Fig. 57.—A method of finger-tip palpation of the radial artery. (Graves.)Fig. 57.—A method of finger-tip palpation of the radial artery. (Graves.)
Fig. 58.—Another method of finger-tip palpation of the radial artery. (Graves.)Fig. 58.—Another method of finger-tip palpation of the radial artery. (Graves.)
It must be borne in mind at the outset that arteriosclerosis and high blood pressure are not always associated. As a matter of fact in the severest grades of senile arteriosclerosis the blood pressure is usually below the normal for the individual's years. However, as high tension is a frequent factor in the production of arterial thickening, blood pressure readings are of importance.
The instrument which one uses is of minor importance provided it is properly standardized. The most important feature of the instrument is the cuff. This must be 12 cm. wide and be long enough to wrap around the arm several times so that the pressure is evenly distributed over the whole arm and not over a small portion. One mercury instrument we had in the hospital was reported to be at great variance with a dial instrument. This mercury instrument was provided with a cuff which was short and was tiedaround the arm by means of a piece of tape. This caused a tight constriction over a small area and rendered the estimation too high. A new, long tailed cuff easily remedied the apparent defect in the instrument.
In taking blood pressures the difference from day to day of 10 or even 15 mm. of systolic pressure has no great significance. Fluctuations of the systolic pressure alone, it is insisted upon, have very little meaning. One must take the whole pressure picture into consideration and determine how the picture changes in order to draw any conclusion in regard to the state of the blood pressure. Failure to pay attention to this evident point has caused much futile work to be written and published.
It is well to emphasize again the point that the blood pressure picture consists of the systolic, the diastolic, the pulse pressure and the pulse rate.
Hoover has called attention to the direct palpation of the femoral artery just below Poupart's ligament as a more accurate index of the pressure in the aorta than the palpation of the radial artery. Possibly one can obtain a more accurate estimate of the blood pressure in this way. This, however, is open to dispute. To estimate the blood pressure by palpating the radial artery is most deceptive. In about 75 per cent of cases one can tell fairly well whether the pressure is abnormally high or abnormally low. Small variations are impossible to determine. Unquestionably it is most advantageous to get into the habit of palpating the femoral artery and checking the result with the sphygmomanometer so that the fingers may be trained to appreciate as accurately as possible changes of pressure.
It may be that one day when the instrument is needed it is not at hand. A well-trained touch then becomes a great asset.
There are certain precautions which must be strictly observed when deductions are drawn from the manometer readings. The psychic factor must be reckoned with. Any emotion may cause marked variations in the pressure. Excitement and anger are especial sources of error. Even the slight excitement arising from taking the first blood pressure on a nervous patient especially is apt to give false values. Usually the readings must be taken many times at the first sitting and the first few may have to be set aside. Worry is a potent factor in raising the pressure. A walk to the physician's office, especially if rapid, has its effect.
The position of the patient when the blood pressure is taken is important. Usually in the office the pressure is taken when the patient sits in a chair. He should assume a relaxed, comfortable attitude. The readings should be made at the same time of day and at the same interval between meals. The pressure in both arms should be measured and comparisons should be made only between readings on the same arm. These precautions may seem useless and even somewhat trivial, and the conditions difficult to control. But unless they are carefully observed the readings will be false, no comparisons can be drawn between the readings on different days, and the instrument will most probably be blamed. I have known this to happen so often that I can not emphasize too strongly the importance of controlling all the essential conditions which go to make accurate work.
In the past few years there has been a veritable avalanche of blood pressure instrument salesmen who have covered the country, sold instruments, and have made many startling claims for the instrument. They have emphasized its value out of proportion to what the instrument can doeven in the hands of one familiar will all the defects. Consequently it is not necessary to emphasize the value of blood pressure. It seems best to utter a few words of caution in regard to its interpretation.
The value lies not in the occasional estimation compared with some other one reading, but in the frequent estimation and in the visualization of the blood pressure picture. For the great majority of diseases the blood pressure has no particular value except to show that the circulation is not materially disturbed. The limits of normal are rather wide, so that consideration of the patient's age, sex, build, etc., will give us some idea of a base line, so to speak, for any one person. Wide departures from relatively normal figures are important, but are not diagnostic or, rather, pathognomonic. I can not help but feel that the diastolic pressure isthemost important part of the blood pressure picture. Persistent high diastolic pressure means increased work for the heart, which, if acting for a long time against the high peripheral resistance, must eventually hypertrophy. The arteries become thickened, lose their wonderful elasticity, fibrous tissue is deposited in their walls, and the vicious circle is established which leads to pathologic hypertension.
Blood pressure readings must be intimately mixed with brains in order to be of any great value in diagnosis or prognosis.
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 slightand 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 ofweight 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.
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 initself 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]inwhich 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.
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 isnot 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 seema priorithat 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.
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 accordingto 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.
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 mustnot, 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.
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.
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 andits 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.
Our conception of arteriosclerosis as a degenerative process affecting the vascular tree rather than a disease, removes the possibility of discussing special symptoms. As a matter of fact, we know of very few organs where even profound pathologic changes in the vascular system produced during life any symptoms which could be laid to these arterial changes. Kind nature has given to us such an excess of organs of every kind that the destruction of large portions of any organ seems to affect the function but little. So only particular groups of organs, which show symptomatic changes as the result of arteriosclerotic processes, will be discussed. It is realized that this may not give Teutonic completeness to the discussion, but it certainly saves paper and has a distinct practical value to the long suffering reader.
Although arteriosclerosis is a disease which affects the whole arterial system, it nevertheless never reaches the same grade all over the body. The difference in the structure and functions of the various organs determines to great extent the eventual symptomatology. Endarteritis obliterans of a small sized artery in the liver or leg would lead to no marked symptoms, as the circulation is so rich that the anastomoses of the blood vessels would soon establish a collateral circulation that would be perfectly competent to sustain the function of the part. Quite different would it be should one of the small arteries of the brain, the lenticulo-striate, for example, which supplies the corpus striatum, become the seat of a thrombosis or embolism caused by arteriosclerosis. The arteries of the brain are terminalarteries and the blood supply would be cut off entirely with a resulting anemic necrosis of the part supplied by the artery and a loss of function of the part. What would be of no moment in the leg or arm might prove even fatal in the brain.
The further symptomatology, therefore, of arteriosclerosis depends entirely on the organ or organs most affected by the interference with the blood supply. The following groups may be recognized:
1. Cardiac.2. Renal.3. Abdominal.4. Cerebral.5. Spinal.6. Local vasomotor effects.7. Pulmonary.
Most cases of arteriosclerosis sooner or later present symptoms referable to the heart. When the organ is hypertrophied and is already working against an enormous peripheral resistance, a slight excess of work put upon it may cause a dilatation of the chambers with the resulting broken compensation. There is dyspnea on slight exertion, possibly some precordial distress, slight edema of the ankles and lower legs and possibly scanty urine. With proper care, a patient with such symptoms may recover, but the danger of another break in compensation is enhanced. The next attack is more severe. The edema is greater, there may be signs of edema of the lungs, effusions into the serous cavities may occur. The heart shows marked dilatation. There is gallop or canter rhythm and there are loud murmurs at the apex. When a patient is first seen in this stage, it may be quite impossible to state whether or not there is true valvular disease of the heart. The muscle is usually diseased in that there is fibroid degeneration of more orless extensive character. This factor causes the heart to lose much of its elasticity and increases the tendency to permanent dilatation. Such cases must be watched before one can say that true valvular insufficiency is not present. The fatal termination of such a case is quite like that of true valvular disease. There is increasing dyspnea, increasing anasarca, and the patient usually succumbs to edema of the lungs, drowned in his own secretions.
Fig. 59.—Aneurysm of the heart wall. (Milwaukee County Hospital.)Fig. 59.—Aneurysm of the heart wall. (Milwaukee County Hospital.)
A very rare complication of the fibroid degeneration of the heart muscle is aneurysm of the heart wall. (Fig. 59.)The apex of the left ventricle is most commonly the site of the aneurysm and rupture occasionally occurs. Such an accident is rapidly fatal. In the arteriosclerotic process which occurs at the root of the aorta, the coronary arteries become involved both at the openings and along the courses of the vessels. A branch or branches or even one artery may become blocked as a result of obliterating endarteritis. The arteries of the heart are not terminal vessels but as a rule blocking of a large branch leads to anemic infarct. These areas become replaced by fibrous tissue which in the gross specimen appears as streaks of whitish or yellowish color in the musculature. Anemic infarcts may not occur. In such cases the anastomosis between branches of the coronary arteries is unusually free. Through arteriosclerosis of the coronary vessels extensive fibrous changes may occur that lead to a myocardial insufficiency with its attending symptoms—dyspnea, irregular and intermittent heart, gallop rhythm, edema, etc. One of the most distressing and dangerous results of sclerosis of the coronary arteries and of the root of the aorta is angina pectoris. While in almost every case of angina pectoris there is disease of the coronary arteries, the contrary does not hold true, for most extensive disease, even embolism, of the arteries is frequently found in persons who never suffered any attacks of pain. This symptom group is more common in males than in females and as a rule occurs only in adult life. "In men under thirty-five syphilitic aortitis is an important factor." (Osler.)
Since the valuable experiments of Erlanger on heart block, considerable attention has been paid to lesions of the Y-shaped bundle of fibers, a bundle arising at the auriculoventricular node and extending to the two ventricles, known also as the auriculoventricular bundle of His. Interference with the transmission of impulses through this bundle gives rise to the symptom group known as the Stokes-Adams syndrome, which is characterized by: (a)slow pulse, (b) cerebral attacks—vertigo, syncope, transient apoplectiform and epileptiform seizures, (c) visible auricular impulses in the veins of the neck. Many of the cases which occur are in elderly people the subjects of arteriosclerosis.
Fig. 60.—Large aneurysm of the aorta eroding the sternum. Death from rupture through the skin preceded by frequent small hemorrhages. (Milwaukee County Hospital.)Fig. 60.—Large aneurysm of the aorta eroding the sternum. Death from rupture through the skin preceded by frequent small hemorrhages. (Milwaukee County Hospital.)
So far as we now know all cases of the Stokes-Adams syndrome are caused by heart block which is only another name for disease in the auriculoventricular bundle. Of interest here is the fact that besides gummata, ulcers, and other lesions of the bundle, definite arteriosclerotic changes have been found.
"The investigation of a typical case of Stokes-Adams disease has shown that the symptoms of this case are caused by some lesion in the heart which gives rise to the conditionnow generally termed heart block. Practically all degrees of heart block have been observed, namely, complete heart block and partial block with 4:1, 3:1, and 2:1 rhythm, and occasionally ventricular silences. These stages occurred during recovery.
"Experiments testing the reaction of the heart to various extrinsic influences demonstrate that when the block is complete the ventricles do not respond to influences presumably of vagus origin, although the auricles still respond normally to such influences, that effects exerted upon the heart presumably through the accelerators still influence the rate of the ventricles as well as that of the auricles.
"When the block is partial the rate of the ventricular contraction varies proportionally with the rate of the auricular contractions but only within certain limits. When these limits are exceeded the block becomes more complete, i. e., a 2:1 rhythm may be changed into a 3:1 rhythm, this into a 4:1 rhythm, and this into complete block, and vice versa.
"The syncopal attacks are, in all probability, directly dependent upon a marked reduction of the ventricular rate. Such reductions of the ventricular rate are always associated with an increase of the auricular rate, and it is believed that the latter is the cause of the former." (Erlanger.)
The epileptiform seizures of the syndrome may be caused by the anemia of the brain resulting from failure of the heart to supply a sufficient quantity of blood.
The apoplectiform attacks are most probably caused by venous congestion when the slowing of the ventricular contractions is not sufficient to cause convulsions, but will just cause complete unconsciousness.
Chronic nephritis, hypertension, arteriosclerosis form a most important trinity. Some stoutly affirm that in all cases of high tension there is chronic renal disease. Certainlythe very highest blood pressures which we see occur in the chronic interstitial forms of kidney disease. The cause is most probably to be sought in some poison which is elaborated in the kidney, is absorbed into the circulation and acts powerfully either on the vasoconstrictor center as a stimulus, or directly on the musculature of the small arteries all over the body. Usually hypertension is progressive but it may be temporary.
A man, 43 years old, entered the Milwaukee County Hospital in uremic coma. The systolic blood pressure was 280-290 mm. Hg, the diastolic pressure 220 mm. (Janeway instrument). Under treatment his blood pressure gradually became lower, at the same period the albumin and casts gradually disappeared from the urine. In two weeks from admission he seemed perfectly well, there were no albumin or casts found in the urine, and the systolic blood pressure was 136 mm., not a high figure for a muscular man of the laboring class. It must be admitted, however, that such cases are the exception, not the rule.
Patients suffering from the association of chronic nephritis with hypertension die slowly, usually. There is gradual development of anasarca. Headache is frequent and severe. Pains all over the body may occur. The sight may suddenly become dim or may even be lost. Dizziness may be complained of and dyspnea is usually marked. Cyanosis comes on, the pulse becomes weak, irregular or intermittent, heart failure sets in, and the patient dies with edema of the lungs.
Another class of renal arteriosclerosis is characterized by a small granular kidney in which fibrous changes of a patchy character have taken place. These scattered areas are the result of obliterating endarteritis of renal arteries here and there with consequent anemia, death of cells, and replacement by fibrous tissue. It occurs as part of a generalized arteriosclerosis in which the whole arterial system is the seat of diffuse (senile) sclerosis. The palpable arteriesare usually beaded or even encircled with calcareous deposits and the aorta is the seat of an extensive nodular and ulcerating sclerosis. The heart is usually small, shows extensive fibrous and fatty changes and possibly the condition known as "brown atrophy;" the blood pressure is low. Such cases do not show any special symptoms. They are anemic, short of breath on exertion, have the appearance and show the signs of senility.
In the first group it is, at times, difficult to say whether the kidney disease or the arterial disease is the most important. From a clinical standpoint the decision is not essential as the end results are much the same in both. However, when actual uremic symptoms dominate the picture, it becomes evident that the disease of the kidney is the chief feature in the causation of the symptoms.
There is an important group of cases to which but little attention has been paid until quite recently. This is the abdominal or visceral type of arteriosclerosis. It has been stated that arteriosclerosis of the splanchnic vessels almost invariably causes high tension. Among others, Janeway has shown that general arteriosclerosis without marked disease of the splanchnic vessels does not cause as a rule increase of blood pressure.
There are cases in which the brunt of the lesion falls upon the abdominal vessels. Such cases have been called "angina abdominalis." It has been suggested (Harlow Brooks) that this type of arteriosclerosis may be determined by constant overloading of the stomach with food, especially rich and spiced food. This causes overwork of the special arteries connected with digestion and so leads to sclerosis of the vessels of the stomach, pancreas, and intestines. Personal habits probably influence to great extent the production of this more or lesslocalizedcondition.
The organs supplied by the diseased arteries suffer fromchanges analogous to those occurring in general or local malnutrition, such as starvation, old age, or local anemias. These changes are atrophy with hemachromatosis (brown atrophy) or fatty infiltration and degeneration. Following the degenerative changes there result connective tissue growth and further limitation of the functionating power of the affected organs.
Pain is a more or less constant symptom of visceral sclerosis. In the early stages there may be only a sense of oppression, of weight, or of actual pressure in the abdomen or pit of the stomach. There may be only recurring attacks of violent abdominal pain accompanied by vomiting. In some cases symptoms of tenderness in the epigastrium, pains in the stomach after eating, vomiting and backache may suggest gastric ulcer. There may be dyspnea and a sense of anguish accompanied with a rapid and feeble pulse. Hematemesis may make the symptom group even more like ulcer of the stomach, and only the course of the disease with the failure of rigid ulcer treatment and the substitution of treatment directed toward relief of the arterial spasm with resulting betterment, enables one to make a diagnosis. The condition may be present for years and the symptoms only epigastric tenderness with dizziness and sweating on lying down after dinner, as in one of Perutz's patients. The attacks are probably due to spasmodic contraction of the sclerosed intestinal vessels with a resulting local rise in blood pressure. The pains are most probably due to the spasm of the intestinal muscles, and some think they are located in the sympathetic and mesenteric plexuses.
This result of arteriosclerosis is not so uncommon, and by keeping this cause of obscure abdominal pain in mind we are now and then enabled to save a patient from operation.
An autopsy on a case which for many years had attacks of abdominal pain and cramp-like attacks, with high blood pressure and heart hypertrophy, showed extensive sclerosisof the abdominal aorta, superior mesenteric and iliacs. These vessels were calcified. Hypertrophy of the left ventricle was found. The kidneys were microscopically normal. There were no changes in the ascending aorta but in the descending portion there were scattered nodules and small calcified plaques.
The attacks of pain from which this patient suffered for many years, the hypertrophy of the left ventricle and the increased blood pressure were thought to be directly due to the sclerosis of the abdominal vessels.
It has been stated that arteriosclerosis is a general disease, yet certain systems of vessels may be affected far more than others, and indeed there may be marked sclerosis at one part of the body and none demonstrable at another part.
In advanced sclerosis there may be one or more of a series of accidents due to embolism, thrombosis, or rupture of the vessels. Such conditions as transient hemiplegia, monoplegia or aphasia may occur. The attacks may come on suddenly and be over in a few minutes; what Allbutt calls "Larval apoplexies." They may last from a few hours up to a day, and are very characteristic. A patient aged 64 years with pipe stem radials and tortuous hard temporals would be lying quietly in bed when suddenly he would stiffen, the eyes would become fixed and the breathing cease. In a few seconds consciousness returned, the patient would shake himself, pass his hand over his brow and ask, "Where am I? Oh, yes, that's all right." He had as many as thirty of these attacks in twenty-four hours, none of them lasting over one minute. To just what such attacks are due, it is hard to say. Some have attributed them to spasm of the smaller blood vessels of the brain, but there have never been demonstrated in the vessels any constrictor fibers.
There is a well recognized form of dementia caused by arteriosclerosis. In general paralysis of the insane and in senile dementia the blood vessels are always diseased. Milder grades of psychic disturbances are accompanied by such symptoms as mental fatigue, persistent headaches, vertigo, memory weakness and fainting. Aphasia, periods of excitement and mental confusion occur in some. Later stages are at times accompanied by inclination to fabulate, loss of judgment, disorientation, narrowing of the external interests, episodes of confusion and hallucinatory delirium.
The hemiplegias, monoplegias and paraplegias may occur again and again and last for one or two days. Unless there has been rupture of the vessels, there is complete recovery as a rule.
In persons who have arteriosclerosis with high tension attacks of melancholia are seen. There are at the same time fits of depression, insomnia, irritability, fretfulness, and a generally marked change in disposition. When the tension is reduced by appropriate treatment these symptoms disappear, to recur when the tension again becomes high. On the contrary, attacks of mania are accompanied by low blood pressure. The dizziness and vertigo in cerebral arteriosclerosis are probably due to the stiffness of the vessels which prevents them from following closely the variations of pressure produced by position, and thus, at times, the brain is deprived of blood and a transient anemia occurs.
Arteriosclerosis of the cerebral vessels is always a serious condition. The greatest danger is from rupture of a blood vessel. Another of the dangers is gradual occlusion of the arteries bringing about necrosis with softening of the brain substance. The latter is more apt to be associated with psychic changes, dementia, etc.; the former, with hemiplegia. It is curious that a small branch of the Sylvian artery, the lenticulo-striate, which supplies the corpus striatum, should be the one which most frequently ruptures.Where the motor fibers from the whole cortex are gathered together in one compact bundle, a very small hemorrhage may and does cause very serious effects. A comparatively large hemorrhage in the silent area of the brain may cause few or no symptoms.
It is conceivable that arteriosclerosis of the vessels of the spinal cord might cause symptoms which would be referred to the areas of the cord where the process was most advanced. The lesions would be scattered and consequently the symptoms might be protean in character.
True epileptic convulsions dependent on arteriosclerotic changes are also seen and are not so uncommon.
This is on the whole a rare condition, much less common than arteriosclerosis of the cerebral vessels. Collins and Zabriskie report the following typical case:
"H., a fireman, fifty-one years old, was in ordinary good health until toward the end of 1902. At that time he noticed that his legs were growing weak and that they tired easily. Later he complained of a jerking sensation in different parts of the lower extremities and at times of sharp pain, which might last from several minutes to two or three hours. The legs were the seat of a heavy, unwieldy sensation, but there was no numbness or other paresthesia. About the same time he began to have difficulty in holding the urine, a symptom which steadily increased in severity. These symptoms continued until March, 1903, i. e., for three months, then he awakened one morning to find that he was unable to stand or walk, and the sphincters of the bowels and bladder relaxed. There was no complaint of pain in the back or legs, no difficulty in moving the arms, in swallowing or in speaking. He says he was able to tell when his lower extremities were touched and he could feel the bed and clothes. He was admitted to the City Hospital three weeks later and the following record was made on April 21, 1903."The patient was a frail, emaciated man of medium height, who had the appearance of being 55-60 years of age. He was unable to stand or walk. When he was lying, he could flex the thigh and the legs slowly and feebly. There was slight atrophy of the anterior and inner muscles, more of the left than of the right side. The knee jerks and ankle jerks were absent. Irritation of the soles caused quite a typical Babinski phenomenon. The patient had fair strength in the upper extremities, but the arms tired very soon, he said. The grip was moderate and alike in each hand. The motility of the face, head, and neck was not noticeably impaired. There was no difficultyin swallowing, and articulation was not defective. Tactile sensibility was slightly disordered in the lower extremities, although he could feel contact of the finger, the point of a pin, and the like. Sensibility was not so acute as normal; there was a quantitative diminution. Sensory perception was not delayed. There was a distinct zone of slight hyperesthesia about as wide as the hand above the femoral trochanters. Above that, sensibility was normal. There was no discernible impairment of thermal sensibility. No part of the body was particularly tender on pressure. A bedsore existed over the sacrum, and there was excoriation of the genitals from constant dribbling of urine."Examination of the chest showed shallow respiratory movements. The heart was regular, weak, there were no murmurs, the second sound was accentuated. Examination of the abdomen showed that the liver and spleen were palpable, but were not enlarged. The abdominal reflexes, both upper and lower, were sluggish. The patient was slow of speech, likewise apparently of thought. He did not seem to show an adequate interest in his condition, still he was fully oriented and seemed to have a fair memory. His mental reflex was slow. There were indications in the peripheral blood vessels and heart of a moderate degree of general arteriosclerosis. The peripheral vessels such as the radial, were palpable, the walls thickened, the blood pressure increased."The patient did not complain of pain while he was in the hospital, a period of four weeks, nor was there any particular change in the patient's symptoms, subjective and objective, during this time. His mental state remained clear until forty-eight hours before death, when he became sleepy, stuporous, and comatose, dying apparently of cardiac weakness, which had set in simultaneously with the clouding of consciousness."At autopsy, except for a few small hemorrhages in the posterior horns of the lower dorsal segments on the right side and a similar condition of the left anterior horns, there was nothing noticed. On microscopic examination, there was found widespread sclerosis of the vessels of the cord to a marked degree with only slight thickening of the vessels of the brain. There were secondary degenerations of ascending and descending type particularly marked at the ninth dorsal segment. They included portions of all the tracts, the pyramidal tract as well. The symptoms in brief were: (1) weakness and easily induced fatigue of the legs; (2) peculiar sensations in the lower extremities, described as jerky, numbness, heaviness, and occasionally sharp pain; (3) progressive incontinence of urine; (4) progressive paraplegia.
"H., a fireman, fifty-one years old, was in ordinary good health until toward the end of 1902. At that time he noticed that his legs were growing weak and that they tired easily. Later he complained of a jerking sensation in different parts of the lower extremities and at times of sharp pain, which might last from several minutes to two or three hours. The legs were the seat of a heavy, unwieldy sensation, but there was no numbness or other paresthesia. About the same time he began to have difficulty in holding the urine, a symptom which steadily increased in severity. These symptoms continued until March, 1903, i. e., for three months, then he awakened one morning to find that he was unable to stand or walk, and the sphincters of the bowels and bladder relaxed. There was no complaint of pain in the back or legs, no difficulty in moving the arms, in swallowing or in speaking. He says he was able to tell when his lower extremities were touched and he could feel the bed and clothes. He was admitted to the City Hospital three weeks later and the following record was made on April 21, 1903.
"The patient was a frail, emaciated man of medium height, who had the appearance of being 55-60 years of age. He was unable to stand or walk. When he was lying, he could flex the thigh and the legs slowly and feebly. There was slight atrophy of the anterior and inner muscles, more of the left than of the right side. The knee jerks and ankle jerks were absent. Irritation of the soles caused quite a typical Babinski phenomenon. The patient had fair strength in the upper extremities, but the arms tired very soon, he said. The grip was moderate and alike in each hand. The motility of the face, head, and neck was not noticeably impaired. There was no difficultyin swallowing, and articulation was not defective. Tactile sensibility was slightly disordered in the lower extremities, although he could feel contact of the finger, the point of a pin, and the like. Sensibility was not so acute as normal; there was a quantitative diminution. Sensory perception was not delayed. There was a distinct zone of slight hyperesthesia about as wide as the hand above the femoral trochanters. Above that, sensibility was normal. There was no discernible impairment of thermal sensibility. No part of the body was particularly tender on pressure. A bedsore existed over the sacrum, and there was excoriation of the genitals from constant dribbling of urine.
"Examination of the chest showed shallow respiratory movements. The heart was regular, weak, there were no murmurs, the second sound was accentuated. Examination of the abdomen showed that the liver and spleen were palpable, but were not enlarged. The abdominal reflexes, both upper and lower, were sluggish. The patient was slow of speech, likewise apparently of thought. He did not seem to show an adequate interest in his condition, still he was fully oriented and seemed to have a fair memory. His mental reflex was slow. There were indications in the peripheral blood vessels and heart of a moderate degree of general arteriosclerosis. The peripheral vessels such as the radial, were palpable, the walls thickened, the blood pressure increased.
"The patient did not complain of pain while he was in the hospital, a period of four weeks, nor was there any particular change in the patient's symptoms, subjective and objective, during this time. His mental state remained clear until forty-eight hours before death, when he became sleepy, stuporous, and comatose, dying apparently of cardiac weakness, which had set in simultaneously with the clouding of consciousness."
At autopsy, except for a few small hemorrhages in the posterior horns of the lower dorsal segments on the right side and a similar condition of the left anterior horns, there was nothing noticed. On microscopic examination, there was found widespread sclerosis of the vessels of the cord to a marked degree with only slight thickening of the vessels of the brain. There were secondary degenerations of ascending and descending type particularly marked at the ninth dorsal segment. They included portions of all the tracts, the pyramidal tract as well. The symptoms in brief were: (1) weakness and easily induced fatigue of the legs; (2) peculiar sensations in the lower extremities, described as jerky, numbness, heaviness, and occasionally sharp pain; (3) progressive incontinence of urine; (4) progressive paraplegia.
Since one of the chief manifestations of syphilis is sclerosis of the arteries, neurologic cases characterized by irregular symptoms and signs which can not be placed in any of the definite system disease groups, are possibly due to irregularly scattered areas of sclerosis throughout the spinal cord caused by obliterating arteritis. Such cases are not so very uncommon. Several have come under myobservation. Further studies of the spinal cords of these cases at autopsy are necessary before a final opinion can be given as to their dependence on arteriosclerosis of the spinal vessels.
When the arteriosclerosis in the peripheral arteries reaches a stage where endarteritis obliterans supervenes, there is usually no chance for a compensatory or collateral circulation to be established. The area supplied by the vessel undergoes dry gangrene. A portion of a toe or finger or a whole foot or hand may shrivel up. It is more common to see the spontaneous amputation take place in the lower extremities. The same effect may be produced by the plugging of a vessel with a thrombus. There may be much pain connected with the sudden blocking, whereas the gradual obliteration of the blood supply of a toe or foot is not as a rule at all painful. The condition is at times revealed more or less accidentally when a patient injures his toe or foot and discovers that there is no sensation in the part and that the wound instead of healing is inclined to grow larger.
Other interesting vasomotor phenomena are frequently connected with arteriosclerosis. Such a one is the curious condition known as Raynaud's disease, a vascular disorder which is divided into three grades of intensity: (1) local syncope, (2) local asphyxia, (3) local or symmetrical gangrene. This is not the place to describe this condition except to say that the condition called "dead fingers" is the most characteristic feature of the first stage. Chilblains represent the mildest grade of the second stage. The parts are intensely congested and there may be excruciating pain. Any one who has ever had chilblains knows how painful they can be. The general health is not impaired as a rule, although the attacks are apt to come on when the person is run down. The third stage may vary from a very mildgrade, with only small necrotic areas at the tips of the fingers, to extensive multiple gangrene.
Another and very rare condition in which chronic endarteritis was the only constant finding is the disease described by S. Weir Mitchell and called by him erythromelalgia (red neuralgia). This is "A chronic disease in which a part or parts—usually one or more extremities—suffer with pain, flushing, and local fever, made far worse if the parts hang down." (Weir Mitchell.)
Probably the most frequently seen result of arteriosclerosis in the leg arteries is the remarkable condition, first described by Charcot, known as intermittent claudication. Persons the subject of this disease are able to walk if they go slowly. If, however, any attempt be made to hurry the step, there results total disability accompanied at times by considerable cramp-like pain. The condition is much more prone to occur in men than in women, and Hebrews seem more frequently affected. The cause is most probably to be sought in the anemia which results from the narrowing of the channels through which the blood reaches the part. The stiff, much narrowed arteries allow sufficient blood to pass along for the nutrition of the part at rest or in quiet motion. Just as soon as more violent exercise is taken, calling for more blood, an ischemia of the part supervenes, for the stiff vessels can not accommodate themselves to changes in the necessary vascularity of the part. A rest brings about a gradual return of blood and the function of the part is restored. Pulsation may be totally absent in the dorsal arteries of the feet and when the legs are allowed to hang down there is apt to be deep congestion.
In this connection a curious case reported by Parkes Weber will not be out of place. The patient, a male, aged 42 years, complained of cramp-like pains in the sole of the left foot and calf of the leg occurring after walking for a few minutes and obliging him to rest frequently. When the legs were allowed to hang over the side of the bed, thedistal portion of the left foot became red and congested looking. No pulsation could be felt in the dorsal artery of the left foot or in the posterior tibial artery. There was no evidence of cardiovascular or other disease. An ulcer on the little toe had slowly healed, but cramp-like muscular pains still occurred on walking. The disease had lasted about five years without the appearance of gangrene.
Weber calls this case one of arteritis obliterans with intermittent claudication.
In the symptomatology of sclerosis of the pulmonary artery the clinical signs and symptoms are mostly referable to the obliterating endarteritis of the smaller vessels, while the physical signs are more apt to reveal the involvement of the main trunk. A history of severe infection in the past is frequent, especially smallpox, and accompanying aortic sclerosis with insufficiency of the mitral valve or stenosis of this valve is the rule. Striking cyanosis is an early symptom, while there is little if any dyspnea and edema. Intermittent dyspragia is common. There seems to be no tendency to clubbed fingers. Repeated hemorrhages from the lungs without the formation of infarcts may occur. There is usually an area of dullness at the upper left margin of the sternum and nearby parts, sensitive to pressure and to percussion, and the heart dullness extends unusually far towards the right. The diagnosis of the right ventricular hypertrophy may be substantiated by a fluoroscopic examination.
Arteriosclerosis is essentially a disease of middle life and old age. It is not unusual, however, to find evidences of the disease in persons in the third decade and even in the second decade. Hereditary influences play a most important rôle, syphilis and the abuse of alcohol in the family history are particularly momentous. The recognition of the early changes in the arteries among young persons depends largely upon how carefully these changes are looked for. The difference in the point of view of one man who finds many cases in the comparatively young, and another man who rarely finds such changes early in life, at times, depends upon the acuity of perception and observation and not upon the fact that one man has had a series of unusually young arteriosclerotic subjects. The diagnosis of arteriosclerosis may be so easily made that the tyro could not fail to make it. It is, however, the purpose of this volume to lay stress on the earliest possible diagnosis and, if possible, to point out how the diagnosis may be arrived at. It is obviously much to the advantage of the patient to know that certain changes are beginning in his arteries, which, if allowed to go on, will inevitably lead to one or more of the symptom groups described in the preceding chapters.
The combination of (1) hypertrophied heart, (2) increased blood pressure, (3) palpable arteries, and (4) ringing, accentuated second sound at the aortic cartilage is, in reality, the picture of advanced arteriosclerosis. If the individual is in good condition much may be done by judiciousadvice and treatment to ward off complications and prolong life with a considerable degree of comfort. But we should not wait until such signs are found before making a diagnosis and instituting treatment. As in all forms of chronic disease the early diagnosis is all important.
The history of the case is the first essential. Often a careful inquiry into the personal habits of a patient, with the record of all the preceding infectious diseases will give us valuable information and may be the means of directing the attention at once to the possible true condition. Particularly must we inquire into the family history of gout and rheumatism. An individual who comes of gouty stock is certainly more prone to arterial degeneration than one who can show a healthy heredity. Alcoholism in the family also is of importance because of the fact that the children of alcoholics start in life with a poor quality of tissue, and conditions that would not affect a man from healthy stock might cause early degeneration of arterial tissue in one of bad ancestry.
What infectious diseases has the patient had? Even the exanthemata may cause degenerations in the arteries, but, as has been shown, such lesions probably heal completely with no resulting damage to the vessel. Should the patient have passed through a long siege of typhoid fever the problem is quite different. Here (vide supra) (Thayer), the palpable arteries do appear to be sclerosed permanently. Probably the length of time that the toxin has had a chance to act determines the permanent damage to the vessel wall. More potent than all other diseases to cause early arteriosclerosis is syphilis, and hence very careful inquiry should be made in regard to the possibility of infection with this virus. Not only the fact of actual infection but the duration and thoroughness of treatment are important matters for the physician to know.
What is the patient's occupation? Has he been an athlete, particularly an oarsman? Has he been under anysevere, prolonged, mental strain? Is he a laborer? If so, in what form of manual labor is he engaged? Such questions as these should never be overlooked, as they form the foundation stones of an accurate diagnosis, and early, accurate diagnosis, we repeat, is essential to successful therapy.
We have called attention to the factor of sustained high pressure in the production of arteriosclerosis. Constant overstretching of the vessels leads to efforts of the body to increase the strength of the part or parts. The material which is used to strengthen the weakened walls has a higher elastic resistance than muscle and elastic tissue, but a lower limit of elasticity, and is none other than the familiar connective tissue. In athletes, laborers, brain workers who are under constant mental strain, and in those whose calling brings them into contact with such poisons as lead, there is every factor necessary for the production of high tension and consequently of arteriosclerosis.
Another question in regard to personal habits is how much tobacco does the patient use and in what form does he use it? Our experience is that the cigar smoker is more prone to present the symptoms of arteriosclerosis than the cigarette smoker, the pipe smoker, or the one who chews the tobacco. A very irritable heart results not infrequently from cigarette smoking but such is almost always found in young men in whom the lesions of arteriosclerosis are exceedingly rare. The probabilities are that the arteriosclerosis in cigar smoking results from the slowly acting poison which causes a rapid heart rate with an increase of pressure.
Last but not least, and perhaps the most important question is, has the patient been a heavy eater? This I believe to be a potent cause of splanchnic arteriosclerosis with the resulting indigestion, cramp-like attacks, high blood pressure, etc. In a joking manner we are accustomed to remark, "Overeating is the curse of the American people." There is, however, much truth in that sentence. Osler, thanwhom there is no keener observer, states that he is more and more impressed with the fact that overloading the stomach with rich or heavy or spiced foods is today one of the first causes of arterial degeneration. It stands to reason that this is true. We know that organs exposed constantly to hard work undergo hypertrophy, and that the blood tension in those organs is high. Blood tension is, after all, dependent on capillary resistance, and if the capillaries are distended with blood, the resistance is great. The digestive organs can be no exception to this rule. Increased work means an increase of blood. This inevitably causes distension of the capillaries with stretching of the arteries and consequent damage to the walls. Once arteriosclerosis is present a vicious circle is established.
A man about forty-five consults us and says that he has noticed recently that he gets out of breath easily; in tying his shoes he experiences some dizziness. He finds that he has palpitation of the heart and possibly pain over the precordial region now and then. He notices also that he is irritable, that is, his family tell him he is, and he notices that things that formerly did not annoy him, now are almost hateful to him. On examination, one finds a palpable radial, a somewhat hypertrophied heart and slightly accentuated second aortic sound. The blood pressure may be high. The urine may or may not reveal any abnormalities. Not infrequently, although no albumin may be found, there are hyaline casts. Such a case of arteriosclerosis is evidently not to be regarded as early. Then the question arises, How are we to recognize early arteriosclerosis? I do not believe that the solution of this problem lies entirely in the hands of the physician. Some men are fortunate enough to come up for an examination for life insurance before an observant doctor who recognizes the palpable artery, makes out the beginning heart hypertrophy and the slightly accentuated second aortic sound. The patient will tell you that he never felt better in his life. He gets up atseven, works all day, plays golf, drinks his three to six whiskies, and is proud of his physical development. But the great mass of people are not fortunate from this standpoint. They do not seek the advice of the physician until they are stretched out in bed. They boast of the fact that for twenty years they have never had a doctor. One may well say that it is a problem how to reach such persons. It seems to me that there can be but one way to do this. The people must be taught that the duty of a physician is just as much to keep them in health as it is to bring them back to health when they are ill. To that end people should be taught that at least twice a year they should be carefully examined. I do not mean that the patient should present himself to the doctor and, after a few questions the doctor say cheerfully, "You are all right." The patient should be systematically examined. That means a removal of the clothing and examination on the bare skin. Such cooperation on the part of patient and doctor would save the patient years of active life and make of the doctor, what his position entitles him to be, the benefactor to the community. Too often careless work on the physician's part lulls the patient into a false sense of security and he wakes up too late to find that he has wasted months or years of life. Early diagnosis of arteriosclerosis is only possible in exceptional cases unless people present themselves to the physician with the thought in mind that he is the guardian of health as well as the healer.
There are patients who go to the ophthalmologist for failing vision. Physically they feel quite well. They have been heavy eaters, hard workers, men and women who have been under great mental strain. On examination of the fundus of the eye there is found slight tortuosity of the vessels with possibly areas of degeneration in the retina. A careful physical examination will usually reveal the signs of arteriosclerosis elsewhere. We have mentioned frequently high tension as an early sign. This must be takenwith somewhat of a reservation, for this reason: not infrequently a persistent high tension is the earliest sign of chronic nephritis. The arteries may be pipe stem in character and the heart small and flabby. However, if one watches for the palpably thickened superficial arteries (always bearing in mind the normal palpability as age advances) and the high tension, he can not go far wrong in his treatment whether the case is one of chronic nephritis or of arteriosclerosis.
There is also this to bear in mind. Arteriosclerosis may be marked in some vessels and so slight in the peripheral vessels that it can not with certainty be made out. But when the radials are sclerosed, it is usually the case that similar changes exist in other parts. Then too, there may be marked changes at the root of the aorta leading to sclerosis of the coronary vessels alone, and the first intimation that the patient or any one else has that there is disease, may be an attack of angina pectoris. Except for symptoms on the part of the heart there is no way to make the diagnosis of sclerosis of the coronary arteries.
In arriving at a diagnosis, when the question is whether or not arteriosclerosis is the main etiologic factor, the most important fact to know is the age of the patient. Other points that have been dwelt on fully must of necessity also be borne in mind.
Possibly the chief conditions that may be confused with some of the results of arteriosclerosis are pseudo angina pectoris which may be mistaken for true angina pectoris, and ulcer of the stomach, appendicitis (?) or other inflammatory abdominal condition which may be mistaken for angina abdominalis.
Differential tables are sometimes of value in fixing the chief points of difference graphically.
In differentiating between ulcer of the stomach and angina abdominalis the following points may be of service: