[Reprinted from The Medical News, October 20 1894.] 
AN UNDESCRIBED HEART-MURMUR. 
By J. N. HALL, M.D., 
PROFESSOR OF THERAPEUTICS* ANX? CLINICAL MEDICINE IN THE 
UNIVERSITY OF COLORADO. 
In quite an extended search in the literature of dis- 
eases of the heart I have been unable to find any note 
of a murmur such as is here described. 
Mrs. C., a widow, thirty-two years of age, a housewife, 
has borne four children and has had two miscarriages, 
the last being only a month ago. Ten years ago she 
had an attack of acute rheumatism confining her to bed 
for five months. She has had several slight attacks 
since. She lost considerable blood at the last miscar- 
riage, and is rather anemic. Upon August 6th, when I 
first saw her, the cardiac area was enlarged to the mam- 
millary line, the apex-beat under the nipple, in the fifth 
space, and the cardiac action decidedly feeble. An apical 
systolic murmur, propagated to the mid-axillary line 
was heard, with accentuation of the pulmonary second 
sound. There was moderate edema of the feet, and 
marked dyspnea ; the respirations were fifty per minute 
while sitting in the chair, the pulse 90, and feeble. No 
pulmonary edema was found. 
I exhibited the patient at the clinic as an example of 
mitral regurgitation, in spite of the fact that the murmur 
was not propagated to the back. The feeble action of 
the heart seemed to me sufficiently to account for this, 
while the lack of such transmission was in my mind 
more than counterbalanced by the presence of edema 
and particularly the marked dyspnea, especially upon 2 
the slightest exertion. In fact, I take decided exception to 
the dictum of Cammann and others, that it is necessary 
to hear a mitral murmur in the back before deciding 
that it indicates regurgitation. I believe I have seen 
several examples that were exceptions to this rule. 
The woman was given iron and a laxative, and re- 
turned on August 29th. Her condition was then about 
the same, excepting that the anemia was a little improved, 
and the murmur followed the first sound and the apex- 
beat, instead of being synchronous with them as before. 
The cardiac action was still so feeble that digitalis was 
prescribed, and a few days later the patient was re- 
examined. 
The edema of the feet at that time had practically 
disappeared. The pulse was 70, and of much better 
strength. The apex-beat was easily visible and palpable. 
The murmur followed the first sound, and the visible beat, 
and was transmitted to the mid-axillary line. The res- 
pirations reached 50 per minute five minutes after slowly 
ascending a short flight of stairs. The basic second 
sound came just at the termination of the murmur, but 
at the apex was obscured by it. The case was exhibited 
to many students, and to Drs. McLauthlin, Lobingier, 
and Hopkins, of the University of Colorado. There 
was no room for disagreement as to the facts, viz., that 
the apex-beat and first sound, with a distinct movement 
imparted to the stethoscope, all preceded the murmur. 
The only explanation of this state of affairs which I can 
conceive, is as follows : 
The mitral valve was incompetent, and regurgitation 
occurred through it, giving rise to the murmur, as is 
usual in such cases. The right ventricle, somewhat 
hypertrophied, gave rise to the apex-beat and a normal 
first sound, and displaced the stethoscope firmly applied 
to the apex region, forming the first element in a redu- 
plication of the first sound of the heart. The second 
part of the reduplication was made by the left ventricle, but instead of a distinct heart-sound a mitral murmur 
was heard, owing to the regurgitation through the mitral 
valve. I believe this explanation sufficiently accounts 
for all the phenomena observed. 
Barr has reported a somewhat similar case in which the 
left ventricle contracted first, with a mitral murmur, and 
was followed by the normal contraction of the right 
ventricle. Sansom reports a case in which, over the 
ventricles " a murmur tailed off from the second redup- 
licatory sound," at the apex only the murmer being 
distinguishable. The case later developed a presystolic 
murmur, and the reduplication disappeared, which 
would appear to confirm his explanation that it was due 
to a presystolic flap of the mitral valve. It obviously 
differs from the case we are considering. 
George Johnson believed that reduplication occurs 
from the contraction first of the hypertrophied auricle, 
followed by that of the ventricle. It is not reasonable, I 
think, to suppose that the auricle could possibly cause 
the distinct apex-beat, even if it could cause the sound. 
Sansom has stated, nevertheless, that in certain cases of 
mitral stenosis the auricle may cause a distinct impulse. 
There has been, I believe, no evidence of mitral stenosis 
in this case, and I consider it opposed to Johnson's 
theory. 
Hayden believed that the reduplication occurred from 
a resolution of the first sound into a muscular sound 
and a valvular element, the latter occurring after the 
former. It seems to be conclusively proved that the 
valve closes early in systole, however, and I certainly 
fail to see any bearing upon the present case. Potain's 
theory that reduplication is generally only apparent, 
being in reality due to a presystolic flapping of the mitral 
valve in association with a normal first sound, evidently 
would not apply here, as the apex-beat accompanied 
the first sound. 
I hope to be able to follow the case, and shall note 
any further developments. 
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