Remarks on failure of the heart from overstrain : being the opening of a discussion in the Section of Pathology at the Annual Meeting of the British Medical Association, held in Glasgow, August, 1888 / by Prof. Roy and J.G. Adami.

  • Roy, Charles Smart, 1854-1897.
Date:
[1888]
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Credit: Remarks on failure of the heart from overstrain : being the opening of a discussion in the Section of Pathology at the Annual Meeting of the British Medical Association, held in Glasgow, August, 1888 / by Prof. Roy and J.G. Adami. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    c or all of the systemic arterioles, as has been supposed by some. Our own observations show that all the blood which reaches the heart is thrown out by it into the arteries until incompetence of the auriculo-ventricular valves results from dilatation of the heart. We do not, of course, for a moment suppose that the causes of heart failure in man ever act with the rapidity or intensity of those present in this experiment. What most usually takes place apparently is that the mitral valve, whether from primary disease or from overstrain, gives way gradually. This gradually-pro- duced regurgitation is in part compensated by rise of pressure in the pulmonary veins, which is kept up until from failure of the right heart the tricuspid gives way. Let us now consider briefly some of the special pathological conditions of the heart, on which light appears to us to be thrown by what we have stated above. The much discussed question as to the possibility of hypertrophy of the heart in plethora with- out increased arterial pressure appears to us to be answered by the detailed facts and considerations. They appear to us to offer a sufficiently simple explanation of this form of hypertrophy. We have, however, never seen such cases. Of acute overstrain of the heart from intense muscular exertion, one of us (R.) has on one occasion had personal experience: when, during convalescence from typhoid, he found himself called upon as a medical man to make a fatiguing and rapid journey with a relieving party over the Mer-de-Glace to the “ J ardin ” to attend to a Chamouni guide who had been severely injured by an Alpine accident. The sensations felt are well described by Clifford All- butt,4 with whose observations on overstrain of the heart our own results fully coincide. The feeling of want of breath and fulness in the region of the heart, as well as the sense of extreme mus- cular limpness, are well-marked subjective phenomena. With regard to the objective phenomena, it did not occur to the one of us personally involved in this matter to percuss out his heart, as was done by the more intelligent Clifford Allbutt, who found the urea of dulness increased; but such characteristics of the condition as are appreciable to the non-medical eye led the injured guide in question to remark, “Mais vous etes essouffle, Monsieur, il faut prendre du cognac,” which treatment with rest was found efficacious, mere rest, however, it may be remarked, not giving the immediate relief obtained from it in cases of breathless- ness from ordinary exertion. Swiss guides, who are exposed to extreme fatigue in cutting steps on ice in mountain climbing, are well acquainted with the condition, as has previously and independently been noted by Clifford Allbutt; they have found that cognac gives a fillip to the system at the right time, and with rest gives relief. Did the time at our disposal admit of it we might say a good deal on the light which, we believe, is thrown by our ob- servations on the pathology of heart failure in chlorosis and some other forms of ansemia and hydrsemia. Much might also be said on the effects of disease of the different valves of the heart and the resulting overstrain thereby thrown on the organ, or part of the organ. We need, however, here only mention that dilatation of the heart in such cases, as well as in cases of primary disease of the heart-wall, is recognisable both at the bed- side and after death. This dilatation we have shown to be a necessary result of increase in the work of the heart, as a result either of increased arterial pressure or of increased output of the organ, and that failure of the heart only takes place when incom- petence of the auriculo-ventricular valves from dilatation of the orifices, makes it impossible for the heart to throw into the arteries all the blood that has reached it by the veins. We have intentionally avoided referring in the above to the influence on the work of the heart of changes in the rate of beat of the organ. We have purposely also avoided entering on the question of hypertrophy, or of the effect on the heart of the vagus and accelerans. These are matters which we hope to deal with in a future communication. Affection of the Valves from Overstrain. We must now return to the relation between overstrain and secondary disease of the valves, and we have first to describe the anatomical changes in the valves which we found to result from artificially produced overstrain, seeing that these appear to us to throw much light on certain forms of val- * St. George’s Hospital Reports, vol. v, 1870, p. 29. ] vular disease. If the ligature by which the aorta is narrowed be placed round the ascending portion of the aortic arch, and then either repeatedly tightened for a short time, or by slower, or by continued slight narrowing, failure of the heart and regurgitation through the auriculo-ventricular valves, be produced, we find that, in nearly every case (six cases at least out of seven), certain portions both of the aortic and mitral, as well as the tricuspid valves are the seat of cedematous thickening. In the aortic valves this thickening is most marked along the line of insertion of the flaps; these flaps themselves presenting also in some cases a varying degree of thickening. With regard to the mitral and tricuspid valves the thickening is situated chiefly along those parts of the flaps which are normally in apposition during systole. In other words, the oedema occupies those parts of the valves which are specially liable to become thickened by formation of fibrous tissue, in such diseases as chronic Bright’s or syphilis, with secondary hypertrophy and valvular disease of the heart. In other of our experiments, in which the aorta has been nar- rowed at a part of its course where there was no possibility of interference with the lymphatics of the heart, there has been no great thickening of the valves, although, in these cases also, we have always found, on killing the animal, some slight thickening along the line of insertion of the aortic valves, and a very charac- teristic-roughening of those parts of the mitral valve which are the seat of oedema in those of our experiments where, besides narrowing the aorta, we presumably interfered, to a certain extent, with the outflow of lymph from the heart. This roughen- ing we could see, with the aid of a hand lens, was due to the distension of the beaded lymphatic vessels of the flaps. Very commonly also a dulness of certain parts of the endocardial covering of the valves led us to suspect a shedding of the endo- thelium. In all cases there were punctiform ecchymoses along the same parts of the mitral flaps, the rest of the endocardial lining showing only exceptionally any appreciable congestion or ecchymosis, and never being found cedematous by us. We may note in passing that we are aware that the left seg- ment of the tricuspid valve of the healthy dog usually presents a variable degree of thickening.6 These anatomical changes in the valves, which result from overstrain, we in- terpret as indicating an increase in the amount of lymph in cer- tain parts of the valves. That such increase or stagnation of lymph tends to formation of fibrous tissue in the affected part, we know is the case in many other tissues. Of these we may mention the fibrous thickening of the subcutaneous tissue of the arm, in the case of persons where cancer of the axillary glands obstructs the outflow of lymph from the limb. We are impressed by the fact that the situation of the oedema of the flaps is strikingly identical with that of the fibrous thicken- ing present in the valves of those cases of heart disease which occur in conjunction with abnormally high arterial pressure. We believe the oedema and the fibrous tissue to be due to the same cause, namely, the increase in the quantity of lymph, which is possibly of a purely mechanical nature. As to the question whether the endothelium be or be not liable to be stripped off the valves in cases of overstrain, and whether such stripping off, if it take place, might not be the cause of deposit of the blood platelets, or of fibrin, and thus lead to socalled “verrucose endocarditis,” this is a matter which we cannot discuss here. Plenty of examples of secondary disease of the valve's from overstrain might be given, but we know of none in which the relation between cause and effect appears to us so evident as in the case of the heart changes present in chronic renal disease ac- companied by high arterial pressure and hydrsemia, both of which, as has been seen, increase the work of the heart. This increased work leads to hypertrophy of the organ; but, over and above this hypertrophy, disease of the valves is of specially common occurrence; Goodhart, for example, in his valuable paper on “ Ansemia as a Cause of Heart Disease,” remarks that where “ there has been prolonged regurgitation on the right side of the heart, the tricuspid flaps are generally considerably thickened.”6 Ste- nosis apparently never occurs in these cases. He says, also, that 5 Reyher, Virchow’s Archiv, xxi, 1861, p. 85, states that in thirty-three dogs examined he constantly found thickening of the septal flap of the tricuspid valve, and the other valves much more frequently diseased than has generally been supposed. We are acquainted with the appearances described by Reyher, and there is no reason to believe that we have been led into error by mistaking these for the results of acute overstrain. 6 Lancet, vol. i, 1880.