Arteriosclerosis and Hypertension Part 12

manifestations of syphilis. That syphilis is responsible for the arterial disease in the vessels of the brain, resulting in apoplexy or sudden cardiac death in middle life, has long been known. In fact, it is claimed (Osler) that all aneurysms occurring in persons under thirty years of age are due to syphilitic aort.i.tis. In the late stages of syphilis the arterial lesions may be of a diffuse character.

=Chronic Drug Intoxications=

Lead, tobacco, and according to some, tea and coffee, are to be cla.s.sed as causal factors in the production of arteriosclerosis. Certain it is that all these substances have a tendency to raise the arterial pressure, but whether the drug itself causes first a degeneration, and later a hypertension results, or vice versa, is not yet positively known. We have just mentioned that lead particularly has a marked effect in producing arterial lesions. Other drugs as adrenalin, barium chloride, physostigmin, etc., while producing experimental arteriosclerosis, hardly could produce the disease in man. =Alcohol= has been blamed for much, and as an etiologic factor in the production of arteriosclerosis formerly was accorded a first place. More recently much doubt has been thrown on this supposition by the work of Cabot, who showed that the mere drinking of even large quant.i.ties of spirits had no effect in producing arterial disease.

This observation has been recently substantiated by Hultgen, who carefully studied clinically 460 cases of chronic alcoholism. He says, "There are no cardiovascular symptoms which might be termed characteristic of chronic alcoholism, unless it be the peculiar fetal qualities of the heart sounds which we know as embryocardia. I find this very frequent among drinkers, but I can offer only a tentative explanation for it, namely the following: Embryocardia can only occur with low tension blood pressure, and in the absence of renal insufficiency. Hence it might be considered as a useful condition of no pathologic significance at all. That alcohol is a sclerogenic pharmakon and productive of arteriosclerosis with its usual train of symptoms may be a fact, but its demonstration would be difficult and is really not shown by my tabulations. There were cardiovascular changes, such as myocarditis, aort.i.tis, valvular heart disease and arteriosclerosis in chronic alcoholics in 54.3 per cent of 461 cases, but this by no means const.i.tutes a proof of the causal relations.h.i.+p between these lesions and the abuse of liquors. I believe it, nevertheless, to be good reasoning to ascribe the bulk of cardiovascular symptoms to the sclerogenic action of alcohol, while abstaining from an interpretation of its pathogenesis." Just what role =tobacco= plays is difficult to say. My own opinion is, that of itself when used in moderation, it has no ill effects. However, as tobacco is a drug that may raise the blood pressure, excessive use must be held responsible for the production of arteriosclerosis. It is difficult to separate its effects from those produced by eating and drinking.

=Overeating=

There can be no doubt but that the constant overloading of the stomach with rich or difficultly digestible food is responsible for a large number of cases of arteriosclerosis. Every one must have noted the increase in force and volume of the heart beat after the ingestion of a large meal. The constant repet.i.tion of such processes conceivably can lead to damage to the vessel walls through hypertension.

In the metabolism of food in the intestines there are substances produced which are poisonous when absorbed directly into the circulation. Ordinarily these substances are rendered harmless either before absorption or are detoxicated in the liver to harmless substances. It is conceivable that a constant overproduction of such poisons would eventually damage the defensive mechanism of the body to such an extent that some of the poisons would circulate in the blood. An expression of a surplus of one, at least, of these decomposition products is the appearance of indican in the urine. It is not believed that indicanuria has the importance attached to it which some authors would have us believe. It is found too often and in too many varying conditions, nevertheless it undoubtedly does reveal the presence of perverted metabolism.

In how far the toxins absorbed from the intestinal tract are responsible for the production of arterial disease, it is not possible to say. Some observers lay great stress on this factor as a cause of arteriosclerosis. The author believes that the role played by the absorption of products of perverted intestinal metabolism is an important one. The primary change is an increased tension in the arterioles which later leads to thickening of the coats of the vessels and to the other consequences of arterial disease. A vicious circle is thus established which has a tendency to become progressively worse.

=Mental Strain=

More and more does one become impressed with the fact that patients with arteriosclerosis are very often those who take life too seriously and either from ambition or from an exalted sense of duty lead especially strenuous lives. Not always are these persons addicted to drug or liquor habit. Many are rather abstemious in their habits. It is not so often that we see as a victim of arteriosclerosis, the carefree person who laughs his way through life without worrying about the morrow. He is not so p.r.o.ne to arteriosclerosis. Worry is a far more potent cause of breakdown than actual manual work. It is the rule to find thickened arteries among neurasthenics. This may be only part of a generalized degeneration of all tissue in the body. The blood pressure in such persons is usually low. So many men of our better cla.s.s live under a continuous mental strain in the business world. The increase in arteriosclerosis cases is real, not apparent. The intense mental strain seems to cause a marked increase in blood pressure (for short periods of mental effort this has been proved) over a period of time sufficient to cause permanent changes in the vessel walls. The same sequence of events repeats itself; high tension, arterial strain, compensatory thickening, hypertrophied heart, etc.

Certainly the character of the arterial tissue has much to do with the determination of degenerative changes which may result from the action of one or more of the etiologic factors.

=Muscular Overwork=

Muscular overwork is to be reckoned with as an etiologic factor. One sees it especially among the laboring cla.s.s in both whites and negroes.

Possibly other factors, as alcohol and coa.r.s.e heavy food, contribute to the early arterial degeneration. Hypertrophy of the heart occurs in athletes, and statistics gathered among the oarsmen especially, show a relatively high mortality at the different decades traceable to the high tension produced while in training. This question deserves more consideration than has been accorded it.

=Renal Disease=

Chronic disease of the kidneys (contracted red kidney) is one of the most certain producers of hypertension; in fact, some maintain that high tension, even without demonstrable kidney lesions, as revealed by careful urine examinations, is a valuable sign pointing to chronic nephritis. This is doubted by others, myself among them. Just what causes the increase in blood pressure sometimes to over 270 mm. of Hg, is not definitely known. It seems most probable that it is some poison elaborated by the diseased kidneys and absorbed into the general circulation. There it acts primarily on the musculature of the arterioles causing tonic contraction and an increase of work on the part of the heart to force the blood through narrowed channels. One fact is certain. We see patients in coma due to renal disease with blood pressure much over 200 mm of Hg. As these cases clear up, the pressure may fall, and should they seemingly recover, the recovery is accompanied with a marked decrease in blood pressure, finally reaching the normal for the individual. Moreover, in the course of a severe acute or subacute nephritis, hypertension is a.s.sociated with headache, partial or total blindness, and drowsiness. When the pressure is reduced, all these symptoms disappear.

There is also the chronically shrunken and scarred kidney known pathologically as the arteriosclerotic kidney. It is probable that there are two groups of cases which we may designate: (1) primary; (2) secondary. In the primary group the kidney disease antedates the sclerosis of the arteries, and the sclerosis is most probably dependent on the constant high tension. We know that prolonged hypertension will produce severe forms of arteriosclerosis. The arterial disease in this group is caused by the renal disease.

In the second group the kidney changes are apparently due to the general arteriosclerosis which, affecting the kidney vessels, causes changes leading to atrophy and subsequent fibrous tissue ingrowth of scattered areas. These cases are not necessarily a.s.sociated with hypertension; on the contrary there is more apt to be hypotension. Where the first group occurs for the most part in young and active middle-aged people, the second group is the result of involutionary processes which accompany advanced age.

However careful a urinalysis may be, there is no a.s.surance that one can predict the pathologic state of the kidney. Often so-called normal urine will be secreted by a badly diseased kidney, whereas a urine which contains considerable alb.u.min and many casts may be secreted by a kidney which is only temporarily the seat of inflammation. What matters after all is not the state of the kidney which the pathologist describes, but the actual functional response of the kidney in the body to the various tests now well known.

=Ductless Glands=

At the present time the tendency among some writers is to make the ductless glands the responsible agents in almost all diseases.

Arteriosclerosis is no exception to this tendency. Sajous, for example, divides the morbid process producing arteriosclerosis into three types; (1) autolytic, (2) adrenal, (3) denutrition. In the first type he finds the pancreas to be the most important gland. It supplies an internal secretion which "takes a direct part in the protein metabolism of the tissue cells, and also in the defensive reactions within these cells, as well as in the phagocytes and in the blood stream." This being the case exaggeration of this digestive process has tissue destruction as its result, arteriosclerosis among them.

In the adrenal type Sajous argues that adrenalin produces lesions experimentally, therefore the adrenal gland has a profound influence by its internal secretion in connection with the sympathetic system in producing degenerations leading to arteriosclerosis.

The denutrition type has as its particular gland the thyroid. The sclerotic process in the arteries is due to the lack of thyroid as in cases of myxedema. After a long resume of his ideas he concludes "that arteriosclerosis is the result of excessive or deficient activity of certain ductless glands, the thyroid and adrenal in particular."

No one can dogmatically deny the part which the ductless glands may play in the production of arteriosclerosis, but it hardly seems that there is enough actual experimental evidence to show that they take such an important part as Sajous believes. Until further and more convincing evidence is offered by competent investigators, I prefer to look with some skepticism upon the ductless gland theory of the causation of arteriosclerosis. The field lends itself too easily to speculation and imagery. Some are already allowing themselves the mental debauch of this nature.

CHAPTER VII

THE PHYSICAL EXAMINATION OF THE HEART AND ARTERIES

=Heart Boundaries=

In order to be able to estimate the departures from normal in the boundaries of the heart, it is essential that there be a definite appreciation of the boundaries of the normal heart in relation to the chest wall.

It is frequently stated that the right limit of cardiac dullness is normally, in the adult, just at the right border of the sternum. This is not strictly accurate. Careful dissections at the autopsy table and x-ray plates of the chest made at a distance of two meters from the tube show that the border of the right auricle is from one to one and a half and even two centimeters from the edge of the sternum at the level of the fourth rib, and on the living subject this can be also demonstrated.

The right border of the heart usually is from 3 to 4 cm. from the midsternal line at the level of the fourth rib.

Again there is a term used in defining the apex, known as the point of maximum impulse. As this does not always coincide with the apex beat and with the outer lower left border of the heart, it would be better to use the term apex beat.

Normally, then, the cardiac dullness, the so-called relative cardiac dullness, begins above at the upper border of the third costal cartilage, as a rule, and taking a somewhat curved line with the concavity inward, descends to the fifth inters.p.a.ce or beneath the fifth rib from 9 to 10 cm. from a line drawn through the center of the sternum parallel to its length, the midsternal line. This seems to me to be a better method of recording the size of the heart than by the lines commonly used; viz., the nipple, or midclavicular, or parasternal line.

Below, the cardiac dullness is merged into the tympany from the stomach and the dullness from the liver. At the sixth right costosternal articulation there is a sharp turn upwards forming at that point with the liver the cardiohepatic angle. At the fourth right cartilage or the third inters.p.a.ce, the dullness is from one to two centimeters from the edge of the sternum. We have then a somewhat pear-shaped area or triangular area with the apex at the apex of the heart. The so-called absolute cardiac dullness does not appear to me to be of any great significance. In reality it is the limit of lung resonance and may be greater or less, not so much on account of variations in the size of the heart, as of variations in size of the lungs and shape of the chest wall.

The really crucial question which should always be asked is, Is the heart enlarged or decreased in size? The position of the apex beat alone can not determine this, neither can the limit to the right of the sternum. The distance between these two points and the depth of the dullness at a distance of 5 cm. from the midsternal line on the left side, will give the size of the heart as nearly as can be obtained in the living subject. A series of measurements in normal adults average 13 to 14 cm. and 9 to 10 cm. respectively. For women they are about 1 cm.

less in each direction.

The elaborate mechanism known as the orthodiagraph is probably the best means of determining the actual limits of the heart, but few men have such an expensive instrument, and, moreover, at the bedside such an instrument could not be used. From comparative measurements I concur in the belief of those who affirm that careful percussion will furnish equally as accurate limits.

The first step in making an examination of the heart is to expose the patient's chest in a good light, and, sitting at his right side, carefully inspect the chest. The position of the apex beat, heaving, bulging, retraction of inters.p.a.ces, etc., can easily be seen if visible. After careful inspection has given all the data which it is possible to obtain, one next lays the palm of the hand over the heart and attempts to palpate the apex beat. The thrust of the apex in a hypertrophied heart can readily be felt, and one can feel whether the heart is regular, irregular, intermittent, or has other change in rhythm. The shock of the closing valves, particularly the aortic, can be felt, and that and the forcible apical impulse are very suggestive signs of hypertrophy and hypertension. Thrills may also be felt and can be timed in relation to the heart cycle.

=Percussion=

It is to percussion that we next proceed, and for the data in regard to the size of the heart, it is, for our purpose, the most valuable of all the physical methods of heart examination.

First and foremost we wish by percussion to learn the actual size of the heart, in other words what is ordinarily called the relative cardiac dullness. With the absolute dullness we are not concerned. That irregular area represents, as has been said, actually the =limits of lung resonance=. The heart may or may not be covered with lung; there may or may not be the incisura cardiaca. What I wish to insist upon is that the size of the area of absolute dullness can give us no data in regard to the size of the heart. What we must endeavor to learn is the actual size of the heart as nearly as our crude means will permit.

Light, very light, almost inaudible percussion, what Goldscheider called "Schwellungsperkussion," must be practiced. Use the middle finger of the right (left) hand as the hammer and the last joint of the middle finger of the left (right) hand pressed firmly against the chest, as pleximeter. I believe it is better to place the pleximeter finger parallel to the boundary to be limited although some place the finger perpendicularly, that is, pointing toward the boundary. Now and then it helps to bend the pleximeter finger at the second joint, hold it perpendicularly to the chest wall, and strike the joint directly in line of the finger. This in my hands has been of great a.s.sistance in percussing the limits of the heart dullness. Pottenger's "light touch palpation" is a modification of the light palpation and, to my mind, has no very special advantages. Auscultatory percussion is of great value at times. The bell of the stethoscope is placed over the portion of heart uncovered by lung (should such be the case), and with this point as a center the chest is lightly and quickly tapped along radii converging toward the stethoscope. One soon learns to recognize the change of pitch as the tapping reaches the border of the heart. It is well to use all methods, especially in difficult cases, and to compare the results.

Personally I have found that by light percussion I can limit with much accuracy the upper, right, and left borders of the heart.

There is much to be gained by using light percussion. Strong blows set in vibration not only the underlying structures, but also more or less of the chest wall. We wish to avoid this source of error, we do not wish to differentiate by pitch alone. Finally one's pleximeter finger becomes, after long practice, so sensitive to changes in the resonance of structures lying below it, that there is actual feeling of impairment to the slightest degree. This delicate touch is what we should endeavor to cultivate.

It is at times of advantage to use immediate percussion. This is done by bending the fingers of the striking hand, bringing the tips in a line and striking the chest lightly with the four fingers as one finger. Some find it easier to percuss the dullness due to the heart in this way than by mediate percussion.

The little hammer and hard rubber, celluloid, bone, or ivory pleximeter does not seem to me to be nearly as good as the fingers. Moreover, one always has his hands, but may forget his hammer and pleximeter.

=Auscultation=