the valves that allows regurgitation, or one that obstructs the onward
blood-current. Valvular insufficiency arises when extensive retraction,
perforation, or partial detachment of the valves prevents them from
completely closing their respective orifices. And when the chordæ
tendineæ have been ruptured, or when calcareous degeneration has made
the valves or the parts in the immediate vicinity abnormally rigid, the
regurgitant current through the aperture thus left gives rise to a
regurgitant murmur.
{654} When the valves are thickened, retracted, adherent,
hypertrophied, or degenerated, so that their edges are prevented from
being accurately applied to the walls of the ventricles or vessels,
they obstruct the current of blood, and the impinging of the
blood-current against the obstruction gives rise to obstructive
murmurs. These conditions--stenosis and insufficiency--are often found
coexisting, but rarely in equal degree, one usually predominating
sufficiently over the other as to give a dominant character to the
murmur.
The lesions which produce these conditions may be temporary or
permanent--temporary when they occur during the course of acute
endocarditis, and permanent when they consist of a new growth either of
connective, fibroid, calcareous, or atheromatous tissue, which alters
the form of the valves and impairs their function. Acute and chronic
valvular disease may produce the same murmurs. The effect of the
valvular deformity depends entirely upon its seat.
In the study of the relations of valvular lesions to cardiac murmurs
physical signs are the important factors in their diagnosis, and it is
necessary always to bear in mind the normal physiological conditions
which constitute a complete cardiac pulsation.
The apex of the normal heart is felt between the fifth and sixth ribs
on the left side, about two inches below the nipple and one inch to its
sternal side. The base of the heart is on a level with the third costal
cartilages. The tricuspid valve lies behind the middle of the sternum,
on a line with the articulations of the cartilages of the fourth ribs
with the sternum. The mitral valve lies behind the cartilage of the
fourth left rib, near the edge of the sternum. The aortic valves lie
behind the sternum, a little below the junction of the cartilages of
the third ribs with the sternum, near its left edge. The pulmonary
valves lie behind the junction of the third left rib with the sternum.
Let it be remembered that the tricuspid orifice is the most
superficial, then the pulmonary, next the aortic, and, deepest of all,
the mitral orifice. Ranged from above downward, the pulmonary orifice
comes first, then the aortic, then the mitral, and lastly the
tricuspid.
Aortic Obstruction, or Stenosis.
Stenosis at the aortic orifice is a common cardiac lesion, and one that
is always accompanied by more or less hypertrophy of the left
ventricular walls.
MORBID ANATOMY.--In aortic obstruction the cardiac valves will be found
to present some or all of the changes which have been described as
taking place in the course of acute and interstitial endocarditis,
together with degenerative changes due to atheromatous, calcareous,
fibroid, fatty, or connective-tissue metamorphosis.
Sometimes the valves may be covered with thick, warty, irregular
excrescences that cause loud murmurs, and yet do not seriously
interfere with the outgoing blood-current. At other times stenosis of
the aortic orifice may be so extensive as to almost obliterate it. When
such is the case, the extent of the lesion will be measured much more
by the consequent hypertrophy and its effects on the systemic
circulation than by the loudness or harshness of the murmur which it
produces.
Very frequently the valves are so rigid that they cannot be pressed
back against the wall of the aorta, and these unyielding prominences
are greater obstacles to the outgoing current of blood than vegetations
on the surface of the valves.
In a few rare cases the outlet may be diminished by constriction of the
{655} aorta at the point of insertion of the valves. Adhesion of the
aortic valves begins at their bases and extends along their free edges
to their tips; sometimes they become fused together into a mass, so
that they project into the blood-stream in the form of a funnel
irregular in shape and studded with calcareous nodules. The line of
attachment of the valves to the aorta frequently becomes entirely
obliterated.
In some instances the contraction of the valves between their points of
attachment causes them to form a deep pocket or pouch, and their points
of attachment may be a quarter of an inch apart.
Obstructions at the aortic orifice are frequently accompanied by
atheromatous changes in the aorta, the result of chronic inflammation
of its tunics--arteritis deformans.
As a result of aortic stenosis the wall of the left ventricle becomes
hypertrophied. This change is a gradual one, and is called compensatory
hypertrophy: it is due to the increased force required to propel the
blood through the constricted orifice.
After a time insufficiency of the mitral valves is apt to occur, caused
either by the extension of endocardial inflammation from the aortic
valves or by the forcible pressure of blood upon the ventricular
surface of the valves.
A slight thickening or roughening of the aortic valves may cause slight
obstruction to the outgoing blood-current, which will interfere but
little with the emptying of the ventricular cavity, and which rarely
leads to hypertrophy of their walls.
ETIOLOGY.--Aortic obstruction is most frequently met with in early and
advanced life, the mean age being forty-seven years. It is not uncommon
in children; valvular lesions have been found in children under two
years of age. It may be induced where the aorta is defectively
developed, and some think that imperfect development of the trachea may
lead to imperfect expansion of the chest, and thus induce disease of
the aortic valve.[6]
[Footnote 6: Barlow in _Guy's Hospital Reports_, S. 1, vol. vi. p.
235.]
Its most frequent cause is acute exudative and interstitial rheumatic
endocarditis. The origin of nearly all valvular disease may be traced
back to an attack of rheumatic fever. Next to acute rheumatism, chorea
is its most frequent cause. Bright's disease and pyæmia may cause it,
and atheroma or arteritis deformans extending to the valves will give
rise to valvular lesions which cause obstruction.
Any of the conditions that cause acute exudative and interstitial
endocarditis may effect changes in the valves, and the tissue thus
developed, undergoing atheromatous, fatty, fibroid, calcareous, or
connective-tissue change, will cause obstruction.
Increased tension of the aorta may be the result of chronic spinal
deformity, and may be regarded as the indirect cause of aortic
stenosis.
The connection between cancer and cardiac valvular disease is to be
noticed, if not as cause and effect, at least as a remarkable and
noteworthy coincidence.
Women are far less subject to aortic obstruction after rheumatism than
men. In men the aortic valves are subject to more pressure and strain
than in women, and hence non-rheumatic disease of these valves is very
common, while in women it is very rare.
Aortic disease especially occurs in men whose occupations involve
repeated, sudden, and great muscular effort.
In old age the walls of the aorta are weakened, and when aortic disease
is met with in young subjects it must be regarded as the result of a
premature senile condition of the vessels. Allbutt says that in Leeds
quite young men have aortic valvular disease, and Peacock mentions
several cases where the {656} disease has occurred in young girls who
have been placed at service before they were fully developed.
Sometimes the valves are found to be studded with vegetations,
apparently of syphilitic origin. Corvisart and Virchow both admit the
possibility of such an origin for valvular disease of the heart, but no
unquestionable case has as yet been advanced in proof of it. It has
been claimed that this is the reason why soldiers so frequently suffer
from heart disease; but sailors are notoriously more subject to
syphilis than soldiers, and heart disease is rare among them.
The reason is evidently to be found in their mode of dress: sailors
wear loose clothes, soldiers have the tightest possible fitting
garments. More force is required to pump the blood through the
constricted vessels, hence arises more strain on the aorta and more
strain on the valves.
Single, sudden muscular efforts have in a limited number of cases
produced disease at the aortic orifice.
Aortic valvular disease more frequently than mitral is of non-rheumatic
origin; it is slower in its development, and is more commonly met with
in advanced life.
SYMPTOMS.--The subjective symptoms of obstruction at the aortic orifice
are not usually well marked. Extensive aortic stenosis is not
incompatible with a state of comparative good health. As the
obstruction to the outflow of blood from the ventricle increases,
compensatory ventricular hypertrophy enables the heart to fill the
arterial system and relieve the pulmonary pressure. As soon as the
ventricular hypertrophy no longer compensates for the obstruction, the
arteries are inadequately filled; the left auricle cannot empty itself
into the left ventricle, and hence the pulmonary vessels are abnormally
full, as is also the entire venous system. The scanty arterial supply
gives the pallor to the face which so frequently accompanies this
condition, and syncope is liable to occur as a result of partial
cerebral anæmia.
These are late effects, and in many cases do not make their appearance
until the mitral valve is secondarily involved. The pulse in aortic
stenosis is normal in frequency, diminished in volume and power,
usually regular in rhythm, though it may be intermittent, and is
compressible and jerky in character.
As a general rule, in aortic stenosis signs of arterial anæmia precede
evidences of venous engorgement. The obstruction to the exit of blood
is shown in the sphygmographic tracing by a slanting or oblique
up-stroke, as seen in the accompanying tracing, or, as Mahomed says,
"the influence of percussion is lost." Tracings of the pulse in aortic
stenosis sometimes show considerable separation between the percussion
and the tidal waves. In some rare instances the pulse is slowed. There
may be slight palpitation, and pain in the chest may sometimes occur in
paroxysms; but pain in the chest is far more common in regurgitation
than in obstruction. Aortic obstruction is more frequently connected
with cerebral embolism than any other valvular lesion.
[Illustration: FIG. 41. Aortic Obstruction (after Foster).]
The left middle cerebral artery is the most common seat of aortic
cardiac emboli. The left lower limb is more subject to embolism from
aortic valvular disease than the right. The splenic and renal vessels
are also the frequent seat of such emboli. Sometimes embolism is due to
small auricular or ventricular {657} clots that form behind the
obstruction. Such clots have occluded the aortic orifice and caused
sudden death.[7]
[Footnote 7: _Pathological Transactions_, vol. ix. p. 91.]
PHYSICAL SIGNS.--The physical signs of aortic obstruction are generally
distinctive and easily appreciated.
Inspection.--The visible area of the cardiac impulse is abnormally
increased. Very extensive increase in the area of impulse is frequently
accompanied by a lifting of the chest-wall over the heart.
Palpation.--The impulse is felt to be forcible, and is sometimes
accompanied by a heaving or lifting motion. The apex is displaced
toward the left and slightly downward. A sensation will sometimes be
imparted to the hand during systole similar to that produced on the
sense of hearing by the whizzing of a missile by the ear. This is often
nothing more than an intensified endocardial thrill. This systolic
frémissement radiates to the ensiform process of the sternum, being
most intense in the second right intercostal space.
Percussion.--The area of cardiac dulness will be increased in
proportion to the displacement of the apex-beat to the left. The
increase in dulness measures the amount of left ventricular
hypertrophy.
Auscultation.--Aortic stenosis produces a systolic murmur which more
frequently accompanies than replaces the first sound of the heart. The
maximum intensity of this murmur is usually at the second sterno-costal
articulation of the right side, but it may be heard with equal
intensity over the whole upper part of the sternum, and followed up the
aorta and along the carotids; again, it may be loudest at the xiphoid
cartilage, or it may be heard with greatest intensity at the junction
of the left third rib with the sternum. In most cases the first sound
is heard with the murmur, but the murmur may entirely replace or
obscure it. This murmur is usually loud and harsh in character, and is
loudest at the beginning of the systole. Harshness is one of its
distinguishing characteristics.
In pure aortic stenosis the aortic second sound may be inaudible, and
is always feeble, but the pulmonic second sound will always be audible.
The area of diffusion of this murmur follows the law that a murmur is
propagated in the direction of the blood-current. It is conveyed along
the aorta into the carotids, and one of its characteristics is that it
is heard in the great vessels of the neck. It may sometimes be heard in
the thoracic and abdominal aorta.
When an aortic obstructive murmur is heard at the apex its intensity is
diminished, and when heard behind it is most distinct at the left of
the third and fourth vertebræ near their spines, and frequently extends
downward along the spine in the course of the aorta, but with
diminished intensity. It is to be noted here that a systolic murmur,
audible at the base, and traceable along the ascending arch toward the
end of the right clavicle, is by no means limited to cases of aortic
stenosis, although aortic stenosis always produces a murmur with these
characteristics.
Arterial murmurs, synchronous with the cardiac systole, are far more
frequent than diastolic murmurs. When the mitral or tricuspid valves
are thickened or incompetent, or when the myocardium is the seat of
extensive fatty degeneration, the murmur of aortic obstruction will
entirely replace the first sound of the heart.
DIFFERENTIAL DIAGNOSIS.--Aortic obstruction may be mistaken for mitral
regurgitation, tricuspid regurgitation; an anæmic bruit, for the murmur
of a thoracic aneurism and for a murmur produced by a scabrous
condition of the ascending arch of the aorta.
1. Both mitral and tricuspid regurgitation, as well as aortic stenosis,
are recognized by a systolic murmur. The murmur of aortic obstruction
is heard with its maximum intensity at the second right sterno-costal
articulation, and {658} diminishes in intensity toward the apex. The
murmur of mitral regurgitation is heard with greatest intensity at the
apex-beat. The murmur of aortic obstruction is conveyed into the
vessels of the neck; that of mitral regurgitation to the left, in the
direction of the apex-beat, and is heard behind, between the fifth and
eighth dorsal vertebræ, at the left of the spine, with very nearly the
same intensity as at the apex. The pulse in aortic stenosis is hard,
firm, and wiry in character, but regular, while in mitral regurgitation
the pulse is irregular in rhythm as well as in force, is never
incompressible, and is easily increased in frequency. Gastric,
intestinal, renal, hepatic, and bronchial symptoms are present in
mitral regurgitation, while the subjective symptoms of aortic
obstruction are cerebral in character. The pulmonic second sound is
generally feeble in aortic stenosis, while in mitral regurgitation it
is intensified. The murmur of aortic stenosis is harsh; the murmur of
mitral regurgitation is soft, and frequently musical in character.
2. Tricuspid regurgitation is also accompanied by a systolic murmur.
But while the murmur of aortic stenosis has its maximum intensity at
the right second sterno-costal articulation, the murmur of tricuspid
regurgitation is very rarely heard above the third rib: this is an
important diagnostic sign. Tricuspid regurgitation is accompanied by
jugular pulsation, while the murmur of aortic obstruction is heard in
the arterial trunks of the neck. To distinguish between intrinsic
pulsation of the jugular vein and throbbing of the carotid arteries
press lightly on the vessel above the clavicle; this arrests pulsation
when due to tricuspid disease, while if due to aortic stenosis the
result is negative. Moreover, respiration influences jugular pulsation,
while it has no influence over carotid throbbing. The area of
transmission of tricuspid regurgitant murmurs is not more than two
inches from the point of their maximum intensity; whereas the aortic
obstructive murmurs are conveyed along the sternum into the vessels of
the neck. There is nothing peculiar or abnormal about the pulse of
tricuspid regurgitation, while the hard and wiry pulse of aortic
obstruction is quite characteristic.
3. An anæmic bruit may be mistaken for aortic stenosis, since the
rhythm and seat of the bruit are often identical with those of the
stenosis. Anæmia, however, produces a murmur that is heard loudest in
the carotids, and is accompanied by a venous hum, the bruit du diable,
which is continuous, and heard best on the right side of the neck. Thus
in anæmia there are three murmurs, arterial, cardiac, and venous. In
aortic disease the murmur has its maximum intensity at the second
sterno-costal articulation of the right side, and is not accompanied by
a venous hum. There is always more or less cardiac hypertrophy in
stenosis, and an increase in the force of the apex-beat, while anæmia
is attended by a feeble cardiac impulse. The murmur is soft and blowing
in anæmia and harsh and rasping in aortic obstruction. The pulse is
characteristic in aortic stenosis; in anæmia it may have a thrill, but
is never hard and wiry. Lastly, the subjective signs of anæmia will
render the diagnosis comparatively easy, especially when the hum in the
veins coexists.
Aortic disease usually occurs in those who have passed middle life as a
rule, and in men, while young females are the chief subjects of anæmic
murmurs.
4. Thoracic aneurism may produce murmurs resembling those of aortic
stenosis. The dilating impulse on palpation, the normal force of the
heart-beat, the single or double bruit, the pain,--all these symptoms
of thoracic aneurism are absent when aortic stenosis alone is present.
Moreover, the history of the case will greatly aid in the diagnosis;
and, lastly, aneurismal murmurs have their maximum intensity at the
seat of the tumor, and not at the base of the heart.
5. A murmur from a scabrous state of the arch of the aorta is
exceedingly {659} rare. It is located higher up than that of aortic
stenosis, is not transmitted into the cervical vessels, and has its
maximum intensity over the transverse portion of the arch.
Aortic Insufficiency, or Regurgitation.
Aortic insufficiency is an abnormal condition of the aortic valves
which prevents their complete closure and allows a backward current of
blood to flow from the aorta into the left ventricle during the
diastole. This lesion is rarely found unassociated with aortic
stenosis, and together they constitute one of the most important and
frequent valvular lesions. It is sometimes called aortic incompetence,
aortic inadequacy, and aortic reflux.
MORBID ANATOMY.--In a normal heart at diastole the aortic semi-lunar
valves are firmly closed, so as to completely fill the orifice between
the left ventricle and the aorta. In aortic insufficiency the valves
are prevented from performing their normal function, on account of the
following anatomical changes. As a result of interstitial endocarditis
the valves may have been thickened, puckered, and shortened, so that
they do not meet when brought into the plane of the orifice.
When the central portion of the segment is indurated, the whole valve
subsequently curls up, either toward the orifice or back against the
wall of the aorta, and in either case there is insufficiency of the
valves. In the first case there is insufficiency with great
obstruction; in the second, with but very slight obstruction.
These processes of thickening and shortening are usually the result of
the train of changes which attend and follow endocardial inflammation,
but they may also come as the result of an atheromatous process
extending from the aorta to the valves; and it may be mentioned here
that the atheromatous changes, by impairing the elasticity of the
aortic walls, become a source of imperfect coronary circulation, and
hence prepare the heart for that dilatation whose other causes will
subsequently be described.
Regurgitation may result not so much from shortening as from adhesion
of the valve-tips to the walls of the aorta. There may be depression of
the valves which comes from over-extension, and then extreme
insufficiency will be the result. When this pathological lesion occurs,
usually only one segment is involved. Complete retroversion of the
valves is a questionable lesion; still, it may occur. Again, one or
more segments may be more or less detached from their points of
insertion, or from the same causes a valvular aneurism or a diseased
valve may be torn or ruptured, and then perforation allows a free
opening for the regurgitant passage of the blood.
After extensive obstruction has existed for a long time little tunnels
may form by the side of the valves and permit a regurgitant current
from the aorta to the ventricle. The aortic valves are more liable to
laceration than any other valves. Not infrequently the ragged edge of a
lacerated or displaced aortic valve is found covered with fibrinous
efflorescences of larger or smaller size.
During a cardiac diastole, normally, the blood is passing from the
auricle into an empty ventricle; when, however, regurgitation has
persisted for a considerable time, there will be added to the primary
stream (which of itself is capable of filling the cavity of the
ventricle) a regurgitant stream from the aorta, and by this combination
of two streams the left ventricle becomes over-distended and
permanently dilated. This dilatation occurs all the more readily since
during the diastole the ventricular walls are relaxed and less capable
of resisting the increased blood-pressure. Thus, permanent dilatation
of the left ventricle occurs in a comparatively short time; and to
overcome {660} the dilatation and the obstruction to the cardiac
circulation the left ventricular walls hypertrophy. The hypertrophy
goes on increasing until it compensates for the dilatation; but before
this point is reached the ventricular cavity sometimes becomes very
much dilated and the left heart reaches an immense size.
This dilatation and hypertrophy may be so extensive that the organ
often weighs twenty or thirty ounces, a case being recorded where the
enormous weight of forty-eight ounces was reached.[8] The heart is then
frequently called the cor bovinum. In such cases the organ has a
peculiar pointed form, the right ventricle appearing like a mere
appendix. The left ventricle is thus capable of containing so much
blood, and such an abnormally large amount is thrown into the aorta at
each cardiac cycle, that the arterial system is largely over-filled.
Hence the arteries are elongated during their pulsations more than in
health, and often become distinctly flexuous with each cardiac
pulsation.
[Footnote 8: See Hilton Fagge, _Diseases of the Valves of the Heart_.]