Pathophysiology of sss. Pathophysiology of the cardiovascular system

1. Circulatory failure, definition of the concept, etiology, forms of circulatory failure. Basic hemodynamic parameters and manifestations. Compensatory and adaptive mechanisms. Circulatory insufficiency is a condition in which the circulatory system does not meet the needs of tissues and organs for blood supply adequate to the level of their function and plastic processes in them. The main causes of circulatory insufficiency: cardiac disorders, disturbances in the tone of the walls of blood vessels and changes in the volume of blood volume and/or rheological properties of the blood. Types of circulatory insufficiency are classified according to the criteria of compensation of disorders, severity of development and course, severity of symptoms. Based on compensation, disorders of the circulatory system are divided into compensated ( signs of circulatory disorders are detected during exercise) and uncompensated (signs of circulatory disorders are detected at rest). According to the severity of the development and course of circulatory failure, acute (develops over several hours and days) and chronic (develops over several months or years) circulatory failure are distinguished. Acute circulatory failure. The most common causes: myocardial infarction, acute heart failure, some arrhythmias (paroxysmal tachycardia, severe bradycardia, atrial fibrillation, etc.), shock, acute blood loss. Chronic circulatory failure. Causes: pericarditis, long-term myocarditis, myocardial dystrophy, cardiosclerosis, heart defects, hyper- and hypotensive conditions, anemia, hypervolemia of various origins. Based on the severity of signs of circulatory failure, three stages of circulatory failure are distinguished. Stage I of circulatory failure - initial - first degree circulatory failure. Signs: decreased rate of myocardial contraction and decreased ejection fraction, shortness of breath, palpitations, fatigue. These signs are detected during physical activity and are absent at rest. Stage II circulatory failure - second degree circulatory failure (moderate or severe circulatory failure). The signs of circulatory failure indicated for the initial stage are detected not only during physical activity, but also at rest. Stage III of circulatory failure - final - circulatory failure of the third degree. It is characterized by significant disturbances in cardiac activity and hemodynamics at rest, as well as the development of significant dystrophic and structural changes in organs and tissues.

2. Heart failure. Heart failure from overload. Etiology, pathogenesis, manifestations. Heart failure is a condition characterized by the inability of the myocardium to provide adequate blood supply to organs and tissues. TYPES OF HEART FAILURE1. Myocardial, caused by damage to myocardiocytes by toxic, infectious, immune or ischemic factors.2. Overload, which occurs when there is volume overload or increased blood volume.3. Mixed. Heart failure due to pressure overload occurs with stenosis of the heart valves and blood vessels, with hypertension of the systemic and pulmonary circulation, and pulmonary emphysema. The compensation mechanism is homeometric, energetically more expensive than heterometric. Myocardial hypertrophy is the process of increasing the mass of individual cardiomyocytes without increasing their number under conditions of increased load. Stages of myocardial hypertrophy according to F.Z. Meyerson I. “Emergency”, or the period of development of hypertrophy.II. The stage of completed hypertrophy and relatively stable hyperfunction of the heart, when normalization of myocardial functions occurs. III. The stage of progressive cardiosclerosis and myocardial depletion. The pathology of the cardiac membrane (pericardium) is most often represented by pericarditis: acute or chronic, dry or exudative. Etiology: viral infections (Coxsackie A and B, influenza, etc.), staphylococci, pneumococci , strepto- and meningococci, tuberculosis, rheumatism, collagenosis, allergic lesions - serum disease (ulcers, drug allergies, metabolic lesions (with chronic renal failure, gout, myxedema, thyrotoxicosis), radiation lesions, myocardial infarction, heart surgery. Pathogenesis: 1 ) hematogenous route of infection is characteristic of viral infections and septic conditions, 2) lymphogenous - with tuberculosis, diseases of the pleura, lung, mediastinum. Cardiac tamponade syndrome - accumulation of a large amount of fluid in the pericardial cavity. The severity of tamponade is influenced by the rate of fluid accumulation in the pericardium. Rapid accumulation of 300-500 ml of exudate leads to acute cardiac tamponade.

3. Myocardial-metabolic form of heart failure (myocardial damage). Causes, pathogenesis. Cardiac ischemia. Coronary insufficiency (l/f, mpf). Myocarditis Myocardial (metabolic, insufficiency from damage) - forms - develops with damage to the myocardium (intoxication, infection - diphtheria myocarditis, atherosclerosis, vitamin deficiency, coronary insufficiency). IHD (coronary insufficiency), degenerative heart disease) is a condition in which there is a discrepancy between the need of the myocardium and its supply with energy and plastic substrates (primarily oxygen). Causes of myocardial hypoxia: 1. Coronary insufficiency2. Metabolic disorders - non-coronary necrosis: metabolic disorders: electrolytes, hormones, immune damage, infections. Classification of IHD: 1. Angina pectoris: stable (at rest) unstable: new-onset progressive (severe) 2. Myocardial infarction. Clinical classification of coronary artery disease: 1. Sudden coronary death (primary cardiac arrest).2. Angina pectoris: a) tension: - new - stable - progressive b) spontaneous angina (special) 3. Myocardial infarction: large focal, small focal 4. Post-infarction cardiosclerosis.5. Heart rhythm disturbances.6. Heart failure. According to the course: acute or chronic latent form (asymptomatic) Etiology: 1. Causes of IHD:1. Coronarogenic: atherosclerosis of the coronary vessels, hypertension, nodular periarteritis, inflammatory and allergic vacculi, rheumatism, obliterating endarteriosis 2. Non-coronary: spasm as a result of the action of alcohol, nicotine, psycho-emotional stress, physical activity. Coronary insufficiency and coronary artery disease according to the development mechanism: 1. Absolute - decrease in flow to the heart through the coronary vessels.2. Relative - when a normal or even increased amount of blood is delivered through the vessels, but this does not meet the needs of the myocardium under conditions of its increased load. Pathogenesis of IHD: 1. Coronary (vascular) mechanism - organic changes in the coronary vessels.2. Myocardiogenic mechanism - neuroendocrine disorders, regulation and metabolism in the heart. The primary violation is at the level of the MCR.3. Mixed mechanism. Cessation of blood flow. Decrease by 75% or more. Ischemic syndrome.

4. Etiology and pathogenesis of myocardial infarction. Differences between myocardial infarction and angina according to laboratory diagnostics. The phenomenon of reperfusion. myocardial infarction. - an area of ​​myocardial necrosis occurs as a result of cessation of blood flow or its supply in quantities insufficient for the needs of the myocardium. At the site of infarction: - mitochondria swell and collapse - nuclei swell, pyknosis of nuclei. transverse striation disappears, loss of glycogen, K + cells die, macrophages form a connective tissue tissue at the site of infarction.1. Ischemic syndrome2. Pain syndrome3. Post-ischemic reperfusion syndrome is the restoration of coronary blood flow in a previously ischemic area. It develops as a result of: 1. Blood flow through collaterals2. Retrograde blood flow through venules3. Dilatation of previously spasmodic coronary arterioles4. Thrombolysis or disaggregation of formed elements.1. Restoration of the myocardium (organic necrosis).2. Additional damage to the myocardium - heterogeneity of the myocardium increases: different blood supply, different oxygen tension, different ion concentration Complications of myocardial infarction: 1. Cardiogenic shock - due to contractile weakness of the left ejection and decreased blood supply to vital organs (brain).2. Ventricular fibrillation (damage to 33% of Purkinje cells and false tendon fibers: vacuolization of the sarcoplasmic reticulum, destruction of glycogen, destruction of intercalated discs, overcontraction of cells, decrease in sarcolemmal permeability. Myocardiogenic mechanism: Causes of nervous stress: discrepancy between biorhythms and heart rhythms. Meyerson, using a model of emotional-painful stress, developed the pathogenesis of damage during stress damage to the heart.

5. Cardiac and extracardiac mechanisms of compensation for heart failure. Myocardial hypertrophy, pathogenesis, stages of development, differences from non-hypertrophied myocardium. Cardiac mechanisms of compensation of cardiac activity: Conventionally, 4 (four) cardiac mechanisms of cardiac activity are distinguished in CH.1. Heterometric Frank-Starling compensation mechanism: If the degree of stretching of muscle fibers exceeds permissible limits, then the force of contraction decreases. With permissible overloads, the linear dimensions of the heart increase by no more than 15-20%. This expansion of the cavities is called tonogenic dilatation and is accompanied by an increase in stroke volume. Dystrophic changes in the myocardium lead to expansion of the cavities without an increase in stroke volume. This is myogenic dilatation (a sign of decompensation).2. Isometric compensation mechanism: During pressure overload Increase in the time of interaction between actin and myosin Increase in pressure and tension of the muscle fiber at the end of diastole The isometric mechanism is more energy-intensive than the heterometric one. The heterometric mechanism is energetically more favorable than the isometric one. Therefore, valvular insufficiency has a more favorable course than stenosis.3. Tachycardia: occurs in situations: = Increased pressure in the vena cava. = Increased pressure in the right atrium and its stretching. = Change in nervous influences. = Change in humoral extracardiac influences. 4. Strengthening sympathoadrenal influences on the myocardium: it turns on when SV decreases and significantly increases the force of myocardial contractions. Hypertrophy is an increase in the volume and mass of the myocardium. Occurs during the implementation of cardiac compensation mechanisms. Heart hypertrophy occurs according to the type of unbalanced growth: 1. Violation of the regulatory support of the heart: the number of sympathetic nerve fibers grows more slowly than the myocardial mass grows.2. The growth of capillaries lags behind the growth of muscle mass - a violation of the vascular supply of the myocardium.3. At the cellular level: 1) The volume of the cell increases more than the surface: cell nutrition, Na+-K+ pumps, oxygen diffusion are inhibited. 2) The volume of the cell increases due to the cytoplasm - the mass of the nucleus lags behind: the provision of the cell with matrix material decreases - plastic supply decreases cells.3) The mass of mitochondria lags behind the growth of myocardial mass. - the energy supply of the cell is disrupted.4. At the molecular level: the ATPase activity of myosin and their ability to use ATP energy are reduced. KGS prevents acute heart failure, but unbalanced growth contributes to the development of chronic heart failure.

6. Left ventricular and right ventricular heart failure. Cellular and molecular basis of heart failure. left ventricular failure, the pressure in the left atrium, in the pulmonary veins increases. a) an increase in pressure in the ventricle in diastole reduces the outflow from the atrium b) stretching of atrioventricular coagulation and relative valve insufficiency as a result of dilatation of the ventricle, regurgitation of blood occurs in the atrium in systole, which leads to increased pressure in the atria. right ventricular failure: congestion in the systemic circle, in the liver, in the portal vein, in the intestinal vessels, in the spleen, in the kidneys, in the lower extremities (edema), dropsy of the cavities. Cell-molecule basis: energy deficiency, accumulation of under-oxidized metabolic products , thread-like substances are the cause of pain in the heart. Excitation of the sympathetic nervous system and the release of stress hormones: catecholamines and glucocorticoids. As a result: hypoxia, activation of LPO in the membranes of cellular and subcellular structures, release of lysosomal hydrolases, cardiomyocyte contractures, cardiomyocyte necrosis. Small foci of necrosis appear - they are replaced by connective tissue (if ischemia is less than 30 minutes Activation of LPO in connective tissue (if ischemia lasts more than 30 minutes) release of lysosomes into the intercellular space - blockage of coronary vessels - myocardial infarction. - an area of ​​myocardial necrosis occurs as a result of cessation of blood flow or its supply in quantities insufficient for the needs of the myocardium.

7. Heart rhythm disorders. Impaired excitability, conductivity and contractility of the heart. Types, causes, mechanism of development, ECG characteristics. Cardiac excitability disorders Sinus arrhythmia. It manifests itself in the form of "unequal duration of intervals between heart contractions and depends on the occurrence of impulses in the sinus node at unequal intervals of time. In most cases, sinus arrhythmia is a physiological phenomenon, more often occurring in children, youth and adolescents, for example, respiratory arrhythmia (increased heart contractions during inhalation and slowdown during the respiratory pause). Sinus arrhythmia also occurred in experiments with the action of diphtheria toxin on the heart. This toxin has an anticholinesterase effect. A decrease in cholinesterase activity promotes the accumulation of acetylcholine in the myocardium and increases the influence of the vagus nerve conduction system, contributing to the occurrence of sinus bradycardia and arrhythmias. Extrasystole is a premature contraction of the heart or its ventricles due to the appearance of an additional impulse from a heterotopic or “ectopic” focus of excitation. Depending on the location of the appearance of the additional impulse, atrial, atrioventricular and ventricular extrasystoles are distinguished. Atrial extrasystoles - additional the impulse originates in the wall of the atrium. The electrocardiogram differs from the normal one in the smaller size of the P wave. Atrioventricular extrasystole - an additional impulse occurs in the atrioventricular node. The excitation wave spreads across the atrial myocardium in the direction opposite to the usual one, and a negative P wave appears on the electrocardiogram. Ventricular extrasystoles and an additional impulse arises in the conduction system of one of the ventricles of the heart and primarily causes excitation of this particular ventricle. A ventricular complex of a sharply changed configuration appears on the electrocardiogram. Ventricular extrasystole is characterized by a compensatory pause—an extended interval between the extrasystole and the following normal contraction. The interval before the extrasystole is usually shortened. Cardiac conduction disorders Impaired conduction of impulses through the conduction system of the heart is called blockade. The blockade can be partial or complete. The conduction interruption can occur anywhere along the path from the sinus node to the terminal branches of the atrioventricular bundle (bundle of His). There are: 1) sinoauricular block, in which the conduction of impulses between the sinus node and the atrium is interrupted; 2) atrioventricular (atrioventricular) blockade, in which the impulse is blocked in the atrioventricular node; 3) blockade of the atrioventricular bundle, when the conduction of impulses along the right or left leg of the atrioventricular bundle is impaired.

8. Vascular form of circulatory failure. Hypertension: etiology, pathogenesis. Symptomatic hypertension. Changes in blood pressure levels are the result of a violation of one of the following factors (usually a combination of them): 1 the amount of blood entering the vascular system per unit time-minute volume of the heart; 2) the value of peripheral vascular resistance; 3) changes in elastic stress and other mechanical properties of the walls of the aorta and its large branches; U), changes in blood viscosity, disrupting blood flow in the vessels. The main influence on blood pressure is exerted by the cardiac output and peripheral vascular resistance, which in turn depends on the elastic tension of the blood vessels. Hypertension and essential hypertension All conditions with increased blood pressure can be divided into two groups: primary (essential) hypertension, or hypertension, and secondary, or symptomatic, hypertension. A distinction is made between systolic and diastolic hypertension. The isolated form of systolic hypertension depends on increased heart function and occurs as a symptom of Graves' disease and aortic valve insufficiency. Diastolic hypertension is determined by narrowing of arterioles and increased peripheral vascular resistance. It is accompanied by increased work of the left ventricle of the heart and ultimately leads to hypertrophy of the left ventricular muscle. Increased heart function and an increase in minute blood volume cause the appearance of systolic hypertension. Symptomatic (secondary) hypertension includes the following forms: hypertension in kidney diseases, endocrine forms of hypertension, hypertension in organic lesions of the central nervous system (tumors and injuries of the interstitial and medulla oblongata, hemorrhages , concussion, etc.). This also includes forms of hemodynamic-type hypertension, i.e., caused by lesions of the cardiovascular system.

9. Vascular hypotension, causes, mechanism of development. Compensatory and adaptive mechanisms. Collapse, different from shock. Hypotension is a decrease in vascular tone and a drop in blood pressure. The lower limit of normal systolic blood pressure is considered to be 100-105 mmHg, diastolic 60-65 mmHg. The average blood pressure is 80 mmHg/art. Average blood pressure figures for people living in the southern regions , tropical and subtropical countries, slightly lower. Blood pressure levels change with age. Hypotension is a condition in which the mean arterial pressure is below 75 mm Hg. Art. A decrease in blood pressure can occur quickly and sharply (acute vascular insufficiency-shock, collapse) or develop slowly (hypotensive conditions). With pathological hypotension, the blood supply to tissues and their supply of oxygen suffers, which is accompanied by dysfunction of various systems and organs. Pathological hypotension can be symptomatic, accompanying the underlying disease (pulmonary tuberculosis, severe forms of anemia, gastric ulcer, Addison's disease, pituitary cachexia and npi). Prolonged fasting causes severe hypotension. With primary or neurocirculatory hypotension, a chronic decrease in blood pressure is one of the first and main symptoms of the disease. Special studies reveal in primary hypotension some dysfunctions of the CENTRAL nervous system - weakening or perversion of vascular reflexes, deviation from the norm vascular reactions to cold, heat, painful stimuli. It is believed that with neurocirculatory hypotension (as well as with hypertension), there is a violation of the central mechanisms of regulation of vascular tone. The main pathological changes with hypotension occur in the same vascular areas as with hypertension - in the arterioles. Violation of the mechanisms of regulation of vascular tone leads in this case to a drop in the tone of the arterioles, expansion of their lumen, a decrease in peripheral resistance and a decrease in blood pressure. At the same time, the volume of circulating blood decreases, and the cardiac output often increases. With collapse, there is a drop in blood pressure and a deterioration in the blood supply to vital organs. These changes are reversible. In shock, multiple organ disturbances occur in the vital functions of the cardiovascular system, nervous and endocrine systems, as well as disturbances in breathing, tissue metabolism, and kidney function. If shock is characterized by a decrease in arterial and venous blood pressure; cold and damp skin with a marbled or pale bluish coloration; tachycardia; breathing problems; decreased amount of urine; the presence of either a phase of anxiety or blackout, then collapse is characterized by severe weakness, pallor of the skin and mucous membranes, coldness of the extremities, and of course, a decrease in blood pressure.

PATHOPHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM

Heart failure.

Heart failure develops when there is a discrepancy between the load placed on the heart and its ability to produce work, which is determined by the amount of blood flowing to the heart and its resistance to expulsion of blood in the aorta and pulmonary trunk. Vascular insufficiency is conventionally distinguished from heart failure; with the second, blood flow to the heart primarily decreases (shock, fainting). In both cases, circulatory failure occurs, that is, the inability to provide the body with a sufficient amount of blood at rest and during physiological stress.

It can be acute, chronic, latent, manifesting itself only during physical activity, or obvious, with disturbances of hemodynamics, the function of internal organs, metabolism, and a sharp limitation of working capacity. Heart failure is primarily associated with impaired myocardial function. It may arise as a result of:

1) overload of the myocardium when excessive demands are placed on it (heart defects, hypertension, excessive physical activity). With congenital malformations, HF is most often observed in the first 3 months of life.

2) myocardial damage (endocarditis, intoxication, coronary circulation disorders, etc.). Under these conditions, failure develops with normal or reduced load on the heart.

3) mechanical limitation of diastole (effusion pleurisy, pericarditis).

4) a combination of these factors.

Heart failure can cause circulatory decompensation at rest or during exercise, which manifests itself in the form of:

1) reducing the strength and speed of contraction, the strength and speed of relaxation of the heart. The result is a subcontracture state and insufficient diastolic filling.

2) a sharp decrease in stroke volume with an increase in residual volume and end-diastolic volume and end-diastolic pressure from overflow, i.e. myogenic dilatation.

3) a decrease in minute volume with an increase in the arteriovenous difference in oxygen.

This symptom is first detected during functional stress tests.

Sometimes heart failure develops against the background of a normal minute volume, which is explained by an increase in the volume of circulating blood due to fluid retention in the body, however, the arteriovenous difference in oxygen also increases in this case, because hypertrophied myocardium consumes more oxygen, performing more work. Stagnation of blood in the pulmonary circle increases blood rigidity and thereby also increases oxygen consumption.

4) an increase in pressure in those parts of the bloodstream from which blood enters the insufficient half of the heart, that is, in the pulmonary veins with insufficiency of the left heart and in the vena cava with right ventricular failure. Increased atrial pressure causes tachycardia. In the early stages, it occurs only during physical activity and the pulse does not normalize earlier than 10 minutes after stopping the exercise. As HF progresses, tachycardia can also be observed at rest.

5) reducing blood flow speed.

In addition to these signs, symptoms of decompensation such as cyanosis, shortness of breath, edema, etc. also appear. It is important to emphasize that the development of heart failure is accompanied by the appearance of heart rhythm disturbances, which significantly affects the course and prognosis. The severity of hemodynamic changes and the manifestation of symptoms of heart failure largely depend on which part of the heart is predominantly damaged.

Features of the pathogenesis of insufficiency
blood circulation according to the left ventricular type.

When the left side of the heart is weakened, the blood supply to the pulmonary circle increases and the pressure in the left atrium and pulmonary veins, capillaries, and arteries increases. This leads to severe, painful shortness of breath, hemoptysis, and pulmonary edema. These phenomena intensify with an increase in venous return to the right heart (with muscle load, emotional stress, horizontal body position). At a certain stage, in many patients, the Kitaev reflex turns on, and as a result of spasm of the pulmonary arterioles, the peripheral vascular resistance of the lungs increases (50, or even 500 times). The long-term spastic state of small arteries leads to their sclerosis and thus, a second barrier is formed in the path of blood flow (the 1st barrier is a defect). This barrier reduces the risk of developing pulmonary edema, but also entails negative consequences: 1) as spasm and sclerosis increase, the blood MO decreases; 2) increased shunting of blood flow bypassing the capillaries, which increases hypoxemia; 3) an increase in the load on the right ventricle leads to its concentric hypertrophy, and subsequently to failure of the right heart. From the moment of the addition of right ventricular failure, the small circle is destroyed. Congestion moves into the veins of the systemic circle, the patient feels subjective relief.

Right ventricular failure.

With right ventricular failure, there is stagnation of blood and an increase in blood supply to the venous part of the systemic circulation, and a decrease in flow to the left side of the heart.

Following a decrease in cardiac output, effective arterial blood flow decreases in all organs, including the kidneys. Activation of the RAS (renin-aldosterone system) leads to the retention of sodium chloride and water and the loss of potassium ions, which

unfavorable for the myocardium. Due to arterial hypovolemia and a decrease in minute volume, the tone of the arterial vessels of the systemic circle increases and the retained fluid moves into the veins of the systemic circle - venous pressure increases, the liver enlarges, edema and cyanosis develop. Due to hypoxia and blood stagnation, liver cirrhosis occurs with the development of ascites, and degeneration of internal organs progresses.

There is no completely isolated right ventricular failure, because the left ventricle also suffers. In response to a decrease in cardiac output, long-term continuous sympathetic stimulation of this part of the heart occurs, and this, in conditions of deterioration of coronary circulation, contributes to accelerated wear of the myocardium.

Secondly, the loss of potassium ions leads to a decrease in the strength of heart contractions.

Thirdly, coronary blood flow decreases and blood supply, as a rule, to the hypertrophied left side of the heart deteriorates.

Myocardial hypoxia

Hypoxia can be of 4 types: respiratory, blood, histotoxic, hemodynamic. Since the myocardium, even under resting conditions, extracts 75% of the incoming blood, and in skeletal muscle 20% of the O2 contained in it, the only way to ensure the increased need of the heart for O2 is to increase coronary blood flow. This makes the heart, like no other organ, dependent on the state of the blood vessels, the mechanisms of regulation of coronary blood flow and the ability of the coronary arteries to adequately respond to changes in load. Therefore, most often the development of myocardial hypoxia is associated with the development of circulatory hypoxia and, in particular, myocardial ischemia. This is what underlies coronary heart disease (CHD). It should be borne in mind that coronary heart disease is a collective concept that unites different syndromes and nosological units. In the clinic, such typical manifestations of coronary artery disease as angina pectoris, arrhythmias, myocardial infarction due to which suddenly, i.e. within an hour after the onset of the attack, more than half of patients with ischemic heart disease die, and it also leads to the development of heart failure due to cardiosclerosis. The pathogenesis of IHD is based on an imbalance between the need of the heart muscle for O2 and its delivery through the blood. This discrepancy may arise as a result of: firstly, an increase in myocardial demand for O2; secondly, reducing blood flow through the coronary arteries; thirdly, when these factors are combined.

The main one (in terms of frequency) is a decrease in blood flow as a result of stenosing atherosclerotic lesions of the coronary arteries of the heart (95%), but there are cases when a person who died from a myocardial infarction does not exhibit an organic decrease in the lumen of blood vessels. This situation occurs in 5% of those who die from myocardial infarction, and in 10% of people suffering from coronary artery disease, in the form of angina, the coronary arteries are not angiographically changed. In this case, they speak of myocardial hypoxia of functional origin. The development of hypoxia may be associated with:

1. With an uncompensated increase in myocardial oxygen demand.

This may occur primarily as a result of the action of catecholamines on the heart. By administering adrenaline, norepinephrine to animals or stimulating sympathetic nerves, necrosis in the myocardium can be obtained. On the other hand, catecholamines increase blood supply to the myocardium, causing dilatation of the coronary arteries, this is facilitated by the accumulation of metabolic products, in particular, adenosine, which has a powerful vasodilator effect, this is also facilitated by an increase in pressure in the aorta and an increase in MO, and on the other hand, they, i.e. e. catecholamines increase myocardial oxygen demand. Thus, the experiment established that irritation of the sympathetic nerves of the heart leads to an increase in oxygen consumption by 100%, and coronary blood flow by only 37%. The increase in myocardial oxygen demand under the influence of catecholamines is associated with:

1) with a direct energy-tropic effect on the myocardium. It is realized through the stimulation of beta‑1‑AR cardiomyocytes and the opening of calcium channels.

2) CAs cause constriction of peripheral arterioles and increase peripheral vascular resistance, which significantly increases the afterload on the myocardium.

3) tachycardia occurs, which limits the possibilities of increasing blood flow in the hard-working heart. (Shortening of diastole).

4) through damage to cell membranes. Catechamines activate lipases, in particular phospholipase A2, which damages the mitochondrial membranes and SPR and leads to the release of calcium ions into the myoplasm, which further damages cellular organelles (see section “Cell Damage”). Leukocytes are retained at the site of damage and release a lot of biologically active substances (BAS). There is a blockage of the microcirculatory bed, mainly by neutrophils. In humans, the number of catecholamines sharply increases in stressful situations (intense physical activity, psycho-emotional stress, trauma, pain) by 10-100 times, which in some people is accompanied by an attack of angina in the absence of organic changes in the coronary vessels. Under stress, the pathogenic effect of catecholamines can be enhanced by overproduction of corticosteroids. The release of mineralocorticoids causes Na retention and causes increased potassium excretion. This leads to increased sensitivity of the heart and blood vessels to the action of catecholamines.

Glucocorticoids, on the one hand, stabilize the resistance of membranes to damage, and on the other, significantly increase the effect of catelolamines and promote Na retention. Long-term excess of Na and lack of potassium causes disseminated non-coronarogenic myocardial necrosis. (Administration of K + and Mg 2+ salts, Ca channel blockers can prevent or reduce myocardial necrosis after coronary artery ligation).

The occurrence of catecholamine cardiac damage is facilitated by:

1) lack of regular physical training, when tachycardia becomes the main compensation factor during physical activity. A trained heart uses energy more economically, and the capacity of O2 transport and utilization systems, membrane pumps, and antioxidant systems increases. Moderate physical activity reduces the effects of psycho-emotional stress and, if it accompanies or follows stress, it accelerates the breakdown of catecholamines and inhibits the secretion of corticoids. The excitement associated with emotions in the nerve centers decreases (physical activity extinguishes the “flame of emotions”). Stress prepares the body for action: flight, fight, i.e. physical activity. Under conditions of inactivity, its negative consequences on the myocardium and blood vessels are more pronounced. Moderate running or walking is a good preventative factor.

The second condition that contributes to catecholamine injury is smoking.

Thirdly, a person’s constitutional characteristics play a very important role.

Thus, catecholamines can cause myocardial damage, but only in combination with the appropriate conditions.

On the other hand, we must remember that disruption of the sympathetic innervation of the heart makes it difficult to mobilize compensatory mechanisms and contributes to faster wear and tear of the heart. The 2nd pathogenetic factor of IHD is a decrease in O2 delivery to the myocardium. It may be related:

1. With spasm of the coronary arteries. Spasm of the coronary arteries can occur at complete rest, often at night in the fast phase of sleep, when the tone of the autonomic nervous system increases or due to physical or emotional overload, smoking, or overeating. A comprehensive study of spasm of the coronary arteries showed that in the vast majority of patients it occurs against the background of organic changes in the coronary vessels. In particular, damage to the endothelium leads to a local change in the reactivity of the vascular walls. In the implementation of this effect, a large role belongs to the products of arachidonic acid - prostacyclin and thromboxane A 2. The intact endothelium produces prostaglandin prostacyclin (PGJ 2) - it has pronounced antiaggregation activity against platelets and dilates blood vessels, i.e. prevents the development of hypoxia. When the endothelium is damaged, platelets adhere to the vessel wall; under the influence of catecholamines, they synthesize thromboxane A2, which has pronounced vasoconstrictor properties and can cause local spasm of the arteries and platelet aggregation. Platelets secrete a factor that stimulates the proliferation of fibroblasts and smooth muscle cells and their migration into the intima, which is observed during the formation of an atherosclerotic plaque. In addition, the unchanged endothelium, under the influence of catecholamines, produces the so-called endothelial relaxation factor (ERF), which acts locally on the vascular wall and is nitric oxide -NO. When the endothelium is damaged, which is more pronounced in older people, the production of this factor decreases, resulting in a sharp decrease in the sensitivity of blood vessels to the action of vasodilators, and with increased hypoxia, the endothelium produces the polypeptide endothelin, which has vasoconstrictor properties. In addition, local spasm of the coronary vessels can be caused by leukocytes (mainly neutrophils) retained in small arteries, releasing the products of the lipoxygenase pathway for the conversion of arachidonic acid - leukotrienes C 4, D 4.

If, under the influence of spasm, the lumen of the arteries decreases by 75%, then the patient develops symptoms of angina pectoris. If the spasm leads to complete closure of the lumen of the coronary artery, then, depending on the duration of the spasm, an attack of resting angina pectoris, myocardial infarction or sudden death may occur.

2. With a decrease in blood flow due to blockage of the arteries of the heart by aggregates of platelets and leukocytes, which is facilitated by a violation of the rheological properties of the blood. The formation of aggregates is enhanced under the influence of catecholamines; their formation can become an important additional factor determining coronary circulatory disorders, pathogenetically associated with arteriosclerosis. plaque and with angiospasmodic reactions. At the site of atherosclerotic damage to the vascular wall, the production of EGF and prostacyclin decreases. Here, platelet aggregates are especially easily formed with all possible consequences, and a vicious circle is completed: platelet aggregates contribute to atherosclerosis, and atherosclerosis promotes platelet aggregation.

3. A decrease in blood supply to the heart may occur due to a decrease in cardiac output as a result of acute. vessel. insufficient, decrease in venous return with a drop in pressure in the aorta and coronary vessels. This can be due to shock or collapse.

Myocardial hypoxia due to organic lesions
coronary arteries.

Firstly, there are cases when myocardial blood circulation is limited as a result of a hereditary defect in the development of the coronary arteries. In this case, symptoms of coronary disease may appear in childhood. However, the most important cause is atherosclerosis of the coronary arteries. Atherosclerotic changes begin early. Lipid spots and streaks are found even in newborns. In the second decade of life, atherosclerotic plaques in the coronary arteries are found in every person after 40 years in 55%, and after 60% of cases. Atherosclerosis develops most quickly in men at the age of 40-50 years, in women later. 95% of patients with myocardial infarction have atherosclerotic changes in the coronary arteries.

Secondly, an atherosclerotic plaque prevents blood vessels from expanding and this contributes to hypoxia in all cases when the load on the heart increases (physical activity, emotions, etc.).

Thirdly, atherosclerotic plaque reduces this lumen. Scar connective tissue, which forms at the site of the plaque, narrows the lumen up to obstructive ischemia. When the contraction is more than 95%, the slightest activity causes an attack of angina. With slow progression of the atherosclerotic process, ischemia may not occur due to the development of collaterals. There is no atherosclerosis in them. But sometimes obstruction of the coronary arteries occurs instantly when hemorrhage occurs in an atherosclerotic plaque.

PATHOPHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM

Heart failure.

Heart failure develops when there is a discrepancy between the load placed on the heart and its ability to produce work, which is determined by the amount of blood flowing to the heart and its resistance to expulsion of blood in the aorta and pulmonary trunk. Vascular insufficiency is conventionally distinguished from heart failure; with the second, blood flow to the heart primarily decreases (shock, fainting). In both cases, circulatory failure occurs, that is, the inability to provide the body with a sufficient amount of blood at rest and during physiological stress.

It can be acute, chronic, latent, manifesting itself only during physical activity, or obvious, with disturbances of hemodynamics, the function of internal organs, metabolism, and a sharp limitation of working capacity. Heart failure is primarily associated with impaired myocardial function. It may arise as a result of:

1) overload of the myocardium when excessive demands are placed on it (heart defects, hypertension, excessive physical activity). With congenital malformations, HF is most often observed in the first 3 months of life.

2) myocardial damage (endocarditis, intoxication, coronary circulation disorders, etc.). Under these conditions, failure develops with normal or reduced load on the heart.

3) mechanical limitation of diastole (effusion pleurisy, pericarditis).

4) a combination of these factors.

Heart failure can cause circulatory decompensation at rest or during exercise, which manifests itself in the form of:

1) reducing the strength and speed of contraction, the strength and speed of relaxation of the heart. The result is a subcontracture state and insufficient diastolic filling.

2) a sharp decrease in stroke volume with an increase in residual volume and end-diastolic volume and end-diastolic pressure from overflow, i.e. myogenic dilatation.

3) a decrease in minute volume with an increase in the arteriovenous difference in oxygen.

This symptom is first detected during functional stress tests.

Sometimes heart failure develops against the background of a normal minute volume, which is explained by an increase in the volume of circulating blood due to fluid retention in the body, however, the arteriovenous difference in oxygen also increases in this case, because hypertrophied myocardium consumes more oxygen, performing more work. Stagnation of blood in the pulmonary circle increases blood rigidity and thereby also increases oxygen consumption.

4) an increase in pressure in those parts of the bloodstream from which blood enters the insufficient half of the heart, that is, in the pulmonary veins with insufficiency of the left heart and in the vena cava with right ventricular failure. Increased atrial pressure causes tachycardia. In the early stages, it occurs only during physical activity and the pulse does not normalize earlier than 10 minutes after stopping the exercise. As HF progresses, tachycardia can also be observed at rest.

5) reducing blood flow speed.

In addition to these signs, symptoms of decompensation such as cyanosis, shortness of breath, edema, etc. also appear. It is important to emphasize that the development of heart failure is accompanied by the appearance of heart rhythm disturbances, which significantly affects the course and prognosis. The severity of hemodynamic changes and the manifestation of symptoms of heart failure largely depend on which part of the heart is predominantly damaged.

Features of the pathogenesis of insufficiency
blood circulation according to the left ventricular type.

When the left side of the heart is weakened, the blood supply to the pulmonary circle increases and the pressure in the left atrium and pulmonary veins, capillaries, and arteries increases. This leads to severe, painful shortness of breath, hemoptysis, and pulmonary edema. These phenomena intensify with an increase in venous return to the right heart (with muscle load, emotional stress, horizontal body position). At a certain stage, in many patients, the Kitaev reflex turns on, and as a result of spasm of the pulmonary arterioles, the peripheral vascular resistance of the lungs increases (50, or even 500 times). The long-term spastic state of small arteries leads to their sclerosis and thus, a second barrier is formed in the path of blood flow (the 1st barrier is a defect). This barrier reduces the risk of developing pulmonary edema, but also entails negative consequences: 1) as spasm and sclerosis increase, the blood MO decreases; 2) increased shunting of blood flow bypassing the capillaries, which increases hypoxemia; 3) an increase in the load on the right ventricle leads to its concentric hypertrophy, and subsequently to failure of the right heart. From the moment of the addition of right ventricular failure, the small circle is destroyed. Congestion moves into the veins of the systemic circle, the patient feels subjective relief.

Right ventricular failure.

With right ventricular failure, there is stagnation of blood and an increase in blood supply to the venous part of the systemic circulation, and a decrease in flow to the left side of the heart.

Following a decrease in cardiac output, effective arterial blood flow decreases in all organs, including the kidneys. Activation of the RAS (renin-aldosterone system) leads to the retention of sodium chloride and water and the loss of potassium ions, which

unfavorable for the myocardium. Due to arterial hypovolemia and a decrease in minute volume, the tone of the arterial vessels of the systemic circle increases and the retained fluid moves into the veins of the systemic circle - venous pressure increases, the liver enlarges, edema and cyanosis develop. Due to hypoxia and blood stagnation, liver cirrhosis occurs with the development of ascites, and degeneration of internal organs progresses.

There is no completely isolated right ventricular failure, because the left ventricle also suffers. In response to a decrease in cardiac output, long-term continuous sympathetic stimulation of this part of the heart occurs, and this, in conditions of deterioration of coronary circulation, contributes to accelerated wear of the myocardium.

Secondly, the loss of potassium ions leads to a decrease in the strength of heart contractions.

Thirdly, coronary blood flow decreases and blood supply, as a rule, to the hypertrophied left side of the heart deteriorates.

Myocardial hypoxia

Hypoxia can be of 4 types: respiratory, blood, histotoxic, hemodynamic. Since the myocardium, even under resting conditions, extracts 75% of the incoming blood, and in skeletal muscle 20% of the O2 contained in it, the only way to ensure the increased need of the heart for O2 is to increase coronary blood flow. This makes the heart, like no other organ, dependent on the state of the blood vessels, the mechanisms of regulation of coronary blood flow and the ability of the coronary arteries to adequately respond to changes in load. Therefore, most often the development of myocardial hypoxia is associated with the development of circulatory hypoxia and, in particular, myocardial ischemia. This is what underlies coronary heart disease (CHD). It should be borne in mind that coronary heart disease is a collective concept that unites different syndromes and nosological units. In the clinic, such typical manifestations of coronary artery disease as angina pectoris, arrhythmias, myocardial infarction due to which suddenly, i.e. within an hour after the onset of the attack, more than half of patients with ischemic heart disease die, and it also leads to the development of heart failure due to cardiosclerosis. The pathogenesis of IHD is based on an imbalance between the need of the heart muscle for O2 and its delivery through the blood. This discrepancy may arise as a result of: firstly, an increase in myocardial demand for O2; secondly, reducing blood flow through the coronary arteries; thirdly, when these factors are combined.

The main one (in terms of frequency) is a decrease in blood flow as a result of stenosing atherosclerotic lesions of the coronary arteries of the heart (95%), but there are cases when a person who died from a myocardial infarction does not exhibit an organic decrease in the lumen of blood vessels. This situation occurs in 5% of those who die from myocardial infarction, and in 10% of people suffering from coronary artery disease, in the form of angina, the coronary arteries are not angiographically changed. In this case, they speak of myocardial hypoxia of functional origin. The development of hypoxia may be associated with:

1. With an uncompensated increase in myocardial oxygen demand.

This may occur primarily as a result of the action of catecholamines on the heart. By administering adrenaline, norepinephrine to animals or stimulating sympathetic nerves, necrosis in the myocardium can be obtained. On the other hand, catecholamines increase blood supply to the myocardium, causing dilatation of the coronary arteries, this is facilitated by the accumulation of metabolic products, in particular, adenosine, which has a powerful vasodilator effect, this is also facilitated by an increase in pressure in the aorta and an increase in MO, and on the other hand, they, i.e. e. catecholamines increase myocardial oxygen demand. Thus, the experiment established that irritation of the sympathetic nerves of the heart leads to an increase in oxygen consumption by 100%, and coronary blood flow by only 37%. The increase in myocardial oxygen demand under the influence of catecholamines is associated with:

1) with a direct energy-tropic effect on the myocardium. It is realized through the stimulation of beta‑1‑AR cardiomyocytes and the opening of calcium channels.

2) CAs cause constriction of peripheral arterioles and increase peripheral vascular resistance, which significantly increases the afterload on the myocardium.

3) tachycardia occurs, which limits the possibilities of increasing blood flow in the hard-working heart. (Shortening of diastole).

4) through damage to cell membranes. Catechamines activate lipases, in particular phospholipase A2, which damages the mitochondrial membranes and SPR and leads to the release of calcium ions into the myoplasm, which further damages cellular organelles (see section “Cell Damage”). Leukocytes are retained at the site of damage and release a lot of biologically active substances (BAS). There is a blockage of the microcirculatory bed, mainly by neutrophils. In humans, the number of catecholamines sharply increases in stressful situations (intense physical activity, psycho-emotional stress, trauma, pain) by 10-100 times, which in some people is accompanied by an attack of angina in the absence of organic changes in the coronary vessels. Under stress, the pathogenic effect of catecholamines can be enhanced by overproduction of corticosteroids. The release of mineralocorticoids causes Na retention and causes increased potassium excretion. This leads to increased sensitivity of the heart and blood vessels to the action of catecholamines.

Glucocorticoids, on the one hand, stabilize the resistance of membranes to damage, and on the other, significantly increase the effect of catelolamines and promote Na retention. Long-term excess of Na and lack of potassium causes disseminated non-coronarogenic myocardial necrosis. (Administration of K + and Mg 2+ salts, Ca channel blockers can prevent or reduce myocardial necrosis after coronary artery ligation).

The occurrence of catecholamine cardiac damage is facilitated by:

1) lack of regular physical training, when tachycardia becomes the main compensation factor during physical activity. A trained heart uses energy more economically, and the capacity of O2 transport and utilization systems, membrane pumps, and antioxidant systems increases. Moderate physical activity reduces the effects of psycho-emotional stress and, if it accompanies or follows stress, it accelerates the breakdown of catecholamines and inhibits the secretion of corticoids. The excitement associated with emotions in the nerve centers decreases (physical activity extinguishes the “flame of emotions”). Stress prepares the body for action: flight, fight, i.e. physical activity. Under conditions of inactivity, its negative consequences on the myocardium and blood vessels are more pronounced. Moderate running or walking is a good preventative factor.

The second condition that contributes to catecholamine injury is smoking.

Thirdly, a person’s constitutional characteristics play a very important role.

Thus, catecholamines can cause myocardial damage, but only in combination with the appropriate conditions.

On the other hand, we must remember that disruption of the sympathetic innervation of the heart makes it difficult to mobilize compensatory mechanisms and contributes to faster wear and tear of the heart. The 2nd pathogenetic factor of IHD is a decrease in O2 delivery to the myocardium. It may be related:

1. With spasm of the coronary arteries. Spasm of the coronary arteries can occur at complete rest, often at night in the fast phase of sleep, when the tone of the autonomic nervous system increases or due to physical or emotional overload, smoking, or overeating. A comprehensive study of spasm of the coronary arteries showed that in the vast majority of patients it occurs against the background of organic changes in the coronary vessels. In particular, damage to the endothelium leads to a local change in the reactivity of the vascular walls. In the implementation of this effect, a large role belongs to the products of arachidonic acid - prostacyclin and thromboxane A 2. The intact endothelium produces prostaglandin prostacyclin (PGJ 2) - it has pronounced antiaggregation activity against platelets and dilates blood vessels, i.e. prevents the development of hypoxia. When the endothelium is damaged, platelets adhere to the vessel wall; under the influence of catecholamines, they synthesize thromboxane A2, which has pronounced vasoconstrictor properties and can cause local spasm of the arteries and platelet aggregation. Platelets secrete a factor that stimulates the proliferation of fibroblasts and smooth muscle cells and their migration into the intima, which is observed during the formation of an atherosclerotic plaque. In addition, the unchanged endothelium, under the influence of catecholamines, produces the so-called endothelial relaxation factor (ERF), which acts locally on the vascular wall and is nitric oxide -NO. When the endothelium is damaged, which is more pronounced in older people, the production of this factor decreases, resulting in a sharp decrease in the sensitivity of blood vessels to the action of vasodilators, and with increased hypoxia, the endothelium produces the polypeptide endothelin, which has vasoconstrictor properties. In addition, local spasm of the coronary vessels can be caused by leukocytes (mainly neutrophils) retained in small arteries, releasing the products of the lipoxygenase pathway for the conversion of arachidonic acid - leukotrienes C 4, D 4.

If, under the influence of spasm, the lumen of the arteries decreases by 75%, then the patient develops symptoms of angina pectoris. If the spasm leads to complete closure of the lumen of the coronary artery, then, depending on the duration of the spasm, an attack of resting angina pectoris, myocardial infarction or sudden death may occur.

2. With a decrease in blood flow due to blockage of the arteries of the heart by aggregates of platelets and leukocytes, which is facilitated by a violation of the rheological properties of the blood. The formation of aggregates is enhanced under the influence of catecholamines; their formation can become an important additional factor determining coronary circulatory disorders, pathogenetically associated with arteriosclerosis. plaque and with angiospasmodic reactions. At the site of atherosclerotic damage to the vascular wall, the production of EGF and prostacyclin decreases. Here, platelet aggregates are especially easily formed with all possible consequences, and a vicious circle is completed: platelet aggregates contribute to atherosclerosis, and atherosclerosis promotes platelet aggregation.

3. A decrease in blood supply to the heart may occur due to a decrease in cardiac output as a result of acute. vessel. insufficient, decrease in venous return with a drop in pressure in the aorta and coronary vessels. This can be due to shock or collapse.

Myocardial hypoxia due to organic lesions
coronary arteries.

Firstly, there are cases when myocardial blood circulation is limited as a result of a hereditary defect in the development of the coronary arteries. In this case, symptoms of coronary disease may appear in childhood. However, the most important cause is atherosclerosis of the coronary arteries. Atherosclerotic changes begin early. Lipid spots and streaks are found even in newborns. In the second decade of life, atherosclerotic plaques in the coronary arteries are found in every person after 40 years in 55%, and after 60% of cases. Atherosclerosis develops most quickly in men at the age of 40-50 years, in women later. 95% of patients with myocardial infarction have atherosclerotic changes in the coronary arteries.

Secondly, an atherosclerotic plaque prevents blood vessels from expanding and this contributes to hypoxia in all cases when the load on the heart increases (physical activity, emotions, etc.).

Thirdly, atherosclerotic plaque reduces this lumen. Scar connective tissue, which forms at the site of the plaque, narrows the lumen up to obstructive ischemia. When the contraction is more than 95%, the slightest activity causes an attack of angina. With slow progression of the atherosclerotic process, ischemia may not occur due to the development of collaterals. There is no atherosclerosis in them. But sometimes obstruction of the coronary arteries occurs instantly when hemorrhage occurs in an atherosclerotic plaque.

The cardiovascular system in children, compared to adults, has significant morphological and functional differences, which are more significant the younger the child. In children, throughout all age periods, the development of the heart and blood vessels occurs: the mass of the myocardium and ventricles increases, their volumes increase, the ratio of the various parts of the heart and its location in the chest, the balance of the parasympathetic and sympathetic parts of the autonomic nervous system change. Until 2 years of a child’s life, differentiation of contractile fibers, conduction system and blood vessels continues. The mass of the left ventricular myocardium, which bears the main burden of ensuring adequate blood circulation, increases. By the age of 7, a child’s heart acquires the basic morphological features of an adult’s heart, although it is smaller in size and volume. Up to 14 years of age, the mass of the heart increases by another 30%, mainly due to an increase in the mass of the left ventricular myocardium. The right ventricle also enlarges during this period, but not as significantly; its anatomical features (elongated lumen shape) make it possible to maintain the same amount of work as the left ventricle and to expend significantly less muscle effort during work. The ratio of the myocardial mass of the right and left ventricles by the age of 14 is 1:1.5. It is also necessary to note the largely uneven growth rates of the myocardium, ventricles and atria, the caliber of blood vessels, which can lead to the appearance of signs of vascular dystonia, functional systolic and diastolic murmurs, etc. All activity of the cardiovascular system is controlled and regulated by a number of neuro-reflex and humoral factors. Nervous regulation of cardiac activity is carried out using central and local mechanisms. The central systems include the vagus and sympathetic nerves. Functionally, these two systems act opposite to each other on the heart. The vagus nerve reduces myocardial tone and automaticity of the sinoatrial node and, to a lesser extent, the atrioventricular node, as a result of which heart contractions are reduced. It also slows the conduction of excitation from the atria to the ventricles. The sympathetic nerve speeds up and enhances cardiac activity. In young children, sympathetic influences predominate, and the influence of the vagus nerve is weakly expressed. Vagal regulation of the heart is established by the 5-6th year of life, as evidenced by well-defined sinus arrhythmia and a decrease in heart rate (I. A. Arshavsky, 1969). However, compared to adults, in children the sympathetic background of regulation of the cardiovascular system remains predominant until puberty. Neurohormones (norepinephrine and acetylcholine) are simultaneously products of the activity of the autonomic nervous system. The heart, compared to other organs, has a high binding capacity for catecholamines. It is also believed that other biologically active substances (prostaglandins, thyroid hormone, corticosteroids, histamine-like substances and glucagon) mediate their effects on the myocardium mainly through catecholamines. The influence of cortical structures on the circulatory apparatus in each age period has its own characteristics, which are determined not only by age, but also by the type of higher nervous activity and the state of general excitability of the child. In addition to external factors affecting the cardiovascular system, there are myocardial autoregulation systems that control the strength and speed of myocardial contraction. The first mechanism of cardiac self-regulation is mediated by the Frank-Sterling mechanism: due to the stretching of muscle fibers by the volume of blood in the cavities of the heart, the relative position of contractile proteins in the myocardium changes and the concentration of calcium ions increases, which increases the force of contraction with an altered length of myocardial fibers (heterometric mechanism of myocardial contractility). The second path of cardiac autoregulation is based on increasing the affinity of troponin for calcium ions and increasing the concentration of the latter, which leads to increased heart function with unchanged muscle fiber length (the homometric mechanism of myocardial contractility). Self-regulation of the heart at the level of the myocardial cell and neurohumoral influences make it possible to adapt the work of the myocardium to the constantly changing conditions of the external and internal environment. All of the above features of the morphofunctional state of the myocardium and the systems that support its activity inevitably affect the age-related dynamics of circulatory parameters in children. Circulatory parameters include the main three components of the circulatory system: cardiac output, blood pressure and blood volume. In addition, there are other direct and indirect factors that determine the nature of blood circulation in the child’s body, all of them are derived from basic parameters (heart rate, venous return, central venous pressure, hematocrit and blood viscosity) or depend on them. Circulating blood volume. Blood is the substance of blood circulation, so assessing the effectiveness of the latter begins with assessing the volume of blood in the body. The amount of blood in newborn children is about 0.5 liters, in adults - 4-6 liters, but the amount of blood per unit of body weight is greater in newborns than in adults. Blood mass in relation to body weight is on average 15% in newborns, 11% in infants, and 7% in adults. Boys have a greater relative amount of blood than girls. A relatively larger blood volume than in adults is associated with a higher level of metabolism. By the age of 12, the relative amount of blood approaches the values ​​typical for adults. During puberty, the amount of blood increases slightly (V.D. Glebovsky, 1988). The bcc can be conditionally divided into a part that actively circulates through the vessels, and a part that is not currently participating in blood circulation, i.e., deposited, participating in circulation only under certain conditions. Blood storage is one of the functions of the spleen (established by age 14), liver, skeletal muscles and venous network. At the same time, the above depots can contain 2/3 bcc. The venous bed can contain up to 70% of the bcc; this part of the blood is in the low-pressure system. The arterial section - the high-pressure system - contains 20% of the bcc; in the capillary bed there is only 6% of the bcc. It follows from this that even a small sudden blood loss from the arterial bed, for example 200-400 ml (!), significantly reduces the volume of blood located in the arterial bed and can affect hemodynamic conditions, while the same blood loss from the venous bed has practically no effect on hemodynamics. The vessels of the venous bed have the ability to expand when blood volume increases and actively narrow when it decreases. This mechanism aims to maintain normal venous pressure and ensure adequate blood return to the heart. A decrease or increase in blood volume in a normovolemic subject (bloc volume is 50-70 ml/kg body weight) is completely compensated by a change in the capacity of the venous bed without changing the central venous pressure. In a child's body, circulating blood is distributed extremely unevenly. Thus, the vessels of the small circle contain 20-25% of the bcc. A significant part of the blood (15-20% of the bcc) accumulates in the abdominal organs. After eating, the vessels of the hepato-digestive region can contain up to 30% of the bcc. When the ambient temperature rises, the skin can hold up to 1 liter of blood. Up to 20% of the bcc is consumed by the brain, and the heart (comparable in metabolic rate to the brain) receives only 5% of the bcc. Gravity can have a significant influence on the bcc. Thus, a transition from a horizontal to a vertical position can cause the accumulation of up to 1 liter of blood in the veins of the lower limb. In the presence of vascular dystopia in this situation, the blood flow to the brain is depleted, which leads to the development of the clinical picture of orthostatic collapse. Violation of the correspondence between the BCC and the capacity of the vascular bed always causes a decrease in the speed of blood flow and a decrease in the amount of blood and oxygen received by the cells, in advanced cases - a violation of venous return and the arrest of a heart “not loaded with blood.” Gynovolemia can be of two types: absolute - with a decrease in the volume of blood volume and relative - with an unchanged volume of blood volume, due to the expansion of the vascular bed. Vasospasm in this case is a compensatory reaction that allows the vascular capacity to adapt to the reduced volume of the bcc. In the clinic, the causes of a decrease in blood volume can be blood loss of various etiologies, exicosis, shock, profuse sweating, and prolonged bed rest. Compensation of the BCC deficiency by the body occurs primarily due to the deposited blood located in the spleen and skin vessels. If the deficit of bcc exceeds the volume of deposited blood, then a reflex decrease in blood supply to the kidneys, liver, spleen occurs, and the body directs all remaining blood resources to supply the most important organs and systems - the central nervous system and heart (circulatory centralization syndrome). The tachycardia observed in this case is accompanied by an acceleration of blood flow and an increase in the rate of blood turnover. In a critical situation, blood flow through the kidneys and liver is reduced so much that acute kidney and liver failure can develop. The clinician must take into account that against the background of adequate blood circulation with normal blood pressure values, severe hypoxia of liver and kidney cells may develop, and adjust therapy accordingly. An increase in blood volume in the clinic is less common than hyiovolemia. Its main causes may be polycythemia, complications of infusion therapy, hydremia, etc. Currently, laboratory methods based on the principle of dye dilution are used to measure blood volume. Arterial pressure. The bcc, being in the closed space of the blood vessels, exerts a certain pressure on them, and the same pressure is exerted by the vessels on the bcc. Thus, blood flow in the vessels and pressure are interdependent quantities. The value of blood pressure is determined and regulated by the magnitude of cardiac output and peripheral vascular resistance . According to the Poiseuille formula, with an increase in cardiac output and unchanged vascular tone, blood pressure increases, and with a decrease in cardiac output, it decreases. With constant cardiac output, an increase in peripheral vascular resistance (mainly arterioles) leads to an increase in blood pressure, and vice versa. Thus, blood pressure determines the resistance that the myocardium experiences when releasing the next portion of blood into the aorta. However, the capabilities of the myocardium are not unlimited, and therefore, with a prolonged increase in blood pressure, the process of depletion of myocardial contractility may begin, which will lead to heart failure. Blood pressure in children is lower than in adults due to wider lumen of blood vessels and greater relative cardiac capacity Table 41. Changes in blood pressure in children depending on age, mm Hg.