In the lungs as elsewhere these two conditions are often associated. Passive hyperaemia in the lungs is nearly always connected with functional disturbance in the heart, and there are two principal forms of heart lesion which are apt to give rise to it. These are, on the one hand, cardiac lesions, chiefly valvular, which interfere mechanically with the pulmonary circulation, and, on the other hand, weakness of the heart, which, as we have seen, is a cause of passive hyperemia in general.
Passive hyperaemia from cardiac lesions occurs under all the different forms of heart disease in which the return of blood to the left auricle and ventricle is hindered by valvular incompetence or otherwise. (See under Valvular Disease of the Heart.) In mitral disease especially there is commonly a direct obstruction to the return of blood from the lungs. This is, in many cases, partly compensated by hypertrophy of the right ventricle, but even when it is so the pulmonary circulation will be at an increased pressure, and a more or less permanent passive hyperemia will exist. This expresses itself during life in the readiness with which dyspnoea develops itself, and also in the frequent coincidence of bronchitis.
The condition of the lungs in cases of prolonged passive hyperaemia is expressed in the designation Brown induration. The whole lung is more consistent than normal, and does not retract so fully when the chest is laid open. The colour is brownish, but the depth of Colour varies considerably in different cases and in different parts of the lung. In this, as in other cases of prolonged hyperaemia, the connective tissue is thickened and increased in density; hence the induration, which Rokitansky thought to be due to inflammatory hypertrophy of the connective tissue. At the same time the capillaries are greatly dilated and tortuous, and haemorrhage by diapedesis is liable to occur as in passive hyperaemia generally. The blood escapes partly into the lung alveoli, giving rise to Haemoptysis, and partly into the surrounding connective tissue, producing the Brown pigmentation. The pigment is in the form of brown granules in the connective-tissue corpuscles.
The condition of the vessels is well shown by separating a piece of lung tissue by ligature, then placing it in nitric acid and afterwards in alcohol. When sections are made the varicose capillaries will be displayed as a brownish-red network, and the larger vessels will also be seen.
Even extreme and prolonged hyperaemia may exist without the development of oedema, the occurrence of which will usually imply the supervention of weakness of the heart.
Passive hyperemia from weakness of the heart is commonly accompanied by oedema of the lungs. In many cases it is developed shortly before death, and is an expression of the fact that failure of the heart is the immediate cause of death. In a large number of debilitating diseases we find just before death the chest full of rales and the breathing much obstructed. In these cases passive hyperaemia and oedema are found after death. On the other hand these phenomena may develop in the course of diseases which specially involve the heart, more particularly the acute fevers, in which passive hypersemia and oedema are frequently of serious import. Existing cardiac lesions, as already mentioned, will predispose to oedema if the heart happens to become exhausted or weakened.
Under these various circumstances gravitation plays an important part in the development of the hyperemia and oedema, and these phenomena are usually most distinct in the parts which during life have been the most dependent. Hence the term Hypostatic engorge ment is often applied. As a general rule, the parts affected are the posterior and basal portions of the lungs. They present after death a dark blue colour, and the tissue is bulkier and more solid than normal. The physical condition is expressed in the term Splenization, the tissue resembling that of the spleen. If the lung be incised and squeezed, a frothy fluid mixed with blood issues from the cut surface. Examined microscopically it is seen that the capillaries are distended and the lung alveoli occupied by serous fluid.
Hypostasis occurs as a post-mortem phenomenon, and this must be borne in mind in the diagnosis of hypostatic engorgement. Even in cases of sudden death from accident the posterior parts of the lung are often of a livid colour from the blood before coagulation having gravitated to the parts of the lung which, in the recumbent position of the body, were dependent.
When passive hyperemia and oedema have persisted for a time they often pass into a condition closely allied to Inflammation. Fibrine and catarrhal cells are present in the lung alveoli, and the lung tissue be-comes more and more consistent, approaching to the condition of hepatization. There is not, however, the complete condensation of proper pneumonia, and an excess of fluid, sometimes of a thickish gromous character, exudes from the cut surface oedema of the lungs sometimes occurs without hyperemia, or at least with very little evidence of the latter visible post mortem. This admits of somewhat ready explanation in cases of Bright's disease, where it is related to the general tendency to oedema. A simple oedema may also occur in consequence of multiple fat embolism in the lung. In other cases there is no apparent cause other than failure of the heart, and the absence of hyperemia may be due to a general anaemia or to some local conditions such as pleural effusion.
In cases of simple oedema the lungs are pale and look bulky. On incision clear frothy fluid exudes, sometimes in large quantity.
Cohnheim has endeavoured to elucidate the pathology of oedema of the lungs by experiment in animals. An extreme passive hypersemia may be produced by paralyzing the left ventricle, while the right ventricle retains its full powers. Cohnheim supposed that a weakening of the left ventricle might explain the hyperremia and oedema occurring immediately before death. This explanation does not seem to the author to be a likely one. Great hyperaemia exists in cardiac-lesions, produced in a somewhat similar fashion to that in these experiments, namely, by obstruction on the left side of the heart, without any oedema, unless, there is a failure in the cardiac contractions. It seems to be rather the extreme stagnation of blood, which such failure implies, that determines the oedema.
Bradford, Dean, and Lewis, (Pulm. circulation) Proc. of Roy. Soc, 1889; Rokitansky, Lehrb., iii.; Zenker, Beitr. z. norm, und pathol. Anat. d. Lungen, 1862; Cohnheim, Allg. Path., i., 501, 1882.