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Philadelphia Medical Journal.
A Weekly Review of Medicine
SATURDAY, OCTOBER 1, 1904
VOL. LXXX, No. 14.
Mitral regurgitation occurs more frequently than any other valvular lesion, and yet physicians are by no means agreed on some of the most important points in connection with it. Should this paper be the means of eliciting discussion on this much discussed subject, its purpose will have been accomplished.
Mitral regurgitation is an abnormal escape-in other words, a leakage of blood from the left ventricle through the left auriculoventricular orifice into the auricle. This leakage may be due to cellular changes in the mitral valves themselves or to a stretching of the mitral opening. As before stated, mitral insufficiency is the least serious when uncomplicated and the most frequent of the valvular diseases. Gibson, of London, found one hundred and fifty-seven out of two hundred cases, or 78 per cent. of his series. Satterthwaite, of New York, out of seventy-one cases, found forty-five to be mitral insufficiency, or 63 per cent. Walsh and Middleton, of London, give about the same per cent. Satterthwaite says that out of ten cases which he examined post mortem, eight, or 80 per cent., were organic, and two, or 20 per cent., were inorganic or relative. About 85 per cent. of the cases have associated with them some other valvular lesion, usually aortic disease.
Probably the most frequent cause of insufficiency is endocarditis, which is caused by a number of diseases, most frequently by rheumatism. Whether or not heart strain produces endocarditis is a disputed point; certain it is that heart strain will produce a relative insufficiency.
Sclerosis of the vessels, extending to the valves and chorda tendineæ, causes them to contract and
hold the valves back, thus preventing them from closing the orifice. New growths in the orifice may prevent the valves from closing. There are
Read before the annual meeting of the University Medical College Alumni Association.
WHOLE NO. 1348.
many causes of relative insufficiency, and, although it is usually a temporary condition, it may be permanent, depending upon whether or not the conditions producing it can be removed. Violent physical exercise and aortic aneurysm, owing to the ensuing largely dilated left heart stretching the mitral opening, are
Properly to appreciate the symptoms of mitral insufficiency it is necessary to thoroughly understand the changes which take place in the heart and the effects these changes have upon the pulmonic and systemic circulation.
It seems to be the consensus of opinion that, when the left ventricle contracts in a normal heart, the blood which it contains is forced through the aortic opening into the aorta; but, because of the failure of the mitral valves to close, a part of the blood is regurgitated into the left auricle. The left auricle, at: this time in the heart's cycle, is constantly receivng its usual supply of blood from the pulmonary veins and now also contains this blood which has been forced back from the left ventricle, so that the left auricle is distended by an excess of blood. This causes it to become dilated, and its walls soon become hypertrophied because of extra work. In like
manner the left ventricle will receive the amount of blood which it normally would and, in addition, it must receive and take care of the extra amount which was regurgitated at the previous systole. On account of this over distention by an excess of blood the left ventricle is the next chamber to be dilated, and, because of the excessive work it is compelled to perform to take care of the blood it contains, its walls are hypertrophied. At this time in the disease there is a congestion of the circulation in the lungs due to the fact that the left side of the heart is not able to dispose of all of the blood coming to it, thus causing a damming back, as it were, of the blood against the oncoming pulmonary circulation. It
will be seen that this condition of venous stasis in the lungs makes it difficult for the right ventricle to force its contents into the pulmonary artery and allows an extra amount of blood to
be in the right ventricle, thus producing dilatation. Here, again, extra work causes the walls of the right ventricle to hypertrophy. By reason of the dilatation of the right ventricle, the tricuspid orifice is held open and the back flow of blood into the right auricle causes it to become dilated, with subsequent hypertrophy of its walls.
This outline of the mechanism of the heart has been deduced from observation and from the literature, and these conclusions seem to be established by the post mortem findings as reported by Dr. Thomas E. Satterthwaite (New York Medical Journal, July 12, 1902).
Some members of the profession do not agree as to this outline, and it was this disagreement that induced me to investigate the matter as closely as possible. Being unable to get information by post mortem findings, I was compelled to resort to the literature. Musser, Da Costa, Hare, Thompson, and Osler were the authors consulted. These authorities agree to what I have just said. Not being satisfied, however, I addressed the following question to a number of prominent physicians: "In what order do the chambers of the heart dilate and walls hypertrophy in mitral regurgitation?" Replies were received from Dr. George W. Webster, of Chicago; Dr. Thomas E. Satterthwaite, of New York; Dr. Albert Abrams, of San Francisco; Dr. William J. Rothwell, of Denver, and Dr. Alexander Lambert, of New York, all of whom are eminent specialists in their respective localities. From these letters it is evident that the profession are by no means agreed upon this point. Dr. Satterthwaite says: "In mitral insufficiency there is such an imperfect closure of the mitral leaflets that, during systolic contraction of the left ventricle, more or less blood leaks back into the left auricle, already partly filled with blood coming from the lungs. Necessarily the left auricle dilates and then hypertrophies because it has more blood to be driven into the left ventricle. And, inasmuch as the left ventricle has to use more force in order to supply the aorta with its proper quantum of blood, it hypertrophies after dilating. But the overfilling of the left auricle dams the blood back on the lungs and offers such resistance to the column coming from the right ventricle that it also hypertrophies and gives way, causing dilatation of the right auricle as soon as the tricuspid yields.
"I hold that the order of events is: I. Dilatation of the left auricle. 2. Hypertrophy of the left auricle. 3. Dilatation of the left ventricle. 4. Hypertrophy of the left ventricle. 5. Dilatation of the right ventricle. 6. Hypertrophy of the right ventricle. 7. Dilatation of the right auricle.
8. Hypertrophy of the right auricle." It will be seen that Dr. Satterthwaite agrees with all of the textbooks cited above. Dr. Webster says: "Gradual increase in the work of the heart causes it to hypertrophy the same as any other muscle, so long as its nutrition remains perfect; when leakage occurs at the mitral valve, part of the blood flows onward in the systemic circulation, and a portion regurgitates backward into the left auricle. This back flow of blood into the left auricle meets the oncoming current from the lungs and is therefore the first chamber of the heart to become engorged or overdistended. If this regurgitation is not extreme and the nutrition remains. perfect, then the left auricle hypertrophies in response to this increased demand made upon it, and, so long as it is able to cope with the additional burden placed upon it, there is no engorgement of the lungs. Soon, however, the auricle dilates and the lungs become engorged and the work of the right ventricle is increased in propelling the blood through the pulmonary circuit. This results in dilatation and hypertrophy of the right ventricle. Ultimately relative insufficiency of the tricuspid may be established and the right auricle becomes dilated dilated and hypertrophied.
When this occurs the work of the left ventricle now becomes increased while, at the same time, its nutrition has been previously impaired because of low blood pressure in the coronary circulation and systemic circulation; it dilates and the dilatation is greater than the hypertrophy."
Dr. Abrams says: "The left auricle first dilates in consequence of its increased supply of blood derived not only from its normal source, the pulmonary veins, but also from the abnormal regurgitant supply through the incompetent mitral orifice. The right ventricle next dilates and then hypertrophies. The dilatation of the ventricle in question is caused by stagnation of the blood in the territory of the pulmonic circulation, which prevents the output of blood from the right ventricle, and, owing to the increased blood pressure in the pulmonary veins, the same ventricle hypertrophies as a compensatory condition to overcome the stasis. Dilatation and hypertrophy of the left ventricle may or may not occur; if it does occur it is because the hypertrophied right ventricle sends the blood in increased quantity and under augmented pressure through the pulmonary capillaries and veins into the left auricle and thence into the left ventricle, which must first dilate to accommodate itself to the increased quantity of blood and then hypertrophy, owing to the increased work thrown upon it."
Dr. Rothwell takes a very conservative view of the matter and says: "The first change is a primary dilatation of the left auricle to accommodate the increased quantity of blood. This is followed by hypertrophy of its walls in so far as its weak musculature will permit. If the lesion is a serious one and the patient's nutrition poor this compensation is soon lost and dilatation of the right ventricle, dropsy, and death will soon occur. On the contrary, with a moderate lesion and good nutrition, both ventricles gradually hypertrophy. I do not think all cases follow the same course with regard to ventricular hypertrophy; which may take the lead in hypertrophic change will depend on the extent of the lesionthe right ventricle if the lesion is considerable, the left if it is slight."
Dr. Lambert says: "I see a good many mitral insufficiencies in Bellevue, but the ones which come to autopsy are those which show the terminal lesions and not the beginning effects of this lesion. Clinically, however, the first sign, when a mitral lesion begins, is the exaggeration of the second pulmonic sound, and this, in my experience, is evident within twenty-four hours after the leak backward begins. This means extra work for the right ventricle, because of increased tension in the pulmonary artery. What goes on simultaneously in the left auricle cannot be made out because it is placed out of our reach for observation. We see, however, at autopsies, left auricles which are both hypertrophied and dilated and also left auricles which are either hypertrophied or dilated, hence we know that changes occur in this chamber. It is the first chamber to feel the strain of a mitral lesion, and I do not see how we can avoid the conclusion that it must respond in some way to the new condition. I believe that it depends upon the extent of the lesion, the rapidity with which the lesion occurs, and the condition of the muscular wall, whether dilatation or hypertrophy, or both, take place. The same is true of the right ventricle, and I think the strain of the lesion comes on the left auricle and right ventricle at about the same time. The real work of holding a good compensation for any considerable mitral lesion must fall on the right ventricle.
"Of course, it is conceivable that a small, slow forming leak may be cared for entirely by the left auricle, and I have seen this occur."
So long as the hypertrophy is sufficient to maintain an equilibrium in the circulation, the various parts of the general organism will receive enough blood to supply their wants and the effects of the engorgement of the lungs and other organs will not be noticed.
The general symptoms are due to the broken compensation in the heart muscle or an increase in the valvular lesion. When the hypertrophy becomes inadequate the symptoms are referable to the heart and to engorgement in the pulmonary and systemic veins. There is very rarely any real pain experienced, but palpitation is usual. The patient will quite often complain of a sinking sensation. Probably the first symptom of which the patient complains will be shortness of breath, especially upon exertion. When shortness of breath exists without exertion we are warned of a most severe cardiac lesion. Because of the stasis of blood in the lungs an exudate escapes into the bronchi and a cough more or less constant results. The expectoration is frequently bloody in character. The cyanosis which always accompanies this passive congestion, due to broken compensation, can usually be anticipated by observing the overdistended veins under the tongue. A very constant symptom to be observed is nausea in the morning. This is the result of stasis of blood in the vessels of the stomach, producing a chronic gastritis. The enlargement of the liver and spleen, the existence of hæmorrhoids, and the congestion of the kidneys are familiar to you.
In severe cases the urine is scanty, contains albumin and frequently casts. Dropsy, which is distinctly a phenomenon of mitral regurgitation, is usually a symptom of late occurrence.
The nervous symptoms in well established cases of mitral insufficiency are generally well marked, but I have been unable to find any explanation of their ætiology. It is generally conceded, however, that lesions of the right heart produce nervousness and excitability, while lesions of the left heart are followed by depression and melancholy.
Physical signs: On inspection the precordial area appears prominent. As a rule the area from the heart to the left clavicle will appear more prominent than the opposite side. The apex can be seen to be displaced to the left and downward, even as low as the sixth interspace, and the area of pulsation is greatly increased in the late stage, owing to the general enlargement of the heart.
Early in the disease, on palpation, the impulse is regular and strong, while after compensation is broken the impulse is weak and irregular. The pulse indicates a diminished amount of blood in the arteries and, as failure of compensation takes place, becomes small in volume, and there will be irregularity both as to time and volume. On percussion the area of heart dulness is increased to the left and downward until the right ventricle is dilated, when the area of dulness is increased also
to the right. It is contended by some that in enlargement of either the right or left ventricle the increase of dulness is to the left. This mistaken idea probably results from the fact that we are unable to distinguish cardiac dulness from hepatic dulness. In order more thoroughly to satisfy myself on this point, I addressed the following question to Dr. Abrams: "In what direction does the dulness on percussion increase in dilatation of the left and in dilatation of the right ventricle?" In reply he said: "In dilatation of the left ventricle the percussional dulness is increased toward the left and downward; in dilatation of the right ventricle, dulness is increased to the right of the sternum, which is specially pronounced if the right auricle is dilated.
"Substernal dulness in the lower sternal region is present and, not infrequently, as my skiascopic studies show that in dilatation of the right ventricle the cardiac shadow corresponding to this chamber of the heart extended downward. This extension of the right ventricle downward cannot be determined by percussion, owing to the juxtaposition of the liver, as one is unable to differentiate hepatic from cardiac dulness. A clue to the preceding condition is afforded, however, by the low position of the liver, a condition which I assume to be compensatory to provide sufficient thoracic space for the enlarged ventricle. I am aware that an enlarged liver is associated with uncompensated mitral lesions, but the condition to which I refer is dissociated with any enlargement of the liver and occurs at a time when the lesion is fully compensated."
Upon auscultation in the mitral area a murmur is heard with the point of greatest intensity in that region. It is systolic in time and, when very loud, it may entirely replace the first sound. and the physician will hear nothing but the murmur. The character of the sound is not the same in all cases, neither does the character of the sound indicate the gravity of the lesion. A very grave lesion may be accompanied by a low, soft murmur, while a loud murmur may attend a slight lesion. The chief characteristics of the murmur are that it is systolic in time and is transmitted to the left, sometimes being heard in the back and sometimes all over the chest and, in children, even over the abdomen.
The most important diagnostic point noticed on auscultation is an accentuation of the pulmonic element of the second sound. It is said to be of sufficient importance to call the attention of the physician to a possible mitral regurgitation even when a murmur cannot be heard at the apex.
This accentuation is due to the increased ten
sion in the pulmonary artery, which occurs, as explained above, on failure of the left heart. The position of the patient influences the murmur, it being heard best when the patient is lying down and often ceasing when the patient stands. It is also increased after exercise. Reduplication of the first sound is very significant of mitral regurgitation when it is present. This is best heard. near the apex. This condition is also found in arterial degeneration, pulmonary emphysema, anæmia and a few other conditions, but does not occur in any other valvular lesion. Of course, if there are other lesions, valvular or otherwise, the signs and symptoms of those lesions will be present.
The diagnosis of this disease is usually not difficult if the heart is examined and attention is given to the physical signs. Patients are frequently treated, however, for chronic gastritis when the gastritis is secondary to a valvular lesion. I knew of one case of mitral insufficiency that was treated for pericarditis. When a murmur is present in pericarditis, it is usually a to and fro murmur and is not transmitted. There is a murmur heard at the apex due to anæmia. This can be distinguished by the history of the case, the unintensified pulmonic second sound, and the absence of cardiac enlargement. The impulse of the heart against the edge of the lung between the heart and chest wall sometimes produces a cardiorespiratory murmur, but it is heard only at the end of a full inspiration and is not transmitted. So that if we have a murmur at the apex, systolic in time, transmitted to the axilla, an accentuated pulmonic second sound, enlargement of the heart, and evidences of blood stasis, we may safely diagnosticate mitral insufficiency.
A New Outdoor Naval Hospital.-The naval authorities will submit an estimate of $50,000 to Congress for the establishment of an outdoor hospital for the treatment of tuberculous patients in the navy. There was some talk of converting the abandoned naval station at Port Royal, S. C., into a resort of this kind, but it is felt that this use of the buildings could not be made without special authority from Congress, and inasmuch as an appropriation would be needed for that purpose, it is considered as economical to buy an old farm somewhere in the hills, not far from the seacoast, where naval consumptives could be treated with a view to their return to the service instead of their discharge on account of disability and the addition to their names to the pension roll. It is proposed to buy a farm and build a hospital with. modern equipments, and carry out the policy of treatment which has been adopted with such success at Pensacola, Fla.
THE PRESENT CONDITION OF TENONTOPLASTY.
the employment of the periosteal method of suture and to the elongation of the flexor tendon by means of artificial tendons. As a matter of fact, the tendon of the quadriceps above the patella is frequently found brittle, and this must undoubtedly arise from the muscular elements which here are intermingled with the tendon, the fatty degeneration of which naturally must loosen the texture of the tendon. It is, therefore, advisable to fasten the flexor tendon not only to the quadriceps tendon, but also to the periosteum of the patella. When I recommend and employ at this place the periosteal suture, I do not think to make myself guilty of an inconsequence, such as Lange has reproached me with, because we here have to deal with quite special conditions, and because here the periosteal suture can be executed on a broad area, in the whole length of the patella; hence, certainly, it is much more reliable than the suture of a simple tendon cross cut to the periosteum. The addition of silk tendon at the knee has been rarely necessary with me, in fact, only in cases of extreme flexion-contraction. Generally the tendon ends of the flexors can be made long enough by careful dissection to be at least sutured to the patella; it is often even possible to draw the tendon down to the ligamentum patellæ proprium. The technics of Lange, which inserts the artificial silk tendon directly into the tuberosity of the tibia, I do not consider rational, because by it a decidedly less advantageous direction of traction is gained than by a transplantation of the tendons to the lower end of the quadriceps or to the patella. By the latter arrangement the conditions of traction are essentially normal.
BY PROFESSOR VULPIUS, M. D.,
(Continued from page 594.)
The attempts at transplantation in the thigh have for their object the replacing of the paralyzed quadriceps. The loss of this muscle in itself does not always demand treatment. In spite of its paralysis, extensive motions of the limb can be observed. Treatment is only necessary either when the ligaments of the knee joint have given way or when the joint is a flail joint or is much overextended, genu recurvatum, the leg deviating to one side, genu velgum paralyticum, when a contracture of the flexors has taken place. In the first case, the treatment can only consist of a fixation of the joint by means of orthopedic apparatus or of arthrodesis. The contracture of the flexors is best removed by the transplantation of the flexors into the quadriceps. It is indeed sufficient simply to cut the flexors, to render possible the extension of the joint, and with it, to render the leg again useful. But by it the strength of the flexors is diminished, without this strength of which they are deprived being again made use of in a rational manner, and moreover, it is not rare for the flexors to shrink again after a tenotomy, so that we have a recurrence of the flexor contracture. Both these disadvantages are obviated if we use the strength derived from the flexors to strengthen extensions. At first the task of replacing functionally the quadriceps seems very difficult. because we have to do with a powerful, and especially functionally much worked, muscle body; however, experience has taught us that a sufficient compensation can very well be accomplished. We, for example, can use for transplantation into this muscle the sartorius, which, like the extensor of the toes, is frequently spared from paralysis-often even proves to be very much hypertrophied. Its anatomical makeup makes it very fit for transplantation in a functional respect, the superficial position of its end tendon behind the condylus internus femoris making its transplantation technically easy. From the same opening, also, an adductor may be laid bare, and, further, both medial flexors may be brought forward. A lateral posterior cut, finally, renders possible the transplantation of the biceps. In bringing the three flexors to the front we by no means lose the power of flexion of the knee joint. It takes place passively and it is further influenced by both bodies of the gastrocnemius. It was this transplantation in the thigh which led Lange to
Since such transplantations were first first tried in America this proceeding has also been employed with us in a large number of cases with fine. results. I myself command a series of about thirty such operations. Generally, though, we have to give a diligent after-treatment to improve and strengthen more and more the motion of extension, which at first is just indicated. But we generally succeed in attaining, if not a normal. yet a sufficiently strong extension of the leg, and through it, as well as through the exclusion of the flexor contraction, in again rendering the limb sufficiently useful.
Also, in the upper extremity, attempts with the transplantation of tendons have been tried in cases of spinal infantile paralysis. Codivilla has tried to replace the opponens pollicis of the hand, although without success. Operation, on the other hand, on account of paralysis in the vicinity of the large nerves of the arm, and especially on account of paralysis of the radialis, has proved