Anatomy and physiology of the cardiovascular system. Physiology of the cardiovascular system: the secrets of the affairs of cardiac ATP-ADP-transferase and creatine phosphokinase
The mass of blood moves through a closed vascular system, consisting of a large and small circles of blood circulation, in strict accordance with the basic physical principles, including the principle of the continuity of the flow. According to this principle, a break in the flow during sudden injuries and injuries, accompanied by a violation of the integrity of the vascular bed, leads to the loss of both a part of the circulating blood volume and a large amount of the kinetic energy of the heart contraction. In a normally functioning circulatory system, according to the principle of the continuity of the flow, the same volume of blood moves per unit time through any cross section of a closed vascular system.
Further study of the functions of blood circulation, both in the experiment and in the clinic, led to the understanding that blood circulation, along with respiration, is one of the most important life-supporting systems, or the so-called "vital" functions of the body, the cessation of functioning of which leads to death within a few seconds or minutes. There is a direct relationship between the general condition of the patient's body and the state of blood circulation, so the state of hemodynamics is one of the determining criteria for the severity of the disease. The development of any serious disease is always accompanied by changes in the circulatory function, manifested either in its pathological activation (tension) or depression of varying severity (insufficiency, failure). The primary lesion of the circulation is characteristic of shocks of various etiologies.
Assessment and maintenance of hemodynamic adequacy are the most important component of the doctor's activity during anesthesia, intensive care and resuscitation.
The circulatory system provides a transport link between the organs and tissues of the body. Blood circulation performs many interrelated functions and determines the intensity of associated processes, which in turn affect blood circulation. All functions implemented by blood circulation are characterized by biological and physiological specificity and are focused on the implementation of the phenomenon of transfer of masses, cells and molecules that perform protective, plastic, energy and informational tasks. In the most general form, the functions of blood circulation are reduced to mass transfer through the vascular system and to mass transfer with the internal and external environment. This phenomenon, most clearly traced in the example of gas exchange, underlies the growth, development and flexible provision of various modes of the organism's functional activity, uniting it into a dynamic whole.
The main functions of the circulation are:
1. Transport of oxygen from the lungs to the tissues and carbon dioxide from the tissues to the lungs.
2. Delivery of plastic and energy substrates to the places of their consumption.
3. Transfer of metabolic products to organs, where they are further converted and excreted.
4. Implementation of the humoral relationship between organs and systems.
In addition, blood plays the role of a buffer between the external and internal environment and is the most active link in the body's hydroexchange.
The circulatory system is made up of the heart and blood vessels. The venous blood flowing from the tissues enters the right atrium, and from there into the right ventricle of the heart. With the reduction of the latter, blood is pumped into the pulmonary artery. Flowing through the lungs, the blood undergoes complete or partial equilibrium with the alveolar gas, as a result of which it gives off excess carbon dioxide and is saturated with oxygen. The pulmonary vascular system (pulmonary arteries, capillaries and veins) forms small (pulmonary) circulation. Arterialized blood from the lungs through the pulmonary veins enters the left atrium, and from there into the left ventricle. With its contraction, blood is pumped into the aorta and further into the arteries, arterioles and capillaries of all organs and tissues, from where it flows through the venules and veins into the right atrium. The system of these vessels forms systemic circulation. Any elementary volume of circulating blood sequentially passes through all the listed sections of the circulatory system (with the exception of blood portions undergoing physiological or pathological shunting).
Based on the goals of clinical physiology, it is advisable to consider blood circulation as a system consisting of the following functional departments:
1. Heart(heart pump) - the main engine of circulation.
2. buffer vessels, or arteries, performing a predominantly passive transport function between the pump and the microcirculation system.
3. Vessels-capacities, or veins, carrying out the transport function of returning blood to the heart. This is a more active part of the circulatory system than the arteries, since the veins are able to change their volume by 200 times, actively participating in the regulation of venous return and circulating blood volume.
4. Distribution vessels(resistance) - arterioles, regulating blood flow through the capillaries and being the main physiological means of regional distribution of cardiac output, as well as venules.
5. exchange vessels- capillaries, integrating the circulatory system into the overall movement of fluids and chemicals in the body.
6. Shunt vessels- arteriovenous anastomoses that regulate peripheral resistance during spasm of arterioles, which reduces blood flow through the capillaries.
The first three sections of the blood circulation (heart, vessels-buffers and vessels-capacities) represent the macrocirculation system, the rest form the microcirculation system.
Depending on the level of blood pressure, the following anatomical and functional fragments of the circulatory system are distinguished:
1. High pressure system (from the left ventricle to the systemic capillaries) of the blood circulation.
2. Low pressure system (from the capillaries of the large circle to the left atrium inclusive).
Although the cardiovascular system is a holistic morphofunctional entity, in order to understand the processes of circulation, it is advisable to consider the main aspects of the activity of the heart, the vascular apparatus, and regulatory mechanisms separately.
Heart
This organ, weighing about 300 g, supplies blood to the "ideal person" weighing 70 kg for about 70 years. At rest, each ventricle of the heart of an adult ejects 5-5.5 liters of blood per minute; therefore, over 70 years, the performance of both ventricles is approximately 400 million liters, even if the person is at rest.
The metabolic needs of the body depend on its functional state (rest, physical activity, severe illness, accompanied by hypermetabolic syndrome). During a heavy load, the minute volume can increase to 25 liters or more as a result of an increase in the strength and frequency of heart contractions. Some of these changes are due to nervous and humoral effects on the myocardium and the receptor apparatus of the heart, others are the physical consequence of the effect of the "tensile force" of venous return on the contractile force of the heart muscle fibers.
The processes occurring in the heart are conventionally divided into electrochemical (automaticity, excitability, conduction) and mechanical, which ensure the contractile activity of the myocardium.
Electrochemical activity of the heart. Contractions of the heart occur as a result of excitation processes that periodically occur in the heart muscle. The cardiac muscle - the myocardium - has a number of properties that ensure its continuous rhythmic activity - automaticity, excitability, conductivity and contractility.
Excitation in the heart occurs periodically under the influence of the processes occurring in it. This phenomenon has been named automation. The ability to automate certain parts of the heart, consisting of special muscle tissue. This specific muscle forms a conduction system in the heart, consisting of a sinus (sinoatrial, sinoatrial) node - the main pacemaker of the heart, located in the wall of the atrium near the mouths of the vena cava, and an atrioventricular (atrioventricular) node, located in the lower third of the right atrium and interventricular septum. From the atrioventricular node, the atrioventricular bundle (His bundle) originates, perforating the atrioventricular septum and dividing into the left and right legs, following into the interventricular septum. In the region of the apex of the heart, the legs of the atrioventricular bundle bend upward and pass into a network of cardiac conductive myocytes (Purkinje fibers) immersed in the contractile myocardium of the ventricles. Under physiological conditions, myocardial cells are in a state of rhythmic activity (excitation), which is ensured by the efficient operation of the ion pumps of these cells.
A feature of the conduction system of the heart is the ability of each cell to independently generate excitation. Under normal conditions, the automation of all the sections of the conduction system located below is suppressed by more frequent impulses coming from the sinoatrial node. In case of damage to this node (generating impulses with a frequency of 60 - 80 beats per minute), the atrioventricular node can become the pacemaker, providing a frequency of 40 - 50 beats per minute, and if this node turns out to be turned off, the fibers of the His bundle (frequency 30 - 40 beats per minute). If this pacemaker also fails, the excitation process can occur in the Purkinje fibers with a very rare rhythm - approximately 20 / min.
Having arisen in the sinus node, the excitation spreads to the atrium, reaching the atrioventricular node, where, due to the small thickness of its muscle fibers and the special way they are connected, there is some delay in the conduction of excitation. As a result, excitation reaches the atrioventricular bundle and Purkinje fibers only after the muscles of the atria have time to contract and pump blood from the atria to the ventricles. Thus, atrioventricular delay provides the necessary sequence of atrial and ventricular contractions.
The presence of a conducting system provides a number of important physiological functions of the heart: 1) rhythmic generation of impulses; 2) the necessary sequence (coordination) of atrial and ventricular contractions; 3) synchronous involvement in the process of contraction of ventricular myocardial cells.
Both extracardiac influences and factors that directly affect the structures of the heart can disrupt these associated processes and lead to the development of various pathologies of the heart rhythm.
Mechanical activity of the heart. The heart pumps blood into the vascular system due to the periodic contraction of the muscle cells that make up the myocardium of the atria and ventricles. Myocardial contraction causes an increase in blood pressure and its expulsion from the chambers of the heart. Due to the presence of common layers of the myocardium in both atria and both ventricles, excitation simultaneously reaches their cells and the contraction of both atria, and then both ventricles, is carried out almost synchronously. Atrial contraction begins in the region of the mouths of the hollow veins, as a result of which the mouths are compressed. Therefore, blood can move through the atrioventricular valves in only one direction - into the ventricles. During diastole, the valves open and allow blood to flow from the atria into the ventricles. The left ventricle has a bicuspid or mitral valve, while the right ventricle has a tricuspid valve. The volume of the ventricles gradually increases until the pressure in them exceeds the pressure in the atria and the valve closes. At this point, the volume in the ventricle is the end-diastolic volume. In the mouths of the aorta and pulmonary artery there are semilunar valves, consisting of three petals. With the contraction of the ventricles, the blood rushes towards the atria and the cusps of the atrioventricular valves close, at this time the semilunar valves also remain closed. The onset of ventricular contraction with the valves fully closed, turning the ventricle into a temporarily isolated chamber, corresponds to the isometric contraction phase.
An increase in pressure in the ventricles during their isometric contraction occurs until it exceeds the pressure in large vessels. The consequence of this is the expulsion of blood from the right ventricle into the pulmonary artery and from the left ventricle into the aorta. During ventricular systole, the valve petals are pressed against the walls of the vessels under blood pressure, and it is freely expelled from the ventricles. During diastole, the pressure in the ventricles becomes lower than in the large vessels, blood rushes from the aorta and pulmonary artery towards the ventricles and closes the semilunar valves. Due to the pressure drop in the chambers of the heart during diastole, the pressure in the venous (bringing) system begins to exceed the pressure in the atria, where blood flows from the veins.
The filling of the heart with blood is due to a number of reasons. The first is the presence of a residual driving force caused by the contraction of the heart. The average blood pressure in the veins of the large circle is 7 mm Hg. Art., and in the cavities of the heart during diastole tends to zero. Thus, the pressure gradient is only about 7 mm Hg. Art. This must be taken into account during surgical interventions - any accidental compression of the vena cava can completely stop the access of blood to the heart.
The second reason for blood flow to the heart is the contraction of skeletal muscles and the resulting compression of the veins of the limbs and trunk. Veins have valves that allow blood to flow in only one direction - towards the heart. This so-called venous pump provides a significant increase in venous blood flow to the heart and cardiac output during physical work.
The third reason for the increase in venous return is the suction effect of blood by the chest, which is a hermetically sealed cavity with negative pressure. At the moment of inhalation, this cavity increases, the organs located in it (in particular, the vena cava) stretch, and the pressure in the vena cava and atria becomes negative. The suction force of the ventricles, which relax like a rubber pear, is also of some importance.
Under cardiac cycle understand a period consisting of one contraction (systole) and one relaxation (diastole).
The contraction of the heart begins with atrial systole, lasting 0.1 s. In this case, the pressure in the atria rises to 5 - 8 mm Hg. Art. Ventricular systole lasts about 0.33 s and consists of several phases. The phase of asynchronous myocardial contraction lasts from the onset of contraction to the closing of the atrioventricular valves (0.05 s). The phase of isometric contraction of the myocardium begins with the slamming of the atrioventricular valves and ends with the opening of the semilunar valves (0.05 s).
The ejection period is about 0.25 s. During this time, part of the blood contained in the ventricles is expelled into large vessels. Residual systolic volume depends on the resistance of the heart and the strength of its contraction.
During diastole, pressure in the ventricles drops, blood from the aorta and pulmonary artery rushes back and slams the semilunar valves, then blood flows into the atria.
A feature of the blood supply to the myocardium is that the blood flow in it is carried out in the diastole phase. There are two vascular systems in the myocardium. The supply of the left ventricle occurs through the vessels extending from the coronary arteries at an acute angle and passing along the surface of the myocardium, their branches supply blood to 2/3 of the outer surface of the myocardium. Another vascular system passes at an obtuse angle, perforates the entire thickness of the myocardium and supplies blood to 1/3 of the inner surface of the myocardium, branching endocardially. During diastole, the blood supply to these vessels depends on the magnitude of intracardiac pressure and external pressure on the vessels. The sub-endocardial network is affected by the mean differential diastolic pressure. The higher it is, the worse the filling of the vessels, i.e., the coronary blood flow is disturbed. In patients with dilatation, foci of necrosis occur more often in the subendocardial layer than intramurally.
The right ventricle also has two vascular systems: the first passes through the entire thickness of the myocardium; the second forms the subendocardial plexus (1/3). The vessels overlap each other in the subendocardial layer, so there are practically no infarcts in the right ventricle. A dilated heart always has poor coronary blood flow but consumes more oxygen than normal.
Anatomy and physiology of the cardiovascular systemThe cardiovascular system includes the heart as a hemodynamic apparatus, arteries, through which blood is delivered to the capillaries, which ensure the exchange of substances between blood and tissues, and veins, which deliver blood back to the heart. Due to the innervation of the autonomic nerve fibers, a connection is made between the circulatory system and the central nervous system (CNS).
The heart is a four-chambered organ, its left half (arterial) consists of the left atrium and left ventricle, which do not communicate with its right half (venous), consisting of the right atrium and right ventricle. The left half drives blood from the veins of the pulmonary circulation to the artery of the systemic circulation, and the right half drives blood from the veins of the systemic circulation to the artery of the pulmonary circulation. In an adult healthy person, the heart is located asymmetrically; about two-thirds are to the left of the midline and are represented by the left ventricle, most of the right ventricle and left atrium, and the left ear (Fig. 54). One third is located to the right and represents the right atrium, a small part of the right ventricle and a small part of the left atrium.
The heart lies in front of the spine and is projected at the level of IV-VIII thoracic vertebrae. The right half of the heart faces forward, and the left back. The anterior surface of the heart is formed by the anterior wall of the right ventricle. On the top right, the right atrium with its ear participates in its formation, and on the left, part of the left ventricle and a small part of the left ear. The posterior surface is formed by the left atrium and minor parts of the left ventricle and right atrium.
The heart has a sternocostal, diaphragmatic, pulmonary surface, base, right edge and apex. The latter lies freely; large blood trunks begin from the base. Four pulmonary veins empty into the left atrium without valves. Both vena cava posteriorly enter the right atrium. The superior vena cava has no valves. The inferior vena cava has a Eustachian valve that does not completely separate the lumen of the vein from the lumen of the atrium. The cavity of the left ventricle contains the left atrioventricular orifice and the orifice of the aorta. Similarly, the right atrioventricular orifice and the orifice of the pulmonary artery are located in the right ventricle.
Each ventricle consists of two sections - the inflow tract and the outflow tract. The path of blood flow goes from the atrioventricular opening to the apex of the ventricle (right or left); the blood outflow path extends from the apex of the ventricle to the orifice of the aorta or pulmonary artery. The ratio of the length of the inflow path to the length of the outflow path is 2:3 (channel index). If the cavity of the right ventricle is able to receive a large amount of blood and increase by 2-3 times, then the myocardium of the left ventricle can sharply increase intraventricular pressure.
The cavities of the heart are formed from the myocardium. The atrial myocardium is thinner than the ventricular myocardium and consists of 2 layers of muscle fibers. The ventricular myocardium is more powerful and consists of 3 layers of muscle fibers. Each myocardial cell (cardiomyocyte) is bounded by a double membrane (sarcolemma) and contains all the elements: the nucleus, myofimbrils and organelles.
The inner shell (endocardium) lines the cavity of the heart from the inside and forms its valvular apparatus. The outer shell (epicardium) covers the outside of the myocardium.
Due to the valvular apparatus, blood always flows in one direction during contraction of the muscles of the heart, and in diastole it does not return from large vessels into the cavity of the ventricles. The left atrium and left ventricle are separated by a bicuspid (mitral) valve, which has two leaflets: a large right and a smaller left. There are three cusps in the right atrioventricular orifice.
Large vessels extending from the cavity of the ventricles have semilunar valves, consisting of three valves, which open and close depending on the amount of blood pressure in the cavities of the ventricle and the corresponding vessel.
The nervous regulation of the heart is carried out with the help of central and local mechanisms. The innervation of the vagus and sympathetic nerves belongs to the central ones. Functionally, the vagus and sympathetic nerves act in exactly the opposite way.
The vagal effect reduces the tone of the heart muscle and the automatism of the sinus node, to a lesser extent of the atrioventricular junction, as a result of which heart contractions slow down. Slows down the conduction of excitation from the atria to the ventricles.
Sympathetic influence speeds up and intensifies heart contractions. Humoral mechanisms also influence cardiac activity. Neurohormones (adrenaline, norepinephrine, acetylcholine, etc.) are products of the activity of the autonomic nervous system (neurotransmitters).
The conduction system of the heart is a neuromuscular organization capable of conducting excitation (Fig. 55). It consists of a sinus node, or Kiss-Fleck node, located at the confluence of the superior vena cava under the epicardium; atrioventricular node, or Ashof-Tavar node, located in the lower part of the wall of the right atrium, near the base of the medial cusp of the tricuspid valve and partly in the lower part of the interatrial and upper part of the interventricular septum. From it goes down the trunk of the bundle of His, located in the upper part of the interventricular septum. At the level of its membrane part, it is divided into two branches: the right and left, further breaking up into small branches - Purkinje fibers, which come into contact with the ventricular muscle. The left leg of the bundle of His is divided into anterior and posterior. The anterior branch penetrates the anterior part of the interventricular septum, the anterior and anterior-lateral walls of the left ventricle. The posterior branch passes into the posterior part of the interventricular septum, the posterolateral and posterior walls of the left ventricle.
The blood supply to the heart is carried out by a network of coronary vessels and mostly falls on the share of the left coronary artery, one quarter - on the share of the right one, both of them depart from the very beginning of the aorta, located under the epicardium.
The left coronary artery divides into two branches:
Anterior descending artery, which supplies blood to the anterior wall of the left ventricle and two-thirds of the interventricular septum;
The circumflex artery that supplies blood to part of the posterior-lateral surface of the heart.
The right coronary artery supplies blood to the right ventricle and the posterior surface of the left ventricle.
The sinoatrial node in 55% of cases is supplied with blood through the right coronary artery and in 45% - through the circumflex coronary artery. The myocardium is characterized by automatism, conductivity, excitability, contractility. These properties determine the work of the heart as a circulatory organ.
Automatism is the ability of the heart muscle itself to produce rhythmic impulses to contract it. Normally, the excitation impulse originates in the sinus node. Excitability - the ability of the heart muscle to respond with a contraction to the impulse passing through it. It is replaced by periods of non-excitability (refractory phase), which ensures the sequence of contraction of the atria and ventricles.
Conductivity - the ability of the heart muscle to conduct an impulse from the sinus node (normal) to the working muscles of the heart. Due to the fact that delayed conduction of the impulse occurs (in the atrioventricular node), the contraction of the ventricles occurs after the contraction of the atria has ended.
The contraction of the heart muscle occurs sequentially: first, the atria contract (atrial systole), then the ventricles (ventricular systole), after contraction of each section, its relaxation (diastole) occurs.
The volume of blood that enters the aorta with each contraction of the heart is called systolic, or shock. Minute volume is the product of stroke volume and the number of heartbeats per minute. Under physiological conditions, the systolic volume of the right and left ventricles is the same.
Blood circulation - contraction of the heart as a hemodynamic apparatus overcomes resistance in the vascular network (especially in arterioles and capillaries), creates high blood pressure in the aorta, which decreases in arterioles, becomes less in capillaries and even less in veins.
The main factor in the movement of blood is the difference in blood pressure on the way from the aorta to the vena cava; the suction action of the chest and the contraction of skeletal muscles also contribute to the promotion of blood.
Schematically, the main stages of blood promotion are:
Atrial contraction;
Contraction of the ventricles;
Promotion of blood through the aorta to large arteries (arteries of the elastic type);
Promotion of blood through the arteries (arteries of the muscular type);
Promotion through the capillaries;
Promotion through the veins (which have valves that prevent the retrograde movement of blood);
Inflow into the atria.
The height of blood pressure is determined by the force of contraction of the heart and the degree of tonic contraction of the muscles of small arteries (arterioles).
Maximum, or systolic, pressure is reached during ventricular systole; minimum, or diastolic, - towards the end of diastole. The difference between systolic and diastolic pressure is called pulse pressure.
Normally, in an adult, the height of blood pressure when measured on the brachial artery is: systolic 120 mm Hg. Art. (with fluctuations from 110 to 130 mm Hg), diastolic 70 mm (with fluctuations from 60 to 80 mm Hg), pulse pressure about 50 mm Hg. Art. The height of capillary pressure is 16–25 mm Hg. Art. The height of venous pressure is from 4.5 to 9 mm Hg. Art. (or 60 to 120 mm of water column).
This article is better to read for those who have at least some idea of the heart, it is written rather hard. I would not advise students. And the circles of blood circulation are not described in detail. Well, so 4+ ...
PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM
PartI. GENERAL PLAN OF THE STRUCTURE OF THE CARDIOVASCULAR SYSTEM. PHYSIOLOGY OF THE HEART
1. General plan of the structure and functional significance of the cardiovascular system
The cardiovascular system, along with respiratory, is key life support system of the body because it provides continuous circulation of blood in a closed vascular bed. Blood, only being in constant motion, is able to perform its many functions, the main of which is transport, which predetermines a number of others. The constant circulation of blood through the vascular bed makes it possible for it to continuously contact with all organs of the body, which ensures, on the one hand, maintaining the constancy of the composition and physicochemical properties of the intercellular (tissue) fluid (actually the internal environment for tissue cells), and on the other hand, maintaining homeostasis of the blood itself.
In the cardiovascular system, from a functional point of view, there are:
Ø heart - pump of periodic rhythmic type of action
Ø vessels- pathways of blood circulation.
The heart provides rhythmic periodic pumping of portions of blood into the vascular bed, giving them the energy necessary for the further movement of blood through the vessels. Rhythmic work of the heart is a pledge continuous circulation of blood in the vascular bed. Moreover, the blood in the vascular bed moves passively along the pressure gradient: from the area where it is higher to the area where it is lower (from arteries to veins); the minimum is the pressure in the veins that return blood to the heart. Blood vessels are present in almost all tissues. They are absent only in epithelium, nails, cartilage, tooth enamel, in some parts of the heart valves and in a number of other areas that are nourished by the diffusion of essential substances from the blood (for example, cells of the inner wall of large blood vessels).
In mammals and humans, the heart four-chamber(consists of two atria and two ventricles), the cardiovascular system is closed, there are two independent circles of blood circulation - big(system) and small(pulmonary). Circles of blood circulation start at ventricles with arterial vessels (aorta and pulmonary trunk ) and end in atrial veins (superior and inferior vena cava and pulmonary veins ). arteries-vessels that carry blood away from the heart veins- return blood to the heart.
Large (systemic) circulation begins in the left ventricle with the aorta, and ends in the right atrium with the superior and inferior vena cava. Blood from the left ventricle to the aorta is arterial. Moving through the vessels of the systemic circulation, it eventually reaches the microcirculatory bed of all organs and structures of the body (including the heart and lungs), at the level of which it exchanges substances and gases with tissue fluid. As a result of transcapillary exchange, blood becomes venous: it is saturated with carbon dioxide, end and intermediate metabolic products, it may receive some hormones or other humoral factors, partly gives oxygen, nutrients (glucose, amino acids, fatty acids), vitamins and etc. Venous blood flowing from various tissues of the body through the vein system returns to the heart (namely, through the superior and inferior vena cava - to the right atrium).
Small (pulmonary) circulation begins in the right ventricle with the pulmonary trunk, branching into two pulmonary arteries, which deliver venous blood to the microcirculatory bed, braiding the respiratory section of the lungs (respiratory bronchioles, alveolar passages and alveoli). At the level of this microcirculatory bed, transcapillary exchange takes place between venous blood flowing to the lungs and alveolar air. As a result of this exchange, the blood is saturated with oxygen, partially gives off carbon dioxide and turns into arterial blood. Through the pulmonary vein system (two out of each lung), arterial blood flowing from the lungs returns to the heart (to the left atrium).
Thus, in the left half of the heart, blood is arterial, it enters the vessels of the systemic circulation and is delivered to all organs and tissues of the body, ensuring their supply.
The end product" href="/text/category/konechnij_produkt/" rel="bookmark"> of the end products of metabolism. In the right half of the heart there is venous blood, which is ejected into the pulmonary circulation and at the level of the lungs turns into arterial blood.
2. Morpho-functional characteristics of the vascular bed
The total length of the human vascular bed is about 100,000 km. kilometers; usually most of them are empty, and only hard-working and constantly working organs (heart, brain, kidneys, respiratory muscles, and some others) are intensively supplied. vascular bed starts large arteries carrying blood out of the heart. The arteries branch along their course, giving rise to arteries of a smaller caliber (medium and small arteries). Having entered the blood-supplying organ, the arteries branch many times up to arteriole , which are the smallest vessels of the arterial type (diameter - 15-70 microns). From the arterioles, in turn, metaarteroils (terminal arterioles) depart at a right angle, from which they originate true capillaries , forming net. In places where capillaries separate from metarterol, there are precapillary sphincters that control the local volume of blood passing through the true capillaries. capillaries represent the smallest blood vessels in the vascular bed (d = 5-7 microns, length - 0.5-1.1 mm), their wall does not contain muscle tissue, but is formed with just one layer of endothelial cells and their surrounding basement membrane. A person has 100-160 billion. capillaries, their total length is 60-80 thousand. kilometers, and the total surface area is 1500 m2. Blood from the capillaries sequentially enters postcapillary (diameter up to 30 μm), collecting and muscle (diameter up to 100 μm) venules, and then into small veins. Small veins, uniting with each other, form medium and large veins.
Arterioles, metarterioles, precapillary sphincters, capillaries and venules constitute microvasculature, which is the path of the local blood flow of the organ, at the level of which the exchange between blood and tissue fluid is carried out. Moreover, such an exchange occurs most effectively in the capillaries. Venules, like no other vessels, are directly related to the course of inflammatory reactions in tissues, since it is through their wall that masses of leukocytes and plasma pass during inflammation.
Koll" href="/text/category/koll/" rel="bookmark">collateral vessels of one artery connecting with branches of other arteries, or intrasystemic arterial anastomoses between different branches of the same artery)
Ø venous(connecting vessels between different veins or branches of the same vein)
Ø arteriovenous(anastomoses between small arteries and veins, allowing blood to flow, bypassing the capillary bed).
The functional purpose of arterial and venous anastomoses is to increase the reliability of the blood supply to the organ, while arteriovenous anastomoses are to provide the possibility of blood flow bypassing the capillary bed (they are found in large numbers in the skin, the movement of blood through which reduces heat loss from the body surface).
Wall all vessels, except for the capillaries , comprises three shells:
Ø inner shell formed endothelium, basement membrane and subendothelial layer(a layer of loose fibrous connective tissue); this shell is separated from the middle shell internal elastic membrane;
Ø middle shell, which includes smooth muscle cells and dense fibrous connective tissue, the intercellular substance of which contains elastic and collagen fibers; separated from the outer shell outer elastic membrane;
Ø outer shell(adventitia), formed loose fibrous connective tissue feeding the vessel wall; in particular, small vessels pass through this membrane, providing nutrition to the cells of the vascular wall itself (the so-called vascular vessels).
In vessels of various types, the thickness and morphology of these membranes has its own characteristics. Thus, the walls of the arteries are much thicker than those of the veins, and to the greatest extent, the thickness of the arteries and veins differs in their middle shell, due to which the walls of the arteries are more elastic than those of the veins. At the same time, the outer shell of the wall of the veins is thicker than that of the arteries, and they, as a rule, have a larger diameter compared to the arteries of the same name. Small, medium and some large veins have venous valves , which are semilunar folds of their inner shell and prevent the reverse flow of blood in the veins. The veins of the lower extremities have the greatest number of valves, while both vena cava, veins of the head and neck, renal veins, portal and pulmonary veins do not have valves. The walls of large, medium and small arteries, as well as arterioles, are characterized by some structural features related to their middle shell. In particular, in the walls of large and some medium-sized arteries (vessels of the elastic type), elastic and collagen fibers predominate over smooth muscle cells, as a result of which such vessels are very elastic, which is necessary to convert pulsating blood flow into a constant one. The walls of small arteries and arterioles, on the contrary, are characterized by the predominance of smooth muscle fibers over connective tissue, which allows them to change the diameter of their lumen over a fairly wide range and thus regulate the level of blood supply to the capillaries. Capillaries, which do not have the middle and outer shells in their walls, are not able to actively change their lumen: it changes passively depending on the degree of their blood filling, which depends on the size of the arteriole lumen.
Fig.4. Scheme of the structure of the wall of the artery and vein
 |
Aorta" href="/text/category/aorta/" rel="bookmark">aorta , pulmonary arteries, common carotid and iliac arteries;
Ø resistive type vessels (resistance vessels)- predominantly arterioles, the smallest vessels of the arterial type, in the wall of which there is a large number of smooth muscle fibers, which allows changing its lumen over a wide range; ensure the creation of maximum resistance to the movement of blood and take part in its redistribution between organs working with different intensities
Ø exchange type vessels(mainly capillaries, partly arterioles and venules, at the level of which transcapillary exchange is carried out)
Ø capacitive (depositing) type vessels(veins), which, due to the small thickness of their middle membrane, are characterized by good compliance and can stretch quite strongly without a concomitant sharp increase in pressure in them, due to which they often serve as a blood depot (as a rule, about 70% of the volume of circulating blood is in the veins)
Ø anastomosing type vessels(or shunting vessels: artreioarterial, venovenous, arteriovenous).
3. Macro-microscopic structure of the heart and its functional significance
Heart(cor) - a hollow muscular organ that pumps blood into the arteries and receives it from the veins. It is located in the chest cavity, as part of the organs of the middle mediastinum, intrapericardially (inside the heart sac - the pericardium). Has a conical shape; its longitudinal axis is directed obliquely - from right to left, from top to bottom and from back to front, so it lies two-thirds in the left half of the chest cavity. The apex of the heart faces down, to the left, and forward, while the wider base faces upwards and backwards. There are four surfaces in the heart:
Ø anterior (sternocostal), convex, facing the posterior surface of the sternum and ribs;
Ø lower (diaphragmatic or back);
Ø lateral or pulmonary surfaces.
The average heart weight in men is 300g, in women - 250g. The largest transverse size of the heart is 9-11 cm, anteroposterior - 6-8 cm, heart length - 10-15 cm.
The heart begins to be laid on the 3rd week of intrauterine development, its division into the right and left half occurs by the 5th-6th week; and it begins to work shortly after its bookmark (on the 18-20th day), making one contraction every second.
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Rice. 7. Heart (front and side view)
The human heart consists of 4 chambers: two atria and two ventricles. The atria take blood from the veins and push it into the ventricles. In general, their pumping capacity is much less than that of the ventricles (the ventricles are mainly filled with blood during a general pause of the heart, while atrial contraction only contributes to additional pumping of blood), but the main role atrial is that they are temporary reservoirs of blood . Ventricles receive blood from the atria and pump it into the arteries (aorta and pulmonary trunk). The wall of the atria (2-3mm) is thinner than that of the ventricles (5-8mm in the right ventricle and 12-15mm in the left). On the border between the atria and ventricles (in the atrioventricular septum) there are atrioventricular openings, in the area of \u200b\u200bwhich are located leaflet atrioventricular valves(bicuspid or mitral in the left half of the heart and tricuspid in the right), preventing the reverse flow of blood from the ventricles to the atria at the time of ventricular systole . At the exit site of the aorta and pulmonary trunk from the corresponding ventricles, semilunar valves, preventing the backflow of blood from the vessels into the ventricles at the time of ventricular diastole . In the right half of the heart, the blood is venous, and in the left half it is arterial.
Wall of the heart comprises three layers:
Ø endocardium- a thin inner shell, lining the inside of the cavity of the heart, repeating their complex relief; it consists mainly of connective (loose and dense fibrous) and smooth muscle tissues. Duplications of the endocardium form the atrioventricular and semilunar valves, as well as the valves of the inferior vena cava and coronary sinus
Ø myocardium- the middle layer of the wall of the heart, the thickest, is a complex multi-tissue shell, the main component of which is cardiac muscle tissue. The myocardium is thickest in the left ventricle and thinnest in the atria. atrial myocardium comprises two layers: superficial (general for both atria, in which the muscle fibers are located transversely) and deep (separate for each of the atria in which muscle fibers follow longitudinally, circular fibers are also found here, loop-like in the form of sphincters covering the mouths of the veins that flow into the atria). Myocardium of the ventricles three-layer: outer (formed obliquely oriented muscle fibers) and interior (formed longitudinally oriented muscle fibers) layers are common to the myocardium of both ventricles, and located between them middle layer (formed circular fibers) - separate for each of the ventricles.
Ø epicardium- the outer shell of the heart, is a visceral sheet of the serous membrane of the heart (pericardium), built according to the type of serous membranes and consists of a thin plate of connective tissue covered with mesothelium.
Myocardium of the heart, providing periodic rhythmic contraction of its chambers, is formed cardiac muscle tissue (a type of striated muscle tissue). Structural and functional unit of cardiac muscle tissue is cardiac muscle fiber. It is striated (the contractile apparatus is represented myofibrils , oriented parallel to its longitudinal axis, occupying a peripheral position in the fiber, while the nuclei are in the central part of the fiber), is characterized by the presence well-developed sarcoplasmic reticulum and T-tubule systems . But him distinctive feature is the fact that it is multicellular formation , which is a collection of sequentially laid and connected with the help of intercalated discs of cardiac muscle cells - cardiomyocytes. In the area of insertion discs, there are a large number of gap junctions (nexuses), arranged according to the type of electrical synapses and providing the possibility of direct conduction of excitation from one cardiomyocyte to another. Due to the fact that the cardiac muscle fiber is a multicellular formation, it is called a functional fiber.
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Rice. 9. Scheme of the gap junction (nexus) structure. Gap contact provides ionic and metabolic conjugation of cells. The plasma membranes of cardiomyocytes in the area of gap junction formation are brought together and separated by a narrow intercellular gap 2-4 nm wide. The connection between the membranes of neighboring cells is provided by a transmembrane protein of a cylindrical configuration - the connexon. The connexon molecule consists of 6 connexin subunits arranged radially and bounding a cavity (connexon channel, 1.5 nm in diameter). Two connexon molecules of neighboring cells are connected in the intermembrane space with each other, resulting in the formation of a single nexus channel, which can pass ions and low molecular weight substances with Mr up to 1.5 kD. Consequently, nexuses make it possible to move not only inorganic ions from one cardiomyocyte to another (which ensures the direct transmission of excitation), but also low-molecular organic substances (glucose, amino acids, etc.)
Blood supply to the heart carried out coronary arteries(right and left), extending from the aortic bulb and making up together with the microcirculatory bed and coronary veins (gathering into the coronary sinus, which flows into the right atrium) coronary (coronary) circulation, which is part of a large circle.
Heart refers to the number of organs working throughout life constantly. For 100 years of human life, the heart makes about 5 billion contractions. Moreover, the intensity of the heart depends on the level of metabolic processes in the body. So, in an adult, the normal heart rate at rest is 60-80 beats / min, while in smaller animals with a larger relative body surface area (surface area per unit mass) and, accordingly, a higher level of metabolic processes, the intensity of cardiac activity is much higher. . So in a cat (average weight 1.3 kg) the heart rate is 240 beats / min, in a dog - 80 beats / min, in a rat (200-400g) - 400-500 beats / min, and in a mosquito tit (weight about 8g) - 1200 beats / min. The heart rate in large mammals with a relatively low level of metabolic processes is much lower than that of a person. In a whale (weight 150 tons), the heart makes 7 contractions per minute, and in an elephant (3 tons) - 46 beats per minute.
The Russian physiologist calculated that during a human life the heart does work equal to the effort that would be enough to lift a train to the highest peak in Europe - Mont Blanc (height 4810m). For a day in a person who is in relative rest, the heart pumps 6-10 tons of blood, and during life - 150-250 thousand tons.
The movement of blood in the heart, as well as in the vascular bed, is carried out passively along the pressure gradient. Thus, the normal cardiac cycle begins with atrial systole , as a result of which the pressure in the atria slightly increases, and portions of blood are pumped into the relaxed ventricles, the pressure in which is close to zero. At the moment following atrial systole ventricular systole the pressure in them increases, and when it becomes higher than that in the proximal vascular bed, blood is expelled from the ventricles into the corresponding vessels. In the moment general pause of the heart there is a main filling of the ventricles with blood, passively returning to the heart through the veins; contraction of the atria provides additional pumping of a small amount of blood into the ventricles.
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Rice. 11. Diagram showing the direction of blood flow in the heart
4. Structural organization and functional role of the conduction system of the heart
The conduction system of the heart is represented by a set of conducting cardiomyocytes that form
Ø sinoatrial node(sinoatrial node, Kate-Flak node, laid in the right atrium, at the confluence of the vena cava),
Ø atrioventricular node(atrioventricular node, Aschoff-Tavar node, is embedded in the thickness of the lower part of the interatrial septum, closer to the right half of the heart),
Ø bundle of His(atrioventricular bundle, located in the upper part of the interventricular septum) and his legs(go down from the bundle of His along the inner walls of the right and left ventricles),
Ø network of diffuse conducting cardiomyocytes, forming Prukigne fibers (pass in the thickness of the working myocardium of the ventricles, as a rule, adjacent to the endocardium).
Cardiomyocytes of the conduction system of the heart are atypical myocardial cells(the contractile apparatus and the system of T-tubules are poorly developed in them, they do not play a significant role in the development of tension in the heart cavities at the time of their systole), which have the ability to independently generate nerve impulses with a certain frequency ( automation).
Involvement" href="/text/category/vovlechenie/" rel="bookmark"> involving the myoradiocytes of the interventricular septum and the apex of the heart into excitation, and then returns to the base of the ventricles along the branches of the legs and Purkinje fibers. Due to this, the apexes of the ventricles first contract, and then their foundations.
In this way, the conduction system of the heart provides:
Ø periodic rhythmic generation of nerve impulses, initiating the contraction of the chambers of the heart with a certain frequency;
Ø certain sequence in the contraction of the chambers of the heart(first, the atria are excited and contract, pumping blood into the ventricles, and only then the ventricles, pumping blood into the vascular bed)
Ø almost synchronous excitation coverage of the working myocardium of the ventricles, and hence the high efficiency of the ventricular systole, which is necessary to create a certain pressure in their cavities, somewhat higher than that in the aorta and pulmonary trunk, and, consequently, to ensure a certain systolic blood ejection.
5. Electrophysiological characteristics of myocardial cells
Conducting and working cardiomyocytes are excitable structures, i.e., they have the ability to generate and conduct action potentials (nerve impulses). And for conducting cardiomyocytes characteristic automation (ability to independent periodic rhythmic generation of nerve impulses), while working cardiomyocytes are excited in response to excitation coming to them from conductive or other already excited working myocardial cells.
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Rice. 13. Scheme of the action potential of a working cardiomyocyte
AT action potential of working cardiomyocytes distinguish the following phases:
Ø rapid initial depolarization phase, due to fast incoming potential-dependent sodium current , arises as a result of activation (opening of fast activation gates) of fast voltage-gated sodium channels; characterized by a high steepness of rise, since the current causing it has the ability to self-update.
Ø PD plateau phase, due to potential dependent slow incoming calcium current . The initial depolarization of the membrane caused by the incoming sodium current leads to the opening slow calcium channels, through which calcium ions enter the inside of the cardiomyocyte along the concentration gradient; these channels are to a much lesser extent, but still permeable to sodium ions. The entry of calcium and partly sodium into the cardiomyocyte through slow calcium channels somewhat depolarizes its membrane (but much weaker than the fast incoming sodium current preceding this phase). In this phase, fast sodium channels, which provide the phase of rapid initial depolarization of the membrane, are inactivated, and the cell passes into the state absolute refractoriness. During this period, there is also a gradual activation of voltage-gated potassium channels. This phase is the longest phase of AP (it is 0.27 s with a total AP duration of 0.3 s), as a result of which the cardiomyocyte is in a state of absolute refractoriness most of the time during the period of AP generation. Moreover, the duration of a single contraction of the myocardial cell (about 0.3 s) is approximately equal to that of AP, which, together with a long period of absolute refractoriness, makes it impossible for the development of tetanic contraction of the heart muscle, which would be tantamount to cardiac arrest. Therefore, the heart muscle is capable of developing only single contractions.
The cardiovascular system is represented by the heart, blood vessels and blood. It provides blood supply to organs and tissues, transporting oxygen, metabolites and hormones to them, delivering CO 2 from tissues to the lungs, and other metabolic products to the kidneys, liver and other organs. This system also transports various cells found in the blood, both within the system and between the vascular system and the extracellular fluid. It ensures the distribution of water in the body, participates in the work of the immune system. In other words, the main function of the cardiovascular system is transport. This system is also vital for the regulation of homeostasis (for example, to maintain body temperature, acid-base balance - ABR, etc.).
HEART
The movement of blood through the cardiovascular system is carried out by the heart, which is a muscular pump, which is divided into right and left parts. Each of the parts is represented by two chambers - the atrium and the ventricle. The continuous work of the myocardium (heart muscle) is characterized by alternating systole (contraction) and diastole (relaxation).
From the left side of the heart, blood is pumped into the aorta, through the arteries and arterioles, into the capillaries, where the exchange between blood and tissues takes place. Through the venules, blood is sent to the vein system and then to the right atrium. it systemic circulation- system circulation.
From the right atrium, blood enters the right ventricle, which pumps it through the vessels of the lungs. it pulmonary circulation- pulmonary circulation.
The heart contracts up to 4 billion times during a person's life, ejecting into the aorta and facilitating the entry of up to 200 million liters of blood into organs and tissues. Under physiological conditions, cardiac output ranges from 3 to 30 l/min. At the same time, the blood flow in various organs (depending on the intensity of their functioning) varies, increasing, if necessary, approximately twice.
shells of the heart
The walls of all four chambers have three membranes: endocardium, myocardium and epicardium.
Endocardium lines the inside of the atria, ventricles and valve petals - mitral, tricuspid, aortic valve and pulmonary valve.
Myocardium consists of working (contractile), conductive and secretory cardiomyocytes.
F Working cardiomyocytes contain a contractile apparatus and a depot of Ca 2 + (cistern and tubules of the sarcoplasmic reticulum). These cells, with the help of intercellular contacts (intercalary discs), are combined into the so-called cardiac muscle fibers - functional syncytium(the totality of cardiomyocytes within each chamber of the heart).
F Conducting cardiomyocytes form the conduction system of the heart, including the so-called pacemakers.
F secretory cardiomyocytes. Part of the atrial cardiomyocytes (especially the right one) synthesizes and secretes the vasodilator atriopeptin, a hormone that regulates blood pressure.
Myocardial functions: excitability, automatism, conduction and contractility.
F Under the influence of various influences (nervous system, hormones, various drugs), myocardial functions change: the effect on the frequency of automatic heart contractions (HR) is denoted by the term "chronotropic action"(can be positive and negative), the effect on the strength of contractions (i.e. on contractility) - "inotropic action"(positive or negative), the impact on the speed of atrioventricular conduction (which reflects the function of conduction) - "dromotropic action"(positive or negative), excitability -
"batmotropic action" (also positive or negative).
epicardium forms the outer surface of the heart and passes (practically merged with it) into the parietal pericardium - the parietal sheet of the pericardial sac containing 5-20 ml of pericardial fluid.
Heart valves
The effective pumping function of the heart depends on the unidirectional movement of blood from the veins to the atria and further to the ventricles, created by four valves (at the entrance and exit of both ventricles, Fig. 23-1). All valves (atrioventricular and semilunar) close and open passively.
Atrioventricular valves:tricuspid valve in the right ventricle and bivalve(mitral) valve in the left - prevent the reverse flow of blood from the ventricles to the atria. The valves close when the pressure gradient is directed towards the atria, i.e. when ventricular pressure exceeds atrial pressure. When the pressure in the atria rises above the pressure in the ventricles, the valves open.
Lunar valves: aortic and pulmonary artery- located at the exit of the left and right ventricles, respectively. They prevent the return of blood from the arterial system to the cavity of the ventricles. Both valves are represented by three dense, but very flexible "pockets", having a crescent shape and attached symmetrically around the valve ring. The “pockets” open into the lumen of the aorta or pulmonary trunk, and when the pressure in these large vessels begins to exceed the pressure in the ventricles (i.e., when the latter begin to relax at the end of systole), the “pockets” straighten out with blood filling them under pressure, and tightly close along their free edges - the valve slams (closes).
Heart sounds
Listening (auscultation) with a stethophonendoscope of the left half of the chest allows you to hear two heart sounds - I
Rice. 23-1. Heart valves. Left- transverse (in the horizontal plane) sections through the heart, mirrored with respect to the diagrams on the right. On right- frontal sections through the heart. Up- diastole, at the bottom- systole.
and II. I tone is associated with the closure of the AV valves at the beginning of systole, II - with the closure of the semilunar valves of the aorta and pulmonary artery at the end of systole. The cause of heart sounds is the vibration of tense valves immediately after closure, together with
vibration of adjacent vessels, the wall of the heart and large vessels in the region of the heart.
The duration of the I tone is 0.14 s, the II tone is 0.11 s. II heart sound has a higher frequency than I. The sound of I and II heart sounds most closely conveys the combination of sounds when pronouncing the phrase "LAB-DAB". In addition to I and II tones, sometimes you can listen to additional heart sounds - III and IV, in the vast majority of cases reflecting the presence of cardiac pathology.
Blood supply to the heart
The wall of the heart is supplied with blood by the right and left coronary (coronary) arteries. Both coronary arteries originate from the base of the aorta (near the insertion of the aortic valve cusps). The posterior wall of the left ventricle, some parts of the septum, and most of the right ventricle are supplied by the right coronary artery. The rest of the heart receives blood from the left coronary artery.
F When the left ventricle contracts, the myocardium compresses the coronary arteries and blood flow to the myocardium practically stops - 75% of the blood flows through the coronary arteries to the myocardium during relaxation of the heart (diastole) and low resistance of the vascular wall. For adequate coronary blood flow, diastolic blood pressure should not fall below 60 mmHg. F During exercise, coronary blood flow increases, which is associated with increased work of the heart, which supplies the muscles with oxygen and nutrients. The coronal veins, collecting blood from most of the myocardium, flow into the coronary sinus in the right atrium. From some areas, located mainly in the "right heart", blood flows directly into the heart chambers.
Innervation of the heart
The work of the heart is controlled by the cardiac centers of the medulla oblongata and the bridge through the parasympathetic and sympathetic fibers (Fig. 23-2). Cholinergic and adrenergic (mainly unmyelinated) fibers form several
Rice. 23-2. Innervation of the heart. 1 - sinoatrial node, 2 - atrioventricular node (AV node).
nerve plexuses containing intracardiac ganglia. Accumulations of ganglia are mainly concentrated in the wall of the right atrium and in the region of the mouths of the vena cava.
parasympathetic innervation. Preganglionic parasympathetic fibers for the heart run in the vagus nerve on both sides. The fibers of the right vagus nerve innervate the right atrium and form a dense plexus in the region of the sinoatrial node. The fibers of the left vagus nerve approach predominantly the AV node. That is why the right vagus nerve affects mainly the heart rate, and the left one - on AV conduction. The ventricles have less pronounced parasympathetic innervation.
F Effects of parasympathetic stimulation: the force of atrial contractions decreases - a negative inotropic effect, the heart rate decreases - a negative chronotropic effect, the atrioventricular conduction delay increases - a negative dromotropic effect.
sympathetic innervation. Preganglionic sympathetic fibers for the heart come from the lateral horns of the upper thoracic segments of the spinal cord. Postganglionic adrenergic fibers are formed by axons of neurons contained in the ganglia of the sympathetic nerve chain (stellate and partly upper cervical sympathetic nodes). They approach the organ as part of several cardiac nerves and are evenly distributed throughout all parts of the heart. The terminal branches penetrate the myocardium, accompany the coronary vessels and approach the elements of the conduction system. The atrial myocardium has a higher density of adrenergic fibers. Every fifth cardiomyocyte of the ventricles is supplied with an adrenergic terminal, ending at a distance of 50 μm from the plasmolemma of the cardiomyocyte.
F Effects of sympathetic stimulation: the force of atrial and ventricular contractions increases - a positive inotropic effect, heart rate increases - a positive chronotropic effect, the interval between contractions of the atria and ventricles (i.e. conduction delay in the AV connection) is shortened - a positive dromotropic effect.
afferent innervation. Sensory neurons of the ganglia of the vagus nerves and spinal nodes (C 8 -Th 6) form free and encapsulated nerve endings in the wall of the heart. Afferent fibers run as part of the vagus and sympathetic nerves.
PROPERTIES OF THE MYOCARDIA
The main properties of the heart muscle are excitability; automatism; conductivity, contractility.
Excitability
Excitability - the property to respond to stimulation with electrical excitation in the form of changes in the membrane potential (MP) with subsequent generation of AP. Electrogenesis in the form of MPs and APs is determined by the difference in ion concentrations on both sides of the membrane, as well as by the activity of ion channels and ion pumps. Through the pores of the ion channels, the ions pass through the electrical
chemical gradient, while ion pumps move the ions against the electrochemical gradient. In cardiomyocytes, the most common channels are for Na +, K +, Ca 2 + and Cl - ions.
The resting MP of the cardiomyocyte is -90 mV. Stimulation generates a propagating AP that causes contraction (Fig. 23-3). Depolarization develops rapidly, as in skeletal muscle and nerve, but, unlike the latter, MP does not return to its original level immediately, but gradually.
Depolarization lasts about 2 ms, the plateau phase and repolarization last 200 ms or more. As in other excitable tissues, changes in the extracellular K+ content affect MP; changes in the extracellular concentration of Na+ affect the AP value.
F Rapid initial depolarization (phase 0) arises as a result of the discovery of potential-dependent fast? + -channels, Na+ ions quickly rush into the cell and change the charge of the inner surface of the membrane from negative to positive.
F Initial fast repolarization (phase 1)- the result of the closing of Na + -channels, the entry of Cl - ions into the cell and the exit of K + ions from it.
F Next long plateau phase (phase 2- MP remains approximately at the same level for some time) - the result of the slow opening of voltage-dependent Ca^-channels: Ca 2 + ions enter the cell, as well as Na + ions, while the current of K + ions from the cell is maintained.
F End fast repolarization (phase 3) occurs as a result of the closure of Ca2+ channels against the background of the continued release of K+ from the cell through K+ channels.
F In the resting phase (phase 4) MP is restored due to the exchange of Na+ ions for K+ ions through the functioning of a specialized transmembrane system - Na+-, K+-pump. These processes relate specifically to the working cardiomyocyte; in pacemaker cells, phase 4 is somewhat different.
Rice.23-3. action potentials. A - ventricle; B - sinoatrial node; B - ionic conductivity. I - AP recorded from surface electrodes, II - intracellular recording of AP, III - mechanical response; G - contraction of the myocardium. ARF - absolute refractory phase, RRF - relative refractory phase. O - depolarization, 1 - initial fast repolarization, 2 - plateau phase, 3 - final fast repolarization, 4 - initial level.
Rice. 23-3.The ending.
Rice. 23-4. The conduction system of the heart (left). Typical AP [sinus (sinoatrial) and AV nodes (atrioventricular), other parts of the conduction system and atrial and ventricular myocardium] in correlation with ECG (right).
Automatism and Conductivity
Automatism - the ability of pacemaker cells to initiate excitation spontaneously, without the participation of neurohumoral control. Excitation, leading to a contraction of the heart, arises in a specialized conducting system of the heart and spreads through it to all parts of the myocardium.
Pconducting system of the heart. The structures that make up the conduction system of the heart are the sinoatrial node, the internodal atrial pathways, the AV junction (the lower part of the atrial conduction system adjacent to the AV node, the AV node itself, the upper part of the His bundle), the His bundle and its branches, Purkinje fiber system (Fig. 23-4).
ATrhythm guides. All parts of the conduction system are capable of generating AP with a certain frequency, which ultimately determines the heart rate, i.e. be the pacemaker. However, the sinoatrial node generates AP faster than other parts of the conduction system, and depolarization from it spreads to other parts of the conduction system before they begin to spontaneously excite. In this way, sinoatrial node - the main pacemaker, or a first-order pacemaker. frequency of it
spontaneous discharges determines the heart rate (average 60-90 per minute).
Pacemaker potentials
MP of pacemaker cells after each AP returns to the threshold level of excitation. This potential, called the prepotential (pacemaker potential), is the trigger for the next potential (Fig. 23-5, A). At the peak of each AP after depolarization, a potassium current appears, which triggers the processes of repolarization. When the potassium current and the output of K+ ions decrease, the membrane begins to depolarize, forming the first part of the prepotential. Two types of Ca 2+ channels open: temporarily opening Ca 2+ channels and long-acting
Rice. 23-5. Spread of excitement through the heart. A - potentials of the pacemaker cell. IK, 1Са d, 1Са в - ion currents corresponding to each part of the pacemaker potential; B-F - distribution of electrical activity in the heart: 1 - sinoatrial node, 2 - atrioventricular (AV-) node. Explanations in the text.
Ca2+d channels. The calcium current flowing through Ca 2+ in channels forms a prepotential, the calcium current in Ca 2+ g channels creates AP.
Spread of excitation through the heart muscle
The depolarization that occurs in the sinoatrial node spreads radially through the atria and then converges (converges) at the AV junction (Figure 23-5). Atrial depolarization is completely completed within 0.1 s. Since conduction in the AV node is slower than conduction in the atrial and ventricular myocardium, an atrioventricular (AV-) delay of 0.1 s occurs, after which excitation spreads to the ventricular myocardium. Atrioventricular delay is reduced by stimulation of the sympathetic nerves of the heart, while under the influence of stimulation of the vagus nerve, its duration increases.
From the base of the interventricular septum, the depolarization wave propagates at high speed through the system of Purkinje fibers to all parts of the ventricle within 0.08-0.1 s. Depolarization of the ventricular myocardium begins on the left side of the interventricular septum and spreads primarily to the right through the middle part of the septum. The wave of depolarization then travels down the septum to the apex of the heart. Along the wall of the ventricle, it returns to the AV node, passing from the subendocardial surface of the myocardium to the subepicardial.
Contractility
The heart muscle contracts if the intracellular calcium content exceeds 100 mmol. This rise in intracellular Ca 2 + concentration is associated with the entry of extracellular Ca 2 + during PD. Therefore, this whole mechanism is called a single process. excitation-contraction. The ability of the heart muscle to develop force without any change in the length of the muscle fiber is called contractility. The contractility of the heart muscle is mainly determined by the ability of the cell to retain Ca 2 +. In contrast to skeletal muscle, AP in cardiac muscle by itself, if Ca2+ does not enter the cell, cannot cause Ca2+ release. Therefore, in the absence of external Ca 2 + contraction of the heart muscle is impossible. The property of myocardial contractility is provided by the contractile apparatus of the cardio-
myocytes bound into functional syncytium by ion-permeable gap junctions. This circumstance synchronizes the spread of excitation from cell to cell and the contraction of cardiomyocytes. Increase in the force of contractions of the ventricular myocardium - positive inotropic effect catecholamines - indirectlyR 1 -adrenergic receptors (sympathetic innervation also acts through these receptors) and cAMP. Cardiac glycosides also increase the contraction of the heart muscle, exerting an inhibitory effect on the K + -ATPase in the cell membranes of cardiomyocytes. In proportion to the increase in heart rate, the force of the heart muscle increases (staircase phenomenon). This effect is associated with the accumulation of Ca 2 + in the sarcoplasmic reticulum.
ELECTROCARDIOGRAPHY
Myocardial contractions are accompanied (and caused) by high electrical activity of cardiomyocytes, which forms a changing electric field. Fluctuations in the total potential of the electric field of the heart, representing the algebraic sum of all AP (see Fig. 23-4), can be recorded from the surface of the body. Registration of these fluctuations in the potential of the electric field of the heart during the cardiac cycle is carried out when recording an electrocardiogram (ECG) - a sequence of positive and negative teeth (periods of electrical activity of the myocardium), some of which are connected by the so-called isoelectric line (periods of electrical rest of the myocardium).
ATelectric field vector (Fig. 23-6, A). In each cardiomyocyte, during its depolarization and repolarization, positive and negative charges closely adjacent to each other (elementary dipoles) appear on the border of the excited and unexcited areas. In the heart, many dipoles simultaneously arise, the direction of which is different. Their electromotive force is a vector characterized not only by magnitude, but also by direction: always from a smaller charge (-) to a larger one (+). The sum of all vectors of elementary dipoles forms a total dipole - the vector of the electric field of the heart, constantly changing in time depending on the phase of the cardiac cycle. Conventionally, it is believed that in any phase the vector comes from one point
Rice. 23-6. Vectors electrical field of the heart . A - scheme for constructing an ECG using vector electrocardiography. The three main resultant vectors (atrial depolarization, ventricular depolarization, and ventricular repolarization) form three loops in vector electrocardiography; when these vectors are scanned along the time axis, a regular ECG curve is obtained; B - Einthoven's triangle. Explanation in the text. α is the angle between the electrical axis of the heart and the horizontal.
ki called the electrical center. For a significant part of the cycle, the resulting vectors are directed from the base of the heart to its apex. There are three main resultant vectors: atrial depolarization, ventricular depolarization and repolarization. Direction of the resulting ventricular depolarization vector - electrical axis of the heart(EOS).
Einthoven triangle. In a bulk conductor (human body), the sum of the electric field potentials at three vertices of an equilateral triangle with an electric field source in the center of the triangle will always be zero. Nevertheless, the potential difference of the electric field between the two vertices of the triangle is not equal to zero. Such a triangle with a heart in its center - Einthoven's triangle - is oriented in the frontal plane of the human body; rice. 23-7, B); when removing the ECG tre-
Rice. 23-7. ECG Leads . A - standard leads; B - enhanced leads from the limbs; B - chest leads; D - options for the position of the electrical axis of the heart depending on the value of the angle α. Explanations in the text.
the square is created artificially by placing electrodes on both hands and the left leg. Two points of the Einthoven triangle with a potential difference between them that changes over time are denoted as derivation of the ECG.
Ocreations ECG. The points for the formation of leads (there are only 12 of them when recording a standard ECG) are the vertices of the Einthoven triangle (standard leads), triangle center (reinforced leads) and points directly above the heart (chest leads).
Standard leads. The vertices of Einthoven's triangle are the electrodes on both arms and left leg. Determining the potential difference in the electric field of the heart between the two vertices of the triangle, they talk about ECG registration in standard leads (Fig. 23-7, A): between the right and left hands - I standard lead, between the right hand and left leg - II standard lead, between left arm and left leg - III standard lead.
Strengthened limb leads. In the center of Einthoven's triangle, when the potentials of all three electrodes are summed up, a virtual "zero", or indifferent, electrode is formed. The difference between the zero electrode and the electrodes at the vertices of Einthoven's triangle is recorded when taking an ECG in enhanced limb leads (Fig. 23-8, B): aVL - between the "zero" electrode and the electrode on the left hand, aVR - between the "zero" electrode and electrode on the right arm, aVF - between the "zero" electrode and the electrode on the left leg. The leads are called reinforced because they have to be amplified due to the small (compared to standard leads) electric field potential difference between the top of Einthoven's triangle and the "zero" point.
chest leads- points on the surface of the body located directly above the heart on the anterior and lateral surfaces of the chest (Fig. 23-7, B). The electrodes installed at these points are called chest ones, as well as the leads that are formed when determining the difference: the potentials of the electric field of the heart between the point of the chest electrode and the "zero" electrode, - chest leads V 1 -V 6.
Electrocardiogram
A normal electrocardiogram (Fig. 23-8, B) consists of the main line (isoline) and deviations from it, called teeth and denoted by Latin letters P, Q, R, S, T, U. ECG segments between adjacent teeth are segments. The distances between different teeth are intervals.
Rice. 23-8. teeth and intervals. A - the formation of ECG teeth during sequential excitation of the myocardium; B - teeth of the normal complex PQRST. Explanations in the text.
The main teeth, intervals and segments of the ECG are shown in fig. 23-8, B.
Prong P corresponds to the coverage of excitation (depolarization) of the atria. Prong duration R equal to the time of passage of excitation from the sinoatrial node to the AV junction and normally in adults does not exceed 0.1 s. Amplitude P - 0.5-2.5 mm, maximum in lead II.
Interval PQ(R) determined from the beginning of the tooth R before the beginning of the tooth Q(or R if Q missing). The interval is equal to the time of passage of excitation from the sinoatrial
node to the ventricles. interval PQ(R) is 0.12-0.20 s with normal heart rate. With tachya or bradycardia PQ(R) varies, its normal values are determined according to special tables.
Complex QRS equal to the depolarization time of the ventricles. Consists of Q waves R and S. prong Q- the first deviation from the isoline downwards, tooth R- the first after the tooth Q upward deviation from the isoline. Prong S- downward deviation from the isoline, following the R wave. Interval QRS measured from the beginning of the tooth Q(or R, if Q missing) until the end of the tooth S. The normal duration in adults QRS does not exceed 0.1 s.
Segment ST - distance between the end point of the complex QRS and the beginning of the T wave. Equal to the time during which the ventricles remain in a state of excitation. Position is important for clinical purposes ST in relation to the isoline.
Prong T corresponds to ventricular repolarization. anomalies T non-specific. They can occur in healthy individuals (asthenics, athletes) with hyperventilation, anxiety, cold water intake, fever, ascent to a high altitude above sea level, as well as with organic myocardial damage.
Prong U - a slight upward deviation from the isoline, recorded in some people after the tooth T, most pronounced in leads V 2 and V 3 . The nature of the tooth is not exactly known. Normally, its maximum amplitude does not exceed 2 mm or up to 25% of the amplitude of the previous tooth. T.
Interval Q-T represents the electrical systole of the ventricles. It is equal to the time of ventricular depolarization, varies depending on age, sex and heart rate. Measured from the beginning of the complex QRS until the end of the tooth T. The normal duration in adults Q-T ranges from 0.35 to 0.44 s, but its duration is very dependent on
from heart rate.
Hnormal heart rhythm. Each contraction originates in the sinoatrial node (sinus rhythm). At rest, the frequency
heart rate fluctuates between 60-90 per minute. Heart rate decreases (bradycardia) during sleep and increases (tachycardia) under the influence of emotions, physical work, fever and many other factors. At a young age, the heart rate increases during inhalation and decreases during exhalation, especially with deep breathing, - sinus respiratory arrhythmia(standard version). Sinus respiratory arrhythmia is a phenomenon that occurs due to fluctuations in the tone of the vagus nerve. During inspiration, impulses from the stretch receptors of the lungs inhibit the inhibitory effects on the heart of the vasomotor center in the medulla oblongata. The number of tonic discharges of the vagus nerve, which constantly restrain the rhythm of the heart, decreases, and the heart rate increases.
Electrical axis of the heart
The greatest electrical activity of the myocardium of the ventricles is found during their excitation. In this case, the resultant of the emerging electrical forces (vector) occupies a certain position in the frontal plane of the body, forming an angle α (it is expressed in degrees) relative to the horizontal zero line (I standard lead). The position of this so-called electrical axis of the heart (EOS) is estimated by the size of the teeth of the complex QRS in standard leads (Fig. 23-7, D), which allows you to determine the angle α and, accordingly, the position of the electrical axis of the heart. The angle α is considered positive if it is located below the horizontal line, and negative if it is located above. This angle can be determined by geometric construction in the Einthoven triangle, knowing the size of the teeth of the complex QRS in two standard leads. Nevertheless, in practice, special tables are used to determine the angle α (they determine the algebraic sum of the teeth of the complex QRS in standard leads I and II, and then the angle α is found in the table). There are five options for the location of the axis of the heart: normal, vertical position (intermediate between the normal position and rightogram), deviation to the right (rightogram), horizontal (intermediate between the normal position and leftogram), deviation to the left (leftogram).
PApproximate assessment of the position of the electrical axis of the heart. To memorize the differences between a right-gram and a left-gram, students
you use a witty school trick, which is as follows. When examining their palms, the thumb and forefinger are bent, and the remaining middle, ring and little fingers are identified with the height of the tooth R."Read" from left to right, like a regular string. Left hand - levogram: prong R it is maximal in standard lead I (the first highest finger is the middle one), decreases in lead II (ring finger), and minimal in lead III (little finger). The right hand is a right-gram, where the situation is reversed: prong R increases from lead I to III (as well as the height of the fingers: little finger, ring finger, middle finger).
Causes of deviation of the electrical axis of the heart. The position of the electrical axis of the heart depends on extracardiac factors.
In people with a high standing diaphragm and / or a hypersthenic constitution, the EOS takes a horizontal position or even a levogram appears.
In tall, thin people with a low diaphragm, the EOS is normally located more vertically, sometimes up to a rightogram.
PUMPING FUNCTION OF THE HEART
Cardiac cycle
Cardiac cycle- this is a sequence of mechanical contractions of the heart during one contraction. The cardiac cycle lasts from the beginning of one contraction to the beginning of the next and begins in the sinoatrial node with the generation of AP. The electrical impulse causes the excitation of the myocardium and its contraction: the excitation sequentially covers both atria and causes atrial systole. Further, the excitation through the AV connection (after the AV delay) spreads to the ventricles, causing the systole of the latter, an increase in pressure in them and the expulsion of blood into the aorta and pulmonary artery. After the ejection of blood, the myocardium of the ventricles relaxes, the pressure in their cavities drops, and the heart prepares for the next contraction. Sequential phases of the cardiac cycle are shown in Fig. 23-9, and a summary of the various events of the cycle - in fig. 23-10 (the phases of the cardiac cycle are indicated by Latin letters from A to G).
Rice. 23-9. Cardiac cycle. Scheme. A - atrial systole; B - isovolemic contraction; C - fast ejection; D - slow expulsion; E - isovolemic relaxation; F - fast filling; G - slow filling.
Atrial systole (A, duration 0.1 s). The pacemaker cells of the sinus node depolarize, and excitation spreads through the atrial myocardium. A wave is registered on the ECGP(See Figure 23-10, bottom of figure). Atrial contraction raises pressure and causes additional (besides gravity) blood flow into the ventricle, slightly increasing end-diastolic pressure in the ventricle. The mitral valve is open, the aortic valve is closed. Normally, 75% of the blood from the veins flows through the atria directly into the ventricles by gravity, before the atrial contraction. Atrial contraction adds 25% of the blood volume as the ventricles fill.
Ventricular systole (B-D duration 0.33 s). The excitation wave passes through the AV junction, His bundle, Purkinje fibers and reaches the myocardial cells. Depolarization of the ventricle is expressed by the complexQRSon the ECG. The onset of ventricular contraction is accompanied by an increase in intraventricular pressure, closure of the atrioventricular valves, and the appearance of a first heart sound.
Rice. 23-10. Summary characteristic of the heart cycle . A - atrial systole; B - isovolemic contraction; C - fast ejection; D - slow expulsion; E - isovolemic relaxation; F - fast filling; G - slow filling.
Period of isovolemic (isometric) contraction (B).
Immediately after the start of contraction of the ventricle, the pressure in it rises sharply, but there are no changes in the intraventricular volume, since all valves are firmly closed, and blood, like any liquid, is incompressible. It takes 0.02-0.03 s for pressure to develop in the ventricle on the semilunar valves of the aorta and pulmonary artery, sufficient to overcome their resistance and opening. Therefore, during this period, the ventricles contract, but the expulsion of blood does not occur. The term "isovolemic (isometric) period" means that there is tension in the muscle, but there is no shortening of the muscle fibers. This period coincides with the minimum systemic
pressure, called diastolic blood pressure for the systemic circulation. Φ Period of exile (C, D). As soon as the pressure in the left ventricle becomes higher than 80 mm Hg. (for the right ventricle - above 8 mm Hg), the semilunar valves open. Blood immediately begins to leave the ventricles: 70% of the blood is ejected from the ventricles in the first third of the ejection period, and the remaining 30% in the next two thirds. Therefore, the first third is called the fast ejection period (C), and the remaining two thirds is called the slow ejection period (D). Systolic blood pressure (maximum pressure) serves as the dividing point between the period of fast and slow ejection. Peak BP follows peak blood flow from the heart.
Φ end of systole coincides with the occurrence of the second heart sound. The contractile force of the muscle decreases very quickly. There is a reverse flow of blood in the direction of the semilunar valves, closing them. The rapid drop in pressure in the cavity of the ventricles and the closing of the valves contributes to the vibration of their strained valves, which create the second heart sound.
Ventricular diastole (E-G) has a duration of 0.47 s. During this period, an isoelectric line is recorded on the ECG until the beginning of the next complex PQRST.
Φ Period of isovolemic (isometric) relaxation (E). During this period, all valves are closed, the volume of the ventricles is not changed. The pressure drops almost as fast as it increased during the period of isovolemic contraction. As blood continues to flow into the atria from the venous system, and ventricular pressure approaches the diastolic level, atrial pressure reaches its maximum. Φ Filling period (F, G). Rapid filling period (F) is the time during which the ventricles rapidly fill with blood. The pressure in the ventricles is less than in the atria, the atrioventricular valves are open, blood from the atria enters the ventricles, and the volume of the ventricles begins to increase. As the ventricles fill, the compliance of the myocardium of their walls decreases and
the filling rate decreases (slow filling period, G).
Volumes
During diastole, the volume of each ventricle increases to an average of 110-120 ml. This volume is known as end-diastolic. After ventricular systole, the blood volume decreases by about 70 ml - the so-called stroke volume of the heart. Remaining after completion of ventricular systole end systolic volume is 40-50 ml.
Φ If the heart contracts more than usual, then the end-systolic volume decreases by 10-20 ml. When a large amount of blood enters the heart during diastole, the end-diastolic volume of the ventricles can increase up to 150-180 ml. The combined increase in end-diastolic volume and decrease in end-systolic volume can double the stroke volume of the heart compared to the norm.
Diastolic and systolic pressure
The mechanics of the left ventricle is determined by diastolic and systolic pressure in its cavity.
diastolic pressure(pressure in the cavity of the left ventricle during diastole) is created by a progressively increasing amount of blood; The pressure just before systole is called end-diastolic. Until the volume of blood in the noncontracting ventricle exceeds 120 ml, the diastolic pressure remains practically unchanged, and at this volume the blood freely enters the ventricle from the atrium. After 120 ml, diastolic pressure in the ventricle rises rapidly, in part because the fibrous tissue of the wall of the heart and pericardium (and partly the myocardium) have exhausted their extensibility.
systolic pressure. During ventricular contraction, systolic pressure increases even under low volume conditions, but peaks at a ventricular volume of 150-170 ml. If the volume increases even more, then the systolic pressure drops, because the actin and myosin filaments of the muscle fibers of the myocardium are stretched too much. Maximum systolic
pressure for a normal left ventricle is 250-300 mm Hg, but it varies depending on the strength of the heart muscle and the degree of stimulation of the cardiac nerves. In the right ventricle, the maximum systolic pressure is normally 60-80 mm Hg.
for a contracting heart, the value of the end-diastolic pressure created by the filling of the ventricle. beating heart - pressure in the artery leaving the ventricle.Φ Under normal conditions, an increase in preload causes an increase in cardiac output according to the Frank-Starling law (the force of contraction of a cardiomyocyte is proportional to the amount of its stretching). An increase in afterload initially reduces stroke volume and cardiac output, but then the blood remaining in the ventricles after weakened heart contractions accumulates, stretches the myocardium and, also according to the Frank-Starling law, increases stroke volume and cardiac output.
Work done by the heart
Stroke volume- the amount of blood expelled by the heart with each contraction. Striking performance of the heart - the amount of energy of each contraction, converted by the heart into work to promote blood in the arteries. The value of shock performance (SP) is calculated by multiplying the stroke volume (SV) by blood pressure.
UP = UO χ HELL.
Φ The higher the blood pressure or SV, the greater the work performed by the heart. The impact performance also depends on the preload. Increasing preload (end-diastolic volume) improves impact performance.
Cardiac output(SV; minute volume) is equal to the product of stroke volume and the frequency of contractions (HR) per minute.
SV = UO χ heart rate.
Minute performance of the heart(MPS) - the total amount of energy converted into work in one minute
you. It is equal to percussion performance multiplied by the number of contractions per minute.
MPS = AP χ HR.
Control of the pumping function of the heart
At rest, the heart pumps from 4 to 6 liters of blood per minute, per day - up to 8,000-10,000 liters of blood. Hard work is accompanied by a 4-7-fold increase in the pumped volume of blood. The basis of control over the pumping function of the heart is: 1) its own cardiac regulatory mechanism, which reacts in response to changes in the volume of blood flowing to the heart (Frank-Starling law), and 2) control of the frequency and strength of the heart by the autonomic nervous system.
Heterometric self-regulation (Frank Starling mechanism)
The amount of blood that the heart pumps every minute depends almost entirely on the flow of blood into the heart from the veins, denoted by the term "venous return". The inherent ability of the heart to adapt to changing volumes of incoming blood is called the Frank-Starling mechanism (law): the more the heart muscle is stretched by the incoming blood, the greater the force of contraction and the more blood enters the arterial system. Thus, the presence of a self-regulatory mechanism in the heart, determined by changes in the length of myocardial muscle fibers, allows us to speak of heterometric self-regulation of the heart.
In the experiment, the influence of the changing value of venous return on the pumping function of the ventricles is demonstrated on the so-called cardiopulmonary preparation (Fig. 23-11, A).
The molecular mechanism of the Frank-Starling effect is that the stretching of myocardial fibers creates optimal conditions for the interaction of myosin and actin filaments, which makes it possible to generate contractions of greater force.
Factors Regulating end-diastolic volume under physiological conditions.
Rice. 23-11. Frank-Starling mechanism . A - scheme of the experiment (preparation "heart-lungs"). 1 - resistance control, 2 - compression chamber, 3 - reservoir, 4 - ventricular volume; B - inotropic effect.
Φ Stretching of cardiomyocytes increases due to an increase in: Φ the strength of atrial contractions; Φ total blood volume;
Φ venous tone (also increases venous return to the heart);
Φ pumping function of skeletal muscles (to move blood through the veins - as a result, venous return increases; the pumping function of skeletal muscles always increases during muscular work);
Φ negative intrathoracic pressure (venous return also increases).
Φ Stretching of cardiomyocytes decreases due to:
Φ vertical position of the body (due to a decrease in venous return);
Φ increase in intrapericardial pressure;
Φ decreased compliance of the walls of the ventricles.
Influence of the sympathetic and vagus nerves on the pumping function of the heart
The efficiency of the pumping function of the heart is controlled by impulses from the sympathetic and vagus nerves.
sympathetic nerves. Excitation of the sympathetic nervous system can increase the heart rate from 70 per minute to 200 and even up to 250. Sympathetic stimulation increases the force of contractions of the heart, thereby increasing the volume and pressure of the pumped blood. Sympathetic stimulation can increase the performance of the heart by 2-3 times in addition to the increase in cardiac output caused by the Frank-Starling effect (Fig. 23-11, B). Inhibition of the sympathetic nervous system can be used to decrease the pumping ability of the heart. Normally, the sympathetic nerves of the heart are constantly tonically discharged, maintaining a higher (30% higher) level of cardiac performance. Therefore, if the sympathetic activity of the heart is suppressed, then, accordingly, the frequency and strength of heart contractions will decrease, as a result of which the level of pumping function will decrease by at least 30% compared to the norm.
Nervus vagus. Strong excitation of the vagus nerve can completely stop the heart for a few seconds, but then the heart usually "escaps" from the influence of the vagus nerve and continues to contract more slowly - 40% less than normal. Vagus nerve stimulation can reduce the force of heart contractions by 20-30%. The fibers of the vagus nerve are distributed mainly in the atria, and there are few of them in the ventricles, the work of which determines the strength of the contractions of the heart. This explains the fact that the excitation of the vagus nerve has more effect on the decrease in heart rate than on the decrease in the force of contractions of the heart. However, a noticeable decrease in heart rate, together with some weakening of the strength of contractions, can reduce the performance of the heart by up to 50% or more, especially when it works with a heavy load.
SYSTEMIC CIRCULATION
Blood vessels are a closed system in which blood continuously circulates from the heart to the tissues and back to the heart.
systemic circulation, or systemic circulation, includes all vessels that receive blood from the left ventricle and end in the right atrium. The vessels located between the right ventricle and the left atrium are pulmonary circulation, or small circle of blood circulation.
Structural-functional classification
Depending on the structure of the wall of the blood vessel in the vascular system, there are arteries, arterioles, capillaries, venules and veins, intervascular anastomoses, microvasculature and hematic barriers(eg, hematoencephalic). Functionally, vessels are divided into shock-absorbing(arteries) resistive(terminal arteries and arterioles), precapillary sphincters(terminal section of precatillary arterioles), exchange(capillaries and venules) capacitive(veins) shunting(arteriovenous anastomoses).
Physiological parameters of blood flow
Below are the main physiological parameters needed to characterize blood flow.
Systolic pressure is the maximum pressure reached in the arterial system during systole. Normal systolic pressure is on average 120 mm Hg.
diastolic pressure- the minimum pressure that occurs during diastole averages 80 mm Hg.
pulse pressure. The difference between systolic and diastolic pressure is called pulse pressure.
mean arterial pressure(SBP) is tentatively estimated by the formula:
SBP \u003d Systolic BP + 2 (diastolic BP): 3.
Φ Average blood pressure in the aorta (90-100 mm Hg) gradually decreases as the arteries branch. In the terminal arteries and arterioles, the pressure drops sharply (up to 35 mm Hg on average), and then slowly decreases to 10 mm Hg. in large veins (Fig. 23-12, A).
Cross-sectional area. The diameter of the aorta of an adult is 2 cm, the cross-sectional area is about 3 cm 2. Towards the periphery, the cross-sectional area of arterial vessels slowly but progressively
Rice. 23-12. Values of blood pressure (A) and linear blood flow velocity (B) in different segments of the vascular system .
increases. At the level of arterioles, the cross-sectional area is about 800 cm 2, and at the level of capillaries and veins - 3500 cm 2. The surface area of the vessels is significantly reduced when the venous vessels join to form a vena cava with a cross-sectional area of 7 cm 2 .
Linear blood flow velocity inversely proportional to the cross-sectional area of the vascular bed. Therefore, the average speed of blood movement (Fig. 23-12, B) is higher in the aorta (30 cm/s), gradually decreases in small arteries and is minimal in capillaries (0.026 cm/s), the total cross section of which is 1000 times greater than in the aorta. The mean flow velocity again increases in the veins and becomes relatively high in the vena cava (14 cm/s), but not as high as in the aorta.
Volumetric blood flow velocity(usually expressed in milliliters per minute or liters per minute). The total blood flow in an adult at rest is about 5000 ml / min. This is the amount of blood pumped out by the heart every minute, which is why it is also called cardiac output.
Circulation rate(blood circulation rate) can be measured in practice: from the moment when the preparation of bile salts is injected into the cubital vein, until a feeling of bitterness appears on the tongue (Fig. 23-13, A). Normally, the speed of blood circulation is 15 s.
vascular capacity. The size of the vascular segments determines their vascular capacity. Arteries contain about 10% of the total circulating blood (CBV), capillaries about 5%, venules and small veins about 54%, and large veins about 21%. The chambers of the heart hold the remaining 10%. Venules and small veins have a large capacity, making them an efficient reservoir capable of storing large volumes of blood.
Methods for measuring blood flow
Electromagnetic flowmetry is based on the principle of voltage generation in a conductor moving through a magnetic field, and the proportionality of the magnitude of the voltage to the speed of movement. Blood is a conductor, a magnet is located around the vessel, and the voltage, proportional to the volume of blood flow, is measured by electrodes located on the surface of the vessel.
Doppler uses the principle of the passage of ultrasonic waves through the vessel and the reflection of waves from erythrocytes and leukocytes. The frequency of the reflected waves changes - increases in proportion to the speed of the blood flow.
Rice. 23-13. Determination of blood flow time (A) and plethysmography (B). 1 -
marker injection site, 2 - end point (tongue), 3 - volume recorder, 4 - water, 5 - rubber sleeve.
Measurement of cardiac output carried out by the direct Fick method and by the indicator dilution method. The Fick method is based on an indirect calculation of the minute volume of blood circulation by arteriovenous O 2 difference and determination of the volume of oxygen consumed by a person per minute. The indicator dilution method (radioisotope method, thermodilution method) uses the introduction of indicators into the venous system and then sampling from the arterial system.
Plethysmography. Information about the blood flow in the limbs is obtained using plethysmography (Fig. 23-13, B).
Φ The forearm is placed in a water-filled chamber connected to a device that records fluctuations in fluid volume. Changes in limb volume, reflecting changes in the amount of blood and interstitial fluid, shift fluid levels and are recorded with a plethysmograph. If the venous outflow of the limb is turned off, then the fluctuations in the volume of the limb are a function of the arterial blood flow of the limb (occlusive venous plethysmography).
Physics of fluid movement in blood vessels
The principles and equations used to describe the motions of ideal fluids in tubes are often applied to explain
behavior of blood in blood vessels. However, blood vessels are not rigid tubes, and blood is not an ideal liquid, but a two-phase system (plasma and cells), so the characteristics of blood circulation deviate (sometimes quite noticeably) from theoretically calculated ones.
laminar flow. The movement of blood in blood vessels can be represented as laminar (i.e. streamlined, with parallel flow of layers). The layer adjacent to the vascular wall is practically immobile. The next layer moves at a low speed, in the layers closer to the center of the vessel the speed of movement increases, and in the center of the flow it is maximum. The laminar motion is maintained until it reaches some critical velocity. Above the critical velocity, laminar flow becomes turbulent (vortex). Laminar motion is silent, turbulent motion generates sounds that, at the proper intensity, are audible with a stethophonendoscope.
turbulent flow. The occurrence of turbulence depends on the flow rate, vessel diameter and blood viscosity. The narrowing of the artery increases the speed of blood flow through the narrowing, creating turbulence and sounds below the narrowing. Examples of noises perceived over the wall of an artery are noises over an area of narrowing of an artery caused by an atherosclerotic plaque, and Korotkoff's tones when measuring blood pressure. With anemia, turbulence is observed in the ascending aorta, caused by a decrease in blood viscosity, hence the systolic murmur.
Poiseuille formula. The relationship between fluid flow in a long narrow tube, fluid viscosity, tube radius and resistance is determined by the Poiseuille formula:
where R is the resistance of the tube,η is the viscosity of the flowing liquid, L is the length of the tube, r is the radius of the tube. Φ Since the resistance is inversely proportional to the fourth power of the radius, the blood flow and resistance in the body change significantly depending on small changes in the caliber of the vessels. For example, blood flow through
courts doubles if their radius increases by only 19%. When the radius is doubled, the resistance is reduced by 6% of the original level. These calculations make it possible to understand why organ blood flow is so effectively regulated by minimal changes in the lumen of arterioles and why variations in arteriole diameter have such a strong effect on systemic BP.
Viscosity and resistance. The resistance to blood flow is determined not only by the radius of the blood vessels (vascular resistance), but also by the viscosity of the blood. The viscosity of plasma is about 1.8 times that of water. The viscosity of whole blood is 3-4 times higher than the viscosity of water. Therefore, blood viscosity is largely dependent on hematocrit, i.e. of the percentage of erythrocytes in the blood. In large vessels, an increase in hematocrit causes the expected increase in viscosity. However, in vessels with a diameter of less than 100 µm, i.e. in arterioles, capillaries and venules, the change in viscosity per unit change in hematocrit is much less than in large vessels.
Φ Changes in hematocrit affect the peripheral resistance, mainly of large vessels. Severe polycythemia (an increase in the number of red blood cells of varying maturity) increases peripheral resistance, increasing the work of the heart. In anemia, peripheral resistance is reduced, partly due to a decrease in viscosity.
Φ In the vessels, erythrocytes tend to settle down in the center of the current blood flow. Consequently, blood with a low hematocrit moves along the walls of the vessels. Branches extending from large vessels at right angles may receive a disproportionately smaller number of red blood cells. This phenomenon, called plasma slippage, may explain why capillary blood hematocrit is consistently 25% lower than in the rest of the body.
Critical pressure of closure of the vessel lumen. In rigid tubes, the relationship between pressure and flow of a homogeneous liquid is linear; in vessels, there is no such relationship. If the pressure in the small vessels decreases, then the blood flow stops before the pressure drops to zero. it
concerns primarily the pressure that promotes red blood cells through capillaries, the diameter of which is smaller than the size of the red blood cells. The tissues surrounding the vessels exert a constant slight pressure on them. If the intravascular pressure falls below the tissue pressure, the vessels collapse. The pressure at which blood flow stops is called the critical closure pressure.
Extensibility and compliance of blood vessels. All vessels are distensible. This property plays an important role in blood circulation. Thus, the extensibility of the arteries contributes to the formation of a continuous blood flow (perfusion) through the system of small vessels in the tissues. Of all the vessels, thin-walled veins are the most pliable. A slight increase in venous pressure causes the deposition of a significant amount of blood, providing a capacitive (accumulating) function of the venous system. Vascular compliance is defined as the increase in volume in response to an increase in pressure, expressed in millimeters of mercury. If the pressure is 1 mm Hg. causes an increase in this volume by 1 ml in a blood vessel containing 10 ml of blood, then the distensibility will be 0.1 per 1 mm Hg. (10% per 1 mmHg).
BLOOD FLOW IN ARTERIES AND ARTERIOLES
Pulse
Pulse - rhythmic fluctuations in the wall of the arteries, caused by an increase in pressure in the arterial system at the time of systole. During each systole of the left ventricle, a new portion of blood enters the aorta. This causes stretching of the proximal aortic wall, as the inertia of the blood prevents the immediate movement of blood towards the periphery. The increase in pressure in the aorta quickly overcomes the inertia of the blood column, and the front of the pressure wave, stretching the wall of the aorta, spreads farther and farther along the arteries. This process is a pulse wave - the spread of pulse pressure through the arteries. The compliance of the arterial wall smooths out pulse fluctuations, constantly decreasing their amplitude towards the capillaries (Fig. 23-14, B).
Sphygmogram(Fig. 23-14, A). On the pulse curve (sphygmogram), the aorta distinguishes the rise (anacrota), which arises
Rice. 23-14. arterial pulse. A - sphygmogram. ab - anacrota, vg - systolic plateau, de - catacrot, d - notch (notch); B - the movement of the pulse wave in the direction of small vessels. There is a damping of the pulse pressure.
under the influence of blood ejected from the left ventricle at the time of systole, and the decline (catacrotic) occurring at the time of diastole. A notch on a catacrot occurs due to the reverse movement of blood towards the heart at the moment when the pressure in the ventricle becomes lower than the pressure in the aorta and the blood rushes back along the pressure gradient towards the ventricle. Under the influence of the reverse flow of blood, the semilunar valves close, a wave of blood is reflected from the valves and creates a small secondary wave of pressure increase (dicrotic rise).
Pulse wave speed: aorta - 4-6 m/s, muscular arteries - 8-12 m/s, small arteries and arterioles - 15-35 m/s.
Pulse pressure- the difference between systolic and diastolic pressure - depends on the stroke volume of the heart and compliance of the arterial system. The greater the stroke volume and the more blood enters the arterial system during each heartbeat, the greater the pulse pressure. The lower the compliance of the arterial wall, the greater the pulse pressure.
Decay of pulse pressure. The progressive decrease in pulsations in the peripheral vessels is called the attenuation of pulse pressure. The reasons for the weakening of pulse pressure are resistance to blood flow and vascular compliance. Resistance weakens the pulsation due to the fact that a certain amount of blood must move ahead of the front of the pulse wave in order to stretch the next segment of the vessel. The more resistance, the more difficulties arise. Compliance causes the pulse wave to decay because more blood must pass in the more compliant vessels ahead of the pulse wave front to cause an increase in pressure. In this way, the degree of attenuation of the pulse wave is directly proportional to the total peripheral resistance.
Blood pressure measurement
direct method.In some clinical situations, blood pressure is measured by inserting needles with pressure sensors into the artery. This direct way definitions showed that blood pressure constantly fluctuates within the boundaries of a certain constant average level. On the records of the blood pressure curve, three types of oscillations (waves) are observed - pulse(coinciding with the contractions of the heart), respiratory(coinciding with respiratory movements) and intermittent slow(reflect fluctuations in the tone of the vasomotor center).
Indirect method.In practice, systolic and diastolic blood pressure is measured indirectly using the Riva-Rocci auscultatory method with the determination of Korotkoff sounds (Fig. 23-15).
Systolic BP. A hollow rubber chamber (located inside a cuff that can be fixed around the lower half of the shoulder), connected by a tube system with a rubber bulb and a pressure gauge, is placed on the shoulder. The stethoscope is placed over the anterior cubital artery in the cubital fossa. Inflating the cuff compresses the upper arm, and the reading on the pressure gauge registers the amount of pressure. The cuff placed on the upper arm is inflated until the pressure in it exceeds the systolic level, and then the air is slowly released from it. As soon as the pressure in the cuff is less than systolic, blood begins to break through the artery squeezed by the cuff - at the time of peak systole -
Rice. 23-15. Blood pressure measurement .
In the anterior ulnar artery, thumping tones begin to be heard, synchronous with heart beats. At this point, the pressure level of the manometer associated with the cuff indicates the value of systolic blood pressure.
Diastolic BP. As the pressure in the cuff decreases, the nature of the tones changes: they become less knocking, more rhythmic and muffled. Finally, when the pressure in the cuff reaches the level of diastolic BP and the artery is no longer compressed during diastole, the tones disappear. The moment of their complete disappearance indicates that the pressure in the cuff corresponds to diastolic blood pressure.
Tones of Korotkov. The occurrence of Korotkoff's tones is due to the movement of a jet of blood through a partially compressed section of the artery. The jet causes turbulence in the vessel below the cuff, which causes vibrating sounds heard through the stethophonendoscope.
Error. With the auscultatory method for determining systolic and diastolic blood pressure, there may be discrepancies from the values obtained by direct measurement of pressure (up to 10%). Automatic electronic blood pressure monitors, as a rule, underestimate the values of both systolic and diastolic
go blood pressure by 10%.
Factors affecting blood pressure values
Φ Age. In healthy people, the value of systolic blood pressure increases from 115 mm Hg. in 15-year-olds up to 140 mm Hg. in 65-year-old people, i.e. an increase in blood pressure occurs at a rate of about 0.5 mm Hg. in year. Diastolic blood pressure, respectively, increases from 70 mm Hg. up to 90 mm Hg, i.e. at a rate of about 0.4 mm Hg. in year.
Φ Floor. In women, systolic and diastolic BP are lower between 40 and 50 years of age, but higher at 50 years of age and older.
Φ Body mass. Systolic and diastolic blood pressure directly correlates with human body weight: the greater the body weight, the higher the blood pressure.
Φ Body position. When a person stands up, gravity alters venous return, decreasing cardiac output and blood pressure. Compensatory increases in heart rate, causing an increase in systolic and diastolic blood pressure and total peripheral resistance.
Φ Muscular activity. BP rises during work. Systolic blood pressure increases due to the fact that the contraction of the heart increases. Diastolic blood pressure initially decreases due to vasodilatation of the working muscles, and then the intensive work of the heart leads to an increase in diastolic blood pressure.
VENOUS CIRCULATION
The movement of blood through the veins is carried out as a result of the pumping function of the heart. Venous blood flow also increases during each breath due to negative intrapleural pressure (suction action) and due to contractions of the skeletal muscles of the extremities (primarily the legs) that compress the veins.
Venous pressure
Central venous pressure - pressure in large veins at the place of their confluence with the right atrium - averages about 4.6 mm Hg. Central venous pressure is an important clinical characteristic necessary to assess the pumping function of the heart. At the same time, it is crucial pressure in the right atrium(about 0 mm Hg) - balance regulator between
the ability of the heart to pump blood from the right atrium and right ventricle to the lungs and the ability of blood to flow from peripheral veins to the right atrium (venous return). If the heart works intensively, then the pressure in the right ventricle decreases. On the contrary, the weakening of the work of the heart increases the pressure in the right atrium. Any influence that accelerates the flow of blood into the right atrium from the peripheral veins increases the pressure in the right atrium.
Peripheral venous pressure. The pressure in the venules is 12-18 mm Hg. It decreases in large veins to about 5.5 mm Hg, since in large veins the resistance to blood flow is reduced or practically absent. Moreover, in the thoracic and abdominal cavities, the veins are compressed by the surrounding structures.
Influence of intra-abdominal pressure. In the abdominal cavity in the supine position, the pressure is 6 mm Hg. It can rise by 15-30 mm Hg. during pregnancy, a large tumor, or the appearance of excess fluid in the abdominal cavity (ascites). In these cases, the pressure in the veins of the lower extremities becomes higher than intra-abdominal.
Gravity and venous pressure. On the surface of the body, the pressure of the liquid medium is equal to atmospheric pressure. The pressure in the body increases as you move deeper from the surface of the body. This pressure is the result of the action of the gravity of water, so it is called gravitational (hydrostatic) pressure. The influence of gravity on the vascular system is due to the mass of blood in the vessels (Fig. 23-16, A).
Muscle pump and vein valves. The veins of the lower extremities are surrounded by skeletal muscles, the contractions of which compress the veins. The pulsation of neighboring arteries also exerts a compressive effect on the veins. Since the venous valves prevent backflow, the blood moves towards the heart. As shown in fig. 23-16, B, the valves of the veins are oriented to move blood towards the heart.
Suction action of heart contractions. Pressure changes in the right atrium are transmitted to large veins. Right atrial pressure drops sharply during the ejection phase of ventricular systole because the atrioventricular valves retract into the ventricular cavity,
Rice. 23-16. Venous blood flow. A - the effect of gravity on venous pressure in a vertical position; B - venous (muscular) pump and the role of venous valves.
increasing atrial capacity. There is an absorption of blood into the atrium from large veins, and in the vicinity of the heart, the venous blood flow becomes pulsating.
Depositing function of veins
More than 60% of the volume of circulating blood is in the veins due to their high compliance. With a large blood loss and a drop in blood pressure, reflexes arise from the receptors of the carotid sinuses and other receptor vascular areas, activating the sympathetic nerves of the veins and causing their narrowing. This leads to the restoration of many reactions of the circulatory system, disturbed by blood loss. Indeed, even after the loss of 20% of the total blood volume, the circulatory system restores its
normal functions due to the release of reserve blood volumes from the veins. In general, the specialized areas of blood circulation (the so-called blood depots) include:
The liver, whose sinuses can release several hundred milliliters of blood for circulation;
The spleen, capable of releasing up to 1000 ml of blood for circulation;
Large veins of the abdominal cavity, accumulating more than 300 ml of blood;
Subcutaneous venous plexus, capable of depositing several hundred milliliters of blood.
TRANSPORT OF OXYGEN AND CARBON DIOXIDE
Blood gas transport is discussed in Chapter 24.
MICROCIRCULATION
The functioning of the cardiovascular system maintains the homeostatic environment of the body. The functions of the heart and peripheral vessels are coordinated to transport blood to the capillary network, where the exchange between blood and tissue fluid takes place. The transfer of water and substances through the wall of blood vessels is carried out by diffusion, pinocytosis and filtration. These processes take place in a complex of vessels known as microcirculatory units. Microcirculatory unit consists of successive vessels. These are terminal (terminal) arterioles - metarterioles - precapillary sphincters - capillaries - venules. In addition, arteriovenous anastomoses are included in the composition of microcirculatory units.
Organization and functional characteristics
Functionally, the vessels of the microvasculature are divided into resistive, exchange, shunt and capacitive.
Resistive vessels
Φ Resistive precapillary vessels - small arteries, terminal arterioles, metarterioles and precapillary sphincters. Precapillary sphincters regulate the functions of capillaries, being responsible for:
Φ number of open capillaries;
Φ distribution of capillary blood flow; Φ speed of capillary blood flow; Φ effective capillary surface; Φ average distance for diffusion.
Φ Resistive post-capillary vessels - small veins and venules containing MMC in their wall. Therefore, despite small changes in resistance, they have a noticeable effect on capillary pressure. The ratio of precapillary and postcapillary resistance determines the magnitude of capillary hydrostatic pressure.
exchange vessels. Efficient exchange between the blood and the extravascular environment occurs through the wall of capillaries and venules. The maximum intensity of the exchange is observed at the venous end of the exchange vessels, because they are more permeable to water and solutions.
Shunt vessels- arteriovenous anastomoses and main capillaries. In the skin, shunt vessels are involved in the regulation of body temperature.
capacitive vessels- small veins with a high degree of compliance.
Blood flow speed. In arterioles, the blood flow velocity is 4-5 mm/s, in veins - 2-3 mm/s. Erythrocytes move through the capillaries one by one, changing their shape due to the narrow lumen of the vessels. The speed of movement of erythrocytes is about 1 mm / s.
Intermittent blood flow. The blood flow in a separate capillary depends primarily on the state of the precapillary sphincters and metarterioles, which periodically contract and relax. The period of contraction or relaxation can take from 30 seconds to several minutes. Such phase contractions are the result of the response of SMCs of vessels to local chemical, myogenic and neurogenic influences. The most important factor responsible for the degree of opening or closing of metarterioles and capillaries is the oxygen concentration in the tissues. If the oxygen content of the tissue decreases, the frequency of intermittent periods of blood flow increases.
The rate and nature of transcapillary exchange depend on the nature of the transported molecules (polar or non-polar
substances, see Ch. 2), the presence of pores and endothelial fenestres in the capillary wall, the basement membrane of the endothelium, as well as the possibility of pinocytosis through the capillary wall.
Transcapillary fluid movement is determined by the relationship, first described by Starling, between the capillary and interstitial hydrostatic and oncotic forces acting through the capillary wall. This movement can be described by the following formula:
V=K fx[(P 1 -P 2 )-(Pz-P 4)], where V is the volume of liquid passing through the capillary wall in 1 min; K f - filtration coefficient; P 1 - hydrostatic pressure in the capillary; P 2 - hydrostatic pressure in the interstitial fluid; P 3 - oncotic pressure in plasma; P 4 - oncotic pressure in the interstitial fluid. Capillary filtration coefficient (K f) - the volume of liquid filtered in 1 min 100 g of tissue with a change in pressure in the capillary of 1 mm Hg. K f reflects the state of hydraulic conductivity and the surface of the capillary wall.
Capillary hydrostatic pressure- the main factor controlling the transcapillary fluid movement - is determined by blood pressure, peripheral venous pressure, precapillary and postcapillary resistance. At the arterial end of the capillary, the hydrostatic pressure is 30-40 mm Hg, and at the venous end it is 10-15 mm Hg. An increase in arterial, peripheral venous pressure and post-capillary resistance or a decrease in pre-capillary resistance will increase capillary hydrostatic pressure.
Plasma oncotic pressure determined by albumins and globulins, as well as the osmotic pressure of electrolytes. Oncotic pressure throughout the capillary remains relatively constant, amounting to 25 mm Hg.
interstitial fluid formed by filtration from capillaries. The composition of the fluid is similar to that of blood plasma, except for the lower protein content. At short distances between capillaries and tissue cells, diffusion provides rapid transport through the interstitium, not only
water molecules, but also electrolytes, nutrients with a small molecular weight, products of cellular metabolism, oxygen, carbon dioxide and other compounds.
Hydrostatic pressure of the interstitial fluid ranges from -8 to + 1 mm Hg. It depends on the volume of fluid and the compliance of the interstitial space (the ability to accumulate fluid without a significant increase in pressure). The volume of interstitial fluid is 15-20% of the total body weight. Fluctuations in this volume depend on the ratio between inflow (filtration from capillaries) and outflow (lymph outflow). Compliance of the interstitial space is determined by the presence of collagen and the degree of hydration.
Oncotic pressure of the interstitial fluid determined by the amount of protein penetrating through the capillary wall into the interstitial space. The total amount of protein in 12 liters of interstitial body fluid is slightly greater than in the plasma itself. But since the volume of interstitial fluid is 4 times the volume of plasma, the protein concentration in the interstitial fluid is 40% of the protein content in plasma. On average, the colloid osmotic pressure in the interstitial fluid is about 8 mm Hg.
The movement of fluid through the capillary wall
The average capillary pressure at the arterial end of the capillaries is 15-25 mm Hg. more than at the venous end. Due to this pressure difference, blood is filtered from the capillary at the arterial end and reabsorbed at the venous end.
Arterial part of the capillary
Φ Promotion of fluid at the arterial end of the capillary is determined by the colloid osmotic pressure of the plasma (28 mm Hg, promotes the movement of fluid into the capillary) and the sum of forces (41 mm Hg) that move the fluid out of the capillary (pressure at the arterial end of the capillary - 30 mm Hg, negative interstitial pressure of the free fluid - 3 mm Hg, colloid osmotic pressure of the interstitial fluid - 8 mm Hg). The pressure difference between the outside and inside of the capillary is 13 mm Hg. These 13 mm Hg.
constitute filter pressure, causing the transition of 0.5% of the plasma at the arterial end of the capillary into the interstitial space. The venous part of the capillary. In table. 23-1 shows the forces that determine the movement of fluid at the venous end of the capillary.
Table 23-1. Fluid movement at the venous end of a capillary
Φ Thus, the pressure difference between the inside and outside of the capillary is 7 mm Hg. is the reabsorption pressure at the venous end of the capillary. The low pressure at the venous end of the capillary changes the balance of forces in favor of absorption. The reabsorption pressure is significantly lower than the filtration pressure at the arterial end of the capillary. However, venous capillaries are more numerous and more permeable. The reabsorption pressure ensures that 9/10 of the fluid filtered at the arterial end is reabsorbed. The remaining fluid enters the lymphatic vessels.
LYMPHATIC SYSTEM
The lymphatic system is a network of vessels and lymph nodes that return interstitial fluid to the blood (Fig. 23-17, B).
Lymph formation
The volume of fluid returning to the bloodstream through the lymphatic system is 2-3 liters per day. Substances with you
Rice. 23-17. Lymphatic system. A - structure at the level of the microvasculature; B - anatomy of the lymphatic system; B - lymphatic capillary. 1 - blood capillary, 2 - lymphatic capillary, 3 - lymph nodes, 4 - lymph valves, 5 - precapillary arteriole, 6 - muscle fiber, 7 - nerve, 8 - venule, 9 - endothelium, 10 - valves, 11 - supporting filaments ; D - vessels of the microvasculature of the skeletal muscle. With the expansion of the arteriole (a), the lymphatic capillaries adjacent to it are compressed between it and the muscle fibers (above), with the narrowing of the arteriole (b), the lymphatic capillaries, on the contrary, expand (below). In skeletal muscles, blood capillaries are much smaller than lymphatic capillaries.
high molecular weight (especially proteins) cannot be absorbed from tissues in any other way, except for the lymphatic capillaries, which have a special structure.
Lymph composition. Since 2/3 of the lymph comes from the liver, where the protein content exceeds 6 g per 100 ml, and the intestine, with a protein content above 4 g per 100 ml, the protein concentration in the thoracic duct is usually 3-5 g per 100 ml. After ingestion of fatty foods, the content of fats in the lymph of the thoracic duct can increase up to 2%. Through the wall of the lymphatic capillaries, bacteria can enter the lymph, which are destroyed and removed, passing through the lymph nodes.
Entry of interstitial fluid into lymphatic capillaries(Fig. 23-17, C, D). The endothelial cells of the lymphatic capillaries are attached to the surrounding connective tissue by the so-called supporting filaments. At the contact points of endothelial cells, the end of one endothelial cell overlaps the edge of another cell. The overlapping edges of the cells form a kind of valves protruding into the lymphatic capillary. When interstitial fluid pressure rises, these valves control the flow of interstitial fluid into the lumen of the lymphatic capillaries. At the moment of filling the capillary, when the pressure in it exceeds the pressure of the interstitial fluid, the inlet valves close.
Ultrafiltration from lymphatic capillaries. The wall of the lymphatic capillary is a semi-permeable membrane, so some of the water is returned to the interstitial fluid by ultrafiltration. The colloid osmotic pressure of the fluid in the lymphatic capillary and interstitial fluid is the same, but the hydrostatic pressure in the lymphatic capillary exceeds that of the interstitial fluid, which leads to fluid ultrafiltration and lymph concentration. As a result of these processes, the concentration of proteins in the lymph increases by about 3 times.
Compression of the lymphatic capillaries. The movements of muscles and organs cause compression of the lymphatic capillaries. In skeletal muscles, lymphatic capillaries are located in the adventitia of precapillary arterioles (see Fig. 23-17, D). As the arterioles expand, the lymphatic capillaries compress
Xia between them and the muscle fibers, while the inlet valves are closed. When the arterioles constrict, the inlet valves, on the contrary, open, and the interstitial fluid enters the lymphatic capillaries.
Lymph movement
lymphatic capillaries. Lymph flow in the capillaries is minimal if the pressure of the interstitial fluid is negative (for example, less than -6 mmHg). An increase in pressure above 0 mm Hg. increases lymph flow by 20 times. Therefore, any factor that increases the pressure of the interstitial fluid also increases the lymph flow. Factors that increase interstitial pressure include:
Increased permeability of blood capillaries;
Increased colloid osmotic pressure of the interstitial fluid;
Increased pressure in arterial capillaries;
Reducing the colloid osmotic pressure of plasma.
Lymphangions. An increase in interstitial pressure is not enough to provide lymphatic flow against the forces of gravity. Passive mechanisms of lymph outflow: pulsation of the arteries, which affects the movement of lymph in the deep lymphatic vessels, contractions of skeletal muscles, movement of the diaphragm - cannot provide lymph flow in a vertical position of the body. This function is actively provided lymphatic pump. Segments of lymphatic vessels bounded by valves and containing SMCs in the wall (lymphangions), able to shrink automatically. Each lymphangion functions as a separate automatic pump. Filling the lymphangion with lymph causes contraction, and the lymph is pumped through the valves to the next segment, and so on, until the lymph enters the bloodstream. In large lymphatic vessels (for example, in the thoracic duct), the lymphatic pump creates a pressure of 50-100 mmHg.
Thoracic ducts. At rest, up to 100 ml of lymph per hour passes through the thoracic duct, about 20 ml through the right lymphatic duct. Every day, 2-3 liters of lymph enter the bloodstream.
MECHANISMS OF BLOOD FLOW REGULATION
Changes in pO 2 , pCO 2 in the blood, the concentration of H +, lactic acid, pyruvate and a number of other metabolites have local impact on the vessel wall and are recorded by chemoreceptors located in the vessel wall, as well as by baroreceptors that respond to pressure in the vessel lumen. These signals enter the nuclei of the solitary tract of the medulla oblongata. The medulla oblongata performs three important cardiovascular functions: 1) generates tonic excitatory signals to the sympathetic preganglionic fibers of the spinal cord; 2) integrates cardiovascular reflexes; and 3) integrates signals from the hypothalamus, cerebellum, and limbic regions of the cerebral cortex. The responses of the CNS are carried out motor autonomic innervation SMC of the walls of blood vessels and myocardium. In addition, there is a powerful humoral regulator system SMC of the vessel wall (vasoconstrictors and vasodilators) and endothelial permeability. The main regulation parameter is systemic blood pressure.
Local regulatory mechanisms
FROM self-regulation. The ability of tissues and organs to regulate their own blood flow - self-regulation. The vessels of many organs have an intrinsic ability to compensate for moderate changes in perfusion pressure by changing the vascular resistance in such a way that blood flow remains relatively constant. Self-regulatory mechanisms function in the kidneys, mesentery, skeletal muscles, brain, liver, and myocardium. Distinguish between myogenic and metabolic self-regulation.
Φ Myogenic self-regulation. Self-regulation is due in part to the contractile response of SMCs to stretch. This is myogenic self-regulation. As soon as the pressure in the vessel begins to rise, the blood vessels stretch and the MMCs surrounding their wall contract. Φ Metabolic self-regulation. Vasodilators tend to accumulate in working tissues, which plays a role in self-regulation. This is metabolic self-regulation. The decrease in blood flow leads to the accumulation of vasodilators (vasodilators) and the vessels dilate (vasodilatation). When blood flow increases
is poured, these substances are removed, which leads to a situation
maintaining vascular tone. FROM vasodilating effects. The metabolic changes that cause vasodilation in most tissues are a decrease in pO 2 and pH. These changes cause relaxation of arterioles and precapillary sphincters. An increase in pCO 2 and osmolality also relaxes the vessels. The direct vasodilating effect of CO 2 is most pronounced in brain tissues and skin. An increase in temperature has a direct vasodilating effect. The temperature in the tissues rises as a result of increased metabolism, which also contributes to vasodilation. Lactic acid and K+ ions dilate the vessels of the brain and skeletal muscles. Adenosine dilates the vessels of the heart muscle and prevents the release of the vasoconstrictor norepinephrine.
Endothelial regulators
Prostacycline and thromboxane A 2 . Prostacyclin is produced by endothelial cells and promotes vasodilation. Thromboxane A 2 is released from platelets and promotes vasoconstriction.
Endogenous relaxing factor- nitric oxide (NO). En-
vascular prethelial cells under the influence of various substances and/or conditions synthesize the so-called endogenous relaxing factor (nitric oxide - NO). NO activates guanylate cyclase in cells, which is necessary for the synthesis of cGMP, which ultimately has a relaxing effect on the SMC of the vascular wall. Suppression of the function of NO-synthase markedly increases systemic blood pressure. At the same time, the erection of the penis is associated with the release of NO, which causes the expansion and filling of the cavernous bodies with blood.
Endothelins- 21-amino acid peptides - represented by three isoforms. Endothelin-1 is synthesized by endothelial cells (especially the endothelium of veins, coronary arteries and arteries of the brain). It is a powerful vasoconstrictor.
Humoral regulation of blood circulation
Biologically active substances circulating in the blood affect all parts of the cardiovascular system. Humoral vasodilating factors (vasodilators)
kinins, VIP, atrial natriuretic factor (atriopeptin) are worn, and humoral vasoconstrictors include vasopressin, norepinephrine, epinephrine and angiotensin II.
Vasodilators
Kinina. Two vasodilatory peptides (bradykinin and kallidin - lysyl-bradykinin) are formed from kininogen precursor proteins by the action of proteases called kallikreins. Kinins cause:
Φ contraction of the SMC of the internal organs, relaxation of the SMC
blood vessels and lowering blood pressure; Φ increase in capillary permeability; Φ increase in blood flow in the sweat and salivary glands and exo-
crinal part of the pancreas.
Atrial natriuretic factor atriopeptin: Φ increases the glomerular filtration rate;
Φ reduces blood pressure, reducing the sensitivity of SMC vessels to
the action of many vasoconstrictor substances; Φ inhibits the secretion of vasopressin and renin.
Vasoconstrictors
Norepinephrine and adrenaline. Norepinephrine is a powerful vasoconstrictor; adrenaline has a less pronounced vasoconstrictive effect, and in some vessels causes moderate vasodilation (for example, with increased contractile activity of the myocardium, it expands the coronary arteries). Stress or muscle work stimulates the release of norepinephrine from sympathetic nerve endings in the tissues and has an exciting effect on the heart, causing narrowing of the lumen of the veins and arterioles. At the same time, the secretion of norepinephrine and adrenaline into the blood from the adrenal medulla increases. Acting in all areas of the body, these substances have the same vasoconstrictive effect on blood circulation as the activation of the sympathetic nervous system.
Angiotensins. Angiotensin II has a generalized vasoconstrictor effect. Angiotensin II is formed from angiotensin I (weak vasoconstrictor action), which, in turn, is formed from angiotensinogen under the influence of renin.
Vasopressin(antidiuretic hormone, ADH) has a pronounced vasoconstrictive effect. Vasopressin precursors are synthesized in the hypothalamus, transported along the axons to the posterior pituitary gland, and from there enter the bloodstream. Vasopressin also increases water reabsorption in the renal tubules.
NEUROGENIC CIRCULATION CONTROL
The basis of the regulation of the functions of the cardiovascular system is the tonic activity of the neurons of the medulla oblongata, the activity of which changes under the influence of afferent impulses from the sensitive receptors of the system - baro- and chemoreceptors. The vasomotor center of the medulla oblongata constantly interacts with the hypothalamus, cerebellum and cerebral cortex for the coordinated function of the cardiovascular system in such a way that the response to changes in the body is absolutely coordinated and multifaceted.
Vascular afferents
Baroreceptors especially numerous in the aortic arch and in the wall of large veins lying close to the heart. These nerve endings are formed by the terminals of the fibers passing through the vagus nerve.
Specialized sensory structures. The reflex regulation of blood circulation involves the carotid sinus and carotid body (see Fig. 23-18, B, 25-10, A), as well as similar formations of the aortic arch, pulmonary trunk, and right subclavian artery.
Φ carotid sinus located near the bifurcation of the common carotid artery and contains numerous baroreceptors, the impulses from which enter the centers that regulate the activity of the cardiovascular system. The nerve endings of the baroreceptors of the carotid sinus are the terminals of the fibers passing through the sinus nerve (Hering) - a branch of the glossopharyngeal nerve.
Φ carotid body(Fig. 25-10, B) reacts to changes in the chemical composition of the blood and contains glomus cells that form synaptic contacts with the terminals of afferent fibers. Afferent fibers for the carotid
the bodies contain substance P and peptides related to the calcitonin gene. Glomus cells also end with efferent fibers passing through the sinus nerve (Hering) and postganglionic fibers from the superior cervical sympathetic ganglion. The terminals of these fibers contain light (acetylcholine) or granular (catecholamines) synaptic vesicles. The carotid body registers changes in pCO 2 and pO 2, as well as shifts in blood pH. Excitation is transmitted through synapses to afferent nerve fibers, through which impulses enter the centers that regulate the activity of the heart and blood vessels. Afferent fibers from the carotid body pass through the vagus and sinus nerves.
Vasomotor center
Groups of neurons located bilaterally in the reticular formation of the medulla oblongata and the lower third of the pons are united by the concept of "vasomotor center" (see Fig. 23-18, C). This center transmits parasympathetic influences via the vagus nerves to the heart and sympathetic influences via the spinal cord and peripheral sympathetic nerves to the heart and to all or almost all of the blood vessels. The vasomotor center includes two parts - vasoconstrictor and vasodilator centers.
Vessels. The vasoconstrictor center constantly transmits signals with a frequency of 0.5 to 2 Hz along the sympathetic vasoconstrictor nerves. This constant stimulation is referred to as sympathetic vasoconstrictor tone, and the state of constant partial contraction of the SMC of blood vessels - by the term vasomotor tone.
Heart. At the same time, the vasomotor center controls the activity of the heart. The lateral sections of the vasomotor center transmit excitatory signals through the sympathetic nerves to the heart, increasing the frequency and strength of its contractions. The medial sections of the vasomotor center transmit parasympathetic impulses through the motor nuclei of the vagus nerve and fibers of the vagus nerves, which slow down the heart rate. The frequency and force of contractions of the heart increase simultaneously with the constriction of the vessels of the body and decrease simultaneously with the relaxation of the vessels.
Influences acting on the vasomotor center:Φ direct stimulation(CO 2 , hypoxia);
Φ exciting influences the nervous system from the cerebral cortex through the hypothalamus, from pain receptors and muscle receptors, from the chemoreceptors of the carotid sinus and aortic arch;
Φ inhibitory influences nervous system from the cerebral cortex through the hypothalamus, from the lungs, from the baroreceptors of the carotid sinus, aortic arch and pulmonary artery.
Innervation of blood vessels
All blood vessels containing SMCs in their walls (i.e., with the exception of capillaries and part of venules) are innervated by motor fibers from the sympathetic division of the autonomic nervous system. Sympathetic innervation of small arteries and arterioles regulates tissue blood flow and blood pressure. Sympathetic fibers innervating the venous capacitance vessels control the volume of blood deposited in the veins. Narrowing of the lumen of the veins reduces venous capacity and increases venous return.
Noradrenergic fibers. Their effect is to narrow the lumen of the vessels (Fig. 23-18, A).
Sympathetic vasodilating nerve fibers. The resistive vessels of the skeletal muscles, in addition to the vasoconstrictor sympathetic fibers, are innervated by vasodilating cholinergic fibers passing through the sympathetic nerves. The blood vessels of the heart, lungs, kidneys, and uterus are also innervated by sympathetic cholinergic nerves.
Innervation of the MMC. Bundles of noradrenergic and cholinergic nerve fibers form plexuses in the adventitial sheath of arteries and arterioles. From these plexuses, varicose nerve fibers are sent to the muscular membrane and terminate on its outer surface, without penetrating to the deeper SMCs. The neurotransmitter reaches the inner parts of the muscular membrane of the vessels by diffusion and propagation of excitation from one SMC to another through gap junctions.
Tone. Vasodilating nerve fibers are not in a state of constant excitation (tonus), while
Rice. 23-18. Control of blood circulation by the nervous system. A - motor sympathetic innervation of blood vessels; B - axon reflex. Antidromic impulses cause the release of substance P, which dilates blood vessels and increases capillary permeability; B - mechanisms of the medulla oblongata that control blood pressure. GL - glutamate; NA - norepinephrine; AH - acetylcholine; A - adrenaline; IX - glossopharyngeal nerve; X - vagus nerve. 1 - carotid sinus, 2 - aortic arch, 3 - baroreceptor afferents, 4 - inhibitory interneurons, 5 - bulbospinal tract, 6 - sympathetic preganglionic, 7 - sympathetic postganglionic, 8 - solitary tract nucleus, 9 - rostral ventrolateral nucleus.
vasoconstrictor fibers usually exhibit tonic activity. If the sympathetic nerves are cut (which is referred to as a sympathectomy), then the blood vessels dilate. In most tissues, the vessels dilate as a result of a decrease in the frequency of tonic discharges in the vasoconstrictor nerves.
Axon reflex. Mechanical or chemical irritation of the skin may be accompanied by local vasodilation. It is believed that when irritated by thin, non-myelinated skin pain fibers, AP not only propagate in the centripetal direction to the spinal cord (orthodromous), but also by efferent collaterals (antidromic) come to the blood vessels of the area of the skin innervated by this nerve (Fig. 23-18, B). This local neural mechanism is called the axon reflex.
Blood pressure regulation
BP is maintained at the required working level with the help of reflex control mechanisms that operate on the basis of the feedback principle.
baroreceptor reflex. One of the well-known neural mechanisms for controlling blood pressure is the baroreceptor reflex. Baroreceptors are present in the wall of almost all large arteries in the chest and neck, especially many baroreceptors in the carotid sinus and in the wall of the aortic arch. The baroreceptors of the carotid sinus (see Fig. 25-10) and the aortic arch do not respond to blood pressure in the range from 0 to 60-80 mm Hg. An increase in pressure above this level causes a response, which progressively increases and reaches a maximum at a blood pressure of about 180 mm Hg. Normal average working blood pressure ranges from 110-120 mm Hg. Small deviations from this level increase the excitation of baroreceptors. They respond to changes in blood pressure very quickly: the frequency of impulses increases during systole and decreases just as quickly during diastole, which occurs within fractions of a second. Thus, baroreceptors are more sensitive to changes in pressure than to its stable level.
Φ Increased impulses from baroreceptors, caused by a rise in blood pressure, enters the medulla oblongata, slows down the
vasoconstrictor center of the medulla oblongata and excites the center of the vagus nerve. As a result, the lumen of the arterioles expands, the frequency and strength of heart contractions decrease. In other words, excitation of baroreceptors reflexively causes a decrease in blood pressure due to a decrease in peripheral resistance and cardiac output. Φ Low blood pressure has the opposite effect, which leads to its reflex increase to a normal level. A decrease in pressure in the carotid sinus and aortic arch inactivates baroreceptors, and they cease to have an inhibitory effect on the vasomotor center. As a result, the latter is activated and causes an increase in blood pressure.
Chemoreceptors in the carotid sinus and aorta. Chemoreceptors - chemosensitive cells that respond to a lack of oxygen, an excess of carbon dioxide and hydrogen ions - are located in the carotid and aortic bodies. Chemoreceptor nerve fibers from the bodies, together with baroreceptor fibers, go to the vasomotor center of the medulla oblongata. When blood pressure drops below a critical level, chemoreceptors are stimulated, since the decrease in blood flow reduces the content of O 2 and increases the concentration of CO 2 and H +. Thus, impulses from chemoreceptors excite the vasomotor center and increase blood pressure.
Reflexes from the pulmonary artery and atria. In the wall of both atria and the pulmonary artery there are stretch receptors (low pressure receptors). Low pressure receptors perceive changes in volume that occur simultaneously with changes in blood pressure. Excitation of these receptors causes reflexes in parallel with baroreceptor reflexes.
Atrial reflexes activating the kidneys. Stretching of the atria causes a reflex expansion of the afferent (bringing) arterioles in the glomeruli of the kidneys. At the same time, a signal is sent from the atrium to the hypothalamus, reducing the secretion of ADH. The combination of two effects - an increase in glomerular filtration rate and a decrease in fluid reabsorption - contributes to a decrease in blood volume and its return to normal levels.
Atrial reflex that controls heart rate. An increase in pressure in the right atrium causes a reflex increase in heart rate (Bainbridge reflex). The atrial stretch receptors that cause the Bainbridge reflex transmit afferent signals through the vagus nerve to the medulla oblongata. Then the excitation returns back to the heart along the sympathetic pathways, increasing the frequency and strength of the contractions of the heart. This reflex prevents the veins, atria, and lungs from overflowing with blood. Arterial hypertension. Normal systolic and diastolic pressure is 120/80 mmHg. Arterial hypertension is a condition when systolic pressure exceeds 140 mm Hg, and diastolic - 90 mm Hg.
Heart rate control
Almost all mechanisms that control systemic blood pressure, in one way or another, change the rhythm of the heart. Stimuli that speed up the heart rate also increase blood pressure. Stimuli that slow down the rhythm of heart contractions lower blood pressure. There are also exceptions. So, if the atrial stretch receptors are irritated, the heart rate rises and arterial hypotension occurs. An increase in intracranial pressure causes bradycardia and an increase in blood pressure. In total increase heart rate decrease in activity of baroreceptors in the arteries, left ventricle and pulmonary artery, increase in activity of atrial stretch receptors, inhalation, emotional arousal, pain stimuli, muscle load, norepinephrine, adrenaline, thyroid hormones, fever, Bainbridge reflex and a sense of rage, and cut down heart rate increased activity of baroreceptors in the arteries, left ventricle and pulmonary artery, exhalation, irritation of pain fibers of the trigeminal nerve and increased intracranial pressure.
Chapter summary
The cardiovascular system is a transport system that delivers the necessary substances to the tissues of the body and removes metabolic products. It is also responsible for delivering blood through the pulmonary circulation to take in oxygen from the lungs and release carbon dioxide into the lungs.
The heart is a muscular pump divided into right and left parts. The right heart pumps blood into the lungs; the left heart - to all remaining body systems.
Pressure is created inside the atria and ventricles of the heart due to contractions of the heart muscle. The unidirectional opening valves prevent backflow between the chambers and ensure the forward flow of blood through the heart.
Arteries transport blood from the heart to the organs; veins - from the organs to the heart.
Capillaries are the main exchange system between blood and extracellular fluid.
Heart cells do not need signals from nerve fibers to generate action potentials.
The cells of the heart exhibit the properties of automatism and rhythm.
Tight junctions connecting cells within the myocardium allow the heart to behave electrophysiologically like a functional syncytium.
The opening of voltage-gated sodium channels and voltage-gated calcium channels and the closure of voltage-gated potassium channels are responsible for depolarization and action potential formation.
Action potentials in ventricular cardiomyocytes have an extended depolarization phase plateau responsible for creating a long refractory period in heart cells.
The sinoatrial node initiates electrical activity in the normal heart.
Norepinephrine increases the automatic activity and speed of action potentials; acetylcholine reduces them.
The electrical activity generated in the sinoatrial node propagates along the atrial musculature, through the atrioventricular node and Purkinje fibers to the ventricular musculature.
The atrioventricular node delays the entry of action potentials into the ventricular myocardium.
An electrocardiogram displays the time-varying electrical potential differences between repolarized and depolarized areas of the heart.
The ECG provides clinically valuable information about the speed, rhythm, patterns of depolarization, and electrically active heart muscle mass.
The ECG displays changes in cardiac metabolism and plasma electrolytes as well as the effects of drugs.
The contractility of the heart muscle changes under the influence of inotropic interventions, which include changes in the heart rate, with sympathetic stimulation or the content of catecholamines in the blood.
Calcium enters the heart muscle cells during the action potential plateau and induces the release of intracellular calcium from stores in the sarcoplasmic reticulum.
The contractility of the heart muscle is associated with changes in the amount of calcium released from the sarcoplasmic reticulum, under the influence of extracellular calcium entering the cardiomyocytes.
The expulsion of blood from the ventricles is divided into fast and slow phases.
Stroke volume is the amount of blood ejected from the ventricles during systole. There is a difference between ventricular end-diastolic and end-systolic volumes.
The ventricles do not empty completely of blood during systole, leaving a residual volume for the next filling cycle.
The filling of the ventricles with blood is divided into periods of rapid and slow filling.
Heart sounds during the cardiac cycle are related to the opening and closing of the heart valves.
Cardiac output is a derivative of stroke volume and heart rate.
The volume of stroke is determined by the end-diastolic length of myocardiocytes, afterload and myocardial contractility.
The energy of the heart depends on the stretching of the walls of the ventricles, heart rate, stroke volume and contractility.
Cardiac output and systemic vascular resistance determine the magnitude of blood pressure.
Stroke volume and compliance of arterial walls are the main factors of pulse pressure.
Arterial compliance decreases as blood pressure rises.
Central venous pressure and cardiac output are interrelated.
Microcirculation controls the transport of water and substances between tissues and blood.
The transfer of gases and fat-soluble molecules is carried out by diffusion through endothelial cells.
The transport of water-soluble molecules occurs due to diffusion through the pores between adjacent endothelial cells.
Diffusion of substances through the wall of capillaries depends on the concentration gradient of the substance and the permeability of the capillary to this substance.
Filtration or absorption of water through the capillary wall is carried out through the pores between adjacent endothelial cells.
Hydrostatic and osmotic pressure are the primary forces for the filtration and absorption of liquid through the capillary wall.
The ratio of post-capillary and pre-capillary pressure is the main factor in capillary hydrostatic pressure.
Lymphatic vessels remove excess water and protein molecules from the interstitial space between cells.
Myogenic self-regulation of arterioles is a response of the SMC of the vessel wall to an increase in pressure or stretch.
Metabolic intermediates cause dilation of arterioles.
Nitric oxide (NO), released from endothelial cells, is the main local vasodilator.
Axons of the sympathetic nervous system secrete norepinephrine, which constricts arterioles and venules.
Autoregulation of blood flow through some organs maintains blood flow at a constant level in conditions where blood pressure changes.
The sympathetic nervous system acts on the heart through β-adrenergic receptors; parasympathetic - through muscarinic cholinergic receptors.
The sympathetic nervous system acts on blood vessels mainly through α-adrenergic receptors.
Reflex control of blood pressure is carried out by neurogenic mechanisms that control heart rate, stroke volume and systemic vascular resistance.
Baroreceptors and cardiopulmonary receptors are important in regulating short-term changes in blood pressure.
The circulatory system is the continuous movement of blood through a closed system of heart cavities and a network of blood vessels that provide all the vital functions of the body.
The heart is the primary pump that energizes the movement of the blood. This is a complex point of intersection of different blood streams. In a normal heart, these flows do not mix. The heart begins to contract about a month after conception, and from that moment its work does not stop until the last moment of life.
During the time equal to the average life expectancy, the heart performs 2.5 billion contractions, and at the same time it pumps 200 million liters of blood. This is a unique pump that is about the size of a man's fist and the average weight for a man is 300g and for a woman is 220g. The heart looks like a blunt cone. Its length is 12-13 cm, width 9-10.5 cm, and anterior-posterior size is 6-7 cm.
The system of blood vessels makes up 2 circles of blood circulation.
Systemic circulation begins in the left ventricle by the aorta. The aorta provides delivery of arterial blood to various organs and tissues. At the same time, parallel vessels depart from the aorta, which bring blood to different organs: arteries pass into arterioles, and arterioles into capillaries. Capillaries provide the entire amount of metabolic processes in tissues. There, the blood becomes venous, it flows from the organs. It flows to the right atrium through the inferior and superior vena cava.
Small circle of blood circulation It begins in the right ventricle with the pulmonary trunk, which divides into the right and left pulmonary arteries. Arteries carry venous blood to the lungs, where gas exchange will take place. The outflow of blood from the lungs is carried out through the pulmonary veins (2 from each lung), which carry arterial blood to the left atrium. The main function of the small circle is transport, the blood delivers oxygen, nutrients, water, salt to the cells, and removes carbon dioxide and end products of metabolism from the tissues.
Circulation- this is the most important link in the processes of gas exchange. Thermal energy is transported with blood - this is heat exchange with the environment. Due to the function of blood circulation, hormones and other physiologically active substances are transferred. This ensures the humoral regulation of the activity of tissues and organs. Modern ideas about the circulatory system were outlined by Harvey, who in 1628 published a treatise on the movement of blood in animals. He came to the conclusion that the circulatory system is closed. Using the method of clamping blood vessels, he established direction of blood flow. From the heart, the blood moves through the arterial vessels, through the veins, the blood moves to the heart. The division is based on the direction of the flow, and not on the content of the blood. The main phases of the cardiac cycle have also been described. The technical level did not allow detecting capillaries at that time. The discovery of the capillaries was made later (Malpighet), which confirmed Harvey's assumptions about the closedness of the circulatory system. The gastro-vascular system is a system of channels associated with the main cavity in animals.
The evolution of the circulatory system.
Circulatory system in shape vascular tubes appears in worms, but in worms, hemolymph circulates in the vessels and this system is not yet closed. The exchange is carried out in the gaps - this is the interstitial space.
Then there is isolation and the appearance of two circles of blood circulation. The heart in its development goes through stages - two-chamber- in fish (1 atrium, 1 ventricle). The ventricle pushes out venous blood. Gas exchange takes place in the gills. Then the blood goes to the aorta.
Amphibians have three hearts chamber(2 atria and 1 ventricle); The right atrium receives venous blood and pushes the blood into the ventricle. The aorta comes out of the ventricle, in which there is a septum and it divides the blood flow into 2 streams. The first stream goes to the aorta, and the second one goes to the lungs. After gas exchange in the lungs, blood enters the left atrium, and then into the ventricle, where the blood mixes.
In reptiles, the differentiation of heart cells into the right and left halves ends, but they have a hole in the interventricular septum and the blood mixes.
In mammals, the complete division of the heart into 2 halves . The heart can be considered as an organ that forms 2 pumps - the right one - the atrium and the ventricle, the left one - the ventricle and the atrium. There is no more mixing of the blood ducts.
Heart located in a person in the chest cavity, in the mediastinum between the two pleural cavities. The heart is bounded in front by the sternum, in the back by the spine. In the heart, the apex is isolated, which is directed to the left, down. The projection of the apex of the heart is 1 cm inward from the left midclavicular line in the 5th intercostal space. The base is directed up and to the right. The line connecting the apex and base is the anatomical axis, which is directed from top to bottom, from right to left and from front to back. The heart in the chest cavity lies asymmetrically: 2/3 to the left of the midline, the upper border of the heart is the upper edge of the 3rd rib, and the right border is 1 cm outward from the right edge of the sternum. It practically lies on the diaphragm.
The heart is a hollow muscular organ that has 4 chambers - 2 atria and 2 ventricles. Between the atria and ventricles are atrioventricular openings, which will be atrioventricular valves. Atrioventricular openings are formed by fibrous rings. They separate the ventricular myocardium from the atria. The exit site of the aorta and pulmonary trunk are formed by fibrous rings. Fibrous rings - the skeleton to which its membranes are attached. There are semilunar valves in the openings in the exit area of the aorta and pulmonary trunk.
The heart has 3 shells.
Outer shell- pericardium. It is built from two sheets - outer and inner, which fuses with the inner shell and is called the myocardium. A space filled with fluid forms between the pericardium and epicardium. Friction occurs in any moving mechanism. For easier movement of the heart, he needs this lubricant. If there are violations, then there are friction, noise. In these areas, salts begin to form, which immure the heart into a “shell”. This reduces the contractility of the heart. Currently, surgeons remove by biting this shell, freeing the heart, so that the contractile function can be carried out.
The middle layer is muscular or myocardium. It is the working shell and makes up the bulk. It is the myocardium that performs the contractile function. The myocardium refers to striated striated muscles, consists of individual cells - cardiomyocytes, which are interconnected in a three-dimensional network. Tight junctions are formed between cardiomyocytes. The myocardium is attached to the rings of fibrous tissue, the fibrous skeleton of the heart. It has attachment to the fibrous rings. atrial myocardium forms 2 layers - the outer circular, which surrounds both atria and the inner longitudinal, which is individual for each. In the area of confluence of the veins - hollow and pulmonary, circular muscles are formed that form sphincters, and when these circular muscles contract, blood from the atrium cannot flow back into the veins. Myocardium of the ventricles formed by 3 layers - outer oblique, inner longitudinal, and between these two layers is located a circular layer. The myocardium of the ventricles begins from the fibrous rings. The outer end of the myocardium goes obliquely to the apex. At the top, this outer layer forms a curl (vertex), it and the fibers pass into the inner layer. Between these layers are circular muscles, separate for each ventricle. The three-layer structure provides shortening and reduction of the clearance (diameter). This makes it possible to expel blood from the ventricles. The inner surface of the ventricles is lined with endocardium, which passes into the endothelium of large vessels.
Endocardium- inner layer - covers the valves of the heart, surrounds the tendon filaments. On the inner surface of the ventricles, the myocardium forms a trabecular meshwork and the papillary muscles and papillary muscles are connected to the valve leaflets (tendon filaments). It is these threads that hold the valve leaflets and do not allow them to twist into the atrium. In the literature tendon threads are called tendon strings.
Valvular apparatus of the heart.
In the heart, it is customary to distinguish between atrioventricular valves located between the atria and ventricles - in the left half of the heart it is a bicuspid valve, in the right - a tricuspid valve, consisting of three wings. The valves open into the lumen of the ventricles and pass blood from the atria into the ventricle. But with contraction, the valve closes and the ability of blood to flow back into the atrium is lost. In the left - the magnitude of the pressure is much greater. Structures with fewer elements are more reliable.
At the exit site of large vessels - the aorta and pulmonary trunk - there are semilunar valves, represented by three pockets. When filling with blood in the pockets, the valves close, so the reverse movement of blood does not occur.
The purpose of the valvular apparatus of the heart is to ensure one-way blood flow. Damage to the valve leaflets leads to valve insufficiency. In this case, a reverse blood flow is observed as a result of a loose connection of the valves, which disrupts hemodynamics. The boundaries of the heart are changing. There are signs of development of insufficiency. The second problem associated with the area of the valves, stenosis of the valves - (for example, the venous ring is stenotic) - the lumen decreases. When they talk about stenosis, they mean either atrioventricular valves or the place where the vessels originate. Above the semilunar valves of the aorta, from its bulb, the coronary vessels depart. In 50% of people, the blood flow in the right is greater than in the left, in 20% the blood flow is greater in the left than in the right, 30% have the same outflow in both the right and left coronary arteries. Development of anastomoses between the pools of the coronary arteries. Violation of the blood flow of the coronary vessels is accompanied by myocardial ischemia, angina pectoris, and complete blockage leads to necrosis - a heart attack. Venous outflow of blood goes through the superficial system of veins, the so-called coronary sinus. There are also veins that open directly into the lumen of the ventricle and right atrium.
Cardiac cycle.
The cardiac cycle is a period of time during which there is a complete contraction and relaxation of all parts of the heart. Contraction is systole, relaxation is diastole. The duration of the cycle will depend on the heart rate. The normal frequency of contractions ranges from 60 to 100 beats per minute, but the average frequency is 75 beats per minute. To determine the duration of the cycle, we divide 60s by the frequency. (60s / 75s = 0.8s).
The cardiac cycle consists of 3 phases:
Atrial systole - 0.1 s
Ventricular systole - 0.3 s
Total pause 0.4 s
The state of the heart in end of the general pause: The cuspid valves are open, the semilunar valves are closed, and blood flows from the atria to the ventricles. By the end of the general pause, the ventricles are 70-80% filled with blood. The cardiac cycle begins with
atrial systole. At this time, the atria contract, which is necessary to complete the filling of the ventricles with blood. It is the contraction of the atrial myocardium and the increase in blood pressure in the atria - in the right up to 4-6 mm Hg, and in the left up to 8-12 mm Hg. ensures the injection of additional blood into the ventricles and atrial systole completes the filling of the ventricles with blood. Blood cannot flow back, as the circular muscles contract. In the ventricles will be end diastolic blood volume. On average, it is 120-130 ml, but in people engaged in physical activity up to 150-180 ml, which ensures more efficient work, this department goes into a state of diastole. Next comes ventricular systole.
Ventricular systole- the most difficult phase of the cardiac cycle, lasting 0.3 s. secreted in systole stress period, it lasts 0.08 s and period of exile. Each period is divided into 2 phases -
stress period
1. asynchronous contraction phase - 0.05 s
2. phases of isometric contraction - 0.03 s. This is the isovalumin contraction phase.
period of exile
1. fast ejection phase 0.12s
2. slow phase 0.13 s.
Ventricular systole begins with a phase of asynchronous contraction. Some cardiomyocytes are excited and are involved in the process of excitation. But the resulting tension in the myocardium of the ventricles provides an increase in pressure in it. This phase ends with the closing of the flap valves and the cavity of the ventricles is closed. The ventricles are filled with blood and their cavity is closed, and the cardiomyocytes continue to develop a state of tension. The length of the cardiomyocyte cannot change. It has to do with the properties of the liquid. Liquids do not compress. In a closed space, when there is a tension of cardiomyocytes, it is impossible to compress the liquid. The length of cardiomyocytes does not change. Isometric contraction phase. Cut at low length. This phase is called the isovaluminic phase. In this phase, the volume of blood does not change. The space of the ventricles is closed, the pressure rises, in the right up to 5-12 mm Hg. in the left 65-75 mm Hg, while the pressure of the ventricles will become greater than the diastolic pressure in the aorta and pulmonary trunk, and the excess pressure in the ventricles over the blood pressure in the vessels leads to the opening of the semilunar valves. The semilunar valves open and blood begins to flow into the aorta and pulmonary trunk.
The exile phase begins, when the ventricles contract, the blood is pushed into the aorta, into the pulmonary trunk, the length of cardiomyocytes changes, the pressure increases and at the height of systole in the left ventricle 115-125 mm, in the right 25-30 mm. Initially, the fast ejection phase, and then the ejection becomes slower. During the systole of the ventricles, 60-70 ml of blood is pushed out, and this amount of blood is the systolic volume. Systolic blood volume = 120-130 ml, i.e. there is still enough blood in the ventricles at the end of systole - end systolic volume and this is a kind of reserve, so that if necessary - to increase the systolic output. The ventricles complete systole and begin to relax. The pressure in the ventricles begins to fall and the blood that is ejected into the aorta, the pulmonary trunk rushes back into the ventricle, but on its way it meets the pockets of the semilunar valve, which, when filled, close the valve. This period is called proto-diastolic period- 0.04s. When the semilunar valves close, the cuspid valves also close, period of isometric relaxation ventricles. It lasts 0.08s. Here, the voltage drops without changing the length. This causes a pressure drop. Blood accumulated in the ventricles. The blood begins to press on the atrioventricular valves. They open at the beginning of ventricular diastole. There comes a period of blood filling with blood - 0.25 s, while a fast filling phase is distinguished - 0.08 and a slow filling phase - 0.17 s. Blood flows freely from the atria into the ventricle. This is a passive process. The ventricles will be filled with blood by 70-80% and the filling of the ventricles will be completed by the next systole.
The structure of the heart muscle.
The cardiac muscle has a cellular structure, and the cellular structure of the myocardium was established back in 1850 by Kelliker, but for a long time it was believed that the myocardium is a network - sencidia. And only electron microscopy confirmed that each cardiomyocyte has its own membrane and is separated from other cardiomyocytes. The contact area of cardiomyocytes is intercalated disks. Currently, cardiac muscle cells are divided into cells of the working myocardium - cardiomyocytes of the working myocard of the atria and ventricles and into cells of the conduction system of the heart. Allocate:
- Pcells - pacemaker
- transitional cells
- Purkinje cells
Working myocardial cells belong to striated muscle cells and cardiomyocytes have an elongated shape, length reaches 50 microns, diameter - 10-15 microns. The fibers are composed of myofibrils, the smallest working structure of which is the sarcomere. The latter has thick - myosin and thin - actin branches. On thin filaments there are regulatory proteins - tropanin and tropomyosin. Cardiomyocytes also have a longitudinal system of L tubules and transverse T tubules. However, T tubules, in contrast to the T tubules of skeletal muscles, depart at the level of the Z membranes (in skeletal muscles, at the border of disc A and I). Neighboring cardiomyocytes are connected with the help of an intercalary disk - the area of \u200b\u200bcontact of the membranes. In this case, the structure of the intercalary disk is heterogeneous. In the intercalary disk, a slot area (10-15 Nm) can be distinguished. The second zone of tight contact is the desmosomes. In the region of desmosomes, a thickening of the membrane is observed, tonofibrils (threads connecting neighboring membranes) pass here. Desmosomes are 400 nm long. There are tight contacts, they are called nexuses, in which the outer layers of neighboring membranes merge, now they are found - conexons - fastening due to special proteins - conexins. Nexuses - 10-13%, this area has a very low electrical resistance of 1.4 Ohm per kV.cm. This makes it possible to transmit an electrical signal from one cell to another, and therefore cardiomyocytes are included simultaneously in the excitation process. The myocardium is a functional sensidium.
Physiological properties of the heart muscle.
Cardiomyocytes are isolated from each other and contact in the area of the intercalated discs, where the membranes of adjacent cardiomyocytes come into contact.
Connexons are connections in the membrane of adjacent cells. These structures are formed at the expense of connexin proteins. The connexon is surrounded by 6 such proteins, a channel is formed inside the connexon, which allows the passage of ions, thus the electric current propagates from one cell to another. “f area has a resistance of 1.4 ohms per cm2 (low). Excitation covers cardiomyocytes simultaneously. They function like functional sensations. Nexuses are very sensitive to lack of oxygen, to the action of catecholamines, to stressful situations, to physical activity. This can cause a disturbance in the conduction of excitation in the myocardium. Under experimental conditions, the violation of tight junctions can be obtained by placing pieces of myocardium in a hypertonic sucrose solution. Important for the rhythmic activity of the heart conducting system of the heart- this system consists of a complex of muscle cells that form bundles and nodes, and the cells of the conducting system differ from the cells of the working myocardium - they are poor in myofibrils, rich in sarcoplasm and contain a high content of glycogen. These features under light microscopy make them lighter with little transverse striation and they have been called atypical cells.
The conduction system includes:
1. Sinoatrial node (or Kate-Flak node), located in the right atrium at the confluence of the superior vena cava
2. The atrioventricular node (or Ashoff-Tavar node), which lies in the right atrium on the border with the ventricle, is the posterior wall of the right atrium
These two nodes are connected by intra-atrial tracts.
3. Atrial tracts
Anterior - with Bachman's branch (to the left atrium)
Middle tract (Wenckebach)
Posterior tract (Torel)
4. The Hiss bundle (departs from the atrioventricular node. Passes through the fibrous tissue and provides a connection between the atrial myocardium and the ventricular myocardium. Passes into the interventricular septum, where it is divided into the right and left pedicle of the Hiss bundle)
5. The right and left legs of the Hiss bundle (they run along the interventricular septum. The left leg has two branches - anterior and posterior. Purkinje fibers will be the final branches).
6. Purkinje fibers
In the conduction system of the heart, which is formed by modified types of muscle cells, there are three types of cells: pacemaker (P), transitional cells and Purkinje cells.
1. P-cells. They are located in the sino-arterial node, less in the atrioventricular nucleus. These are the smallest cells, they have few t-fibrils and mitochondria, there is no t-system, l. system is underdeveloped. The main function of these cells is to generate an action potential due to the innate property of slow diastolic depolarization. In them, there is a periodic decrease in the membrane potential, which leads them to self-excitation.
2. transition cells carry out the transfer of excitation in the region of the atrioventricular nucleus. They are found between P cells and Purkinje cells. These cells are elongated and lack the sarcoplasmic reticulum. These cells have a slow conduction rate.
3. Purkinje cells wide and short, they have more myofibrils, the sarcoplasmic reticulum is better developed, the T-system is absent.
Electrical properties of myocardial cells.
Myocardial cells, both working and conducting systems, have resting membrane potentials and outside the membrane of the cardiomyocyte is charged "+", and inside "-". This is due to ionic asymmetry - there are 30 times more potassium ions inside the cells, and 20-25 times more sodium ions outside. This is ensured by the constant operation of the sodium-potassium pump. Measurement of the membrane potential shows that the cells of the working myocardium have a potential of 80-90 mV. In the cells of the conducting system - 50-70 mV. When cells of the working myocardium are excited, an action potential arises (5 phases): 0 - depolarization, 1 - slow repolarization, 2 - plateau, 3 - fast repolarization, 4 - resting potential.
0. When excited, the process of depolarization of cardiomyocytes occurs, which is associated with the opening of sodium channels and an increase in the permeability for sodium ions, which rush inside the cardiomyocytes. With a decrease in the membrane potential of about 30-40 millivolts, slow sodium-calcium channels open. Through them, sodium and additionally calcium can enter. This provides a process of depolarization or overshoot (reversion) of 120 mV.
1. The initial phase of repolarization. There is a closing of sodium channels and some increase in the permeability to chloride ions.
2. Plateau phase. The depolarization process is slowed down. Associated with an increase in the release of calcium inside. It delays charge recovery on the membrane. When excited, potassium permeability decreases (5 times). Potassium cannot leave cardiomyocytes.
3. When the calcium channels close, a phase of rapid repolarization occurs. Due to the restoration of polarization to potassium ions, the membrane potential returns to its original level and diastolic potential occurs
4. Diastolic potential is constantly stable.
The cells of the conduction system have distinctive potential features.
1. Reduced membrane potential during the diastolic period (50-70mV).
2. The fourth phase is not stable. There is a gradual decrease in the membrane potential to the threshold critical level of depolarization and gradually continues to slowly decrease in diastole, reaching a critical level of depolarization, at which self-excitation of P-cells occurs. In P-cells, there is an increase in the penetration of sodium ions and a decrease in the output of potassium ions. Increases the permeability of calcium ions. These shifts in ionic composition lead to the fact that the membrane potential in P-cells decreases to a threshold level and the p-cell self-excites, giving rise to an action potential. The Plateau phase is poorly expressed. Phase zero smoothly transitions to the TB repolarization process, which restores the diastolic membrane potential, and then the cycle repeats again and P-cells go into a state of excitation. The cells of the sino-atrial node have the greatest excitability. The potential in it is especially low and the rate of diastolic depolarization is the highest. This will affect the frequency of excitation. P-cells of the sinus node generate a frequency of up to 100 beats per minute. The nervous system (sympathetic system) suppress the action of the node (70 strokes). The sympathetic system can increase automaticity. Humoral factors - adrenaline, norepinephrine. Physical factors - the mechanical factor - stretching, stimulate automaticity, warming also increases automaticity. All this is used in medicine. The event of direct and indirect heart massage is based on this. The area of the atrioventricular node also has automaticity. The degree of automaticity of the atrioventricular node is much less pronounced and, as a rule, it is 2 times less than in the sinus node - 35-40. In the conduction system of the ventricles, impulses can also occur (20-30 per minute). In the course of the conductive system, a gradual decrease in the level of automaticity occurs, which is called the gradient of automaticity. The sinus node is the center of first-order automation.
Staneus - scientist. The imposition of ligatures on the heart of a frog (three-chamber). The right atrium has a venous sinus, where the analogue of the human sinus node lies. Staneus applied the first ligature between the venous sinus and the atrium. When the ligature was tightened, the heart stopped its work. The second ligature was applied by Staneus between the atria and the ventricle. In this zone there is an analogue of the atria-ventricular node, but the 2nd ligature has the task of not separating the node, but its mechanical excitation. It is applied gradually, exciting the atrioventricular node and at the same time there is a contraction of the heart. The ventricles get contracted again under the action of the atria-ventricular node. With a frequency of 2 times less. If you apply a third ligature that separates the atrioventricular node, then cardiac arrest occurs. All this gives us the opportunity to show that the sinus node is the main pacemaker, the atrioventricular node has less automation. In a conducting system, there is a decreasing gradient of automation.
Physiological properties of the heart muscle.
The physiological properties of the heart muscle include excitability, conductivity and contractility.
Under excitability heart muscle is understood as its property to respond to the action of stimuli with a threshold or above the threshold force by the process of excitation. Excitation of the myocardium can be obtained by the action of chemical, mechanical, temperature irritations. This ability to respond to the action of various stimuli is used during heart massage (mechanical action), the introduction of adrenaline, and pacemakers. A feature of the reaction of the heart to the action of an irritant is what acts according to the principle " All or nothing". The heart responds with a maximum impulse already to the threshold stimulus. The duration of myocardial contraction in the ventricles is 0.3 s. This is due to the long action potential, which also lasts up to 300ms. The excitability of the heart muscle can drop to 0 - an absolutely refractory phase. No stimuli can cause re-excitation (0.25-0.27 s). The heart muscle is completely unexcitable. At the moment of relaxation (diastole), the absolute refractory turns into a relative refractory 0.03-0.05 s. At this point, you can get re-stimulation on over-threshold stimuli. The refractory period of the heart muscle lasts and coincides in time as long as the contraction lasts. Following relative refractoriness, there is a short period of increased excitability - excitability becomes higher than the initial level - super normal excitability. In this phase, the heart is particularly sensitive to the effects of other stimuli (other stimuli or extrasystoles may occur - extraordinary systoles). The presence of a long refractory period should protect the heart from repeated excitations. The heart performs a pumping function. The gap between normal and extraordinary contraction is shortened. The pause can be normal or extended. An extended pause is called a compensatory pause. The cause of extrasystoles is the occurrence of other foci of excitation - the atrioventricular node, elements of the ventricular part of the conducting system, cells of the working myocardium. This may be due to impaired blood supply, impaired conduction in the heart muscle, but all additional foci are ectopic foci of excitation. Depending on the localization - different extrasystoles - sinus, pre-medium, atrioventricular. Ventricular extrasystoles are accompanied by an extended compensatory phase. 3 additional irritation - the reason for the extraordinary reduction. In time for an extrasystole, the heart loses its excitability. They receive another impulse from the sinus node. A pause is needed to restore a normal rhythm. When a failure occurs in the heart, the heart skips one normal beat and then returns to a normal rhythm.
Conductivity- the ability to conduct excitation. The speed of excitation in different departments is not the same. In the atrial myocardium - 1 m / s and the time of excitation takes 0.035 s
Excitation speed
Myocardium - 1 m/s 0.035
Atrioventricular node 0.02 - 0-05 m/s. 0.04 s
Conduction of the ventricular system - 2-4.2 m/s. 0.32
In total from the sinus node to the myocardium of the ventricle - 0.107 s
Myocardium of the ventricle - 0.8-0.9 m / s
Violation of the conduction of the heart leads to the development of blockades - sinus, atriventricular, Hiss bundle and its legs. The sinus node may turn off.. Will the atrioventricular node turn on as a pacemaker? Sinus blocks are rare. More in atrioventricular nodes. The lengthening of the delay (more than 0.21 s) excitation reaches the ventricle, albeit slowly. Loss of individual excitations that occur in the sinus node (For example, only two out of three reach - this is the second degree of blockade. The third degree of blockade, when the atria and ventricles work inconsistently. Blockade of the legs and bundle is a blockade of the ventricles. accordingly, one ventricle lags behind the other).
Contractility. Cardiomyocytes include fibrils, and the structural unit is sarcomeres. There are longitudinal tubules and T tubules of the outer membrane, which enter inward at the level of the membrane i. They are wide. The contractile function of cardiomyocytes is associated with the proteins myosin and actin. On thin actin proteins - the troponin and tropomyosin system. This prevents the myosin heads from bonding to the myosin heads. Removal of blocking - calcium ions. T tubules open calcium channels. An increase in calcium in the sarcoplasm removes the inhibitory effect of actin and myosin. Myosin bridges move the filament tonic toward the center. The myocardium obeys 2 laws in the contractile function - all or nothing. The strength of the contraction depends on the initial length of the cardiomyocytes - Frank Staraling. If the cardiomyocytes are pre-stretched, they respond with a greater force of contraction. Stretching depends on filling with blood. The more, the stronger. This law is formulated as "systole - there is a function of diastole." This is an important adaptive mechanism that synchronizes the work of the right and left ventricles.
Features of the circulatory system:
1) the closure of the vascular bed, which includes the pumping organ of the heart;
2) the elasticity of the vascular wall (the elasticity of the arteries is greater than the elasticity of the veins, but the capacity of the veins exceeds the capacity of the arteries);
3) branching of blood vessels (difference from other hydrodynamic systems);
4) a variety of vessel diameters (the diameter of the aorta is 1.5 cm, and the capillaries are 8-10 microns);
5) a fluid-blood circulates in the vascular system, the viscosity of which is 5 times higher than the viscosity of water.
Types of blood vessels:
1) the main vessels of the elastic type: the aorta, large arteries extending from it; there are many elastic and few muscle elements in the wall, as a result of which these vessels have elasticity and extensibility; the task of these vessels is to transform the pulsating blood flow into a smooth and continuous one;
2) vessels of resistance or resistive vessels - vessels of the muscular type, in the wall there is a high content of smooth muscle elements, the resistance of which changes the lumen of the vessels, and hence the resistance to blood flow;
3) exchange vessels or "exchange heroes" are represented by capillaries, which ensure the flow of the metabolic process, the performance of the respiratory function between blood and cells; the number of functioning capillaries depends on the functional and metabolic activity in the tissues;
4) shunt vessels or arteriovenular anastomoses directly connect arterioles and venules; if these shunts are open, then blood is discharged from the arterioles into the venules, bypassing the capillaries; if they are closed, then the blood flows from the arterioles into the venules through the capillaries;
5) capacitive vessels are represented by veins, which are characterized by high extensibility, but low elasticity, these vessels contain up to 70% of all blood, significantly affect the amount of venous return of blood to the heart.
Blood flow.
The movement of blood obeys the laws of hydrodynamics, namely, it occurs from an area of higher pressure to an area of \u200b\u200blower pressure.
The amount of blood flowing through a vessel is directly proportional to the pressure difference and inversely proportional to the resistance:
Q=(p1—p2) /R= ∆p/R,
where Q-blood flow, p-pressure, R-resistance;
An analogue of Ohm's law for a section of an electrical circuit:
where I is the current, E is the voltage, R is the resistance.
Resistance is associated with the friction of blood particles against the walls of blood vessels, which is referred to as external friction, there is also friction between particles - internal friction or viscosity.
Hagen Poiselle's law:
where η is the viscosity, l is the length of the vessel, r is the radius of the vessel.
Q=∆ppr 4 /8ηl.
These parameters determine the amount of blood flowing through the cross section of the vascular bed.
For the movement of blood, it is not the absolute values \u200b\u200bof pressure that matters, but the pressure difference:
p1=100 mm Hg, p2=10 mm Hg, Q=10 ml/s;
p1=500 mm Hg, p2=410 mm Hg, Q=10 ml/s.
The physical value of blood flow resistance is expressed in [Dyne*s/cm 5 ]. Relative resistance units were introduced:
If p \u003d 90 mm Hg, Q \u003d 90 ml / s, then R \u003d 1 is a unit of resistance.
The amount of resistance in the vascular bed depends on the location of the elements of the vessels.
If we consider the resistance values that occur in series-connected vessels, then the total resistance will be equal to the sum of the vessels in the individual vessels:
In the vascular system, blood supply is carried out due to the branches extending from the aorta and running in parallel:
R=1/R1 + 1/R2+…+ 1/Rn,
that is, the total resistance is equal to the sum of the reciprocal values of the resistance in each element.
Physiological processes are subject to general physical laws.
Cardiac output.
Cardiac output is the amount of blood pumped out by the heart per unit of time. Distinguish:
Systolic (during 1 systole);
Minute volume of blood (or IOC) - is determined by two parameters, namely systolic volume and heart rate.
The value of the systolic volume at rest is 65-70 ml, and is the same for the right and left ventricles. At rest, the ventricles eject 70% of the end-diastolic volume, and by the end of systole, 60-70 ml of blood remains in the ventricles.
V system avg.=70ml, ν avg.=70 beats/min,
V min \u003d V syst * ν \u003d 4900 ml per minute ~ 5 l / min.
It is difficult to determine V min directly; an invasive method is used for this.
An indirect method based on gas exchange has been proposed.
Fick method (method for determining the IOC).
IOC \u003d O2 ml / min / A - V (O2) ml / l of blood.
- O2 consumption per minute is 300 ml;
- O2 content in arterial blood = 20 vol %;
- O2 content in venous blood = 14% vol;
- Arterio-venous oxygen difference = 6 vol% or 60 ml of blood.
IOC = 300 ml / 60 ml / l = 5 l.
The value of systolic volume can be defined as V min/ν. The systolic volume depends on the strength of contractions of the ventricular myocardium, on the amount of blood filling of the ventricles in diastole.
The Frank-Starling law states that systole is a function of diastole.
The value of the minute volume is determined by the change in ν and the systolic volume.
During exercise, the value of the minute volume can increase to 25-30 l, the systolic volume increases to 150 ml, ν reaches 180-200 beats per minute.
The reactions of physically trained people relate primarily to changes in systolic volume, untrained - frequency, in children only due to frequency.
IOC distribution.
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Aorta and major arteries |
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small arteries |
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Arterioles |
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capillaries |
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Total - 20% |
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small veins |
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Large veins |
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Total - 64% |
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small circle |
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Mechanical work of the heart.
1. the potential component is aimed at overcoming the resistance to blood flow;
2. The kinetic component is aimed at giving speed to the movement of blood.
The value A of resistance is determined by the mass of the load displaced over a certain distance, determined by Genz:
1.potential component Wn=P*h, h-height, P= 5kg:
The average pressure in the aorta is 100 ml Hg st \u003d 0.1 m * 13.6 (specific gravity) \u003d 1.36,
Wn lion yellow \u003d 5 * 1.36 \u003d 6.8 kg * m;
The average pressure in the pulmonary artery is 20 mm Hg = 0.02 m * 13.6 (specific gravity) = 0.272 m, Wn pr zhl = 5 * 0.272 = 1.36 ~ 1.4 kg * m.
2. kinetic component Wk == m * V 2 / 2, m = P / g, Wk = P * V 2 / 2 *g, where V is the linear velocity of blood flow, P = 5 kg, g = 9.8 m / s 2, V = 0.5 m / s; Wk \u003d 5 * 0.5 2 / 2 * 9.8 \u003d 5 * 0.25 / 19.6 \u003d 1.25 / 19.6 \u003d 0.064 kg / m * s.
30 tons per 8848 m raises the heart for a lifetime, ~ 12000 kg / m per day.
The continuity of blood flow is determined by:
1. the work of the heart, the constancy of the movement of blood;
2. elasticity of the main vessels: during systole, the aorta is stretched due to the presence of a large number of elastic components in the wall, they accumulate energy that is accumulated by the heart during systole, when the heart stops pushing blood, the elastic fibers tend to return to their previous state, transferring blood energy, resulting in a smooth continuous flow;
3. as a result of contraction of skeletal muscles, the veins are compressed, the pressure in which increases, which leads to pushing the blood towards the heart, the valves of the veins prevent the backflow of blood; if we stand for a long time, then the blood does not flow, since there is no movement, as a result, blood flow to the heart is disturbed, as a result, fainting occurs;
4. when blood enters the inferior vena cava, the factor of the presence of “-” interpleural pressure comes into play, which is designated as a suction factor, while the more “-” pressure, the better the blood flow to the heart;
5.pressure force behind VIS a tergo, i.e. pushing a new portion in front of the lying one.
The movement of blood is estimated by determining the volumetric and linear velocity of blood flow.
Volumetric velocity- the amount of blood passing through the cross section of the vascular bed per unit time: Q = ∆p / R , Q = Vπr 4 . At rest, IOC = 5 l / min, the volumetric blood flow rate at each section of the vascular bed will be constant (pass through all vessels per minute 5 l), however, each organ receives a different amount of blood, as a result of which Q is distributed in% ratio, for a separate organ it is necessary know the pressure in the artery, vein, through which the blood supply is carried out, as well as the pressure inside the organ itself.
Line speed- velocity of particles along the vessel wall: V = Q / πr 4
In the direction from the aorta, the total cross-sectional area increases, reaches a maximum at the level of capillaries, the total lumen of which is 800 times greater than the lumen of the aorta; the total lumen of the veins is 2 times greater than the total lumen of the arteries, since each artery is accompanied by two veins, so the linear velocity is greater.
The blood flow in the vascular system is laminar, each layer moves parallel to the other layer without mixing. The near-wall layers experience great friction, as a result, the velocity tends to 0, towards the center of the vessel, the velocity increases, reaching the maximum value in the axial part. Laminar flow is silent. Sound phenomena occur when laminar blood flow becomes turbulent (vortices occur): Vc = R * η / ρ * r, where R is the Reynolds number, R = V * ρ * r / η. If R > 2000, then the flow becomes turbulent, which is observed when the vessels narrow, with an increase in speed at the points of branching of the vessels, or when obstacles appear on the way. Turbulent blood flow is noisy.
Blood circulation time- the time for which the blood passes a full circle (both small and large). It is 25 s, which falls on 27 systoles (1/5 for a small one - 5 s, 4/5 for a large one - 20 s). Normally, 2.5 liters of blood circulates, the turnover is 25 s, which is enough to provide the IOC.
Blood pressure.
Blood pressure - the pressure of blood on the walls of blood vessels and chambers of the heart, is an important energy parameter, because it is a factor that ensures the movement of blood.
The source of energy is the contraction of the muscles of the heart, which performs a pumping function.
Distinguish:
Arterial pressure;
venous pressure;
intracardiac pressure;
capillary pressure.
The amount of blood pressure reflects the amount of energy that reflects the energy of the moving stream. This energy is the sum of potential, kinetic energy and potential energy of gravity:
E = P+ ρV 2 /2 + ρgh,
where P is the potential energy, ρV 2 /2 is the kinetic energy, ρgh is the energy of the blood column or the potential energy of gravity.
The most important is the blood pressure indicator, which reflects the interaction of many factors, thereby being an integrated indicator that reflects the interaction of the following factors:
Systolic blood volume;
Frequency and rhythm of contractions of the heart;
The elasticity of the walls of the arteries;
Resistance of resistive vessels;
Blood velocity in capacitive vessels;
The speed of circulating blood;
blood viscosity;
Hydrostatic pressure of the blood column: P = Q * R.
Arterial pressure is divided into lateral and end pressure. Lateral pressure- blood pressure on the walls of blood vessels, reflects the potential energy of blood movement. final pressure- pressure, reflecting the sum of potential and kinetic energy of blood movement.
As the blood moves, both types of pressure decrease, since the energy of the flow is spent on overcoming resistance, while the maximum decrease occurs where the vascular bed narrows, where it is necessary to overcome the greatest resistance.
The final pressure is greater than the lateral pressure by 10-20 mm Hg. The difference is called shock or pulse pressure.
Blood pressure is not a stable indicator, in natural conditions it changes during the cardiac cycle, in blood pressure there are:
Systolic or maximum pressure (pressure established during ventricular systole);
Diastolic or minimal pressure that occurs at the end of diastole;
The difference between the systolic and diastolic pressures is the pulse pressure;
Mean arterial pressure, reflecting the movement of blood, if there were no pulse fluctuations.
In different departments, the pressure will take on different values. In the left atrium, systolic pressure is 8-12 mm Hg, diastolic is 0, in the left ventricle syst = 130, diast = 4, in the aorta syst = 110-125 mm Hg, diast = 80-85, in the brachial artery syst = 110-120, diast = 70-80, at the arterial end of the capillaries syst 30-50, but there are no fluctuations, at the venous end of the capillaries syst = 15-25, small veins syst = 78-10 (average 7.1), in in the vena cava syst = 2-4, in the right atrium syst = 3-6 (average 4.6), diast = 0 or "-", in the right ventricle syst = 25-30, diast = 0-2, in the pulmonary trunk syst = 16-30, diast = 5-14, in pulmonary veins syst = 4-8.
In the large and small circles, there is a gradual decrease in pressure, which reflects the expenditure of energy used to overcome resistance. The average pressure is not the arithmetic average, for example, 120 over 80, the average of 100 is an incorrect given, since the duration of ventricular systole and diastole is different in time. Two mathematical formulas have been proposed to calculate the average pressure:
Ср р = (р syst + 2*р disat)/3, (for example, (120 + 2*80)/3 = 250/3 = 93 mm Hg), shifted towards diastolic or minimal.
Wed p \u003d p diast + 1/3 * p pulse, (for example, 80 + 13 \u003d 93 mm Hg)
Methods for measuring blood pressure.
Two approaches are used:
direct method;
indirect method.
The direct method is associated with the introduction of a needle or cannula into the artery, connected by a tube filled with an anticoagulant substance, to a monometer, pressure fluctuations are recorded by a scribe, the result is a recording of a blood pressure curve. This method gives accurate measurements, but is associated with arterial injury, is used in experimental practice, or in surgical operations.
The curve reflects pressure fluctuations, waves of three orders are detected:
The first - reflects fluctuations during the cardiac cycle (systolic rise and diastolic decrease);
Second - includes several waves of the first order, associated with breathing, since breathing affects the value of blood pressure (during inhalation, more blood flows to the heart due to the "suction" effect of negative interpleural pressure, according to Starling's law, blood ejection also increases, which leads to increase in blood pressure). The maximum increase in pressure will occur at the beginning of exhalation, however, the reason is the inspiratory phase;
Third - includes several respiratory waves, slow fluctuations are associated with the tone of the vasomotor center (an increase in tone leads to an increase in pressure and vice versa), are clearly identified with oxygen deficiency, with traumatic effects on the central nervous system, the cause of slow fluctuations is blood pressure in the liver.
In 1896, Riva-Rocci proposed testing a cuffed mercury sphygnomanometer, which is connected to a mercury column, a tube with a cuff where air is injected, the cuff is applied to the shoulder, pumping air, the pressure in the cuff increases, which becomes greater than systolic. This indirect method is palpatory, the measurement is based on the pulsation of the brachial artery, but diastolic pressure cannot be measured.
Korotkov proposed an auscultatory method for determining blood pressure. In this case, the cuff is superimposed on the shoulder, a pressure above systolic is created, air is released and the appearance of sounds on the ulnar artery in the elbow bend is listened to. When the brachial artery is clamped, we do not hear anything, since there is no blood flow, but when the pressure in the cuff becomes equal to the systolic pressure, a pulse wave begins to exist at the height of the systole, the first portion of blood will pass, therefore we will hear the first sound (tone), the appearance of the first sound is an indicator systolic pressure. The first tone is followed by a noise phase as the motion changes from laminar to turbulent. When the pressure in the cuff is close to or equal to the diastolic pressure, the artery will expand and the sounds will stop, which corresponds to the diastolic pressure. Thus, the method allows you to determine systolic and diastolic pressure, calculate pulse and mean pressure.
The influence of various factors on the value of blood pressure.
1. The work of the heart. Change in systolic volume. An increase in systolic volume increases the maximum and pulse pressure. The decrease will lead to a decrease and decrease in pulse pressure.
2. Heart rate. With a more frequent contraction, the pressure stops. At the same time, the minimum diastolic begins to increase.
3. Contractile function of the myocardium. The weakening of the contraction of the heart muscle leads to a decrease in pressure.
condition of the blood vessels.
1. Elasticity. Loss of elasticity leads to an increase in maximum pressure and an increase in pulse pressure.
2. The lumen of the vessels. Especially in the vessels of the muscular type. An increase in tone leads to an increase in blood pressure, which is the cause of hypertension. As the resistance increases, both the maximum and minimum pressure increase.
3. Blood viscosity and amount of circulating blood. A decrease in the amount of circulating blood leads to a decrease in pressure. An increase in volume leads to an increase in pressure. An increase in viscosity leads to an increase in friction and an increase in pressure.
Physiological constituents
4. The pressure in men is higher than in women. But after the age of 40, the pressure in women becomes higher than in men.
5. Increasing pressure with age. The increase in pressure in men is even. In women, the jump appears after 40 years.
6. Pressure during sleep goes down, and in the morning is lower than in the evening.
7. Physical work increases systolic pressure.
8. Smoking increases blood pressure by 10-20 mm.
9. Pressure rises when you cough
10. Sexual arousal increases blood pressure to 180-200 mm.
Blood microcirculation system.
Represented by arterioles, precapillaries, capillaries, postcapillaries, venules, arteriolovenular anastomoses and lymphatic capillaries.
Arterioles are blood vessels in which smooth muscle cells are arranged in a single row.
Precapillaries are individual smooth muscle cells that do not form a continuous layer.
The length of the capillary is 0.3-0.8 mm. And the thickness is from 4 to 10 microns.
The opening of capillaries is influenced by the state of pressure in arterioles and precapillaries.
The microcirculatory bed performs two functions: transport and exchange. Thanks to microcirculation, the exchange of substances, ions, and water takes place. Heat exchange also occurs and the intensity of microcirculation will be determined by the number of functioning capillaries, the linear velocity of blood flow and the value of intracapillary pressure.
Exchange processes occur due to filtration and diffusion. Capillary filtration depends on the interaction of capillary hydrostatic pressure and colloid osmotic pressure. The processes of transcapillary exchange have been studied starling.
The filtration process goes in the direction of lower hydrostatic pressure, and the colloid osmotic pressure ensures the transition of the liquid from less to more. The colloid osmotic pressure of blood plasma is due to the presence of proteins. They cannot pass through the capillary wall and remain in the plasma. They create a pressure of 25-30 mm Hg. Art.
Substances are carried along with the liquid. It does this by diffusion. The rate of transfer of a substance will be determined by the rate of blood flow and the concentration of the substance expressed as mass per volume. Substances that pass from the blood are absorbed into the tissues.
Ways of transfer of substances.
1. Transmembrane transfer (through the pores that are present in the membrane and by dissolving in membrane lipids)
2. Pinocytosis.
The volume of extracellular fluid will be determined by the balance between capillary filtration and fluid resorption. The movement of blood in the vessels causes a change in the state of the vascular endothelium. It has been established that active substances are produced in the vascular endothelium, which affect the state of smooth muscle cells and parenchymal cells. They can be both vasodilators and vasoconstrictors. As a result of the processes of microcirculation and metabolism in the tissues, venous blood is formed, which will return to the heart. The movement of blood in the veins will again be influenced by the pressure factor in the veins.
The pressure in the vena cava is called central pressure .
arterial pulse is called the oscillation of the walls of arterial vessels. The pulse wave moves at a speed of 5-10 m/s. And in the peripheral arteries from 6 to 7 m / s.
The venous pulse is observed only in the veins adjacent to the heart. It is associated with a change in blood pressure in the veins due to atrial contraction. The recording of a venous pulse is called a phlebogram.
Reflex regulation of the cardiovascular system.
regulation is divided into short-term(aimed at changing the minute volume of blood, total peripheral vascular resistance and maintaining the level of blood pressure. These parameters can change within a few seconds) and long term. Under physical load, these parameters should change rapidly. They quickly change if bleeding occurs and the body loses some of the blood. Long term regulation It is aimed at maintaining the value of blood volume and the normal distribution of water between the blood and tissue fluid. These indicators cannot arise and change within minutes and seconds.
The spinal cord is a segmental center. Sympathetic nerves innervating the heart (upper 5 segments) come out of it. The remaining segments take part in the innervation of blood vessels. The spinal centers are unable to provide adequate regulation. There is a decrease in pressure from 120 to 70 mm. rt. pillar. These sympathetic centers need a constant influx from the centers of the brain in order to ensure the normal regulation of the heart and blood vessels.
Under natural conditions - a reaction to pain, temperature stimuli, which are closed at the level of the spinal cord.
Vascular center.
The main center of regulation will be vasomotor center, which lies in the medulla oblongata and the opening of this center was associated with the name of the Soviet physiologist - Ovsyannikov. He performed brain stem transections in animals and found that as soon as the brain incisions passed below the inferior colliculus of the quadrigemina, there was a decrease in pressure. Ovsyannikov found that in some centers there was a narrowing, and in others - an expansion of blood vessels.
The vasomotor center includes:
- vasoconstrictor zone- depressor - anteriorly and laterally (now it is designated as a group of C1 neurons).
Posterior and medial is the second vasodilating zone.
The vasomotor center lies in the reticular formation. The neurons of the vasoconstrictor zone are in constant tonic excitation. This zone is connected by descending pathways with the lateral horns of the gray matter of the spinal cord. Excitation is transmitted through the mediator glutamate. Glutamate transmits excitation to the neurons of the lateral horns. Further impulses go to the heart and blood vessels. It is excited periodically if impulses come to it. Impulses come to the sensitive nucleus of the solitary tract and from there to the neurons of the vasodilating zone and it is excited. It has been shown that the vasodilating zone is in an antagonistic relationship with the vasoconstrictor.
Vasodilating zone also includes vagus nerve nuclei - double and dorsal nucleus from which efferent paths to the heart begin. Seam cores- they produce serotonin. These nuclei have an inhibitory effect on the sympathetic centers of the spinal cord. It is believed that the nuclei of the raphe participate in reflex reactions, are involved in the processes of excitation associated with emotional stress reactions.
Cerebellum affects the regulation of the cardiovascular system during exercise (muscle). Signals go to the nuclei of the tent and the cortex of the cerebellar vermis from the muscles and tendons. The cerebellum increases the tone of the vasoconstrictor area. Receptors of the cardiovascular system - aortic arch, carotid sinuses, vena cava, heart, small circle vessels.
The receptors that are located here are divided into baroreceptors. They lie directly in the wall of blood vessels, in the aortic arch, in the region of the carotid sinus. These receptors sense changes in pressure, designed to monitor pressure levels. In addition to baroreceptors, there are chemoreceptors that lie in the glomeruli on the carotid artery, the aortic arch, and these receptors respond to changes in the oxygen content in the blood, ph. Receptors are located on the outer surface of blood vessels. There are receptors that perceive changes in blood volume. - volume receptors - perceive changes in volume.
Reflexes are divided into depressor - lowering pressure and pressor - increasing e, accelerating, slowing down, interoceptive, exteroceptive, unconditional, conditional, proper, conjugated.
The main reflex is the pressure maintenance reflex. Those. reflexes aimed at maintaining the level of pressure from baroreceptors. Baroreceptors in the aorta and carotid sinus sense the level of pressure. They perceive the magnitude of pressure fluctuations during systole and diastole + average pressure.
In response to an increase in pressure, baroreceptors stimulate the activity of the vasodilating zone. At the same time, they increase the tone of the nuclei of the vagus nerve. In response, reflex reactions develop, reflex changes occur. The vasodilating zone suppresses the tone of the vasoconstrictor. There is an expansion of blood vessels and a decrease in the tone of the veins. Arterial vessels are expanded (arterioles) and veins will expand, pressure will decrease. Sympathetic influence decreases, wandering increases, rhythm frequency decreases. The increased pressure returns to normal. The expansion of the arterioles increases the blood flow in the capillaries. Part of the fluid will pass into the tissues - the volume of blood will decrease, which will lead to a decrease in pressure.
Pressor reflexes arise from chemoreceptors. An increase in the activity of the vasoconstrictor zone along the descending pathways stimulates the sympathetic system, while the vessels constrict. The pressure rises through the sympathetic centers of the heart, there will be an increase in the work of the heart. The sympathetic system regulates the release of hormones by the adrenal medulla. Increased blood flow in the pulmonary circulation. The respiratory system reacts with an increase in breathing - the release of blood from carbon dioxide. The factor that caused the pressor reflex leads to the normalization of the blood composition. In this pressor reflex, a secondary reflex to a change in the work of the heart is sometimes observed. Against the background of an increase in pressure, an increase in the work of the heart is observed. This change in the work of the heart is in the nature of a secondary reflex.
Mechanisms of reflex regulation of the cardiovascular system.
Among the reflexogenic zones of the cardiovascular system, we attributed the mouths of the vena cava.
bainbridge injected into the venous part of the mouth 20 ml of physical. solution or the same volume of blood. After that, there was a reflex increase in the work of the heart, followed by an increase in blood pressure. The main component in this reflex is an increase in the frequency of contractions, and the pressure rises only secondarily. This reflex occurs when there is an increase in blood flow to the heart. When the inflow of blood is greater than the outflow. In the region of the mouth of the genital veins, there are sensitive receptors that respond to an increase in venous pressure. These sensory receptors are the endings of the afferent fibers of the vagus nerve, as well as the afferent fibers of the posterior spinal roots. The excitation of these receptors leads to the fact that the impulses reach the nuclei of the vagus nerve and cause a decrease in the tone of the nuclei of the vagus nerve, while the tone of the sympathetic centers increases. There is an increase in the work of the heart and blood from the venous part begins to be pumped into the arterial part. The pressure in the vena cava will decrease. Under physiological conditions, this condition can increase during physical exertion, when blood flow increases and with heart defects, blood stagnation is also observed, which leads to increased heart rate.
An important reflexogenic zone will be the zone of the vessels of the pulmonary circulation. In the vessels of the pulmonary circulation, they are located in receptors that respond to an increase in pressure in the pulmonary circulation. With an increase in pressure in the pulmonary circulation, a reflex occurs, which causes the expansion of the vessels of the large circle, at the same time the work of the heart is accelerated and an increase in the volume of the spleen is observed. Thus, a kind of unloading reflex arises from the pulmonary circulation. This reflex was discovered by V.V. Parin. He worked a lot in terms of the development and research of space physiology, headed the Institute of Biomedical Research. An increase in pressure in the pulmonary circulation is a very dangerous condition, because it can cause pulmonary edema. Since the hydrostatic pressure of the blood increases, which contributes to the filtration of blood plasma and due to this state, the liquid enters the alveoli.
The heart itself is a very important reflexogenic zone. in the circulatory system. In 1897, scientists Doggel it was found that there are sensitive endings in the heart, which are mainly concentrated in the atria and to a lesser extent in the ventricles. Further studies showed that these endings are formed by sensory fibers of the vagus nerve and fibers of the posterior spinal roots in the upper 5 thoracic segments.
Sensitive receptors in the heart were found in the pericardium and it was noted that an increase in fluid pressure in the pericardial cavity or blood entering the pericardium during injury, reflexively slows down the heart rate.
A slowdown in the contraction of the heart is also observed during surgical interventions, when the surgeon pulls the pericardium. Irritation of the pericardial receptors is a slowing of the heart, and with stronger irritations, temporary cardiac arrest is possible. Switching off sensitive endings in the pericardium caused an increase in the work of the heart and an increase in pressure.
An increase in pressure in the left ventricle causes a typical depressor reflex, i.e. there is a reflex expansion of blood vessels and a decrease in peripheral blood flow and at the same time an increase in the work of the heart. A large number of sensory endings are located in the atrium, and it is the atrium that contains stretch receptors that belong to the sensory fibers of the vagus nerves. The vena cava and atria belong to the low pressure zone, because the pressure in the atria does not exceed 6-8 mm. rt. Art. Because the atrial wall is easily stretched, then an increase in pressure in the atria does not occur and the atrial receptors respond to an increase in blood volume. Studies of the electrical activity of atrial receptors showed that these receptors are divided into 2 groups -
- Type A. In type A receptors, excitation occurs at the moment of contraction.
-TypeB. They are excited when the atria fill with blood and when the atria are stretched.
From the atrial receptors, reflex reactions occur, which are accompanied by a change in the release of hormones, and the volume of circulating blood is regulated from these receptors. Therefore, atrial receptors are called Value receptors (responding to changes in blood volume). It was shown that with a decrease in the excitation of atrial receptors, with a decrease in volume, the parasympathetic activity reflexively decreased, i.e., the tone of the parasympathetic centers decreases and, conversely, the excitation of the sympathetic centers increases. Excitation of the sympathetic centers has a vasoconstrictive effect, and especially on the arterioles of the kidneys. What causes a decrease in renal blood flow. A decrease in renal blood flow is accompanied by a decrease in renal filtration, and sodium excretion decreases. And the formation of renin increases in the juxtaglomerular apparatus. Renin stimulates the formation of angiotensin 2 from angiotensinogen. This causes vasoconstriction. Further, angiotensin-2 stimulates the formation of aldostron.
Angiotensin-2 also increases thirst and increases the release of antidiuretic hormone, which will promote water reabsorption in the kidneys. Thus, there will be an increase in the volume of fluid in the blood and this decrease in receptor irritation will be eliminated.
If the volume of blood is increased and the atrial receptors are excited at the same time, then inhibition and release of antidiuretic hormone reflexively occur. Consequently, less water will be absorbed in the kidneys, diuresis will decrease, the volume then normalizes. Hormonal shifts in organisms arise and develop within a few hours, so the regulation of circulating blood volume refers to the mechanisms of long-term regulation.
Reflex reactions in the heart can occur when spasm of the coronary vessels. This causes pain in the region of the heart, and the pain is felt behind the sternum, strictly in the midline. The pains are very severe and are accompanied by cries of death. These pains are different from tingling pains. At the same time, pain sensations spread to the left arm and shoulder blade. Along the zone of distribution of sensitive fibers of the upper thoracic segments. Thus, heart reflexes are involved in the mechanisms of self-regulation of the circulatory system and they are aimed at changing the frequency of heart contractions, changing the volume of circulating blood.
In addition to the reflexes that arise from the reflexes of the cardiovascular system, reflexes that occur when irritated from other organs can occur are called coupled reflexes in an experiment on the tops, the scientist Goltz found that sipping the stomach, intestines, or lightly tapping the intestines in a frog is accompanied by a slowdown in the heart, up to a complete stop. This is due to the fact that impulses from the receptors arrive at the nuclei of the vagus nerves. Their tone rises and the work of the heart is inhibited or even stopped.
There are also chemoreceptors in the muscles, which are excited by an increase in potassium ions, hydrogen protons, which leads to an increase in the minute volume of blood, vasoconstriction of other organs, an increase in mean pressure and an increase in the work of the heart and respiration. Locally, these substances contribute to the expansion of the vessels of the skeletal muscles themselves.
Surface pain receptors speed up the heart rate, constrict blood vessels and increase mean pressure.
Excitation of deep pain receptors, visceral and muscle pain receptors leads to bradycardia, vasodilation and pressure reduction. In the regulation of the cardiovascular system the hypothalamus is important , which is connected by descending pathways with the vasomotor center of the medulla oblongata. Through the hypothalamus, with protective defensive reactions, with sexual activity, with food, drink reactions and with joy, the heart began to beat faster. The posterior nuclei of the hypothalamus lead to tachycardia, vasoconstriction, increased blood pressure and increased blood levels of adrenaline and norepinephrine. When the anterior nuclei are excited, the work of the heart slows down, the vessels dilate, the pressure drops and the anterior nuclei affect the centers of the parasympathetic system. When the ambient temperature rises, the minute volume increases, the blood vessels in all organs, except the heart, shrink, and the skin vessels expand. Increased blood flow through the skin - greater heat transfer and maintenance of body temperature. Through the hypothalamic nuclei, the influence of the limbic system on blood circulation is carried out, especially during emotional reactions, and emotional reactions are realized through the Schwa nuclei, which produce serotonin. From the nuclei of the raphe go the way to the gray matter of the spinal cord. The cerebral cortex also takes part in the regulation of the circulatory system and the cortex is connected with the centers of the diencephalon, i.e. hypothalamus, with the centers of the midbrain and it was shown that irritation of the motor and premator zones of the cortex led to a narrowing of the skin, celiac and renal vessels. . It is believed that it is the motor areas of the cortex, which trigger the contraction of skeletal muscles, that simultaneously include vasodilating mechanisms that contribute to a large muscle contraction. The participation of the cortex in the regulation of the heart and blood vessels is proved by the development of conditioned reflexes. In this case, it is possible to develop reflexes to changes in the state of blood vessels and to changes in the frequency of the heart. For example, the combination of a bell sound signal with temperature stimuli - temperature or cold, leads to vasodilation or vasoconstriction - we apply cold. The sound of the bell is given beforehand. Such a combination of an indifferent bell sound with thermal irritation or cold leads to the development of a conditioned reflex, which caused either vasodilation or constriction. It is possible to develop a conditioned eye-heart reflex. The heart does work. There were attempts to develop a reflex to cardiac arrest. They turned on the bell and irritated the vagus nerve. We don't need cardiac arrest in life. The organism reacts negatively to such provocations. Conditioned reflexes are developed if they are adaptive in nature. As a conditioned reflex reaction, you can take - the pre-launch state of the athlete. His heart rate increases, blood pressure rises, blood vessels constrict. The situation itself will be the signal for such a reaction. The body is already preparing in advance and mechanisms are activated that increase the blood supply to the muscles and blood volume. During hypnosis, you can achieve a change in the work of the heart and vascular tone, if you suggest that a person is doing hard physical work. At the same time, the heart and blood vessels react in the same way as if it were in reality. When exposed to the centers of the cortex, cortical influences on the heart and blood vessels are realized.
Regulation of regional circulation.
The heart receives blood from the right and left coronary arteries, which originate from the aorta, at the level of the upper edges of the semilunar valves. The left coronary artery divides into the anterior descending and circumflex arteries. The coronary arteries function normally as annular arteries. And between the right and left coronary arteries, the anastomoses are very poorly developed. But if there is a slow closing of one artery, then the development of anastomoses between the vessels begins and which can pass from 3 to 5% from one artery to another. This is when the coronary arteries are slowly closing. Rapid overlap leads to a heart attack and is not compensated from other sources. The left coronary artery supplies the left ventricle, the anterior half of the interventricular septum, the left and partly the right atrium. The right coronary artery supplies the right ventricle, the right atrium, and the posterior half of the interventricular septum. Both coronary arteries participate in the blood supply of the conducting system of the heart, but in humans the right one is larger. The outflow of venous blood occurs through the veins that run parallel to the arteries and these veins flow into the coronary sinus, which opens into the right atrium. Through this path flows from 80 to 90% of venous blood. Venous blood from the right ventricle in the interatrial septum flows through the smallest veins into the right ventricle and these veins are called vein tibesia, which directly remove venous blood into the right ventricle.
200-250 ml flows through the coronary vessels of the heart. blood per minute, i.e. this is 5% of the minute volume. For 100 g of the myocardium, from 60 to 80 ml flows per minute. The heart extracts 70-75% of oxygen from arterial blood, therefore, the arterio-venous difference is very large in the heart (15%) In other organs and tissues - 6-8%. In the myocardium, capillaries densely braid each cardiomyocyte, which creates the best condition for maximum blood extraction. The study of coronary blood flow is very difficult, because. it varies with the cardiac cycle.
Coronary blood flow increases in diastole, in systole, blood flow decreases due to compression of blood vessels. On diastole - 70-90% of coronary blood flow. The regulation of coronary blood flow is primarily regulated by local anabolic mechanisms, quickly responding to a decrease in oxygen. A decrease in the level of oxygen in the myocardium is a very powerful signal for vasodilation. A decrease in oxygen content leads to the fact that cardiomyocytes secrete adenosine, and adenosine is a powerful vasodilating factor. It is very difficult to assess the influence of the sympathetic and parasympathetic systems on blood flow. Both vagus and sympathicus change the way the heart works. It has been established that irritation of the vagus nerves causes a slowdown in the work of the heart, increases the continuation of diastole, and the direct release of acetylcholine will also cause vasodilation. Sympathetic influences promote the release of norepinephrine.
There are 2 types of adrenergic receptors in the coronary vessels of the heart - alpha and beta adrenoreceptors. In most people, the predominant type is beta-adrenergic receptors, but some have a predominance of alpha receptors. Such people will, when excited, feel a decrease in blood flow. Adrenaline causes an increase in coronary blood flow due to an increase in oxidative processes in the myocardium and an increase in oxygen consumption and due to the effect on beta-adrenergic receptors. Thyroxine, prostaglandins A and E have a dilating effect on the coronary vessels, vasopressin constricts the coronary vessels and reduces coronary blood flow.
Cerebral circulation.
It has many features in common with the coronary, because the brain is characterized by high activity of metabolic processes, increased oxygen consumption, the brain has a limited ability to use anaerobic glycolysis and cerebral vessels react poorly to sympathetic influences. Cerebral blood flow remains normal with a wide range of changes in blood pressure. From 50-60 minimum to 150-180 maximum. The regulation of the centers of the brain stem is especially well expressed. Blood enters the brain from 2 pools - from the internal carotid arteries, vertebral arteries, which then form on the basis of the brain Velisian circle, and 6 arteries supplying the brain with blood depart from it. For 1 minute, the brain receives 750 ml of blood, which is 13-15% of the minute blood volume and cerebral blood flow depends on cerebral perfusion pressure (the difference between mean arterial pressure and intracranial pressure) and the diameter of the vascular bed. The normal pressure of the cerebrospinal fluid is 130 ml. water column (10 ml Hg), although in humans it can range from 65 to 185.
For normal blood flow, perfusion pressure should be above 60 ml. Otherwise, ischemia is possible. Self-regulation of blood flow is associated with the accumulation of carbon dioxide. If in the myocardium it is oxygen. At a partial pressure of carbon dioxide above 40 mm Hg. The accumulation of hydrogen ions, adrenaline, and an increase in potassium ions also expand the cerebral vessels, to a lesser extent, the vessels react to a decrease in oxygen in the blood and the reaction is observed to decrease in oxygen below 60 mm. rt st. Depending on the work of different parts of the brain, local blood flow can increase by 10-30%. Cerebral circulation does not respond to humoral substances due to the presence of the blood-brain barrier. Sympathetic nerves do not cause vasoconstriction, but they affect smooth muscle and the endothelium of blood vessels. Hypercapnia is a decrease in carbon dioxide. These factors cause expansion of blood vessels by the mechanism of self-regulation, as well as a reflex increase in mean pressure, with subsequent slowing of the heart, through excitation of baroreceptors. These changes in systemic circulation - Cushing reflex.
Prostaglandins- are formed from arachidonic acid and as a result of enzymatic transformations 2 active substances are formed - prostacyclin(produced in endothelial cells) and thromboxane A2, with the participation of the enzyme cyclooxygenase.
Prostacyclin- inhibits platelet aggregation and causes vasodilation, and thromboxane A2 formed in the platelets themselves and contributes to their clotting.
The drug aspirin causes inhibition of the inhibition of the enzyme cyclooxygenases and leads to decrease education thromboxane A2 and prostacyclin. Endothelial cells are able to synthesize cyclooxygenase, but platelets cannot do this. Therefore, there is a more pronounced inhibition of the formation of thromboxane A2, and prostacyclin continues to be produced by the endothelium.
Under the action of aspirin, thrombosis decreases and the development of a heart attack, stroke, and angina pectoris is prevented.
Atrial Natriuretic Peptide produced by the secretory cells of the atrium during stretching. He renders vasodilating action to the arterioles. In the kidneys, expansion of the afferent arterioles in the glomeruli and thus leads to increased glomerular filtration, along with this, sodium is also filtered, an increase in diuresis and natriuresis. Reducing the sodium content contributes pressure drop. This peptide also inhibits the release of ADH from the posterior pituitary gland and this helps to remove water from the body. It also has an inhibitory effect on the system. renin - aldosterone.
Vasointestinal peptide (VIP)- it is released in the nerve endings along with acetylcholine and this peptide has a vasodilating effect on arterioles.
A number of humoral substances have vasoconstrictor action. These include vasopressin(antidiuretic hormone), affects the narrowing of arterioles in smooth muscles. Affects mainly diuresis, and not vasoconstriction. Some forms of hypertension are associated with the formation of vasopressin.
Vasoconstrictor - norepinephrine and epinephrine, due to their action on alpha1 adrenoreceptors in the vessels and cause vasoconstriction. When interacting with beta 2, vasodilating action in the vessels of the brain, skeletal muscles. Stressful situations do not affect the work of vital organs.
Angiotensin 2 is produced in the kidneys. It is converted to angiotensin 1 by the action of a substance renin. Renin is formed by specialized epithelioid cells that surround the glomeruli and have an intrasecretory function. Under conditions - a decrease in blood flow, the loss of organisms of sodium ions.
The sympathetic system also stimulates the production of renin. Under the action of angiotensin-converting enzyme in the lungs, it is converted to angiotensin 2 - vasoconstriction, increased pressure. Influence on the adrenal cortex and increased aldosterone formation.
Influence of nervous factors on the state of blood vessels.
All blood vessels, except for capillaries and venules, contain smooth muscle cells in their walls and smooth muscles of blood vessels receive sympathetic innervation, and sympathetic nerves - vasoconstrictors - are vasoconstrictors.
1842 Walter - cut the sciatic nerve of a frog and looked at the vessels of the membrane, this led to the expansion of the vessels.
1852 Claude Bernard. On a white rabbit, he cut the cervical sympathetic trunk and observed the vessels of the ear. The vessels dilated, the ear turned red, the temperature of the ear increased, the volume increased.
Centers of sympathetic nerves in the thoracolumbar region. Here lie preganglionic neurons. The axons of these neurons leave the spinal cord in the anterior roots and travel to the vertebral ganglia. Postganglionics reach the smooth muscles of the blood vessels. Expansions form on the nerve fibers - varicose veins. Postganlionars secrete norepinephrine, which can cause vasodilation and constriction, depending on the receptors. The released norepinephrine undergoes reverse reabsorption processes, or is destroyed by 2 enzymes - MAO and COMT - catecholomethyltransferase.
The sympathetic nerves are in constant quantitative excitation. They send 1, 2 pulses to the vessels. The vessels are in a somewhat narrowed state. Desimpotization removes this effect.. If the sympathetic center receives an exciting influence, then the number of impulses increases and an even greater vasoconstriction occurs.
Vasodilating nerves- vasodilators, they are not universal, they are observed in certain areas. Part of the parasympathetic nerves, when excited, cause vasodilation in the tympanic string and lingual nerve and increase the secretion of saliva. The phasic nerve has the same expanding action. In which the fibers of the sacral department enter. They cause vasodilatation of the external genitalia and small pelvis during sexual arousal. The secretory function of the glands of the mucous membrane is enhanced.
Sympathetic cholinergic nerves(Acetylcholine is released.) To the sweat glands, to the vessels of the salivary glands. If sympathetic fibers affect beta2 adrenoreceptors, they cause vasodilation and afferent fibers of the posterior roots of the spinal cord, they take part in the axon reflex. If the skin receptors are irritated, then the excitation can be transmitted to the blood vessels - into which substance P is released, which causes vasodilation.
In contrast to the passive expansion of blood vessels - here - an active character. Very important is the integrative mechanisms of regulation of the cardiovascular system, which are provided by the interaction of nerve centers and the nerve centers carry out a set of reflex mechanisms of regulation. Because the circulatory system is vital they are located in different departments- cerebral cortex, hypothalamus, vasomotor center of the medulla oblongata, limbic system, cerebellum. In the spinal cord these will be the centers of the lateral horns of the thoraco-lumbar region, where the sympathetic preganglionic neurons lie. This system ensures adequate blood supply to the organs at the moment. This regulation also ensures the regulation of the activity of the heart, which ultimately gives us the value of the minute volume of blood. From this amount of blood, you can take your piece, but peripheral resistance - the lumen of the vessels - will be a very important factor in the blood flow. Changing the radius of the vessels greatly affects the resistance. By changing the radius by 2 times, we will change the blood flow by 16 times.
