Circulatory Disorders – Disturbance of Blood and Lymph Circulation

There are three types of circulatory disorders.

  1. Disturbance in the blood supply of the vessels (hyperemia and anemia, which may be arterial or venous).
  2. Develops in disturbance of the rheological properties of blood (stasis, thrombosis, and embolism).
  3. Due to disruption of the permeability of the vessel wall (bleeding, hemorrhage, hemorrhage).

Classification of circulatory disorders: – 

Types of circulatory disorders

  • ·       Hyperemia: 1) Arterial 2) Venous
  • ·       Anemia (ischemia)
  • ·       Bleeding, hemorrhage
  • ·       Haemorrhagia
  • ·       Stasis: lymphostasis, hemostasis
  • ·       Thrombosis
  • ·       Embolism
  • ·       Shock
  • ·       DIC
  • ·       Necroses: 1) Coagulation (dry) 2) Colliquative (moist)
  • ·       Infarcts: anemic or ischemic; hemorrhagic; anemic with hemorrhagic rim
  • ·       Gangrene (dry and wet)
  • ·       Bedsores
  • ·       Sequestration
  • ·       Mummification


HYPEREMIA (circulatory disorder)

In circulatory disorders, There is an increased blood supply of an organ or tissue due to the increased inflow of arterial blood

In circulatory disorders, It can be general or local.

General arterial hyperemia characterized by an increase in blood volume (hypertension) or the number of red blood cells (erythremia), which leads to increased blood supply of organs and tissues – “at a certain portion of the blood channel per unit time”.

Macroscopically: – redness of the skin, mucous membranes, and in increased blood pressure.

Types of arterial hyperemia:

  1. Angioneurotic hyperemia(neuroparalytic): -As a result of stimulation of vasodilator nerves or paralysis of vasoconstrictor nerves.
  2. Collateral hyperemia: –When blood flow through great blood vessels is disturbed (thrombosis, embolism), and the blood runs in collaterals.
  3. Postanemic hyperemia: – Cause leading to compression of blood vessel (tumor, ligature, accumulation of fluid in the cavity, a blood clot, and others) is accounted for hyperemia above the localization of causative factor, and lower the localization of causative factor – anemia. In the case of rapid removal of causative factor, there is hyperemia in the organs, which were in a state of anemia, and there is acute anemia in the organs, which were in a state of hyperemia. Therefore, the causative factor should be eliminated gradually restoring blood circulation.
  4. Vacuum hyperemia: – Develops due to a decrease in barometric pressure. i.e. for divers (at caisson work) and astronauts (at the sudden change in barometric pressure), which contributes to the development of gas embolism. Local vacuum hyperemia may be on the skin due to medical suction cups.
  5. Peristatic hyperemia: – Develops due to the increased blood flow in the focus of inflammation.
  6. Hyperemia caused by arteriovenous fistulaoccurs in the presence of anastomosis between the artery and vein, f.e. in wounds or injuries.


In circulatory disorders, Venous hyperemia is characterized by increased blood supply of an organ or tissue due to the reduced blood outflow. Blood inflow is not changed or reduced. Venous stasis leads to congestive hyperemia and to venous and capillary dilatation, which is accompanied by hypoxia, increased permeability of the capillary basement membranes.

In circulatory disorders, Venous hyperemia may be general or local.

General venous hyperemia develops in cardiac pathology, which leads to the development of acute or chronic cardiovascular insufficiency. Acute general venous hyperemia is a manifestation of acute cardiac insufficiency, o.f. in myocardial infarction, acute myocarditis, when there is a deficiency of myocardial contractile function.

Morphological changes in acute general venous hyperemia are due to hypoxic injury of histohematological barrier. This results in increased permeability of the walls of blood vessels, plasmorrhagia, edema, stasis in the capillaries, multiple diapedesis hemorrhage, degenerative and necrobiotic changes in parenchymal organs.

Chronic general venous hyperemia develops in the syndrome of chronic cardiac insufficiency. For example, heart defects, ischemic heart disease, chronic myocardites, cardiomyopathies, endocardial fibroelastosis and other causes.



Morphogenesis of brown in duration of the lungs (Table 7)

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In circulatory disorders, The morphological changes in chronic general venous hyperemia develop due to chronic tissue hypoxia, wherein there is injury of histohematological barrier, increased permeability of the walls of blood vessels, followed by plasmenorrhagia, edema, stasis in the capillaries, multiple diapedesis hemorrhage and degenerative and necrobiotic changes.

The release of red blood cells outside the bloodstream due to increased vascular permeability, the formation of hemosiderin pigment, macrophagy lead to the development of hemosiderosis; and organs and tissues become brown.

Along with these changes, atrophic and sclerotic processes develop in the tissues of internal organs. The parenchyma of the organs is full-blooded, dark cherry.

In circulatory disorders, Chronic hypoxia in organs stimulates the synthesis of collagen by fibroblasts and fibroblast-like cells; this leads to the following changes: the connective tissue replaces parenchymal elements; congestive hardening or induration of organs and tissues develops, in particular, in the lung, liver, spleen, and kidneys. Due to venous stasis, “cyanotic spleen or kidney” develops.


Morphogenesis of congestive liver fibrosis (Table 7)

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Macroscopic changes in “brown induration of the lung” are characterized by parenchyma firmness, it has few air-filled structures, becomes brown due to hemosiderosis. The cut tissue is full-blooded.

Microscopic changes in the lung, in hemosiderosis, are characterized by an accumulation of brown hemosiderin pigment in the interstitial tissue, the lumens of the alveoli and bronchi, Siderophages are discolored to dark brown color having been stained with hematoxylin and eosin, and in Perls test, they become emerald-green – “Prussian blue” due to the restoration of Fe3.


Figure 31 and 32

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Morphological equivalent of venous hyperemia is macroscopic changes in the lung which are referred to as “brown induration of the lung”, and in the liver – “Nutmeg liver”, in the spleen – “cyanotic spleen”, in the kidney – “cyanotic kidney”. The organs are increased in size, spotty full-blooded, their edges are rounded, there is dripping dark blood on the surface of the cut.

Local venous hyperemia develops due to hindered venous return from an organ or body part. The cause is related to the closure of the lumen of the vein by a clot, embolus or by squeezing of the vessel from outside, for example, by tumor, overgrowth of connective tissue, the accumulation of fluid in the cavities and others.

In local venous hyperemia, skin becomes cyanotic, cold to the touch. Organs also become cyanotic, slightly increased in volume, have rounded edges, the surface is full-blooded, and the capsule is tense; there is dripping dark blood on the surface of the cut.


Figure 31 and 32

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In circulatory disorders, Thrombosis is intravital blood coagulation in the lumen of the vessel or cavity of the heart. Formed (as a result of this process) blood clot is called a thrombus.

The process of blood coagulation is multistaged: there is sequential activation of proteins – precursors, clotting factors found in the blood internal) and tissue (external).

In circulatory disorders, There also is the anticoagulant system that provides regulation of the hemostatic system, i.e. liquid state of the blood in the vessels; dysregulation of hemostasis leads to thrombosis.

Causes of thrombosis:

Local factors – damage to the integrity of the vessel wall (endothelium), it may be vasculitis, venous hyperemia or disturbed blood flow velocity.

General factors – dysregulation of hemostatic systems (coagulation and anticoagulation), changes in the composition of blood.

Characteristics of the phases of clot formation:

Phase 1 – platelet agglutination – there is directed movement and platelet adhesion to the site of endothelial damage. This releases the lipoprotein complex of the peripheral zone of the platelets – hyalomere, which has agglutinative properties. Platelet agglutination results in their degranulation, release of serotonin and platelet thromboplastin factor, which leads to the formation of active thromboplastin, and the beginning of the next phase.

Phase 2 – coagulation of fibrinogen and fibrin formation, which are related to the enzymatic reaction. There is a process of transition thromboplastin – thrombin – fibrinogen-fibrin”. The central part of blood platelets – granulomere containing an enzyme becomes the template for fibrin. Both this enzyme and serotonin have vasoconstrictor properties.

Phase 3 – agglutination of red blood cells, uptake with white blood cells.

Phase 4 – precipitation of plasma proteins and the formation of a clot -thrombus.


Figure 36

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In circulatory disorders, The structure of a blood clot depends on the rate of its formation. Microscopically, blood clot is composed of fibrin and blood corpuscles.

According to its structure, a clot may be: white – white blood cells predominate; red – red blood cells predominate; mixed – there is a layered structure consisting of red blood cells and white blood cells; hyaline thrombus – in the coregulation of plasma proteins.

According to its localization, a clot may be: parietal – when the most part of the vessel lumen is free; obstructive – when vessel lumen is partially or completely closed; in aneurysm dilated thrombus. The shape and length of the thrombus are different and have the structure of the vessel.

Anatomically – it has a head, body and tail.


Figure 37

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Macroscopic changes of thrombus – corrugated surface is typical, it is dull and dry, the consistency is dense, it has layered structure on the cut; having been cut, it crumbles; the head of the thrombus is very tightly fixed to the damaged site of the endothelium of the vessel wall.


Figure 38

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Microscopically, thrombus is composed of fibrin, platelets, erythrocytes, leukocytes and plasma proteins. One of the causes of clot formation is an in flammation of the vessel wall – vasculitis in phlebitis. These changes are referred to as thrombovascular disease, and thrombus is often mixed.


Figure 39

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In the red thrombus, erythrocytes with the presence of fibrin strands and platelets predominate.


Figure 40

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In clinical practice, it is of great importance to be able to diagnose and differentiate thrombus and post-mortem blood clot.

Macroscopically, post-mortem blood clot is different from a thrombus on the following grounds: the surface is smooth, shiny; the clot lies freely in the lumen of the vessel, its structure is homogeneous, elastic, and it can be easily removed from the lumen.

Outcomes of a blood clot:

Favorable – aseptic autolysis, which occurs due to proteolytic activity of the enzymes of leukocytes; vascularization, when the channels are lined with endothelium; calcification (petrification); phleboliths (stone formation in the veins).

Adverse – thromboembolic outcome, septic autolysis, thrombo bacterial embolism (in sepsis), which may lead to necrosis or infarction.

The significance of the outcome of thrombosis for the body is determined by the rate of thrombosis development, the localization of the process and the

type of the vessel


EMBOLISM (circulatory disorder)

In circulatory disorders, Embolism is a pathological process when substances which do not normally occur and lead to circulatory failure circulate in the bloodstream.

In circulatory disorders, Types of embolism depending on the reason may be gas, air, tissue (tumor), thromboembolism, fat, microbial (in sepsis), foreign substances embolism.

  1. Gas embolism is when there is a blockage of the lumen with nitrogen gas bubbles. It occurs in people employed in caisson work: in divers, astronauts, test pilots when there is an abrupt change in barometric pressure from high to low and rapid decompression develops. Nitrogen does not have time to go through the lungs and accumulates as bubbles in the blood. In such a case, they block the capillaries of the brain, spinal cord, liver, kidneys and other organs.
  2. Thromboembolism is a pathological process when fragmentations or separation of anatomical parts of a thrombus occur, that lead to circulatory failure in the form of necrosis or infarction. Its tail section migrates mostly. Macroscopic and microscopic pictures of thromboembolism with localization in various organs and vessels are shown in figures 41, 42, 43 and 44.


Figure 41, 42, 43 and 44

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In circulatory disorders, Tissue embolism (tumor, cellular) develops when some pieces of tissue or tumor enter the blood stream in damaging the integrity of the vessel walls. The process, when tumor cells from a primary focus with their migration enter the bloodstream in tissue embolism, is called metastatic spread, tissue embolus is denoted as metastasis (Fig. 45).


Figure 45

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In circulatory disorders, Fat embolism is a type of embolism, the cause of which is when fat drops occur in the lumen of blood vessels, mostly capillaries. Progression of fat embolism may occur in the subcutaneous tissue injury. in so-called “crush syndrome”, in bone fractures, in cases of improper oil-based drug administration.

The meaning and the outcome of fat embolism depend on the extent and localization of the process. For example, pulmonary fat embolism is dangerous to human life, if the process of fat embolism covers more than 2/3 of the lung capillaries.

In circulatory disorders, It is difficult to diagnose fat embolism grossly, it is possible only under microscopic examination by means of special staining by the method of Sudan III, when fat droplets are detected in the lumen of the pulmonary capillaries and discolour to yellow.


Figure 46

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When stained lung tissue in fat embolism with hematoxylin and eosin fat droplets dissolve in alcohol during coloring of a material and look like clear vacuoles in the lumens of pulmonary vessels (Fig. 47).


Figure 47

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Microbial embolism develops in infectious diseases, in sepsis. The reason may be bacteria, animal parasites, protozoa, fungi (Fig. 48).


Figure 48. Microbial embolus in the vessel lumen of the myocardium in sepsis.

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In circulatory disorders, Air embolism occurs when atmospheric air falls in the bloodstream. For example, air embolism can occur in wounds with damage of the integrity of blood vessels, particularly veins of the neck, where the pressure is negative and the air as though absorbs into the lumen of the vessel, in violation of the intravenous infusion procedure, in opening veins of the uterus during pregnancy, incases of premature detachment of placenta as well as in pneumothorax, etc. The air accumulates in the cavity of the right heart and stretches it; blood becomes frothy in the veins and air bubbles accumulate.

Foreign substances embolism is a pathological process when the flow of blood falls in a variety of foreign particles, e.g. a bullet, particles from shells or other substances.

The significance of emboli to the human body is directly related to the cause of development, type of embolism, its location and the extent and early clinical diagnostics.

Outcome of embolism is poor circulation, progression of ischemia, necrosis or myocardial infarction.


In circulatory disorders, Disseminated intravascular coagulation syndrome (DIC) is characterized by the formation of multiple blood clots in the vessels of the microvasculature of various organs and tissues due to activation of blood coagulation factors, imbalance between coagulation and anticoagulation systems followed by intensifying and developing of multiple hemorrhages.

Causes of DIC: it often develops in shock of any origin (hemorrhagic, carcinogenic, anaphylactic, traumatic and other forms), in the transfusion of in compatible blood group, malignant tumors, severe intoxication, obstetric pathology, organ transplantation, extensive injuries, operations and other states.

Stages of DIC:

  1. first the stage of hypercoagulation and thrombus formation is characterized by intravascular aggregation of blood cells, as well as disseminated coagulation with the formation of multiple blood clots in the microvasculature of tissues and organs;
  2. second – progressive consumption coagulopathy – is characterized by a significant decrease in platelets and fibrinogen, a transition occurs from hyper coagulation to incoagulability with hemorrhagic diathesis;
  3. third the stage of deep in coagulability and fibrinolysis activation, leading to lysis of microthrombi formed earlier, and then degradation of coagulation factors and progression of absolute incoagulability, which leads to bleeding and hemorrhage;
  4. fourth – recovery stage (residual symptoms) is characterized by degenerative, necrotic and hemorrhagic lesions in all organs and tissues, acute multiple organ failure. Multiple blood clots in the vessels of the microvasculature, diaper disc hemorrhage, and necrosis are morphologically characteristic.

In severe cases of DIC mortality rate is 50% due to the development of acute multiple organ failure, mortality in newborns is up to 75-90%.


SHOCK. TYPES OF SHOCK (circulatory disorders)

In circulatory disorders, Shock is an abruptly developing pathological process that threatens life, due to the action of super strong stimuli and is characterized by severe impairment of the central nervous system, autoregulation of the microvasculature, respiration and metabolism, which lead to destructive changes of organs and tissues and as a result it involves the emergency medical care.

The pathogenesis of shock – the trigger is an impairment of tissue perfusion.

Classification of shock:

  • Hypovolemic shock (hemorrhagic)- it is based on the acute disorder of circulating blood volume.
  • Transfusion shock – incompatible blood transfusion reaction
  • Hemolytic shock – it is based on intravascular hemolysis of red blood cells.
  • Cardiogenic shock is the result of the rapid fall of the contractile function of the myocardium and the increase of the flow of afferent impulses, particularly in acute myocardial infarction due to acute circulatory disorders accompanied by acute myocardial ischemia.
  • Anaphylactic shock is a pathological reaction in response to any agent (allergen), they are frequently drugs or other toxic agents.
  • Traumatic shock – it is based on excessive afferent impulses and pain syndrome. As a rule, this type of shock is often accompanied by hemorrhage and intoxication that worsen its course and prognosis.
  • Septic shock (its other names are endotoxic or toxic infectious). Is caused by endotoxins of pathogenic flora.

In circulatory disorders, Progression of shock of different genesis is based on a universal complicated polyphasic mechanism; in this context 3 phases of shock may be noted:

1-phase of compensated shock – the early period of this phase is characterized by the preservation of relatively specific characteristics due to the etiological factor and its pathogenesis; hemodynamic parameters are within normal limits.

2 – phase of decompensated shock develops when the causative factor remains in effect, marked hemodynamic failure is noted, specific features associated with the etiological factor and pathogenesis are lost; clinical and morphological manifestations of shock are stereotyped.

3 – phase of irreversible shock – at this stage of the pathological process deep irreversible damage of all organs and systems is taking place, and multiple organ failure is developing.



In circulatory disorders, A hemorrhage is a flow of blood from a vessel (or heart), the cause of which is the injury of the integrity of the vascular wall. According to the source hemorrhage may be: arterial, venous, arterial venous (mixed), capillary, parenchymal and heart.

A common type of hemorrhage is bleeding, in which blood accumulates

in tissues extravascularly followed by focal or diffuse suffusion (Fig. 49, 50, 51,

52, 53).

There are 4 types of bleeding:

  1. Hematoma is a local accumulation of blood to form clots and disruption of the structure of tissues, which results in the cavity formation.
  2. Hemorrhagic suffusion is the infiltration of tissue with blood while maintaining its integrity.
  3. Bruises are planar hemorrhages in the skin, subcutaneous tissue, and mucous membranes.
  4. Petechiae are minor bleeding in the skin, mucous and serous mem branes of internal organs.


Causes hemorrhage and bleeding:

Diapedesis is increased vascular permeability often microvasculature vessel that can develop in severe intoxication, hypoxia, infection, coagulopathy, systemic vasculitis, uremia, leukemia, hemophilia, hemorrhagic diathesis:

Break is an affection that occurs as a result of injuries in damage to the vascular wall;

Corrosion of the vessel wall is in this case we speak of arrosivo hemorrhage due to the injury of the integrity of the vascular wall, corrosion, for instance, by a tumor, in purulent inflammation, exposure to chemicals, and vascular invasion of fallopian tube with villi in ectopic pregnancy. Depending on the cause of hemorrhage, and which organ it is localized in.

macroscopic changes may be different and have their names. Bleeding may be of 2 types:

In circulatory disorders, External hemorrhage occurs when there is an outlot of the blood from the vessel lumen, or the heart cavity into the surrounding tissue. For example. spitting up blood, bloody nose, metrorrhagia is uterine hemorrhage, melena is a discharge of blood in the feces, and others; Internal hemorrhage occurs when there is an accumulation of blood in the body cavities and organs.

For example, hemothorax is an accumulation of blood in the pleural cavity; hemoperitoneum is an accumulation of blood in the abdominal cavity, hemopericardium is in the heart cavity, hemothorax is in the pleural cavity, etc.

(Fig. 54).


Figure 54.

Hemothorax. The accumulation of blood in the pleural cavity, the lungs are pneumatic (pulmonary atelectasis is pointed out with an arrow).


The significance of bleeding and hemorrhage is determined by their appearance, distribution, localization in some organs, as well as the extent of blood loss.


In circulatory disorders, Menorrhagia is a process that is characterized by the outlet of the blood plasma from the vessel lumen due to increased vascular permeability and suffusion, and it is called plasmatic suffusion. In this pathological process occurs transendothelial outlet of blood plasma due to the ultrafiltration through the pores of the basal membrane of the endothelium of the vessel wall. Accumulation of plasma components leads to damage to the cells and the intercellular substances as in the vascular wall and in the perivascular tissue, as a result of which fibrinoid necrosis (fibrinoid) or hyalinosis of vessel wall develop.