Hyperemia – Arterial Hyperemia & Venous Hyperemia

Hyperemia is also known as Plethora or Congestion, depending on the spread of the process, can be Arterial Hyperemia and Venous Hyperemia.

Arterial hyperemia

Arterial Plethora or Congestion is a type of circulatory disorders when there is an increased blood supply of an organ or tissue due to the increased inflow of arterial blood. Arterial hyperemia may be general or local.

General arterial hyperemia is a type of Plethora, which is characterized by an increase in blood volume (hypertension) or the number of red blood cells (erythremia), which leads to the eased blood supply of organs and tissues.

Local arterial hyperemia is characterized by an increase in blood volume at a certain portion of the blood channel per unit of time.

Macroscopically, there is redness of the skin, mucous membranes, and increased blood pressure in hyperemia.

Types of arterial hyperemia:

  1. Angioneurotic hyperemia (neuroparalytic) occurs as a result of stimulation of vasodilator nerves or as a result of paralysis of vasoconstrictor nerves.
  2. Collateral hyperemia occurs when blood flow through great blood vessels is disturbed (thrombosis, embolism), and the blood runs in collaterals.
  3. Postanemic hyperemia – when the cause leading to compression of a 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 the 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, It may be common, for example, 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 fistula occurs in the presence of anastomosis between the artery and vein, i.e. in wounds or injuries.

Venous hyperemia

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.

Venous Plethora may be general or local.

General venous Congestion 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, fe in myocardial infarction, acute myocarditis when there is a deficiency of myocardial contractile function.

Morphological changes in acute general venous Congestion are due to hypoxic injury of the histo-hematological barrier. This results in increased permeability of the walls of blood vessels, plasmorthagia, edema, stasis in the capillaries, multiple diapedetic hemorrhages, 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 myocarditis, cardiomyopathies, endocardial fibroelastosis, and other causes. Morphogenesis of brown induration of the lungs is shown in table 7.

Table 7

Morphogenesis of brown induration of the lungs

Chronic venous hyperemia, pulmonary hypertension, tissue hypoxia

Adaptive restructuring of the pulmonary veins and arteries

Vascular sclerosis of the lung, adaptation failure

Increased tissue hypoxia

Dilatation and hyperemia of the capillaries Activation of fibroblasts of pneumo-sclerosis Dilatation and hyperemia of the capillaries
Increased vascular permeability Increased vascular permeability
Diapedetic hemorrhage hemosiderosis Insufficiency of the lymphatic system Penetration of plasma proteins into the tissues

The morphological changes in chronic general venous hyperemia develop due to chronic tissue hypoxia, wherein there is an injury of histohematological barrier, increased permeability of the walls of blood vessels, followed by plasmorrhagia, edema, stasis in the capillaries, multiple diapedetic hemorrhages, and degenerative and necrobiotic changes.

The release of red blood cells outside the bloodstream due to increased vascular permeability, the formation of hemosiderin pigment, macrophages 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.

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 nutmeg liver is represented in table Given Below.

Morphogenesis of congestive liver fibrosis

Chronic venous stasis, hypoxia


Hyperemia, hemorrhage. destruction of the hepatocytes in the center of the liver acinus Sclerosis of the walls and obliteration of the lumens of the central and collecting veins


The growth of connective tissue in the center of the liver acini The proliferation of fibroblasts of the adventitia of the veins and lipocytes acting as fibroblasts Shunting of blood

Capillarization of sinusoids

Progressive liver fibrosis

Insufficiency of the lymphatic system


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 Perl’s test, they become emerald-green – “Prussian blue” due to the restoration of Fe3 (Fig. 31, 32).

Figure 31. Brown induration of the lung: Brown siderophages. Stained with hematoxylin and cosin 200-fold.


Figure 32. Hemosiderosis of the lung. Accumulation of siderophages in the lumens of alveoli and interstitial tissue of the lung. Perls test (reaction of Prussian blue). 100-fold.

The 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 (Fig. 33, 34, 35).


Figure 33. Nutmeg liver. Liver parenchyma is spotty full-blooded, dark-cherry

Local venous Plethora or Congestion 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 the 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. Or gans 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 34. Nutmeg liver Intralobular capillaries are full-blooded stained with hematoxylin and eosin. 100-fold


Figure 35. Cyanotic spleen in venous hyperemiaHyperemia of the parenchyma