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.
In the early stage there may be a mere swelling of the valves, with as
yet a smooth, unbroken surface, but with enlargement and increase of the
connective tissue cells, later fungous vegetations start out from the
surface, and on these the fibrine of the blood is deposited in layers.
Besides the formation of clots on their surfaces other changes occur on
the cardiac valves as the result of inflammation. The organization of
the exuded lymph within and upon them leads to rigidity, loss of
elasticity, unevenness of their surface, contraction and puckering so
that they can no longer approximate to each other, but leave the orifice
imperfectly closed. They may, moreover, have gristle or bone deposited
in their substance. The osseous degeneration of such new products
appears to be the most common cause of those ossifications of the heart,
of which specimens are to be found in nearly all veterinary museums.
=Chronic valve disease= is thus found to be a common result of
endocarditis, and from the obstacle presented to the flow of blood
through the different cardiac orifices by the rigid, inelastic and
distorted valves, hypertrophy of the heart frequently supervenes.
In our domestic quadrupeds ante-mortem clots and fibrinous polypi have
been chiefly formed in the right side of the heart, and diseased valves
in the left.
_Symptoms._ The general symptoms agree in many respects with those of
_pericarditis_. There are the same general symptoms of fever
(temperature 102° to 106°), the same pinched, anxious countenance, the
same shortness of breath and oppression when moved, the same violent
heart’s action, and the same rapid, excitable pulse tending to be
irregular and intermittent. Among the more specific symptoms are a very
violent impulse of the heart against the left side, varying in force,
however, in successive beats; a metallic tinkling accompanying the
impulse and sometimes heard at some little distance from the body, a
blowing murmur as soon as the changes in the valves render them
insufficient to close the orifices, and, if the obstruction exists on
the right side, venous pulse, general venous congestion, and dropsical
swellings.
The pulse may at first have considerable force but, as insufficiency of
the valves ensues, it becomes small and weak, its weakness forming a
most marked contrast to the violence of the heart’s impulse against the
side. The irregularity and intermission of the pulse is to be ascribed
at first to the impaired nervous energy of the heart though later it is
often due to the obstacle presented by clots to the flow of blood from
the heart, so that a beat sometimes takes place without a corresponding
pulsation. It may reach 80 or 160 per minute in horse or ox.
The blowing murmur when heard is one of the most characteristic symptoms
but must be carefully distinguished from other allied heart sounds. If
very loud it may be confounded with the friction sound of pericarditis,
but may be differentiated by its invariable coincidence with some
particular portion of the heart’s beat. The absence of local tenderness
is another distinctive symptom. Again in pericarditis effusion takes
place early annulling friction sound, and diminishing alike the impulse
and the sounds of the heart.
It is of less practical value to be able to distinguish the precise seat
of the murmur, yet the following data will guide to such a conclusion.
=Simple induration or insufficiency of the Left Auriculoventricular
(Mitral) valve.= Paroxysms of palpitation, oppression, and difficulty of
breathing; vertigo with loss of control over the limbs and vacillating
gait; stupor, coma; slight tremor and blowing noise with the first sound
of the heart; heart’s impulse, violent, but irregular in force,
sometimes double; pulse feeble, irregular, unequal, or intermittent;
sometimes though not at all constantly a venous pulse in the lower end
of the jugulars. In chronic induration of this valve, or in osseous, or
cartilaginous degeneration the same symptoms are shown. The more general
symptoms may, however, require exercise to develop them.
=Induration, etc., of the Right Auriculo-Ventricular (tricuspid) valve.=
The symptoms are almost identical with the last. Venous pulse is
constant, and, particularly after exertion, the veins generally are
distended. Dropsies are more common.
=Narrowing of the Mitral orifice.= In addition to the same general
symptoms as the last named lesions, there is a sighing, blowing, purring
or rasping sound, according to the degree of narrowing, heard _before_
the first sound of the heart. It is the noise of the blood rushing
through the narrowed orifice between auricle and ventricle. It is
usually loudest behind the middle of the shoulder on the left side.
Feeble pulse, frequent imminence of suffocation and filling of the
limbs, etc., are nearly constant.
=Narrowing of the Tricuspid orifice.= Symptoms nearly identical with the
last. Venous pulse more constant. Blowing murmur sometimes loudest on
the _right_ side of the chest.
=Induration or insufficiency of the aortic valves.= Blowing murmur with
the second sound of the heart. Double rushing sound in the carotid with
each heart’s beat. There is an appreciable interval between the beat of
the heart and corresponding pulsation at the jaw.
=Induration or insufficiency of the pulmonary valves.= Blowing murmur
with the second heart sound, but no corresponding double sound in the
carotid, nor any marked retarding of the pulse.
=Loose coagula in the heart= or _adherent ones_ (_polypi_) produce one
or other of the above class of symptoms, according to the particular
orifice they tend to block or the valves whose function they impair.
Anæmia and leukæmia may have blowing murmurs with the first or second
heart sound.
=Embolism.= =Plugging of arteries.= Another class of symptoms sometimes
supervenes because of loose clots being washed on into the arteries, and
blocking them when they reach those that are too small to transmit them.
These symptoms will be as varied as the organs whose arteries are
plugged. If in the brain there may be dulness, stupor, vertigo,
somnolence, delirium; if in the liver, biliary and digestive
derangement; if in the lungs, cough with the other signs of pneumonia
and abscess; and if in the limbs lameness and paralysis, (brought on or
aggravated by exercise, and often removed by a few minutes’ rest),
wasting of the muscles, etc. (_See Embolism_).
_Causes._ These are in the main the same as those of _pericarditis_.
Weak health, exposure to extremes of weather, punctures with foreign
bodies, but above all, the rheumatic constitution are common causes.
Indeed rheumatism appears more prone to attack the serous membrane
lining the heart cavities than that enveloping it externally. One reason
for this is to be found in the great and incessantly recurring strain on
the fibrous structure of the valves, and particularly in hard worked
horses and hunting dogs in which the strain is often extreme. It has
been argued that the increased blood pressure caused by digitalis is an
appreciable cause. Its frequent connection with rheumatism is shown in
the rheumatic lesions of joints and fibrous structures seen in carcasses
dead of endocarditis.
Diseases in the muscular substance of the heart as cysts, abscess, etc.,
frequently extend to the endocardium.
Among other causes must be mentioned disease-changes in the blood. These
may act on the valves directly as in the case of lactic acid injected by
Dr. Richardson, into the peritoneum with the view of producing
rheumatism and successfully as regards the lesions of the cardiac
valves; or indirectly by determining coagulation and irritation of the
lining membrane coming into contact with the clot. The very fibrinous
and plastic state of the blood in extensive inflammations is a probable
cause of the occurrence of clots in the heart, and the frequency of such
clots in the dog has been ascribed to the plasticity of his blood
(Leblanc). The injection of pus into the blood or the absorption of
microbes from diseased surfaces will sometimes produce ulcerative
disease of the valves. The same is true as regards the germs of
omphalitis, pneumonia, arthritis and other infectious diseases.
Lafosse records certain cases of endocarditis due to extension of the
disease from inflamed veins.
_Prognosis._ Endocarditis is always attended with great danger to life,
but it is more likely to terminate in chronic valvular disease which
quite unfits the animal for useful work. Mild cases may terminate in
complete recovery.
_Treatment._ This is in the main the same as that adopted in the early
stages of pericarditis. Absolute rest is of prime importance. Laxatives,
sedatives and counterirritants are to be mainly relied upon. Belladonna
and chloroform on the chest behind the left elbow may be used. As there
is not the same danger from effusion, diuretics need not be pushed to
the same extent. Digitalis must be avoided if possible until the high
fever subsides. In infective cases, quinia, salicylate of soda, salol,
or hyposulphite of soda may be given. Later give tincture of muriate of
iron.
In rhemuatic cases, treat as for an acute attack of rheumatism. Frequent
large doses of salicylate of soda or salol, large doses of acetate of
potass and colchicum, warm clothing and counterirritants to the region
of the heart are especially demanded. (See Rheumatism.)
When clots are suspected, and when endocarditis threatens to lapse into
the chronic form, it is recommended to give iodide of potassium (horse
and ox 1 drachm, dog 5 grains, twice daily) with carbonate of ammonia or
of potass and bitter tonics. A lengthened rest after apparent recovery
is essential to avoid permanent valve lesions.