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ally formed and the heart is able to adapt itself to the increased work
demanded of it. The chief burden falls upon the left ventricle which
often becomes enormously hypertrophied. The heart of aortic insuffi-
ciency is one of the largest met with and is often referred to as the cor
bovinum (see Figs. 181 and 193). Great hypertrophy of the heart, how-
ever, is not a constant accompaniment of aortic insufficiency as the
opening may be very slight and the amount of blood which regurgitates
small.

Relative insufficiency of the aortic valve rarely occurs as the result
of cardiac dilatation but a permanent stretching of the aortic ring is
not infrequent secondarily to syphilitic aortitis. In this case the valve
segments themselves are intact but the leakage is produced by the in-
ability of the valve to close the enlarged opening.

Disease of the first part of the aorta is also apt to involve the ori-
fices of the coronary arteries and thus cause attacks of true angina.
Even without involvement of the coronary openings the circulation in the
coronary arteries may be embarrassed as a result of the lowering of the
pressure in the aorta due to the backward leak.

In most cases of aortic insufficiency there is an associated arterio-
sclerosis and the systolic blood-pressure is high.

Pathological Physiology. — Failure of the aortic valves to properly
close the aortic opening results in the back flow or regurgitation of a
portion of the blood which has been thrown into the systemic arteries.
The problem which the left ventricle faces is to expel during each systole
the normal amount of blood which it receives from the left auricle plus
the amount which regurgitates from the aorta. This naturally increases
its work and results in hypertrophy. The latter is proportional to
the amount of regurgitated blood. In cases which are recognizable
clinically the hypertrophy is usually of an extreme grade. Another
change produced in the left ventricle, as the result of the regurgitation
from the aorta, is dilatation. This is brought about by the increased
amount of blood it is forced to accommodate during diastole. Just as in
the case of hypertrophy the degree of dilatation is dependent on the
amount of the regurgitant flow from the aorta. In spite of the excessive
amount of blood the left ventricle must expel at each systole, it empties
itself in about the same length of time as the normal ventricle, although
it does not always do so as completely. Whereas in aortic stenosis the
left ventricle requires an increased amount of time to empty itself, a
shortening of the systole is an advantage in aortic insufficiency, as it then
has less blood to handle by reason of the curtailment of the diastolic
period.

As the result of the great hypertrophy of the left ventricle the blood
is driven into the aorta with tremendous force. This produces a high
systolic pressure 1 in the systemic arteries. On (lie other hand, the
sudden regurgitation of a portion of the blood from the aorta into the left



678 DISEASES OF THE PERICARDIUM, HEART, AND AORTA

ventricle leads to a sudden recoil of the blood column and consequently
to a low diastolic pressure. The filling of the systemic arteries under
great pressure, and the sudden drop in this pressure due to the regurgita-
tion can be seen in the short, abrupt pulsation of the visible arteries
and can also be felt by palpating the radial artery. The incessant pound-
ing of the hypertrophied left ventricle, the high systolic pressure and the
low diastolic pressure tend to produce a very intermittent blood supply
in the whole arterial system and especially in the coronary vessels. The
latter result is particularly serious as it interferes with the nutrition of
the heart muscle and this eventually leads to exhaustion through degen-
erative changes. When the left ventricle reaches the limit of hyper-
trophy or becomes exhausted, dilatation ensues and with it relative
insufficiency of the mitral valve. This in turn is followed by the usual
phenomena of broken compensation.

Symptoms. — Aortic regurgitation may exist in a latent form for years
without giving rise to any symptoms whatsoever. Among the earliest
symptoms noted are those due to alternations in the circulation, espe-
cially cerebral anemia. There may be headaches, attacks of vertigo or
flashes of light before the eyes. Anemia is often a marked feature
in these cases, the face especially presenting a pale grayish color. Even
prior to any evidence of failing compensation, pain may be a prominent
symptom. It may be in the nature of true angina, or a sense of sub-
sternal oppression and pain, or it may be an annoying palpitation or
throbbing sensation in the precordium. Shortness of breath, especially
after exertion, is often the first symptom noticed by the patient. Later,
there may be cough and occasionally blood-streaked sputum. Cyanosis
is unusual unless there is an associated mitral lesion.

In patients subject to this lesion, distressing dreams and sleep
which is broken at frequent intervals, are more common than in any other
form of heart disease. Mental symptoms, such as delirium, halluci-
nations and even suicidal tendencies, are also occasionally encountered.

In cases of aortic insufficiency, sudden death is not infrequent and
may occur with but slight premonitory symptoms. The foregoing
symptoms are, for the most part, somewhat distinctive of aortic valvular
trouble. Failure to maintain compensation may be brought about by
a gradual weakening of the left ventricle and the establishing of mitral
incompetency. The symptoms then assume the character of those
due to broken compensation from any cause, although the symptoms
peculiar to the lesion itself may become accentuated.

Physical Signs. — Inspection. — A diagnosis of aortic insufficiency can
be made in a large number of cases from inspection alone. This is due
to the arterial phenomena which constitute the most distinctive feature
of the disease.

All of the peripheral arteries are seen to strongly pulsate. Not
only is this true of the large superficial vessels but even the small arteries
in the hand and face may be seen to throb, and on ophthalmoscopic
examination the retinal arteries may be seen pulsating. The arterial
pulsation may be so strong that the foot is jerked when the knee is crossed
or the head may be moved slightly with each systole.

In addition the so-called capillary pulse is usually present. This is
caused by the rapid filling and emptying of the capillaries.

The pulsatile movement may even reach the veins. This may be



ENDOCARDITIS 679

noted in the veins in the back of the hands. The phenomenon may
be brought out by holding the hand so as to drop the wrist. This aids
in filling the veins and if pulsation is present it will not be sharp and abrupt
as in the arteries, but slow and deliberate. Capillary pulsation is some-
times seen in asthenic conditions accompanied with a low blood-pressure.

In well-marked cases the apex beat is displaced downward and to
the left. It is commonly in the sixth interspace but may be as low
as the seventh in the anterior axillary line. If the hypertrophy is well-
marked, the cardiac impulse is heaving and forcible and may move the
entire precordium. In children and young adults the precordium may
bulge. If dilatation has occurred the impulse is diffuse and often wavy.

Palpation. — This enables one to appreciate more fully the forcible,
heaving character of the impulse. Thrills are not constant but may be
felt occasionally. They are either presystolic or systolic at the apex or
diastolic and systolic over the base of the heart. The arteries feel large
and are usually thickened. When one of the radial arteries is palpated,
the pulse beat is felt to impinge against the finger with an abrupt, forcible
stroke and immediately recede, hence the terms water-hammer or collaps-
ing pulse. It is also frequently referred to as the Corrigan pulse. The
features of this type of pulse are sometimes best appreciated by grasping
the wrist and holding it up above the level of the heart, thus accentuating
the effect of gravity. The distention of the large vessels at the root of the
neck may be so marked as to simulate aneurism. The sphygmographic
tracing is characteristic. The upstroke is high and almost perpendicular
and forms a very acute angle with the sharply descending downstroke
(see Fig. 131). It is in marked contrast to the sphygmographic record
of aortic stenosis which is exactly the reverse, namely a slow and low up-
stroke and a very gradual descent of the downstroke. Auricular fibrilla-
tion which is so commonly encountered in mitral disease is not common in
aortic lesions unless dilatation of the left ventricle and auricle supervenes.

Percussion.- — The area of cardiac dulness is usually increased to the left
and in extreme cases may reach the anterior axillary line. The upper
border may reach the third rib. There is usually some dulness to the right
of the sternum. This may be due to extreme hypertrophy of the left
ventricle which causes an extension of the whole heart to the right or it
may be brought about by dilatation of the right ventricle when compensa-
tion is no longer complete (see Fig. 172).

In some cases a slight area of dulness may be made out, over the ster-
nal end of the second right intercostal space due to dynamic dilatation of
the aorta.

Auscultation. — The murmur of aortic insufficiency is caused by the
backward rush of blood from the aorta into the left ventricle during the
ventricular diastole. While the seat of the production of the murmur is
over a point close to the left border of the sternum opposite the third
costal cartilage it is, as a rule, not best heard in this situation. The
punctual maximum for the murmur of aortic incompetency is placed, by
most authorities, at the second costal cartilage on the right, although
there are some who believe that the murmur, in many instances, is best
heard in the fourth interspace on the left side close to the sternum. Our
experience is in accordance with the latter view. The murmur is in most
instances soft and low-pitched. It may be very loud, but it rarely has the
coarse rasping quality so commonly heard in other valvular murmurs



680 DISEASES OF THE PERICARDIUM, HEART, AND AORTA

although at times it has a distinct musical tone. The murmur of aortic
insufficiency is transmitted downward along the right border of the
sternum or towards the cardiac apex. It also may be heard upwards along
the sternal margin as far as the sterno-clavicular articulation or in the
carotids. In such instances there is usually a dilatation of the aorta asso-
ciated with stretching of the aortic ring. In well-marked cases, with a
loud murmur, it may be heard all over the chest (see Figs. 194 and 196).
In some cases the murmur of Duroziez may be heard over one of the
large arteries, such as the femoral This murmur is said never to occur
except in the presence of aortic leakage. Traube's double sound is some-
times heard in cases complicated by tricuspid insufficiency.

The murmur may be long drawn out and occupy the whole of diastole
or it may be short and take up but part of the second sound. Generally
speaking, a long loud diastolic murmur shows a considerable degree of
pressure kept up in the aorta, which is desirable and a proof that the heart
is acting with vigor; also that the valve leakage is not excessive. This is
a favorable augury. A weak short murmur indicates the opposite and
may be a note of impending danger although there are many exceptions
to this (Broadbent).

The pulse pressure may also be utilized to determine the degree of
damage. In order to maintain the mean aortic pressure the systolic
pressure must be abnormally high in order to compensate for the rapid
fall of pressure during diastole. The pulse pressure, however, serves as a
useful gauge of the degree of the leak only when compensation is effective.

In some instances the murmur of aortic incompetency is heard by the
unaided ear much better than with a stethoscope (Flint).

Associated with the diastolic murmur there is very often heard a
systolic murmur. This is usually due to some degree of obstruction but
it not infrequently happens that a systolic murmur may occur without
stenosis. This is explained by Rosenbach as follows : At the beginning
of the left ventricular systole the regurgitating flow has not entirely
ceased and when this encounters the opposing current a murmur, systolic
in time, is produced.

If compensation is complete the first sound at the apex is usually
clear. If dilatation of the left ventricle occurs, the first sound at the apex
is replaced by a systolic murmur due to relative insufficiency. If com-
pensation is again restored, this murmur disappears and the first sound
becomes normal.

In a very considerable percentage of cases of aortic incompetency there
is heard at the apex a murmur presystolic in time and which is usually
referred to as Flint's murmur.

Since Flint's time several hypotheses have been advanced to explain
the mechanism of this murmur. (1) That the regurgitant stream tends
to lift the great anterior mitral curtain and so to obstruct the mitral orifice
at the end of diastole as to impede the current from the auricle. (2)
That the mitral valve is thrown into vibration by the two currents, the
regurgitant from the aorta and the direct from the auricle. (3) That in
the absence of aortic valve disease, but in the presence of adherent peri-
cardium, vibrations may be set up by the current propelled from a dilated
and hypertrophied auricle into a ventricle whose muscular walls are
deficient in tone. (4) That shortening of the chordae tendinese, or
dilatation of the left ventricle, may bring about a vertical narrowing of



ENDOCARDITIS 681

the aperture through which the blood passes from auricle to ventricle, the
auricular muscle continuing to be sufficiently powerful to generate a
fluid vein. 1 The differentiation of this murmur from that due to mitral
stenosis has been considered under the latter condition (see Fig. 136).

Diagnosis. — If due consideration is given to the arterial phenomena asso-
ciated with the diastolic murmur heard at the base of the heart little or no
confusion should arise. If, however, the diagnosis is made on the presence
of a murmur alone mistakes may occur as a diastolic murmur is sometimes
heard in other conditions. In addition to aortic regurgitation a diastolic
murmur may be heard at the base of the heart as the result of insuffi-
ciency of the pulmonary valves. This murmur, sometimes called the
Graham Steell murmur, is associated with chronic mitral disease and is
caused by stretching of the conus arteriosus and the orifice of the pul-
monary artery. The time and location of the murmur are all that it
has in common with aortic regurgitation. In Graves' disease a diastolic
bruit is sometimes heard over the sternum and rarely a cardio-respirator y
murmur is diastolic in time. The chief point of distinction between the
murmur of aortic insufficiency and other occasional murmurs occurring
during the diastolic phase is the presence or absence of the arterial
phenomena.

It is not easy to distinguish between aortic regurgitation due to
disease of the semilunar valves and relative insufficiency associated with
dilatation of the aorta. In the latter condition the murmur is often
transmitted high over the sternum or even into the carotids; in addition
there is dulness to the right in the second interspace due to the dilated
aorta.

The following peripheral arterio-venous signs may be met with in
cases of aortic insufficiency, and while they are more commonly and strik-
ingly met with in this condition than in any other, they are none of them
pathognomonic of this lesion. (1) Collapsing pulse, (2) visible arterial
pulsation, (3) capillary pulse, (4) venous pulse, (5) hepatic pulse, (6)
femoral snap, (7) double femoral murmur (Duroziez's sign), (8) Double
femoral tones (Traube's sign). 2

AORTIC STENOSIS

Etiology. — This is the rarest of the left-sided valvular lesions. True
aortic stenosis unassociated with another valvular lesion is not often
encountered. In the autopsy records of the Pennsylvania and Philadel-
phia General Hospitals, Norris found 48 instances of aortic stenosis out
of a total of 9940 cases having cardiac lesions. It is important to bear this
in mind as a systolic murmur at the aortic cartilage is relatively common
and on this evidence alone a diagnosis of aortic stenosis is made far too
frequently. The interpretation of systolic murmurs heard at the aortic
area has been considered on page 730. The great majority of cases
of aortic stenosis are encountered in those past the middle period of life
and in those who are the subjects of atheromatous changes in the arteries,
especially the aorta. It is rare among women. Occurring as a single
lesion it is not often caused by acute rheumatic fever.

1 Sansom and GlBSON, Au.bittt and Rolleston: "System of Medicine," vol. vi,
p. 362.

2 Tick, F. : "The Clinical Determination and Significance of Some Peripheral
Signs of Aortic Insufficiency," Illinois Med. Jour., September, 1911.



682 DISEASES OF THE PERICARDIUM, HEART, AND AORTA

Morbid Anatomy. — The anatomical changes which take place in the
semilunar valves are precisely similar to those which occur in the intima
of the blood-vessels and ending in atheromatous degeneration. As a
result, the leaflets become fused, stiff, and rigid and obstruct the free
escape of the blood from the left ventricle into the aorta (see Fig.
385). In some instances the obstruction is made worse by vegetations




Fig. 385. — Aortic obstruction from above. The margins of the leaflets are fused to-
gether, thickened and calcified, reducing the orifice to about one-third of its normal caliber.
The mitral and tricuspid orifices are also sclerosed and contracted.

which develop during an attack of secondary endocarditis (see Fig.
386). The resistance offered adds to the work of the left ventricle which,
as a consequence, becomes hypertrophied. It is in this variety of val-
vular lesion that the so-called " concentric hypertrophy" is most nearly
approximated. Practically, however, some degree of dilatation is always
present. When the heart can no longer overcome the obstruction, dila-
tation and the phenomena of broken compensation ensue.



ENDOCARDITIS



683



Pathological Physiology. — The mechanism of aortic stenosis is quite
simple. Owing to the obstruction to the ventricular outflow, the
blood-pressure in the left ventricle is increased, sometimes to twice
the normal. Another effect caused by the obstruction is to prolong
the time of emptying the ventricle and as a result the ventricular systole
may consume from 5 to 50 per cent, more than the normal time. If
the obstruction become^ too great or the muscle becomes exhausted, an




FlG. 386. — Aortic obstruction, seen from above. The leaflets are fused together, thick-
ened, and indurated. They are covered with small vegetations.



insufficient amount of blood reaches the systemic circulation and as a
result the pulse pressure becomes small and symptoms of cerebral
anemia may develop. In cases of aortic stenosis the left ventricle
occupies the same position in maintaining compensation that the right
ventricle does in mitral disease. As long as the hypertrophy keeps in
advance of the obstruction, the circulatory equilibrium is maintained.
If, however, the obstruction becomes too great or, what is more apt to



684 DISEASES OF THE PERICARDIUM, HEART, AND AORTA

occur, the muscle becomes exhausted, the ventricle dilates and then there
develops relative mitral insufficiency with the usual sequence of events
which characterize broken compensation. Some observers have ex-
pressed the opinion that stretching of the mitral ring and a certain
amount of leakage through the auriculo-ventricular opening is to be looked
upon as being in the nature of a safety valve action. There is little to sup-
port this view, however.

Symptoms. — Of all the valvular lesions aortic stenosis is the most apt
to occur in a latent form. It may be present for years without causing
serious symptoms. Failure of the left ventricle manifests itself by the
occurrence of symptoms which may be brought on by slight exertion,
or excitement. They consist of shortness of breath, palpitation, a sense
of oppression in the precordium, and substernal pain or anginal attacks.
In addition a curtailment of the amount of blood thrown into the sys-
temic arteries may manifest itself by evidences of cerebral anemia, such
as vertigo or dizziness. If the left ventricle become dilated from exhaus-
tion, the usual phenomena attending broken compensation are present.
Sudden death is not uncommon and may occur as the result of sudden
cardiac failure or an attack of angina.

Physical Signs. — Inspection does not reveal much of importance;
extreme hypertrophy is not often marked as a result of this lesion.
Furthermore, occurring as it does in elderly people, the size of the heart
is often obscured by a rigid chest wall and emphysematous lungs.

Palpation. — A very common feature of aortic stenosis, although not
peculiar to it, is a systolic thrill felt over the base of the heart on the
right side. One of the most distinctive features of this lesion is the slow
retarded pulse felt at the wrist and graphically shown by a sphygmo-
graphic tracing. The pulse is often slow, between 50 and 60 beats per
minute and the pulse wave is much prolonged. This is well shown in a
pulse tracing but may also be appreciated by the palpating finger as the
artery is gradually filled with blood. In addition to the slow slanting up-
stroke the tracing may show an anacrotic pulse or the pulsus bisferiens.

Percussion. — This is relatively unimportant and is often valueless
owing to pulmonary emphysema.

Auscultation. — As we have repeatedly emphasized, a systolic murmur
at the aortic area, even when transmitted to the vessels in the neck, is
not pathognomonic of true stenosis but is more often associated with
changes in the aorta itself, usually a roughening of the intima or a dilata-
tion of the artery. The murmur of true aortic stenosis is transmitted
not only upward to the carotids but is frequently audible along the right
border of the sternum as low as the fourth or fifth ribs. In some in-
stances it is very loud and may be heard all over the precordium and in
such instances the question always arises as to whether the murmur
heard at the apex is the same as that heard at the aortic cartilage or
is a second murmur due to mitral insufficiency. Even more distinctive
of stenosis than the slow retarded pulse is the character of the second
aortic sound. This is either very feeble or inaudible due to the fact that
the stiff and rigid valve segments are incapable of snapping together.
If, therefore, the second aortic sound is normal and especially if it is
loud and ringing in character, the murmur originates in the aorta and is
not due to rigid and diseased valves. Some leakage is probably always
present but this is often so slight that no murmur can be heard.



ENDOCARDITIS 685

Diagnosis. — The diagnosis of true aortic stenosis rests upon the fol-
lowing facts: (1) A systolic thrill felt over the base of the heart to the
right of the sternum; (2) a slow retarded pulse; (3) a systolic murmur
heard at the aortic cartilage and transmitted to the vessels of the neck;
and last, but most important, a feeble or inaudible second aortic sound.

TRICUSPID INSUFFICIENCY

Etiology. — Lesions involving the tricuspid valve may be (1) organic
and (2) functional.

1. Organic disease of the tricuspid leaflets is rare although not so un-
usual as was once believed to be the case. Formerly it was taught that
organic lesions of the valves in the right heart were almost invariably
congenital in origin. Recent investigations, however, have shown that
these lesions are more frequently the result of acquired disease than of a
congenital defect.

(a) The tricuspid leaflets may be the seat of an acute inflammatory
process which develops during the course of one of the acute infections
such as puerperal fever and other forms of general sepsis, gonorrhea,
pneumonia, diphtheria, scarlet fever and acute rheumatic fever. The
last-named infection is by far the most important etiological factor.
Statistical studies indicate that acute rheumatic fever is the apparent
cause of organic tricuspid disease in from 35 to 62 per cent, of cases. 1



Online LibraryGeorge William NorrisDiseases of the chest and the principles of physical diagnosis → online text (page 68 of 79)