contained in the ventricles and thrown against the aortic walls leads
to endarteritis and subsequent atheromatous degeneration of the
arterial walls, and the arteries become so brittle that during
excitement they may suddenly rupture and cerebral apoplexy result;
aneurism is also liable to be developed under such conditions.
In the normal heart the aortic recoil is the force which propels the
blood into the coronary arteries. When the aortic valves are
insufficient, and furnish little or no resistance to the return
blood-current, the coronary blood-supply is consequently diminished.
When perfect compensation has existed for some time, it begins to fail,
and dilatation again commences at the expense of the walls of the
heart. This dilatation is aided, first, by the condition of the
coronary arteries above referred to, and, secondly, by the fact that
aortic recoil is now expended as much in driving a regurgitant current
into the ventricle as in forcing blood through the coronary vessels.
In some cases atrophy of the papillary muscles allows the mitral flaps
to swing back into the left auricle when increased pressure is exerted
upon them. When from any one of these causes mitral incompetence
becomes secondary to, and coexistent with, aortic insufficiency, all
the signs of impeded venous circulation will be present. These changes
will be considered under the head of Mitral Disease.
When over-distension of the left ventricle causes incomplete emptying
of the left auricle, a greater or less amount of passive hyperæmia of
the lungs may be present without mitral insufficiency.
ETIOLOGY.--The etiology of aortic insufficiency is similar to that of
aortic stenosis. Rheumatic endocarditis is undoubtedly its most
frequent cause, but it may also have its origin in sudden and violent
muscular effort, atheroma of the aorta, endarteritis, congenital
malformation, and enlargement of the aortic orifice. Congenital
malformation or congenital non-development is, according to Virchow, a
frequent cause in chlorotic females.
In many cases the atheroma that causes the incompetence is of gouty
origin, especially when gouty kidneys coexist or when alcoholismus is
associated with a gouty diathesis.
Sometimes aortic incompetence is the result of imperfect development of
the aortic valves. A rare case is recorded in the _Pathological
Transactions_ (vol. xvi. p. 77), where a young man fell from a height
upon his side and tore off an entire flap of the semi-lunar valve:
there was no external mark of injury, and the rupture was plainly due
to the transmission of rapid vibrations from the jarred surface.
Valvular inadequacy sometimes results from dilatation of the aorta at
its origin.
{661} There can be little doubt but that the interstitial inflammation
which gives rise to the valvular changes which allow aortic
regurgitation is often excited by the violence with which the aortic
valves are closed by the backward rush of blood on the aortic recoil
during prolonged and violent physical exertion.
Thus, although rheumatism plays a very important part in its
development, it is so far from being its sole cause that C. Hilton
Fagge says that in at least half the cases of this form of valvular
disease met with in London hospitals one fails to elicit a rheumatic
history.
SYMPTOMS.--Rational Signs.--So long as hypertrophy of the left
ventricle compensates for its dilatation, the individual will suffer
little or no inconvenience, even though the regurgitation is extensive.
When the regurgitant stream is a very small one there will also be
little or no disturbance of the general health.
But the compensation is only maintained for a short time. When the
equilibrium is lost the eccentric hypertrophy induces excessive
heart-action during mental excitement or violent muscular effort. The
action of the heart then becomes labored, and the patient becomes
anxious, nervous, and fretful. Sufferers from aortic regurgitation are
generally aware that exercise will augment all their uncomfortable
symptoms. Their respirations are accelerated by moderate exercise, and
are accompanied by cardiac palpitation. As the insufficiency increases
attacks of headache and vertigo become more and more prolonged and
severe; the patient complains of muscæ volitantes, dyspnoea, giddiness,
and is compelled to sleep with his head elevated. Palpitation is now a
constant symptom, and a visible carotid impulse is persistently
present.
A comparatively frequent symptom of aortic regurgitation is a
distinctly paroxysmal shooting or stabbing pain over the heart, in the
left shoulder, or extending down the left arm. Sometimes this pain is
accompanied by numbness and a peculiar whiteness of the skin along the
line of the pain. In other cases the pain passes from the middle of the
sternum to the right arm. This pain is increased by mental excitement
and muscular exertion, and sometimes by over-distension of the stomach.
In a few cases patients will complain of a sickening fluttering of the
heart.
When the nutrition of the hypertrophied ventricular walls becomes
markedly interfered with, or when insufficiency of the mitral valves
occurs, the veins of the systemic circulation become overloaded, as is
evidenced by cyanosis and dropsy; the dropsy appears first as oedema of
the feet, and gradually extends upward until a condition of general
anasarca is reached. The cyanosis is increased after slight exertion,
and is accompanied by dyspnoea, carotid pulsation, and puffiness of the
face.
In the advanced stages of the disease there is orthopnoea, sudden
starting in sleep, angina pectoris, and in some cases albuminuria and
enlargement and tenderness of the liver. Attacks of syncope at first
occur only after active muscular exercise, but later they occur
independently of it, and are extremely distressing. These patients are
in danger of death at any moment, either during a state of the utmost
calm or the most intense excitement; the danger is greater, however,
during exertion.
The pulse is the most characteristic subjective symptom of this form of
valvular lesion. It was first accurately described by Sir Dominick
Corrigan,[9] and it is frequently called Corrigan's pulse. He
especially said that the disease was indicated by visible pulsation of
the vessels of the head, neck, and upper extremities. On account of the
elongation of the arteries during their pulsation, and their becoming
distinctly flexuous, the pulse is frequently called the locomotive
pulse. It is large and distinct, rapidly projected against the finger,
and just as quickly the arterial tension sinks to its minimum and the
{662} impulse vanishes. It is sometimes accompanied by a vibrating jar,
on account of which it is called the water-hammer, jerking, splashing,
or collapsing pulse. Its characteristics are more apparent when the arm
is raised above the head. Although slightly infrequent, quick, and
jerking, it is always regular in rhythm; the radial impulse is felt a
little after the apex-beat. Thus the pulse-wave of aortic regurgitation
travels slowly along the arteries. This delay in the pulse is constant.
[Footnote 9: _Edin. Med. and Surq. Journ._, April, 1832.]
As soon as the systemic circulation is overloaded from insufficiency of
the heart or from secondary mitral insufficiency, the pulse becomes
feeble and irregular upon the slightest exertion, and may intermit, but
it is still of the same peculiar jerking character. The sphygmographic
tracings of this pulse show a high upstroke and absence of the dicrotic
wave.
[Illustration: FIG. 42. Aortic Regurgitation.]
[Illustration: FIG. 43. Aortic Obstruction and Regurgitation (from a
Patient in Bellevue Hospital).]
This vibrating pulse or pulse of unfilled arteries is usually possessed
of fulness of volume, but when obstruction coexists it may be small and
flickering unless the arteries are calcified or atheromatous. The pulse
of aortic insufficiency taken by the sphygmograph resembles strongly
the pouls des vieillards, but the senile pulse gives a rounded instead
of a pointed summit. Still, in old age the two tracings may be
indistinguishable.[10] The peculiar crochet or beak is noticeable in
graphic tracings of the pulse of aortic inadequacy.
[Footnote 10: Marey, _Phys. Méd. de Circ. du Sang_, Paris, 1863.]
Stokes has described, under the designation of steel-hammer pulse, a
peculiar and characteristic pulsation of the arteries which occurs in
cases of acute rheumatic arthritis supervening upon chronic inadequacy
of the aortic valves. The pulse is abrupt and energetic, as the rebound
of a smith's hammer from the anvil; it is exhibited, however, only in
the arteries adjacent to the affected joints.[11]
[Footnote 11: _Continued Fever_, 1874, p. 244.]
PHYSICAL SIGNS.--Inspection.--There is an increase in the area of the
apex-beat, which is plainly more forcible and is visible over a wider
area than in aortic obstruction. After compensation has ceased to
balance the forces in the heart the apex-beat becomes more and more
feeble and diffused. One of the most important points obtained by
inspection is pulsation of the carotids and the vessels of the upper
extremities. Becker and Quincke have observed pulsation of the retinal
vessels in cases of extensive aortic regurgitation.[12]
[Footnote 12: _London Ophth. Hosp. Rep._, Feb., 1873.]
Palpation.--On placing the hand over the præcordial region a heaving,
lifting impulse will be perceived, which is transmitted over a large
portion of the thoracic walls. The apex-beat is displaced downward and
toward the left, sometimes as far as the eighth rib and two and a half
inches to the left of the left nipple. Occasionally a continuous
diastolic thrill, equally intense during the whole of the diastole, is
felt over the sternum, most distinctly at the site of the aortic
valves. In some cases there is a slight pulsation in the scrobiculus
cordis.
{663} Percussion.--The area of percussion dulness corresponds to the
extent of the cardiac enlargement. Deep dulness is elicited below and
to the left of the normal area, and its outline has more of an oval
contour than in health. So soon as the cardiac dilatation exceeds the
hypertrophy, the area of dulness will extend horizontally rather than
vertically, and it may be carried slightly upward, the apex beating in
the axillary space. The area of dulness may extend six and a half
inches from right to left, and from the upper edge of the third rib to
the line of the liver dulness. The superficial area of dulness is
likewise increased horizontally and toward the left.
Auscultation.--Aortic regurgitation is characterized by a diastolic
murmur, which may take the place of, or immediately follow, the second
sound of the heart. It is very distinct at any point over the base of
the heart, but usually has its maximum intensity either at the sternal
end of the second right costal cartilage, in the second right
intercostal space, or at the sternal junction of the third rib on the
left side. It is transmitted over the sternum, and sometimes will be
loudest at the xiphoid cartilage, and is thence transmitted in the
direction of the apex. Its area of diffusion is greater than that of
any other cardiac murmur: it is not only conducted down the sternum to
the xiphoid cartilage and to the apex, but it may be heard at the sides
of the chest along the spinal column, and sometimes faintly in the
ascending and transverse portions of the arch, in the carotids, and in
rare instances as far as the radial arteries. The murmur of aortic
reflux is accompanying rather than substitutive, for the pulmonic
second sound is audible at the right base.
Foster[13] regards incompetency of the posterior segment of the valve
as producing a murmur which is conducted to the apex, whereas
inadequacy of either or both of the anterior segments is accompanied by
a murmur which is conducted to the ensiform cartilage. This point has a
practical bearing on account of the relationship of the anterior
segments of the valve to the coronary arteries. If the murmur indicates
a lesion of the posterior flap of the valve, the prognosis will be
better. When the second sound of the heart is distinct the murmur
immediately follows it. Many English writers call the murmur a
post-diastolic aortic murmur.
[Footnote 13: _Med. Times and Gaz._, 1873, vol. ii. p. 658 _et seq._]
Although having the greatest area of diffusion, aortic reflux has not
the loudest murmur; it is soft, blowing, sometimes rough, and
frequently musical. It is loudest at the beginning of diastole,
gradually decreasing in intensity, although it may preserve its
rushing, blowing character during all the diastole.
An aortic regurgitant murmur may temporarily disappear if a plug of
fibrin closes the orifice, or if the walls of the left ventricle are
the seat of extensive fatty degeneration, the aorta being rigid and
inelastic.[14] When aortic stenosis coexists there will be a double
murmur, audible over a very large space, having its maximum intensity
at the right edge of the sternum in the second interspace.
[Footnote 14: _Brit. Med. Journ._, 30th March, 1882.]
Systolic and diastolic murmurs, though sometimes separated by a
well-defined pause, may run into each other. If mitral regurgitation
occurs with aortic regurgitation, each murmur retains its own location
of maximum intensity. In rare instances, when two segments of the valve
are healthy, a clear aortic second sound is heard, which is preceded by
a faint reflux murmur. Such a murmur is said to be prediastolic in
rhythm. Aortic reflux murmurs are often very indistinct, and can only
be heard when the patient is in the recumbent posture. There is no
necessary connection between the amount of reflux and the loudness of
the murmur.
A diastolic murmur heard at or below the level of the aortic valves,
chiefly {664} audible in the line of the sternum, indicates
considerable aortic incompetence. If a diastolic murmur is inaudible in
the carotids, it is usually preceded by a systolic murmur, which has
its maximum intensity at the aortic valves or in the so-called aortic
area: such a murmur indicates comparatively trifling incompetence with
considerable obstruction, probably produced by calcified semi-lunar
valves.
If a diastolic murmur is distinctly audible in the carotid arteries, it
is invariably preceded by a loud systolic murmur in them, the systolic
portion of the murmur not being very plainly audible in the aortic nor
in any part of the cardiac area: this indicates very considerable
incompetence with comparatively trifling obstruction.
DIFFERENTIAL DIAGNOSIS.--The diagnosis of aortic regurgitation is
generally not difficult, as it rests almost exclusively upon the
existence or nonexistence of a diastolic murmur. It may, however, be
mistaken for aortic stenosis, for mitral obstruction, for pericarditis
localized over the aorta, for aneurism of the aorta, for aneurism of
the aorta immediately above the valves, patency of the ductus
arteriosus, for insufficiency of the pulmonic semi-lunar valves, and,
occasionally, for a rough and inelastic condition of the ascending
aorta.
1st. Mitral obstruction gives a presystolic murmur, while aortic reflux
produces a diastolic murmur. Mitral stenosis is accompanied by no
hypertrophy or dilatation of the left ventricle, whereas these
conditions are always present with aortic reflux. The quality of a
presystolic mitral murmur is harsh and rough, and it has a churning,
blubbering, or grinding character, while aortic reflux has a murmur of
low pitch and of a soft, blowing, or musical character. Mitral stenosis
is accompanied by a purring thrill which is absent in aortic
regurgitation. The murmur of mitral stenosis is the longest of all the
cardiac murmurs. The murmur of mitral stenosis is never heard behind,
whereas that of aortic regurgitation is often heard at the sides of the
chest and along the spinal column. Finally, mitral stenosis is attended
by well-marked pulmonary symptoms during active physical exertion,
which are rarely present in aortic insufficiency.
2d. A pericardial friction sound over the aorta has its maximum
intensity over the seat of its production, and is usually audible
during both the cardiac systole and diastole. In aortic regurgitation
the character of the pulse, the existence of hypertrophy and dilatation
of the left ventricle, and the carotid pulsation will establish the
diagnosis.
3d. An aneurism at the sinuses of Valsalva is diagnosticated by the
history of the case, the presence of the murmur over the pulmonary
artery, the evidences of arterial degeneration, the absence of left
ventricular dilatation and hypertrophy, and the peculiar jerking pulse.
An aneurismal murmur is circumscribed, has a booming quality, and is
usually systolic in rhythm and never transmitted to the apex of the
heart.
4th. Patency of the ductus arteriosus is a rare condition: in a case
where this was diagnosticated[15] the murmur was audible at the left of
the sternum, was not everywhere continuous with the second sound, was
only transmitted very feebly to the left, and had a wavy character,
sufficient of itself to distinguish it from an aortic regurgitant
murmur.
[Footnote 15: _Guy's Hosp. Rep._, Ser. 3, vol. xviii., 1872-73.]
5th. Insufficiency of the pulmonic semi-lunar valves is the rarest of
all valvular lesions: the murmur should be diastolic, having its
maximum intensity in the second intercostal space of the left side; it
should be transmitted only downward and toward the right apex; and
should not be attended by arterial pulsation, a jerking pulse, or by
left ventricular hypertrophy and dilatation.
6th. A diastolic murmur in the ascending arch, due to roughening,
rigidity, {665} and dilatation of the artery, is also rare, while the
condition which some say can produce it is very common.
Two cases are recorded in which the diagnosis rested upon the character
of the pulse, throbbing of the arteries, and the absence of hypertrophy
and dilatation of the left ventricle.[16]
[Footnote 16: Bellingham _Dis. of Heart_, 1857, p. 152; also _Trans.
Path. Society_, vol. iii., March, 1868, p. 3, article by Prof. Law.]
Mitral Stenosis.
Stenosis, or obstruction of the auriculo-ventricular opening of the
left heart, is due partially to constriction at the base of the mitral
valves, and partially to adhesions of the valve-tips or chordæ
tendineæ. It usually occurs as a consequence of rheumatic endocarditis,
rarely of atheromatous degeneration, and is most likely to occur in
endocarditis affecting young persons.
Mitral disease is present in one-half the cases of valvular diseases of
the heart. Usually, insufficiency and stenosis of the mitral orifice
occur together, and stenosis probably never occurs without some
insufficiency.
MORBID ANATOMY.--As a result of acute exudative or interstitial
endocarditis, the valves are rendered shorter and narrower, as well as
thicker and more cartilaginous, than normal. These rigid valvular
projections not only obstruct the flow of blood from the auricle to the
ventricle, but allow of its regurgitation from the ventricle into the
auricle. In mitral stenosis there is not only thickening and
contraction of the valves, but the valve-tips or the chordæ tendineæ
become adherent, and sometimes each papillary muscle gives rise to a
corrugated, cylindrical mass pierced with one or more slits, indicating
the chordæ of which it was originally made up. The wall of the valve,
especially toward its free edge, is greatly thickened, and these
thickened portions are so dense that they have a distinctly
cartilaginous feel. On the valvular flaps that have undergone this
sclerotic change calcareous masses are very frequently developed, and
are especially liable to form when a gouty diathesis exists.
When the chordæ tendineæ and papillary muscles have become adherent,
the edges of the valves are drawn down toward the apex of the heart;
and since the flaps are adherent for a greater or less distance upward
from their bases, the valve presents a funnel-shaped appearance with
its base looking toward the auricle and its apex toward the ventricle,
whose smaller opening, rarely circular, usually resembles a slit with
its axis in the line which unites the original segments of the valve.
This button-hole slit may scarcely admit the tip of the little finger,
while the normal mitral orifice permits the easy introduction of three
fingers.
Annular (ring-like) stenosis is far more common at the mitral than at
the aortic orifice. Hard, wart-like vegetations frequently develop on
the puckered and seamed flaps, which increase the already existing
obstruction. Sometimes the funnel-shaped appearance is wanting, and the
flaps are stretched horizontally across, with a small opening in the
centre, like a diaphragm: looked at it from the auricle, this slit is
often crescentic in shape.
In cases of long standing the vegetations may become calcified. If the
new tissue in the diseased valves undergoes fatty change and softens,
ulcerative processes are set up and the chordæ tendineæ may rupture. On
the floor of such ulcers calcareous masses and débris are frequently
found.
Hayden thinks that "all funnel-shaped mitral stenosis is the result of
primary acute inflammation and thickening of the valve-segments, with
cohesion of their adjacent edges." Out of 62 cases of mitral stenosis,
59 assumed the button-hole form, and 3 only the funnel-shape (Fagge and
Hayden).
{666} In rare instances the tendons will adhere to the wall of the
heart as well as become matted together. Adjacent to the valves the
endocardium will usually be found slightly thickened.
The following changes are developed in the heart and vessels as the
result of mitral stenosis: The left ventricle becomes smaller, and
sometimes its walls are thinner than normal. The aorta is also small
and thin-walled. An almost necessary result of mitral stenosis is
dilatation, with subsequent hypertrophy of the left auricle. Sometimes
the auricular cavity is enormously dilated--so much so that fifty years
ago Thurman described it as true aneurism of the left auricle.[17] Not
infrequently the left auricular walls are from one-eighth to one-fourth
of an inch in thickness. Its appendix is elongated, assuming a peculiar
curved form, the aperture between it and the auricle becoming wider
than normal. Moxon records a case of extensive mitral stenosis where
the appendix was two and three-quarter inches long.
[Footnote 17: _Med.-Chir. Trans._, vol. iii., Ser. 2, p. 244.]
As soon as the auricular hypertrophy ceases to be compensatory and
dilatation begins, the pulmonary circulation becomes obstructed,
causing increased tension in and distension of the pulmonary vessels.
The walls of the pulmonary vessels, especially those of the main trunk,
are thickened and hypertrophied; in rare cases they have been found
twice the thickness of those of the aorta.
Although mitral stenosis is a disease of youth, and atheroma one of old
age, yet it not infrequently happens that even before the age of
puberty atheromatous degeneration occurs in the pulmonary vessels,
especially in the small branches, as a result of the increased
blood-tension in the pulmonary system.[18]
[Footnote 18: _Trans. Path. Society_, vol. xvii. p. 90.]
The passive pulmonary hyperæmia which results from the obstructed
pulmonary circulation may lead to those changes which collectively
constitute brown induration of the lung. Another occasional occurrence,
directly due to extensive mitral stenosis, is nodular hemorrhagic
infarction. Hemorrhagic infarction of the lungs is in nearly every case
preceded by thrombosis of the right side of the heart.