arterial hypertension may be a delay in the body of sodium due to excessive consumption of salt and insufficiency of natriuretic factors. An increased content of 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 long-acting antihypertensive drugs. 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, cardiac output and the tone of blood vessels (arterial and venous) decrease - 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 taking the drug, a pronounced withdrawal syndrome develops: 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.

Clonidine solutions in the form of eye drops are 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 the contractions of the heart and the 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 not suitable 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 intravenously slowly in 20 ml of isotonic sodium chloride solution in case of a 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 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 (with 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-adrenergic blockers: bradycardia, heart failure, difficulty in atrioventricular conduction, a decrease in HDL levels in blood plasma, an increase in the tone of the bronchi and peripheral vessels (less pronounced in β 1 -blockers), increased action of hypoglycemic agents, decreased 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 responses to the 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 the organism as an independent individual and its adaptation to the environment.

The ANS innervates not only the internal organs, but also the sense organs and the 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 the autonomic, parasympathetic fibers of the 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 go directly from the spinal cord or the corresponding nucleus of the cranial nerve directly to the working organ, as somatic, but are interrupted in the nodes of the sympathetic trunk and other nodes of the ANS, a diffuse reaction is created when one or more preganglionic nerves are stimulated. fibers.

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 one Schwann sheath, so excitation can be transmitted along them in a cable type, i.e., an excitation wave running through one fiber can be transmitted to fibers that are currently 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.

The main biological function of the 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 support of various forms of adaptive purposeful behavior (mental and physical activity, the implementation of biological motivations - food, sexual, motivations of fear and aggression, adaptation to changing environmental conditions ).

The ANS implements its functions mainly in the following ways: 1) regional changes in vascular tone; 2) adaptive-trophic action; 3) management of the functions of 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) are 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. The adrenal medulla hormone (adrenaline) and the thyroid hormone (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 the general integration of physiological processes carried out by the ANS, of particular importance are the permanent 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 the 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 influence of various blood and cerebrospinal fluid factors on the centers.

The autonomic (autonomous) nervous system regulates all the internal processes of the body: the functions of internal organs and systems, glands, blood and lymphatic vessels, smooth and partially striated muscles, and sensory organs. It provides homeostasis of the body, i.e. the relative dynamic constancy of the internal environment and the stability of its basic physiological functions (blood circulation, respiration, digestion, thermoregulation, metabolism, excretion, reproduction, etc.). In addition, the autonomic nervous system performs an adaptive-trophic function - the regulation of metabolism in relation to environmental conditions.

The term "autonomic nervous system" reflects the control of the involuntary functions of the body. The autonomic nervous system is dependent on the higher centers of the nervous system. There is a close anatomical and functional relationship between the autonomic and somatic parts of the nervous system. Autonomic nerve conductors pass through the cranial and spinal nerves.

The main morphological unit of the autonomic nervous system, as well as the somatic one, is the neuron, and the main functional unit is the reflex arc. In the autonomic nervous system, there are central (cells and fibers located in the brain and spinal cord) and peripheral (all its other formations) sections. There are also sympathetic and parasympathetic parts. Their main difference lies in the features of functional innervation and is determined by the attitude to the means that affect the autonomic nervous system. The sympathetic part is excited by adrenaline, and the parasympathetic part by acetylcholine. Ergotamine has an inhibitory effect on the sympathetic part, and atropine on the parasympathetic part.

Sympathetic part of the autonomic nervous system.

Its central formations are located in the cerebral cortex, hypothalamic nuclei, brain stem, in the reticular formation, and also in the spinal cord (in the lateral horns). The cortical representation has not been sufficiently elucidated. From the cells of the lateral horns of the spinal cord at the level from VIII to LII, peripheral formations of the sympathetic part begin. The axons of these cells are sent as part of the anterior roots and, having separated from them, form a connecting branch that approaches the nodes of the sympathetic trunk.

This is where part of the fibers ends. From the cells of the nodes of the sympathetic trunk, the axons of the second neurons begin, which again approach the spinal nerves and end in the corresponding segments. The fibers that pass through the nodes of the sympathetic trunk, without interruption, approach the intermediate nodes located between the innervated organ and the spinal cord. From the intermediate nodes, the axons of the second neurons begin, heading to the innervated organs. The sympathetic trunk is located along the lateral surface of the spine and basically has 24 pairs of sympathetic nodes: 3 cervical, 12 thoracic, 5 lumbar, 4 sacral. So, from the axons of the cells of the upper cervical sympathetic ganglion, the sympathetic plexus of the carotid artery is formed, from the lower - the upper cardiac nerve, which forms the sympathetic plexus in the heart (it serves to conduct accelerating impulses to the myocardium). The aorta, lungs, bronchi, abdominal organs are innervated from the thoracic nodes, and the pelvic organs are innervated from the lumbar nodes.

Parasympathetic part of the autonomic nervous system.

Its formations start from the cerebral cortex, although the cortical representation, as well as the sympathetic part, has not been sufficiently clarified (mainly it is the limbic-reticular complex).

There are mesencephalic and bulbar sections in the brain and sacral - in the spinal cord. The mesencephalic section includes cells of the cranial nerves: the third pair is the accessory nucleus of Yakubovich (paired, small cell), which innervates the muscle that narrows the pupil; Perlia's nucleus (unpaired small cell) innervates the ciliary muscle involved in accommodation. The bulbar section makes up the upper and lower salivary nuclei (VII and IX pairs); X pair - the vegetative nucleus that innervates the heart, bronchi, gastrointestinal tract, its digestive glands, and other internal organs. The sacral region is represented by cells in the SIII-SV segments, the axons of which form the pelvic nerve that innervates the urogenital organs and the rectum.

Features of autonomic innervation.

All organs are under the influence of both the sympathetic and parasympathetic parts of the autonomic nervous system. The parasympathetic part is more ancient. As a result of its activity, stable states of organs and homeostasis are created. The sympathetic part changes these states (i.e., the functional abilities of organs) in relation to the function being performed. Both parts work in close cooperation. However, there may be a functional predominance of one part over another. With the predominance of the tone of the parasympathetic part, a state of parasympathotonia develops, the sympathetic part - sympathotonia. Parasympathotonia is characteristic of the state of sleep, sympathotonia is characteristic of affective states (fear, anger, etc.).

In clinical conditions, conditions are possible in which the activity of individual organs or body systems is disrupted as a result of the predominance of the tone of one of the parts of the autonomic nervous system. Parasympathotonic crises manifest bronchial asthma, urticaria, angioedema, vasomotor rhinitis, motion sickness; sympathotonic - vasospasm in the form of symmetrical acroasphyxia, migraine, intermittent claudication, Raynaud's disease, transient form of hypertension, cardiovascular crises in hypothalamic syndrome, ganglionic lesions. The integration of vegetative and somatic functions is carried out by the cerebral cortex, the hypothalamus and the reticular formation.

Suprasegmental division of the autonomic nervous system. (Limbico-reticular complex.)

All activity of the autonomic nervous system is controlled and regulated by the cortical divisions of the nervous system (limbic region: parahippocampal and cingulate gyrus). The limbic system is understood as a number of cortical and subcortical structures that are closely interconnected and have a common pattern of development and functions. The limbic system also includes the formations of the olfactory pathways located at the base of the brain, the transparent septum, the vaulted gyrus, the cortex of the posterior orbital surface of the frontal lobe, the hippocampus, and the dentate gyrus. Subcortical structures of the limbic system: caudate nucleus, putamen, amygdala, anterior tubercle of the thalamus, hypothalamus, frenulum nucleus.

The limbic system is a complex interweaving of ascending and descending pathways, closely associated with the reticular formation. Irritation of the limbic system leads to the mobilization of both sympathetic and parasympathetic mechanisms, which has corresponding vegetative manifestations. A pronounced vegetative effect occurs when the anterior parts of the limbic system are irritated, in particular the orbital cortex, amygdala and cingulate gyrus. At the same time, salivation, a change in breathing, increased intestinal motility, urination, defecation, etc. appear. The rhythm of sleep and wakefulness is also regulated by the limbic system. In addition, this system is the center of emotions and the neural substrate of memory. The limbic-reticular complex is under the control of the frontal regions of the cerebral cortex.

In the suprasegmental department, senior researcher distinguish ergotropic and trophotropic systems (devices). Division into the sympathetic and parasympathetic parts in the suprasegmental section of the VNS. impossible. Ergotropic devices (systems) provide adaptation to environmental conditions. Trophotropic are responsible for ensuring homeostatic balance and the course of anabolic processes.

Autonomic innervation of the eye.

The autonomic innervation of the eye provides expansion or contraction of the pupil (mm. dilatator et sphincter pupillae), accommodation (m. ciliaris), a certain position of the eyeball in the orbit (m. orbitalis) and partially - raising the upper eyelid (smooth muscle - m. tarsalis superior) . - The sphincter of the pupil and the ciliary muscle, which serves for accommodation, are innervated by parasympathetic nerves, the rest are sympathetic. Due to the simultaneous action of sympathetic and parasympathetic innervation, the loss of one of the influences leads to the predominance of the other.

The nuclei of parasympathetic innervation are located at the level of the superior colliculus, are part of the third pair of cranial nerves (the nucleus of Yakubovich - Edinger - Westphal) - for the sphincter of the pupil and the nucleus of Perlia - for the ciliary muscle. The fibers from these nuclei go as part of the III pair and then enter the ganglion ciliarae, from where the posttanglion fibers originate to m.m. sphincter pupillae et ciliaris.

The nuclei of sympathetic innervation are located in the lateral horns of the spinal cord at the level of the Ce-Th segments. The fibers from these cells are sent to the border trunk, the upper cervical node, and then along the plexuses of the internal carotid, vertebral and basilar arteries they approach the corresponding muscles (mm. tarsalis, orbitalis et dilatator pupillae).

As a result of the defeat of the nuclei of Yakubovich - Edinger - Westphal or the fibers coming from them, paralysis of the sphincter of the pupil occurs, while the pupil expands due to the predominance of sympathetic influences (mydriasis). With the defeat of the nucleus of Perlia or the fibers coming from it, accommodation is disturbed.
The defeat of the ciliospinal center or the fibers coming from it leads to a narrowing of the pupil (miosis) due to the predominance of parasympathetic influences, to the retraction of the eyeball (enophthalmos) and a slight drooping of the upper eyelid. This triad of symptoms - miosis, enophthalmos and narrowing of the palpebral fissure - is called the Bernard-Horner syndrome. With this syndrome, depigmentation of the iris is sometimes also observed. Bernard-Horner syndrome is more often caused by damage to the lateral horns of the spinal cord at the level of Ce-Th, the upper cervical sections of the borderline sympathetic trunk or the sympathetic plexus of the carotid artery, less often by a violation of the central influences on the ciliospinal center (hypothalamus, brain stem).

Irritation of these departments can cause exophthalmos and mydriasis.
To assess the autonomic innervation of the eye, pupillary reactions are determined. Examine the direct and friendly reaction of the pupils to light, as well as the pupillary reaction to convergence and accommodation. When identifying exophthalmos or enophthalmos, the state of the endocrine system, family features of the structure of the face should be taken into account.

Vegetative innervation of the bladder.

The bladder has dual autonomic (sympathetic and parasympathetic) innervation. The spinal parasympathetic center is located in the lateral horns of the spinal cord at the level of S2-S4 segments. From it, parasympathetic fibers go as part of the pelvic nerves and innervate the smooth muscles of the bladder, mainly the detrusor.

Parasympathetic innervation ensures contraction of the detrusor and relaxation of the sphincter, i.e., it is responsible for emptying the bladder. Sympathetic innervation is carried out by fibers from the lateral horns of the spinal cord (segments T11-T12 and L1-L2), then they pass as part of the hypogastric nerves (nn. hypogastrici) to the internal sphincter of the bladder. Sympathetic stimulation leads to contraction of the sphincter and relaxation of the bladder detrusor, i.e., it inhibits its emptying. Consider that defeats of sympathetic fibers do not lead to disturbances of an urination. It is assumed that the efferent fibers of the bladder are represented only by parasympathetic fibers.

Excitation of this section leads to relaxation of the sphincter and contraction of the bladder detrusor. Urination disorders can be manifested by urinary retention or incontinence. Urinary retention develops as a result of spasm of the sphincter, weakness of the detrusor of the bladder, or as a result of a bilateral violation of the connection of the organ with the cortical centers. If the bladder overflows, then under pressure, urine can be released in drops - paradoxical ischuria. With bilateral lesions of the cortical-spinal influences, temporary urinary retention occurs. Then it is usually replaced by incontinence, which occurs automatically (involuntary periodic urinary incontinence). There is an urgent urge to urinate. With the defeat of the spinal centers, true urinary incontinence develops. It is characterized by the constant release of urine in drops as it enters the bladder. As part of the urine accumulates in the bladder, cystitis develops and an ascending infection of the urinary tract occurs.

Vegetative innervation of the head.

The sympathetic fibers that innervate the face, head, and neck originate from cells located in the lateral horns of the spinal cord (CVIII-ThIII). Most of the fibers are interrupted in the superior cervical sympathetic ganglion, and a smaller part goes to the external and internal carotid arteries and forms periarterial sympathetic plexuses on them. They are joined by postganglionic fibers coming from the middle and lower cervical sympathetic nodes. In small nodules (cell clusters) located in the periarterial plexuses of the branches of the external carotid artery, fibers terminate that have not been interrupted at the nodes of the sympathetic trunk. The remaining fibers are interrupted in the facial ganglia: ciliary, pterygopalatine, sublingual, submandibular and auricular. Postganglionic fibers from these nodes, as well as fibers from the cells of the upper and other cervical sympathetic nodes, go either as part of the cranial nerves or directly to the tissue formations of the face and head.

In addition to the efferent, there is afferent sympathetic innervation. Afferent sympathetic fibers from the head and neck are sent to the periarterial plexuses of the branches of the common carotid artery, pass through the cervical nodes of the sympathetic trunk, partially contacting their cells, and through the connecting branches come to the spinal nodes.

Parasympathetic fibers are formed by axons of the stem parasympathetic nuclei, they go mainly to the five autonomic ganglia of the face, in which they are interrupted. A smaller part goes to the parasympathetic clusters of cells of the periarterial plexus, where it is also interrupted, and the postganglionic fibers go as part of the cranial nerves or periarterial plexuses. The anterior and middle sections of the hypothalamic region through the sympathetic and parasympathetic conductors affect the function of the salivary glands, mainly of the side of the same name. In the parasympathetic part there are also afferent fibers that go in the vagus nerve system and are sent to the sensory nuclei of the brainstem.

Features of the activity of the autonomic nervous system.

The autonomic nervous system regulates the processes occurring in organs and tissues. With dysfunction of the autonomic nervous system, various disorders occur. Characterized by the periodicity and paroxysmal violation of the regulatory functions of the autonomic nervous system. Most of the pathological processes in it are caused not by the loss of functions, but by irritation, i.e. increased excitability of central and peripheral structures. A feature of the autonomic nervous system is repercussion: a violation in some parts of this system can lead to changes in others.

Clinical manifestations of lesions of the autonomic nervous system.

Processes localized in the cerebral cortex can lead to the development of vegetative, in particular trophic disorders in the zone of innervation, and in case of damage to the limbic-reticular complex, to various emotional shifts. They often occur with infectious diseases, injuries of the nervous system, intoxication. Patients become irritable, quick-tempered, quickly exhausted, they have hyperhidrosis, instability of vascular reactions, trophic disorders. Irritation of the limbic system leads to the development of paroxysms with pronounced vegetative-visceral components (cardiac, epigastric auras, etc.). With the defeat of the cortical part of the autonomic nervous system, sharp autonomic disorders do not occur. More significant changes develop with damage to the hypothalamic region.

At present, an idea has been formed of the hypothalamus as an integral part of the limbic and reticular systems of the brain, which carries out the interaction between regulatory mechanisms, the integration of somatic and autonomic activity. Therefore, when the hypothalamic region is affected (tumor, inflammatory processes, circulatory disorders, intoxication, trauma), various clinical manifestations can occur, including diabetes insipidus, obesity, impotence, sleep and wakefulness disorders, apathy, thermoregulation disorder (hyper- and hypothermia), widespread ulceration in the mucous membrane of the stomach, lower esophagus, acute perforation of the esophagus, duodenum and stomach.

The defeat of autonomic formations at the level of the spinal cord is manifested by pilomotor, vasomotor disorders, disorders of sweating and pelvic functions. With segmental disorders, these changes are localized in the zone of innervation of the affected segments. In the same areas, trophic changes are noted: increased dryness of the skin, local hypertrichosis or local hair loss, and sometimes trophic ulcers and osteoarthropathy. With the defeat of segments CVIII - ThI, Bernard-Horner syndrome occurs: ptosis, miosis, enophthalmos, often - a decrease in intraocular pressure and dilation of facial vessels.

With the defeat of the nodes of the sympathetic trunk, similar clinical manifestations occur, especially pronounced if the cervical nodes are involved in the process. There is a violation of sweating and a disorder of the function of the pilomotors, vasodilation and an increase in temperature on the face and neck; due to a decrease in the tone of the muscles of the larynx, hoarseness of the voice and even complete aphonia, the Bernard-Horner syndrome, may occur.

In case of irritation of the upper cervical node, there is an expansion of the palpebral fissure and pupil (mydriasis), exophthalmos, a syndrome reciprocal of the Bernard-Horner syndrome. Irritation of the upper cervical sympathetic ganglion may also manifest itself as sharp pains in the face and teeth.

The defeat of the peripheral parts of the autonomic nervous system is accompanied by a number of characteristic symptoms. Most often there is a kind of syndrome called sympathalgia. In this case, the pains are burning, pressing, arching in nature, they are distinguished by a tendency to gradually spread around the area of ​​\u200b\u200bprimary localization. Pain is provoked and aggravated by changes in barometric pressure and ambient temperature. There may be changes in the color of the skin due to spasm or expansion of peripheral vessels: blanching, redness or cyanosis, changes in sweating and skin temperature.

Autonomic disorders can occur with damage to the cranial nerves (especially the trigeminal), as well as the median, sciatic, etc. It is believed that paroxysms in trigeminal neuralgia are mainly associated with lesions of the autonomic parts of the nervous system.

The defeat of the autonomic ganglia of the face and oral cavity is characterized by the appearance of burning pains in the zone of innervation related to this ganglion, paroxysmal, the occurrence of hyperemia, increased sweating, in case of damage to the submandibular and sublingual nodes - increased salivation.

Research methodology.

There are numerous clinical and laboratory methods for studying the autonomic nervous system. Usually their choice is determined by the task and conditions of the study. However, in all cases, it is necessary to take into account the initial state of the autonomic tone and the level of fluctuations relative to the background value.

It has been established that the higher the initial level, the smaller the response in functional tests. In some cases, even a paradoxical reaction is possible. The study is best done in the morning on an empty stomach or 2 hours after eating, at the same time, at least 3 times. In this case, the minimum value of the received data is taken as the initial value.

To study the initial autonomic tone, special tables are used that contain data that clarify the subjective state, as well as objective indicators of autonomic functions (nutrition, skin color, condition of the skin glands, body temperature, pulse, blood pressure, ECG, vestibular manifestations, respiratory functions, gastrointestinal tract, pelvic organs, performance, sleep, allergic reactions, characterological, personal, emotional characteristics, etc.). Here are the main indicators that can be used as criteria underlying the study.

After determining the state of autonomic tone, autonomic reactivity is examined under the influence of pharmacological agents or physical factors. As pharmacological agents, the introduction of solutions of adrenaline, insulin, mezaton, pilocarpine, atropine, histamine, etc. is used.

The following functional tests are used to assess the state of the autonomic nervous system.

cold test . With the patient lying down, the heart rate is counted and blood pressure is measured. After that, the hand of the other hand is lowered for 1 minute into cold water at a temperature of 4 °C, then the hand is taken out of the water and the blood pressure and pulse rate are recorded every minute until they return to the initial level. Normally, this happens after 2-3 minutes. With an increase in blood pressure by more than 20 mm Hg. the reaction is assessed as pronounced sympathetic, less than 10 mm Hg. Art. - as moderate sympathetic, and with a decrease in pressure - as parasympathetic.

Oculocardial reflex (Dagnini-Ashner). When pressing on the eyeballs in healthy individuals, heart contractions slow down by 6-12 per minute. If the number of contractions slows down by 12-16, this is regarded as a sharp increase in the tone of the parasympathetic part. The absence of a slowdown or acceleration of heart contractions by 2-4 per minute indicates an increase in the excitability of the sympathetic part.

solar reflex . The patient lies on his back, and the examiner makes pressure with his hand on the upper abdomen until a pulsation of the abdominal aorta is felt. After 20-30 seconds, the number of heartbeats slows down in healthy individuals by 4-12 per minute. Changes in cardiac activity are assessed as in the oculocardial reflex.

Orthoclinostatic reflex . The study is carried out in two stages. In a patient lying on his back, the number of heart contractions is counted, and then they are asked to stand up quickly (orthostatic test). When moving from a horizontal to a vertical position, the heart rate increases by 12 per minute with an increase in blood pressure by 20 mm Hg. When the patient moves to a horizontal position, the pulse and pressure indicators return to their original values ​​within 3 minutes (clinostatic test). The degree of pulse acceleration during an orthostatic test is an indicator of the excitability of the sympathetic part of the autonomic nervous system. A significant slowing of the pulse during the clinostatic test indicates an increase in the excitability of the parasympathetic part.

Pharmacological tests are also carried out.

Adrenaline test. In a healthy person, subcutaneous injection of 1 ml of a 0.1% solution of adrenaline causes blanching of the skin, an increase in blood pressure, an increase in heart rate, and an increase in blood glucose levels after 10 minutes. If these changes occur faster and are more pronounced, this indicates an increase in the tone of sympathetic innervation.

Skin test with adrenaline . A drop of 0.1% adrenaline solution is applied to the skin injection site with a needle. In a healthy person, blanching and a pink corolla around appear in this area.

Test with atropine . Subcutaneous administration of 1 ml of a 0.1% solution of atropine causes dry mouth and skin, increased heart rate and dilated pupils in a healthy person. Atropine is known to block the M-cholinergic systems of the body and is thus an antagonist of pilocarpine. With an increase in the tone of the parasympathetic part, all reactions that occur under the action of atropine are weakened, so the test can be one of the indicators of the state of the parasympathetic part.

Segmental vegetative formations are also investigated.

Pilomotor reflex . The goosebumps reflex is caused by a pinch or by applying a cold object (a tube of cold water) or a coolant (a cotton swab soaked in ether) to the skin of the shoulder girdle or the back of the head. On the same half of the chest, "goosebumps" appear as a result of contraction of smooth hair muscles. The arc of the reflex closes in the lateral horns of the spinal cord, passes through the anterior roots and the sympathetic trunk.

Acetylsalicylic acid test . With a glass of hot tea, the patient is given 1 g of acetylsalicylic acid. There is diffuse sweating. With damage to the hypothalamic region, its asymmetry can be observed. With damage to the lateral horns or anterior roots of the spinal cord, sweating is disturbed in the zone of innervation of the affected segments. With damage to the diameter of the spinal cord, taking acetylsalicylic acid causes sweating only above the site of the lesion.

Trial with pilocarpine . The patient is injected subcutaneously with 1 ml of a 1% solution of pilocarpine hydrochloride. As a result of irritation of the postganglionic fibers going to the sweat glands, sweating increases. It should be borne in mind that pilocarpine excites peripheral M-cholinergic receptors, which cause increased secretion of the digestive and bronchial glands, constriction of the pupils, increased tone of the smooth muscles of the bronchi, intestines, gallbladder and bladder, uterus. However, pilocarpine has the strongest effect on perspiration. With damage to the lateral horns of the spinal cord or its anterior roots in the corresponding area of ​​​​the skin, after taking acetylsalicylic acid, sweating does not occur, and the introduction of pilocarpine causes sweating, since the postganglionic fibers that respond to this drug remain intact.

Light bath. Warming the patient causes sweating. The reflex is spinal, similar to the pilomotor. The defeat of the sympathetic trunk completely excludes sweating on pilocarpine, acetylsalicylic acid and warming the body.

Skin thermometry (skin temperature ). It is investigated with the help of electrothermometers. Skin temperature reflects the state of skin blood supply, which is an important indicator of autonomic innervation. Areas of hyper-, normo- and hypothermia are determined. A difference in skin temperature of 0.5 °C in symmetrical areas is a sign of autonomic innervation disorders.

Dermographism . Vascular reaction of the skin to mechanical irritation (hammer handle, blunt end of a pin). Usually, a red band appears at the site of irritation, the width of which depends on the state of the autonomic nervous system. In some individuals, the strip may rise above the skin (sublime dermographism). With an increase in sympathetic tone, the band has a white color (white dermographism). Very wide bands of red dermographism indicate an increase in the tone of the parasympathetic nervous system. The reaction occurs as an axon reflex and is local.

For topical diagnostics, reflex dermographism is used, which is caused by irritation with a sharp object (swipe across the skin with the tip of a needle). There is a strip with uneven scalloped edges. Reflex dermographism is a spinal reflex. It disappears when the posterior roots, spinal cord, anterior roots and spinal nerves are affected at the level of the lesion.

Above and below the affected area, the reflex usually persists.

pupillary reflexes . The direct and friendly reactions of the pupils to light, their reaction to convergence, accommodation and pain are determined (dilation of the pupils with a prick, pinch and other irritations of any part of the body)

Electroencephalography is used to study the autonomic nervous system. The method makes it possible to judge the functional state of the synchronizing and desynchronizing systems of the brain during the transition from wakefulness to sleep.

With damage to the autonomic nervous system, neuroendocrine disorders often occur, therefore, hormonal and neurohumoral studies are carried out. They study the function of the thyroid gland (basic metabolism using the complex radioisotope absorption method I311), determine corticosteroids and their metabolites in the blood and urine, carbohydrate, protein and water-electrolyte metabolism, the content of catecholamines in the blood, urine, cerebrospinal fluid, acetylcholine and its enzymes, histamine and its enzymes, serotonin, etc.

Damage to the autonomic nervous system can be manifested by a psychovegetative symptom complex. Therefore, they conduct a study of the emotional and personal characteristics of the patient, study the anamnesis, the possibility of mental trauma, and carry out a psychological examination.

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. In 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, the vagus nerve (the main nerve of the parasympathetic nervous system) is stimulated. 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. Taking certain medications (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. There are pathological conditions in which irritation of the vagus nerve (its fibers located in the internal organs, or nerve nuclei in the brain) is observed.

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 are also characteristic. The skin is 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 disturbed. 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 must pass. This method is based on the study of the passage of a bioelectrical impulse in the heart. So, with sinus bradycardia (when the sinus node rarely generates an impulse), there is a decrease in heart rate while maintaining a 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, a greater number of atrial contractions than the number of QRS complexes will indicate the presence of AV blockade 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 of 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.

Drug therapy consists in prescribing 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.

If hemodynamic disorders occur (weakness, fatigue, dizziness), the doctor may prescribe tonic drugs for the patient: ginseng tincture, caffeine. These drugs increase heart rate and increase blood 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. A stable set heart rate favors 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. There are primary arterial hypertension, or hypertension (essential hypertension), as well as secondary (symptomatic) hypertension, for example, arterial hypertension in glomerulonephritis and nephrotic syndrome (renal hypertension), with narrowing of the 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 of 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 (hypotensive agents of 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 the 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. The pheochromocytoma is removed surgically, but before the operation, during the operation or, if the operation is not possible, lower the blood pressure with the help of oc-blockers.

A frequent cause of arterial hypertension may be a delay in the body of sodium due to excessive consumption of salt and insufficiency of natriuretic factors. An increased content of 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 long-acting antihypertensive drugs. 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, cardiac output and the tone of blood vessels (arterial and venous) decrease - 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 taking the drug, a pronounced withdrawal syndrome develops: 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.

Clonidine solutions in the form of eye drops are 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 the contractions of the heart and the 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 not suitable 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 intravenously slowly in 20 ml of isotonic sodium chloride solution in case of a 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 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 (with 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-adrenergic blockers: bradycardia, heart failure, difficulty in atrioventricular conduction, a decrease in HDL levels in blood plasma, an increase in the tone of the bronchi and peripheral vessels (less pronounced in β 1 -blockers), increased action of hypoglycemic agents, decreased 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.

Bradycardia is called an arrhythmia of the heart, in which their frequency decreases to less than 60 beats per minute ( by some authors less than 50). This condition is more a symptom than an independent disease. The appearance of bradycardia can accompany a variety of pathologies, including those not directly related to cardiovascular system. Sometimes the heart rate ( heart rate) falls even in the absence of any disease, being a natural reaction of the body to external stimuli.

In medical practice, bradycardia is much less common than tachycardia ( increased heart rate). Most patients do not attach much importance to this symptom. However, with recurring episodes of bradycardia or a severe decrease in heart rate, it is worth making a preventive visit to a general practitioner or cardiologist to rule out more serious problems.

Anatomy and physiology of the heart

Heart is a hollow organ with well-developed muscular walls. It is located in the chest between the right and left lungs ( approximately one third to the right of the sternum and two thirds to the left). The heart is fixed on large blood vessels that branch off from it. It has a rounded or sometimes more elongated shape. In the filled state, it is approximately equal in size to the fist of the person under study. For convenience in anatomy, two ends are distinguished. The base is the upper part of the organ, into which large veins open and from where large arteries exit. The apex is the free lying part of the heart in contact with the diaphragm.

The cavity of the heart is divided into four chambers:

• right atrium;
• right ventricle;
• left atrium;
• left ventricle.

The atrial cavities are separated from each other by the atrial septum, and the ventricular cavities by the interventricular septum. The cavities of the right side of the heart and the left side do not communicate with each other. The right side of the heart pumps venous blood, rich in carbon dioxide, and the left side - arterial, saturated with oxygen.

The wall of the heart consists of three layers:

• outdoor - pericardium (its inner leaf, which is part of the wall of the heart, is also called the epicardium);
• middle - myocardium;
• internal - endocardium.

The myocardium plays the greatest role in the development of bradycardia. This is the heart muscle that contracts to pump blood. First, there is a contraction of the atria, and a little later - a contraction of the ventricles. Both of these processes and the subsequent relaxation of the myocardium are called the cardiac cycle. The normal functioning of the heart ensures the maintenance of blood pressure and the supply of oxygen to all tissues of the body.

The most important properties of the heart are:

• excitability- the ability to respond to an external stimulus;
• automatism- the ability to contract under the action of impulses that have arisen in the heart itself ( normal - in the sinus node);
• conductivity- the ability to conduct excitation to other myocardial cells.

Under normal conditions, each heartbeat is initiated by a pacemaker - a bundle of special fibers located in the interatrial septum ( sinus node). The pacemaker gives an impulse that goes to the interventricular septum, penetrating into its thickness. Further, the impulse along the interventricular septum along special conductive fibers reaches the apex of the heart, where it is divided into the right and left legs. The right leg extends from the septum to the right ventricle and penetrates into its muscle layer, the left leg extends from the septum to the left ventricle and also penetrates into the thickness of its muscle layer. This whole system is called the conduction system of the heart and contributes to the contraction of the myocardium.

In general, the work of the heart is based on the alternation of relaxation cycles ( diastole) and abbreviations ( systole). During diastole, a portion of blood enters the atrium through large vessels and fills it. After that, systole occurs, and blood from the atrium is ejected into the ventricle, which at this time is in a relaxed state, that is, in diastole, which contributes to its filling. The passage of blood from the atrium to the ventricle occurs through a special valve, which, after filling the ventricle, closes and the ventricular systole cycle occurs. Already from the ventricle, blood is ejected into large vessels that exit the heart. At the outlet of the ventricles, there are also valves that prevent the return of blood from the arteries to the ventricle.

The regulation of the heart is a very complex process. In principle, the sinus node, which generates impulses, sets the heart rate. It, in turn, can be affected by the concentration of certain substances in the blood ( toxins, hormones, microbial particles) or the tone of the nervous system.

Different parts of the nervous system have the following influence on the heart:

• parasympathetic nervous system, represented by branches of the vagus nerve, reduces the rhythm of heart contraction. The more impulses enter the sinus node along this path, the greater the likelihood of developing bradycardia.
• Sympathetic nervous system raises heart rate. It seems to oppose the parasympathetic. Bradycardia can occur with a decrease in its tone, because then the influence of the vagus nerve will prevail.

In an adult at rest, the heart rate ranges from 70 to 80 beats per minute. However, these boundaries are conditional, because there are people who are normally characterized by an accelerated or slow heart rate throughout their lives. In addition, the limits of the norm may vary somewhat depending on age.

Age norms of heart rate

Patient's age	Normal heart rate (beats per minute)	Heart rate, which can be regarded as bradycardia (beats per minute)
Newborn baby	About 140	Less than 110
Child under 1 year old	130 - 140	Less than 100
16 years	105 - 130	Less than 85
6 – 10 years	90 - 105	Less than 70
10 – 16 years old	80 - 90	Less than 65
Adult	65 - 80	Less than 55 - 60

In general, physiological norms can have large deviations, but such cases are quite rare. Given the dependence of heart rate on age and many other external or internal factors, self-diagnosis and treatment of bradycardia is not recommended. A person without a medical education may not understand the situation and incorrectly assess the limits of the norm, and taking medication will only worsen the patient's condition.

Causes of bradycardia

Bradycardia can be caused by quite a few different things. As noted above, not all bradycardia is a symptom. Sometimes the heart rate slows down due to some external cause. Such bradycardia is called physiological and does not pose a danger to the patient's health. In contrast, pathological bradycardia is the first symptom of serious diseases that must be diagnosed in time. Thus, all reasons can be divided into two large groups.


The physiological causes of bradycardia are:

• good physical preparation;
• hypothermia ( moderate);
• stimulation of reflex zones;
• idiopathic bradycardia;
• age-related bradycardia.

Good physical fitness

Paradoxically, bradycardia is a frequent companion of professional athletes. This is due to the fact that the heart of such people is accustomed to increased stress. At rest, it contracts strongly enough to keep blood flowing even at a low heart rate. In this case, the rhythm slows down to 45 - 50 beats per minute. The difference between such bradycardia is the absence of other symptoms. A person feels absolutely healthy and is able to perform any load. This indicator, by the way, is the main difference between physiological and pathological bradycardia. During exercise, even in a professional athlete, the heart rate begins to rise. This suggests that the body adequately responds to an external stimulus.

Most often, physiological bradycardia is observed in the following athletes:

• runners;
• rowers;
• cyclists;
• football players;
• swimmers.

In other words, the training of the heart muscle is facilitated by those sports in which a person performs a moderate load for a long time. At the same time, his heart works in an enhanced mode and additional fibers appear in the myocardium. If such a trained heart is left unloaded, it will be able to circulate blood even at a low heart rate. A case is known when a professional cyclist had bradycardia with a frequency of 35 beats per minute and was recognized as physiological and did not require treatment. However, doctors recommend even professional athletes whose heart rate remains at a level of less than 50 beats per minute for a long time to undergo a preventive examination by a cardiologist.

Hypothermia

Hypothermia is called hypothermia to less than 35 degrees. In this case, we do not mean frostbite, which occurs with local exposure to cold, but a complex cooling of all organs and systems. Bradycardia with moderate hypothermia is a protective reaction of the body to adverse effects. The heart switches to an “economical” mode of operation so as not to exhaust energy resources. There are cases when patients with hypothermia survived, although at some point their body temperature reached 25 - 26 degrees.

Bradycardia in these cases is one of the components of the general protective reaction. The heart rate will rise again as the body temperature rises. This process is similar to hibernation ( hibernation) in some animals.

Stimulation of reflex zones

In the human body, there are several reflex zones that affect the functioning of the heart. The mechanism of this effect is to stimulate the vagus nerve. His irritation leads to a slowdown in heart rate. An attack of bradycardia in these cases can be artificially induced, but it will not last long and will reduce the heart rate slightly. Sometimes doctors themselves resort to such maneuvers to quickly bring down an attack of tachycardia in a patient.

It is possible to artificially induce an attack of bradycardia by stimulating the following zones:

• eyeballs. With gentle pressure on the eyeballs, the nucleus of the vagus nerve is stimulated, which leads to the appearance of bradycardia. This reflex is called the Ashner-Dagnini reflex or the ocular reflex. In healthy adults, pressure on the eyeballs lowers heart rate by 8 to 10 beats per minute on average.
• Carotid bifurcation. At the site of the bifurcation of the carotid artery into internal and external is the so-called carotid sinus. If you massage this area with your fingers for 3-5 minutes, it will lower your heart rate and blood pressure. The phenomenon is explained by the close location of the vagus nerve and the presence of special receptors in this area. Massage of the carotid sinus is usually performed on the right side. Sometimes this technique is used in diagnostic or ( less often) for medicinal purposes.

Thus, bradycardia can be artificially induced even in a completely healthy person by stimulating the reflex zones. At the same time, stimulation is not always intentional. A person may, for example, vigorously rub their eyes due to dust getting into them, which will cause the Ashner reflex and bradycardia. Irritation of the vagus nerve in the area of ​​the carotid artery is sometimes the result of an excessively tight tie, scarf, or narrow collar.

Idiopathic bradycardia

Idiopathic is called constant or periodic ( in the form of seizures) bradycardia, in which doctors cannot determine its cause. The patient does not play sports, does not take any medications, and does not report other factors that could explain this symptom. Such bradycardia is considered physiological if there are no other disorders with it. That is, the slowing of the heart rate is successfully compensated by the body itself. No treatment is required in this case.

age-related bradycardia

As noted above, heart rate in children is usually significantly higher than in adults. In older people, on the contrary, the pulse rate usually decreases. This is due to age-related changes in the heart muscle. Over time, tiny islands of connective tissue appear in it, scattered throughout the myocardium. Then they talk about age-related cardiosclerosis. One of its consequences will be worse contractility of the heart muscle and changes in the conduction system of the heart. All this leads to bradycardia at rest. This is also facilitated by the slow metabolism characteristic of older people. The tissues no longer need oxygen so much, and the heart does not have to pump blood at an increased intensity.

Bradycardia is usually noted in people after 60-65 years of age and is permanent. In the presence of acquired cardiac pathologies, it can be replaced by bouts of tachycardia. The decrease in heart rate at rest is usually small ( rarely below 55 - 60 beats per minute). It does not cause any accompanying symptoms. Thus, age-related bradycardia can be safely attributed to the natural processes occurring in the body.

The causes of pathological bradycardia can be the following diseases and disorders:

• taking medications;
• increased tone of the parasympathetic nervous system;
• poisoning;
• some infections;
• heart pathology.

Taking medications

Bradycardia is a fairly common side effect with long-term use of many drugs. Usually in these cases it is temporary and does not pose a threat to the life or health of patients. However, if episodes of bradycardia recur regularly after taking any drug, you should consult your doctor or pharmacist. It is possible that you need to change the dosage of the drug or even replace it with another drug with a similar effect.

The most pronounced attacks of bradycardia can cause the following drugs:

• quinidine;
• digitalis;
• amisulpride;
• beta blockers;
• calcium channel blockers;
• cardiac glycosides;
• adenosine;
• morphine.

The most common cause of bradycardia is the misuse of these drugs and the violation of the dosage. However, even when taken correctly, prescribed by a specialist, side effects may occur due to the patient's individual sensitivity to a particular drug. In medical practice, there are also cases of poisoning with the above drugs ( intentional or accidental). Then the heart rate may drop to levels that threaten the patient's life. Such bradycardia requires urgent qualified medical care.

Increased tone of the parasympathetic nervous system

Parasympathetic innervation of the heart, as noted above, is carried out by the branches of the vagus nerve. With its increased tone, the heart rate will be greatly slowed down. Among the physiological causes of irritation of the vagus nerve, the points of its artificial excitation have already been noted. However, irritation can also occur in a number of diseases. With them, there is a mechanical effect on the nerve nuclei located in the brain, or its fibers.

The following factors can cause an increased tone of the parasympathetic innervation of the heart:

• neuroses;
• traumatic brain injury;
• increased;
• hemorrhagic stroke ( brain hemorrhage) with the formation of a hematoma in the cranial cavity;
• neoplasms in the mediastinum.

In addition, increased vagal tone is often observed in the postoperative period in patients who have undergone surgery in the head, neck, or mediastinum. In all these cases, the vagus nerve may be pinched due to swelling. When it is squeezed, the tone rises, and it generates more impulses going, including to the heart. The result is bradycardia, in which heart rate is directly related to how severely the nerve is damaged or compressed. A normal heart rhythm usually returns after the underlying cause is removed. Bradycardia caused by an increase in the tone of the vagus nerve is sometimes also called neurogenic.

poisoning

Bradycardia can be a sign of poisoning not only with drugs, but also with other toxic substances. Depending on the chemical properties of a certain substance, different organs and systems of the body are affected. In particular, bradycardia can be caused by a direct lesion of the heart muscle, and an effect on the cells of the conduction system, and a change in the tone of the parasympathetic or sympathetic nervous system. In any case, a slowdown in heart rate will not be the only symptom. For other signs and manifestations, an experienced specialist can preliminarily determine the toxin, and laboratory analysis will confirm the diagnosis.

Poisoning with the following substances can lead to bradycardia:

• lead and its compounds;
• organophosphates ( including pesticides);
• nicotine and nicotinic acid;
• some drugs.

In all these cases, bradycardia develops quickly and heart rate directly depends on the amount of toxin that has entered the bloodstream.

Hypothyroidism

Hypothyroidism is a decrease in the concentration of thyroid hormones in the blood ( thyroxine, triiodothyronine). These hormones are involved in many processes in the body, including general metabolism. One of their effects is to maintain the tone of the nervous system and regulate the work of the heart. Excess thyroid hormones ( hyperthyroidism) leads to increased heart rate, and their lack leads to bradycardia.

Hypothyroidism occurs due to diseases of the gland itself or due to a lack of iodine in the body. In the first case, the tissue of the organ is directly affected. Thyroid cells, which should normally produce hormones, are replaced by connective tissue. There are many reasons for this process. Iodine plays a significant role in the formation of the hormone itself in the thyroid gland. It is he who is the main component in the molecule of thyroxine and triiodothyronine. With a lack of iodine, iron increases in size, trying to compensate for the reduced level of hormones with the number of its cells. This condition is called thyrotoxic goiter or myxedema. If it is observed in a patient with bradycardia, it can be said for sure that the cause of this symptom is a violation of the thyroid gland.

Thyroid diseases leading to hypothyroidism and bradycardia are:

• congenital disorders in the development of the thyroid gland ( hypoplasia or aplasia);
• transferred operations on the thyroid gland;
• ingestion of toxic isotopes of iodine ( including radioactive);
• inflammation of the thyroid gland thyroiditis);
• some infections;
• injuries in the neck;
• autoimmune diseases ( autoimmune Hashimoto's thyroiditis).

With the above diseases, at first bradycardia will appear in the form of frequent attacks, but over time it will be observed constantly. Heart problems are not the only symptom of hypothyroidism. It can be suspected for other manifestations of the disease.

In parallel with bradycardia, patients with hypothyroidism experience the following symptoms:

• pathological weight gain;
• poor tolerance to heat and cold;
• menstrual irregularities ( among women);
• impairment of the central nervous system decreased concentration, memory, attention);
• decrease in the level of erythrocytes ( anemia);
• tendency to constipation;
• swelling in the face, tongue, limbs.

Infectious diseases

Infectious diseases are most often accompanied by tachycardia ( acceleration of the heartbeat), which explains the increase in body temperature. However, with some infections, the heart rate may slow down. In addition, sometimes they talk about relative bradycardia, which in practice is quite common. It is called relative because the heart rate does not drop much, and sometimes, on the contrary, it even rises. The problem is that if the patient has a temperature of, say, 38.5 degrees, his normal heart rate will be approximately 100 beats per minute. If at the same time he has a heart rate of 80 beats per minute, this can be considered bradycardia. This phenomenon is characteristic of some infections. In some cases, it is even a typical symptom, which is referred to when making a preliminary diagnosis.

Infections that may cause relative bradycardia include:

• severe sepsis;
• some variants of the course of viral hepatitis.

In addition, bradycardia can develop with very severe infection ( almost any), when the body is no longer able to fight the disease. Then the heart stops working normally, blood pressure drops, and all organs and systems gradually fail. Usually such a severe course indicates a poor prognosis.

Heart pathologies

Bradycardia of various types can be observed in various diseases of the heart itself. First of all, it concerns inflammatory processes and sclerosis processes ( proliferation of connective tissue) that affect the conduction system. The tissue of which this system consists conducts a bioelectric impulse very well. If it is affected by a pathological process, the impulse passes more slowly and the heart rate decreases, since not all cardiomyocytes contract in time. If this process is a point process, then only one section of the heart or one section of the heart muscle can “lag behind” in contraction. In such cases, they speak of blockades.

During blockades, impulses are produced at a normal frequency, but do not propagate along the fibers of the conducting system and do not lead to corresponding contractions of the myocardium. Strictly speaking, such blockades are not full-fledged bradycardia, although the pulse rate and heart rate slow down with them. Rhythm disturbances are typical in these cases ( arrhythmias), when heart contractions occur at different intervals.

Bradycardia and blockade of the conduction system can occur with the following pathologies of the heart:

• diffuse cardiosclerosis;
• focal cardiosclerosis;

In all these cases, bradycardia is a non-permanent symptom. It all depends on to what extent and in what place the nodes and fibers of the conductive system are damaged. Bradycardia can be observed constantly for a long time or occur in the form of seizures, followed by periods of tachycardia. Thus, it is very difficult to navigate by this symptom to make a diagnosis. It is necessary to conduct a thorough diagnosis to identify the causes of bradycardia and the nature of the heart lesions.

Types of bradycardia

There is no single and generally accepted classification of bradycardia into certain types, since in medical practice there is no particular need for this. However, when formulating a diagnosis, doctors usually try to characterize this symptom as accurately as possible. In this regard, several characteristics of bradycardia have appeared, which allow us to conditionally divide it into several types.

According to the severity of the symptom, the following types can be distinguished:

• mild bradycardia. With it, the pulse rate is more than 50 beats per minute. In the absence of other cardiac pathologies, this does not cause any discomfort to the patient, and the symptom often goes unnoticed. Mild bradycardia includes most of the physiological causes that cause a decrease in heart rate. In this regard, there is usually no need for specific treatment for mild bradycardia.
• Moderate bradycardia. Moderate is called bradycardia, in which the heart rate is from 40 to 50 beats per minute. In trained or elderly people, it may be a variant of the norm. With this type of bradycardia, various symptoms associated with oxygen starvation of tissues are sometimes observed.
• Severe bradycardia. Severe bradycardia is characterized by a decrease in heart rate below 40 beats per minute, which is most often accompanied by various disorders. In this case, a thorough diagnosis is required to identify the causes of a slow heart rate and drug treatment as needed.

Many physicians prefer not to classify bradycardia by heart rate, as this classification is very arbitrary and does not apply to all patients. More often they talk about the so-called hemodynamically significant bradycardia. This means that the slowdown of the heart has led to circulatory disorders. Such bradycardia is always accompanied by the appearance of appropriate symptoms and manifestations. If the bradycardia is not hemodynamically significant, there are no such symptoms. This classification very often coincides with the division of bradycardia into physiological and pathological.

Another important criterion by which bradycardia can be classified is the mechanism of its occurrence. It should not be confused with the causes of this symptom, because most of the above causes work by similar mechanisms. This classification is very important for understanding the pathological process and choosing the right treatment.

From the point of view of the mechanism of occurrence of bradycardia, they are divided into two types:

• Violation of impulse production. In case of violation of the production of a bioelectric impulse, they speak of sinus bradycardia. The fact is that this impulse originates in the sinus node, the activity of which largely depends on external innervation. Thus, the heart rate will decrease for reasons other than heart disease. In rare cases, inflammatory processes in the heart itself, affecting the sinus node, can also be observed. However, there will always be a characteristic feature on examination. This is the rhythm of contractions. The myocardium contracts at regular intervals, and on the electrocardiogram ( ECG) reflects the timely and consistent contraction of each of the cavities of the heart.
• Violation of impulse conduction. Violation of impulse conduction is almost always caused by pathological processes in the heart muscle itself and the conduction system. There is a blockade of impulse conduction in a certain area ( for example, atrioventricular block or bundle branch block). Then bradycardia will be observed only in that cavity of the heart, the innervation of which turned out to be blocked. Often there are situations when, with atrioventricular blockade, the atria contract in the normal mode, and the ventricles - 2-3 times less often. This greatly disrupts the process of pumping blood. Arrhythmias occur, and the risk of blood clots increases.

In addition, as noted above, there are absolute or relative bradycardias. The latter are sometimes also called paradoxical. They speak of absolute bradycardia when the heart rate drops below 50-60 beats per minute, keeping in mind the generally accepted norm for a healthy person at rest. Paradoxical bradycardia is diagnosed when the pulse should be quickened, but it remains normal or slightly increased.

Sometimes bradycardia is also divided by diagnostic feature. Everyone knows that this symptom implies a decrease in heart rate, but heart rate is often measured by the pulse on the radial artery in the wrist. It should be borne in mind that one contraction of the heart does not always lead to one contraction of the artery. Sometimes even the pulsation of the carotid artery in the neck does not correctly reflect the work of the heart. In this regard, we can talk about bradycardia, in which the pulse is slow, but the heart contracts in a normal mode ( false bradycardia). The differences are explained by tumors that compress the arteries, arrhythmias, narrowing of the lumen of the vessels. The second option is, respectively, true bradycardia, when the heart rate and pulse on the arteries coincide.

Symptoms of bradycardia

In most cases, a slight decrease in heart rate is not accompanied by the appearance of any serious symptoms. Various complaints appear mainly in the elderly. In athletes and young people, certain symptoms are observed only when the heart rate drops below 40 beats per minute. Then they talk about pathological bradycardia, affecting the overall blood flow.

The main symptoms of bradycardia are:

• dizziness;
• inadequate increase in heart rate during exercise;
• pale skin;
• increased fatigue;

Dizziness

With a significant decrease in heart rate or the presence of concomitant heart diseases, a deterioration in systemic blood flow is observed. This means that the heart cannot maintain blood pressure at a normal level ( 120/80 mmHg). The slowing of the rhythm is not compensated by strong contractions. Due to the drop in blood pressure, the supply of oxygen to all tissues of the body worsens. First of all, nervous tissue, namely the brain, reacts to oxygen starvation. During an attack of bradycardia, dizziness occurs precisely because of disturbances in its work. As a rule, this feeling is temporary, and as the normal rhythm of the heart is restored, the dizziness disappears.

fainting

Fainting occurs for the same reason as dizziness. If an attack of bradycardia lasts long enough, then blood pressure drops, and the brain seems to temporarily turn off. In people with low blood pressure ( against the background of other chronic diseases) attacks of bradycardia are almost always accompanied by syncope. Especially often they occur during physical or intense mental stress. At these moments, the body's need for oxygen is especially high and its shortage is felt by the body very acutely.

Inadequate increase in heart rate during exercise

Normally, in all people, physical activity causes a rapid heartbeat. From a physiological point of view, this is necessary to compensate for the increased oxygen demand of the muscles. In the presence of pathological bradycardia ( for example, in people with increased tone of the parasympathetic nervous system) this mechanism does not work. Physical activity is not accompanied by an adequate increase in heart rate. This symptom indicates the presence of a certain pathology and makes it possible to distinguish physiological bradycardia in athletes from pathological. The fact is that even in trained people with a normal pulse of about 45 - 50 beats per minute, during the load, the heart rate gradually increases. In people with certain diseases, the pulse rate increases slightly or an arrhythmia attack occurs.

Dyspnea

Shortness of breath occurs mainly during physical exertion. In people with bradycardia, blood is pumped more slowly. The pumping function of the heart is impaired, which causes stagnation of blood in the lungs. Crowded vessels of the pulmonary circulation are not able to maintain normal gas exchange. In such cases, respiratory failure occurs when a person cannot catch his breath after physical exertion for a long time. Sometimes a reflex dry cough may occur.

Weakness

Weakness is the result of poor oxygen supply to the muscles. It is observed in people with pathological bradycardia with frequent attacks. For a long time, the muscles do not receive the right amount of oxygen. Because of this, they cannot contract with the necessary force and the patient is unable to perform any physical work.

Pale skin

The pallor of the skin is due to low blood pressure. The body tries to compensate for insufficient blood flow and mobilizes blood from a kind of "depot". One of these "depot" is the skin. An increase in the volume of circulating blood, it would seem, should increase blood pressure, but in reality this does not happen. The reason usually lies in the increased tone of the parasympathetic nervous system.

Fatigue

Increased fatigue in people with bradycardia is due to the rapid depletion of energy resources in the muscles. Prolonged episodes of oxygen starvation disrupt the metabolism, due to which there is no accumulation of energy in the form of special chemical compounds. In practice, the patient performs some physical work, but quickly gets tired. The recovery period is longer than in healthy people. Usually, patients with bradycardia quickly notice this symptom and report it to the doctor themselves at the time of admission.

Chest pain

Chest pains appear only with a serious violation of the heart. They usually occur during exercise or when the heart rate falls below 40 beats per minute. The fact is that not only the striated muscles of the limbs react to the deterioration of blood flow. The heart muscle also needs a constant supply of oxygenated blood. With severe bradycardia, angina pectoris occurs. The myocardium suffers from a lack of oxygen and its cells begin to gradually die. This causes pain in the chest. Attacks of angina pectoris usually occur during a violent emotional outburst or physical activity.

Thus, almost all the symptoms of bradycardia, one way or another, are associated with oxygen starvation of the body. In most cases, these manifestations of the disease are temporary. However, even episodic attacks of dizziness, and even more so fainting, can greatly impair the quality of life of patients.

The above symptoms are not typical only for attacks of bradycardia. They can be caused by other, more serious and dangerous pathologies. In this regard, their appearance should be regarded as a reason for a visit to the doctor.

Diagnosis of bradycardia

In the vast majority of cases, preliminary diagnosis of bradycardia itself does not present any particular difficulties and can be performed by the patient himself or by another person without medical education. The main condition is the knowledge of the points on the human body where you can feel the pulsation of the arteries. In most cases, we are talking about radiation ( on the wrist) or sleepy ( on the neck) arteries. However, as noted above, the rhythm of the heart contraction does not always coincide with the pulsation rate of the arteries. In this regard, a patient who suspects that he has bradycardia ( especially with heart rate less than 50 beats per minute), should consult a doctor for a more thorough diagnosis.

Bradycardia itself can be confirmed by the following diagnostic methods:

• auscultation;
• electrocardiography ( ECG);
• phonocardiography.

Auscultation

Auscultation is an instrumental examination method. With it, the doctor, using a stethophonendoscope, listens to murmurs and heart sounds through the anterior chest wall. This method is fast, painless and fairly accurate. Here the work of the heart itself is evaluated, and not the beating of the arteries. Unfortunately, even auscultation does not give one hundred percent correct confirmation of the diagnosis. The fact is that with bradycardia accompanied by arrhythmias, it is very difficult to correctly measure the heart rate. Because of this, during auscultation, approximate data are obtained.

A big plus is that during this examination, the work of the heart valves is evaluated in parallel. The doctor has the opportunity to immediately suspect some diseases and continue the search in the right direction.

Electrocardiography

Electrocardiography is a study of the conduction of a bioelectrical impulse in the heart by creating an artificial electric field. This procedure lasts 5-15 minutes and is absolutely painless. This makes the ECG the most common and effective method for studying cardiac activity.

With sinus bradycardia, the ECG differs little from normal, with the exception of a rarer rhythm. This is easy to see by calculating the speed of the tape passing through the electrocardiograph and comparing it with the duration of one cardiac cycle ( distance between the peaks of two identical teeth or waves). It is somewhat more difficult to diagnose blocks in normal sinus rhythm.

The main electrocardiographic signs of atrioventricular blockade are:

• increase in the duration of the interval P - Q;
• severe deformation of the ventricular QRS complex;
• the number of atrial contractions is always greater than the number of ventricular QRS complexes;
• loss of ventricular QRS complexes from the general rhythm.

Based on these signs, the doctor can not only confirm the presence of bradycardia with high accuracy, but also determine its type or even the cause of development. In this regard, ECG is prescribed for all patients with reduced heart rate, regardless of the presence of other symptoms. If the patient complains of bradycardia attacks, 24-hour Holter ECG monitoring can be performed. In this case, the schedule of the heart will be removed within 24 hours, and the doctor will be able to notice even small periodic rhythm disturbances.

Phonocardiography

Phonocardiography is considered a somewhat outdated research method. In fact, its purpose is also to study the tones and murmurs of the heart. It differs from auscultation only in a higher recording accuracy and saving the examination results in the form of a special schedule. Heart contractions, their duration and frequency are easily determined by a specialist. However, the accuracy of this method is not as high as that of the ECG. Therefore, if the doctor sees signs of bradycardia on the phonocardiogram, he will still prescribe an ECG to clarify the causes of this symptom.

Diagnosis of bradycardia ( especially pronounced and with hemodynamic disturbances) is by no means limited to a decrease in heart rate. The doctor is obliged to determine whether the decrease in rhythm is a physiological feature of the body or a sign of a more serious pathology. For this, a wide range of different analyzes and examinations can be prescribed, which will reflect structural and functional changes in the heart and other organs or systems.

To clarify the diagnosis, patients with bradycardia may be prescribed the following diagnostic methods of examination:

• General and biochemical analysis of blood. This laboratory method can indicate the presence of an inflammatory process in the body, help to suspect an infection or poisoning.
• General and biochemical analysis of urine. It is prescribed for the same reasons as a blood test.
• Blood test for hormones. The most common test is thyroid hormone levels to confirm hypothyroidism.
• echocardiography ( echocardiography). This method is a study of the heart using ultrasound radiation. It gives an idea of ​​the structure of the organ and hemodynamic disorders. It is prescribed without fail in the presence of other symptoms ( along with bradycardia).
• Analysis for toxins. For lead or other chemical poisoning, blood, urine, feces, hair, or other body tissues may be tested ( depending on the circumstances under which the poisoning occurred).
• bacteriological research. Bacteriological examination of blood, urine or feces is necessary to confirm the diagnosis of an infectious disease.

Thus, the process of diagnosis in a patient with bradycardia can take quite a long time. But after determining the cause of the decrease in heart rate, the doctor will be able to prescribe the most effective treatment and prevent other health problems.

Treatment of bradycardia

Before starting treatment, it should be established whether bradycardia is a physiological norm for the patient or whether it is a symptom of some other pathology. In the first case, no treatment is required. In the second, the treatment will be aimed at eliminating the causes that caused bradycardia. Medical acceleration of the heart rate may be needed only if other symptoms are present that indicate a hemodynamic disorder ( shortness of breath, dizziness, weakness, etc.).

The decision to start treatment is made by the therapist. The patient himself, due to the lack of proper medical education, cannot unambiguously say whether bradycardia occurs at all ( even if the heart rate is slightly reduced). If the general practitioner has doubts about the causes of this symptom, he sends the patient for examination to a cardiologist. It is this specialist who is the most competent in matters of cardiac arrhythmias.

Indications for starting treatment for bradycardia are:

• dizziness, fainting and other symptoms that indicate circulatory disorders;
• low blood pressure;
• frequent attacks of bradycardia, causing the patient a feeling of discomfort;
• inability to work normally temporary disability);
• chronic diseases causing bradycardia;
• decrease in heart rate below 40 beats per minute.

In all these cases, treatment of bradycardia is started in order to maintain proper circulation and reduce the risk of complications. In most cases, hospitalization is not required. In a hospital setting, only patients with concomitant heart pathologies or if bradycardia is caused by other serious diseases that pose a threat to life and health are treated. The final recommendations on the need for hospitalization are given by the cardiologist based on the patient's condition.

For the treatment of tachycardia, there are the following methods:

• conservative ( medical) treatment;
• surgery;
• treatment with folk remedies;
• prevention of complications.

Conservative treatment

Conservative or drug treatment is the most common and fairly effective method of dealing with bradycardia. Various medications affect the heart in certain ways, increasing heart rate and preventing other symptoms. An important action of drugs against bradycardia is to increase heart rate and increase blood pressure, as this compensates for circulatory disorders.

Drug treatment for reduced heart rate should be prescribed only by a specialist with a medical background. The fact is that improper use of drugs for the heart can lead to overdose and severe heart rhythm disturbances. In addition, bradycardia may be a symptom of another disease that the patient himself is not able to recognize. Then drugs that increase heart rate may not help at all or cause a worsening of the condition ( depending on the nature of the pathology). In this regard, drug self-treatment is strictly prohibited.

Drugs used to treat bradycardia

Name of the drug	pharmachologic effect	Recommended dose
Atropine	This drug belongs to the group of anticholinergics. Prevents excitation of the parasympathetic nervous system. The vagus nerve tone narrows and the heart rate rises.	0.6 - 2.0 mg 2 - 3 times a day. It is administered intravenously or subcutaneously.
Isoprenaline (intravenously)	These drugs are one of the analogues of adrenaline. They accelerate and increase heart rate through stimulation of adrenergic receptors in the myocardium and an increase in the tone of the sympathetic nervous system.	2 - 20 mcg per 1 kg of the patient's weight per minute until the heart rate stabilizes.
Isoprenaline by mouth (as tablets)		2.5 - 5 mg 2 - 4 times a day.
Isadrin (intravenously)		0.5 - 5 mcg per minute until the heart rate stabilizes.
Isadrin (sublingual - under the tongue)		2.5 - 5 mg until complete resorption 2 - 3 times a day.
Eufillin	This drug belongs to bronchodilators ( expanding bronchi) means, but has many effects useful in bradycardia. It increases and enhances heart rate, and improves oxygen delivery to tissues.	240-480 mg IV slowly ( no faster than 5 minutes), 1 per day.

Almost all of these drugs are taken as needed, that is, during episodes of bradycardia and until a normal heart rhythm returns. In some cases, a doctor may prescribe their use for a long time ( weeks, months).

If the bradycardia is a symptom of another disorder, other drugs may be prescribed ( thyroid hormones for hypothyroidism, antibiotics for infectious diseases, etc.). Eliminating the root cause will effectively eliminate the symptom itself.

Surgery

Surgical treatment for bradycardia is used very rarely and only in cases where a decrease in heart rate significantly affects hemodynamics. The place and nature of the surgical intervention are determined by the cause that caused the bradycardia. With congenital anomalies in the development of cardiac tissues, surgical correction is done as far as possible in childhood to ensure normal growth and development of the child.

Surgical treatment is also necessary in the presence of tumors or formations of a different nature in the mediastinum. In rare cases, it is even necessary to remove tumors directly from the parasympathetic and sympathetic fibers. Usually, after such operations, a normal heart rhythm is quickly restored.

In some cases, there is severe persistent bradycardia leading to heart failure, but the cause is unknown or cannot be corrected. In these cases, surgical treatment will consist of implanting a special pacemaker. This device independently generates electrical impulses and delivers them to the desired points of the myocardium. Thus, the lower rhythm of the sinus node will be suppressed, and the heart will begin to pump blood normally. Today, there are many different types of pacemakers that help to fully restore the ability to work and eliminate all the symptoms associated with a heart rhythm disorder. In each case, the pacemaker model is selected individually based on the degree of circulatory disorders and the causes that caused bradycardia.

Treatment with folk remedies

Folk remedies can help with bradycardia with a heart rate of at least 40 beats per minute. Most recipes use medicinal plants that lower the tone of the parasympathetic nervous system, increase myocardial contractions, or maintain blood pressure. They partly restore normal heart rhythm, partly prevent the development of complications. With hemodynamically significant bradycardia, it is not recommended to resort to alternative methods of treatment until a final diagnosis is made. Also, do not take medicinal plants in parallel with drug treatment, as this increases the likelihood of unpredictable side effects.

In the treatment of bradycardia with folk remedies, the following recipes are used:

• Immortelle Flask. 20 g of dried flowers pour 0.5 liters of boiling water. Infusion lasts several hours in a dark place. Take this remedy 20 drops 2-3 times a day. It is not recommended to take it after 19.00.
• Tatar decoction. 100 g of dry baskets are poured with 1 liter of boiling water. The mixture continues to boil over low heat for 10 - 15 minutes. The infusion lasts about 30 minutes. After that, the broth is filtered and cooled. You need to take it 1 tablespoon before meals.
• Infusion of Chinese lemongrass. Fresh fruits are poured with alcohol at the rate of 1 to 10. After that, the alcohol tincture should stand for at least a day in a dark place. Added to tea about 1 teaspoon tincture per cup of tea or boiled water). You can add sugar or honey to taste. The tincture is taken 2-3 times a day.
• Decoction of yarrow. For a glass of boiling water, you need 20 g of dry grass. Usually the product is prepared immediately for 0.5 - 1 liter. The mixture is boiled over low heat for 8-10 minutes. Then it is infused and gradually cooled for 1 - 1.5 hours. Take a decoction of 2 - 3 teaspoons several times a day.

Prevention of complications

Prevention of complications of bradycardia is mainly aimed at eliminating its symptoms, which affect the quality of life of people. From bad habits, it is necessary to give up, first of all, smoking, since chronic nicotine poisoning affects the functioning of the heart and the entire circulatory system. Physical activity is usually limited only in cases where bradycardia is pathological. Then it can lead to heart failure. To prevent this, the patient is not recommended to load the heart muscle.

Particular attention in the prevention of complications is given to the diet. The fact is that certain nutrients in various foods can affect the functioning of the heart to one degree or another. The importance of this method of prevention should not be underestimated, since non-compliance with the diet sometimes nullifies even the entire course of drug treatment.

In the diet, patients with bradycardia should adhere to the following principles:

• limiting the consumption of animal fats ( especially pork);
• refusal of alcohol;
• reduction in caloric intake up to 1500 - 2500 kcal per day depending on the work performed);
• limited intake of water and salt ( only by special order of the attending physician);
• the use of nuts and other plant foods rich in fatty acids.

All this helps to prevent the development of heart failure and the formation of blood clots, which are the main danger in pathological bradycardia.

Consequences of bradycardia

Bradycardia in most patients occurs without pronounced symptoms and serious circulatory disorders. Therefore, compared with other diseases of the cardiovascular system, the risk of developing any residual effects, complications or consequences with bradycardia is low.

Most often, patients with bradycardia face the following problems:

• heart failure;
• thrombus formation;
• chronic attacks of bradycardia.

Heart failure

Heart failure develops relatively rarely and only with a strong decrease in heart rate. With it, the left ventricle does not supply enough blood to organs and tissues and cannot maintain blood pressure at the desired level. In this regard, the risk of developing coronary disease and myocardial infarction increases. It is especially important for such patients to limit physical activity, since during it the myocardium consumes much more oxygen.

Thrombus formation

The formation of blood clots in the heart is observed mainly with heart blockade and bradycardia with a violation of the normal heart rhythm. Blood is pumped through the chambers of the heart slowly, and a small part of it constantly remains in the cavity of the ventricle. This is where the gradual formation of blood clots occurs. The risk increases with prolonged or frequent attacks.

Blood clots formed in the heart can get into almost any vessel, leading to its blockage. In this regard, a number of serious complications can develop - from extensive myocardial infarction to ischemic stroke. Patients with bradycardia in whom thrombi are suspected are referred for echocardiography to assess the risk of complications. After that, specific treatment is prescribed with drugs that prevent blood clotting. As an extreme measure to prevent the formation of blood clots, the implantation of a pacemaker remains. Correctly set rhythm will prevent stagnation of blood in the ventricle.

Chronic attacks of bradycardia

Chronic attacks of bradycardia are observed mainly for physiological reasons, when it is almost impossible to eliminate them with medication. Then the patient often suffers from dizziness, weakness, loss of attention and concentration. Unfortunately, it is very difficult to deal with these symptoms in such cases. Doctors select symptomatic treatment individually for each patient, depending on his complaints.