BLOOD CIRCULATION DISORDERS

BLOOD CIRCULATION DISORDERS

Circulatory disorders can be divided into 3 groups: abnormal blood supply (arterial plethora, venous plethora, anemia), impaired vascular wall permeability (bleeding, hemorrhage, plasmorrhage), and disorders of the course and blood condition (stasis, thrombosis).

Disorders of blood circulation

Arterial plethora (hyperemia)

Arterial plethora = increased blood supply to the organ, tissue due to increased arterial blood flow.

General arterial plethora. It occurs with an increase in circulating blood volume.

Local arterial plethora. Occurs when the innervation is disturbed (angioedema) due to impaired blood flow through the arterial trunk (collateral hyperemia), after elimination of the factor (tumor, ligature, fluid) that squeezes the artery (hyperemia after ischemia), due to a decrease in barometric pressure (vacant blood pressure). ), with inflammation (inflammatory hyperemia), in the presence of arteriovenous shunt.

Venous plethora

Venous plethora = increased blood supply to an organ or tissue due to a decrease (difficulty) in the outflow of blood; blood flow is not changed or reduced.

• Stagnation of venous blood leads to the expansion of veins and capillaries, slowing blood flow in them, to the development of hypoxia, which is the main pathogenetic factor determining changes in the organs in venous plethora.

• Venous plethora can be general and local, acute and chronic.

General venous plethora. It is a morphological substrate of heart failure syndrome.

a. Common acute venous plethora.

• Occurs with acute heart failure, complicating large-focal myocardial infarction, acute myocarditis, etc.

• Due to hypoxia and an increase in hydrostatic pressure, the permeability of capillaries increases dramatically, plasma saturation (plasmorrhage) and edema, stasis in capillaries and multiple diapedes hemorrhages develop in the stroma of organs; in the parenchyma - dystrophic and necrotic changes.

Morphological changes.

Edema and hemorrhages develop in the lungs; Acute pulmonary edema is one of the main causes of death in patients with acute cardiovascular insufficiency.

Kidney dystrophy and necrosis of the epithelium of the tubules occur.

In the liver, centrolobular hemorrhages and necrosis develop.

b. General chronic venous plethora.

• Occurs with chronic cardiovascular insufficiency (heart defects, coronary heart disease, chronic myocarditis, cardiomyopathy, etc.).

• Long maintaining the state of tissue hypoxia, it leads not only to plasmorrhagia, edema, stasis and hemorrhages, dystrophy and necrosis, but also to atrophy and sclerosis: a congestive seal (induration) of organs and tissues develops.

Morphological changes.

• In hypodermic cellulose at venous stagnation common edema - anasarka - develops.

• Fluid accumulates in serous cavities, hydrothorax, hydropericardium, ascites develops (fluid usually appears in the abdominal cavity in the presence of congestive nutmeg fibrosis of the liver).

• Cyanotic induration develops in the skin, kidneys, spleen; the liver becomes nutmeg; brown induration occurs in the lungs.

а. The skin (especially of the lower limbs) becomes cold and becomes bluish (cyanosis). The veins of the skin and subcutaneous tissue are dilated, filled with blood; lymphatic vessels are also enlarged and filled with lymph. Swelling of the dermis and subcutaneous tissue, proliferation of connective tissue in the skin.

b. Kidneys are enlarged, dense, bluish.

с. The spleen is enlarged, dense, on a cut of dark cherry color, no scraping of the pulp.

Liver.

Macroscopic picture: the liver is enlarged, dense, its edges are rounded, the cut surface is variegated, gray-yellow with dark red specks and resembles nutmeg.

Microscopic picture: only the central sections of the lobules are full of blood, where hemorrhages are noted, hepatic beams are complexed and hepatocytes are killed; these sections on the liver section look dark red. At the periphery of the lobules, hepatocytes are in a state of fatty degeneration, which explains the gray-yellow color of the liver tissue. The spread of venous plethora from the centers to the periphery of the lobules is prevented by high pressure in the sinusoids of the lobules' periphery - the place where the branch of the hepatic artery falls. In the outcome of chronic venous stasis, nutmeg fibrosis develops in the liver; rarely, with prolonged venous stasis, sclerosis in the liver progresses, the liver tissue undergoes restructuring and the process ends with the formation of small-node cirrhosis of the liver (nutmeg, cardiac fibrosis).

In the lungs brown induration develops: they are enlarged, brown in color, of a dense consistency.

Microscopic picture: in the lumens of the alveoli, bronchi, in the interalveolar septa and peribronchial connective tissue, there is an accumulation of cells loaded with brown pigment hemosiderin. The growth of connective tissue in the interalveolar septa and around the bronchi is also noted. During the Perls reaction, the brown pigment-hemosiderin gives a positive reaction to iron, its grains are painted in bluish-green color.

Pulmonary hemosiderosis in venous plethora is associated with an increase in vascular permeability and the development of multiple diapedesic hemorrhages (local hemosiderosis, see “Disorders of endogenous pigment metabolism” in the topic “Mixed dystrophies”).

Local venous plethora.

• Occurs when there is difficulty in venous blood outflow from a specific organ or part of the body due to the closure of the vein lumen (thrombus or embolus) or compression from the outside (tumor, growing tissue).

• In organs, the same changes occur as with general congestion.

• Muscat liver and nutmeg cirrhosis can occur with thrombophlebitis of the hepatic veins, which is characteristic of the Budd-Chiari disease (syndrome).

Anemia.

Anemia, or ischemia, is a decrease in the blood supply to a tissue, organ, or part of the body as a result of insufficient blood flow.

• Anemia may occur during arterial spasm (angiospastic anemia), closure of the artery through a thrombus or embolus (obstructive), with artery compression by a tumor, effusion, tourniquet, ligature (compression), as a result of redistribution of blood (for example, anemia of the brain during extraction of fluid from the abdominal cavity, where most of the blood rushes).

• Changes in tissue in case of anemia are associated with the duration of hypoxia resulting from this and the degree of sensitivity of the tissue to it.

• With acute anemia, dystrophic and necrotic changes occur in the organs.

• At chronic anemia, atrophy of parenchymal elements and stroma sclerosis develops.

Pulmonary embolism.

• The source is usually the blood clots of the lower extremities, the veins of the tissue of the small pelvis that occur during venous stasis, as well as blood clots of the right heart.

• One of the most common causes of sudden death in patients in the postoperative period and in patients with heart failure.

• In the genesis of death in pulmonary thromboembolism, both the closure of the vessel lumen with the development of acute right ventricular insufficiency and the pulmonary-coronary reflex are important: a spasm of the bronchial tree, branches of the pulmonary artery, and coronary arteries of the heart.

• At an autopsy, usually in the general trunk of the pulmonary artery, loosely lying gray-red color of worm-like masses with a dull surface is visible.

• Thromboembolism of the small branches of the pulmonary artery usually develops a hemorrhagic pulmonary infarction.

b. Arterial thromboembolism (arteries of the systemic circulation).

• The source of arterial thromboembolism is more often blood clots that form in the left half of the heart (with endocarditis, malformations, myocardial infarction, etc.) and in the aorta (or large arteries) with atherosclerosis.

• Organs develop heart attacks and gangrene.

Thromboembolic syndrome with heart attacks in many organs often develops.

 

Fat embolism.

Develops when fat enters the bloodstream:

a) in case of traumatic damage to the bone marrow (at the fracture of long tubular bones);

b) at crushing of subcutaneous fatty tissue;

c) in case of erroneous intravenous administration of oil solutions of medicinal or contrast agents.

• Fat droplets that enter the veins occlude the capillaries of the lungs and through the arteriovenous anastomoses enter the circulation, obturating the capillaries of the kidneys, brain and other organs.

• Massive fat embolism leads to acute pulmonary insufficiency: when examining histological lung preparations stained with Sudan III, droplets of orange-red color are detected in the capillaries of the interalveolar septa.

• Fatal outcome can also occur in adipose embolism of brain capillaries, which leads to the appearance of numerous point hemorrhages in the brain tissue.

 

Air embolism.

• It develops when air enters the bloodstream when the veins of the neck are wounded (which is facilitated by negative pressure in them), after childbirth or abortion, if the sclerosing lung is damaged, and if intravenous air is accidentally injected along with the drug.

• air bubbles trapped in the blood cause an embolism of the capillaries of the pulmonary circulation; If air bubbles get into the systemic circulation, brain capillary embolism may develop.

• At the autopsy, an air embolism is recognized by the release of air from the right side of the heart when piercing them, if you pre-fill the cavity of the heart shirt with water. The blood in the cavities of the heart has a foamy appearance.

Gas embolism.

• Characteristic of caisson disease: it develops with rapid decompression (i.e., a rapid transition from elevated atmospheric pressure to normal atmospheric pressure).

• The bubbles of nitrogen released from high pressure in a dissolved state cause blockages in the capillaries of the brain and spinal cord, liver, kidneys and other organs, which is accompanied by the appearance of small foci of ischemia and necrosis (especially often in the brain tissue).

• A characteristic symptom is myalgia.

A special tendency to the development of caisson disease is noted in obese people, since most of the nitrogen is retained by fatty tissue.

Tissue embolism.

It may occur during tissue destruction due to injury or pathological process leading to the entry of pieces of tissue (cells) into the blood. Amniotic fluid embolism in parturients can be accompanied by the development of disseminated intravascular coagulation syndrome and lead to death.

Embolism by malignant tumor cells underlies the metastasis of tumors: in the organs, numerous round tumor nodes often come to light with depressions in the center (necrosis).

Microbial embolism.

Occurs in cases where bacteria circulating in the blood (as well as fungi, animal parasites, protozoa) occlude the lumen of the capillaries. Often, bacterial emboli are formed when a thrombus is purulently melted. Thrombobacterial embolism.

At the site of the blockage of the vessel with bacterial emboli, metastatic abscesses are formed. An example of bacterial embolism is the embolic purulent nephritis that is often found in septicopyemia: the kidney is enlarged; multiple small yellowish foci (foci of purulent inflammation) are visible in the cortex and medulla.

Embolism by foreign bodies. It is observed when catheters, fragments of metal objects (projectiles, bullets, etc.) enter the blood. Foreign bodies also include embolism with lime and cholesterol crystals of atherosclerotic plaques, which propogates in the vessel lumen when they are ulcerated.

Shock

Shock - circulatory collapse, accompanied by hypoperfusion of tissues and a decrease in their oxygenation.

Causes of shock.

1. Reduction of cardiac output (more often with blood loss or severe heart failure).

2. Common peripheral vasodilation (usually with sepsis or severe injury, accompanied by hypotension).

Types of shock.

1. Hypovolemic shock. The basis is an acute decrease in the volume of circulating blood (severe blood loss, fluid loss from burns, indomitable vomiting and diarrhea, etc.).

2. Cardiogenic shock occurs due to a decrease in cardiac output (with extensive myocardial infarction and other conditions leading to acute heart failure).

Vascular shock:

a) anaphylactic;

b) neurogenic (traumatic shock).

 

Stages of shock.

1. Non-progressive (early) stage. Included are mechanisms that compensate for a decrease in cardiac output to maintain the perfusion of vital organs.

2. Progressive stage. Depletion of compensatory mechanisms: tissue hypoperfusion and metabolic acidosis develop, blood is “sequestered” in a sharply expanded capillary bed; there is a deep collapse.

3 Irreversible stage. Organ damage and metabolic disorders, incompatible with life, develop.

BLOOD CIRCULATION DISORDERS

Circulatory disorders can be divided into 3 groups: abnormal blood supply (arterial plethora, venous plethora, anemia), impaired vascular wall permeability (bleeding, hemorrhage, plasmorrhage), and disorders of the course and blood condition (stasis, thrombosis).

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