The pericardium in its anatomical and pathological relations corresponds to the other serous sacs, and, to a certain extent, to the synovial cavities. The pleura, peritoneum, and pericardium are to be regarded, as we previously found in studying cedema and dropsy, as large lymphatic spaces. These sacs are composed of connective tissue, and lined with a single layer of flat endothelium. By means of numerous stomata they are in communication with the lymphatic vessels, and to some extent with one another. The pericardium is in less direct communication with the pleura and peritoneum than these are with each other, but by circuitous routes there is some communication, especially with the pleura. It is to be remembered also that through each serous cavity there is a certain circulation of serous fluid. This fluid does not accumulate in the sac, because it is carried off as quickly as it is transuded from the vessels, but if the transudation increase greatly there may be an accumulation and consequent dropsy.
In considering the Causes of this disease it is of some consequence to note that the inflammation usually affects the whole surface at once. This seems to indicate that an irritant has found admission to the pericardial sac, and by the motions of the heart and the natural currents of the fluid in the sac, has been carried hither and thither throughout it. There are many cases in which the tubercular virus is the irritant; we find tubercles in the inflamed tissue of the pericardium. (See afterwards under Tubercular Pericarditis.) The majority of cases of simple pericarditis is associated with acute rheumatism. There are some cases in which the disease appears to be of spontaneous origin; it is ascribed to cold. Bright's disease in its various forms strongly predisposes to inflammations of the serous membranes, especially the pericardium and pleura.
In regard to the Phenomena which manifest themselves at the onset of an acute pericarditis, we may presume that the irritant induces the •changes in the vessels which have been described in treating of inflammatioii in general, but opportunities are wanting for observing the consequent redness as patients survive this early stage. Exudation from the vessels soon follows, and serous fluid begins to accumulate in the sac. As the inflammation affects the surface of the sac, the endothelial lining is very directly involved. The flat endothelial cells are to a considerable extent shed, being apparently killed by the irritant, but they may also 1be found showing signs of germination. The exudation consists primarily of exuded liquor sanguinis with contractile cells, but soon Fibrine is deposited on the inflamed surface. (See Fig. 57, p. 168.) The detachment of the endothelium seems to be the circumstance which determines the coagulation, on principles already explained. The deposition of fibrine occurs on both visceral and parietal layers of the aac, but it is usually thickest on the visceral surface, where it may present shaggy masses on the surface of the heart (see Fig. 229). It is whitish in appearance, and of soft, almost gelatinous consistence. The fibrinous layers on the opposed surfaces of the pericardium are usually Mparated by serous fluid which occupies the sac, but an appearance is often presented which suggests the application and withdrawal of the layers while still in a soft plastic condition. This appearance is variously described'as the Honeycomb or Pine-apple condition, and it has been aptly' compared to that presented when two pieces of bread, thickly buttered, are stuck loosely together and then separated. This honeycomb appearance, it will be understood, is most markedly present on those parts of the pericardium where the heart in its movement comes most frequently against the parietes.
Fig. 229. - Acute pericarditis. The surface of both visceral and parietal layers of the pericardium is coated with fibrine.
If the inflammation has been slight and transient, there may be little beyond a small serous and fibrinous exudation, which is gradually absorbed. But as a general rule further changes develop, and these are mainly in the connective tissue of the pericardial sac. This shows evidence of inflammation by the presence of innumerable cells, so that by degrees it is converted into Granulation tissue. This inflammatory transformation, according to the intensity of the irritation, penetrates deeply, extending frequently to the interstitial connective tissue in the muscular substance of the heart. A layer of vascular granulations thus forms beneath the fibrinous exudation. The layer of granulations has the general tendencies as well as the structure of granulation tissue elsewhere; it tends to develop into connective tissue as soon as the inflammatory irritation becomes sufficiently mild. With the subsidence of the inflammation there is a reduction of the serous exudation. The fibrine is also disposed of, partly undergoing fatty degeneration and so becoming absorbed, and is partly eaten into from beneath by the granulation tissue. The result of this is that the granulations are, as it were, laid bare, and a vascular layer occupies the place of the former fibrinous deposit.
With the absorption of the exudation the two layers of the pericardium come in contact, and a coalescence of the granulating surfaces,, more or less complete, occurs. The vessels intercommunicate, and the two layers, so far as they are in contact, become virtually one. As the granulation tissue passes on in its development into connective tissue, the Pericardial sac undergoes partial or complete obliteration, the uniting agent being vascular connective tissue, and so we have the condition of Adherent pericardium. The connection will at first be delicate, and may be torn through, but as time goes on it gets firmer, and a condition results in which the two layers are absolutely inseparable. Under certain circumstances the coalescence of the two layers is not complete, and there is only a partial adhesion; in that case the adhesions are sometimes greatly stretched by the movements of the heart, so that tags or ligaments may unite the surface of the heart to the parietal layer.
In some intense and prolonged cases of acute pericarditis, Suppuration occurs, and the serous exudation in the pericardium gives place to pus. This, however, is a rare occurrence. On the subsidence of the inflammation the pus dries in by the absorption of its fluid, and its debris remains as dead matter, which subsequently gets infiltrated with lime salts; this may ultimately become consolidated so as to form calcareous plates in the midst of thick adhesions. (See ante, p. 184).
Septic inflammations, such as those which occur in pyaemia when an abscess in the substance of the heart extends to the surface and bursts into the pericardium or gives off septic microbes, or in the rarer case of perforation of an ulcer of the stomach or oesophagus into the pericardium, are purulent from the outset.
Adherent pericardium frequently leads to Hypertrophy and Dilatation of the heart. It does so both directly by interfering with the muscular tissue, and indirectly by requiring the heart to use increased exertion in performing its task.
It is to be remembered that adhesion of the pericardium takes origin in inflammation, and from this circumstance it results that in several ways the action of the heart is interfered with. During the acute stage of the inflammation there is fluid in the sac of the pericardium, and by the mere mechanical pressure of this fluid the cardiac contractions are interfered with, and if the effusion continue long enough there may be hypertrophy to overcome the obstacle. But again, the inflammation extends a certain distance into the muscular wall of the heart beneath the pericardium. A certain portion of muscle is thus interfered with in its action, and more vigorous contraction is required of the rest. There may even be considerable thickening of the pericardium by development of connective tissue, and this extending some distance in the connective tissue between the muscular fibres may seriously compromise them. But further, when adhesion is complete, the heart in contracting must drag in with it the parietal as well as the visceral pericardium. In the normal state the two surfaces of the pericardium glide on one another, and the parietal layer accommodates itself to the movements of the heart. If there is adhesion, however, unless the adhesion be very loose, there can be no such gliding, and there must be some loss of force in dragging the parietal layer inwards. But the parietal layer is normally attached to the under surface of the sternum and to other structures around, and the attachment may be rendered closer by the inflammation. The heart will drag on these parts in contracting, and this will greatly add to its work. It is well known that dragging in of the intercostal spaces is a common sign of adherent pericardium. As these causes vary to a considerable extent, the amount of hypertrophy varies in proportion. As the causes also act nearly uniformly on the heart, the hypertrophy is general, that is, it usually affects all the cavities of the heart. Such a hypertrophy may almost completely compensate, so that a person with adherent pericardium and a very large heart may have no cardiac symptoms.
As observed above, acute pericarditis often becomes chronic, and, in that case, usually results in adhesion of the pericardium. A more direct chronic inflammation results in the condition designated White spots, Milk spots, or Soldier's spots, which are very common pathological conditions. They occur in about half the cases examined post-mortem, and their frequency seems nearly in direct proportion to age. They are in the form of well-defined, whitish, opaque areas on the surface of the heart, of very various size, sometimes very small, at other times so large as almost to cover the anterior surface. Their edges are usually abrupt and well defined, but they may merge gradually in the pericardium. They have often a brilliant white tendinous appearance, but may be more dull. They are most frequently situated on the anterior surface of the right ventricle, and next on that of the left ventricle, especially near the apex. They are also met with on the posterior surface, especially near the base of the heart, and on the intrapericardial portions of the great vessels. They are more uncommon on the parietal layer of the sac.
These spots actually consist in a thickening of the pericardium, presenting merely dense connective tissue covered with endothelium (see Fig. 230).
Fig. 230. - Soldier's spot on pericardium, b, Muscular wall of heart; a, pericardium, thickening at c so as to form spot, x 25.
We have here a circumscribed inflammation affecting by preference certain districts, and the cause must be a local one. It seems to be due to the irritation resulting from the projection of the heart against its surroundings. The commonest seat is where the anterior surface of the right ventricle comes against the sternum at the place where the edges of the lungs turn aside and expose the pericardium. The sternum is less yielding than most surrounding parts, and so the irritation is greater here. The spot where the left ventricle near the apex strikes against the fifth rib is the next most frequent site.