[=Notice=: 1. _In situ_—exact position and relation to surrounding
organs; shape; size; degree of firmness or flabbiness. 2. _After
removal_—amount and kind of blood discharged from divided vessels;
shape of heart; round or elongated; apex formed by which ventricle;
amount of fat on surface; relative size of each cavity. 3. _Right
auricle_—character and quantity of blood contained; fibrinous clot.
Lining membrane; general condition of; foramen ovale; open or closed;
thickness, consistence, etc., of muscular walls. Auriculo-ventricular
opening; its shape; estimate of size by introducing fingers; rough or
smooth; fibrous or calcareous deposits; circumference. 4. _Right
ventricle_—nature and quantity of contents; fluid blood; blood clot;
fibrinous clot; size; attachments of same to muscular columns; firm or
soft; size of cavity; thickness and condition of muscular walls;
color, firmness, etc. 5. _Tricuspid valves_—natural, thickened,
thinned or contracted; granulations; patches of calcareous matter;
degree of flexibility; can they close the opening? Condition of chordæ
tendineæ; length, thickness, flexibility, rupture, etc. 6. _Pulmonary
opening_—size and shape; smooth or rough. Semilunar valves; thin and
smooth, or thick, rough and inflexible; power of closing the opening;
will water pass through when poured in from above? 7. _Left side of
heart_—observe same as on right. 8. _Generalities_—weight after
removal of blood; wounds; morbid growths; abscesses; malformations;
aneurism; rupture, etc.]
The several morbid conditions of the heart may be classified as follows:
1. Inflammation │of muscular walls. │Carditis.
„ │of serous membranes. │Pericarditis.
„ │ „ │Endocarditis.
│ │
2. Diseases of valves. │Thickening.
„ │ „ │Ossification.
„ │ „ │Atrophy.
│ │
3. Changes in the walls of the heart, │Hypertrophy.
influencing the size of the cavities. │
„ │ „ │Dilation.
„ │ „ │Atrophy.
│ │
4. Morbid conditions of the walls alone. │Fatty degeneration.
„ │ „ │Morbid growths.
„ │ „ │Ossification of
│ │ coronary arteries.
„ │ „ │Malformations.
„ │ „ │Abscess.
„ │ „ │Aneurism.
„ │ „ │Rupture.
│ │
5. Displacements. │Congenital. │Ectopia cordis.
„ │Pathological. │Transposition.
│ │
6. Contents of cavities. │Heart clots.
1. Inflammatory Affections.
=Carditis.= Inflammation of the muscular substance of the heart is by no
means a common disease, and when present, is probably always associated
either with endocarditis, or more frequently pericarditis. We may
recognize this condition after death, by the light yellow color of the
heart; with a relaxed, flabby, and in some instances a softened
condition of the walls. Upon cutting into the muscular walls, there will
be found exuding a semi-purulent fluid and often small cavities, varying
in size from a pin’s head to a small pea, will be found filled with pus.
This condition may involve the whole heart, or may be confined to one or
more portions. Inflammation of the muscular substance of the heart, may,
undoubtedly, be one of the primary causes leading to aneurism or even to
rupture. The symptoms of this disease are not readily recognized during
life, being always combined with inflammation of the peri- or
endocardium.
=Pericarditis.= Affections of the pericardium have been noticed in the
previous section.
=Endocarditis.= Inflammation of the lining membrane of the heart
(_endocardium_) most frequently occurs in connection with an attack of
articular rheumatism. It may, however, result from blows or injuries of
the chest, and has been induced by violent muscular efforts. It is said
also, to be often connected with some vitiated condition of the blood,
as in pyæmia or Bright’s disease of the kidneys, and has been noticed
also in cases of measles, typhus and puerperal fever.
Endocarditis more frequently attacks the left, than the right side of
the heart. The anatomical appearances, are a loss of smoothness and
transparency of the membrane, with an injected condition of its vessels.
Deposits of lymph may be found adhering to the free surface at various
points, or to the tendinous cords or valves, giving a roughened, or even
warty appearance to all those parts. These may become detached, and
swept on with the blood, and finally lodging in some of the arteries of
the head or extremities, where they are known as _emboli_, they may
become a source of serious trouble. The inflammation may extend to the
muscular structure, resulting in softening or the formation of purulent
cysts.
It is, however, upon those folds of the lining membrane constituting the
valves, and particularly upon the left side of the heart, that the
effects of endocardial inflammations are especially manifested. In this
way originates most of the so-called
2. Valvular Affections of the Heart.
One of the most common of the results of inflammation extending to the
valves, is
=Thickening.= This may depend either upon a deposit of lymph beneath or
between the layers of membrane constituting the valves, thus rendering
them thick and inflexible while the surface is left smooth, or, at the
same time, a deposit upon the exterior may be found, rendering them
rough and even warty in appearance, and so stiffened and irregular upon
their borders as to greatly interfere with the performance of their
functions, and thus permitting _regurgitation_ to take place at the
imperfectly closed opening.[8] The tendinous cords, at the same time,
may be found thickened, hardened, and contracted, or even ruptured,
while the auriculo-ventricular openings may also be found greatly
contracted from the thickening of the base of the valves and the fibrous
tissues forming the borders of the openings. In one case the contraction
on the left side of the heart was so great as scarcely to admit the
little finger, while the thumb should readily pass that opening.
The semilunar valves of the aorta are liable to the same changes, their
thickened condition preventing their folding back completely into the
sinuses of the artery during the systolic action of the heart, or of
completely closing the vessel upon pressure from above.
=Calcification.= This condition of the valves may result from a
progressive change from simple thickening with fibrinous deposits, to a
cartilaginous state, accompanied with so-called bony, or more properly
_calcareous_ patches, which may involve large portions of the valves.
Ossification of the valves upon the right side of the heart, is but
rarely found; upon the left, both the mitral and aortic valves are
liable to this affection.
=Atrophy.= The aortic, pulmonary, and sometimes mitral valves, are
occasionally found greatly thinned; and this condition may result either
in a gradual stretching of the central portion of the valve from
pressure of the blood, giving rise to _aneurism_ of the valves, or, it
may become _perforated_ with small irregular openings, or, from its
weakened condition, _rupture_ may take place, producing sudden death.
This condition appears to consist in a gradual wearing away of the
substance of the valves, from unusual brittleness of their structure,
the result probably of chronic inflammation.
Again, the valves may be found greatly contracted, (_stenosis_) hard and
rigid, which will be attended with imperfect closure and consequent
regurgitation. Dilatation of the orifices without any change in the
valves, may also be found, resulting in the same imperfect closure.
Disease of the valves of the heart, by obstructing the orifices, is
likely to result in
3. Changes Affecting the Size of the Cavities.
=Hypertrophy.= Hypertrophy of the heart, is a condition in which there
is an increased thickness of its walls, and generally also enlargement
of its cavities. Yet there may be thickening—very rarely however—with a
diminution in the size of the cavities. It may affect both sides of the
heart, but is frequently confined to the left ventricle.
The main cause of hypertrophy of the heart, is the existence of some
obstruction to the circulation, either in the heart, or some portion of
the arterial system, as by aneurism, pressure of tumors, etc., or by
disease of the kidneys. It is most frequently, however, associated with
disease of the valves or large arteries. It may sometimes result from
continued functional excitement, and generally accompanies cases of
partial adhesion of the surfaces of the pericardium, while complete
adhesion is more likely to be followed by dilatation or atrophy. On the
right side of the heart, hypertrophy is usually the result of some
obstruction to the circulation through the lungs, as in an emphysematous
condition of that organ.
The following measurements, &c., of the normal heart, will serve as a
guide in judging of cases of enlargement:
_Size._ Lænnec has stated, that the heart in its normal condition, is
about the size of the closed fist of the individual. This comparison,
however, is not very satisfactory. It will be usually found to measure
about 5 inches in length, 3½ in its greatest width, and 2½ in its
extreme thickness, from its anterior to its posterior surface.
_Weight._ From an examination of four hundred cases, the average weight
was found to be 9½ ounces in the male, and 8¼ ounces in the female. In a
robust, muscular male, the heart may, however, be found to weigh as much
as 12 ounces, and still be normal in all its parts.
_Thickness of Walls._ Right auricle, 1 line; left, 1½ lines. Right
ventricle, 1½ lines, and left, a little over 5 lines, or half an inch,
at its middle, being a little thinner both at the base and apex.
_Size of Orifices._ Circumference of auriculo-ventricular opening of the
right side, nearly 4 inches; of left side, 3½ inches; of the pulmonary
artery, 2⅝ inches; of aorta, 2⅜ inches.
When enlarged, the heart may be found measuring 6 to 7 inches in length,
as much in breadth, and 12 to 16 inches in circumference. The weight may
also be increased to 15, 20 or 25 ounces, and the walls may increase in
thickness to nearly a-half inch, and upon the left to over an inch.
Hypertrophy of the heart, has been divided into three forms:—1st,
_simple_ hypertrophy; 2d, _eccentric_; and 3d, _concentric_ hypertrophy.
In the first form, the walls are thickened, while the cavities remain
unchanged. (Simple hypertrophy.)
In the second form, the thickening of the walls is attended with an
_enlargement_ or _dilatation_ of the cavities. (Eccentric
hypertrophy.[9])
In the third form, the thickening is attended with a _diminution_ in the
capacity of the cavities. (Concentric hypertrophy.)
It has been observed in cases where an examination has been made very
soon after a sudden, violent death, attended with loss of blood, as in
decapitation, etc., that the cavities have been nearly obliterated,
while the walls were greatly thickened. By maceration for a few days,
the ventricles have become relaxed to their natural size and capacity.
This state of the heart has been observed in persons in whom, during
life, none of the symptoms of disease of the heart had been manifested,
and hence the condition is to be considered as the immediate effect of
the peculiar character of the cause of death.
=Dilatation.= Dilatation of the cavities of the heart, is a condition
which may also result from the presence of obstacles or impediments to
the circulation, as from ossification of the valves; narrowing of the
pulmonary or aortic orifices; employments requiring powerful muscular
efforts; and in consolidation, tubercular induration, emphysematous
condition of the lungs, or fatty degeneration.
The muscular substance is usually soft and flaccid, sometimes of a
violet color, again pale and yellowish. The thinning may be so great, as
to reduce the thickest part of the left ventricle to two lines or even
less, when the walls will appear to be composed of but little more than
a thin layer of fat covered with the pericardium.
Three forms of dilatation are recognized: _active_, _simple_ and
_passive_.
Active dilatation is associated with _hypertrophy_ of walls,
constituting eccentric hypertrophy.
In simple hypertrophy, the walls retain their _normal thickness_, while
the shape may be changed according to the cavity affected.
Passive dilatation, on the other hand, is accompanied with _thinning_ of
the walls, and usually results from fatty degeneration, atrophy, or some
other change in the muscular fibre.
=Atrophy.= In this condition there is a uniform decrease in the size of
the heart. Its cavities becomes small, and its walls thin. It usually
attends diseases accompanied with great impoverishment of the blood, as
in cancer, diabetes, etc., or may result from obstruction of the
coronary arteries from calcification, atheroma or thrombi.
Paget mentions a case where the heart of a cancerous man, fifty years
old, weighed only five ounces, four drachms; and that of a diabetic
woman, which weighed only five ounces, one drachm. It is usually
accompanied with a general wasting of the tissues and organs of the
body, and frequently will be found associated with fatty degeneration,
which will now be noticed.
4. Morbid Condition of the Walls Alone.
=Fatty Degeneration.= Two forms of fatty diseases of the heart have been
recognized. In the first, which should be known as “_fatty growth_,” to
distinguish from “_fatty degeneration_,” there is an unusual quantity of
adipose matter in those parts of the heart where more or less is usually
found, viz.:—Along the furrows through which the vessels run, and
particularly about the base of the heart. The fatty masses may dip more
or less into the substance of the walls, displacing the muscular fibres,
although the latter are generally normal in color and density, even when
imbedded in masses of fat. This condition may be found in persons who
are otherwise thin, as well as in the obese.
But the more frequent form of fatty disease, is that known as _fatty
degeneration_. In this, we find upon opening the heart, that it has lost
the reddish-brown color characteristic of the muscular fibre in its
normal condition, and is pale, soft and flabby. The whole organ feels
soft, doughy and inelastic, much like a heart beginning to decompose. If
the wall of the left ventricle be partly cut through, the remainder is
easily torn, and the surfaces have a granulated appearance.
Upon the inner surface, beneath the endocardium, numerous small thickly
set spots, or sometimes wavy lines, of a pale buff, or light yellow
color, may be noticed. This appearance does not depend upon a deposit of
fat among the muscular fibres, but rather upon a change in that tissue;
and an examination with the microscope, will show fatty degeneration of
the fibre.
This condition of the heart, may involve the whole organ, or may be
confined to one or more portions. It is much less common in the
auricles, than in the ventricles, and more frequent in the left
ventricle than in the right. It will be generally found more advanced in
the upper portion of the septum of the ventricles, and in the large,
fleshy columns of the left side; or it may be found in these columns
alone, which accounts for the occasional rupture of the latter.
_Fatty Degeneration_ may be associated with _fatty growth_, or with
hypertrophy, or thinning and dilatation, and may be the cause of
rupture. The general character of softness, paleness, and mottled color,
should lead to _suspicion_ of the existence of this disease, when a
microscopic examination being resorted to, the conclusion would be
decisive. A small portion of fibre, examined with a power of 300 or 400
diameters, will present, in fatty degeneration, instead of the striated
appearance of the normal fibre, a granular appearance, with numerous
minute oil globules scattered through the fibre. In the palest part of
the heart, the disease will be generally most advanced; but even here,
the microscope will show some fibres in a healthy condition, while
others around them are rendered completely granular.
Exhausting diseases of various kinds, typhus and other severe fevers,
phosphorus poisoning, etc., may result in this peculiar condition of the
heart.
5. Morbid Growths.
Under this head may be placed _tumors_, _cancers_, _melanosis_, and
_hydatids_.
=Tumors= of various kinds are occasionally found in connection with the
heart. _Fibrous_ tumors of a small size may develop within the muscular
walls, while _syphilitic_ growths, _cysts_, and _tubercular_ deposits
may also, in rare cases, be discovered.
=Cancer.= Cancer of the heart has been noticed in two forms—_epithelial_
and _medullary_. A man, fifty-eight years old, had an epithelial cancer
of the eye, which was removed. Two years after, the man died with a
large cancerous tumor over the parotid gland. A post-mortem examination
revealed a cancerous mass, about an inch and a-half in diameter,
imbedded in the apex of the right ventricle and septum of the heart. A
microscopic examination revealed its epithelial character.[10]
_Medullary_ cancer of the heart has been usually found associated with
the same disease in the lungs and liver, and forms an investing mass
which may involve the whole organ.
=Melanosis= of the heart presents the same character as in other parts
of the body, and is considered but a variety of the medullary cancer,
pigmentary matter being added. It may be developed upon the surface, or
may infiltrate the substance of the whole organ.
=Hydatids= have been occasionally found in the heart, the most of which
have probably been animal in their character, (_acephalocysts_.) A
female, forty years old, who had been suffering pain in the region of
the heart for some months, suddenly died, after running rapidly up
stairs. One ounce of fluid was found in the pericardium. A considerable
tumor was found at the apex of the heart, which slightly fluctuated.
This tumor was about three inches in diameter, globular in form, and
encroached considerably upon the cavity of the right ventricle. When
laid open, it was found to contain a large number of small cysts or
hydatids, varying in size from that of a small pea to that of a pigeon’s
egg, the space between which was filled with a soft curdlike substance,
of a yellow color.[11]
=Ossification of Coronary Arteries.= That condition of the arteries of
the heart usually termed _ossification_ is more properly one of
_calcification_, consisting of a deposit of hard, gritty, calcareous
matter, in which there is none of the true character of real bone, no
trace of bone-corpuscle or vascular canals ever being discovered in
them. Chemical analysis has shown the deposits to be composed of 50
parts of animal matter, with 47½ of the phosphate and 2 of the carbonate
of lime in every 100. This matter being deposited in circular layers,
the artery becomes gradually converted into a hard, bony-like tube,
which may be traced with the finger along the grooves of the heart
through which the coronary artery runs. This is peculiarly a disease of
old people, and may accompany a similar condition of the arch of the
aorta or of the semilunar valves, and by interfering with the proper
nutrition of the heart may result in other forms of disease, as fatty
degeneration, dilatation, &c.
=Abscess.= Abscess of the heart, may unquestionably follow an attack of
carditis, or inflammation of the muscular substance. The cut surface of
the heart in these cases, not unfrequently shows small cavities
containing a purulent fluid, and in some instances a distinct abscess is
found.
A man, sixty years old, was suddenly attacked, while at work, with coma
and great feebleness, followed by death on the third day. The left
ventricle being opened, an abscess was discovered near the apex,
irregular in form, and containing a bloody, purulent-looking fluid. The
coronary arteries were much ossified.
=Malformations= of the heart, are extremely rare in adults, or even in
children that have passed the early days of infancy. They consist
frequently in arrest of development of the auricular septum, or, in
other words, of a patulous foramen ovale, which, by permitting of a
mixture of arterial and venous blood upon the left side of the heart,
results in early death. I have in several instances found this foramen
imperfectly closed in the adult heart, but the opening has been so
small—barely sufficient to permit the passage of a probe—as to offer
little or no obstacle to the proper performance to the heart’s function.
Malformation of the heart is undoubtedly one of the many causes of death
in utero, which might be demonstrated by a post-mortem examination.
=Aneurism.= Partial aneurism, or false aneurism of the heart, consists
in the formation of a sac or pouch, in some portion of the walls of the
organ, communicating with the cavity of the chamber, in the walls of
which it has been formed. They may form in any part of the muscular
walls of the heart, but are more frequent in the left ventricle. They
would seem to result from a separation of some of the muscular fibres,
when, by their retraction, a cavity or pouch, of a rounded or oval form
results, which, in some instances, has its walls composed of the
pericardium alone, there being a complete destruction of the muscular
fibres.
The interior of these pouches, may be found filled with layers of
coagulated fibrinous deposits, as in the case of aneurism of arteries;
or, if they communicate with the ventricular cavity by a large opening,
they may be filled with a simple soft clot of blood.
The size of these aneurismal pouches, vary from that of a cherry, to a
pigeon’s egg, or larger, when they change much the usual figure of the
heart, by their projection upon the external surface.
The following conditions have been supposed to favor the formation of
these aneurismal sacs:—1st, softening of the muscular tissue of the
heart; 2d, ulceration of the lining membrane; and 3d, rupture of the
muscular fibres.
=Rupture= of the walls of the heart sometimes happens, producing sudden
death. It may result from severe contusions of the chest, in which case,
the auricles are more likely to give way. More frequently, rupture will
result from softening of the walls in fatty degeneration or ulceration,
or from the bursting of an aneurism of the heart, or from stenosis of
the aorta. In the latter cases, the left ventricle will be usually the
seat of the rupture.
6. Displacements.
_Changes of Position_ of the heart, are by no means unfrequent. They may
be congenital in their origin, or the result of disease in the
surrounding organs. Of congenital displacement, we may mention first:
_Ectopia Cordis_, where, from some arrest of development, in the
inclosing parts, the heart may be found in some position other than its
normal one. From deficiency of the sternum and ribs, the heart has been
found protruding from the chest, (_ectopia pectoralis_,) or from absence
or deficiency of the diaphragm, it may be found in the abdomen with the
abdominal viscera. Such cases live but a short time after birth.
_Transposition_ of the heart is found in those cases where all the
viscera, abdominal and thoracic, are exactly reversed in position. A
case of this kind was discovered in the dissecting-room a few years ago,
by Dr. R. B. Weaver, demonstrator of anatomy, in the Hahnemann Medical
College. The heart was here upon the right side, the aorta curving to
the left; the liver upon the left; the stomach with its pylorus to the
left; the colon commencing in the left iliac fossa; in short, everything
completely reversed in position. The subject was a female of about
thirty years, and undoubtedly suffered no inconvenience from the
abnormal positions.
The more frequent displacements of the heart, however, are those
resulting from disease in the surrounding structures. It may be crowded
from its normal position, by pleuritic effusions, accumulations of air
(pneumothorax), or even by a highly emphysematous lung. Displacements
may also result from the presence of aneurismal or other tumors in the
chest; curvatures of the spine; or from a hernial protrusion of some of
the abdominal viscera through an opening in the diaphragm; or the
presence of tumors, enlarged viscera, dropsies, etc., within the
abdomen.
7. Contents of the Cavities.
=Heart Clots.= This subject is one that has until recently, been but
imperfectly understood; and now even, our knowledge relating to it, is
by no means complete. Enough is known, however, to convince us that
_heart clots_, are a more frequent cause of sudden death, than has been
heretofore supposed.
Having in a recent paper, read before the Philadelphia County
Homœopathic Medical Society, quite fully treated of this subject, I
shall here merely transcribe the leading points of the same.[12]
_Fibrinous heart clots_, _polypus of the heart_, _or fatty deposits_, as
they are sometimes called, differ from ordinary clots of blood, in the
absence of the blood corpuscles, and hence, presenting the buff color
characteristic of the coagulated fibrin of the blood. Ordinary blood
clots, with the corpuscles entangled with the fibrin—and hence
presenting the red color of blood—are usually found in the cavities of
the heart and large blood-vessels after death, but in greater quantity
upon the right side.
_Color._ The shade of color presented by the fibrinous clot varies in
different cases. While _buff_ is the prevailing color, the shade varies
from a light drab to a decided yellow.
_Consistency._ In this respect a good deal of variation is also found;
the difference depending, probably, in part upon the character of the
disease, and in part upon the rapidity or slowness of the formation;
those of a rapid or very recent formation, having a soft, fatty, or
jelly-like character;[13] while, on the other hand, those of a more
gradual formation, and with more sthenic forms of disease, acquire a
considerable degree of density, the surface presenting a smooth
appearance, as if acted upon by a current of blood, and in all respects
resembling the dense fibrinous masses, found blocking up the cavities of
aneurismal tumors.
_Position._ In every case reported below, the clot has been on the
_right_ side of the heart, although in some, a small, soft clot has been
found on the _left_. I am not sure that I have ever found one of these
clots on the left side of the heart of such a size and consistency, or
under such circumstances, as to have led me to suppose that it might
have been a cause of death.
The body of the clot is usually found in the ventricle, extending from
this, either up into the pulmonary artery, or through the opening into
the auricle. In all cases, the clot has been more or less entangled with
the tendinous cords of the valves and muscular columns of the heart,
requiring, in some instances, considerable force to tear it away from
its attachments.
_Time of formation._ An important question to be decided in regard to
these heart clots, is the time of their formation. Are they _ante_ or
_post_-mortem in their origin? And upon the solution of this query
depends the conclusion as to whether they are the _cause_ or the
_result_ of death in the cases where found. That a fibrinous clot may
sometimes be formed in the coagulation of the blood _outside_ of the
body, is a fact well known; as in the blood drawn from patients
suffering from acute inflammatory affections, where, from the retarding
of the coagulation, the blood corpuscles, from their greater specific
gravity, have time to fall towards the bottom of the vessel, thus giving
the “buffy coat” to the upper portion of the clot. The same
cause—retarded coagulation—unquestionably may give rise to a clot _in
the heart_ after death, presenting the same character, viz., with the
upper portion, of the buff, fibrinous character, while the lower
portion, from the presence of corpuscles, will present the appearance of
an ordinary blood clot. Such clots are not unfrequently found after
death.
But have we any evidence that the fibrin of the blood may be deposited,
forming clots within the vessels during life? In proof of this, we have
only to refer to the result of the application of a ligature to an
artery; where the interval between the point of application and the
first vessel coming off above, will be filled with a fibrinous clot,
which performs an important part in the closing up of the vessel; or, to
the well-known deposits of fibrinous layers within aneurismal tumors,
sufficient, in many cases, to so fill up the sac as to result in a cure;
therefore, the favoring conditions being present, it is not unreasonable
to claim that fibrinous clots _may_ form within the heart, of such size
and in such positions as to be an immediate cause of death.
_Causes._ In looking for the causes, or conditions promoting the
formation of these fibrinous deposits, we have to consider, first,
variations in the character of the blood itself; and secondly,
peculiarities in its circulation and in the circulatory apparatus.
Fibrin, one of the normal constituents of the blood, is estimated by
physiologists as forming from 2 to 3 parts in 1000, while it may fall as
low as 1, or rise to 7½ parts. We find it reduced to the minimum
quantity in all diseases which present a hæmorrhagic tendency, as in
true typhus, yellow fever, certain malignant forms of disease, and as
the effect of many poisons, both animal and vegetable. In these cases,
the loss of fibrin results in the effusion of blood into the tissues,
producing petechial spots, or upon the mucous surfaces, giving rise to
epistaxis, black vomit, hæmaturia, etc., while very feeble, if any,
coagulation of the blood will be found after death.
In scurvy, however, where we have a condition of the blood not unlike
that above referred to, there appears to be a marked tendency to the
formation of clots, as has been noticed by many observers, and as has
been verified by Dr. J. C. Morgan, in several cases which came under his
notice while in the army.
But it is in cases where there is at least a _relative increase_ of
fibrin, that heart clots are more liable to form. Such a condition we
find in cases where, while the fibrin remains normal in quantity, the
water of the blood, the menstruum in which the fibrin is held in
solution, is below the normal standard, this reduction favoring the
tendency to deposit. Thus, in all cases where there has been an
exhausting and rapid flux from the bowels, as in cholera, or excessive
purging from drastic cathartics, or from the colliquative sweating of
phthisis, we have the favoring condition, and death may be the immediate
result of a fibrinous clot in the heart.
The _most_ favorable condition, however, for the formation of heart
clots, is undoubtedly that in which there is an _absolute_ increase of
fibrin, and this we find in a large number of diseases marked by acute
inflammatory symptoms; as in pleurisy, pneumonia, diphtheria, croup,
acute rheumatism, erysipelas, puerperal fever, etc. In a large number of
deaths from these diseases, a post-mortem examination would undoubtedly
bring to light a heart clot, which has at least served to hasten, if it
has not been the immediate cause of the fatal termination.
Again, the formation of heart clots is evidently promoted by any
circumstances or conditions, resulting in great feebleness or languor of
the circulation, independent of variations in the amount of fibrin. A
complete stasis of the blood is certain to be followed by coagulation;
as in employment of pressure in the treatment of aneurism; so in cases
of great prostration of the powers of life, attended with extreme
feebleness of the circulation, as 1st. In cases of shock, where life is
not immediately destroyed; 2d. In certain cases of poisoning, as by
opium, where the action of the heart is greatly depressed; and 3d. In
syncope, either with or without loss of blood. In all of these cases the
danger of the formation of the heart clot is very great, and probably in
a large number this is the immediate cause of death.
It is a fact well established, that loss of blood, either by hæmorrhages
or venesection, is followed by an increased coagulability of that fluid;
hence, the fearful hæmorrhages which sometimes attend parturition, if
accompanied with syncope, are in great danger of being followed by the
formation of the heart clot, and thus ending in death.[14]
Another circumstance tending to promote the formation of fibrinous clots
in the heart, is evidently to be found in the peculiar formation of the
valves guarding the auriculo-ventricular openings. It is well known how
fibrin may be collected from fresh blood, by beating the same with a
bundle of twigs, the latter soon becoming coated with shreds of fibrin;
so the _chordæ tendineæ_ and fleshy columns of the heart, between which
the blood is continually being driven, affords convenient points for
collecting the same from the feebly circulating or overcharged blood;
and from the close intermingling of the tendinous cords, with the
substance of the clot, it is probably upon these that the deposit first
begins to form.
In explanation of the fact that fibrinous clots are almost universally
found on the _right_ or _venous_ side of the heart, notwithstanding that
arterial blood is richer in fibrin than venous, the following has been
suggested to my mind: _First._ While venous blood contains a smaller
proportion of fibrin, may not its deoxydized condition favor the more
ready deposit of this substance, than by the more highly vitalized
arterial blood? _Second._ The feebler muscular power of the right side
of the heart would necessarily be attended with a slower circulation
through its cavities, the partial stasis of the blood giving another
condition favorable for the formation of a clot; and _Third._ The valves
of the right side of the heart, present three flaps or folds, instead of
two as on the left, and hence, with their numerous tendinous cords,
offer an increased number of obstructing points, around which the
deposit may be made. These several circumstances would seem sufficient
to account for the admitted fact.
_Symptoms._ The symptoms attending the formation of fibrinous clots in
the heart, are usually sudden in their accession, frequently attended
with a chill, and marked by great oppression in breathing, coldness of
surface, and _pallor of face and lips_, the latter symptom
distinguishing from the dyspnœa attending croup, asthma, pneumonia,
etc., where the face is _livid_ from venous congestion. The pulse is
usually rapid and feeble; the action of the heart labored, palpitating,
and sometimes intermitting, while auscultation will reveal a tumultuous
churning-like action, the normal sounds being quite undistinguishable.
Pulsation of the jugulars will be present in most cases, and where the
clot greatly obstructs the play of the tricuspid valves, a double
pulsation will be likely to be noticed. In the last stage, a copious
cold perspiration appears upon the whole surface of the body.
As might be anticipated, fibrinous formations, while of small size, are
sometimes washed away from their attachments and swept on with the
current of blood into the arteries and carried to distant parts of the
body, as is sometimes the case also in aneurism, thus producing the
embolic masses often found blocking up arteries in different parts of
the body. When upon the right side, the embolus would be carried into
the pulmonary artery, obstructing the circulation through the lungs, and
producing symptoms more or less grave, according to the size of the
clot. Upon the left side of the heart, from the greater force of the
circulation, these bodies are probably more frequently swept away from
their attachments and carried into the aorta, and thus on, perhaps,
through the carotids to the head, or into the subclavian, or down the
aorta, finally lodging in some of the branches of the lower extremities.
Convulsions, paralysis, etc., are not unfrequently produced by the
lodgment of emboli in some of the arteries of the brain, while, when
carried into the arteries of the extremities, pain, falling of
temperature, impairment of sensation, contraction of muscles, atrophy,
and even gangrene may result.
The following examples will serve to illustrate the class of cases to
which I refer:
CASE I.—_Death from Heart Clot in Anæmia._
A lad, 11 years old, and very anæmic, went to school in the morning in
his usual health; while there was taken with a chill. On his way home
vomited freely. The chill lasted for a long time, and was accompanied
with an oppression in breathing, which gradually increased through the
day and night, and until the time of my first visit at 11 o’clock A.
M. the next day. I then found him extremely pallid, lips bloodless,
perspiring freely, suffering from great restlessness and distress,
with extreme dyspnœa; mind wandering, pulse irregular and feeble;
action of the heart very tumultuous, the normal sounds being
unrecognizable. In the neck noticed a rapid rolling pulsation of the
jugulars, which presented two beats to one of the artery at the wrist.
At my second visit, made at 4 o’clock P. M., the patient had just
expired.
The autopsy, made twenty hours after death, gave the following
results: Upon opening the abdomen found the liver presenting a dark
mottled appearance, and highly congested; other abdominal organs
natural; pericardium contained about one ounce of serum. Upon opening
the right auricle of the heart, found a firm fibrinous mass, extending
downwards through the ventricular opening, and which, upon the latter
cavity being opened, was found firmly attached to the tricuspid
valves, and entangled with the fleshy columns and tendinous cords.
The presence of such a body in this position, and with such
attachments, it was evident, must have so interfered with the passage
of the blood from the auricle to the ventricle, as, upon the
contraction of the former cavity, to have caused a backward pressure
into the veins, and thus have produced the _first_ of the double
pulsations of the jugulars.
Again, the position of this clot, preventing the closure of the valves
upon the contraction of the ventricle, there would have been a
regurgitation into the auricle, and the same backward flow into the
veins, thus producing the _second_ pulsation of the jugulars seen
during life.
CASE II.—_Death from Heart Clot in Pregnancy._
A lady, 28 or 30 years old, also very anæmic, and three months
pregnant, had been suffering occasional fainting spells. For some days
before her decease she had suffered from dyspnœa, and on that day,
after ascending a flight of stairs, fell upon the floor, and before a
physician could be obtained breathed her last. A post-mortem showed
all the thoracic and abdominal viscera in a healthy condition, while
the right side of the heart contained a large fibrinous clot, with
attachments similar to those found in Case I.
CASE III.—_Death from Heart Clot in Diphtheria._
A boy, 3 years old, had an attack of diphtheria. The case presented no
unfavorable symptoms until about the fourth day, when he was taken
with great restlessness and oppression in breathing, and while sitting
on the chamber at stool, suddenly died. The autopsy here again
revealed the heart clot, as in the other cases.
CASE IV.—_Death from Heart Clot in Consumption._
A man, 30 years of age, a furrier by trade, was suffering from
tubercular disease of the lungs. He had never given up his work,
though he was much reduced in flesh, had a bad cough, diarrhœa, and
night sweats. While at his employment, he was one day taken with great
oppression, increased cough, etc., and in twenty-four hours expired.
The post-mortem showed that, while the upper portion of both lungs
contained large deposits of tubercles, there were no abscesses, and
the lower portions presented sufficient sound lung tissue to have
maintained life. Upon opening the heart the usual fibrinous clot was
found in the right ventricle, extending upwards into the auricle.
CASE V.—_Death from Heart Clot in Rheumatism._
A strong colored man, of 25 years, had an attack of inflammatory
rheumatism. The disease presented the usual characters, the
inflammation wandering from joint to joint. During the second week he
was suddenly attacked with great difficulty in breathing, violent and
irregular action of the heart, and great distress, followed by rapid
prostration and death. The post-mortem examination revealed thickened
tricuspid valves, with a firm clot of large size adhering to the same.
CASE VI.—_Death from Heart Clot in Debility._
A gentleman, 55 years old, who had been for some time in feeble
health, was taken, upon rising in the morning, with oppression and
distress in the region of the heart, dying in twelve hours. The heart
clot was found here, as in the other cases, upon the right side of the
heart.
CASE VII.—_Heart Clot in Death from Over-dose of Morphia._
A gentleman, of about 50 years, a physician, was found one morning
dead in his bed. His health had been previously good, excepting that
he was troubled with neuralgia which gave him sleepless nights, and
for which he sometimes took morphia. On the night previous to his
death he came home and retired at a late hour. An open bottle of
morphia and small spatula were found on his desk next morning, the
spatula showing evidence of having been thrust deeply into the
morphia, and probably a large and over-dose carelessly removed and
taken. The autopsy here again revealed a large and firm fibrinous
heart clot.
CASE VIII.—_Death from Heart Clot in Acute Gastritis._
A lady of about 60 years, had an attack of acute gastritis, but was
considered convalescing, and her physician (Dr. Martin) made his last
visit in the evening. The next morning she was found dead in her bed.
The post-mortem showed the spleen somewhat enlarged, and its capsule
greatly thickened.[15] Other organs healthy, while the heart contained
an unusually large fibrinous clot, which has been preserved in the
College Museum.[16]
The above include the more marked cases of death that have come under
my notice, where that result could, in my mind, be fairly attributed
to the formation of fibrinous clots in the heart.
The following inferences may, we think, be fairly deduced from the
several cases reported:
_First._ In some instances the fibrinous clots are apparently the _sole
cause_ of death. (Cases 1, 2, and 3.)
_Second._ In other, and a larger number of diseases, as in acute
rheumatism, pneumonia, croup, etc., which otherwise would recover, a
fatal termination results from the formation of heart clots. (Cases 3
and 5.)
_Third._ In still other diseases, which are of themselves necessarily
fatal, as in phthisis, cholera, etc., death is often hastened by these
formations. (Case 4.)