Chapter L: Part 50

In spite, however, of these investigations, and those of Allibert (1828), Louis (1837), Baron (1838), and Paget,[6] who showed how the blood could coagulate in the heart and by transport block up the pulmonary capillaries, we cannot dispute the glory to Virchow of having in some sort created this study. Owing to his great sagacity, he was able to seal his studies and experiments with the stamp of a master-mind. The new words embolus and embolism introduced by him refer to a process which was previously but badly understood, and which now fix, as it were, a domain in modern pathology. The theory of Virchow found many advocates--many who were opposed to it in the beginning. In consequence of this it was the origin of numerous works undertaken in this new direction. Amongst the most important are the communication of Schützenberger,[7] the thesis of Lancereaux (1862), the great work of Cohn (Berlin, 1862), the article of Weber in the treatise of Pitta and Billroth--which contains recent theories about coagulation of the blood and the transformation of clots--and the memoir of Polaillon upon cardiac embolism (Paris, 1879).

[Footnote 6: _Med.-Chir. Trans._, 1844, pp. 162-188.]

[Footnote 7: _Gazette médicale de Strasbourg_, 1857.]

ETIOLOGY.--So soon as the blood is withdrawn from the influence of life it no longer remains fluid, but rapidly coagulates. Thus it is we find frequently after death coagula filling the cavities of the heart and extending in long ribbon-like bands into the larger vessels, more particularly in the veins. What occurs here is very similar to what we notice in a bowl which receives the blood of a venesection. Here the blood thickens rapidly, the clot forms, leaves the sides of the bowl, assumes the appearance of jelly more or less colored owing to the corpuscles enclosed in the meshes of fibrin, and is bathed in a quantity of ambient serum. A similar change takes place in the heart: the serum is imbibed by the tissues and the clot remains in its cavities.

Coagulation of the blood is a very complex problem. Many theories seek to explain it. On the one hand, it has been said the fibrin pre-exists in the blood, and by the fact of the slowing of the circulation, the reduction of the {722} temperature, etc. the fibrin separates from the blood and coagulates. Again, it is admitted that the fibrin does not exist formed in the blood, but that a fibrinogenous material is present which is acted upon by the hæmoglobin or globulin contained in the red globules, the leucocytes, and the corpuscles of connective tissue, and sometimes is, sometimes is not, caused to precipitate as fibrin (Virchow). The exact conditions which occasion the activity of the globulin are unknown. The reaction which takes place has been said to resemble that which takes place between amygdalin and emulsin when prussic acid is formed, or between myrosin and myronic acid when the volatile oil of mustard is produced. Further, it is stated, in accordance with accurate chemical investigations, that the plasma of the blood contains a substance called plasmin, which separates itself into fibrin which coagulates and into fibrin which remains dissolved in the blood (metalbumen, Robin). These fibrins are evidently of two kinds. The plasmin divides itself under the influence of slowing of the circulation, the action of acids, of foreign bodies, of oxygen in excess, etc.; it remains intact in a fluid condition when the vascular walls and globules are healthy, the blood circulating with normal rapidity, and in presence of alkaline principles.[8] According to Foster,[9] "Coagulation is the result of the interaction of two bodies, paraglobulin and fibrinogen, brought about by the agency of a third body, fibrin ferment." Schmidt concludes that when blood is shed a number of white and intermediate corpuscles fall to pieces, by which act a quantity of fibrin ferment and of paraglobulin is discharged into the plasma. These meeting there with the already present fibrogen give rise to fibrin, and coagulation results.

[Footnote 8: _Dict. de Méd. et de Chirurgie pratique_, vol. viii. p. 569.]

[Footnote 9: _A Textbook of Physiology_, p. 22, New York, 1880.]

As regards the formation of clots within the body, it is supposed that injured or diseased spots or foreign bodies first attract, and then, as it were, by irritation cause the death of, a certain number of corpuscles.[10] The views of Schmidt of the fibrino-plastic function of paraglobulin are not accepted by all investigators; and some authors believe that the fibrinogen as well as the fibrin ferment arises from the white corpuscles.[11]

[Footnote 10: _Pflüger's Archiv_, vi. (1872), p. 413; xi. (1875), pp. 291 and 515; xiii. (1876), pp. 93 and 146; quoted by Foster.]

[Footnote 11: Frédericq, L., _Recherches sur la Coagulation du Sang_, Bruxelles, 1877, quoted by Foster.]

According to Bristowe,[12] the frequency of sanguineous concretions does not depend upon sex, but is in a certain relation with age. He has remarked, for example, that they are proportionately more often met with at the extremes of life than toward middle age. This might be explained satisfactorily, perhaps, on the supposition that at these periods the circulation is at times very feeble, owing either to congenital feebleness on the one hand or chronic organic affections on the other. At all events, when we seek for the causes which have most influence in determining the formation of cardiac concretions previous to death, we find--I. the mechanical, or those which act specially in slowing the current of blood through the heart. These causes may exist within the heart or may be removed from it. II. The vital or pathological. These causes are of somewhat difficult determination at times, and pertain usually to affections in which there is notable blood-change, in which the quantity of the fibrin has been augmented absolutely or relatively, or to those of infectious type--viz. diphtheria; or to those constitutional in nature--phthisis, cancer, etc. III. The inflammation of the endocardium or endocarditis. This is admitted by Andral, in a note upon the etiology of cardiac concretions in the work of Laennec, as having special importance. Bouillaud also attributed their formation in certain cases to the chemical action of pus which was present in the economy.

[Footnote 12: _Pathol. Society's Trans._, vol. xiv. p. 71, quoted by Bartholow.]

{723} I. Amongst the mechanical causes we should mention all organic lesions of the heart, all obstacles in the pulmonary circulation, and possibly, by analogy, certain badly-defined lesions of the pneumogastric nerves. All the stenoses and dilatations of orifices, all irregularities of the valves or heart-walls, all depressions or roughened parts of the walls,[13] may determine the beginning of a concretion. In the same way, a small mass of fibrin deposited on a calcareous valve after transport from one of the veins of the limbs may originate a voluminous heart-clot. Dilatation of the heart, pericarditis, every cardiac change which weakens the contractile power, is a predisposing cause of cardiac thrombosis. Every organic lesion of the heart tending toward that final stage of asystolism so often encountered, and which weakens so greatly cardiac contractility; pouching of different portions of the cardiac wall, or aneurism; pressure upon the right heart by a mediastinal tumor or a sacculated aneurism of the arch of the aorta,[14]--all these have great power in producing intra-cardiac thrombi. The mechanism of these different lesions was familiar to Kreyssig, Laennec, and Hope. At the same time it must be admitted that these changes in the heart are not of themselves always sufficient to give rise to fibrinous deposits. We encounter stenoses and regurgitations at orifices very frequently, and concretions, on the other hand, are relatively rare. Moreover, we find heart-clot at times when there is no cardiac alteration. We believe, therefore, that the heart lesion is an aiding factor--that in the last moments of life, when the force of the heart's contraction is weakened and the conditions of the blood favor coagulation, they will act with special power.

[Footnote 13: _Pathol. Society's Trans._, vol. xiv. p. 71, cases by J. W. Ogle.]

[Footnote 14: Walshe, _Dis. of the Heart_, Lond., 1873.]

Among the mechanical causes which are removed or distant should be mentioned all those which interfere with the pulmonary circulation. Such are the effects left behind by pneumonia, pleuro-pneumonia, or the compression of the blood-vessels by old congestion of the lungs. In these cases, when the vis a tergo is impaired somewhat, and an obstacle is placed in the pulmonary capillary circulation, even if cardiac thrombosis does not directly result at first, we may have thrombi form in the pulmonary veins. In the same way, the nervous affections which are accompanied with slowing of the circulation tend to produce coagulation of the blood. All lesions, as we have said, of the pneumogastrics act in the same direction. In proof of this we should cite the experiments of Meyer of Bonn, of Longet, and of Blondet, who produced fibrinous concretions in the hearts of animals by tying or cutting the pneumogastric nerves. At the same time, the heart-beats became more rapid, wavering, unequal, and less energetic than in ordinary physiological conditions. After all, however, all these mechanical causes are but predisposing causes, for they do not always produce cardiac concretions. Frequently, as we have said already, the obstruction to the circulation may be present, and yet at the autopsy no fibrinous deposit be found in the heart. In order that the mechanical causes act efficiently to produce coagula, it is essential that they be aided by the conditions of the blood which favor it.

All concretions do not form with the same rapidity nor are they of the same size. At times their production is sudden, and but a few hours elapse before the fatal termination is reached. Again, it is affirmed that weeks, and even months, may pass before the concretion has reached a volume sufficient to cause entire stoppage of the heart's contractions. In the former category are found, of course, the softer, least consistent coagula--usually, however, very voluminous; in the latter are the smaller, more elastic, and resistant concretions, at times even presenting a stratified structure[15] and {724} surrounded habitually by a clot formed during the latter moments of life, and having a large proportion of cruor in its composition. The heart affected with fatty degeneration should, if we consider its weakened power and deficient contractility, be a predisposing cause of stagnation first, and finally of the formation of intra-cardiac thrombi. As a matter of observation in the dead-house, however, such hearts are not frequently accompanied with fibrinous deposits in their cavities.

[Footnote 15: According to Legroux, roughening of the walls or valves gives rise to stratified coagula of moderate size, or else to those small clots which deposit on the surface or margin of the valves (_Dict. Encycl. des Sci. méd._, article "Concrétions sanguines," Paris, 1876).]

All diseases which by their nature and duration produce great exhaustion of the vital powers tend strongly to produce fibrinous coagula in the heart. This is eminently true of those which at the same time do not occasion a diminished plasticity of the blood. It is often assumed that mere stasis in the blood-current through the heart is essential to the formation of clots in its cavities, and to lend support to this belief reference is made to the phenomena which take place in bleeding. It is not true, however, that stasis is necessary to coagulation, and the proof is afforded when we take a bundle of twigs and by beating the blood forcibly produce the separation of the fibrin. Besides a slowness of the circulation, there must be, once again, an obstacle in the heart itself, and even then polypoid concretions are not always formed.[16]

[Footnote 16: _Gaz. hébdomadaire_, Paris, 1856.]

II. The Vital or Pathological Causes.--In this class of conditions leading to cardiac thrombosis are included all diseases in which certain special changes have taken place in the blood itself. Among these we should mention, first, certain sthenic inflammatory affections in which the proportion of the plasmin (fibrin and metalbumen) is notably elevated, and in which, on this account, there is a strong tendency to the separation of fibrin from the blood and to the formation of cardiac concretions. In fibrinous pneumonia and acute rheumatism this is particularly true, and amongst the numerous accidents we have to dread in the course of these diseases none strike us with more dread than the possible production of intra-cardiac thrombi. In fibrinous pneumonia this complication is so frequent that Bouillaud has enunciated the following pathological law: "Fibrinous concretions exist constantly in patients who succumb to a frank, acute pleuro-pneumonia, well characterized, which has reached the second stage."[17] According to Raynaud, this is without question a great exaggeration, and results from the confusion this learned author evidently made between terminal clots and those formed some time previous to death. Nevertheless, there is here a proof of the great frequency of coagula occasioned by this disease, and of the strong tendency to their formation which the condition of the blood must afford. What we have said of fibrinous pneumonia and acute articular rheumatism is not true, singular to say, of lobular or broncho-pneumonia. The lesions of this form of pneumonia are those of a catarrhal inflammation of the lung, and the blood does not offer during its course the remarkable tendency to coagulation that is shown in fibrinous pneumonia. Usually, the heart-cavities and the vessels are filled after death with a liquid of a black or violet-brown color, very often sticky.[18] The fibrin in the heart-cavities in pneumonia is fibrillar, and does not present those changes which indicate that it has been deposited for a long while. Moreover, these coagula do not present physical characters which show any considerable degree of age. They are usually terminal coagula, or at least formed within a few days of the fatal termination. Do globular vegetations occur in pneumonia? At times they do, but they are at least very rare as compared with the fibrinous conditions just referred to.

[Footnote 17: _Gazette méd._, 1843, vol. xi. p. 270, quoted by Armand, _Thèse de Paris_, 1857, p. 41.]

[Footnote 18: Damaschino, _Thèse de Paris_.]

There are other general conditions in which there is a marked tendency to {725} the formation of cardiac coagula. In the puerperal state, according to Simpson, it is occasioned by the resorption of many new elements which vitiate its composition and thus occasion this result. In the poisoning following upon glanders or pyohæmia intra-cardiac thrombi are often found. Lancereaux has found in this latter disease fibrinous deposits in the right ventricle and pulmonary artery around small masses composed of pus-cells. In the different cachectic states, such as those caused by chronic Bright's disease,[19] advanced phthisis, and cancer, although we have a diminution in the proportion of red globules, there is present at the same time a relative increase of fibrin; and the consequence is that concretions are often formed in the heart. In fact, it is in these cachexiæ that we often encounter those fibrinous cysts which will be described under the title of Morbid Anatomy.

[Footnote 19: Here the retention of the excreta is an important factor in the formation of cardiac thrombosis (Bristowe).]

Many well-known authors have declared that diphtheria was very powerful in producing fibrinous concretions in the right heart some time previous to death. Among those who have written specially on this subject we would mention Winkler,[20] Richardson,[21] Meigs[22] and Robinson.[23] According to the latter writer, elastic fibrinous clots twisted in the valves and adherent to the cardiac walls are developed frequently in children at a period quite removed from that of the agony, and at a time when they are not as yet in a condition of extreme weakness. Except in exceptional instances this influence of diphtheria to produce cardiac coagula is doubted by Parrot.[24] He admits its power, particularly when it is complicated with membranous croup, and in these examples he believes the precocious formation of coagula is determined probably by the asphyxic condition. Whilst denying the influence of diphtheria, Parrot freely acknowledges that measles, especially when complicated with broncho-pneumonia, tends to produce cardiac concretions. The same tendency is recognized by Harley in the early stage of scarlet fever where there is high pyrexia.[25]

[Footnote 20: _Die Bluthlumpen dann der Häutiger Bräune_, Wien, 1852.]

[Footnote 21: _Med. Times_, vol. i. p. 23, 1860.]

[Footnote 22: _Am. Journ. Med. Sci._, April, 1864.]

[Footnote 23: _De la Thrombose cardiaque dans la Diphthérie_, Paris, 1872.]

[Footnote 24: _Dict. Encycl. des Sci. méd._, vol. xviii. p. 484.]

[Footnote 25: _Medico-Chirurg. Trans._, vol. lv.]

Notwithstanding the diminished proportion of fibrin in typhoid fever, and the impossibility of explaining, in many cases, any increase of the plasticity by local inflammatory disorders, cardiac concretions have been observed by Huss, Virchow, and Hardy.[26] Bucquoy also relates, after Huxham, an epidemic which reigned at Plymouth in 1742 amongst sailors who came from a long cruise, characterized by dyspnoea, cardiac palpitations, and intermittences of the pulse. Many of those attacked died, and at the autopsies made polypoid concretions of considerable elasticity and adherent to the walls of the heart were found. Another similar occurrence took place amongst the soldiers of the garrison of Rocroy in 1746. Quite a number succumbed after having shown symptoms similar to those of the sailors of Huxham. Cadaveric sections discovered in the left ventricle several hard, consistent cardiac thrombi.

[Footnote 26: Quoted by Bucquoy, _Des Concrétions sanguines_, Paris, 1863, p. 36.]

III. Endocarditis.--Whatever may be the opinion of different authors in regard to the frequency of endocarditis when intra-cardiac thrombi are present, it is certain that if it does exist the explanation of the presence of these deposits is clear and ample. In endocarditis we have both a local and mechanical cause and also a vital condition of fibrinous deposits in the heart. As a mechanical cause we know that often it is the cause of the stenoses of orifice which are present, and that further, by its effect in producing roughening or fissuring of surface, it offers a strongly predisposing cause of the {726} deposit of fibrin. Ulcerative endocarditis acts still more efficiently in this direction, owing to the fact that it produces its effects as much on the surface of the valve, aortic and mitral, near the adherent portion and in the neighborhood of the cardiac orifice, as between its layers. The result is, that the surface is rough, unequal, presenting often cauliflower excrescences, and showing sometimes, in the midst of a mass of fibrin that has become deposited by degrees, portions of a softened, partially-detached valve which was the nucleus of the outer layers of fibrin. Further, endocarditis of both forms acts as a vital and efficient cause of cardiac thrombosis, in that it belongs to the class of inflammatory diseases which occasions an absolute increase in the proportion of fibrin of the blood (from 25/1000, concrete fibrin 3, and metalbumen 22, to 56/1000, concrete fibrin 17, metalbumen 36); and also, more especially in ulcerous endocarditis, by the transport of infectious materials into the blood, which still further tend to cause coagulation.[27]

[Footnote 27: At times there is complete deprivation of epithelium over a limited area, and in rare cases slight ulcerations of membrane. These two conditions are efficient factors of the exudation of plastic lymph.]

SYMPTOMATOLOGY.--According to Laennec,[28] it is equally erroneous to attribute to cardiac thrombosis many symptoms which properly belong to an organic lesion of the heart (notably hypertrophy) as it is to believe that intra-cardiac thrombi never begin to form until the terminal period of life. According to him, Haller, Vinckler, Staneari, and Bonaroli[29] have observed obliterations of the internal jugular vein and carotid artery by very firm concrete fibrin, and he himself has seen a similar production in the inferior vena cava for the space of four fingers' breadth. Although these concretions were evidently formed during life, they occasioned no symptoms indicative of their presence, nor were there any obstructions in the course of the circulation which could explain their origin. Reasoning from these facts and from the phenomena which occur in aneurismal tumors, it seems highly probable that the blood should coagulate in the heart also during life. Later writers frankly admitted that coagulations in the veins caused partial dropsies, a usual instance of which is the white swelled leg, or phlegmasia alba dolens, from obliteration of the femoral vein.[30] This is not invariable, for I have seen, in patients who have succumbed to diphtheria, both venæ cavæ obstructed by coagula, without having observed during life either local or general oedema.[31]

[Footnote 28: _A Treatise on Diseases of the Chest_, p. 183, Philada., 1823.]

[Footnote 29: Quoted by Morgagni, _Epist._ 64.]

[Footnote 30: Vide Bouillaud, _Archiv. gén. de, Méd._, t. ii. et v., quoted by Hope.]

[Footnote 31: _Thrombose cardiaque dans la Diphthérie_, Paris, 1872, p. 43.]

Scarcely any contemporary author doubts that cardiac thrombosis gives rise to more or less well-defined symptoms. What these are we shall now consider. Of course we are far less liable to-day, when the diagnosis of organic cardiac disease is so accurate, to attribute to intra-cardiac thrombi the signs, physical or rational, which properly belong to them, and which ancient observers could not differentiate. Nevertheless, there are complex cases in which one is at fault even in regard to this problem.

The symptoms of cardiac thrombosis vary naturally with their size, situation, and rapidity of formation. Certain authors have affirmed, for example, that the concretions formed in an auricle cause a greater amount of interference with the circulation than those elsewhere situated. This they do partly by reason of their size and the less contractile power possessed by the auricle, partly because from the auricle prolongations are sent off which occlude the cardiac orifices. When cardiac concretions form suddenly a few days previous to death, they always aggravate all the symptoms of an obstructed circulation.[32] If the case be one of pre-existing disease of the heart, they soon obliterate the cardiac cavities and lead to a rapid fatal {727} termination. According to Grisolle,[33] when the concretions are small and form an obstacle neither to the play of the valves nor to the cardiac circulation, they are not revealed by any appreciable functional trouble. The opinion of Grisolle in regard to small coagula is also shared by Legroux, especially when they are fixed at a distance from a cardiac orifice or concealed in a sinus. When, however, the thrombi are larger and interfere more or less with the course of the blood, they occasion very marked symptoms.

[Footnote 32: Hope, _On the Heart_, p. 486, Philada., 1846.]

[Footnote 33: _Pathologie interne_, p. 467, Paris, 1865.]

Even before the days of auscultation there were certain rational signs which were dwelt upon with much force as showing the presence of cardiac concretions. Thus, Senac[34] writes that the patients thus afflicted feel a weight or oppression in the præcordial region which sometimes becomes extremely painful. Palpitations and irregularities of the pulse were also noted as symptomatic of these productions. Laennec believes that coagula of any size may be recognized; "when, in a patient who till then had presented regular pulsations of the heart, these suddenly became so anomalous, confused, and obscure that they can no longer be analyzed, we may suspect the formation of a polypous concretion."[35] He further adds that if the trouble takes place on one side alone of the heart, the fact is almost certain. When the coagula occupy the cavities of the right heart, the sounds of the left heart may remain normal whilst those of the right side are more or less distant and muffled (Legroux). Several authors, amongst whom we should mention Legroux, Bouillaud, Barth, and Roger, have mentioned amongst the physical characters which show the existence of intra-cardiac thrombi the sudden development of a blowing murmur limited to the præcordial region or propagated into the aorta. Sometimes this bruit was soft, sometimes harsh and rough. These writers have also noticed, in conjunction with grave general symptoms, the doubling of the first sound of the heart, making occasionally a sort of galloping murmur. As regards the recognition of concretions on one side alone, I acknowledge that after auscultating carefully several cases in which the autopsy showed coagula formed during life, I have been unable to note signs sufficient to justify a differential diagnosis.

[Footnote 34: _Traité de la Structure du Coeur, de son Action et de ses Maladies_, t. ii. p. 470 _et suix_, quoted by Bucquoy.]

[Footnote 35: _De l'Auscult._, t. ii. p. 597, quoted by Hope.]

The distinction appears to me difficult in like cases, for how explain 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.]

COMPLICATIONS AND SEQUELÆ.--One, if not the gravest, complication which can arise during the formation and duration of heart-clot is the production of an embolus of the pulmonary artery, completely filling up its cavity, arresting respiration, and causing sudden death by asphyxia. More frequently smaller portions of heart-clot become detached and are transported farther along by the blood-current. Finally, they become arrested in vessels of smaller calibre. In these they may remain for a short time, and then become dissolved and resorbed, leaving the calibre of the vessel free after their disappearance, or else they form permanent plugs and give rise to inflammation, coagulation, or hemorrhage. According to the investigations of Lefeuvre,[55] which are both clinical and experimental, it would appear that the obstruction of the arterial distribution to any given part is almost immediately followed by engorgement of tissue and hyperæmia of the capillaries of the affected region. Feltz[56] has further shown that this condition is brought about by reflux from the veins and paralysis of the capillaries. It is not infrequent, moreover, to find hemorrhage into the tissues as a direct sequela of this changed condition of circulation.

[Footnote 55: _Brit. and Foreign Med.-Chir. Review_, Oct., 1871.]

[Footnote 56: _Traité clinique et expérimentale des Embolies capillaires_, Strasburg, 1870.]

These are, in fact, the conditions described under the name of infarctions. Small detached particles may be detached from the cardiac clot, if it be found in the left cavity, and transported after a similar manner by the blood-current of the aorta and its divisions until finally arrested in the different {734} viscera of the economy (spleen, kidney, liver) or in the arteries of the extremities.[57] In these different situations they give rise, when finally arrested, to results which differ considerably according to the structure of the organs or tissues where they become impacted. In certain instances, carefully studied by Senhouse Kirkes, the disintegrated and puriform contents of old fibrinous coagula are carried throughout the vascular system and determine marked typhoid phenomena. The patient is attacked with irregular paroxysms of fever of intermittent type, diarrhoea, vomiting, and extreme feebleness. Kirkes explains these symptoms partly by the obstructions occasioned by small emboli, partly by a sort of poisoning due to the transformation of the fibrin. The accidents thus occasioned at times very closely resemble those which characterize pyæmia.[58] The fluid contained in the interior of the old clots, which give rise to these accidents by reason of their transformation, is thick, grumous, and puriform. It is surrounded by a sort of pseudo-cyst, and is composed mainly of altered fibrin and red and white blood-corpuscles.[59]

[Footnote 57: _Gazette hébdomadaire_, 1856. Legroux reports a case of acute rheumatism accompanied by endocarditis and followed by concretions in the left cavities of the heart, and obliterations of the arteries of the limbs by emboli without gangrene ensuing.]

[Footnote 58: _Dict. Encycl. des Sci. méd._, _loc. cit._]

[Footnote 59: _Pathol. Soc. Transact._, vol. xiv. p. 65, cases by J. W. Ogle.]

Pulmonary apoplexy and hæmoptysis often take place in connection with the presence of a fibrinous clot of the right heart. This connection, however, is not absolute, and many cases of right cardiac coagulum have been observed in which neither of these complications became manifest. When there has been pre-existent valvular disease, especially of the mitral, these sequelæ more surely follow than when there has not been this organic disease. The connection between the pulmonary apoplexy and the valvular affection is even more intimate than that of the hæmoptysis, and the same statement is also true of its relationship with cardiac thrombosis.

Upon this subject Hayden[60] writes as follows: "Pulmonary apoplexy seeming to require it as a necessary antecedent condition, while hæmoptysis, though generally associated with thrombosis in the last moments of life, frequently does occur independently of it."

[Footnote 60: _Dis. of the Heart_, vol. i. p. 529.]

The doctrine of Ludwig, as supported by Niemeyer,[61] that the pulmonary apoplexy is directly due to stasis and deposit in the capillaries of blood-corpuscles, does not appear possible if we accord faith to the researches of Waters,[62] who has shown an intercommunication between the bronchial vessels and pulmonary veins; and reasoning upon this basis we have a strong confirmation of Virchow's theory of hemorrhagic infarction (Hayden) consequent upon embolism.

[Footnote 61: _A Textbook of Practical Medicine_, 1869, vol. i. p. 156.]

[Footnote 62: _The Human Lung_, 1860, p. 201.]