The trochar or aspirator needle should be pushed in a direction upward and inward until resistance ceases or it is felt that the heart has been touched. A caoutchouc tube may now be attached to it and allowed to depend twelve or eighteen inches, and its lower end should be plunged in a weak solution of boric acid or other antiseptic. This avoids the entrance of air and insures against the introduction of ærial bacteria.
When the vital powers are being exhausted stimulants must be given to support the animal, combined with iodide of potassium. (See advice concerning the allied condition in Hydrothorax).
In the chronic pericarditis of oxen the fatality is greater. Treatment consists mainly in counterirritants and powerful diuretics employed in doses determined by the strength of the animal, and combined with stimulants and tonics as in the advanced stages of the acute disease.
In complicated forms of pericarditis attention must be given mainly to the constitutional affection, thus in influenza a stimulating and supporting treatment is demanded, and in rheumatism colchicum, acetate of potass, salicylate of soda, salol and similar agents must be freely administered, though not to the exclusion of counterirritants to the region of the heart, and other measures demanded by the heart diseases.
ENDOCARDITIS.
Definition. Pathology and lesions, congestion of the endocardium covering the valves, valves liable through friction and strain, exudation in or on the serosa rendering it opaque, coagula of fibrine on the surface, secondary endocarditis mycotic, microbes, changes in serosa, distortions and degenerations of valves. Symptoms, as in pericarditis, with violent heart impulse of varying force, clear metallic sound, blowing murmurs, weak pulse decreasing in force, irregular, intermittent, absence of local tenderness, no friction sound, no increase in area of dulness, if lesions are in right heart—venous pulse, venous congestion, dropsies. Valve lesions, in mitral valve—general heart symptoms and murmur with 1st heart sound, 2d sound may be repeated and exceptionally a venous pulse—in tricuspid valve—same with constant venous pulse, venous congestion and dropsy; narrowing of the mitral orifice—general heart symptoms and blowing murmur before the 1st sound; narrowing of the tricuspid orifice—same with murmur sometimes audible on the right side; insufficiency of aortic valves—general heart symptoms and murmur with 2d heart sound, double rushing sound in arteries and delay of pulse beat at jaw; lesions in pulmonary valves—same but without double rush in arteries, or delay of pulse beat at jaw. Loose coagula. Embolism. Causes, as in pericarditis and strain on valves, and poisons and microbes in the blood. Prognosis grave. Treatment, as in the early stages of pericarditis, antirheumatics and germicides more, and diuretics less desirable. For clots iodides, alkalies.
Definition. Inflammation of the serous membrane lining the chambers and covering the valves of the heart.
Pathology and Morbid Anatomy. The causes and symptoms will be better understood after the diseased conditions have been comprehended. The earliest changes are the reddening and thickening of the lining membrane of the heart but above all of that covering the valves. The valves are particularly exposed to inflammation by reason of the friction of the blood when violently forced through the narrow opening in excited conditions of the heart, by the strain thrown upon them from the violent contractions of the heart or the recoil of blood in the arteries, and by their susceptibility in common with all other fibrous structures to rheumatic inflammation. The redness is of the ramified or branching kind characteristic of inflammation, and is neither removable by washing the surface nor does it correspond in position with the colored portion only of a clot which the cavity in question may contain, as seen in bloodstaining occurring after death.
There is further exudation of plastic lymph into and beneath the serous membrane, rendering it opaque, white and thick, or on its surface forming granular elevations, and in the case of the valves becoming moulded into ridges or festoons by the mutual pressure of the different flaps on each other. The inflamed surfaces are further liable to be covered by masses of blood clot in successive layers, deposited by the action of the fibrinogenous matter developed in the inflamed part. These clots sometimes accumulate in considerable masses, firmly adherent to the heart’s walls or valves by their attached surface, but soft and filamentous on their free aspect. These clots or polypi, as they have been called, are soft and loose on their free surface, and become firmer toward their points of attachment. In other words their consistency is in direct ratio to their age. If of old standing they are usually pale yellow or white and streaked with red, while if recent they are mostly red throughout. They vary in size from a thin film to a mass filling up nearly the entire cavity in which they are lodged, and as they frequently extend through the auriculo-ventricular openings or become applied against this or the opening of the great artery, they seriously and sometimes fatally interfere with the circulation. Leblanc asserts that large masses of this kind may be deposited in a few days or even hours, causing sudden deaths, and especially in dogs. He has found other circumstances than endocarditis to cause these fibrinous deposits, and especially the absorption of pus, or the sudden suppression of a long standing discharge, as in catarrh of the air passages. If death does not immediately ensue, these fibrinous deposits may become vascular, as is the case with false membranes in the pleuræ, becoming organized into fibrous tissue, or even degenerating into calcareous matter, necrotic debris, or pus, several instances of which as occurring in horse and cow are on record.
These cases illustrate endocarditis by infection (mycotic, malignant, or ulcerative endocarditis), which occurs independently, or as an extension of a bacteridian disease, primarily localized elsewhere in the system. Thus it is a secondary lesion in infectious omphalitis, pneumonia, pleurisy, arthritis, abscess, pyæmia, etc. Beside the general lesions of endocarditis and a great tendency to molecular death of the new formations and the underlying tissues, there is the presence of specific germs which have been the occasion of the disease. Among these the staphylococcus pyogenes aureus, the streptococcus pyogenes, and the diplococcus pneumoniæ, have been particularly noted. In case the valves were already diseased, they become especially liable to be colonized by any such bacteria that may be circulating in the blood.