CHAPTER VIII

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 piesô 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.