In my own observations I have always found the veins of the neck manifest, without in a single instance reaching any great size, and never have I noticed the prominence of the eyes noted by Walshe. In these cases cyanosis was limited, and was notable in a marked degree only upon the lips, the cheeks, and in the upper extremities. The general or local infiltration of tissue I have never remarked, although closely looked for on several occasions. Some authors, indeed, have described a bluish appearance of the entire surface of the body, together with signs of general infiltration. The explanation given of these phenomena is that there is a general obstruction of the capillary circulation, and that the return of the venous blood to the cavities of the heart is rendered almost impossible. In other words, we have here a well-marked asphyxic condition. If this be true, it is only partially so, and there must be great variation in different instances of fibrinous deposition in the right heart. The rational symptom which was for me one of great value in the diagnosis of these cases was that of excessive pallor, not only of the face, but of the limbs and the entire trunk. This pallor appeared constantly to increase until the last moments of life.
Richardson indeed says the symptoms are those of syncope, not of asphyxia. The different processes of life are arrested on account of a simple absence of arterial blood, not owing to the presence of blood unfitted to reconstitute the tissues. The tendency to fainting is probably due, therefore, to the fact that the right ventricle being more or less completely filled by a fibrinous coagulum, the blood is prevented from passing through its cavity and entering the lungs. As a result, there will be but a relatively small portion of blood which becomes oxygenized after each right cardiac systole. When the clot occupies the left ventricle and auricle, there will be a reflux of blood into the pulmonary tissue, thus causing great congestion of this structure. So intense will this congestion become that occasionally hæmoptysis results and pulmonary apoplexy may be developed, due, doubtless, to rupture of the capillary vessels. This condition occurs before the right heart is much or at all obstructed by coagula. We can appreciate that the physical signs must, if properly noted, show manifestly in which cavity the clot is located. If it be in the right heart, anæmia and emphysema of the lung should follow; hence breathlessness and increased pulmonary resonance. If it be in the left cardiac cavity, the lungs become engorged very rapidly, and we should find dulness on percussion, moist râles, and perhaps an equal or even greater amount of dyspnoea.
Difficulty of breathing appears to belong as well to the symptoms which indicate cardiac thrombus on one side of the heart as to those which characterize its presence upon the other. This symptom was first accurately described by Hope, since his day by Richardson and Meigs.43 It has something special in its features which strikes one particularly, but may deceive unless closely observed. It takes place not because the movements of the thorax are interfered with, not because the entrance of air into the lungs is prevented, for the vesicular respiratory murmur is easily distinguished, but because the amount of blood furnished by the pulmonary artery is diminished. The anguish of the patient is sometimes terrible. The nares dilate, the chest expands spasmodically with each inspiration, and the patient is agitated, moans, and shows that extreme craving for air described by Van Swieten in the summæ anxietates. Under these circumstances, Hayden44 states, the surface is cold, and often humid with perspiration. Pain and great oppression in the præcordial region have occasionally been referred to, as in the patient of Beau, who said, in placing his hand to his chest, "I have there a weight which has suddenly formed and which stifles me." Often the anxiety is extreme, and the painful sensations continue to increase steadily until death occurs. In rare instances the suffering, when it has reached a certain degree of intensity, may remain stationary, or even become considerably less. If such a respite occur, it is only temporary, however, and the anguish soon recommences. In milder cases sometimes, and apparently after dissolution or disintegration of the clot, the severe symptoms may by degrees disappear, and from this period the patient makes a steady, uninterrupted march toward recovery. I have only lately witnessed a similar example in a youth attacked with typhoid fever, which had reached the third week. There are constant and intense effort to breathe, extreme restlessness, and the patient will throw himself from one side of the bed to the other, and scarcely remain quiet for a few moments. These symptoms are usually more developed when there is concomitant cardiac disease of organic nature, and unless this be present may not be so pronounced as to concentrate attention upon them.
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.