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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    [4] enough, been overlooked by -writers on the subject. We may say, first of all, that the quantity of blood within the vascular system influences greatly the volume of blood which the heart has to expel in a given time. This can easily be seen on injecting blood, three-quarter per cent, salt solution, or other appropriate fluid, into one of the veins. For example, we find in one experiment (illustrated by Fig. 4) that injection of 50 cubic centimetres of salt solution produced an increase in the mechanical work done by the heart equal to about 34 per cent. The calibre of the veins also necessarily affects the quantity of blood which reaches the heart in a given time. This fact can be very well shown by applying gentle pressure to the abdomen, as is well shown by the tracing in Fig. 5. Narrowing of the veins has, therefore, the same effect as increasing the volume of blood in the vascular system. There are many other ways by which this factor in the work done by the heart can be varied, without any change in the arterial pressure, but we do not propose to occupy your time with this sub- ject, seeing that what concerns us here is the effect of change in the work of the heart, however, produced on the organ itself. It need hardly be said that where the rapidity and force of beat remain constant, any increase in the amount of blood which reaches the heart must necessarily in- crease the diastolic expan- sion of the organ. Within physiological limits, there appears to be no great harm in such variations in the dia- stolic expansion of the heart, which, we may note in pass- ing, are very much greater than is generally supposed. We have no reason to be- lieve that, with an increased degree of expansion in dia- stole, more energy is expended in throwing out a given volume of blood against a given arterial pressure. Sup- posing the arterial pressure and the force of the muscular contractions to remain con- stant, any increase in the dia- stolic expansion of the ven- tricle necessarily implies a diminished degree of . con- traction in systole, although the volume of blood expelled by the heart with each con- traction may be, and in physiological conditions always is, increased. This is well seen in Fig. 5. When the work of the heart is raised owing to increase in the volume of the blood reach- ing it by the veins in a given time, the extent and the efficiency of contraction is increased, although the degree of contraction of the individual muscle fibres at the end of systole is diminished. It is generally asserted that, at the end of each contraction, the ventricle is always completely empty of blood, a view which is evidently opposed to what we have just said as to the varying amount of residual blood in the ventricles at the end of systole. The following experiment, even were there no other evidence at hand, conclusively shows, we think, that the generally received views upon this subject are erroneous. The experiment consists in introducing the little finger through the apex into the interior of the left ventricle of the living animal, the heart having been exposed. This, at first sight, very difficult operation, is perfectly easy, and need not cause any escape of blood. The finger is in- troduced in the same way as the cannula of the instrument first .described by us—namely, by being pushed through an incision which has penetrated two-thirds of the distance between the pericardium and endocardium. The heart continues to beat, as far as can be seen, quite normally under these circumstances, and by the finger so introduced it can be felt that, at each contrac- tion, the lower part of the ventricular cavity closes completely, the musculi papillares coming into contact with one another; the upper part of the cavity, however, lying between the valves and the papillary muscles does not become emptied. We must assume that, cceteris paribus, beyond a certain limit, in- crease in the work of the heart due to increase in the volume of blood thrown out in a given time tends to fatigue or weaken the organ. We find, then, that the work of the heart varies very greatly within physiological limits as a result both of the changes in the arterial pressure and in the amount of blood which reaches the organ, and that variations in the latter are of even more frequent occurrence than in the former. There is also the fact that increase in the work done, other things being equal, produces diminished completeness of contraction in systole, and therefore an increase in the residual blood in the ventricle. This physiological dilatation of the heart with increased work becomes, when excessive, the cause of failure of the organ from overwork or overstrain, as it is generally called; in other words, the heart goes on contracting and sending out all the blood which reaches it (excepting, of course, the residual blood) until the moment when, either from increase Fig. 5.—Cardiometer tracing, showing effect of abdominal compression on the amount of blood thrown out by the heart. The time-curve gives intervals of one second. During the period between the two vertical lines at A the heart gave 32 contractions, the average height of the movements of the lever-point resulting from these being 27 millimetres. Multiplying 27 by 32 we obtain 861 millimetres of upward movement during that time. Between the vertical lines B, during whicli the abdomen was being compressed, the heart gave the same number of con- tractions as during the same period of time before compression. The average height was now 35 millimetres, which number multiplied by 32 gives 1,120 millimetres of upward movement. This is equal to an increase of almost 30 per cent.—more correctly. 29.6. As abdominal pressure does not lower the aortic pressure, this amount represents an equal increase in the work done by the heart. The curve also shows that the increased inflow to the heart, re- sulting from abdominal pressure, leads to diminished contraction of the heart in systole, as well as to a relatively greater expansion in diastole. The period of compression begins immediately before the third vertical line, and finishes immediately after the fourth. in the arterial pressure, or from weakness of the heart muscle resulting from fatigue or from disease of its walls, the muscles at the basis of the ventricles no longer in systole narrow the auriculo-ventricular orifices to a degree which permits of these orifices being closed by their valves, these not being capable of expanding to the same extent as the muscular substance of the heart. This fact is very prettily illustrated by an experiment, we believe, of Cohnheim’s, and which we have frequently per- formed and seen performed; it consists in narrowing the ascend- ing arch of the aorta by a screw clamp while the arterial pressure is recorded by a mercury manometer connected with one of the carotids, the clamp therefore being placed between the heart and the point at which the arterial pressure is measured. As the clamp is gradually screwed up there is no corresponding fall in the manometric pressure, such as might a priori be expected. What happens is that when the aorta has been narrowed to a con- siderable extent, which varies in different animals, the arterial pressure suddenly falls, and if the clamp be not removed the animal dies. This continuance of the normal pressure up to the time when the sudden fall occurs is not due to narrowing of any