Chapter LI: Part 51

PATHOLOGY AND MORBID ANATOMY.--In the great majority of cases clots presenting different physical characters are found in one or more of the cavities of the heart after death. According to the supposed time of their formation, they have been very properly divided into--1, cadaveric (post-mortem); 2, terminal (in actu mortis); 3, ancient (ante-mortem). It is important at the very beginning of the considerations which I shall make in regard to these formations to determine, if possible, the physical characters of cadaveric and terminal clots, so as to be able afterward to more clearly separate from them the true cardiac concretions or those formed at a time more or less removed from the period of death. Without much question, it is owing to the indifference or neglect of later writers in making these necessary distinctions that uncertainty has arisen in the minds of many with respect of the age of many heart-clots. The cadaveric and terminal clots would indeed have but slight pathological interest attached to them were it not that occasionally during {735} life, in a spontaneous manner, cardiac thrombosis suddenly takes place, and is always the cause of symptoms of considerable gravity and which often occasion a fatal termination.

I. Cadaveric Clots.--These present the characters of blood drawn from the arm by venesection and which is allowed to coagulate in a vase. 1. Sometimes they are large, soft, homogeneous, friable masses, distending one or more of the cardiac cavities, and having an appearance very similar to badly-cooked currant-jelly, and there is no apparent separation of the fibrin and the globules. Such an aspect is found particularly when the relative quantity of fibrin is below the normal or the blood is deficient in plasticity. In alkaline poisoning and many adynamic forms of disease this is notably the case.[63] It may likewise occur in forms of death in which there has been considerable obstruction to the circulation. 2. In a somewhat similar manner, when the blood is removed from the influences which give it life and stagnates, or is arrested within the heart, coagulation takes place and the blood separates into two layers. The upper is fibrinous, and resembles the buffy coat covering a clot after bloodletting; the under layer is mainly cruoric, and encloses within its meshes by far the larger proportion of the red globules. This latter mass always forms the lowest stratum by relation with the position of the body after death. Between these two layers, and from the fact of their smaller density, we find more of the leucocytes. This formation of blood-clot in distinct strata has been accomplished experimentally by Pasta,[64] who poured some blood of an animal into the heart of an ox and allowed it to deposit. The cruoric mass is always soft, and may be readily washed from the fibrin by a stream of water. Frequently these clots distend the cardiac cavities to such an extent that when they are opened at the autopsy a portion will fall upon the table and the rest is readily detached from them. The microscope shows the same condition of globules and fibrin in these coagula as it does in those of a venesection. According to Walshe, these cadaveric coagula are usually voluminous, jelly-like masses of fibrin of a pale straw-color, semi-transparent, and containing a quantity of serum in their meshes. Never do they show the slightest signs of stratification, and are not really adherent to the cardiac walls. Occasionally their prolongations may be intertwined amongst the papillary muscles and fleshy columns. According to Legroux, it appears difficult to understand how these large masses of fibrin become separated from the blood and deposited in the heart during life, and yet he is indisposed to regard them as a strictly post-mortem production. They are for him simply the result of the agony.[65] After death the serum is expelled from the clot in larger or smaller quantity, and for a longer or shorter time according to its own spontaneous retractility.

[Footnote 63: Magendie, "Lectures on the Blood," _Lancet_, 1839.]

[Footnote 64: _Dict. de Médecine_, t. viii. p. 560, Paris, 1868.]

[Footnote 65: _Gaz. hébdomadaire_, 1856.]

There are instances in which death has taken place very suddenly (chloroform, lightning, blow on epigastrium), and the blood remains liquid in the cardiac cavities and shows no tendency to coagulation (Walshe). The intimate cause of this condition is difficult to state, although the sudden shock to the nervous system is doubtless the main explanation. Under these circumstances the lining membrane of the heart is apt to become stained with the coloring matter of the blood.[66] At times the ventricles of the heart contain no blood at the autopsy. This is more frequently true of the left than of the right ventricle. Even then the auricles are more or less full.

[Footnote 66: Bristowe, in _Reynolds's System of Medicine_, vol. v. p. 106.]

II. Terminal Clots.--These clots are found at a period more or less removed from the time of death. It may be that they have been present in the heart many days before the fatal termination is reached, or indeed that the act of dying, when the whole organism is overcome by the {736} numerous conditions which inevitably tend in this direction, is mainly instrumental in their rapid production. Of course their outward aspect as well as their intimate structure will vary greatly with their age and with the disease which has been present. Never are they formed entirely of cruor; frequently they are composed of a large quantity of fibrin. Their coloration varies with the quantity of red globules, leucocytes, and serum shut up in the meshes of the latter. In the cruoric as well as the fibrinous clots time also works changes of coloration. In the latter by the mere expression of the fibrin the coagula become less shiny and take on a darker tint, and when deeply colored by red globules they may go through many changes of tint from a violet or red-brick color to a pink. Usually, however, these latter changes require a much longer time to be effected than is properly understood in the term terminal clot. The latter is white, with a yellow or green tint, or again of a fleshy color with spots of deeper hue upon their surface. These are nothing more than small masses of blood, although to superficial inspection they may appear vascular. In structure they may be homogeneous throughout, but this is extremely rare, for in the same clot we habitually find different parts which are evidently of different ages; and not only is this true, but what leads more to confusion in regard to the precise age of a given clot is the fact that a relatively old one is at times juxtaposed or intimately annexed to a purely cadaveric one. To make the distinction of what portion of clot has been formed some time, and what part in the agony, is occasionally almost impossible. Owing to the manner of death or to certain rapid chemical changes which may take place, the interior of terminal clots is at times softened and filled with a puriform material which is probably only softened fibrin.[67] These clots are more or less firm and elastic. They adhere quite intimately by a number of roots to the walls of the heart, and are twined around the chordæ tendineæ, the musculi pectinati, and are closely attached after this manner in the depressions between the columnæ carneæ. Sometimes they send off long projections into the large vessels which proceed from the base of the heart. These latter may be cylindrical in form and fill up the vascular calibre, or appear like so many flattened and ribbon-like strips. The elasticity of these clots is made especially evident when we attempt to tear them away from the cavities in which they are adherent. They come away in small pieces, and show a rough, irregular surface where they have been torn asunder. Upon pressure the terminal clots allow a smaller or larger amount of serum to exude from their surface, according to their age and the site of their formation. If the quantity be large, the clot is much reduced in size and changes considerably its physical characters. It must be evident, therefore, that if a clot be contained in the ventricle, and be submitted for any notable length of time to active and forcible contractions, it cannot contain any large amount of serum. In the auricles near the appendages the clot does not bear any very strong outward pressure--not much more, in fact, than it would in an aneurismal sac. Clots in this situation may have existed, therefore, for quite a time before all or even a great part of their serum has exuded (Legroux). Rarely, terminal clots are somewhat stratified. The form of these clots is variable; usually flat, they may also be globular, ovoid, or thick. As they pass through the cardiac orifices they are narrowed. At a level with the sigmoid valves the full margin of the cusps is marked upon their surface, and discoid masses, formed usually almost exclusively of fibrin, fill the cavities of the cusps and are moulded to their surface. To this condition great importance has been attached as indicating the formation of the coagula prior to death. In fact, Poullet[68] has endeavored to prove irrecusably by experiments upon animals {737} that in all cases where these masses were present the clot had been formed quite a length of time during life. Raynaud,[69] although admitting the ante-mortem foundation of these imprints, nevertheless holds that they are produced in the act of dying. The author,[70] owing to the fact that he has found more than once the amount of fibrin and globules about equally proportioned in the deposits of the sigmoid sacs, considers that they may be formed after death. In this opinion he is upheld by Walshe, who goes even farther, and states that he has seen coagula filling the right ventricle, the infundibulum, pulmonary artery, and its branches, and tightly grasped by all these parts in which this mark was apparent,[71] and yet the coagulum was certainly formed post-mortem. This opinion was further sustained by more than one case observed during life, and in which the final symptoms were not at all those usually assigned to cardiac thrombosis. According to Richardson,[72] the fact that the clot is grooved upon its surface or contains a canicula through its interior is a positive proof of the passage of the blood-current, and hence of its formation during life.

[Footnote 67: _Cycl. of Anatomy and Physiology_, p. 114, 1848.]

[Footnote 68: _Thèse de Montpellier_, 1866. In this sign Poullet also endeavored to show a distinguishing feature between clots formed within the heart and those transported from one of the large veins of the extremities and arrested in the heart. Before Poullet, these sigmoid prolongations had been mentioned by Gallard and studied by Chauveau of Lyons and Gardner of Glasgow.]

[Footnote 69: _Dict. de Méd. et de Chirurgie_, vol. viii. pp. 562 and 565.]

[Footnote 70: _De la Thrombose cardiaque dans la Diphthérie_, Paris, 1872.]

[Footnote 71: V. (after Walshe) such a specimen, No. 3636 Univ. College Museum, London.]

[Footnote 72: _On Fibrinous Deposits of the Heart_, 1860.]

Whilst attaching a certain amount of importance to the signs just mentioned as indicating the age of a clot, Parrot[73] is disposed to consider the color, consistence, intimate attachments, and histological structure of far greater importance in determining their formation some time prior to death. Usually speaking, the terminal coagula have gone through no retrogressive changes as regards their primary elements. The red globules are perhaps paler than normal, but the fibrillæ of fibrin are still distinct and the leucocytes show well-defined nuclei and do not contain any fat-granules. These coagula, both terminal and cadaveric, are found more frequently in the right than the left side of the heart (Bouillaud). For the terminal especially the right auricle is a frequent location (Parrot). This does not coincide with the following table, taken from Legroux, and which shows the relative frequency of the products in the different cardiac cavities: In 48 cases concretions were found "in all the cavities at the same time, 8 times; the right cavities and the left ventricle, 2; the left cavities and the right ventricle, 2; the two ventricles, 4; the two right cavities, 5; the two left cavities, 3; the right auricle, 1; the right ventricle, 7; the left auricle 8; the left ventricle, 8 = 48 times."

[Footnote 73: _Dict. Encyc. des Sci. méd._, Paris, 1876.]

III. Ancient Clots.--There are several varieties which differ considerably in their outward conformation and appearances, and are formed at a period more or less removed from the time of death: _(a)_ Stratified coagula, which are attached intimately to the cardiac walls, and present frequently an aspect which has been confounded with that of true vascularization. So intimate is their adherence at times that to effect their separation the scalpel has to be used, and in the attempt the endocardium is detached. This membrane is frequently affected at the level of their attachments with an alteration of atheromatous nature. The volume of these coagula differs considerably. According to the old writers, they may have become large enough to fill the cavities entirely of one side of the heart and weigh at least a pound.[74] This is evidently an exaggeration, and coagula of this size could only be formed after death. Still, very large clots, formed some time previous to death, have been carefully described by Bouillaud.[75] These should be considered very {738} exceptional cases, and according to Raynaud[76] such masses would inevitably cause immediate death. Notwithstanding this affirmation, an ancient clot so voluminous as to fill an entire cavity has occasionally been found. Such an instance is the one referred to by Parrot,[77] where the left auricle was found distended by a stratified coagulum, whilst the other cavities were relatively empty. Generally, the volume of these clots varies from that of a walnut to that of a grain of millet. Sometimes they are flattened out, cover a large surface, and extend from one cavity into another. It is extremely infrequent to encounter a coagulum which fills more than the one-third or one-half of the cavity which contains it. These coagula have different shapes. They are ovoid, globular, sessile, pedunculated. Their number is usually in inverse proportion with their volume. When they have a certain mass and occupy the cardiac cavities they are often unique.

[Footnote 74: Cited by Bucquoy, _Des Concrétions sanguines_, Paris, 1863, p. 62.]

[Footnote 75: _Traité des Maladies du Coeur_.]

[Footnote 76: _Dict. de Médecine et de Chirurgie_, vol. viii. p. 565.]

[Footnote 77: _Dict. Encyc. des Sci. méd._, 1 Série, vol. xviii. p. 481.]

_(b)_ Warty excrescences, which deposit generally upon the surfaces or margins of the aortic or mitral valves, although they may be found adherent to other portions of the endocardium. These warty growths or vegetations are only so in appearance, for their real structure is mainly that of fibrin. Rarely do we find them in the right heart. They have a jagged mulberry or cauliflower aspect, and adhere to an otherwise healthy endocardial lining or to points where an alteration or fissure already exists. Sometimes they are in the form of rounded pedunculated masses, as described by Laennec,[78] and have given rise to no obvious symptoms during life. These deposits of fibrin should be distinguished from morbid growths and exuded lymph. The latter may be augmented in size by layers of fibrin, and may require close inspection to clearly differentiate them. The two preceding varieties of clot are often apparently due to some constitutional dyscrasia.

[Footnote 78: "Végétations globuleuses," _Traité d'Auscultation médiate_, t. ii. p. 630.]

_(c)_ Globular concretions or fibrinous cysts, the latter term being adopted on account of the well-known contents, which have a grumous or purulent appearance[79] and are of fluid consistence. They are limited by a cyst-wall, and are firmly attached to the walls of the heart either by a single pedicle or by a series of roots intertwined with the columnæ carneæ or musculi pectinati. Usually they occupy situations in the cardiac cavities somewhat removed from the direct current of the blood. The favorite situations for them are at the apex of the left ventricle or in the appendix of the right auricle. According to Rokitansky,[80] they almost invariably occupy the left ventricle, but the observations of later writers show conclusively that this is an error (Bristowe). Thus, Hayden states that in his belief the right chambers are much more frequently the seat of thrombosis than the left chambers. This difference is explained by the greater tendency to stasis in the right heart, where also there is less considerable muscular development. Of 44 fatal cases of valvular lesion, he cites 24 instances of cardiac thrombosis on the right side of the heart, and 12 instances on the left side. No case is reported by him in which the coagulum existed solely on the left side.[81] They have been found inserting upon the cardiac valves, and in this situation, owing to their pedunculated formation and varying position, have sometimes occasioned curious physical phenomena. A rare instance of this kind is cited by Walshe,[82] where, the mitral valve being perforated, the concretion caused at one time a systolic, at another a diastolic, murmur. They vary in size from a pullet's egg to that of a hazelnut, and exist singly in a cardiac cavity or are in considerable {739} numbers. When we attempt to detach them from the cardiac parietes, we frequently tear through some of their roots and leave small masses behind. When quite numerous they are also small in size, and may then be wholly lodged in the interspaces between the fleshy columns. Under these circumstances they are usually continuous with one another and extend their processes underneath the muscular bands, which are only attached by their extremities to the walls of the heart.[83] These clots have been found in the heart free of all attachments. In one such instance reported by Pitres[84] they were very numerous and were contained in all the cavities of the heart. This was a rare example. Their surface is usually smooth and the cyst-wall occasionally very thin. The cyst itself may be unilocular or divided into a number of smaller intercommunicating cavities. Occasionally, through rupture of the sac-wall, the contents have been emptied into the cardiac cavity outside. The color of these globular or ovoid concretions is buff or brick-red, and corresponds very nearly with the fluid contained in their interior. The different coloration of the contents is due mainly to the larger or smaller proportion of the coloring matter of the blood mingled with them. Sometimes these ancient concretions are covered by coagula of later formation, and it is only after close inspection that we can determine their real character. The endocardium is usually intact at their level, and rarely shows signs even of irritative inflammation. Hence we conclude that in an analogous manner with preceding forms of coagula they owe their existence to a constitutional alteration of the blood. Whilst the rule is that on section these globular concretions offer an interior consistence which is more or less softened, yet occasionally we encounter one in which the structure is homogeneous throughout, and presents very closely the appearance everywhere revealed by its external aspect. The elements, under these circumstances, of the sac-wall and the interior part of the concretion are almost identical. Under the microscope these are recognized as being mainly compound granular bodies, oil-globules, some imperfect cells, or altered blood-corpuscles surrounded by a network of fibrin. After a brief period, and in consequence of disintegration, the contents of these cysts may resemble pus and show certain differences in their constituents according to their appearance. "When white or buff-colored they consist almost solely, if not solely, of molecular matter, oil, and broken-down corpuscles, with which are frequently mixed compound granular cells and colorless acicular crystals. When presenting a brick-red or chocolate hue they exhibit, in addition to the elements just mentioned, numerous blood-corpuscles more or less altered, and consequently more or less indistinct, and occasionally also ruby-colored, rhomboidal, hæmatoid crystals."[85]

[Footnote 79: _Pathol. Society's Trans._, vol. xiv. p. 65 _et seq._]

[Footnote 80: _Path. Anat._ (Syd. Soc. trans.), vol. iv. p. 217.]

[Footnote 81: _Dis. of the Heart and Aorta_, Part ii. p. 1020.]

[Footnote 82: _Dis. of the Heart_, 4th ed., p. 106 _(b)_.]

[Footnote 83: Bristowe, in _Reynolds's System of Medicine_, vol. v. p. 107.]

[Footnote 84: _Bull. Soc. anatomique_, Feb. 5, 1875.]

[Footnote 85: Bristowe, on "Softening Clots in the Heart," _Path. Society's Trans._, vol. xiv.]

It is to the rupture of cysts of similar characters with those just detailed that may be properly ascribed pyæmic symptoms occasioned by the diffusion of their contents in the circulation.[86]

[Footnote 86: Ogle, _loc. cit._]

Coloration.--The color of ancient coagula varies from a dull white to that of a grayish, slightly yellowish, or slate tint. These extremes of color and all intermediary shades depend upon the age of the clot, the manner of its formation, the larger or smaller number of red corpuscles shut up in its fibrinous texture, and the chemical transformations it has undergone. In order that the opinion at first formed of the age of a clot by its coloration may be of some value, it is essential that this ocular examination may be further aided by the results of microscopic investigation. Occasionally, as already stated, the ancient coagula are covered by clots of late formation, but these may ordinarily be distinguished by even slight inspection.

{740} Consistence.--Usually the ancient coagula are firm, friable, and without elasticity. They are then readily detached from their insertions by traction, and always come away in small masses. On other occasions they offer considerable cohesion, and preserve their form when we attempt to tear through or break them. The degree of friability is in proportion with the regressive alteration of their substance. Sometimes the clinical history apparently indicates that a heart-clot has remained soft during several years (Walshe). Coagula, however, which have evidently been formed for a considerable period are frequently fibrinous or cartilaginous in their structure, and a deposit of calcareous material in their interior or upon their surface is occasionally found.

Organization.--The question as to whether the coagula formed within the cavities of the heart can become organized has been variously determined. Amongst those authors who speak of the progressive evolution of the clot, some admit the possibility, others absolutely deny it. That these cardiac clots are frequently coherent, firm, fibrous, or lamellated is no proof that they may become organized, since the same features prevail in the old coagula contained in an aneurismal sac. These latter, as we are aware, are readily separated from the membranous walls which surround them, and never take on a similar structure to theirs or give evidence of a new vascular formation in their interior (Legroux). Cruveilhier, Monneret, and Robin consider these coagula to be dead structures incapable of organization. Those who believe in the possibility of the clot becoming organized support their convictions by referring to certain rude resemblances with organized tissues; yet even these (Hunter, Laennec, Bouillaud) have never established their statements by any unquestioned examples. Moreover, we should remember that formerly investigations were made in a very imperfect manner. The instruments employed were insufficient and poorly adapted to accurate research of this kind. Whenever the organization of a clot was admitted, it was in connection with a preceding inflammation of the endocardium, which itself occasioned a plastic exudation. This exudation, becoming organized, was the means, according to them, of introducing a new vascular formation into the clot. According to the later researches of Virchow, Billroth, Feltz, etc., there can be no doubt as to the vascularization at times of ancient coagula contained in the vessels. In regard to cardiac coagula, we should urge the facts of their greater size and different situation as rendering their organization very improbable. Moreover, hitherto no experimenter has injected any vascular twigs in a cardiac thrombus. To sum up: whilst it appears possible that a cardiac clot may become organized in view of what has been shown to take place in vessels, still the facts thus far closely observed do not corroborate strongly this opinion, and we cannot pronounce ourselves in an absolute manner (Raynaud). Amongst the coagula least likely to become organized are the very large ones and those connected with the heart-walls by a narrow pedicle.

DIAGNOSIS.--From the preceding signs and symptoms can an accurate diagnosis be established of the presence within the cardiac cavities of fibrinous coagula? Evidently not if these formations be of small size and be situated where they do not interfere notably with the circulation. This is eminently true of those which are formed slowly in the auricular appendix or at the apex of the ventricle. In order that even a probable diagnosis of cardiac thrombosis should be made, it is essential that the coagulum should occupy a certain space, that it should be fixed near or at one of the orifices, or interfere in a perceptible degree with the valvular play. Due consideration is always to be had for etiological conditions when these can be wholly or in part known. If, for example, there be present an acute or chronic affection of the heart, and in a sudden manner, without apparent or sufficient {741} cause, the symptoms and physical signs pointing to greater disturbance of the function of this organ become developed, we naturally suspect the formation of a cardiac coagulum. And this is true, although the signs of this production are not dissimilar to those indicating structural heart disease. Thus, the rapid development of præcordial dyspnoea, of rapid, tumultuous action of the heart, of feeble, depressible, irregular pulse, and of extreme pallor or lividity of surface, combined with coldness of the extremities and extreme anxiety, gasping for breath, and jactitation, indicate under like circumstances the formation of heart-clot. This diagnosis is further confirmed when upon listening to the respiration we find that the air enters and goes out of the lungs freely, and that there is no evidence in the lungs of any sudden obstruction or inflammatory condition. Of course it is very important for the physician to be familiar with the patient's previous condition and antecedents. If the accidents just referred to become developed without these facts being known, it would be far more difficult to make a diagnosis of cardiac clot than when the accidents take place whilst the patient is being constantly watched and when the physical state never varies without being observed and noted. If there be a venous obstruction in one of the large veins of the limbs, either at the time or prior to the formation of the cardiac thrombus, the symptoms occasioned by it will give even more significance to those which show heart trouble. The same information is also afforded by sudden obstructions in different portions of the arterial channels; and whenever these embolic transports take place they show, with tolerable certainty, the pre-existence of an intra-cardiac thrombus. As we can readily understand, it is far less practicable to make the diagnosis of a clot which develops slowly, and therefore gives rise to symptoms gradually, than of one which has manifested itself more or less suddenly.

The physical signs of cardiac thrombosis as a complication of cardiac disease are not necessarily very significative. This is true, first, because there may not be an abnormal murmur owing to the weakness of the cardiac contractions; second, because (even if it be present) the murmur may be readily confounded with one already existing which is occasioned by organic heart disease. Theoretically, the first sound of the heart should be muffled by the presence of a coagulum of any notable size which interferes with the play of the valves, but this might be also occasioned by the presence of chronic cardiac valvulitis. Still, if an abnormal murmur, harsh or soft in character, become suddenly developed over the pulmonary or aortic orifice, where it was known not to have previously existed, it is a physical sign which points with much certainty to the presence of a heart-clot. Whenever the signs and symptoms given above which show disturbance in the heart's action occur in a similar sudden manner in the course of an inflammatory or cachectic disease, such as pneumonia, cancer, or phthisis, we should properly suspect the formation of an autochthonous or embolic clot in the heart. These formations arise also, not infrequently, as an instantaneous complication in the duration of acute articular rheumatism, certain of the eruptive or acute fevers[87]--_i.e._ measles, scarlatina, etc.--and the puerperal state, as we have already pointed out in another portion of this article. In pneumonia, as in the other affections just mentioned, if no fresh inflammatory area either in the lungs or in another viscus can be discovered which is sufficient to explain the occurrence of new alarming symptoms of obstructed circulation, the difficulties of a correct diagnosis are much less than if organic heart disease be present. And this is particularly true because another solution of the cause of the patient's condition is less available (Flint). Besides, if it be sure that suddenly an endocardial murmur is developed where none existed previously, this sign, {742} taken with the striking rational and other symptoms referable to the heart, is one of great corroborative value as regards diagnosis. Not only does cardiac thrombosis occur under the circumstances mentioned already when we have a certain right to expect it by reason of its relative frequency, but occasionally it will become evident by its symptoms under conditions where we have no right to look for its development. In these instances it is only by a diagnosis of exclusion that we can discover the correct interpretation of the phenomena presented. In the obstruction caused by a heart-clot developed in the right cardiac cavities there is of course stasis in the systemic venous circulation in consequence of the small quantity of blood which can pass through the heart on its way to the lungs. This condition, moreover, develops a peculiar dyspnoea which has been very striking at times, and which has been particularly considered by Richardson,[88] so as to differentiate it with an analogous but dissimilar state which prevails when the obstruction exists in the lungs or other portions of the respiratory tract. In the former case if we listen carefully to the breathing the vesicular murmur is normal in quality and pitch, although of exaggerated intensity, and the dyspnoea is evidently due to the fact that the air lacks, so to speak, a sufficient quantity of blood to arterialize it. Consequently, the surface of the body is pale rather than cyanosed, and the heart-sounds and pulse are feeble, tumultuous, or notably irregular. In the latter case the lungs are congested or there is some other evident obstruction of the larynx, trachea, or bronchial tubes which prevents the entrance into the alveoli of a sufficient quantity of blood for the purposes of hæmatosis. Hence a rapidly generalized cyanosis becomes developed, the superficial veins are generally turgescent over the surface of the body, and what with the irregular, feeble action of the heart, although its normal sounds are distinctly defined, the violent convulsive movements of the voluntary muscles, the abolition of the intelligence of the patient toward the fatal termination, we have a sufficient number of signs which point distinctly to an asphyxic state. Finally, at the end of life in the former case it is the heart which first comes to a stop, whereas in the latter the lungs are the organs which are primarily arrested in their movements. These differential signs have great practical importance. Unfortunately, there are instances in which it is extremely difficult to assign in proper degree the symptoms occasioned by the heart-clot on the one hand or obstructed respiration on the other.

[Footnote 87: Keating, _Am. Journ. Med. Science_, Jan., 1885, p. 122, v.--an able article, entitled "Heart-Clot as a Fatal Complication in the Acute Fevers of Childhood."]

[Footnote 88: _Medical Times_, vol. i. p. 330, 1856.]

We have in another place pointed out this fact where at the same time there was present a membranous deposit of diphtheritic membrane blocking up the calibre of the larynx and a cardiac coagulum distending the right cardiac cavities.[89] In like manner, there may be an inflammatory complication in the lungs themselves--_i.e._ broncho-pneumonia--which by its sudden beginning and the rapid rise in the number of the respirations and the pulse should awaken a suspicion as to the cause of these symptoms. An error in regard to the modifying influence of this accident would be possible were it not that broncho-pneumonia, even of limited extent, reveals itself by stethoscopic signs, and, moreover, would not explain all the phenomena which arise. These are: the excessive pallor, the special kind of anxiety, the weakness and inequality of the pulse, the muffled heart-sounds, and the very rapid death. In exceptional instances, when the lungs are merely affected with hyperæmia, the characteristic signs of cardiac thrombosis are more readily recognized.

[Footnote 89: Robinson, _loc. cit._, p. 48.]

That form of uræmia known as the dyspnoeic or respiratory, which has been well described by Fournier, is sometimes confounded with heart-clot. Its commencement is often sudden. Soon labored respiratory action is very marked, and approximates true orthopnoea, although there is absence of {743} pulmonary lesion. From the cardiac disturbance it can be differentiated by the pulse, the cardiac rhythm, bodily pallor, and the usual evidences of kidney disease.

The distinguishing features between pulmonary embolism or thrombosis and the deposit of fibrinous coagula in the heart are extremely difficult to delineate. At times the cardiac coagula manifest their existence quite as suddenly as does pulmonary embolism. Nothing, moreover, prevents the formation[90] at a simultaneous moment of a coagula in the veins as well as in the heart. The puerperal condition, which is a predisposing cause of an excessive relative amount of fibrin, is likewise an efficient cause of both these formations. Besides, we should add, there is no reason why the fibrinous coagulum of the heart in changing position should not throw off a plug which will block up the pulmonary artery completely. To separate these conditions or to make a diagnosis between them other than one based upon probabilities is not possible.[91]

[Footnote 90: Ball, _Des Embolies pulmonaires_, Paris, 1862.]

[Footnote 91: Vernay, _Gaz. médicale de Lyon_, Nos. des 13 Mars et 22 Mars, 1868.]

We do not consider it essential in this place to go farther and make known the signs by which we shall be able to distinguish cardiac thrombosis from certain affections of the larynx, such as laryngitis stridulosa, oedema glottidis, and membranous laryngitis, or indeed from asthma or functional disturbance of the heart. It is easy, indeed, to confound this affection with organic cardiac disease, but what we have already said should enable us to make the distinction with facility. In certain infectious diseases, and more particularly diphtheria, death by cardiac paralysis has been described. In these instances there would seem to be a real impairment, functional or organic, of the structure of the pneumogastric nerves, which is accompanied by an irregular action of the pharyngeal muscles, by vomiting,[92] extreme slowness of the pulse,[93] a remittent form of syncopal attacks, and powerless action of the heart. No such combined symptoms appear in our description of cardiac thrombosis, and they are therefore sufficient, in our opinion, to substantiate the opinion of a morbid entity which can be satisfactorily explained by recognizing solely a lesion of nerve.

[Footnote 92: Jenner, _Diphtheria, its Symptoms and Treatment_, London, 1861, p. 42 _et seq._]

[Footnote 93: Maingault, _Actes de la Société méd. des Hôpitaux_, 5^{ème} Fascicule, 1861, Obs. 40.]

In many examples of death by heart-clot the aspect of the patient is very much that of one who dies in the period of a collapse from cholera (Flint), the great difference between the two states consisting in the fact that in the latter there is no notable degree of dyspnoea.

The diagnosis between coagulum of the right and left side of the heart can be determined with some accuracy if strict attention be paid to the effect of the presence of the clot on the normal cardiac murmurs. If, for example, the clot is situated in the right ventricle, it is probable that by interference with the tricuspid play it will render the valvular sound occasioned by closure less distinct, and for this reason the first sound of the heart will not be heard as well to the right as to the left of the sternum. In a similar way, the diminution of sound at the pulmonary orifice in the left second intercostal space may be explained, for the extension of the concretion into the origin of the pulmonary artery will almost certainly prevent the perfect closure of its cusps (Richardson). In deposits of fibrin in the left cavities of the heart we naturally distinguish less well the cardiac sounds along the left border of the sternum than toward its right margin. We also have congestion of the lungs, owing to the fact that a smaller quantity of blood is able to pass through the partially-filled left heart. To this is added a tumultuous, irregular action of the heart and a feeble pulse. It is proper to add, however, that excepting cases of chronic organic heart disease with dilatation or {744} degeneration of the walls deposits of fibrin in the left heart are relatively very infrequent.

In cases of acute endocarditis we have no means usually to distinguish between the general symptoms of nervous shock and the physical signs occasioned by cardiac thrombosis on the one hand, and rupture of a valve or tendinous cord on the other. According to Walshe, this could scarcely be otherwise, as clotting to a greater or less extent must necessarily deposit around the spot where the tear takes place. In view of a case reported by Hammer[94] of sudden cardiac failure in which the symptoms prior to death pointed to possible intra-cardiac thrombosis, and where at the autopsy thrombotic occlusion of one of the coronary arteries was found, it is well to bear in mind the possibility of this rare occurrence. The principal features of this case were the suddenness of the collapse, pallor, slight dyspnoea, and extremely slow pulse, ranging from 23 to 8 to the minute!

[Footnote 94: _Abstract of Med. Science_, 1878, p. 208; _Lond. Med. Rec._, March 15th.]

PROGNOSIS.--The prognosis of fibrinous coagula in the cavities of the heart is always extremely serious. The gravity of the situation is, however, in some degree proportionate to their size, their situation, and the rapidity of their formation. Thus, for example, those which are spread out like a membrane over the interior surface of the heart, as has been noted after endocarditis, are of less serious a nature than those which are polypiform. As regards the polypiform concretions which we encounter singly, which are small and formed slowly, they will be so much more dangerous as the lobe held by the pedicle can become engaged in the orifices of the heart or the vessels which take origin from it.[95] Certain well-known observers, it is true, such as Bouillaud, Barth, Roger, Racle, Meigs, and Armand, have stated their belief that in rare instances these coagula may become dissolved and disappear. Indeed, we ourselves have become convinced in more than one exceptional case that the morbid phenomena manifested, both local and general, were but the evident proofs of the beginning of fibrinous deposit in the right ventricle of the heart, and yet we have seen these evidences change their characters and finally disappear under proper treatment, leaving the patients ultimately in as good health as they were previous to their formation.[96]

[Footnote 95: Armand, _Des Concrétions fibrineuses polypiformes du Coeur_, Paris, 1857, p. 49.]

[Footnote 96: We are more assured in regard to this possibility than we were ten years ago (v. Thesis).]

Legroux does not believe cardiac concretions can be reabsorbed, and with Cruveilhier he admits them to be dead formations. Nevertheless, he admits that fibrinous cysts may entirely disappear by a process of progressive liquefaction. Moreover, a case reported in his exhaustive article which he observed makes him acknowledge that a fibrinous coagulum may diminish, retract, atrophy, form adhesions with the cardiac walls, and thus not interfere notably with the cardiac functions.[97] The fact, however, that there may be no present suffering does not shield such a patient surely from future accidents of a serious nature brought on by his intra-cardiac condition. About the diagnosis, however, of intra-cardiac thrombi, especially when a perfect cure has been established, there always will remain an element of justifiable doubt, and particularly in those conditions where an underlying constitutional dyscrasia of grave import was present. This latter state of itself often becomes either rapidly or eventually mortal. Apart from the gravity of cardiac thrombosis in view of its evidently pernicious influence upon the heart, it is likewise a very serious affection on account of the possibility of its giving rise to embolic transports into different viscera (brain, lungs, etc.), which themselves may bring about a direct and speedy fatal termination. Even when the embolic plugs do not occasion such considerable obstructions {745} of important vascular channels as to cause rapid death, they may fill up numerous capillaries of the economy with material of a kind which shall be followed, sooner or later, by septic symptoms or those of pyæmic poisoning.

[Footnote 97: _Gazette hébdomadaire_, 1856.]

TREATMENT.--According to certain well-known authors, all curative treatment of heart-clot is useless (Bucquoy). Others, more sanguine, repose confidence in the internal use of alkalies, even when a fibrinous deposit in the cavities of the heart has commenced to form. A third class of observers, whilst they doubt the efficacy of any treatment under these circumstances in causing the disaggregation or absorption of an intra-cardiac coagulum, nevertheless believe we can limit the rapidity and size of its formation, and also retard the fatal termination, by giving time sufficient for adhesions to form with the cardiac walls. Richardson has proposed the administration of minim x doses of liquor ammoniæ at short intervals in an ounce of water, in order to dissolve existing coagula, and reports favorably upon its use. Gerhardt[98] counts upon better results from the use of a saline spray of bicarbonate of sodium of the strength of ½° to 1½°. This spray should be frequently inhaled, and in this manner, he believes, the heart is reached more directly and effectually. Successes are claimed by the use of this method of treatment. According to Flint,[99] the idea of giving any remedies with a view to dissolve solidified fibrin is absurd, whereas as a preventive treatment it is legitimate in circumstances where this state is likely to occur, and may even become an important therapeutic object.

[Footnote 98: _Deutsches Archiv für klinische Medicin_, vol. v. p. 207, summarized in the _Dublin Quarterly Journal of Medical Sciences_, May, 1869, p. 421, quoted by Walshe.]

[Footnote 99: _Diseases of the Heart_, p. 285.]

Alkaline remedies are said to have the power of holding the fibrin of the blood in solution. If this be true, they are certainly indicated to prevent coagulation. Moreover, if the fibrin in normal blood be held in solution owing to the presence of ammonia, it must be evident that this remedy is specially indicated in carrying out a secondary object of the prophylactic treatment. Bartholow[100] still maintains, however, that frequent small doses of ammonium carbonate afford the best chances of relief even when the coagulum is already formed. The latter distinguished author advises in cases which are most imminent intravenous injections of ammonia. The proportions should be one part of ammonia to three of water. The vein selected must be the jugular, and special precautions taken to avoid the entrance of air or a foreign body into the circulation. With attention to this formal indication there is little or no danger from these injections, as has been many times proven experimentally. Walshe[101] regards the use of carbonate of ammonium, combined with bicarbonate of potassium, in five-grain doses, repeated three times daily, as a mere prophylactic, but as the best, after all, we possess, and recognizes from its use the only practical outcome from the enormous sacrifices of canine life made by Magendie in his experiments to illustrate his lectures on the blood. In spite of the numerous attempts to fluidify the blood, these efforts have always remained unsuccessful (Raynaud), and Legroux, who first proposed it, in his later writings abandoned the alkaline treatment as useless. The most he affirms that can be done is to combat with energy cardiac inflammations.

[Footnote 100: _Practice of Medicine_, New York, 1880, p. 285.]

[Footnote 101: _Diseases of the Heart_, 4th ed., London, 1873.]

There is, however, a palliative medication which is indicated by the presence of the obstacles to the circulation within the heart. The general condition must be kept in view in carrying out treatment rather than the local signs. A properly combined therapeutic method in which the derivatives and counter-irritants play an important rôle offers, in Legroux's estimation, the best solacing means to oppose to the developed accidents. We must, however, maintain the patient in a quiet attitude and administer drugs which {746} shall tranquillize pain and diminish anxiety. The counsel to keep the patient absolutely at rest is of primary importance in view of the sudden fatal accidents which have frequently occurred either in getting into bed after descending from it, or in sitting up and reaching for something the patient needs. The patient should be placed in bed in a semi-recumbent position, properly supported, and arrangements must be made so that all fatigue of eating and drinking or attending to his excrementitial functions are provided against. Of course we should treat a case of cardiac thrombosis complicating a frank inflammatory condition, such as acute endocarditis, certain forms of pleurisy or pneumonia, very differently from a case in which the state is one of relative feebleness or adynamia, as in the advanced stages of diphtheria, or after profuse uterine hemorrhage during or after confinement. In the first category of cases it may be in a few rare instances that local depletion of the blood by means of leeches or venesection is still indicated, especially if the patient be one of more than usual vigorous frame. In any example of this sort it is obvious that the internal use of the alkalies, the employment of revulsives (_i.e._ dry cups), and counter-irritants over the chest (as previously mentioned), adjoined, perhaps, to the action on the emunctories by diluent drinks, are the means which offer us the best guarantee of success. But how shall we act with our second class of cases? Certainly, we ought not for one moment, with our actual physiological knowledge, to consider the propriety of taking blood from a patient thus affected. May we use the alkaline treatment with reasonable hopes of benefit in a curative way? Yes, if we employ certain of the stimulating salts, like carbonate of ammonium, or even this salt combined with moderate doses of bicarbonate of potassium. We should remember, however, that these drugs are intended particularly to combat the pathological condition of the blood which apparently underlies the formation of fibrinous concretions in the heart.

Against the possible fatty degeneration of the cardiac muscular fibre, or the functional or organic affection of the pneumogastrics, which predispose to or accompany the production of cardiac coagula, we must make use of digitalis in small, repeated doses, and nux vomica or some other preparation containing strychnine. I have on more than one occasion seen these agents do evident good,[102] and on this account am encouraged to urge their exhibition. With Hertz, we are not disposed to believe that digitalis, when given with a little precaution, and especially in urgent cases, is contraindicated by the danger feared by Gerhardt and Penzoldt, that it favors thrombosis of the right side of the heart and gives rise to new emboli.[103]

[Footnote 102: _Loc. cit._, p. 68.]

[Footnote 103: _Ziemssen's Cyclopædia_, vol. v. p. 326.]

It is almost needless to add that under like circumstances we should insist upon the frequent use of stimulants, like alcohol, chloroform, and ether, in the form of brandy, whiskey, spiritus chloroformi, or spiritus ætheris, or repeated doses of strong black coffee with one of the preceding preparations added to it. In regard to the prophylactic use of alkaline treatment continued during several days and in large or frequently-repeated doses, we advise against it for the reasons, first, that we do not know, in advance, the precise conditions in which fibrinous intra-cardiac coagula will form; and second, because though the alkalies have a well-known antiplastic action, they act as depressants to the general economy when employed in the manner mentioned, which is the sole method in which their internal use would be of some practical advantage.

Whenever we have in diphtheria a case in which there is at the same time obstruction of the glottis by a false membrane and clogging of the heart by a fibrinous coagulum, we should abstain from performing tracheotomy on account of its evident uselessness.[104]

[Footnote 104: _Medical Times_, vol. ii. p. 617.]

{747}

NEUROSES OF THE HEART.

FUNCTIONAL DISORDERS OF THE HEART'S ACTION; ANGINA PECTORIS; EXOPHTHALMIC GOITRE.

BY AUSTIN FLINT, M.D.

The neuroses of the heart are those affections relating to this organ which do not necessarily involve either inflammation or structural lesion of any of its component parts. The larger proportion of these affections may be grouped under the name functional disorders of the heart's action. The affection called angina pectoris is characterized by pain more or less intense. It is generally associated with disordered action of the heart, and also with cardiac lesions. It may, however, exist without either disordered action or lesion, and hence it is with propriety included among the neuroses of the heart. Exophthalmic goitre is invariably associated with disordered action of the heart, but it has other very marked symptomatic traits which give to it a distinctive character. The name of the affection refers to these. The cardiac disorder is, however, the most constant, and, pathologically, the most important, and therefore the affection may be considered as one of the neuroses of the heart. In this article the functional disorders of the heart's action, irrespective of angina pectoris and exophthalmic goitre, will be first considered, and afterward these two affections will receive separate consideration.

Functional Disorders of the Heart's Action.

The disorders of the heart's action which agree in respect of their functional character present marked variations as regards the manner in which the action is disordered. An account of these will be given under the name Varieties, together with the symptomatology.

VARIETIES AND SYMPTOMATOLOGY.--The term palpitation denotes a violent or tumultuous action of the heart. A type of this variety of disorder is afforded when the heart is much excited by fear or some other intense mental emotion. The fact that emotional excitement will produce in some persons notable palpitation, and in others little or no disturbance of the heart's action, illustrates differences inherent in the organ itself as regards susceptibility to disorder. These innate differences are exemplified in cases of disease. In certain persons the heart readily takes on a morbid functional disorder from causes which in other persons do not produce this effect. A peculiar susceptibility to disorder is expressed by the term irritable heart, a term introduced by DaCosta. Instead of the violence which characterizes palpitation, there may be irregularity, with notable feebleness of the heart's action. The patient often describes this variety of disorder as a fluttering of the heart. The consciousness of the disorder is less distinct than when the {748} disordered action is violent. With irregularity are generally associated increased frequency of the heart's action and præcordial distress. The degree of disorder as respects either violence or feebleness and irregularity of action differs in different cases within wide limits. Intermittence is another variety of disorder. The intermission may extend over a period of one, two, three, or more beats. It is sometimes preceded or followed by increased frequency of action, and it sometimes occurs without any other rhythmical disturbance. The patient is usually conscious of the intermittence, and it is apt to occasion great alarm, especially before the mind has become accustomed to it. The intermissions occur more or less frequently in different cases and at different periods in the same case. In the cases of palpitation in which the heart acts with violence it is not probable that the power of the heart's action is increased. The systolic ventricular movements are quick and have a spasmodic violence, without actual increase of force. The first sound of the heart over the apex under these circumstances is short and its quality valvular. The valvular element of this sound is predominant and intensified in consequence of the quickness of the systolic movements and the small quantity of blood in the ventricles when the ventricular systole takes place. Owing to the latter physical condition the range of movement of the auriculo-ventricular valves is greater and the valvular sound proportionately increased. The systolic movements of the apex against the chest-wall sometimes give rise to a ringing or metallic sound (cliquetis métallique).