Volume 3 — DISEASES OF THE BLOOD, AND OF THE HÆMATOPOIETIC SYSTEM. (continued 6)

⁴³ Am. Journ. Med. Sciences, April, 1864.

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 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

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.

⁴⁶ Med. Times and Gazette, vol. i., 1873, p. 58; also Pathol. Soc. Trans., vol. xxvii. p. 70.

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 diphtheria⁴⁸ and pneumonia such examples are not infrequently encountered. As Austin Flint⁴⁹ 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. Bristowe⁵⁰ 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.

⁴⁸ Robinson, loc. cit.

⁴⁹ Diseases of the Heart, p. 276, Philada., 1870.

⁵⁰ Reynolds's System of Medicine, vol. v. p. 113.

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 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 (Laennec⁵²). 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

⁵² Dict. Encycl. des Sci. méd., article "Concrétions sanguines."

⁵³ Edin. Med. Journal, April, 1868, v.—case by H. Douglas.

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. Feltz⁵⁶ 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.

⁵⁵ Brit. and Foreign Med.-Chir. Review, Oct., 1871.

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 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

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.

⁵⁸ Dict. Encycl. des Sci. méd., loc. cit.

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 Hayden⁶⁰ 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."

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.

⁶¹ A Textbook of Practical Medicine, 1869, vol. i. p. 156.

⁶² The Human Lung, 1860, p. 201.

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 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.

⁶³ Magendie, "Lectures on the Blood," Lancet, 1839.

⁶⁴ Dict. de Médecine, t. viii. p. 560, Paris, 1868.

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.

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 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, Poullet⁶⁸ has endeavored to prove irrecusably by experiments upon animals 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.

⁶⁷ Cycl. of Anatomy and Physiology, p. 114, 1848.

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.

⁶⁹ Dict. de Méd. et de Chirurgie, vol. viii. pp. 562 and 565.

⁷⁰ De la Thrombose cardiaque dans la Diphthérie, Paris, 1872.

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

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, Parrot⁷³ 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."

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 exceptional cases, and according to Raynaud⁷⁶ 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.

⁷⁴ Cited by Bucquoy, Des Concrétions sanguines, Paris, 1863, p. 62.

⁷⁵ Traité des Maladies du Coeur.

⁷⁶ Dict. de Médecine et de Chirurgie, vol. viii. p. 565.

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.

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 appearance⁷⁹ 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 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 Pitres⁸⁴ 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

⁷⁹ Pathol. Society's Trans., vol. xiv. p. 65 et seq.

⁸⁰ Path. Anat. (Syd. Soc. trans.), vol. iv. p. 217.

⁸¹ Dis. of the Heart and Aorta, Part ii. p. 1020.

⁸² Dis. of the Heart, 4th ed., p. 106 (b).

⁸³ Bristowe, in Reynolds's System of Medicine, vol. v. p. 107.

⁸⁴ Bull. Soc. anatomique, Feb. 5, 1875.

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

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.

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 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 fevers⁸⁷—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, 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.

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."

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.

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 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 formation⁹⁰ 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

⁹⁰ Ball, Des Embolies pulmonaires, Paris, 1862.

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.

⁹² Jenner, Diphtheria, its Symptoms and Treatment, London, 1861, p. 42 et seq.

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 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 Hammer⁹⁴ 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!

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

⁹⁵ Armand, Des Concrétions fibrineuses polypiformes du Coeur, Paris, 1857, p. 49.

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 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.

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. Gerhardt⁹⁸ 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.

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.

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. Bartholow¹⁰⁰ 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. Walshe¹⁰¹ 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.

¹⁰⁰ Practice of Medicine, New York, 1880, p. 285.

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 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

¹⁰² Loc. cit., p. 68.

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

¹⁰⁴ Medical Times, vol. ii. p. 617.

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 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).

A rare variety of functional disorder which has received but little attention is notable infrequency of the heart's action. The revolutions of the organ were reduced to sixteen per minute in a case reported by Thornton.¹ In 1876, I reported 5 cases, the reduction in frequency varying from 26 to 40 per minute.² In one of these cases there was marked intermittency, and in another case the action of the heart was irregular. With these exceptions the rhythm was regular. I have met with a few additional instances since these cases were reported. In this variety the disorder continues for several successive days, and it may be for a much longer period. A persistent infrequency sometimes remains as a sequel, recovery in other respects being complete. In one of my reported cases the revolutions were 36 for several weeks after recovery. In these instances the infrequency of the heart's action, which is sometimes a congenital peculiarity, is acquired. Hewan has reported his own case as an illustration of this fact. His normal frequency had been 72, but after a period of intense study the frequency gradually decreased, and finally remained at from 28 to 32 per minute.³ This variety of disorder will claim distinct consideration with reference to diagnosis and etiology. It may or may not be accompanied by præcordial distress.

¹ Trans. Clinical Society of London, vol. viii., 1875.

² American Practitioner, January, 1876.

³ London Med. Times and Gazette, March, 1875.

The more frequent varieties of disorder of the heart's action occur in most instances in paroxysms. The paroxysms differ widely in duration as well as in their intensity. They may last for an instant only or for many continuous days. Exceptionally the duration is much longer. I have known a persistent and very great increase of frequency of the heart's action with irregularity, and such a degree of weakness that the pulse could with difficulty be counted, to continue for several weeks, leading to oedema of the lower limbs, prostration, and pallor, so that the patient's appearance was that of one moribund. In this case before the attack and after recovery there was no evidence of any other affection than functional disorder of the heart, and to this the patient had long been subject. In another case an extremely irregular action of the heart continued unceasingly for more than two months, there being no signs of either an inflammatory or a structural affection of the organ, and the functional disorder at length ceasing. As a rule, an attack of functional disorder of the heart implies a liability thereto; other attacks occur after variable intervals. This fact involves a peculiar susceptibility, or, in other words, an irritable heart.

The symptoms referable to the heart may be combined with those of coexisting affections. Disturbances of digestion are frequently associated. Paroxysms of disordered action of the heart are often accompanied by gastric flatulence, and gaseous eructations afford relief. Patients are apt to endeavor to eructate by voluntary efforts. Other evidences of indigestion are not infrequent. The mind is much disturbed, especially if previous paroxysms have not occurred. The facial expression shows anxiety. The apprehension is of organic disease of the heart and of sudden death. This apprehension is excited in a marked degree by intermittence of the heart's action. It is often extremely difficult to convince patients of the absence of immediate danger. They require to be assured of this fact over and over again, and whenever a paroxysm occurs. This statement applies even to medical men who suffer from functional disorders of the heart's action. The surface is usually cool or cold. It is sometimes bathed in perspiration—a symptom probably due, in a great measure, to the condition of mind. Exclusive of angina pectoris, paroxysms of functional disorder are not attended by præcordial pain. The paroxysms may cease either suddenly or after a gradual improvement. The cessation is abrupt in the instances in which the paroxysms last but an instant or but a few moments, and not infrequently when the paroxysms are of much longer duration the normal rhythmical action is at once resumed.

The variety of disorder characterized by diminished frequency of the heart's action is often associated with cerebral disturbance. In 2 cases cited in my paper there were severe epileptiform seizures, together with frequent epileptoid attacks; in 2 cases there was mental excitability amounting to delirium; and in 1 case there was great mental and physical prostration with gastric irritability, the latter due apparently to cerebral disturbance. In 1 case only there was no evidence of disorder of the brain. Of 3 cases which have fallen under observation since the publication of my paper, in 1 there was notable mental disturbance, the mind remaining intact in the other 2 cases.

DIAGNOSIS.—Certain facts pertaining to functional disorders of the heart's action in their ordinary paroxysmal forms render the diagnosis probable. One of these is the occurrence in paroxysms, the action of the heart being normal in the intervals. Another fact is the occurrence of the paroxysms at night oftener than in the daytime. The ability of the patient to take active exercise without exciting a paroxysm and without discomfort is evidence that the paroxysmal affection is functional. A diagnostic feature of a purely functional disorder is great apprehension connected with the disordered action of the heart. The patient is apt to feel that there is imminent danger of sudden death. So strong is this apprehension that it is sometimes difficult to overcome it by positive assertions of the absence of danger. On the other hand, disordered action of the heart, when incident to structural affections, occasions comparatively little mental disturbance; the patient suffers chiefly or exclusively from the physical ailments. In a purely functional affection the patient generally is vividly conscious of the disordered action, whereas the action in structural affections may be greatly disordered and the patient take no cognizance of it. The existence of certain causes to be mentioned under the head of the Etiology bears upon the diagnosis. The liability to functional disorders, as evidenced by previous attacks, is also to be taken into account. These facts, however, are not fully adequate for the exclusion of structural affections of the heart. Moreover, the persistence in some cases of notable disorder for days, weeks, or even months, would seem to render highly probable the existence of some structural affection. The basis of a positive diagnosis is the exclusion, by the absence of their physical signs, of inflammatory affections and lesions of structure.

The physician who undertakes to diagnosticate functional disorders of the heart by symptoms alone—that is, without physical exploration—must often be in doubt, and if not prudently distrustful of his ability as a diagnostician, he is liable to commit errors which are sometimes extremely unfortunate. I was requested to see a young woman who was represented as suffering from a disease of the heart from which she might die at any moment. It was stated to me that her situation was perfectly understood by herself and her family, and that the object of my visit was simply to satisfy some of her friends. I found her in a dark room, with every arrangement to prevent the least mental excitement and physical exertion. Fearing that my questions and the examination of the chest might occasion disturbance which would prove fatal, it was proposed that one of her family be made the medium of the former, and that the latter be dispensed with. This was of course objected to on my part. My questions she answered in a feeble whisper. The examination of the chest showed the absence of all physical signs of disease. The affection was purely functional and wholly devoid of danger. I could cite from cases which have come under my observation not a few in which the error of imputing functional disorders to organic lesions has occasioned the loss of years as regards the duties and pleasures of life, together with the unhappiness incident to living in daily expectation of sudden death. With a degree of practical knowledge of auscultation and percussion sufficient to recognize the signs of inflammatory and structural diseases, and self-confidence sufficient to decide upon the absence of these signs, there is but little liability to error in the diagnosis of functional disorders.

If the apex-beat be in its normal situation, and the areas of the superficial and deep cardiac regions be not extended, the heart is not enlarged; and if there be no endocardial murmur it may be inferred that the valves and orifices are normal. The exclusion of structural lesions under these circumstances is almost positive. It is open only to the exception that certain occult lesions may exist, such as fatty degeneration and obstruction of the coronary arteries. Aside from the infrequency of these, the history and symptoms may render their existence extremely improbable. A hæmic murmur at the aortic or the pulmonic orifices or at both orifices is not uncommon. That the murmur is inorganic may generally be determined by other evidences of anæmia, by an arterial murmur in the neck, and by the venous hum. With the results of physical exploration as just stated, whatever may be the form of disorder, whatever may be its intensity, whatever may be its duration, and whatever may be the associated symptoms, it may be declared to be purely functional.

The diagnosis is less simple and easy when functional disorders occur in connection with structural lesions, but without any relation of cause and effect. Lesions affecting the valves or orifices of the heart often exist without giving rise to any appreciable disturbance. They are either innocuous or their effects do not occasion any inconvenience of which notice is taken. How often is it that an examination of the chest reveals the signs of cardiac lesions which had not been suspected by either the patient or the physician! How often are applicants for life insurance astonished when told that they are not insurable on account of the signs of a cardiac affection! Now these persons are liable to functional disorders of the heart from the causes which produce them in those with perfectly sound organs, the cardiac lesions having no part in the etiology, but perhaps contributing to render the disorders more intense. The problem of diagnosis in these cases is to determine that the functional disorders are not dependent on the lesions. Were they thereon dependent they might denote grave disease, but if not thus dependent they have little or no gravity. This diagnostic problem is to be solved, in the first place, by attention to the inquiry whether the lesions are in proportion to the disturbance of the heart's action. Valvular lesions, if the heart be but little or not at all enlarged, are either innocuous or occasion small inconvenience. This fact will often suffice for the solution of the problem. Moreover, the physical signs may show that the lesions involve neither valvular insufficiency nor obstruction, or, at all events, not in a degree adequate to account for the disturbed action; in the second place, the symptoms are to be considered with reference to the inquiry whether they belong to the clinical history of structural affections or of functional disorders; and, in the third place, the existence of any of the well-known causes of functional disorders is to be taken into consideration. The error is not uncommon of attributing functional disorders to coexisting lesions when the connection is one of mere coincidence. This error may be as unfortunate as that of supposing that functional disorders denote structural affections when the latter are entirely wanting.

Certain considerations, aside from the exclusion of organic affections of the heart, apply particularly to the diagnosis of that variety of functional disorder characterized by infrequency of the heart's action. It is to be ascertained that the infrequency is not a normal peculiarity, either congenital or acquired. Napoleon the Great was a well-known instance of normal infrequency, the number of beats being 40 per minute. As a rule, if an intelligent adult person has habitually a notably infrequent pulse he becomes acquainted with the fact, and therefore if he be ignorant of such a peculiarity it may be inferred that it is not normal.

There is a curious form of functional disorder which would lead to the error of inferring infrequency of the heart's action from the pulse. The disorder is characterized by the regular alternation of a ventricular systole giving rise to a radial pulse, with one too feeble to be appreciated at the wrist. Assuming the number of ventricular systoles to be 70 per minute, in such a case the radial pulse would be 35 per minute. I have met with several examples of this form of disorder in which, as may be said, there is a regular irregularity of the heart's action. The carotid pulse in these cases represents each ventricular systole, and on auscultation of the heart's sounds there will be found to be four sounds to each radial pulse. This form of disorder is liable to lead to the error of supposing reduplication of both the first and the second sound of the heart. It is hardly necessary to add that in cases of obstructive and regurgitant lesions with feebleness of the heart's action the diminished quantity of blood expelled from the left ventricle, with some of its contractions, may be too small to produce an appreciable radial pulse. The existence of these cardiac lesions is easily ascertained by auscultation.

Infrequency of the heart's action is a well-known symptom in cases of injury of the skull and in certain intra-cranial affections. Cerebral hemorrhage, embolism, and thrombosis are easily excluded by the absence of paralysis, but the exclusion of subacute or chronic meningitis is not so easy. But infrequency of the heart's action, when a symptom of the latter affection, is accompanied by cerebral symptoms denoting compression of the brain—symptoms which are wanting when the infrequency is the characteristic of a functional disorder of the heart's action. Moreover, the absence of fever, of increased sensibility to light and sounds, and of the symptoms embraced in the clinical history of cerebral meningitis, will render the exclusion of that affection positive. The heart's action is abnormally infrequent in some cases of cholæmia and of uræmia, but these affections are easily excluded. Certain drugs—namely, aconite, digitalis, and veratrum viride—diminish the frequency of the heart's action. These drugs, given to a person in health, produce, in fact, a transient effect which is equivalent to the functional disorder of the heart thereby characterized.

PATHOLOGY AND ETIOLOGY.—The neuroses of the heart are functional disorders involving the relations of this organ to the nervous system. The functional disorders of the heart's action affect the frequency, the rhythm, and the force of the cardiac movements. The pathology of these disorders would be more fully understood were our knowledge of the physiology of the heart's movements more complete. We know that contractions of the heart continue when it is separated from all its nervous connections and after removal from the body, especially in cold-blooded animals. The rhythm, frequency, and force of its normal movements are evidently dependent on influences derived through the sympathetic and pneumogastric nerves. Experiments show that the movements continue, but with increased frequency and with irregularity, after division of the pneumogastrics; hence this nerve is regarded as exercising an inhibitory and regulating influence over the action of the heart. Disorders of the heart's action from causes which pertain to the brain doubtless involve especially this nerve. Other causes act through the relations with the different organs of the body by means of the sympathetic system of nerves.

Impoverishment of the blood occasions disorder, probably by affecting the nutrition of the heart. Toxical agents in the blood enter into the pathology in certain cases.

The etiology of functional disorders of the heart's action involves, as an important factor, a predisposition inherent either in the organ or in its nervous connections. A peculiar susceptibility to the causes which induce disorder is an idiosyncrasy. Causes which produce disorder in those who have this idiosyncrasy are inoperative upon others. Some persons are liable to functional disorders of this organ all their lives, whereas some appear to be exempt from any liability thereto. In this respect the cardiac muscular fibres are analogous to those of the pulmonary bronchi. A peculiar susceptibility of the latter is requisite for the capability of having bronchial asthma. The susceptibility of the heart-muscle varies in different persons, and a reasonable supposition is that in proportion to the degree of this susceptibility will the causes of functional disorder be more readily and actively operative.

Clinical observation furnishes evidence of various causes giving rise to functional disorders of the heart. The more prominent are—over-exertion of the faculties of the mind, prolonged mental anxiety, the use of tobacco, tea and coffee taken in excess, too great indulgence in venery, the unnatural abuse of the sexual system, dyspeptic ailments, uricæmia, and anæmia. These causes are often combined in individual cases. With reference to effective treatment, inquiries should be directed in every case to facts relating to these several causes.

Long-continued violent muscular exertions are supposed to lead to functional disorders of the heart. DaCosta has described cases occurring among soldiers during the late Civil War in which the cardiac disorder seemed to him referable to severe marches. He applied the name irritable heart to the condition in these cases.⁴ It is probable that mental excitement had more or less to do with the causation. Albutt, Seitz, and other observers have attributed functional disorders to over-straining of the heart by occupations which call for severe exercise of the muscles.

⁴ Medical Memoirs of the United States Sanitary Commission, 1867. See Address before the Philadelphia Medical Society, by A. Stillé, 1883, p. 18. See also Diseases of the Heart among Soldiers, by A. B. R. Myers, London, 1870.

Paroxysmal disorder of the heart belongs among the multifarious symptoms referable to the nervous system in cases of hysteria. It is among the toxical manifestations embraced in the clinical history of gout, being referable, when it occurs in this pathological connection, to uricæmia. It may have this causation in cases in which the ordinary gouty manifestations do not occur.

In the variety of disorder characterized by infrequency of the heart's action it may be assumed that the causative agency is exerted through the pneumogastrics. The inhibitory function of this nerve is affected in the same way as by the galvanic current in the experimental observations on animals in illustration of this function. This view is corroborated by the frequent association of this variety of disorder with notable cerebral disturbance.

PROGNOSIS.—A purely functional disorder of the heart's action may be said to be devoid of danger to life. This is a remarkable fact, taking into view the importance of the organ, together with the degree and the duration of disordered action in some cases. Of many thousand cases which have come under my observation, I am not aware of having met with a single instance in which death was fairly attributable to an uncomplicated functional disorder. It is readily understood that functional disorders superadded to, albeit not dependent upon, organic affections of the heart may contribute to a fatal termination. But the tolerance of functional disorders under these circumstances is often very remarkable.

The assurance of the absence of all danger frequently lifts from the minds of patients a heavy load of anxiety and apprehension. To be able to give such an assurance is one of the delights of medical practice. Patients often find it difficult to believe that the disorder from which they suffer can take place while the heart is organically sound. Many require very positive and repeated assurances in order to secure their belief. The question is many times asked, "How is it possible that I should suffer so much, and yet the heart be free from disease?" Another question which is apt to be asked is, "How can you ascertain so quickly that there is no disease?" In anticipation of the latter question, in order to ensure the desirable moral effect, it is sometimes good policy to prolong the examination, inasmuch as for the exclusion of all the physical signs of organic disease a few moments only are required. Another question, still, is, "Will not organic disease be likely to be produced by the functional disorders?" The physician is fully warranted in giving a negative answer. Exclusive of the cases of exophthalmic goitre, functional disorders of the heart do not involve liability to either inflammatory or structural affections.

Recurrences of functional disorders of the heart constitute the rule rather than the exception. Their frequency will depend much on the degree of the predisposition, but of course more or less on the causes therewith associated. The mental anxiety and apprehensions which they at first occasion after a time wear away, and they are at length reckoned as belonging among those annoyances of life to which may be applied the common expression, "What cannot be cured must be endured."

TREATMENT.—Prompt relief or palliation of suffering is often the immediate object of treatment when cases first come under observation. The medicinal remedies for this object are the ethereal or alcoholic stimulants, the different antispasmodics, and opium. Chloric ether and the compound spirit of ether (Hoffman's anodyne) often act efficiently. An eligible prescription is the combination of one of these with an equal part of the compound tincture of lavender, of which a teaspoonful, properly diluted, may be given after short intervals. Brandy, whiskey, or some other form of spirit in many cases will afford prompt relief. It should be given not much diluted. These remedies are especially indicated in paroxysms of irregular or intermittent and enfeebled action of the heart. They are less adapted to cases in which the heart's action is violent. Of antispasmodics, valerian, the valerianate of ammonia, camphor, and asafoetida are appropriate. Some one of the preparations of opium is to be employed if the disorder be not relieved by other remedies. Of the different forms of opiate, codeia is the least objectionable, and perhaps as efficient as any other. With a view to promptness of relief in certain cases of severity, morphia may be administered hypodermically. Other palliative measures are a sinapism to the præcordia, and, if the extremities be cold, a mustard pediluvium. Of the efficacy of the ice-bag applied over the heart, which is recommended by German writers, I cannot speak from personal observation. The testimony in behalf of its usefulness is, to say the least, sufficient for resorting to it without apprehension of doing harm. In some cases of obstinate persistence of disorder the opportunity is afforded for trying in succession the various remedies which have been named. Digitalis is sometimes useful. Concomitant disorders which may have originated or which tend to keep up the disordered action of the heart are to be appropriately treated. Flatulence and other ailments referable to indigestion and constipation not infrequently are in this category. Paroxysms may be sometimes arrested by certain mechanical means, such as pressure upon the abdomen, holding the breath after a deep inspiration, and compression of the vagus and sympathetic nerves in the neck.

In some cases of functional disorder there is a persistent increase of the frequency of the heart's action without irregularity in rhythm. The action of the heart in these cases is the same as in cases of exophthalmic goitre, the enlargement of the thyroid body and the prominence of the eyeballs which characterize the latter affection being wanting. In these cases aconite in small doses is to be recommended. From one minim to three minims of the tincture of the root may be given, repeated after intervals of four or six hours and continued indefinitely. In cases the opposite to the foregoing—namely, those in which the disorder is characterized by infrequency of the heart's action—a rational indication is to give remedies with a view to excite the heart. In the cases which have come under my observation alcoholics have had but little effect upon the heart, although apparently useful as regards the nervous symptoms which are apt to accompany this variety of cardiac disorder. As this disorder does not, as a rule, occasion distress, the patient perhaps not being conscious of any disturbances of the heart's action, and as the infrequency does not appear to involve danger, the treatment may be directed to fulfilling other symptomatic indications.

Positive assurances of the absence of danger have often a potential influence in relieving paroxysms of functional disorder. The disorder is not infrequently increased and kept up by mental apprehension, and these assurances therefore do away with an active causative agency. They are also useful in the way of preventing the recurrence of paroxysms. It is evident that in order to exert this moral influence the physician must be competent to decide that the disorder is purely functional. He can so decide only if he have confidence in his ability to exclude inflammatory and structural affections or to determine that the disorder is not dependent on lesions which may coexist. If he have not sufficient confidence in his opinion, he will naturally and properly not give positive assurances, and a lack of positiveness will be likely to lead the patient to infer that the disorder is not devoid of danger. The good effect of certain measures of treatment is in part attributable to a mental influence. This is legitimately a therapeutic object here as in other affections.

The more important part of the treatment in the majority of the cases of functional disorders of the heart's action is that which relates to prevention. The preventive treatment, in addition to the moral influences already referred to, consists chiefly in removing as far as practicable the causes of the disorder. The predisposition cannot be removed, but the causes which are auxiliary thereto in producing disorder are, to a greater or less extent, controllable.

Prolonged mental anxiety is often inseparable from the events of life. "Therein the patient must minister unto himself" The voluntary exercise of the mental faculties, however, can be restrained within physiological limits. Tobacco can be abstained from, and, as a rule, total abstinence is easier than moderate indulgence. Tea and coffee can be used moderately if at all. Dyspeptic ailments are amenable to appropriate dietetic and medicinal treatment. On no account should the diet be reduced below the requirements for ample nutrition. Anæmia, which exists in a large proportion of cases, especially in women, calls for chalybeate tonics, to be continued persistently as long as the blood remains impoverished. It is needless to add that in these cases the causes of the anæmia are, if possible, to be removed, and that chalybeates are to be supplemented by proper dietetic and regiminal treatment. Sexual excess and abuses are to receive adequate attention. There can be no question as to unnatural sexual excitation. But a question often arises in individual cases concerning the physiological limitations of natural indulgence. These limitations probably differ widely in different persons. They are, however, always exceeded if the indulgence exceed the instinctive demand—that is, if its increase be made an object for voluntary efforts. Long-continued and violent muscular exertions should be interdicted. Uricæmia or the gouty diathesis claims appropriate remedies and hygienic regulations.

Several of the various causes just recapitulated are frequently combined, so that the preventive treatment is by no means always limited to the removal of a single cause. The treatment will prove successful in proportion as the efforts to remove the causes are effectual.

Angina Pectoris.

The name angina pectoris was introduced by Heberden in 1768 to designate a group of symptoms which from that date has been regarded as constituting an individual affection. The word angina, signifying strangulation, has but little pertinency in this application of it, and various other names have been proposed in its stead. For the most part these are based on pathological views which are either erroneous or hypothetical, and at the present time the name angina pectoris is generally adopted in all countries.

The affection may be defined as a paroxysmal neuralgia, the pain of which is seated within or near the præcordia, shooting thence in most cases into the left shoulder, and extending downward to a greater or less extent into the left upper extremity, the right upper extremity being sometimes similarly affected. In some instances the pain extends to the lower limbs; the paroxysms often accompanied by a feeling of anguish and of impending death, the affection in the great majority of cases being incident to organic disease of either the heart or the aorta and involving liability to sudden death.

SYMPTOMATOLOGY.—The foregoing definition embraces the prominent traits of a severe paroxysm. The pain may extend into situations other than those mentioned—namely, in different directions throughout the chest, into the neck, the jaws, and the temples, the abdomen, and the groin. In describing the pain patients use such terms as constricting, tearing, burning, etc. Perhaps in its most severe form there is no disease attended with more intense suffering. It is related that the description of the affection by Heberden led to a communication to him from an unknown correspondent who gave an account of his own case, and bequeathed to Heberden his body to be examined after death. The examination was made by John Hunter, who himself fell a victim to the affection. An analogous instance occurred in my own experience. A patient was led by the intensity of his sufferings to request that I should make a post-mortem examination in his case, with the hope that something might be thereby ascertained which would prove useful to others. This request was complied with. Associated with the pain in severe paroxysms is what has been called a breast-pang, giving rise to a sensation as if death were at hand. A choking sensation, which is implied in the name angina, is an occasional symptom, resembling the globus hystericus. Respiration is not obstructed, but the patient may voluntarily restrain the respiratory movements lest they increase the suffering. Dyspnoea, if present, is thereby produced. During the continuance of the paroxysm the patient refrains from movements of the body or limbs, keeping a fixed position and grasping some firm support in order better to remain motionless while the pain lasts. A sensation of numbness in the affected limbs accompanies the pain. The circulation is usually more or less disturbed. There is sometimes increased and sometimes diminished frequency of the pulse. The action of the heart is often intermittent and otherwise irregular. It may be strong, but oftener it is weak. At the beginning the arterial tension has been found to be increased, but later is diminished. The face is generally pallid, but sometimes livid. The disturbances of the circulation are often modified by coexisting organic disease of the heart, but superadded are those of functional disorder incident to the paroxysm. The countenance is haggard and anxious. The surface of the body is cold, and may be bathed in perspiration. The mind remains unaffected. The paroxysms usually commence suddenly, and, as a rule, so end. Eructations of gas are apt to follow their cessation, together with a free discharge of limpid urine. The duration of a paroxysm may be but a few seconds; it is rarely longer than a few minutes. When it appears to be protracted for a considerable period, there is generally a series of attacks occurring in quick succession, instead of one continuous paroxysm.