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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Licence: Public Domain Mark

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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    [2] this increase in pressure having a limit, and this limit varying in different animals. The intra-ventricular pressure in the left ven- tricle during systole, which in the dog is normally something under 130 millimetres mercurial pressure, can, by gradual narrow- ing of the ascending aorta, be raised to 250 millimetres, 300 milli- metres, or even a little more, in certain cases. Beyond a certain point further narrowing, and even complete closure (which of course is only possible for a few seconds without causing death) does not raise the pressure within the ventricle beyond the limit above referred to, which limit varies with the animal and with the condition of the heart at the time. With two successive momentary closures of the aorta the maximum pressure obtained in the left ventricle is the same. With fatigue of the heart, produced either by continued slight narrowing, or often repeated great narrowing, or complete clo- sure of the aorta, this maximum limit gradually falls. We may add also that the curves show a rise in the pres- sure during dia- stole, which is relatively less than the rise of systolic pressure. This is well shown by the curve. Such nar- rowing of the aorta produces a very evident dis- tension of both ventricles, which, nevertheless, go on contracting and expanding in what to the eye seems a per- fectly normal manner. Exami- nation of the large veins, however, shows that in them, with the great or extreme narrowing just re- ferred to, there is a very visible wave proceeding from the heart with each ven- tricular systole ; in other words, this narrowing of the aorta pro- duces regurgita- tion through both mitral and tri- cuspid valves. The effect, then, of greatly increasing the resistance which the ventricles have to overcome in the evacuation of their contents, is to raise the intra-ventricular pressure during systole to a height varying with the individual heart under observation, and to cause great expansion of the chambers of the heart with regurgi- tation eventually through the auriculo-ventricular valves. It may further be noted that the supply of blood to the heart muscle influences, the height of this limit. This is shown by the fact that narrowing the aorta raises the maximum pressure ob- tainable in the right ventricle by narrowing the pulmonary artery. The experiment on which this statement is founded runs as follows:—the pulmonary artery is first narrowed (the pressure- gauge being connected with the right ventricle), and the maxi- mum pressure thereby produced is recorded. When this is Fig. 2’—Simultaneous tracings of cardiac pressure-gauge and cardiac myograph, applied to lett ventricle of dog. The time-curve gives intervals of one second. The signal-curve shows during the slightly raised part t]ie time during which the ascending aorta was slightly constricted, while the middle part of the curve, which is raised higher, gives the time during which the aorta was completely closed. The point of this curve, at which it returns to its original level, indicates the moment when the ligature round the aorta was completely removed. The upper curve was taken by an instrument which permits of a graphic record being obtained of the distance between any two points on the heart wall. [This instru- ment we hope to describe elsewhere.] The two points on the front of the left ventricle from which the curve was taken lay in a line parallel with the interventricular sulcus, and were situated about halfway between apex and base of the ventricle. Upward movement of the lever point corresponds to approxima- tion of the points chosen—in other words, to contraction of the wall of the ventricle. The individual con- tractions of the heart, as well as the effect of the respirations, can be readily recognised, together with the great expansion of the ventricle during the period of closure of the aorta. During this time, also, it can be seen that the shortening of the muscular fibres of the ventricle in systole is greatly diminished. The larger curve gives the intraventricular pressure rise of the lower point corresponding to rise of pres- sure. The slight rise of pressure in systole during the period of slight constriction of the aorta is well shown, as well as the fact that the pressure in diastole remains unchanged. During the period of com- plete closure of the aorta the systolic pressure soon rises to its maximum limit, which in the case of the heart in question was about 250 millimetres mercurial pressure, During the same period of time the diastolic pressure rises gradually to an extent relatively much less than the rise in systolic pressure. repeated shortly after the aorta has been greatly narrowed, a very much higher systolic pressure is found to result. We see no reason to doubt that here, with the increased pressure resulting from constriction of the aorta, the coronary arteries receive an augmented blood-supply, which improves the nutrition of the right ventricle. After overstrain of the heart produced in this way, the valves are found to present certain anatomical changes, to which we will presently have to refer. In the meantime it is more convenient to proceed to the consideration of the second factor which influ- ences the work of the heart, namely, the quantity of blood thrown out by it in a given time. Changes in the Amount of Blood Expelled. Ludwig’s Stro* muhr2 is capable, it need hardly he said, of giving information on this subject, but it is not specially suited for our purpose, seeing that it gives no indication of the effect on the heart itself of variations in the quantity of blood thrown out by that organ, nor can it be conve- niently employed without very seri- ous interference with the circula- tion in the sys- temic arteries. The method which we employed is one which per- mits measurement both ot the amount of blood thrown out of the heart in a given time, and the effect on the heart itself of variations in that volume. It con' sists in enclosing the living working heart in what is for all practical purposes a rigid air-tight box, the variations in whose contents can be recorded graphically. In other words, it is a cardiac plethysmo- graph, or onco- graph. We will in the following pages refer to it the by the name cardiometer.3 The construction of this instrument will readily be understood on looking at the diagram. Here, also, we need not trouble you with technical details, and will only say that round the root of the heart is placed a metal ring, which is made in two pieces, for convenience of adjustment, and which is grooved outside, so as to retain in position a ring of india-rubber, something like an ordinary umbrella ring. This double ring having been placed round the root of the heart, the outer or parietal layer of the pericardium is then drawn tight over it, while against it, and firmly pressing the pericardium, are screwed the two halves of the 2 Stolnikow, Die Aichung des Blutstromes. Dubois-Eeyraond's Archiv, 1886. 1 Both cardiemeter and pressure-gauge were made for us by the Cambridge Scientific Instrument Company