This is a condition in which the blood stagnates in the vessels; they are overfilled with blood which, as it remains too long in the vessels, has a venous character, hence passive hyperemia is also called Venous Hyperemia.


Passive hyperemia frequently occurs as a consequence of Weakness of the heart. In the normal state the forces of the circulation in order to remove the blood from depending parts, have to overcome gravitation. The force of the heart propagated through arteries and capillaries to the veins is generally sufficient to do this. It is, however, assisted by the muscular movements, which, in conjunction with the valves in the veins, materially assist the venous current; also by the aspiration effected by the inspiratory movements. But if the heart is weak, the blood is apt to linger in depending parts or in parts far removed from the centre; hence the name Hypostasis or Hypostatic hypersemia applied to such conditions. Weakening of the heart occurs in many forms of disease. It is often very marked in fevers, such *as typhus and typhoid, or in long-continued debilitating diseases, which produce anaemia. In these cases the blood often stagnates in the dependent parts of the lungs, or in depending parts of the skin, over the sacrum and shoulder blades in persons lying on their backs, over the trochanters in persons lying on their sides. In these latter situations the weakness of the circulation along with the mechanical effects of the weight of the body and the irritation of decomposing material, lead frequently to necrosis of the skin and the formation of bed-sores. In fevers there may be passive hyperemia of the extremities of the fingers or toes, resulting even in necrosis or gangrene.

Again, there may be difficulty in overcoming gravitation on account of the force of the heart being partly lost by reason of Obstruction of arteries. Thus atheroma, by producing a thickening of the internal coat, may cause a partial obstruction, which is often increased by the formation of thrombi on the affected surface. In consequence of this, the force of the heart may be insufficient and the blood may stagnate in the parts supplied. Complete occlusion of an artery will under certain circumstances produce extreme passive hyperemia. (Hsemor-rhagic infarction, see under Embolism).

Obstruction of veins is the most direct and obvious cause of passive hyperemia. This may be produced by pressure of tumours, exudations, bandages, the pregnant uterus, even hard masses of faeces, by coagulation of blood within the veins, or by the bursting of tumours into veins, or their growth through their walls.

Lastly, Disease of the valves of the heart produces in a large proportion of cases a general venous hypersemia (see under Heart).

Phenomena Of Passive Hyperemia

Taking the simplest case, that of obstruction of a venous stem, the first result is an increase of bloodpressure in the veins behind the point of obstruction, and an accumulation of blood in the part. If the veins have abundant anastomoses, then the blood will soon to a considerable extent find its way by other channels and the normal conditions be restored. But from the list of causes of passive hyperaemia it will be seen that most of these involve sets of veins, or whole regions of the body; even in the case of thrombosis, the coagulation usually extends to a number of veins; hence, relief by anastomosis may not be obtained. The local increase of pressure remains, and it affects capillaries.

The further effects are to be traced to the excessive pressure of the accumulated blood in the capillaries and to the nutritive changes in their walls from the stagnation of the blood. The blood accumulates in excessive quantity in these vessels and at an excessive pressure. In consequence of this an increase in the natural transudation of fluid through the capillaries occurs, and the blood-corpuscles, especially the red ones, escape from the vessels. Each of these phenomena merits more special consideration.

Haemorrhage by diapedesis is the escape of the red corpuscles from the blood-vessels without rupture of their walls. This process occurs mainly, if not entirely, in the capillaries, and it can be shown by experiment that it does not involve rupture of these vessels. If the tongue of a frog is ligatured at its base so as to include all the veins, but excluding the artery, there will be the phenomena of hyperemia greatly intensified, and among these phenomena diapedesis. But if the ligature be loosened within a moderate period, the circulation is restored, and the phenomena disappear. If the escape of blood-corpuscles had been by rupture, it would have continued after resumption of the circulation. As to the manner in which corpuscles escape, it is probable that they pass between the endothelial cells. Fig. 24 shows the appearance of the endothelium of a capillary mapped out by treatment with nitrate of silver, and Fig. 25 shows capillaries similarly treated after passive hyperemia had existed. The latter illustration is taken from Arnold, who asserts that while in the normal condition there are minute apertures between the endothelial cells, chiefly at the angles where two or three meet, these are found much enlarged in passive hyperemia. The small apertures may be called stigmata, and the larger ones stomata. The excessive pressure in the capillaries seems to be the chief agent in causing the escape of the corpuscles as well as the increased transudation of fluid, but we have also as a considerable element, in many cases, a nutritive defect in the walls of the vessels from their long exposure to venous blood, allowing of the escape of the corpuscles. The haemorrhage is usually inconsiderable, but in some cases it attains to large dimensions. (See under Thrombosis of cerebral sinuses).

The author has observed of late a loose way of using the term diapedesis by applying it to the emigration of the leucocytes. As this use is confusing and is opposed to the original employment by Strieker, Cohnheim, Arnold, and others, to designate a form of haemorrhage, it seems unadvisable. The author therefore limits the term to the escape of red corpuscles without rupture, reserving the term emigration for the more active penetration of the white corpuscles.

That there is an increased Transudation of fluid can be directly proved by experiment. The flow in the lymphatic vessels has been proved to be excessive. If the lymphatics are not capable of disposing of the entire excess, then the fluid accumulates in the serous spaces and cavities of the body, giving rise to (Edema and Dropsy (see further on). This accumulation will occur if, on the one hand, the transudation be too great for the lymphatics to dispose of it, or if, on the other, for some reason, the lymphatics do not take it up sufficiently. The current in the lymphatics depends on the blood-pressure, and we have just seen that the cause of the increased transudation is excess of blood-pressure, and so the same condition which determines the increase will, to a certain extent, cause it to be more rapidly disposed of. • In cases of hypostasis, however, there is a special tendency to oedema. The hyperemia here is due, as we have seen, to weakness of the heart associated with the action of gravitation. Both of these causes will equally act on the lymphatic circulation, and induce the transuded fluid to linger and accumulate.

Normal capillary, with endothelium mapped out by treatment with nitrate of silver.

Fig. 24. - Normal capillary, with endothelium mapped out by treatment with nitrate of silver.

Capillaries after passive hyperemia.

Fig. 25. - Capillaries after passive hyperemia. Apertures between the cells greatly enlarged; the so-called stomata. (Arnold).

The exuded fluid, as may be inferred, contains red corpuscles, but it does so to a much less extent in actual pathological conditions than might be supposed from experiments in animals. In the latter there is a sudden obstruction, with exaggerated results; in actual disease in man the processes usually develop slowly, and there is some accommodation of the vessels. It should be added that the white corpuscles pass out of the vessels as well as the red, but not to such an extent, and that the corpuscles, both red and white, escape from the small veins as well as from the capillaries.

The part which is the seat of passive hyperemia is unduly red, and the tint is dark or livid, hence the term Cyanosis, which is applied when the lividity is extensive. The part is swollen, both from the over-filling of the vessels and from the oedema, and is usually lowered in temperature. In organs readily capable of increase in bulk, there may be considerable Enlargement as a result of passive hypersemia. This is especially the case in the spleen.

Two other consequences frequently follow in prolonged passive hypersemia. The distended capillaries exerting pressure on the surrounding structures may through time produce Atrophy. This is seen especially in passive hypersemia of the liver, where the central parts of the lobules often show a striking absence of hepatic cells. It is also seen in the kidney and the retina.

An opposite result is often effected by prolonged passive congestion, namely, Hypertrophy of the connective tissue, induced by the increased transudation which bathes this tissue. The hypertrophied connective tissue is dense, and it gives increased density to the organs affected, hence the term Cyanotic induration. This is very common as a result of valvular disease of the heart and is seen in the heart itself, the lungs, kidneys, liver, etc. In the lungs the induration is associated with pigmentation, due to the haemorrhage by diapedesis, hence the term Brown induration.

Necrosis or death of parts is not a common result of passive hypersemia. It occurs when the conditions are such as to produce complete stagnation of blood. If a loop of intestine be caught in a hernia in such a way as to obstruct all the veins, then passive hypersemia may be followed by gangrene. Similarly ligature of the femoral vein or its obstruction by a tumour may produce gangrene, as this vein has few and insufficient anastomosis. This only occurs if the vein be suddenly obstructed.


For a good account of passive hyperemia from experimental side, see Cohnheim's Allgem. Pathologie, 2nd ed., vol. i., p. 138. See also Recklinghausen, Allgem. Path., p. 28; Arnold, Virchow's Archiv, lviii., 1873; Zielonko,. ibid., lvii., 1873.