Arteriosclerosis and Hypertension Part 14

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. Allb.u.t.t 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 cla.s.s. 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 pa.s.sive 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 circ.u.mstances. 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, pus.h.i.+ng the palpating hand forcibly up from the chest wall.

The visible area of pulsation may occupy three inters.p.a.ces 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 m.u.f.fled 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 pract.i.tioners 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 rec.u.mbent and becomes hyperemic later when placed horizontally. In health this change occurs more rapidly.

CHAPTER IX

SYMPTOMS AND PHYSICAL SIGNS

=Special=

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 terminal arteries 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.

=Cardiac=

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 or less 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 succ.u.mbs to edema of the lungs, drowned in his own secretions.