on a bronchus, reduce its calibre one-half, and thus interfere with the
functional activity of the left lung. When the pulmonary hyperæmia is
extensive violent physical exertion or violent coughing may cause a
rupture of one of the larger pulmonary vessels, and true pulmonary
apoplexy result.
Bronchorrhoeal expectoration of large quantities of glairy mucus is a
very frequent result of the intense hyperæmia of the mucous membrane of
the bronchial tubes which sometimes occurs in mitral stenosis. The
secretion is increased with every increase in the passive hyperæmia.
The lungs are at all times so liable to congestion and oedema that any
sudden or violent exercise may lead to a rapidly fatal result. Again,
when the conditions enumerated have existed for some time, mitral
stenosis may lead to hypertrophy of the right heart. In some rare cases
the tricuspid orifice has become slightly insufficient.
ETIOLOGY.--Mitral disease is especially met with in the young, and in
the child it is almost invariably a stenosis. The average age is about
thirty-one; it is very rare to find it occurring after the fiftieth
year of life. It seems from statistics that it is nearly twice as
frequent in females as in males.
It is not infrequently of congenital origin. Acute rheumatic
endocarditis is its most frequent cause. The mitral valves are more
frequently affected in chorea than the aortic. In some few instances
stenosis results from extension of the inflammatory process from the
aortic semi-lunar valves, or prolonged aortic regurgitation and
stenosis may lead mechanically to mitral disease, but not to stenosis.
Niemeyer regards atheroma as an exceptional cause of mitral stenosis.
No other authority regards it as a possible cause.
{667} It is a question whether scarlatina or diphtheria tends to
produce in children a valvular endocarditis which is followed by mitral
stenosis. It seems plausible, since in many young children it is
certain that mitral stenosis has not resulted from either rheumatism or
chorea. Finally, with the exception of atheroma, all the causes
enumerated in the etiology of aortic stenosis may be the cause of
mitral stenosis.
SYMPTOMS.--Rational Signs.--The subjective cardiac symptoms of mitral
stenosis are few. There may be no such symptoms. Usually, after violent
exercise there is more or less cardiac palpitation, but this will cease
as soon as the auricle can relieve itself, which is readily
accomplished by the patient's assuming a recumbent position on the
right side with the head slightly elevated. This class of patients as a
rule are pale and anæmic. There is a sharp pain frequently felt in the
region of the apex, which is always suggestive of mitral stenosis. The
pulse is regular and normal in character so long as the auricular
hypertrophy compensates for the auricular dilatation.
When the ventricle is unable to receive and discharge its normal
quantity of blood with normal regularity, the pulse becomes small in
volume, feeble in force, rapid and irregular in rhythm. The
sphygmograph exhibits a tracing, frequently called the mitral pulse;
the sphygmograph tracing is the same as when the ventricle throws a
greatly diminished blood-current into the aorta (Fig. 44). This is
asystolism, and the pulse is a clear indication of the condition.
[Illustration: FIG. 44. Mitral Obstruction (from Patient in Bellevue
Hospital).]
Balfour differs from other authorities in the statement that among the
most remarkable subsidiary phenomena of mitral stenosis is irregularity
of cardiac rhythm, which, always present in a greater or less degree,
is sometimes a diagnostic phenomenon. The auricular systole commences
earlier than normal on account of its hypertrophy. This premature
contraction of the auricle, stimulating ventricular contraction, is
indicated by a second ventricular systole which is much less forcible
than the first.
The passive pulmonary hyperæmia attending the advanced stages of this
form of cardiac disease causes habitual dyspnoea, which is exaggerated
by physical exertion and is attended by a dry, hacking, teasing cough
which resembles the so-called nervous cough.
After violent or prolonged exertion there may be bronchorrhoea, a pint
of glairy, watery mucus often being expectorated in a few moments. Not
infrequently severe exercise induces attacks of profuse, watery,
blood-stained expectoration, indicative of pulmonary congestion and
oedema. Sometimes the exertion of walking rapidly against a strong wind
will induce such intense congestion and oedema of the lungs in one with
extensive mitral stenosis as to cause sudden death.
Hæmoptysis is not infrequent, small quantities of pure florid blood
being expectorated.
Orthopnoea is not a frequent symptom of mitral stenosis, for even in
extensive and long-standing cases the pulmonary congestion is not
constant, as the auricle is able ordinarily to empty itself, and only
becomes engorged during active physical exertion or great mental
excitement.
It should be mentioned here that the old idea, that "mitral stenosis
sometimes produces hypertrophy of the left ventricle," is fallacious.
In no instance can it be attributable to mitral stenosis.
{668} Physical Signs.--Inspection.--As the left ventricle does not
receive its normal quantity of blood, the cardiac impulse is feeble.
Sometimes it has a visible undulating movement.
Palpation.--On palpation, although the apex-beat is less forcible than
normal, a distinct purring thrill will be communicated to the hand:
this thrill is a constant attendant of mitral stenosis, and may be
regarded as its diagnostic sign. It should be remembered, however, that
a purring thrill does not always indicate mitral stenosis. It is most
distinct at the apex-beat, although it may be diffused over the whole
præcordial space. It either continues through the entire diastole or is
only present just before the systole. It is sometimes called a
presystolic thrill. It ceases with the apex-beat. The only conditions
besides mitral stenosis which will cause a purring thrill at the
cardiac apex are mitral regurgitation, with extensive dilatation of the
left ventricle, and left ventricular aneurism; in both instances the
thrill will not be presystolic, but systolic.
Percussion.--The increased size of the left auricle may cause an
increase in the area of cardiac dulness upward and to the left at the
inner part of the second left interspace. This increased area of
dulness will only be recognized on careful percussion during
expiration.
Auscultation.--Mitral stenosis is characterized by a loud churning,
grinding, or blubbering presystolic murmur; this murmur is of longer
duration than any other cardiac murmur, on account of the time required
for the blood to pass through the narrowed and obstructed orifice. It
ends with the commencement of the first sound and the apex-beat, being
synchronous with the purring thrill. The murmur is heard with its
maximum intensity a little above the apex-beat.
Cryan records a case where the murmur was absent, but the diagnosis of
mitral stenosis was made from the other symptoms. At the autopsy the
orifice would barely admit the tip of the little finger, and the
absence of the murmur was accounted for by the smallness of the
aperture.[19]
[Footnote 19: _Trans. Path. Society_, Dublin, Part 2, vol. iv., 1870.]
As a rule, mitral stenosis is accompanied by the loudest as well as the
longest cardiac murmur. The murmur is always louder when the patient is
erect than when in the recumbent posture. For a few days before death,
and at any time when there is great constitutional debility, the murmur
may be held in abeyance. A presystolic murmur is never present when
auriculo-ventricular narrowing does not exist. When this lesion does
exist it is never permanently, and very seldom temporarily, absent. A
prolonged murmur and a sharp first sound indicate a funnel-shaped
stenosis. A murmur immediately following the second sound, and running
through the apex-beat, indicates great contraction of the
orifice--diaphragmatic contraction. The murmur of mitral stenosis is
very rarely, if ever, conveyed to the left of the apex-beat, and it is
rarely heard more than two inches to the right of the apex. The second
sound of the heart is intensified over the pulmonary valves. When
mitral reflux and mitral obstruction coexist, the two murmurs run into
each other, constituting a single murmur that may be mistaken for a
systolic murmur. The harsh character of the presystolic element of the
murmur can always be recognized.
A mitral obstructive murmur is never soft or musical, but there is a
rare form of presystolic mitral which is so short as to resemble a
tone. A mitral stenotic murmur does not often merge into the first
sound of the heart, but is usually separated from it by a short
interval. Sometimes a stenotic murmur only becomes audible when the
patient sits up. In about one-third of all cases of stenosis of the
mitral orifice the second sound is reduplicated. It is best heard at
the apex and when the heart's action is slow. The reduplication may be
temporarily absent. Pulmonary congestion efficiently accounts for {669}
this reduplication. Geigel ascribes it to "non-coincidence in the
closure of the valves." Guttman regards it as originating at the
stenotic orifice itself. Balfour thinks that thrill and reduplication
of the second sound are sufficient to make a diagnosis in the absence
of murmur. Some regard the length of the pause between the murmur and
the first sound as a measure of the stenosis--the shorter the pause,
the greater the stenosis.
DIFFERENTIAL DIAGNOSIS.--The diagnosis of mitral stenosis is not
difficult; it mainly depends upon the existence of two physical
signs--the purring thrill and a loud, long, blubbering presystolic
murmur.
Mitral obstruction may be mistaken for the murmur of aortic
regurgitation (see page 657), for a pericardial friction located over
the apex, for a prolonged systolic murmur replacing the first sound at
the apex, and for a prediastolic basic murmur transmitted to the apex.
1. To diagnosticate between local pericarditis and mitral stenosis, the
same methods are employed and the same rules are to be observed as were
mentioned in the diagnosis between aortic reflux and local pericarditis
(p. 664).
2. A prolonged systolic apexial murmur, enduring as it does for the
period of the first sound, that of the short pause, and reaching the
second sound, is often accompanied by a muffled second sound readily
mistaken for the first. The diagnosis of this murmur rests upon its
soft and blowing character, the synchronism of the murmur with the
systolic impulse and carotid pulsation, and the fact that there is no
murmur with the second sound at the base.
[Illustration: FIG. 45. Mitral and Aortic Obstruction and Regurgitation
(from a Patient in Bellevue Hospital).]
A prediastolic murmur is distinguished from a mitral stenotic murmur by
its progressively diminishing intensity from the base to the apex, by
its being accompanied by hypertrophy of the left ventricle, and by a
jerking, irregular pulse. The preceding tracings explain themselves.
Mitral Regurgitation.
Regurgitation at the mitral orifice is due to a condition of the mitral
valves which allows the blood to flow back from the left ventricle into
the left auricle. The backward effects of mitral reflux are more varied
than those of any other valvular lesion.
It is a common form of valvular disease, and in the majority of cases
is the result of acute exudative or interstitial endocarditis.
MORBID ANATOMY.--The most common lesions which give rise to mitral
regurgitation are thickening, induration, and shortening of the mitral
valves. In rare instances it may occur independent of valvular disease
from displacement of one or more of the segments of the valve, the
result of changes in the papillary muscles, chordæ tendineæ, or the
ventricular walls. It may also occur in extreme anæmia, or from
relaxation of the papillary muscles and dilatation of the left
ventricle, without a corresponding elongation of the papillary muscles,
and from rupture of the chordæ tendineæ. In most instances, however,
the valves are shortened, thickened, and indurated.
In some instances lime salts and large masses of chalky matter are
found {670} imbedded in the indurated valves. In such cases the surface
and edges of the valves are so rough and jagged that more or less
obstruction accompanies the regurgitation.
All these changes, except calcification, may also occur in the chordæ
tendineæ and columnæ carneæ. The valves may also become adherent to the
walls of the ventricles, or as a result of the shrinking and shortening
of the chordæ tendineæ the valve-flaps may not pass back to the plane
of the orifice.
Again, the valves or the chordæ tendineæ may be ruptured, so that the
valves are pressed during the cardiac systole back into the auricle. If
the chordæ tendineæ which are inserted nearest the centre of the valve
become lengthened, that part of the flap will be bent upon itself,
having evidently yielded to the blood-pressure, and this allows of
regurgitation. Sometimes, when the valves appear perfectly healthy, by
the application of the water test they will be found to be
insufficient.
The first effect of mitral regurgitation is dilatation of the left
auricle, due to the pressure of the two blood-currents during its
diastole--one from the lungs, and the other from the left ventricle.
This dilatation leads to thickening and hypertrophy of the left
auricular walls. Following this, the pulmonary circulation is impeded,
the pulmonary vessels enlarge, and they may undergo degeneration as a
result of the continued regurgitant pressure.
Passive congestion of the lungs with brown or pigment induration is an
early pathological sequel of mitral regurgitation. The constant
interference with the return circulation from the lungs obstructs more
or less the outward current of blood to the lungs from the right
ventricle. As the obstruction is a gradual one, the right ventricle
becomes so hypertrophied as to overcome it. Consequently, the
hypertrophied right ventricle compensates at first for the mitral
regurgitation, and as long as the right ventricle is able to fully
overcome the abnormal pressure of the blood in the lungs from the
mitral regurgitation, so long the patients are comfortable. Sooner or
later, however, the compensatory hypertrophy of the right ventricle
ceases, and a secondary dilatation occurs which admits of no
compensation.
This final dilatation of the right ventricle is favored by the
myocardial degeneration, which occurs as a result of defective
nutrition of the heart-walls; when this condition is reached the veins
throughout the body are placed in a similar condition to those in the
lungs.
This general venous congestion is indicated by passive hyperæmia of the
abdominal viscera and by cyanosis of the surface during active physical
exercise.
The liver is the organ first affected, on account of its great
vascularity and from the fact that the hepatic veins do not collapse
readily and possess no valves. Thus the liver becomes enlarged and
stony (the nutmeg liver) as a result of the obstruction to the emptying
of the hepatic vein, and when there is coexistent obstruction of the
bile-ducts jaundice will be present.
This portal obstruction induces passive hyperæmia of the intestines and
stomach, enlargement of the spleen, and large and painful hemorrhoidal
tumors. The impediment to the return of blood from the brain causes
cerebral congestion; from the kidney, renal congestion; and, finally,
the obstruction to the systemic venous return leads to the accumulation
of fluid in the areolar tissue and in the cavities. This dropsy
generally begins in the feet and extends upward. In females the
obstruction in the vena cava inferior induces derangements of the
menstrual functions. Ascites, hydrothorax, hydro-pericardium, and
pulmonary oedema may subsequently develop.
In addition to these changes, the dilated and hypertrophied left
auricle throws an abnormal quantity of blood with abnormal force into
the left ventricle during its diastole, which leads to dilatation of
its cavity and necessitates a compensatory hypertrophy of the left
ventricular walls. This {671} hypertrophy of the left ventricle
increases the force of the reflux current, so that during excitement
and active physical exertion pulmonary congestion, oedema, and cerebral
apoplexy are liable to occur. In many cases of mitral regurgitation,
when the venous engorgement is excessive, general dropsy is favored by
the anæmia produced by the obstruction of the thoracic duct.
Friedreich maintains that the augmented tension in the venous system
causes an increased resistance in the systemic arteries, which leads to
left ventricular hypertrophy.
ETIOLOGY.--Mitral regurgitation may occur at any age; it is especially
liable to follow rheumatic endocarditis in the young.
Acute exudative and interstitial endocarditis of rheumatic origin is
the primary cause of most of the changes which lead to mitral
insufficiency. These changes cause the extensive retractions and
thickenings which are present in most cases.
It may occur in conditions of extreme anæmia or where there is
degeneration of the walls of the left ventricle.
It is not infrequently secondary to changes at the aortic orifice,
produced either by an extension of endocarditis from the aortic to the
mitral valves and their appendages, or by the secondary mitral
valvulitis excited by regurgitant blood-currents from the aorta.
Mitral insufficiency may also be the result of the enlargement of the
left auriculo-ventricular orifice which accompanies excessive
dilatation of the left ventricle.
Disease of the columnæ carneæ and chordæ tendineæ, when their
structures are so weakened as to allow the flaps of the valve to pass
back of the plane of the orifice, will also cause mitral insufficiency.
Ulcerative endocarditis may cause it, either by perforation and rupture
of the valves or by rupture of the chordæ tendineæ.
SYMPTOMS.--During the early stage of mitral insufficiency, when the
hypertrophy of the right ventricle compensates for the regurgitation,
there are no rational symptoms which would lead one to suspect its
existence; but when the right ventricle is unable to overcome the
obstruction to the pulmonary circulation caused by the regurgitant
blood-current, there will be more or less dyspnoea, accompanied by a
short, hacking cough, with an abundant expectoration of frothy serum.
Sometimes the watery expectoration is blood-stained.
Frequently, the blood-stained expectoration is accompanied by free
hæmoptysis, although it should be remembered that profuse hæmoptysis is
far more frequent with stenosis than with regurgitation at the mitral
orifice. But a cough and watery expectoration with occasional dark
blood-stains are usually present as an advanced symptom of mitral
regurgitation. Active physical exertion increases the dyspnoea and
causes cardiac palpitation.
In advanced cases the extremities, face, and lips become blue, the
result of the interference with the capillary circulation, and the
liver becomes enlarged and hardened--conditions easily recognized by
palpation and percussion.
The patient will complain of a sense of weight and fulness in the right
hypochondrium, and there will be anorexia, nausea, and a sense of
oppression in the epigastrium. Sometimes the hepatic circulation
becomes so obstructed that the biliary secretion is interfered with,
and jaundice will be added to the cyanotic discoloration, which gives
to the surface a peculiar greenish hue.
Following the hepatic derangement are frequent attacks of gastric and
intestinal catarrh and evidences of embarrassed renal circulation.
The urine is diminished in quantity, high-colored, and loaded with
lithates. Sometimes albumen and fibrinous or blood casts are found in
it.
{672} Headache, dizziness, vertigo, stupor, somnolence, and sometimes a
peculiar form of delirium of short duration, result from the passive
cerebral hyperæmia induced by obstruction in the superior vena cava.
A late symptom of mitral regurgitation is dropsy, which results both
from impaired general nutrition and the abnormal blood-pressure in the
venous system, both together causing an exudation of the watery portion
of the blood through the walls of the vessels. Dropsy, from mechanical
causes having their seat in the heart, first appears in the lower
extremities, the ankles becoming oedematous, and thence may extend over
the whole body. For this condition to be reached it may require several
years or only a few months, depending upon the general condition of the
patient and the amount of the reflux. With the general anasarca the
dyspnoea becomes extreme; the serous cavities of the body as well as
the lungs become oedematous; erythema may occur in the region of the
groins, the skin exhibiting a tendency to diffuse gangrene.
Late in the disease pulmonary hemorrhagic infarction may occur as a
result of metastasis, and this, in the vast majority of cases, lights
up a rapidly fatal pneumonia.
All these changes, however grave and urgent they may be, are gradual in
their development, so that the condition of the patient is not so
insufferable as its description would lead one to suppose.
The pulse of mitral regurgitation is at first in no respect
characteristic. It remains regular in force and rhythm, but later it
becomes somewhat diminished in force and volume, irregular in its
rhythm, and increased in frequency, but never jerking in character.
This tracing illustrates my meaning. While it remains full it is feeble
and always compressible. When the heart's action is excited, it has a
certain tremulousness: these last-named characteristics are to be
regarded more as the result of the failure of the left ventricle than
of changes in the valvular insufficiency. If a mitral regurgitant pulse
has any distinctive peculiarity, it is its diminution in volume.
[Illustration: FIG. 46. Mitral Regurgitation (from a Patient in
Bellevue Hospital).]
Coincident mitral or aortic stenosis may render the pulse regular even
in extensive mitral regurgitation.
[Illustration: FIG. 47. Mitral and Aortic Regurgitation (from a Patient
in Bellevue Hospital).]
Physical Signs.--Inspection.--The area of visible cardiac impulse
extends over an abnormal space, and is more or less distinct according
as the right ventricular hypertrophy is moderate or extensive.
Sometimes the thoracic wall is seen to rise and fall with each cardiac
cycle, and not infrequently the epigastrium exhibits slight pulsation
corresponding in rhythm with the heart-beats.
The epigastric pulsation is due to the right ventricular hypertrophy
always found with extensive mitral regurgitation.
Skoda, Bamberger, and Leyden record a few instances in which inspection
revealed a double impulse accompanying, with more or less regularity,
each cardiac systole. This double impulse only occurs in aggravated
cases of {673} mitral insufficiency, and arises from non-coincidence of
contraction of the two ventricles.
The jugular veins appear swollen, and this is always most conspicuous
when the patient is lying down.
Palpation.--The apex-beat is displaced to the left. When hypertrophy
predominates over dilatation, the apex-beat is felt lower than normal.
When the dilatation exceeds the hypertrophy, the apex-beat is carried
outward and often slightly upward. The impulse is diffused and more or
less forcible according as the right or left ventricular hypertrophy
predominates. This systolic frémissement is most noticeable when the
base of the heart lies close to the chest-wall from retraction of the
margin of the left lung.
Purring tremor, systolic in rhythm, felt most intensely at the apex and
becoming feebler the farther the hand is removed from that part, either
to the right or upward, is invariably due to mitral reflux.