SYMPTOMS AND PHYSICAL SIGNS
=General=
Well developed arteriosclerosis shows four pathognomonic signs: (1)
hypertrophy of the heart; (2) accentuation of the aortic second sound;
(3) palpable thickening of the arteries; and (4) heightened blood
pressure. However, it must not be inferred that these signs must be
present in order to diagnose arteriosclerosis. It has already been said
that a very marked degree of thickening, with even calcification of the
palpable arteries, may occur with absolutely no increase of blood
pressure, and at autopsy a small flabby heart may be found.
While arteriosclerosis is usually a disease which is of slow maturation,
nevertheless cases are occasionally seen which develop rather rapidly.
The peripheral arteries have been noticed to become stiff and hard in as
relatively brief a time as two years from the recognized onset of the
disease.
Since involution processes are physiologic, as has been described (vide
infra), arteriosclerosis may assume an advanced grade and run its course
devoid of symptoms referable to diseased arteries. It is doubtful
whether the sclerosis itself could produce symptoms, except in cases
later to be described, were it not that the organs supplied by the
diseased arteries suffer from an insufficient blood supply and the
symptoms then become a part of the symptom-complex of any or all the
affected organs.
There are cases, however, in comparatively young persons where a
combination of certain ill-defined symptoms gives a clue to the
underlying pathologic processes. These symptoms of early
arteriosclerosis are the result of slight and variable disturbances in
the circulation of the various organs. Normally there are frequent
changes in the blood pressure in the organs, but the vasomotor control
of normal elastic vessels is so perfect that no symptoms are noted by
the individual. When the arteries are sclerosed, they are less elastic
and the blood supply is, therefore, less easily regulated. At times
symptoms occur only after effort. The patient may tire more readily than
he should for a given amount of mental or bodily exercise; he is weary
and depressed, and occasionally there is noted an unusual intolerance of
alcohol or tobacco. Vertigo is common, especially on rising in the
morning or in suddenly changing from a sitting to a standing position.
Some complain of constant roaring or ringing in the ears. There may be
dull headache that the accurate fitting of glasses does not alleviate.
Unusual irritability or somnolency with a disinclination to commence a
new task may be present. Sometimes the effort of concentrating the
attention is sufficient to increase the headache. This has been called
"the sign of the painful thought." Numbness and tingling in the hands,
feet, arms, or legs are also complained of, and neuralgias, not
following the course of the nerves but of the arteries, also occur. It
is important to remember that the train of symptoms resembling
neurasthenia in a person over forty-five years old may be due to
incipient arteriosclerosis. This tardy neurasthenia frequently
accompanies cancer, tuberculosis, diabetes, and incipient general
paralysis, as well as incipient arteriosclerosis.
Bleeding from the nose, epistaxis, taking place frequently in a
middle-aged person, sometimes is an early symptom. The bleeding may be
profuse, but is rarely so large as to be positively harmful. In fact, it
may do much good in relieving tension. Slight edema of the ankles and
legs is seen. Dyspnea on slight exertion is not uncommon. Dyspeptic
symptoms are not infrequent, pyrosis (heartburn), a feeling of fullness
after meals with belching or a feeling of weight in the epigastrium.
The dyspeptic symptoms may be so marked that one might almost speak of a
variety of arteriosclerosis, the dyspeptic type. For quite a while
before any symptoms that would definitely fix the case as one of
undoubted arteriosclerosis, the patient complains that foods which
previously were digested with no difficulty now give him gastric
distress. The examination of the stomach contents of a patient
presenting gastric symptoms reveals usually a subacidity. The total
acidity measured after the Ewald test meal may be only 20 and the free
HCl may be absent. Attention has been called to an unnatural pallor of
the face in early arteriosclerosis. Progressive emaciation is sometimes
seen in cases of arteriosclerosis and may be the only symptom of which
the patient complains.
=Hypertension=
Not all cases of arteriosclerosis are accompanied by increased arterial
tension. As has been stated in a previous chapter, the blood pressure in
the arterial system depends chiefly on two factors; viz., the degree of
peripheral (capillary) resistance, and the force of the ventricular
contraction. The highest arterial pressures recorded with the
sphygmomanometer occur not in pure arteriosclerosis but in cases where
there is concomitant chronic interstitial disease of the kidneys. When
this is found there is always arteriosclerosis more or less marked. In
cases where the arteries are so sclerosed that they feel like pipe stems
there may be an actual decrease in the blood pressure. Hence the
clinical measuring of the pressure in the brachial artery alone is not
sufficient for a diagnosis of arteriosclerosis. A persistent high blood
pressure even with normal urinary findings is not a sign of
arteriosclerosis. The high tension later may lead to the production of
sclerosis of the arteries, but in these cases the kidney may be
primarily at fault.
The impression must not be gained that hypertension in itself always
constitutes a disease or even a symptom of disease. Hypertension itself
is practically always a compensatory process. That is to say, it is the
attempt on the part of the body to equalize the distribution of blood in
the body when there is some poison causing constriction of the small
arteries. In this sense hypertension is not only essential, but actually
life-saving. A heart which is so diseased that it can not respond to the
call for increased action by hypertrophy of its fibers, would shortly
wear out. The very fact that the heart becomes enlarged and the tension
in the arteries becomes high, indicates that in such a heart there was
great reserve power. But while hypertension is largely an effort at
adjustment among the various parts of the circulation, it nevertheless
tends to increase, provided the cause or causes which produced it act
continuously. Moreover, as has been said (Chap. II), the arterioles do
not respond to increased work on the part of the heart by expanding, but
by contracting. A vicious circle is thus maintained which eventually
must lead to serious consequences.
Hypertension is then, if anything, only a symptom which may or may not
demand treatment. That hypertension leads to the production of sclerosis
of the arteries has been repeatedly affirmed here. In certain cases it
is good and should not be experimented with. In other cases it is bad
and some treatment to reduce the tension must be tried. The main point
is to regard hypertension as one regards a compensated heart lesion.
Prof. T. Clifford Allbutt divides the causes of arteriosclerosis
clinically into three classes: (1) The toxic class--the results of
poisons of the most part of extrinsic origin, chiefly those of certain
infections. In some of these diseases, the blood pressures, as for
example, in syphilis, are ordinarily unaffected; in others, as in lead
poisoning, they are raised. (2) The class he calls hyperpietic,[15] in
which an arteriosclerosis is the consequence of tensile strength, of
excessive arterial blood pressure persisting for some years. A
considerable example of this class is the arteriosclerosis of granular
kidney, but in many cases kidney disease is, clinically speaking,
absent. (3) The involutionary class, in which the change depends upon a
senile, or quasisenile degradation. This may be no more than wear and
tear, a disposition of all or of certain tissues to premature
failure--partly atrophic, partly mechanical--under ordinary stresses; or
it also may be toxic, a slow poisoning by the "faltering rheums of age."
In ordinary cases of this class the blood pressures for the age of the
patient are not excessive. Although the toxins of the specific fevers,
notably typhoid, as stated above, and influenza, have been shown to
produce arteriosclerosis, this, under favorable circumstances he
believes tends to disappear. This has been shown by Wiesel.
[15] From pieso to squeeze, oppress or distress. Hyperpiesis,
therefore, signifies excessive pressure.
As the blood pressure is dependent on the resistance offered by the
capillaries and arterioles, there are only two ways in which increased
pressure can be brought about; either by rendering the blood more
viscous, or by the generation of some poison from the food taken into
the body which, acting on the vasomotor center or directly on the finer
vessels, arteriolar or capillary, sets up a constriction over any large
area, and mainly in the splanchnic area. In regard to the liability to
arteriosclerosis, this area stands second only to the aortic and
coronary areas. He believes that arteriosclerosis itself has little
effect in raising arterial pressure. Many cases are seen in which with
extreme arteriosclerosis there was no rise in blood pressure, and some
in which pressures have been rising even long before the appearance of
arterial disease. Prof. Allbutt also believes that in the hyperpietic
cases the arteries undergo a transient thickening, which can be removed
if the causes can be reached and overcome.
Clinically speaking, then, hyperpietic arteriosclerosis is not a
disease, but a mechanical result of disease. If the narrowing of the
arterioles is brought about by thickening due to arteriosclerosis, then
it would seem _a priori_ that such obliteration should cause a rise in
pressure. Were the vascular system a mere mechanical set of tubes and a
pump, this would happen, but other factors of great importance must be
taken into consideration besides the mechanical factors; viz., chemical
and biological factors. Thus, whole parts may be closed and with
compensatory dilatation in other parts there would be little or no
change in pressure, unless there were hyperpiesis. In established
hyperpiesis, we note two conditions in the radial artery: first, a
comparatively straight vessel with a small diameter; secondly, a larger,
more tortuous vessel, "the large leathery artery." In the cases of the
first group, hyperpiesis is often more marked, although not appearing so
to the examining finger, than in the second class. In view of the
difficulty of estimating by touch alone the amount of hyperpiesis in a
contracted hard artery, it is often overlooked until a ruptured vessel
in the brain startles us to a realization of our mistake. The "narrow"
artery is more dangerous than the tortuous one, for with every change in
pressure the passive vessels of the brain must receive blood that under
normal conditions would go to other parts of the circulation.
In involutionary sclerosis there is a gradual thickening and tortuosity
of the vessel, which although it may be greater than in the hyperpietic
cases, yet is never so dangerous to life. The heart in hyperpiesis
hypertrophies and dilates, but such a heart is the result, not an
integral part, of the arterial disease.
=The Heart=
When the arterial tree becomes narrowed and the resistance offered to
the flow of blood thereby is increased, more muscular work is required
of the left ventricle and according to the general laws which govern
muscles the ventricle hypertrophies. There is an actual increase in
number of fibers as well as an increase in the size of the individual
fibers. Some of the best examples of simple hypertrophy of the left
ventricle are found under such circumstances. The chambers as a rule do
not dilate until the resistance becomes greater than the contraction can
overcome, when symptoms of broken compensation of the heart take place.
The hypertrophy of the left ventricle brings more of this portion of the
heart toward the anterior chest wall. The enlargement is toward the
left, also, consequently the apex-beat is found below and to the left of
its usual site, even an inch or more beyond the nipple line. The impulse
is heaving, pushing the palpating hand forcibly up from the chest wall.
The visible area of pulsation may occupy three interspaces and the
precordium is seen to heave with every systole. On auscultation the
second sound at the aortic cartilage is ringing, clear, and accentuated.
Not infrequently, too, the first sound is loud and booming, but has a
curious muffled sound that may even be of a murmurish quality. The
leaflets of the mitral valve may be the seat of sclerosis, the edges are
slightly thickened and do not quite approximate, thus causing a definite
murmur with every systole. This murmur may be transmitted out into the
axilla and be heard at the inferior angle of the left scapula.
=Palpable Arteries=
Not every artery that can be felt is the subject of arteriosclerosis,
and, as has been stated, palpable arteries being more or less a
condition of advancing years, judgment as to whether the artery is
pathologically or physiologically thickened may be a matter of
individual opinion. A radial artery that lies close to the lower end of
the radius and can actually be seen to pulsate when the hand is held
slightly extended on the back of the wrist, is easily felt, but must
not, therefore, be considered a sclerosed artery. The radial may be so
deeply situated in the wrist of a fat subject that it is difficultly
palpable. Yet the two cases just described may have arteries of
identical structure, there being no more retrogressive changes in the
one than in the other. "Experience is fallacious and judgment
difficult."
The small, contracted, wiry artery of a chronic nephritic may feel like
a pipe stem, but if properly felt the mistake will not be made of
considering such an artery an unusually sclerosed one. When the wave is
pressed out of such a high tension artery, it is found that what seemed
to be a firm sclerosed vessel, was in reality an artery tightly
stretched over the column of blood.
=Ocular Signs and Symptoms=
It would not exaggerate too much to say that the examination of the eye
grounds with the ophthalmoscope is the most important aid in the early
diagnosis of arteriosclerosis. Long before there are any subjective
symptoms, changes can be seen in the blood vessels of the retina which,
while not always diagnostic, at least call attention to a beginning
chronic disease. As I become more proficient in the use of the
ophthalmoscope, I am impressed with the importance of the ocular signs
of arterial disease. I would urge practitioners to familiarize
themselves with this instrument. The electrically lighted instruments on
the market now have so simplified the technic that any physician should
be able to see the grosser changes which take place in the arteries and
veins of the retina and in the disc. Frequently the ophthalmologist is
the first to recognize early arteriosclerosis. In the fundus are seen
increased tortuosity of the retinal vessels and their terminal twigs
with more or less bending of the vessels at their crossings. The
arteries are terminal ones, and small patches of retinitis are therefore
found. The changes have been divided into (1) suggestive, (2)
pathognomonic.
Under (1) are:
(a) Uneven caliber of the vessels,
(b) Undue tortuosity,
(c) Increased distinctness of the central light streak,
(d) An unusually light color of the breadth of the artery.
Under (2) are:
(a) Changes in size and breadth of the retinal arteries so that they
look beaded,
(b) Distinct loss of translucency,
(c) Alternate contractions and dilatations in the veins,
(d) Most important of all, the indentation of the veins by the stiffened
arteries.
There is yet another sign which appears to be pathognomonic. The
arteries are pale, appear rigid and through the center, parallel to the
course, is a rather bright, fine threadlike line. The appearance is
known as the "silverwire" artery. It is particularly constant in
hypertension where the most beautiful examples are seen.
Moreover, there is the arcus senilis, the fine translucent to opaque
circle surrounding the outer portion of the iris. Practically every one
with a well-marked arcus senilis has arteriosclerosis, but vice versa
not every one with even marked arteriosclerosis has an arcus senilis.
In general, the symptoms are gradual loss of acute vision, and attacks
of transient loss of vision. The explanation which has been offered for
these phenomena is the contraction in a diseased central artery.
=Nervous Symptoms=
The onset of arteriosclerosis is, in the majority of cases, so insidious
that certain nervous manifestations, due in all probability to
disturbances in blood pressure, are present long before the actual
sclerosis of the arteries can be felt. These nervous symptoms are at
times the sign posts to show us the way to accurate diagnosis. There may
be gradual increase in irritability of temper, inability to sleep,
vertigo even extending to transient attacks of unconsciousness. Loss of
memory for details frequently is an early symptom of sclerosis of the
cerebral arteries. Nervous indigestion may be present. Various
paresthesias as numbness, tingling, a sense of coldness or of heat or
burning, a sense of stiffness or even actual stiffness or weakness may
occur in the arms and legs, more frequently in the legs. The pain
complained of may be due to occlusion of an artery, although evidence
for this is lacking. It has been thought by some that the pain in angina
pectoris might be due to this cause.
Several curious and interesting diseases which have been thought by some
to have arteriosclerosis as a basis are accompanied by pain. Such are
erythromelalgia, Raynaud's disease, "dead fingers," and intermittent
claudication.
Erb has reported a large series of intermittent limp (claudication) from
his private practice. He finds that the large majority of the cases
occur in men. The abuse of tobacco was evidently the main etiologic
factor in about half of the cases. Repeated exposure to cold and the
abuse of alcohol were responsible for most of the other cases. Curiously
enough he finds that a history of syphilis was present in only a small
proportion of his cases. It is his firm conviction that intermittent
limping--which he thinks should be called angiosclerotic dysbasia--is
frequently incorrectly diagnosed. It is mistaken for other troubles and
treated wrongly. As gangrene may develop this is particularly dangerous.
The affection generally develops gradually, although he has seen cases
where the onset was rather acute. The partial or complete lack of the
pulse in the foot is the one striking sign, together with the varying
behavior of the pulse, its disappearance when the feet are cold and its
return after a warm foot bath or under other treatment. Signs of general
arteriosclerosis were present in nearly every case. When there is a
tendency to the development of intermittent limp he finds that a
valuable sign is the manner in which the leg blanches when it is lifted
repeatedly while the patient is recumbent and becomes hyperemic later
when placed horizontally. In health this change occurs more rapidly.