that a trouble so considerable, even though it exists on one side only,
should not influence the entire cardiac circulation? Moreover, it
should be emphasized that the phenomena dwelt upon do not always
manifest themselves when the cardiac contractions are perfectly normal.
The heart-beats may be increased in frequency and the rhythm be
changed. The passage, therefore, from a state of relative calm merely
to that of extreme agitation is appreciated less readily. This is
particularly true of the symptoms usually described as pertaining to
the presence of terminal coagula. For here, at a period approximating
the fatal termination, it is wellnigh impossible to determine
accurately special symptoms. For this reason it is not surprising how
authors have varied in their descriptions, and at best none of them are
completely full and satisfactory. I have myself many times sought to
recognize the blowing murmur given by Bouillaud as a physical sign of
cardiac concretions, but in not a single instance have I been able to
satisfy myself as to its existence. True it is that the cases I have
watched with greatest care were those of children affected with toxic
diphtheria, and it is possible, on account of the infrequency of
valvular diseases during childhood, that more than once there may have
been confusion between the signs afforded by newly-formed thrombi and
those which belonged exclusively to a pre-existing disease of the
endocardium.
Moreover, these murmurs have been heard and described by too many good
{728} observers (Walshe, Flint, Richardson) for any small negative
evidence to weigh against that which is very positive. Sometimes they
have been but the exaggeration of a bruit previously heard and which
characterized an organic affection of the heart. Sometimes the presence
of the thrombus has caused the diminution or complete disappearance of
the pre-existing structural murmur. Again, these murmurs are discovered
for the first time when the other signs indicate the existence of
intra-cardiac thrombi. When they are heard under these circumstances
they prove positively that the coagula have sent prolongations between
the cavities of the heart or into the great vessels, so as to prevent
the accurate coaptation of the valves or to obstruct the onward current
of the blood. In the first case a regurgitant murmur is occasioned,
tricuspid or mitral, which is heard at the apex; in the second case a
basic murmur is detected, which is pulmonary or aortic. Usually these
murmurs are systolic, although they may in rare conditions be
diastolic. The murmurs have been heard more frequently on the right
side of the heart, and have pointed by their location of greatest
intensity to the obstruction of the infundibulum and pulmonary orifice.
They are then basic or suprabasic, and carried upward toward the
infra-clavicular region on the left side. These murmurs are heard very
rarely on the left side--so infrequently, indeed, that Walshe cannot
affirm that he has ever observed clinically one in this region.
Theoretically, of course, such murmurs may be heard at any spot in the
præcordial region, and with the first or second sounds provided their
size and position in relation to orifices or valves could sufficiently
account for them. Whilst there can be little question that murmurs do
take place in the præcordial region wholly due to the presence of
heart-clot, it is probable that their frequency and diagnostic
importance is less than superficial consideration would cause one to
believe. Thus, Flint[36] states that "the presence of coagula may
occasion an endocardial murmur, but as a rule it is wanting, probably
in consequence of the enfeebled action of the heart." Richardson[37]
holds an analogous opinion, and writes: "There are sometimes abnormal
sounds, but it is difficult to distinguish these from murmurs the
results of valvular lesions." Walshe[38] is at variance with this view,
especially in regard to the thrombal de novo murmur, and has "heard
such a murmur when the examination post-mortem showed the fibrinous
coagulum as the only probable cause of it."
[Footnote 36: _Disease of the Heart_, Philada., 1870, p. 280.]
[Footnote 37: _The Coagulation of the Blood_, Lond., 1858, p. 428.]
[Footnote 38: _Op. cit._ (foot-note).]
Auscultation.--In the heart the single, constant sign that has been
observed consists in the modified tonality of the normal sounds. These
are rapid, irregular, muffled, obscured, and distant. There is notable
inequality also in the strength of successive beats, which is obviously
explained by the great difficulty the blood encounters in traversing
the heart. Now, as I have seen in frequent autopsies that the valvular
mechanism of the left heart is ordinarily free from any fibrinous
deposit, it is readily understood that it can produce the two sounds
normal as regards situation and time, but greatly modified in
transmission.
Percussion.--Percussion, except in particular cases which are rare, and
in which the cavities are much distended by their contents, will only
furnish us with negative signs. When the ventricles are swollen by
large coagula, the percussion dulness will be extended laterally. As
the right cavity is usually the seat of the deposit, it will be
particularly marked toward the right of the sternum. In those instances
where the area of præcordial dulness had been determined before the
formation of the fibrinous concretion this extension becomes a physical
sign of great value. It is to Piorry and the use of the plessimeter
that we owe whatever of exactness belongs in like cases to this method
of examination.
{729} Inspection and Palpation.--The cardiac impulse may be unaffected
by the presence of the thrombus, and if it has been regular in rhythm
previous to its formation it may still remain so. This condition is
infrequent, however, and usually the pulsations become irregular,
tumultuous, and rapid. The force of successive beats will also be
different. These signs can be determined by the sight and touch.
Pulse.--The characters of the pulse are variable. Sometimes it presents
manifest inequalities, occasional intermittences, and is extremely
frequent. It may be quite feeble in the beginning, and afterward gain
in strength. Sometimes, in spite of its weakness and depressibility, it
retains its regularity and its rhythm is unchanged. The coagulum
existing in the cardiac cavities, especially on the right side,
explains the variations of the pulse. Effectively, at each contraction
of the ventricle this chamber, containing a less quantity of liquid
blood, projects a smaller amount of venous blood to the lungs. Besides,
this quantity is insufficient to replace the volume of revivified blood
which leaves the lung with each inspiration. Soon the left cardiac
cavities contract with but small power upon an amount of blood below
the normal, and yet it is with this supply that the left heart must
satisfy the needs of all the organs. The arteries during life become
nearly empty, and it is to this condition, as well as to the lack of
synchronism between the action of the two sides of the heart, should be
attributed the signs we recognize in the characters of the pulse.[39]
[Footnote 39: Robinson, _loc. cit._]
In some instances of cardiac concretions the sonority of the chest
remains normal. In others it is obviously augmented, and even by
percussion very lightly performed a sound of raised pitch is produced.
According to Richardson, this acute emphysema is the direct result of
an insufficient blood-supply in the capillaries which surround the
pulmonary alveoli. Whilst such a condition may often be observed
amongst children, it is not unknown with adults. The affirmation,
therefore, of Walshe, that it can only be observed in young people, and
that in adults its place is supplied by considerable pulmonary
congestion, is not exact. Since Richardson first called attention to
the exaggerated sonority of the lungs in cases of heart-clot, other
observers have also referred to it. Lavirotte (1864) particularly has
insisted on it as a proof of fibrinous deposition in the right heart,
and has demonstrated with pathological specimens that it was occasioned
by the exsanguinated state of the lungs and their hyperdistension with
air.[40] On the other hand, Raynaud[41] states that when the left
cavities are the seat of the concretion there is considerable
stagnation in the lungs, and they show signs of great congestion.
Thoracic percussion becomes less resonant, and subcrepitant râles are
heard in an extended area. Sometimes, even, a moderate hæmoptysis takes
place. These signs of emphysema on one hand, of congestion on the
other, are not spoken of by the majority of writers on this subject;
yet when they are present they will serve to fix our diagnosis and
render it more certain. With respect to emphysema, especially amongst
children, we should mention its great frequency, and on this account
perhaps proper value has not been given to it when found at the autopsy
of a child whose death has been occasioned by cardiac thrombosis. When
the cardiac thrombus is present in the right side of the heart,
Legroux[42] has shown that there will be a more or less turgid
condition of the veins of the neck, and perhaps also of the right upper
limb. With this distension of the veins we shall remark, according to
him, a partial or general infiltration of the subcutaneous tissues.
Sometimes the oedematous condition is limited to the face and neck;
occasionally it extends below the diaphragm, especially on the right
side of the body. The extent of the oedema will depend upon the number
and size of the prolongations which are {730} given out by the main
coagulum. Occasionally these prolongations have been found not only
blocking up the pulmonary artery, but also filling one or both venæ
cavæ and branching out as far as the jugular and subclavian veins.
[Footnote 40: _Congrès Medico-Chirurgical_, Lyon, 1864.]
[Footnote 41: _Dict. de Méd. et de Chirurgie_, vol. viii. p. 573.]
[Footnote 42: _Gazette hébdomadaire_, 1856.]
In my own observations I have always found the veins of the neck
manifest, without in a single instance reaching any great size, and
never have I noticed the prominence of the eyes noted by Walshe. In
these cases cyanosis was limited, and was notable in a marked degree
only upon the lips, the cheeks, and in the upper extremities. The
general or local infiltration of tissue I have never remarked, although
closely looked for on several occasions. Some authors, indeed, have
described a bluish appearance of the entire surface of the body,
together with signs of general infiltration. The explanation given of
these phenomena is that there is a general obstruction of the capillary
circulation, and that the return of the venous blood to the cavities of
the heart is rendered almost impossible. In other words, we have here a
well-marked asphyxic condition. If this be true, it is only partially
so, and there must be great variation in different instances of
fibrinous deposition in the right heart. The rational symptom which was
for me one of great value in the diagnosis of these cases was that of
excessive pallor, not only of the face, but of the limbs and the entire
trunk. This pallor appeared constantly to increase until the last
moments of life.
Richardson indeed says the symptoms are those of syncope, not of
asphyxia. The different processes of life are arrested on account of a
simple absence of arterial blood, not owing to the presence of blood
unfitted to reconstitute the tissues. The tendency to fainting is
probably due, therefore, to the fact that the right ventricle being
more or less completely filled by a fibrinous coagulum, the blood is
prevented from passing through its cavity and entering the lungs. As a
result, there will be but a relatively small portion of blood which
becomes oxygenized after each right cardiac systole. When the clot
occupies the left ventricle and auricle, there will be a reflux of
blood into the pulmonary tissue, thus causing great congestion of this
structure. So intense will this congestion become that occasionally
hæmoptysis results and pulmonary apoplexy may be developed, due,
doubtless, to rupture of the capillary vessels. This condition occurs
before the right heart is much or at all obstructed by coagula. We can
appreciate that the physical signs must, if properly noted, show
manifestly in which cavity the clot is located. If it be in the right
heart, anæmia and emphysema of the lung should follow; hence
breathlessness and increased pulmonary resonance. If it be in the left
cardiac cavity, the lungs become engorged very rapidly, and we should
find dulness on percussion, moist râles, and perhaps an equal or even
greater amount of dyspnoea.
Difficulty of breathing appears to belong as well to the symptoms which
indicate cardiac thrombus on one side of the heart as to those which
characterize its presence upon the other. This symptom was first
accurately described by Hope, since his day by Richardson and
Meigs.[43] It has something special in its features which strikes one
particularly, but may deceive unless closely observed. It takes place
not because the movements of the thorax are interfered with, not
because the entrance of air into the lungs is prevented, for the
vesicular respiratory murmur is easily distinguished, but because the
amount of blood furnished by the pulmonary artery is diminished. The
anguish of the patient is sometimes terrible. The nares dilate, the
chest expands spasmodically with each inspiration, and the patient is
agitated, moans, and shows that extreme craving for air described by
Van Swieten in the summæ anxietates. Under these circumstances,
Hayden[44] states, the surface is cold, and often humid with
perspiration. Pain and great oppression {731} in the præcordial region
have occasionally been referred to, as in the patient of Beau, who
said, in placing his hand to his chest, "I have there a weight which
has suddenly formed and which stifles me." Often the anxiety is
extreme, and the painful sensations continue to increase steadily until
death occurs. In rare instances the suffering, when it has reached a
certain degree of intensity, may remain stationary, or even become
considerably less. If such a respite occur, it is only temporary,
however, and the anguish soon recommences. In milder cases sometimes,
and apparently after dissolution or disintegration of the clot, the
severe symptoms may by degrees disappear, and from this period the
patient makes a steady, uninterrupted march toward recovery. I have
only lately witnessed a similar example in a youth attacked with
typhoid fever, which had reached the third week. There are constant and
intense effort to breathe, extreme restlessness, and the patient will
throw himself from one side of the bed to the other, and scarcely
remain quiet for a few moments. These symptoms are usually more
developed when there is concomitant cardiac disease of organic nature,
and unless this be present may not be so pronounced as to concentrate
attention upon them.
[Footnote 43: _Am. Journ. Med. Sciences_, April, 1864.]
[Footnote 44: Cases 106, 107, and 111.]
The brain scarcely shows the effect of congestion when the patient
dozes for a few moments even in the midst of his great distress. These
times of repose are frequent, but very temporary. In a little while the
patient goes off in delirium or has a convulsion. Again, he relapses
into coma, in which state death may take place. In some instances there
has been obstinate vomiting during several days preceding a fatal
termination. It is possible that this symptom favored the rapid
development of the thrombus.
The preceding signs and symptoms will sometimes declare themselves
suddenly in the midst of an inflammatory or cachectic affection, and
will then point directly to the presence of a cardiac thrombus of
considerable size which has rapidly formed, and which obstructs an
orifice or interferes with the normal play of the valves. Again, there
are all the physical evidences of an old organic affection of the
heart, or those of acute endocarditis or pericarditis, and rapidly all
the symptoms referable to the heart become greatly increased, whilst
orthopnoea, pallor, and coldness of the extremities take place. If a
careful examination of the chest reveals no intercurrent and pulmonary
nor superadded cardiac affection, we may then fairly assume the
existence of an intra-cardiac concretion. Nevertheless, we should
remember that in many of these cases there is a close resemblance of
the symptoms with those occasioned by a sudden rupture of one of the
chordæ tendineæ in the course of acute endocarditis (Walshe).
We should not lose sight of the fact that at times a clot will form in
the heart without giving rise to manifest symptoms unless the attention
be specially directed to its formation. This will be true in instances
where the coagulum forms slowly, is small, or occupies a place removed
from orifices or valves. In a cardiac sinus, for example, a coagulum of
inconsiderable size may remain fixed and latent for a long period. Such
is not the case, as we already have shown, when the coagulum fills in
part one or more of the cardiac cavities, is situated near an orifice,
is attached to the walls by a pedicle which allows it to float freely
in the ventricle, or is intertwined with the valves or chordæ tendineæ.
Under all these circumstances, they give rise to the signs and symptoms
we have dwelt upon above, and which ordinarily make known their
presence. Occasionally, however, there is such a combination of
symptomatic morbid phenomena relating to different organs that we are
at a loss to separate them accurately and to determine how this or that
symptom is occasioned. This statement is particularly true in regard to
the distinguishing symptoms which indicate the presence of terminal
coagula. At a period when the fatal termination is not far removed, and
when it is extremely difficult both to recognize and interpret special
{732} symptoms, it is readily understood why those pertaining directly
to cardiac thrombosis have not hitherto been fully and accurately
described.
COURSE, DURATION, AND TERMINATIONS.--Cardiac concretions may form more
or less rapidly, and in certain situations occasion death
instantaneously and surely. This is eminently true of large coagula
which fill up the infundibulum and pulmonary artery. Cases of this sort
have been mentioned by various authors. Amongst others, we would
specially direct attention to those instances in which sudden death has
taken place during the puerperal state after severe post-partum
hemorrhage. The patient has at times, in assuming an erect sitting
posture, been attacked with a syncopal attack resulting in a few
instances fatally.[45] In the same category we should include those
examples in which sudden death has followed severe surgical
operations.[46] Two cases of this termination, due to coagula in the
right heart, are reported by Robert Lawson.[47]
[Footnote 45: _Philada. Medical Examiner_, March, 1849, paper by
Charles D. Meigs; vide also Spiegelberg, _Lerbuch der Geburtshülfe_,
and Lusk, _The Science and Art of Midwifery_, p. 597.]
[Footnote 46: _Med. Times and Gazette_, vol. i., 1873, p. 58; also
_Pathol. Soc. Trans._, vol. xxvii. p. 70.]
[Footnote 47: _Med. Times and Gazette_, Feb. 8, 1873.]
In cardiac dilatation this mode of death is not infrequently seen. It
here seems to depend mainly upon stasis of blood caused by weakened
power of contractility in the right heart and "by impairment of
respiratory and nutritive attraction arising from feeble respiration
and arrested tissue-change" (Hayden). The post-mortem revelation has
afterward shown cardiac thrombosis to be the efficient cause of death.
In diphtheria[48] and pneumonia such examples are not infrequently
encountered. As Austin Flint[49] remarks, however, these coagula
present almost identical physical characters with those formed after
death, and consequently to fix precisely the moment of their production
will at best be but a matter for conjecture. According to Walshe, it
would be difficult to determine whether or not some of these almost
instantaneous deaths occurred as a coincidence or as an effect.
Besides, it is frequently impossible to determine the length of time
they have existed before completely obstructing the circulation through
the pulmonary artery into the lungs, and hence causing fatal syncopal
or asphyxic phenomena. Bristowe[50] goes so far even as to affirm in
the great majority of cases that cardiac concretions are unaccompanied
with appreciable symptoms. In this statement he includes coagula of
large size entirely filling one or more of the cardiac cavities, and
doubtless formed within a few hours of the final termination. To quote
his own words, "We ought to require very strong testimony indeed to
convince us in any case that concretions found in the heart at the time
of death have caused death, still more to convince us that those clots
which resemble in every point the clots which are the mere result of
dying have had this effect." How different does this sound from the
opinions of B. W. Richardson,[51] who attributes so many well-marked
symptoms to the formation of voluminous moulded clots in the heart!
And, indeed, is it not at variance with the views of a host of the best
medical observers? We believe Bristowe goes too far, and that cardiac
concretions are not infrequently the cause of very sudden death both in
acute and chronic diseases.
[Footnote 48: Robinson, _loc. cit._]
[Footnote 49: _Diseases of the Heart_, p. 276, Philada., 1870.]
[Footnote 50: _Reynolds's System of Medicine_, vol. v. p. 113.]
[Footnote 51: "Lectures" in the _British Medical Journal_, 1860.]
There are numerous instances in which the coagulum formed in the heart
is of smaller size, does not form so rapidly, and besides occupies a
position in which, as it does not interfere greatly with the function
of the heart, death does not of necessity immediately take place.
Little by little, however, the clot is added to, and before many days
have elapsed symptoms of gravest {733} import are pronounced. So usual
is it for the phenomena connected with the formation of a large cardiac
concretion to be accompanied by those which properly belong to another
serious affection which may likewise occasion rapid death (pneumonia,
endocarditis, typhoid fever, diphtheria, etc.) that we with the
greatest difficulty separate the symptoms, and can assign to the
intra-cardiac condition those doubtless occasioned by it.
The cases referred to above are not the only ones. Occasionally we meet
with cardiac concretions after death which have evidently existed for a
number of years, and sometimes without having ever revealed their
presence by notable interference with the circulation or in any way
affecting the habitual good health of the individual (Laennec[52]).
This is perhaps not to be wondered at when the coagulum is small and
situated near the apex of the heart, in one of the auricular
appendages, or in such a position as not to alter the play of the
cardiac valves or obstruct the orifices. But when we see a whole
cavity, as an auricle, forcibly distended by an old concretion which
fills its entire cavity, the absence of all symptoms during life
pointing to its existence occasions much surprise. Some of these large
coagula have nevertheless, by a sudden change in their position, caused
instantaneous death; others again, after giving rise to obscure
symptoms affecting both the pulmonary and cardiac circulation, have
likewise brought about a rapidly fatal termination.[53] Sometimes, in
consequence of the condensation or atrophy of the clot, the phenomena
which took place suddenly with great intensity and indicated its
presence became gradually modified, and we have known one remarkable
instance in a youth during the third week of an attack of typhoid fever
where the accidents thus occasioned completely disappeared, and the
patient left the hospital apparently cured.[54]
[Footnote 52: _Dict. Encycl. des Sci. méd._, article "Concrétions
sanguines."]
[Footnote 53: _Edin. Med. Journal_, April, 1868, v.--case by H.
Douglas.]
[Footnote 54: What occurred in this case I am of course unable to state
in a positive manner. All I know is, that the heart became suddenly
obstructed, followed by weak, irregular pulse and dusky countenance,
and that in twenty-four hours, under treatment with frequently-repeated
doses of digitalis and carbonate of ammonia, the accidents subsided.
Was there a solution and disintegration of an incompletely formed
heart-clot? It seems to me probable.]