mitral reflux. I have never found it except in those cases where left
ventricular dilatation greatly exceeded the hypertrophy.
Percussion.--Percussion reveals an increase in the area of cardiac
dulness, especially laterally; it extends both to the left and right of
the normal line, as well as downward. The area of superficial as well
as deep-seated dulness will be increased laterally and downward.
Auscultation.--Mitral insufficiency is attended by a systolic murmur
which either completely or partially replaces the first sound of the
heart. The quality of the murmur is variable, and not in itself as
distinctive as that of mitral stenosis. It is usually a soft and
blowing bellows murmur; sometimes, toward its end, the murmur will
assume a distinctly musical character.
While the first sound of the heart may be heard distinctly in the early
stages of mitral reflux, later the murmur in nearly all cases takes the
place of the heart-sounds. Hence many English writers rightly
denominate this murmur as post-systolic rather than systolic in its
nascent stages. It is heard with its maximum intensity at the
apex-beat. Its area of diffusion is to the left on a line corresponding
to the apex-beat. It is audible at or near the inferior angle of the
left scapula. It can be heard between the lower border of the fifth and
the upper border of the eighth vertebra, at the left of the spine, with
nearly the same intensity as at the apex. The murmur may be absent from
the latter situation until cardiac hypertrophy is developed.
The second sound of the heart over the pulmonary valves is accentuated,
while below the junction of the third rib with the sternum on the left
side both heart-sounds are feeble. Skoda first drew attention to
exaggeration of the second pulmonary arterial sound as a positive and
unerring indication of mitral regurgitation.
An intensified pulmonary second sound requires a strong right ventricle
and an intact tricuspid valve, and is not always present. In general
terms, the area of diffusion of a mitral regurgitant murmur is toward
the left of the apex-beat. Whatever may be its character, the murmur is
generally loudest at its commencement. A loud systolic murmur at the
apex, and not heard at the back, is probably not produced by mitral
reflux.
As at the aortic orifice, so at the mitral, stenosis and regurgitation
are apt to occur in the same individual, giving rise to a combined
presystolic and systolic murmur, which is a continuous murmur that
begins shortly after the second sound of the heart and often continues
until the second sound commences. The two sounds, although mingling to
form one murmur, can, in the majority of cases, be readily
distinguished from each other, for the point of maximum intensity and
the very limited area of diffusion of a presystolic murmur readily
distinguish it from a mitral systolic which is audible in the left
scapular region. It is important to recognize the existence of both
these {674} murmurs in estimating the prognosis in any case. Guttman
mentions a case where five distinct murmurs were combined and yet
clearly distinguishable.
DIFFERENTIAL DIAGNOSIS.--It is usually not difficult to recognize
mitral regurgitation. The seat and rhythm of the murmur and its area of
diffusion are sufficient to distinguish it from other cardiac murmurs.
The character of the pulse, the symptoms referable to the right heart,
and the pulmonary complications will also assist in its diagnosis.
It may, however, be mistaken for aortic obstruction, since both give
rise to a systolic murmur, for tricuspid regurgitation, for fibroid
disease of the heart, and for roughening of the ventricular surface of
the mitral valve or of the ventricular wall near the aortic orifice.
The diagnosis between mitral regurgitation and aortic stenosis has
already been given (see page 657).
Mitral and tricuspid insufficiency both produce a systolic murmur, but
a mitral regurgitant murmur has its maximum of intensity at the apex,
and is conveyed toward the left axillary and scapular regions, while
the maximum intensity of a tricuspid regurgitant murmur is to the right
of the base of the xiphoid cartilage, and it is transmitted upward and
to the right: the area of transmission establishes the diagnosis.
Pulmonary symptoms are prominent in mitral reflux, and absent in
tricuspid regurgitation. The pulmonary second sound is markedly
enfeebled in tricuspid regurgitation, and markedly intensified in
mitral regurgitation.
Fibroid disease of the heart may produce a systolic apex murmur, but it
is an exceedingly rare disease, a pathological curiosity.[20]
[Footnote 20: In the _Pathological Transactions_ (1874, vol. xxv. p.
64) Fagge records a few cases, and mentions that perhaps one positive
indication of fibroid disease of the heart, rather than of a valvular
lesion, may be found in its resisting treatment with greater
obstinacy.]
Roughening of the ventricular wall gives rise to a murmur which has its
maximum intensity at the base of the heart, and is transmitted along
the aortic arch and into the vessels which spring from it in the
thorax.
The vibration of an irregular chordæ tendineæ stretched across the
aortic orifice, its extremities being inserted into opposite walls of
the ventricle, may produce a systolic musical murmur, but the line of
its transmission will correspond to that of an aortic obstruction. A
systolic mitral murmur due to the sudden rupture of one or a number of
the valve-flaps, of the papillary muscles or tendons, is accompanied by
a loud systolic blowing murmur, which is immediately accompanied by all
the urgent symptoms of acute pulmonary congestion.
Pulmonary Obstruction.
On account of the infrequency of disease of the pulmonic valves very
little is known of the phenomena to which such diseases may give rise.
In fact, they are so rare that there is no written history of their
subjective symptoms; their diagnosis is only arrived at by exclusion,
and they cannot be recognized except by the physical signs which attend
them.
As has been already stated, endocarditis in the right heart is rare,
except in intra-uterine life, and the various conditions of the aorta,
atheroma, aortitis, etc., which I have mentioned in the etiology of
aortic valvular disease have no analogues in the pulmonary vessels.
Usually, valvular disease of the right heart is the sequela of lesions
in the left. It must be remembered, however, that the pulmonary artery
may become atheromatous. I have already shown (see p. 666) how certain
valvular diseases of the left heart may induce such a pathological
condition. But even under such conditions disease of the pulmonary
valves is rare. Balfour {675} believes that constriction of the
pulmonary artery may occur at various periods of intra-uterine life. As
a rule, the pulmonary valves are subject to no lesions except
congenital malformation.
MORBID ANATOMY.--Bertin records an instance of pulmonary obstruction
where the valves, distorted and adherent, formed a horizontal septum
across the orifice, it being barely one-fourth of an inch.
A rigid tricuspid valve has been found to be the cause of obstruction
at the pulmonary orifice, the pulmonary valves themselves being normal.
A few autopsies have revealed obstructions at the pulmonary artery,
caused not so much by valvular defect as by aneurisms, tumors of the
pericardium or of the anterior mediastinum, enlarged bronchial glands,
or pressure of a solidified lung.
The pulmonary artery may be occluded just beyond the valves by a
cancerous tumor, and there are examples where a phthisical process in
the left lung has induced it.
A murmur indicative of pulmonary obstruction may be produced by a
cardiac thrombosis.
I have placed these statements under the head of its morbid anatomy for
the reason that they cannot be appreciated and their pathological
significance realized during life.
Reasoning from analogy, obstruction at the pulmonary orifice ought to
be followed by compensatory hypertrophy of the right ventricle and
accompanied by tricuspid regurgitation and dilatation of the right
auricle.
Ormerod records 3 cases[21] where pulmonary obstruction was
diagnosticated during life, and where the post-mortem proved the
accuracy of the diagnosis: 2 of these cases occurred in men under
twenty-eight, and the other in a woman of twenty-one. In 2 of these
cases all the other cardiac valves were healthy. The pulmonic orifice
would barely admit the introduction of a goosequill. Warburton Bigbie
mentions a case (man æt. eighteen) where reflux and stenosis at the
pulmonary orifice coexisted. There were four valves, and these were
incompetent. All the other valves were normal.
[Footnote 21: _Edin. Med. and Surg. Journ._]
Congenital stenosis of the infundibulum of the right ventricle is the
probable result of foetal myocarditis or of syphilis.
I have never met but two pulmonic obstructive murmurs where subsequent
autopsies were obtained. In both cases it was found that the murmur had
been produced by mediastinal tumors pressing on the pulmonic artery so
as to diminish the calibre.
ETIOLOGY.--Pulmonary stenosis is rarely the result of endocarditis or
of degenerative changes in the pulmonary artery. Bertin states that
when abnormal communication between the two sides of the heart has
existed, the arterial blood has excited endocarditis in the right
heart.
Syphilis has been advanced as a possible cause of degenerations at the
pulmonic orifice.
SYMPTOMS.--The only rational symptoms that have been noted in the few
recorded cases of pulmonic disease admit of manifold explanations, and
no one is either constant or diagnostic. In some cases anæmia existed,
in others there were cardiac palpitation, dyspnoea, cyanosis, and
dropsy; but none of these belong exclusively to a pulmonic lesion nor
do they necessarily depend upon it.
Physical Signs.--Inspection, palpation, and percussion give negative
rather than positive results. In a few instances palpation may give a
systolic thrill confined to the second left intercostal articulation.
Such a frémissement results both from roughness and contraction of the
pulmonic orifice.
Auscultation.--A systolic murmur is heard with its maximum intensity
directly over the pulmonic valves; it is very superficial, and
consequently {676} very distinct, and it is limited in its diffusion.
It is never heard at the xiphoid cartilage nor along the course of the
aorta. If it has an area of diffusion, it is toward the left shoulder.
The murmur is loud and soft in character, sometimes bellows. It is not
audible in the vessels of the neck nor is it attended by arterial
pulsation.
When phthisical consolidation partially occludes the pulmonary artery,
a loud but soft systolic murmur is heard, which is sometimes
high-pitched and musical, and often entirely suspended during a full
inspiration. In some few instances there is a bruit de diable in the
jugular veins.
DIFFERENTIAL DIAGNOSIS.--It is possible to confound a pulmonic
obstructive murmur with a mitral regurgitation which is propagated
upward into the left auricular appendix. But the area of a mitral
regurgitant is also backward, and by this it could be distinguished
from a pulmonic obstruction. Besides, in mitral disease the pulse is
very different from the pulse of pulmonary stenosis.
Aortic stenosis can hardly be mistaken for pulmonary obstruction, for
the arterial pulsation, the peculiar pulse, and the transmission of the
murmur into the arteries of the neck will suffice to discriminate
between them.
An aneurism at the sinus of Valsalva may produce a systolic pulmonary
murmur by the pressure which it produces upon the pulmonary artery. It
would be impossible to distinguish it from a pulmonic stenosis.
The diagnosis of pulmonary obstruction is usually reached only by
exclusion.
Pulmonary Regurgitation.
This form of valvular lesion is exceedingly rare; indeed, many doubt
its occurrence. The lesion seldom occurs except as the result of injury
or congenital defect, and there are but few well-authenticated cases in
medical literature.[22]
[Footnote 22: _Path. Trans._, vol. xvi. p. 74.]
The statement[23] that the pulmonary valves exhibit a cribriform
condition nearly as often as the aortic is not sustained in this
country by the results of post-mortems. In one of the cases to which I
have referred (p. 675) as an example of pulmonary stenosis the valves
were likewise found insufficient. In Bigbie's case (referred to on p.
675), where there were four flaps to the valve (producing obstruction),
there was marked insufficiency coexisting.
[Footnote 23: _Dis. of the Heart_, Bellingham.]
The morbid anatomy, etiology, and rational symptoms do not require a
separate consideration. The anatomical appearances are the same as
those found in similar conditions of the aortic valves, and the
etiology and rational symptoms are the same as those of pulmonic
stenosis.
Physical Signs.--Theoretically, pulmonic regurgitation should be
accompanied by a diastolic murmur having its maximum intensity over the
pulmonic valves, and its area of diffusion should be downward and
toward the xiphoid cartilage. It should be soft and blowing in
character. This murmur is rarely heard alone: it is usually associated
with obstruction at the same orifice or with some murmur whose origin
is on the left side of the heart.
Niemeyer states that dyspnoea, hemorrhagic infarction, and consumption
of the lungs have followed insufficiency at the pulmonary orifice. No
other authority mentions any such symptoms, while the assignment of
valvular disease as a cause of phthisis is not based upon clinical
facts.
With a pulmonic regurgitant murmur there should be on palpation and
percussion physical evidences of hypertrophy and dilatation of the
right heart, the rationale of whose production would be identical with
that which was considered in aortic regurgitation. I have never heard a
regurgitant pulmonic murmur.
{677} DIFFERENTIAL DIAGNOSIS.--The murmur of pulmonary regurgitation
may be mistaken for that of aortic regurgitation. The points in
connection with their differentiation are fully discussed on p. 664.
The PROGNOSIS and TREATMENT are identical with those of the former
lesion.
Tricuspid Stenosis.
This valvular lesion is so rare that there are no established rules for
its diagnosis.
Its MORBID APPEARANCES and ETIOLOGY are the same as those of pulmonic
stenosis.
The SYMPTOMS of tricuspid stenosis would be those due to obstruction to
the entire venous circulation. The right auricle would be dilated, and
there would be visceral enlargements in the abdomen, cyanosis of the
face and extremities, scanty and albuminous urine, hemorrhoidal tumors,
headache, dizziness and vertigo due to passive cerebral hyperæmia, and
finally general anasarca. The few recorded cases were associated with
mitral stenosis with one exception, a case of Bertin's.[24]
[Footnote 24: _Traité des Maladies du Coeur_, Obs. 17.]
In a case exhibited by Quain the tricuspid flaps, thick and opaque,
were united for one-third of their extent. In the other cases the
valve-flaps formed a diaphragm whose central opening varied in size,
admitting only the point of one finger. In every condition of tricuspid
stenosis the heart was enlarged.
Tricuspid stenosis (as in pulmonic stenosis) may be the result of
pressure of tumors.
In all well-authenticated cases the chief symptoms seem to be extreme
lividity, palpitation, and dyspnoea.
Physical Signs.--Inspection reveals general cyanosis. The jugulars are
turgescent and exhibit presystolic pulsation. This pulsation is
sometimes the only inconvenience the patient suffers.
Palpation may discover a venous thrill at the base of the neck.
Percussion may show the right auricle to be greatly enlarged, and
cardiac dulness will be increased laterally and toward the right.
Auscultation.--Tricuspid stenosis should be attended by a presystolic
murmur whose maximum intensity would be at the lower portion of the
sternum just above the xiphoid cartilage. This murmur may be propagated
faintly toward the base, but never toward the apex of the heart. It is
sometimes accompanied by fremitus.
Hayden offers the following diagnostic point: The murmur of mitral
stenosis (without which tricuspid stenosis never occurs) is limited to
the apex region; a murmur of the same rhythm is produced at the sternum
by tricuspid stenosis, "and between these two localities there is a
point where no murmur can be heard."
It is unnecessary to consider its differential diagnosis.
The lesion would be diagnosticated (if at all) by exclusion, and
prognosis and treatment would depend on the gravity and sequelæ of the
accompanying condition--viz. Mitral Stenosis (q. v.), for the rule is,
that stenosis of the tricuspid never occurs unless there is extensive
mitral obstruction, and the latter condition is always the predominant
one.
Tricuspid Regurgitation.
Regurgitation at the tricuspid orifice is generally secondary to mitral
stenosis or regurgitation; primary disease of the tricuspid valves,
however, is not infrequent.
{678} MORBID ANATOMY.--The valvular lesions which lead to tricuspid
insufficiency are similar to those which produce mitral insufficiency.
The valves are thickened, shrunken, and opaque, the papillary muscles
are shortened, thickened, and the chordæ tendineæ undergo similar
changes and are sometimes adherent.
The valves or the chordæ tendineæ and columnæ carneæ may rupture; in
either case acute and extensive insufficiency results, as has been
stated. Acute endocarditis of the right heart is rare in adult life,
but when it occurs the tricuspid valves are its primary and principal
seat.
The reason for this is found in their anatomical structure and in the
tension to which they are subject in diseases of the mitral valves.
They are rarely the seat of rheumatic endocarditis or calcareous
degenerations.
Ulcerative endocarditis is seldom met with in the right heart. In a
case recorded by Charcot and Vulpian one of the tricuspid valves was
softened and perforated, presenting numerous vegetations. Scattered
abscesses in the lungs were found in this case.
Any infection through emboli from the tricuspid flaps will produce
secondary effects within the thoracic cavity. The first effect of
tricuspid regurgitation is dilatation of the right auricle; following
this there will be more or less hypertrophy of its walls. As soon as
the valves in the subclavian and jugular veins are no longer able to
resist the regurgitant current jugular pulsation follows. But before
this occurs the tributaries of the inferior cava and the organs to
which they are distributed will become greatly engorged, for they have
no valves to resist the regurgitant current, as are found in the veins
coming from the upper part of the body. The inferior cava and the
hepatic veins sometimes become enormously distended under these
circumstances, and the liver will show the peculiar section that has
gained for it the name of nutmeg liver.
Following the hepatic changes, the skin assumes a dingy yellow hue.
When this is combined with cyanosis it produces a peculiar greenish
tint which is only met with in heart disease. The spleen enlarges and
hardens; the mucous membrane of the stomach is congested, ecchymotic,
and often presents numerous hemorrhagic erosions. Intestinal catarrh is
subsequently developed, and the general venous congestion within the
abdominal cavity is exhibited by hemorrhoids and ascites. The kidneys
become congested and stony, and thrombi may form in the femoral vein
and induce subsequent pulmonary infarctions.
The stasis in the veins below the diaphragm is accompanied by
transudation of serum--first in the ankles, and thence the dropsy
progresses upward until the patient may finally reach a condition of
general anasarca. The obstruction to the general systemic circulation
which results may subject the left ventricle to so much extra labor
that it hypertrophies, and then we have the infrequent occurrence of
disease of the left heart following that of the right.
Since tricuspid reflux has mitral disease for its principal cause in
abnormal cases, the heart becomes greatly enlarged and a condition of
extreme cardiac dilatation and hypertrophy is reached.
ETIOLOGY.--As has been stated, the most frequent cause of tricuspid
regurgitation is mitral disease, either stenosis or regurgitation. Any
condition of the lungs which will produce hypertrophy and dilatation of
the right ventricle will lead to it; it is met with in extensive
pulmonary emphysema, in cirrhosis of the lung, and in extensive chronic
bronchitis. Balfour regards chronic bronchitis as its most frequent
cause after mitral stenosis.
It is possible for any valvular disease in the left heart, when of long
duration, to lead to tricuspid regurgitation. From all these causes the
rationale is {679} the same: the abnormal amount of blood in the right
ventricle presses with undue force against a valve, which physiologists
regard as normally slightly insufficient; the stress upon the
valve-flaps and the valvular attachments is such that endocardial
inflammation is excited at the part subject to the greatest strain, and
valvular insufficiency is the result.
It is possible for disease of the tricuspid valves to result from any
of the causes which have been enumerated on p. 666 as etiological
factors in valvular diseases.
SYMPTOMS.--Tricuspid regurgitation being in the majority of cases
secondary to some other valvular disease or some chronic pulmonary
affection, its symptoms during the early stages are vague and masked by
those of the primary disease. But as soon as the valves become so
insufficient that the venous return is markedly impeded, a train of
symptoms is developed which has its origin in the visceral derangements
already referred to.
In addition to these symptoms there may be, with extensive tricuspid
regurgitation, cardiac palpitation, cardiac dyspnoea, and marked
irregularity in the force and rhythm of the heart. The liver and spleen
are enlarged, the skin becomes dingy, and there is obstinate
constipation with hemorrhoids. The liver is likewise rendered very
liable under such circumstances to attacks of interstitial hepatitis.
Venous stasis is evinced by dyspepsia, nausea, vomiting, and
hæmatemesis. The secretion of the kidneys is scanty, dark-colored, of
high specific gravity, often containing albumen and casts.
Passive cerebral hyperæmia is marked by headache, dizziness, vertigo,
and muscæ volitantes, and there is a peculiar mental disturbance which
is not met with in any other form of heart disease.
Late in the disease, if the patient is placed in a horizontal position,
the face becomes turgid and blue, and if he remain long in the
recumbent position stupor and coma may supervene. Jugular and
epigastric pulsation are characteristic physical signs.
A very late symptom is dropsy, which begins at the ankles and extends
upward until there is general anasarca. It is a point to be noticed
that in the dropsy from tricuspid reflux the genital organs suffer
slightly if at all.
[Illustration: FIG. 48. Tricuspid Regurgitation (after Galabin): _a_,
_a_, anadicrotic wave synchronous with the auricular systole, and
caused by reflux into the large veins.]
Physical Signs.--Inspection.--In extensive tricuspid disease the area
of the cardiac impulse is increased more than in any other valvular
lesion. This area sometimes extends from the nipple to the xiphoid
cartilage, and it may reach as high as the second right intercostal
space. There is a visible impulse in the jugular veins, more apparent
in the right than in the left. Sometimes the veins in the face, arms,
and hands, or even the thyroid and mammary veins, are seen to pulsate.