The Elevation of the Diaphragm.-But we find here a condition which makes it plain that in our patient the heart-dulness is increased without any hypertrophy of the heart itself. We find, namely, an elevation of the diaphragm. We find in both sides of the thorax the explanation of this symptom. We have shown that the lung is one intercostal space and one rib too high, the liver-dulness on the right side being in the parasternal and nipple lines, at the upper border of the fifth rib. On the left side, instead of uniting with the tympanitic sound of the stomach at the seventh rib, the clear lung tympanitic note is found in the fifth intercostal space, except in the region of the heart. Besides, we find the apex-beat one intercostal space too high. There can be no doubt, therefore, that the diaphragm is elevated.

Cause of the Elevation of the Diaphragm.-To account for this elevation, our attention is first directed to the condition of the abdomen. There is no particular distention: its conformation is normal. The tension of the abdomen is not increased, as is readily seen by laying on the hand. The cause of the elevation of the diaphragm must be sought for in another source. There is no reason to believe that there is an enlargement of the upper part of the liver, as is seen in certain diseases of that organ, as abscess or echinococcus. Contraction of the lung resulting from fibroid thickening after old inflammatory processes is not present, nor is adhesive pleuritis. The existence of a loud percussionnote and vesicular breathing over both lungs testifies to their condition. In the deep inspiration which we now ask the patient to take, the lung and the border of the liver on the right recede to the upper border of the seventh rib,—that is, two ribs lower, and on the left the heartdulness becomes as small as in the healthy person under the same circumstances. The lungs have, therefore, thoroughly proved their power of expansion. When the lungs are apparently abnormally contracted and the diaphragm is drawn correspondingly farther upward, and yet both are normal, we can explain the condition only as the result of an abnormal type of respiration. In fact, this type of respiration has been observed in many cases of chlorosis,-a somewhat quickened but superficial breathing,—and it is reasonable to expect that the lung, by a long continuation of this form of breathing, will become retracted, which condition, naturally, can be detected only by an examination of the border of the lung. You will find this superficial breathing in all cases of severe chlorosis, especially where the patient has lain in bed for a long time. When the patient, on the other hand, has not been confined to bed, this condition will be less frequently found. You

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will find, if you give your attention to this detail, that the elevation of the diaphragm disappears as the patient grows better.

The Influence of an Elevated Diaphragm upon the Position of the Heart.-As soon as we discover the high position of the diaphragm we can explain the increased heart-dulness and the outward displacement of the apex-beat. You find in all books on physical diagnosis that the heart is more closely pressed to the anterior thoracic wall. In most cases where an elevation of the diaphragm exists it is caused by a pressing up of the contents of the abdomen, as in pregnancy, tympanites, or ascites. The same anatomical condition must be produced by insufficiently deep inspiration in the thorax, with shrinking of the lung, as is seen in our patient. Retraction of the borders of the lung and the high position of the diaphragm explain the form and extent of the heart-dulness. These conditions are here, widening out to right and left, and an elevation of the upper border (third rib instead of fourth).

Further, the position of the apex-beat to the left is explained by the fact that the base of the pericardium, which is found by the average from the examination of many cases to rest upon the diaphragm, would be carried upward only a little, since the middle portion of the diaphragm, held down as it is by its close connection with the vascular trunks, would be less movable than the lateral portions. The movement of the heart by the raising of the diaphragm must, therefore, be greatest at the point farthest removed from the middle; that is, at the apex. The heart would be rotated on an axis which is anteroposterior, the apex describing an arc which is not only from below upward, but also from within outward. We find, when we have diagnosed the condition produced by an elevation of the diaphragm and the displacement of the apex towards the left, even as little change from the dilatation and hypertrophy of the left ventricle as is found in pregnancy.

Evidently the rotation of the heart upon an antero-posterior axis, through the elevation of the diaphragm, is not the only alteration in position which the heart makes. It has already been shown that the heart leans strongly forward. The cause of this forward movement is explained by the greater bending of the left portion of the diaphragm during its change of form than of the right portion, and its consequent action upon the heart. The greater pressure is from behind and to the left, so that the heart is also rotated a little upon its long axis. The portion that extends outward towards the left would be pressed forward; that is, the apex, the anterior border of the left ventricle, a portion of

the left auricle, the orifice of the arteria pulmonalis, and the arteria pulmonalis itself. Because of this we find an exceedingly strong apexbeat. The apex is here entirely free from lung; and, besides, we find a full and easily-felt pulsation of the pulmonary artery. The portion of lung that lies between the pulmonary artery and the thoracic wall is thinner than normal. A careful examination of this spot shows a distinct upheaval and sinking of the intercostal space. On the other hand, every short diastolic action which the movement of the pulmonary valves makes cannot be perceived. This is a noteworthy fact, since it shows that the impulse in the region of the pulmonary artery is not perceptibly heightened; otherwise, with the superficial position of the artery, the recoil of the blood must be clearly felt.

The Influence of the Elevation of the Diaphragm upon the Results of Auscultation of the Heart.-For the same reason, the deductions from auscultation are to be modified. The second pulmonary sound is louder than the second aortic; this difference is very marked, as great as we find it in the failure of the mitral valve. Yet I must warn you as to the increase of the second pulmonary sound in these cases: do not mistake it for increased pressure in the region of the pulmonary artery in your diagnosis, and thereby contradict the result of palpation. Then it is clear that an increase of the second pulmonary tone can come about in two different ways: (1) when it is really louder than the aortic sound; (2) when the attendant condition is more favorable for the arteria pulmonalis than for the aorta. The latter is true in those cases in which the orifice of the pulmonary artery approaches the thoracic wall, while the overlying aorta, over which we hear the aorta sounds, through the rotation of the heart upon its long axis, is somewhat farther removed from the thoracic wall. On that account we hear over the aorta both tones softly, while over the pulmonary artery both the systolic and the diastolic sounds appear very loud. The understanding of these conditions-namely, the simultaneous systolic and diastolic strengthening of the pulmonary tones-is important, and would in other cases besides chlorosis help to a better understanding of the differences in sounds.

In order to confirm the above, we should not forget the other points over which the second tone of the heart can be heard,—that is, over the apex and the fifth costal cartilage. It is already known that the diastolic sound which can be heard at this point of the thorax is the result of the valvular closure. You must in all cases of mitral stenosis, mitral insufficiency, and other diseases in which there are pressure-symptoms in the pulmonary circulation and increase of the

second pulmonary sound, remember that the second sound over the tricuspid valves is louder than at the apex; and, further, that in most cases the second sound over the tricuspids is louder than the first at the same place. The second sound here at the apex laps over the second tone on the tricuspid, and this is less than the first sound in intensity.

Conclusions.-We come to the conclusions that the changed position of the apex-beat, the strong heart-impulse, the perceptible pulsation of the pulmonary artery, the loud pulmonary sounds, and the increased heart-dulness, are explained by the retraction of the lung margins from the heart, and by the elevation of the diaphragm; and that we are not justified in allowing ourselves, because of these symptoms in connection with the systolic murmur, to make a diagnosis of mitral insufficiency.

As you see, we base our diagnosis entirely upon objective examination. We do not need to infer from past experience with chlorotic patients that there is never any physical change in the heart. This is always important, as it confirms our diagnosis and excludes the supposition that perhaps she had a definite lesion of the heart-valves as a result of the articular rheumatism. Before we make our comparative conclusions between the two cases, I should like to call your attention to two symptoms which we observed in the arterial system of our chlorotic patient.

I. The Quality of the Pulse in the Radial Artery.—The pulse is full, soft, and dierotic. You will not find such a pulse in every case of chlorosis. You will not observe it if you make the mistake of confusing it with chronic cases of anæmia and oligamia which have originated in childhood in a hyperplasia of the arterial system (Virchow); also in true chlorosis the dicrotic pulse is not always found; but when you have a case before you where the finger is on the pulse of a strong and well-nourished girl suffering from an acute and severe chlorosis, then you will always have the chance to observe a full dicrotic pulse. We will not fail to recognize both these appearances as signs of a marked dilatability of the vessels, or, in other words, of atonicity of the arteries.

II. The Quality of the Sound-Symptoms in the Arteria Cruralis.— It is well known that normally, by carefully applying the stethoscope, one hears either nothing at all or an arterio-diastolic tone; on applying the stethoscope with more force, one hears an arterio-diastolic stenosis murmur; and by still further pressing the stethoscope, one hears the so-called pressure-sound. Here, in this chlorotic girl, we can perceive,

as any beginner can distinguish, two distinct sounds during one pulsation. With this, however, we ought not to be satisfied, as in the crural artery there are several kinds of double sounds.

The phenomenon of double sounds is not infrequent. It was first observed in cases of aortic insufficiency; later, in mitral stenosis, in anæmia, in pregnancy, in fevers, in contracted kidney, in arterio-sclerosis, and in chlorosis.

I have for a long time observed the symptoms, and find that there are three kinds of double tones in the arteria cruralis :

(a) A double arterio-diastolic sound. The sounds generally follow quickly one upon the other; the first is not finished when the second begins; there is a separation as well as a doubling. This form is found in mitral stenosis, in saturnism, in chronic contracted kidney, in arteriosclerosis, and often in pregnancy.

(b) A simple arterio-diastolic followed quickly by an arterio-systolic sound. The second sound begins immediately, or after a trifling pause, after the first sound. Often one can notice only that he has to do with two sounds, and cannot determine the quality of them. This form is found in aortic insufficiency, and in some cases of very high fevers.

(c) Simple arterio-diastolic and delayed arterio-systolic sounds. In these cases the pause is longer, even longer than that between the first and second heart-sounds. This condition is, therefore, very easy to diagnose. This form is found in severe anæmia, in chlorosis, in pernicious anæmia, in high fevers, seldom in pregnancy.

With this last-named form we have to do here. You can see by the collected evidence that we have here such a condition as is shown by the tension of the vessels.

In the following table I have summarized the symptoms which we have found in the circulatory system. A further explanation of this table is not necessary. The similarities, as well as the dissimilarities, in the symptoms in mitral stenosis and in chlorosis with elevation of the diaphragm are both shown. The comparative value of the several symptoms in diagnosis can be seen by reference to the

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