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Peripheral circulatory disorders. What are the dangers of peripheral circulatory disorders?

PERIPHERAL CIRCULATION DISORDER

THROMBOSIS AND EMBOLISM

PLAN

1. The concept of peripheral circulation.

2. Arterial hyperemia.

2.1. Physiological hyperemia.

2.2. Pathological arterial hyperemia.

2.3. Neurogenic arterial hyperemia of the neurotonic type.

2.4. Neurogenic arterial hyperemia of the neuroparalytic type.

3. Venous hyperemia.

4. Ischemia.

4.1. Compressive ischemia.

4.2. Obstructive ischemia.

4.3. Angiospastic ischemia.

6. Thrombosis.

6.1. Definition of thrombosis.

6.2. The main factors of thrombosis.

6.3. Outcome of thrombosis.

7. Embolism.

7.1. Embolism of exogenous origin.

7.2. Embolism of endogenous origin.

7.2.1. Fat embolism.

7.2.2. Tissue embolism.

7.2.3. Amniotic fluid embolism.

7.3. Embolism of the pulmonary circulation.

7.4. Embolism of the systemic circulation.

7.5. Portal vein embolism.

Blood circulation in the area of the peripheral vascular bed (small arteries, arterioles, capillaries, postcapillary venules, arteriovenular anastomoses, venules and small veins), in addition to blood movement, ensures the exchange of water, electrolytes, gases, essential nutrients and metabolites through the blood-tissue-blood system .

The mechanisms of regulation of regional blood circulation include, on the one hand, the influence of vasoconstrictor and vasodilator innervation, on the other, the effect on the vascular wall of nonspecific metabolites, inorganic ions, local biologically active substances and hormones brought by the blood. It is believed that with a decrease in the diameter of blood vessels, the importance of nervous regulation decreases, and metabolic regulation, on the contrary, increases.

In an organ or tissue, in response to functional and structural changes in them, local circulatory disorders may occur. The most common forms of local circulatory disorders: arterial and venous hyperemia, ischemia, stasis, thrombosis, embolism.

ARTERIAL HYPEREMIA.

Arterial hyperemia is an increase in the blood supply to an organ as a result of excess blood flow through the arterial vessels. It is characterized by a number of functional changes and clinical signs:

diffuse redness, dilatation of small arteries, arterioles, veins and capillaries, pulsation of small arteries and capillaries,

· increase in the number of functioning vessels,

local increase in temperature,

· increase in the volume of the hyperemic area,

· increased tissue turgor,

increased pressure in arterioles, capillaries and veins,

· Accelerate blood flow, increase metabolism and enhance organ function.

The causes of arterial hyperemia can be: the influence of various environmental factors, including biological, physical, chemical; increased load on an organ or tissue area, as well as psychogenic effects. Since some of these agents are ordinary physiological stimuli (increased load on the organ, psychogenic effects), arterial hyperemia that occurs under their influence should be considered physiological. The main type of physiological arterial hyperemia is working, or functional, as well as reactive hyperemia.

Working hyperemia - this is an increase in blood flow in an organ, accompanying an increase in its function (hyperemia of the pancreas during digestion, skeletal muscle during its contraction, an increase in coronary blood flow with increased heart function, a rush of blood to the brain during mental stress).

Reactive hyperemia represents an increase in blood flow after its short-term restriction. It usually develops in the kidneys, brain, skin, intestines, and muscles. The maximum response is observed a few seconds after resumption of perfusion. Its duration is determined by the duration of the occlusion. Due to reactive hyperemia, the “debt” in blood flow that arose during occlusion is thus eliminated.

Pathological arterial hyperemia develops under the influence of unusual (pathological) irritants (chemicals, toxins, metabolic products formed during inflammation, burns; fever, mechanical factors). In some cases, the condition for the occurrence of pathological arterial hyperemia is an increase in the sensitivity of blood vessels to irritants, which is observed, for example, with allergies.

Infectious rash, redness of the face in many infectious diseases (measles, typhus, scarlet fever), vasomotor disorders in systemic lupus erythematosus, redness of the skin of a limb when certain nerve plexuses are damaged, redness in half the face in neuralgia associated with irritation of the trigeminal nerve, etc. etc., are clinical examples of pathological arterial hyperemia.

Depending on the factor causing pathological arterial hyperemia, we can talk about inflammatory, thermal hyperemia, ultraviolet erythema, etc.

According to pathogenesis, two types of arterial hyperemia are distinguished - neurogenic (neurotonic and neuroparalytic type) and caused by the action of local chemical (metabolic) factors.

Neurogenic arterial hyperemia of neurotonic type may occur reflexively due to irritation of extero- and interoreceptors, as well as irritation of vasodilator nerves and centers. Mental, mechanical, temperature, chemical (turpentine, mustard oil, etc.) and biological agents can act as irritants.

A typical example of neurogenic arterial hyperemia is redness of the face and neck during pathological processes in the internal organs (ovaries, heart, liver, lungs).

Arterial hyperemia, caused by the cholinergic mechanism (the influence of acetylcholine), is also possible in other organs and tissues (tongue, external genitalia, etc.), the vessels of which are innervated by parasympathetic nerve fibers.

In the absence of parasympathetic innervation, the development of arterial hyperemia is caused by the sympathetic (cholinergic, histaminergic and beta-adrenergic) system, represented in the periphery by the corresponding fibers, mediators and receptors (H2 receptors for histamine, beta-adrenergic receptors for norepinephrine, muscarinic receptors for acetylcholine).

Neurogenic arterial hyperemia of the neuroparalytic type can be observed in the clinic and in animal experiments during transection of sympathetic and alpha-adrenergic fibers and nerves that have a vasoconstrictor effect.

Sympathetic vasoconstrictor nerves are tonically active and under normal conditions constantly carry impulses of central origin (1-3 impulses per 1 second at rest), which determine the neurogenic (vasomotor) component of vascular tone. Their mediator is norepinephrine.

In humans and animals, tonic pulsation is inherent in sympathetic nerves going to the vessels of the skin of the upper extremities, ears, skeletal muscles, alimentary canal, etc. Transection of these nerves in each of these organs causes an increase in blood flow in the arterial vessels. The use of periarterial and ganglion sympathectomy for endarteritis accompanied by prolonged vascular spasms is based on this effect.

Arterial hyperemia of the neuroparalytic type can also be obtained chemically by blocking the transmission of central nerve impulses in the area of the sympathetic nodes (using ganglion blockers) or at the level of sympathetic nerve endings (using sympatholytic or alpha-blocking agents). Under these conditions, voltage-dependent slow Ca 2+ channels are blocked, the entry of extracellular Ca 2+ into smooth muscle cells along the electrochemical gradient, as well as the release of Ca 2+ from the sarcoplasmic reticulum is disrupted. Contraction of smooth muscle cells under the influence of the neurotransmitter norepinephrine thus becomes impossible. The neuroparalytic mechanism of arterial hyperemia partially underlies inflammatory hyperemia, ultraviolet erythema, etc.

The idea of the existence of arterial hyperemia (physiological and pathological), caused by local metabolic (chemical) factors, is based on the fact that a number of metabolites cause vasodilation, acting directly on the non-striated muscle elements of their walls, regardless of innervation influences. This is also confirmed by the fact that complete denervation does not prevent the development of either working, reactive, or inflammatory arterial hyperemia.

An important role in increasing blood flow during local vascular reactions is played by changes in the pH of the tissue environment - a shift in the reaction of the environment towards acidosis promotes vasodilation due to an increase in the sensitivity of smooth muscle cells to adenosine, as well as a decrease in the degree of oxygen saturation of hemoglobin. Under pathological conditions (burn, injury, inflammation, exposure to UV rays, ionizing radiation, etc.), along with adenosine, other metabolic factors also become significant.

The outcome of arterial hyperemia may be different. In most cases, arterial hyperemia is accompanied by increased metabolism and organ function, which is an adaptive reaction. However, adverse consequences are also possible. In atherosclerosis, for example, a sharp dilation of a vessel may be accompanied by rupture of its wall and hemorrhage into the tissue. Such phenomena are especially dangerous in the brain.

VENOUS HYPEREMIA.

Venous hyperemia develops due to an increase in blood supply to an organ or tissue area as a result of obstructed blood outflow through the veins.

Reasons for its development:

· blockage of veins by a thrombus or embolus;

· compression by a tumor, scar, enlarged uterus, etc.

Thin-walled veins can also be compressed in areas of sharp increase in tissue and hydrostatic pressure (at the site of inflammation, in the kidneys with hydronephrosis).

In some cases, the predisposing factor of venous hyperemia is the constitutional weakness of the elastic apparatus of the veins, insufficient development and reduced tone of the smooth muscle elements of their walls. Often this predisposition is familial in nature.

Veins, like arteries, although to a lesser extent, are rich reflexogenic zones, which suggests the possibility of a neuro-reflex nature of venous hyperemia. The morphological basis of vasomotor function is the neuromuscular apparatus, which includes smooth muscle elements and effector nerve endings.

Venous hyperemia also develops when the function of the right ventricle of the heart is weakened, the suction effect of the chest is reduced (exudative pleurisy, hemothorax), and difficulty in blood flow in the pulmonary circulation (pneumosclerosis, pulmonary emphysema, weakened function of the left ventricle).

The main factor causing local changes in venous hyperemia is oxygen starvation (hypoxia) of the tissue.

In this case, hypoxia is initially caused by a restriction in the flow of arterial blood, then by the effect of metabolic products on tissue enzyme systems, which results in a violation of oxygen utilization. Oxygen starvation with venous hyperemia causes disruption of tissue metabolism, causes atrophic and dystrophic changes and excessive growth of connective tissue.

Along with local changes in venous hyperemia, especially if it is caused by general causes and is of a generalized nature, a number of general hemodynamic disorders with very serious consequences are also possible. Most often they occur when large venous collectors are blocked - the portal vein, the inferior vena cava. The accumulation of blood in these vascular reservoirs (up to 90% of all blood) is accompanied by a sharp decrease in blood pressure and disruption of nutrition of vital organs (heart, brain). Death may occur due to heart failure or respiratory paralysis.

A disturbance of peripheral circulation, which is based on a limited or complete cessation of arterial blood flow, is called ischemia (from the Greek ischeim - to delay, stop, haima - blood) or local anemia.

Ischemia is characterized by the following symptoms:

blanching of the ischemic area of the organ;

· decrease in temperature;

· disturbance of sensitivity in the form of paresthesia (feeling of numbness, tingling, “crawling”);

· pain syndrome;

· decrease in blood flow speed and organ volume;

· decreased blood pressure at the artery site;

located below the obstacle, a decrease in oxygen tension in the ischemic area of the organ or tissue;

· impaired formation of interstitial fluid and decreased tissue turgor;

· dysfunction of an organ or tissue;

· dystrophic changes.

The cause of ischemia can be various factors: compression of the artery; obstruction of its lumen; effect on the neuromuscular apparatus of its wall. In accordance with this, compression, obstructive and angiospastic types of ischemia are distinguished.

Compressive ischemia occurs from compression of the adductor artery by a ligature, scar, tumor, foreign body, etc.

Obstructive ischemia is a consequence of partial narrowing or complete closure of the artery lumen by a thrombus or embolus. Productive-infiltrative and inflammatory changes in the arterial wall that occur with atherosclerosis, obliterating endarteritis, periarteritis nodosa, also lead to limitation of local blood flow as obstructive ischemia.

Angiospastic ischemia occurs as a result of irritation of the vasoconstrictor apparatus of blood vessels and their reflex spasm caused by emotional influence (fear, pain, anger), physical factors (cold, injury, mechanical irritation), chemical agents, biological irritants (bacterial toxins), etc. In pathological conditions, vasospasm is characterized by a relative duration and significant severity, which can cause a sharp slowdown in blood flow, even stopping it completely. Most often, vasospasm develops in arteries of relatively large diameter inside the organ according to the type of vascular unconditioned reflexes from the corresponding interoreceptors. These reflexes are characterized by significant inertia and autonomy.

The nature of metabolic, functional and structural changes in the ischemic area of the tissue or organ is determined by the degree of oxygen starvation, the severity of which depends on the rate of development and type of ischemia, its duration, location, the nature of collateral circulation, the functional state of the organ or tissue.

Ischemia that occurs in areas of complete obstruction or compression of the arteries, other things being equal, causes more severe changes than with spasm. Rapidly developing ischemia, like long-term ischemia, is more severe compared to slowly developing or short-term ischemia. Sudden tissue obstruction is especially important in the development of ischemia, since this may result in a reflex spasm of the branching system of a given artery.

Ischemia of vital organs (brain, heart) has more severe consequences than ischemia of the kidneys, spleen, lungs, and ischemia of the latter is more severe than ischemia of skeletal, muscle, bone or cartilage tissue. These organs are characterized by a high level of energy metabolism, at the same time, their collateral vessels are functionally absolutely or relatively unable to compensate for circulatory disorders. On the contrary, skeletal muscles and especially connective tissue, due to the low level of energy metabolism in them, are more stable under ischemic conditions.

Stasis is a slowing down and stopping of blood flow in capillaries, thin arteries and veins.

There are true (capillary) stasis, which occurs as a result of pathological changes in the capillaries or a violation of the rheological properties of the blood, ischemic - due to the complete cessation of blood flow from the corresponding arteries into the capillary network, and venous.

Venous and ischemic stasis are a consequence of a simple slowdown and cessation of blood flow. These conditions arise for the same reasons as venous hyperemia and ischemia. Venous stasis can be the result of compression of the veins, blockage by a thrombus or embolus, and ischemic stasis can be a result of spasm, compression or blockage of the arteries. Elimination of the cause of stasis leads to the restoration of normal blood flow. On the contrary, the progression of ischemic and venous stasis contributes to the development of true.

With true stasis, the column of blood in the capillaries and small veins becomes motionless, the blood is homogenized, red blood cells swell and lose a significant part of their pigment. The plasma, together with the released hemoglobin, extends beyond the vascular wall. In the tissues of the focus of capillary stasis there are signs of severe malnutrition and necrosis.

The cause of true stasis there may be physical (cold, heat), chemical (poisons, concentrated solution of sodium chloride, other salts, turpentine, mustard and croton oils) and biological (microorganism toxins) factors.

The mechanism of development of true stasis explained by intracapillary aggregation of erythrocytes, i.e. their gluing and formation of conglomerates, impeding blood flow. This increases peripheral resistance.

In the pathogenesis of true stasis, slowing down of blood flow in capillary vessels due to blood thickening is important. The leading role here is played by the increased permeability of the walls of capillary vessels located in the zone of stasis. This is facilitated by etiological factors causing stasis and metabolites formed in tissues. Particular importance in the mechanism of stasis is given to biologically active substances (serotonin, bradykinin, histamine), as well as the acylotic shift of the tissue reaction of the medium and its colloidal state. As a result, there is an increase in the permeability of the vascular wall and dilation of blood vessels, leading to blood thickening, slowing of blood flow, aggregation of red blood cells and, as a result, stasis.

Particularly important is the release of plasma albumin into the tissue, which helps to reduce the negative charge of erythrocytes, which may be accompanied by their loss from a suspended state.

Thrombosis is the process of intravital formation on the inner surface of the wall of blood vessels of blood clots consisting of its elements.

Blood clots can be parietal (partially reduce the lumen of blood vessels) or obstructive. The first type of blood clots most often occurs in the heart and trunks of great vessels, the second - in small arteries and veins.

Depending on which components predominate in the structure of the blood clot, white, red and mixed blood clots are distinguished. In the first case, the thrombus is formed by platelets, leukocytes, and also a small amount of plasma proteins; in the second - red blood cells held together by fibrin threads; mixed thrombi are alternating white and red layers.

The main factors of thrombus formation (in the form of Vikhrov’s triad).

1. Damage to the vascular wall that occurs under the influence of physical (mechanical trauma, electric current), chemical (NaCl, FeCl3, HgCl2, AgNO3) and biological (endotoxins of microorganisms) factors as a result of disturbances in its nutrition and metabolism. These disorders are also accompanied by atherosclerosis, hypertension, and allergic processes.

2. Violation of the activity of the blood coagulation and anticoagulation system of the vascular wall. An increase in the activity of the blood coagulation system due to an increase in the concentration of procoagulants in it (thrombin, thromboplastin), as well as a decrease in the activity of the anticoagulant system (a decrease in the content of anticoagulants in the blood or an increase in the activity of their inhibitors), as a rule, leads to intravascular blood coagulation (IBC). VSSK is caused by a rapid and significant entry into the vascular bed of blood coagulation factors (tissue thromboplastin), which is observed with premature placental abruption, amniotic fluid embolism, traumatic shock, and acute massive hemolysis of red blood cells. The transition of VSSK to thrombosis occurs under the influence of coagulation factors of the vascular wall and platelets when they are damaged.

3. Slowing of blood flow and its disturbances (turbulence in the area of the aneurysm). This factor is probably of less importance, but it helps explain why blood clots form in veins 5 times more often than in arteries, in the veins of the lower extremities 3 times more often than in the veins of the upper extremities, as well as the high incidence of thrombosis during decompensation blood circulation, long-term bed rest.

The consequences of thrombosis can be different. Considering its importance as a hemostatic mechanism in acute trauma accompanied by bleeding, thrombosis should be considered from a general biological point of view as an adaptive phenomenon.

At the same time, thrombus formation in various diseases (atherosclerosis, diabetes mellitus, etc.) can be accompanied by severe complications caused by acute circulatory disorders in the area of the thrombosed vessel. The development of necrosis (infarction, gangrene) in the basin of a thrombosed vessel is the final stage of thrombosis.

The outcome of thrombosis can be aseptic (enzymatic, autolytic) melting, organization (resorption with replacement by connective tissue), recanalization, septic (purulent) melting. The latter is especially dangerous, as it contributes to septicopyemia and the formation of multiple abscesses in various organs.

Embolism (from the Greek emballein - throw inside) is a blockage of blood vessels by bodies (emboli) brought by the blood or lymph flow.

Depending on the nature of the emboli, embolism is distinguished:

· endogenous, caused by a blood clot, fat, various tissues, amniotic fluid, gas (with decompression sickness).

Embolism is classified according to location:

systemic circulation,

· pulmonary circulation;

Portal vein system.

In all cases, the movement of emboli is usually carried out in accordance with the natural forward movement of blood.

Embolism of exogenous origin. Air embolism occurs when large veins are injured (jugular, subclavian, dural sinuses), which collapse weakly and the pressure in which is close to zero or negative. This circumstance can also cause air embolism during medical procedures - when infusion of solutions into these vessels. As a result, air is sucked into the damaged veins, especially at the height of inspiration, with subsequent embolism of the vessels of the pulmonary circulation. The same conditions are created when the lung is injured or has destructive processes in it, as well as when pneumothorax is applied. In such cases, however, embolism of the vessels of the large circulation occurs. Similar consequences result from the entry of a large amount of air from the lungs into the blood when a person is exposed to an explosive shock wave (air, water), as well as during “explosive decompression” and rapid ascent to a high altitude. The resulting sharp expansion of the pulmonary alveoli, rupture of their walls and the entry of air into the capillary network lead to inevitable embolism of the vessels of the systemic circulation. With anaerobic (gas) gangrene, gas embolism is also possible.

The sensitivity of different animals and humans to air embolism varies. A rabbit dies from intravenous injection of 2-3 ml of air, dogs tolerate injections of air in a volume of 50-70 ml/kg. Man in this regard occupies an intermediate position.

Embolism of endogenous origin. The source of thromboembolism is a particle of a detached thrombus. The separation of a blood clot is considered a sign of its inferiority (“sick blood clot”). In most cases, “sick blood clots” form in the veins of the systemic circulation (veins of the lower extremities, pelvis, liver), which explains the high frequency of pulmonary embolism. Only when blood clots form in the left half of the heart (with endocarditis, aneurysm) or in the arteries (with atherosclerosis) does embolism occur in the vessels of the systemic circulation. The reason for the inferiority of a blood clot, the detachment of its particles and thromboembolism is its aseptic or purulent melting, a violation of the retraction phase of thrombus formation, as well as blood coagulation.

Fat embolism occurs when drops of fat, most often of endogenous origin, enter the bloodstream. The cause of fat droplets entering the bloodstream is damage (crushing, severe concussion) to the bone marrow, subcutaneous or pelvic tissue and fat accumulations, and fatty liver.

Since the source of embolism is located primarily in the veins of the systemic circulation, fat embolism is possible primarily in the vessels of the pulmonary circulation. Only later is it possible for fatty droplets to penetrate through the pulmonary capillaries (or arteriovenous anastomoses of the pulmonary circulation) into the left half of the heart and the arteries of the systemic circulation.

The amount of fat causing fatal fat embolism varies in different animals within the range of 0.9-3 cm 3 /kg.

Tissue embolism observed in case of injury, when scraps of various body tissues, especially those rich in water (bone marrow, muscles, brain, liver) are released into the blood circulation system, primarily the pulmonary circulation. Of particular importance is vascular embolism by malignant tumor cells, since it is the main mechanism for the formation of metastases.

Amniotic fluid embolism occurs when amniotic fluid enters damaged vessels of the uterus during childbirth in the area of the separated placenta.

Gas embolism is the main pathogenetic link in the state of decompression, in particular decompression sickness. The difference in atmospheric pressure from high to normal (for divers) or vice versa from normal to sharply low (rapid rise to altitude, depressurization of the aircraft cabin) leads to a decrease in the solubility of gases (nitrogen, oxygen, carbon dioxide) in tissues and blood and clogging of these gases with bubbles (primarily nitrogen) capillaries located mainly in the systemic circulation basin.

Embolism of the pulmonary circulation. The most important functional change in vascular embolism of the pulmonary circulation is a sharp decrease in blood pressure in the systemic circulation and an increase in pressure in the pulmonary circulation.

There are several hypotheses explaining the mechanisms of the hypotensive effect in pulmonary embolism. The opinion that an acute decrease in blood pressure is considered as reflex hypotension (Schwingk-Parin unloading reflex) has become widespread. It is believed that the depressor reflex is caused by irritation of receptors located in the bed of the pulmonary artery.

A certain significance in lowering blood pressure during pulmonary embolism is attributed to weakening of heart function due to myocardial hypoxia, which is the result of an increase in the load on the right half of the heart and a sharp decrease in blood pressure.

The obligatory hemodynamic effect of vascular embolism in the pulmonary circulation is an increase in blood pressure in the pulmonary artery and a sharp increase in the pressure gradient in the pulmonary artery-capillary area, which is considered as a result of a reflex spasm of the pulmonary vessels.

Embolism of the systemic circulation. As mentioned above, embolism of the vessels of the systemic circulation is most often based on pathological processes in the left half of the heart, accompanied by the formation of blood clots on its inner surface (thromboendocarditis, myocardial infarction), thrombus formation in the arteries of the systemic circulation followed by thromboembolism, gas or fat embolism . Places of frequent localization of emboli are the coronary, middle cerebral, internal carotid, and renal splenic arteries. All other things being equal, the localization of emboli is determined by the angle of origin of the lateral vessel, its diameter, and the intensity of blood supply to the organ. A large angle of origin of the lateral branches in relation to the upstream segment of the vessel, their relatively large diameter, and hyperemia are factors predisposing to one or another localization of emboli.

With gas embolism accompanying decompression sickness or “explosive decompression,” a predisposing factor to the localization of emboli in the vessels of the brain and subcutaneous tissue is the good solubility of nitrogen in tissues rich in lipoids.

Portal vein embolism. Portal vein embolism, although much less common than embolism of the pulmonary and systemic circulation, attracts attention with its characteristic clinical symptom complex and extremely severe hemodynamic disturbances.

Due to the large capacity of the portal bed, blockage of the main trunk of the portal vein or its main branches by an embolus leads to an increase in blood supply to the abdominal organs (stomach, intestines, spleen) and the development of portal hypertension syndrome (increased blood pressure in the portal vein system from 8-10 to 40-60 cm water column). In this case, as a consequence, a characteristic clinical triad develops (ascites, expansion of the superficial veins of the anterior abdominal wall, enlargement of the spleen) and a number of general changes caused by circulatory disorders (decreased blood flow to the heart, stroke and minute volume of blood, decreased blood pressure), respiration (shortness of breath, then a sharp decrease in breathing, apnea) and functions of the nervous system (loss of consciousness, respiratory paralysis).

The basis of these general disorders is primarily a decrease in the mass of circulating blood caused by its accumulation (up to 90%) in the portal bed. Such hemodynamic disturbances are often the direct cause of death in patients.

Literature.

1. N.N. Zaiko. Pathological physiology - K., 1985.

2. A.D.Ado, L.M.Ishimova. Pathological physiology - Medicine, 1980.

3. G.E. Arkadyeva, N.N. Petrintseva. Mechanisms of impaired platelet-vascular hemostasis - L., 1988.

4. V.S.Paukov, N.K.Khitrov. Pathology - M.: Medicine, 1989.

Blood circulation is a continuous process of blood circulation in the body, necessary to provide all cells with nutrition and oxygen. The blood also removes metabolic products and carbon dioxide from the body. The central organ of blood circulation is the heart. It consists of arterial (left) and venous (right) halves. Those, in turn, are divided into the atrium and ventricle, which communicate with each other. In the human body, there are two circles of blood circulation: large (systemic) and small (pulmonary).

In the systemic circulation, blood from the left atrium flows into the left ventricle, then into the aorta, after which it flows through the arteries, veins and capillaries to all organs. In this case, gas exchange occurs, the blood gives nutrients and oxygen to the cells, and carbon dioxide and harmful metabolic products enter it. The capillaries then become venules, then veins, which merge into the superior and inferior vena cava, which drain into the right atrium of the heart, ending the systemic circulation.

The pulmonary circulation is when blood saturated with carbon dioxide enters the lungs from the right ventricle through the pulmonary arteries. Oxygen penetrates through the thin walls of the alveoli into the capillaries, while carbon dioxide, on the contrary, is released into the external environment. Oxygenated blood flows through the pulmonary veins into the left atrium.

A circulatory disorder is a condition when the cardiovascular system is unable to ensure normal blood circulation to tissues and organs. This disorder is manifested not only by a failure in the pumping function of the heart, but also by disorders in organs and tissues. According to the nature of circulatory disorders, the following are distinguished:

Initial manifestations of insufficient blood circulation,

· Acute circulatory disorders,

· Chronic slowly progressive circulatory disorders.

Causes of acute and chronic circulatory disorders

The most common causes of circulatory disorders (hemodynamics) include smoking, diabetes mellitus, old age, homocysteine (more than 30% of normal). After seventy years of age, problems with peripheral arteries occur in every third person.

Chronic circulatory disorders in the lower extremities can be caused by diseases such as arterial stenosis, obliterating endarteritis, diabetes mellitus, and varicose veins. Chronic cerebral circulatory disorders are associated with atherosclerosis, arterial hypertension, coronary heart disease, and smoking.

In general, circulatory disorders are either a result, a consequence, or support and provision of general pathological processes, because blood flows to all cells of our body. Almost all diseases known to man are accompanied by more or less pronounced blood flow disorders.

Symptoms of acute and chronic circulatory disorders

If we consider the symptoms of acute and chronic cerebral circulatory failure, they may not bother the patient until something provokes an abundant blood supply to the brain, and this is physical labor, an unventilated room, etc. They manifest themselves as impaired coordination and vision, noise in the head, decreased performance, insomnia, memory impairment, numbness of the face or limbs, and speech impairment.

If symptoms persist for a long time, sometimes more than a day, this is a clear sign of a stroke - an acute circulatory disorder of the brain, often fatal. If such symptoms appear, you should immediately take appropriate measures and call a doctor.

If we consider the symptoms of circulatory disorders in the upper and lower extremities, the most common of them is intermittent claudication, i.e. pain or discomfort that occurs when walking and disappears in a quiet position. The temperature of the hands and feet may be low; doctors call this “cold hands” or “cold feet.”

Venous stars and networks form on the legs, indicating the initial stage of varicose veins. The patient may experience a feeling of heaviness, weakness, or cramps in the lower extremities. The reason for all this is poor blood circulation in the arms and legs.

Chronic and acute disorders coexist etiologically. In patients with acute impairment, symptoms of chronic failure are common.

Diagnosis of circulatory disorders

Today, many methods for diagnosing circulatory disorders are used:

Ultrasound duplex scanning (examination of veins and arteries with ultrasound);

Selective contrast venography (examination after administration of a contrast agent into a vein);

Scintigraphy (nuclear analysis, harmless and painless);

Computed tomography (layer-by-layer study of the structure of an object);

Magnetic resonance imaging (the study is based on the use of a magnetic field and radio waves);

Magnetic resonance angiography (a special case of MRI, provides images of blood vessels).

Prevention of circulatory disorders

An integral condition for a healthy human life is normal blood circulation. To maintain it, there are various methods of prevention. First of all, try to lead an active lifestyle. Baths, saunas, contrast showers, hardening, massage and all sorts of vasodilators that reduce the tone of the vascular muscles also stimulate blood circulation.

Treatment of peripheral circulation

Peripheral circulation is the movement of blood through capillaries, arterioles, small arteries, small veins, metarterioles, venules, arteriovenular anastomoses and postcapillary venules according to the principle from blood to tissue, then from tissue to blood. At a young age, problems with blood circulation occur less often, but with age they are almost inevitable.

There are many drugs that improve blood circulation - antispasmodics, antiplatelet agents (prevent platelet aggregation), anticoagulants (normalize blood microcirculation), angioprotectors (reduce vascular permeability) and others, but phyto or homeopathic drugs are considered safer at the initial stage of the disease. However, self-medication in such cases is dangerous. To avoid harming yourself, you should consult a doctor. It will help you choose the most optimal option for medications for the treatment and prevention of peripheral circulation.

Education: Moscow Medical Institute named after. I. M. Sechenov, specialty - "General Medicine" in 1991, in 1993 "Occupational diseases", in 1996 "Therapy".

PERIPHERAL CIRCULATION DISORDER

THROMBOSIS AND EMBOLISM

PLAN

1. The concept of peripheral circulation.

2. Arterial hyperemia.

2.1. Physiological hyperemia.

2.2. Pathological arterial hyperemia.

2.3. Neurogenic arterial hyperemia of the neurotonic type.

2.4. Neurogenic arterial hyperemia of the neuroparalytic type.

3. Venous hyperemia.

4. Ischemia.

4.1. Compressive ischemia.

4.2. Obstructive ischemia.

4.3. Angiospastic ischemia.

6. Thrombosis.

6.1. Definition of thrombosis.

6.2. The main factors of thrombosis.

6.3. Outcome of thrombosis.

7. Embolism.

7.1. Embolism of exogenous origin.

7.2. Embolism of endogenous origin.

7.2.1. Fat embolism.

7.2.2. Tissue embolism.

7.2.3. Amniotic fluid embolism.

7.3. Embolism of the pulmonary circulation.

7.4. Embolism of the systemic circulation.

7.5. Portal vein embolism.

ARTERIAL HYPEREMIA.

diffuse redness, dilatation of small arteries, arterioles, veins and capillaries, pulsation of small arteries and capillaries,

· increase in the number of functioning vessels,

local increase in temperature,

· increase in the volume of the hyperemic area,

· increased tissue turgor,

increased pressure in arterioles, capillaries and veins,

· Accelerate blood flow, increase metabolism and enhance organ function.

Depending on the factor causing pathological arterial hyperemia, we can talk about inflammatory, thermal hyperemia, ultraviolet erythema, etc.

According to pathogenesis, two types of arterial hyperemia are distinguished - neurogenic (neurotonic and neuroparalytic type) and caused by the action of local chemical (metabolic) factors.

A typical example of neurogenic arterial hyperemia is redness of the face and neck during pathological processes in the internal organs (ovaries, heart, liver, lungs).

VENOUS HYPEREMIA.

Venous hyperemia develops due to an increase in blood supply to an organ or tissue area as a result of obstructed blood outflow through the veins.

Peripheral circulation (local, organ tissue, regional) refers to blood flow in small arteries, veins, capillaries, and arteriovenous anastomoses. In turn, blood circulation in arterioles, precapillaries, capillaries, postcapillaries and venules and arteriovenous shunts is called microcirculation. The main role of peripheral circulation is to provide cells and tissues with oxygen, nutrients, and eliminate metabolic products.

Typical disorders of regional circulation include arterial and venous hyperemia, ischemia, stasis, thrombosis, embolism, bleeding and hemorrhage, which complicate the development of various forms of pathology of infectious and non-infectious nature. Depending on the duration of development, blood flow disorders can be (1) transient (2) persistent, (3) irreversible. According to the degree of prevalence, blood flow disorders can be (1) diffuse, (2) generalized, (3) local in nature.

Common forms of peripheral circulatory disorders may result from cardiac dysfunction, and vascular damage or changes in blood condition lead to focal local disturbances of blood flow.

Arterial hyperemia

Arterial hyperemia (Greek hyper – over, haima – blood) is a state of increased blood supply to an organ and tissue, resulting from increased blood flow through dilated arteries. Arterial hyperemia can be local and general. General arterial plethora is characteristic of plethora - a significant increase in the volume of circulating blood [for example, with erythrocytosis, hyperthermia (overheating) of the body], fever in patients with infectious diseases, with a rapid drop in barometric pressure. According to the clinical course, arterial hyperemia can be acute or chronic.

According to their biological significance, physiological and pathological forms of arterial hyperemia are distinguished. Physiological forms of arterial hyperemia are associated with increased function of certain organs, for example, muscles during physical activity, the brain during psycho-emotional stress, etc.

Pathological arterial hyperemia occurs in response to the action of pathogenic stimuli and does not depend on the metabolic needs of the organ. In accordance with the characteristics of etiological factors and development mechanisms, the following types of pathological arterial hyperemia are distinguished:

neuroparalytic;

neurotonic;

post-ischemic;

vacant;

inflammatory;

collateral;

hyperemia due to arteriovenous fistula.

The pathogenesis of arterial hyperemia is based on myoparalytic And neurogenic (angioneurotic) mechanisms:

The myoparalytic mechanism, being the most common mechanism for the development of arterial hyperemia, is caused by a decrease in vasomotor tone of vessels under the influence of metabolites (organic and inorganic acids, for example, carbon dioxide, lactate, purines, etc.), mediators of inflammation, allergies, etc., changes in electrolyte balance , hypoxia. It underlies post-ischemic, inflammatory, physiological working arterial plethora.

The essence of the neurogenic mechanism is a change in vasomotor influences (vasoconstriction and vasodilation), leading to a decrease in the neurogenic component of vascular tone. This mechanism underlies the development of neurotonic and neuroparalytic hyperemia, as well as inflammatory arterial plethora during the implementation of the axon reflex.

Neuroparalytic arterial hyperemia characterized by a decrease in the tone of the sympathetic vasoconstrictor component, which is observed when the sympathetic nerves, ganglia or adrenergic nerve endings are damaged.

Neurotonic arterial hyperemia occurs when the tone of the parasympathetic or sympathetic cholinergic vasodilator nerves increases or when their centers are irritated by a tumor, scar, etc. This mechanism is observed only in some tissues. Under the influence of sympathetic and parasympathetic vasodilators, arterial hyperemia develops in the pancreas and salivary glands, tongue, cavernous bodies, skin, skeletal muscles, etc.

Postischemic arterial hyperemia is an increase in blood flow in an organ or tissue after a temporary cessation of circulation. It occurs, in particular, after removing the constricting tourniquet and quickly removing ascitic fluid. Reperfusion not only promotes positive changes in tissue. The intake of excessive amounts of oxygen and its increased use by cells lead to intensive formation of peroxide compounds, activation of lipid peroxidation processes and, as a consequence, direct damage to biological membranes and free radical necrobiosis.

Vacatnaya hyperemia I (Lat.vacuus – empty) is observed when barometric pressure drops over any part of the body. This type hyperemia develops with rapid release from compression of the vessels of the abdominal cavity, for example, with the rapid resolution of labor, removal of a tumor compressing the vessels, or rapid evacuation of ascitic fluid. Vacuum hyperemia is observed in divers when working in caissons in cases of rapid transition from conditions of increased barometric pressure to normal. In such situations, there is a danger of a sharp decrease in venous return to the heart and, accordingly, a drop in systemic blood pressure, since the vascular bed of the abdominal cavity can accommodate up to 90% of the volume of circulating blood. Vacat hyperemia is used as a local healing factor when prescribing medical cupping.

Inflammatory arterial hyperemia occurs under the influence of vasoactive substances (inflammatory mediators), causing a sharp decrease in basal vascular tone, as well as due to the implementation of neurotonic or neuroparalytic mechanisms and axon reflex in the alteration zone.

Collateral arterial hyperemia It is adaptive in nature and develops as a result of a reflex dilation of collateral vessels when blood flow through the main arteries is obstructed.

Hyperemia due to arteriovenous fistula observed when arterial and venous vessels are damaged as a result of the formation of an anastomosis between an artery and a vein. In this case, arterial blood rushes under pressure into the venous bed, ensuring arterial plethora.

Arterial hyperemia is characterized by the following changes in microcirculation:

dilatation of arterial vessels;

increase in linear and volumetric blood flow rates in microvessels;

increased intravascular hydrostatic pressure;

increase in the number of functioning capillaries;

increased lymph formation and acceleration of lymph circulation;

reducing the arteriovenous oxygen difference.

External signs of arterial hyperemia include redness of the hyperemic zone, caused by dilation of blood vessels, an increase in the number of functioning capillaries, and an increase in the content of oxyhemoglobin in venous blood. Arterial hyperemia is accompanied by a local increase in temperature, which is explained by the increased influx of warmer arterialized blood and an increase in the intensity of metabolic processes. Due to an increase in blood flow and lymphatic filling in the hyperemic zone, an increase in turgor (tension) and the volume of hyperemic tissue occurs.

Physiological arterial hyperemia has, as a rule, a positive value, as it leads to increased tissue oxygenation, intensified metabolic processes and increased organ function. It can be relatively short-term and does not cause significant morphological changes in organs and tissues and develops with such physiological adaptive reactions as thermoregulation, erection, and stress changes in muscle blood flow. Pathological arterial hyperemia, characterized by excessive vasodilation and a sharp increase in intravascular pressure, can lead to vascular rupture and hemorrhage. Similar consequences can be observed in the presence of defects in the vascular wall (congenital aneurysms, atherosclerotic changes, etc.). With the development of arterial hyperemia in organs enclosed in a closed volume, symptoms associated with increased hydrostatic pressure arise: joint pain, headaches, tinnitus, dizziness, etc. Pathological arterial hyperemia can contribute to hypertrophy and hyperplasia of tissues and organs and accelerate their development.

If arterial hyperemia is generalized, for example, with skin hyperemia over a large surface, then it can seriously affect systemic hemodynamics: cardiac output, total peripheral vascular resistance, systemic blood pressure.

Peripheral circulatory disorders

In the circulatory system, three interconnected links are conventionally distinguished:

1 central blood circulation: carried out in the cavities of the heart and large vessels, and ensures the maintenance of systemic blood pressure, the direction of blood flow, and levels out significant fluctuations in blood pressure during the ejection of blood from the ventricles of the heart.

2 peripheral (organ, local, tissue, regional) is carried out in the arteries, veins of organs and tissues, provides the volume of blood supply and levels of perfusion pressure in tissues and organs in accordance with their functional activity.

3. blood circulation in the vessels of the microvasculature: realized in capillaries, arterioles, venules, arteriovenous shunts. Provides optimal blood delivery to tissues, transcapillary exchange of substrates and metabolic products, as well as blood transport to tissues.

Arterial hyperemia:

This is an increase in blood supply to an organ or tissue due to an increase in blood flow through dilated vessels.

The following types of arterial hyperemia are distinguished by mechanism:

1 physiological: working and reactive

2 pathological: neurogenic, humoral, neuromyoparalytic.

Neurogenic arterial hyperemia occurs:

Neurotonic: occurs due to the predominance of the parasympathetic nervous system over the sympathetic. (irritation of the parasympathetic ganglia by a tumor, scars, or due to an increase in the cholinoreactive properties of blood vessels (with an increase in H + I K + extracellular))

Neuroparalytic: occurs when the activity of sympathetic impulses decreases (damage to ganglia) or when the adrenoreactive properties of blood vessels decrease (adrenoreceptor blockade)

Humoral: occurs when vasoactive substances accumulate, causing a vasodilator effect. These include biologically active substances (histamine, serotonin), ADP, adenosine, organic acids of the Krebs cycle, lactate, pyruvate, prostaglandins E, I 2

Non-myoparalytic: consists in the depletion of CA in the vesicles of sympathetic nerve endings and/or a significant decrease in the tone of the muscle fibers of the arterioles. This usually occurs with prolonged exposure to various factors, most often of a physical nature, on the tissue. For example, with prolonged use of heating pads, mechanical pressure initially corresponds to the pressure of the abdominal vessels during ascites, and the removal of ascitic fluid is accompanied by art. hyperemia of tissue and organs of the abdominal cavity.

Physiological WORKING: develops due to increased function of organs and tissue. (arterial hyperemia of skeletal muscles during work)

REACTIVE: develops with short-term ischemia of an organ or tissue to eliminate the backlog of blood supply (after measuring blood pressure in the forearm)

Manifestations of arterial hyperemia:

1.increase in the number and diameter of visible arterial vessels, which is a consequence of an increase in their lumen

2.redness of an organ or tissue. This is due to an increase in arterial blood flow, an increase in the number of functioning capillaries and a decrease in the arteriovenous difference in oxygen, i.e. arterialization of venous blood.

3. local increase in temperature, as a result of increased metabolism and increased heat production, as well as due to the influx of heated blood.

4.increase in the volume and turgor of tissue due to an increase in their blood and lymph filling.

5. for tissue microscopy:

increase: the number of functioning capillaries, the diameter of arterioles and precapillaries, acceleration of blood flow through microvessels, decrease in the diameter of the axial cylinder.

Consequences of arterial hyperemia:

Activation of specific tissue and organ functions

Potentiation of nonspecific functions and processes in particular: local immune reactions, increased plastic processes, lymph formation.

Ensuring hypertrophy and hyperplasia of the structural elements of tissue cells.

Overstretching and micro-tears of the walls of microvasculature vessels

Bleeding external and internal.

VENOUS HYPEREMIA:

This is an increase in blood supply to organs or tissue due to difficulty or cessation of blood outflow through the veins.

Causes:

1. Mechanical obstruction to blood flow: this may be a consequence

narrowing of the vein

a) compression (squeezing from outside) by a tumor, scar, bandage, exudate.

b) obstruction: thrombus, embolus.

2.Heart failure

3.decreased suction function of the chest

4. low elasticity of the venous walls, insufficient development and reduced tone of the smooth muscle elements in them.

Mechanisms of development of venous hyperemia:

They are associated with the creation of a mechanical obstacle to the outflow of venous blood from tissues and disruption of its flow.

Signs of venous hyperemia:

1increase in the number and diameter of visible venous vessels

2cyanosis: caused by an increased content of reduced hemoglobin

3 local decrease in temperature, due to a decrease in metabolic processes in tissues and a decrease in arterial blood flow.

Edema: develops as a result of an increase in blood pressure in the capillaries, post-capillaries and venules, this leads to an imbalance in Starling’s equilibrium and causes increased filtration of fluid through the vessel wall and a decrease in its reabsorption in the venous part of the capillary. With prolonged venous hyperemia, edema is potentiated due to an increase in the permeability of the capillary wall due to the accumulation of acidic metabolites in the tissues. This is due to a decrease in oxidative processes in the tissue and the development of local acidosis. That leads to:

A) to peripheral hydrolysis of components of the basement membrane of capillaries

B) to the activation of proteases, in particular hyaluronidase, which causes enzymatic hydrolysis of the components of the basement membrane of capillaries.

During microscopy in the area of venous hyperemia:

Increased diameter of capillaries and postcapillaries, venules

At the initial stages, the number of capillaries increases and then decreases

Slowing down until blood flow stops

Significant expansion of the axial cylinder

Pendulum-like movement of blood in venules

Pathophysiological significance of venous hyperemia:

Decreased specific and nonspecific function of an organ and tissue.

Hypoplasia and hypotrophy of structural elements

Necrosis of parenchymal cells and development of connective tissue.

ISCHEMIA

This violation of peripheral circulation, which is based on restriction or complete cessation of blood flow.

Types of ischemia:

1 compression: with arterial pressure, scar, tumor, ligature

2 obstructive: reduction, up to the closure of the lumen of the vessel - thrombus, embolus, atherosclerotic plaque.

3 angiospastic: occurs due to arterial spasm, which may be associated with:

1) with activation of sympathetic neuroeffector influences or with an increase in the release of CA

2) with an increase in the adrenoreactive properties of arterioles (with an increase in Na + in the muscle fibers of the arteriole walls)

3) with the accumulation in the tissue and blood of substances causing vasoconstriction (angiotensin 2, thromboxane, prostaglandin ef

Manifestations of ischemia:

1.Reducing the diameter and number of visible arterial vessels

2. Pallor of an organ or tissue is due to a decrease in their blood supply and a decrease in the number of functioning capillaries

3. Decrease in the magnitude of arterial pulsation as a result of a decrease in their systolic filling with blood

4. Decrease in temperature of the ischemic area, due to a decrease in the flow of warm blood, and then due to a decrease in metabolism in the tissue

5.Decreased volume and turgor due to lack of blood in the vessels and decreased lymph formation.

By microscopy:

1. Reducing the diameter of arterioles and capillaries

2.Reducing the number of functioning capillaries

3. Slowing blood flow

4.Expansion of the axial cylinder

The consequences of ischemia depend on:

The nature of the consequences depends on the time of ischemia and the diameter of the vessel, as well as on the significance of the organ.

1.rate of development of ischemia

2.vessel diameter

3.sensitivity of the organ to hypoxia

4. the significance of an ischemic organ for the body

5.degree of development of collateral circulation

Consequences of ischemia:

1. Decrease in specific and nonspecific functions of an organ or tissue

2. Development of dystrophy and atrophy

3. Development of a heart attack

STASIS:

THIS is the cessation of blood flow in the microcirculatory bed.

Causes of stasis:

2.venous hyperemia

3. factors causing pathological changes in capillaries or disruption of the rheological properties of blood.

Types of stasis depending on the reasons:

1.true formation of stasis begins with damage to the capillary wall and activation of their blood cells and adhesion and aggregation.

2. ischemic outcome of ischemia due to a decrease in arterial blood flow, a slowdown in its flow and the turbulent nature of blood movement, which secondarily determines the adhesion and aggregation of formed elements

3.venous congestive stasis is the result of a slowdown in the outflow of venous blood, its thickening, cell damage with the subsequent release of proaggregants and cell aggregation and adhesion.

Mechanisms of stasis

The main mechanism of stasis is due to the cessation of blood flow in the microcirculatory unit.

1. aggregation and agglutination of blood cells under the influence of BAS proaggregants, these include ADP, thromboxane, prostaglandins F and E, CA. Their effect on blood cells leads to adhesion, aggregation and agglutination. This process is combined with the release of new biologically active substances from blood cells, including proaggregants, which potentiates agglutination reactions up to the cessation of blood flow.

2.aggregation of blood elements

due to a decrease in their negative charge and even a change to positive under the influence of an excess of potassium, calcium, sodium, magnesium ions, which are released from blood cells and vascular walls when they are damaged by causal factors causing stasis. Having a positive charge, damaged cells stick tightly to undamaged cells, forming aggregates that adhere to the intima of microvessels. This causes activation of blood cells and the release of new biologically active substances, which increase aggregation and adhesion.

3. aggregation of cells as a result of the adsorption of protein micelles on them, since the latter have the following factors:

1) being amphoteric, they are able to reduce the surface charge of cells by connecting with them using amino groups.

2) proteins are fixed on the surface of blood cells and facilitate the processes of adhesion and aggregation on the surface of the vascular wall

Consequences of stasis:

When the cause of stasis is quickly eliminated, blood flow is quickly restored and no damage is observed in tissues and cells.

Prolonged stasis causes degenerative changes in tissues and foci of micronecrosis.

EMBOLISM

This is the transfer and/or blockage of blood vessels by bodies that are not normally in the blood.

Embolism classification:

According to the nature of emboli:

Endogenous (gas, thromboembolism, tissue, amniotic fluid)

E xogenic:

air-

reasons: injury to large veins in which the pressure is close to zero (jugular, dural sinuses, subclavian); injury to the lung or its destruction (embolism of the pulmonary circulation); the entry of a large amount of air from the lungs into the blood during a blast wave.

Endogenous:

Gas: the main link in the pathogenesis is decompression, in particular with decompression sickness.

Atmospheric pressure difference from:

Increased to normal in divers

From normal to reduced when climbing mountains, depressurizing the plane.

Thromboembolism:

The source of blood clots is often defective blood clots; most often such blood clots form in the lower extremities.

Causes of inferior blood clots:

Aseptic or purulent melting

Impaired blood clot retraction

Blood clotting disorder

Fat

Occurs when disemulsified fatty pennies of less than 6-8 microns in size appear in the vessels.

Crushing of tubular bones

Severe damage to subcutaneous fat tissue

Lymphography

Parenteral administration of fat emulsion

Carrying out artificial circulation

Closed heart massage

Separation of atheromatous masses from an atherosclerotic plaque

fat enters the vessels, first clogs the capillaries, then the drops are retained in the pulmonary vessels, pass through the pulmonary filter and enter the systemic circulation, settling in the vessels of the brain, kidneys, and pancreas. The manifestations are caused, on the one hand, by the degree of mechanical blockage of the blood vessels of a particular organ, and on the other, by the chemical action of fatty acids formed as a result of fat hydrolysis.

Fabric:

A) in case of injury, fragments of body tissue (muscles, bone marrow, liver) can be carried in

B) tumor metastasis

Amniotic fluid: during childbirth, amniotic fluid enters the damaged vessels of the uterus in areas of the separated placenta. Since at this time the fetus has hypoxia, meconium appears in the amniotic fluid, its dense particles clog the vessels. Features of this embolism include sharply activated fibrinolysis in the blood. Since tissue fibrinokinases enter the bloodstream and fibrinolytic purpura may develop.

Classification of embolism and directions of movement of emboli:

1.orthograde embolism: movement of the embolus along the bloodstream

2.retrograde: against the blood flow

a) under the influence of gravity from the inferior vena cava to the veins of the lower limb

b) with increased intrathoracic pressure, with sharp exhalations (when coughing from the inferior vena cava into the veins of the liver)

3. paradoxical: unfused IVS and IVS. As a result, emboli from the right half of the heart move to the left, bypassing the right circle.

By localization they distinguish:

Small circle embolism

Large circle embolism

Portal vein embolism

Pulmonary embolism: with an increase in blood pressure in the pulmonary trunk, with a decrease in blood pressure in the pulmonary circulation, this leads to a decrease in blood flow to the left side of the heart and a decrease in blood ejection and, accordingly, cardiac output, which further leads to a decrease in arterial pressure and hypoxia in brain.

This is the intravital formation of dense masses consisting of blood elements on the walls of the vessel.

Stages of thrombosis:

1.adhesion:

Adhesion of blood elements to the vascular wall due to the release of vasoconstrictors, ATP, adrenaline, histamine, serotonin, prostaglandin D 2, E 2, and a simultaneous decrease in the synthesis of prostaglandin in the vascular wall

Changing the wall potential from negative to positive

Platelets adhere to the vascular wall due to the synthesis of von Willebrand factor in them, which is also synthesized in the vascular wall.

2.aggregation: crowding of platelets with subsequent release of aggregation factors such as thromboxane and vasoconstrictors. Degranulation leading to a second wave of aggregation

3.agglutination (gluing) is the formation of pseudopods by platelets and flattening of the thrombus in the capillaries

4.blood clot retraction. Due to thrombostenin and calcium ions.

Causes of thrombosis according to Virchow:

Damage to the vascular wall

Activation of the coagulation system

Changes in the rheological properties of blood

pathophysiological significance: - blockage of the lumen by a thrombus leads to circulatory disorders at the microcirculatory level

Prevent bleeding