Fig. 54.—Blood pressure record from a normal reaction to ether. Note that the systolic and diastolic rise and fall together. At the end of the anesthetization the pulse pressure is practically the same as at the beginning. Compare this with the record in Fig. 55, where the operation had to be discontinued on account of the onset of shock.Fig. 54.—Blood pressure record from a normal reaction to ether. Note that the systolic and diastolic rise and fall together. At the end of the anesthetization the pulse pressure is practically the same as at the beginning. Compare this with the record in Fig. 55, where the operation had to be discontinued on account of the onset of shock.
Fig. 55.—Beginning of operative shock. Chart showing the method of recording blood pressure during operation. Note that the pulse and respiration show no remarkable changes, but the blood pressure steadily fell, the systolic more than the diastolic so that the pulse pressure was gradually reaching the danger point. Further work on this case was stopped following the warning given by the blood pressure. The patient was returned to the ward and a week later anesthesia was again given, the operation was completed, and the patient had a satisfactory convalescence.Fig. 55.—Beginning of operative shock. Chart showing the method of recording blood pressure during operation. Note that the pulse and respiration show no remarkable changes, but the blood pressure steadily fell, the systolic more than the diastolic so that the pulse pressure was gradually reaching the danger point. Further work on this case was stopped following the warning given by the blood pressure. The patient was returned to the ward and a week later anesthesia was again given, the operation was completed, and the patient had a satisfactory convalescence.
A method which is widely used is as follows: The anesthetist wraps the cuff of one of the dial instruments around the patient's arm, and arranges the dial so that it can easilybe seen by him at all times. This does not in any way interfere with the work of the surgeon. Over the brachial artery below the cuff is the bell of a binaural stethoscope held in place by the strap attachment now on the market. The tubes of the stethoscope are long enough to reach conveniently to the ear pieces. A watch is pinned to the sheet of the table. He has a chart, as illustrated (Fig. 56) on a board and makes a dot in every space for five minute intervals. By joining the lines a curve is obtained which tells at a glance what the circulation is doing. I feel sure that more attention and care exercised on the part of the anesthetist would be the means of conserving many lives lost from shock following operation.
Fig. 56.—Showing method of using blood pressure instrument during operation without interfering with the operator or assistants. Sheet thrown back to show cuff on arm of patient. Anesthetist has chart on table beside him, dial pinned to pad in full view, bulb near hand. Extra tubing must be put on the blood pressure instrument.Fig. 56.—Showing method of using blood pressure instrument during operation without interfering with the operator or assistants. Sheet thrown back to show cuff on arm of patient. Anesthetist has chart on table beside him, dial pinned to pad in full view, bulb near hand. Extra tubing must be put on the blood pressure instrument.
A sudden drop in the pressure picture may mean a large hemorrhage. The gradual return of the pressure picture means that the vasomotor mechanism has acted to keep up the pulse pressure. Should the diastolic pressure continually fall, it may mean that the hemorrhage is still taking place (Wiggers).
One might affirm almost without fear of contradiction that the constant determination of blood pressure during pregnancy is more important than the examination of the urine. Within recent years a number of observers having access to a large material, have given the results of their findings. There is a striking unanimity of opinion, although now and then a difference in minor details.
The blood pressure should be taken frequently during pregnancy. The usual and highly essential precautions in taking pressure in general apply most particularly in these cases. Towards the end of pregnancy the pressure should if possible be taken daily and oftener if necessary.
Pressure in women is usually below 120 mm. Many patients have a temporary rise in blood pressure during pregnancy, due oftenest to constipation, without developingother symptoms. This is common to all conditions and has no significance. Some think that an abnormally low pressure, that is, a systolic below 90 mm., suggests that the patient is likely to react unduly to the strain of labor. This is denied by others. Among 1000 cases (Irving) the pressure was below 90 in only one case. A gradually rising pressure precedes albuminuria, as a rule. If there is albumin without change in pressure the albumin may usually be disregarded. Some think that a pressure over 130 mm. systolic should be carefully watched. The danger limit is set by some at 150 mm. If the blood pressure from the very first is high, it may mean only that that was the patient's normal pressure. This calls for increased watchfulness. It is held by some that high blood pressure favors hemorrhage and probably explains the hemorrhagic lesions in the placenta and some viscera in eclampsia and albuminuria.
All are agreed that the most significant change is the gradual but sure rise from a low pressure. When this is combined with albuminuria the danger of toxemia is imminent. The high blood pressure in those under thirty years of age seems to be a more certain sign of approaching toxemia than the same pressure in those older. The pressure falls within a few days to its normal after delivery in the toxic cases.
Although the emesis gravidarum is held to be a sign of a toxemia of some unknown nature, the blood pressure is never raised even in the pernicious form.
In all infectious diseases the blood pressure tends to be lower than normal. During chills the systolic may rise to great height due to the violent muscular contractions.
We found the blood pressure of great value in giving information concerning the circulation. Again we repeatthat it is not the systolic alone or the diastolic alone but the pulse pressure which we wish to keep informed about. In pneumonia we have tried out Gibson's law only to discard it. This so-called law is that in pneumonia the systolic pressure in millimeters should remain above the figure for the pulse rate. When the figure in mm. of pressure is equalled by or exceeded by the pulse rate the prognosis is grave.
In typhoid fever we have made many estimations at various stages of the disease. We can only say that the pressure picture tends to fall during the course. The systolic falls more than the diastolic so that it is not uncommon to see pulse pressures of 20 mm. at the beginning of convalescence in spite of the high caloric feeding practiced. At the time of perforation the systolic pressure may be raised. This is only the reflex from the initial pain. Soon the pressure falls and if peritonitis sets in, the pressure is exceedingly low and the pulse pressure gradually falls until the circulation can no longer be carried on. In large hemorrhage the pressure suddenly falls. If only one hemorrhage has occurred a gradual rise takes place, but the general pressure picture remains at a lower level for days, gradually returning where it was before the hemorrhage.
In beginning failure of the circulation we found elevation of the foot of the bed about nine inches to be of such value that we felt there must be some increase in blood pressure. Numerous readings were made covering a period of several months. Although we felt certain that the circulation was improved, we rarely needed cardiac stimulation, we never could prove any increase of blood pressure with the sphygmomanometer.
In all infectious diseases there is no help offered by blood pressure estimations in diagnosis. The sole and important use is that of keeping track of the circulation.
No rules can be laid down for blood pressure in valvular heart disease. Aortic stenosis, the rarest of the valvular lesions, is practically always accompanied by high pressure picture. Mitral stenosis on the contrary usually shows a low pressure picture. Mitral insufficiency may show an exceedingly low picture or an exceedingly high picture. Aortic insufficiency also may be accompanied by a high systolic or by a normal systolic pressure. It depends on the etiology. Practically all the rheumatic cases have low pressure, the syphilitic cases have a high pressure. It is characteristic of all cases of aortic insufficiency that the diastolic pressure is low, even as low as 30 mm. The pulse pressure is invariably high. Usually there is no difficulty in determining the diastolic pressure. The intense third tone suddenly becomes dull at the point of diastolic pressure and frequently the dull sound can be distinctly heard over the artery down to the zero of the scale. If difficulty is found in reading the diastolic as the pressure is reduced, the estimation may be reversed and the pressure gradually increased from zero to the point where the dull tone suddenly becomes loud and clear. These points always coincide.
This has already been discussed somewhat fully in Chapter III and will receive more consideration later. It might be remarked in passing that in a case of seeming coma where albumin is found in the urine but where the blood pressure is low or normal, I have found at autopsy in several cases pyonephrosis and not chronic nephritis. The blood pressure may be useful in differentiating uremic coma from the coma of pyonephrosis. Also in the cases of coma with anasarca, either the acute, subacute or chronic form the blood pressure is not raised as a rule. Other diseases of the kidney, as tuberculosis, cancer, infection with pyogenicorganisms, are not accompanied with any notable changes in blood pressure.
Blood pressure is only of value in the above diseases in affording information concerning the state of the circulation. There is nothing characteristic about the pressure in any of these diseases.
The causes of arteriosclerosis are many and varied. No two persons have the same resisting power toward poisons that circulate in the blood. Some go through life exposed to all the infectious diseases without ever becoming infected, while others fall easy victims to every disease that comes, no matter how careful they may be, and it is quite the same in regard to the resistance of the arterial tissues. If the tubing is of first class quality and the individual does not place too much strain on it, he may live to the biblical three-score years and ten, and possess arteries which have undergone such slight changes that they are not palpable. Such a person is, however, the exception. On the other hand, if the tissue is of poor quality, even the ordinary wear and tear of life causes early changes in the vessels, and a person of forty may have hard arteries.
We have described in a previous chapter the changes which normally occur in the arteries as age advances. An artery that is normal for a man of fifty years would be distinctly abnormal for a boy of fifteen.
Two broad divisions of arteriosclerosis may be made: (1) congenital, or the result of inherited tendency; (2) acquired.
When Dr. O. W. Holmes was asked how to live to the age of seventy, he replied that a man should begin to pick his ancestors one hundred years before he was born. Our parents determine the character of the tissues with which we start in life, and this determines our general resistance. We might properly speak of congenital arteriosclerosiswhere the affected individual had poor arterial tissue with which to begin life, for that, in a sense, is a congenital defect, and arterial tissue that is poor in quality is prone to disease.
The author is more and more impressed with the part that heredity plays in the determination of arterial degeneration. Especially does syphilis in the parents or grandparents leave its stigma in the succeeding generations in the shape of poor arterial tissue which is prone to early degeneration. Recently W. W. Graves has called attention to a malformation of the vertebral border of the scapula which consists in a concavity instead of the normal convexity of the bone. To this malformation he has given the name, scaphoid scapula. He considers this to be but one manifestation of a general lack of development in the individual. He speaks of this maldevelopment as a blight and considers that syphilis in the ancestors is responsible for the condition in the offspring. He finds that even in children, the subjects of the scaphoid scapula, the arteries are very definitely thickened. While confirmation of his observations is lacking, there is no doubt that we must lay the blame for much of the arteriosclerosis in our patients to the poor quality of arterial tissue transmitted by ancestors who have acquired some constitutional disease. It may have been syphilis, it may have been the degeneration produced by alcohol or other drug. We can not ignore the part which heredity plays. The various factors to be considered in the production of the acquired form of arteriosclerosis appear to me to be but contributory factors to a very great extent, the essential and fundamental factor being the quality of arterial tissue with which the individual is endowed.
Arteriosclerosis may occur in infants. Cases have been reported of calcification of the arteries in infants and children. The arteriosclerosis may occur without nephritis or rise of blood pressure. Cerebral hemorrhage in a childof two years has been seen. Heredity in these cases plays a most important rôle. In many of the reported cases there was no question of congenital syphilis. Aneurysms, single or multiple, have been found in the arteries of children, and even the pulmonary artery may show sclerotic changes.
As a rule the cases usually seen belong in this group because it seems as if a connection could be established almost always between one or more of the etiologic factors to be described and the disease. While this apparently is the case, we must never lose sight of the part which the quality of the tissue plays. When we leave this out of our calculations we undoubtedly make many false deductions. When two men of the same age who have been exposed to the same conditions as far as we can learn, are found to have quite different arteries, the one normal, the other thickened, we must postulate congenitally poor tissue on the part of the latter. Such tissue readily becomes diseased following conditions which would very likely have produced no noticeable effect on perfectly normal, healthy tissue.
Hypertension must still be reckoned with in the etiology of arteriosclerosis although the rôle that it was thought to play does not seem so important. Changes of blood pressure alone are not considered by many to be sufficient for the production of arteriosclerosis. This may play some part, but there are many other factors mostly unknown which determine in any case the production of arterial lesions.
With every systole of the heart, blood is forced out into the arterial system against a certain amount of resistance represented by the tonicity of the capillary area, and the amount of cohesion between the viscous blood and the wallsof arterioles. When a dilatation of the capillaries over any large area takes place, the blood pressure falls, provided there is no compensatory contraction in other areas to make up for the decreased resistance in the dilated vessels. The viscosity of the blood, as such, probably has very little effect on the resistance to the flow. With the systole of the heart there is a sudden dilatation of the arch of the aorta, and a wave of expansion follows, which is transmitted to the periphery and is lost only in the capillaries.
The blood pressure is constantly changing. Physiologically there are relatively wide variations in the pressure in a perfectly normal individual. There are some persons who have hypotension, a blood pressure much below the normal. Such persons have usually small hearts, small aortas, and they seem to have but little resistance to disease. Many diseases, especially the prolonged fevers, diminish markedly the blood pressure. Whether the hypertension is the cause of the structural changes that are found in the walls of the vessels, or is the result of the diminished area of the arterial tree through which the same amount of blood has to be driven as before the vessel walls became narrowed, is still disputed. As has been stated, experimental evidence would tend to place the initial blame upon the poisons circulating in the blood, which first damage the vessel walls. The subsequent changes then produce thickening and inelasticity. Some think (Allbutt) that the hypertension is primary. There are cases seen clinically that lend support to this view and there is experimental evidence also (v. Chap. II). Not infrequently individuals in middle life begin to show increase of arterial blood pressure without discoverable cause. In such case it may be that there is slowly progressing chronic nephritis. The urine if examined only superficially in single specimens may not reveal any abnormalities. Careful functional examination by means of the newer tests may reveal functionaldeficiency. It must not be supposed that all cases of increasing hypertension are cases of chronic nephritis. The opinion has already been expressed (Chap. III) concerning this point. Experience has convinced me that the opinion expressed in former editions is not altogether correct.
No age is exempt from the lesions of arteriosclerosis if we consider the two groups. However, the disease is seen for the most part in persons past middle life. The relative frequency with which it is found in the different decades depends on so many factors that it is of no value to tabulate them. As has been stated, arteriosclerosis of all types is an involution process that advances with age. Longevity is a question of the integrity of the arterial tissue, and no one can tell what sort of "vital rubber" (Osler) any one of us has. However, many with poor tubing may make such use of it that it will outlast good tubing that is badly treated. Unfortunately we have no way of telling early enough with just what sort of arterial tissue we are starting life.
There is no doubt that men are far more prone to arterial disease than women are; all statistics are in accord on this point. This is explained by the greater exposure of men to those conditions of life which tend to produce circulatory strain, and so to produce arteriosclerosis, or vice versa. Arteriosclerosis in women is not often seen until after the fiftieth year. Cases of the most extreme grade of pipe stem arteries are, however, seen in old women, and calcified arteries are not hard to find among the inmates of an old woman's home.
Some of the most beautiful examples of arteriosclerosis in this country are seen in the negro. Not only is thisdisease more frequent in the black race, but the age of onset is much earlier than in the Caucasian. The accidents of arteriosclerosis, viz., aneurysm, cerebral hemorrhage, etc., are more common among the negro males. The etiologic factors that are most often found in the history are the prevalence of syphilis and hard physical labor.
Certain occupations have a distinct causal relationship to arteriosclerosis; among such are particularly those entailing prolonged muscular exercise, especially if much lifting is necessary. Every one is familiar with the phenomena accompanying the exertion of lifting. The breath is drawn in, the glottis is closed, and the muscles of the chest wall are held rigidly while the exertion lasts. This causes a great increase in blood pressure, and constant repetition of this will produce permanent high tension. In hospitals, the stevedores as a class have marked arteriosclerosis, and, almost without exception, they are comparatively young men. Occupations that are accompanied with prolonged mental strain, such as now occur to the heads of large manufacturing and financial institutions, also predispose to early arterial changes. Psychic activity, especially when it is accompanied by worry, is a potent factor in the production of the increased blood pressure which is the chief factor in producing arterial disease. It has been suggested that sexual continence in high-strung men produces changes in the nervous system which can conceivably lead to the production of high tension and further to arteriosclerosis. This, however, I can not think has any foundation in fact except in so far as such men are prone to live at high speed and wear themselves out sooner than the normal person. The sexual continenceper seis not harmful. There are, however, men who seem not to be harmed by the constant wear and tear of our modern life. These are the exceptions.
Workers in factories where paint is made and the ingredientshand-mixed, are prone to develop arteriosclerosis early in life. It has been found that the laborers most apt to be victims of lead intoxication are those who are careless in their habits of cleanliness, particularly in regard to the fingernails. The continuous absorption of lead into the system, brings about a condition of hypertension that has its inevitable results.
The fact is that any occupation which entails either the absorption of toxic substances, or prolonged muscular labor, will hasten markedly the onset of arterial disease.
The opinion that arteriosclerosis is due in large part to poisoning by end products or by-products of protein digestion is now receiving much support. Experiments on dogs and rabbits have lent some confirmation to chemical observations. It has been shown that dogs fed for a long time on putrefied meat developed inflammation and degeneration of the adventitia and media, with hyperplasia and calcification of the intima of many arteries. In the pulmonary and carotid arteries, in the vena cavas and myocardium, there were extensive necroses and hyaline degeneration. Moreover, injections of sodium urate and ergot caused necroses in the muscularis and elastica of the aorta, pulmonary artery, vena cavas inferior and heart muscle, but there was no calcification. Guinea pigs which were fed indol in small doses by the mouth over a long period showed atheromatous degeneration of the aorta.
As more study has been given to the arteries in persons who have died of the acute infectious diseases, more has come to light concerning the effects of the toxins of these diseases on the vessel walls. In the arteries of children who have died of measles, scarlet fever, diphtheria, cerebrospinalmeningitis, etc., degenerative changes in the arteries occur, modified only by the length of time that the toxins have acted.
Thayer has shown that the arteries of those who have passed through an attack of moderately severe or severe typhoid fever are as a rule more readily palpable than are the vessels of persons of corresponding years who have never had the disease. Clinically the typhoid toxin appears to cause the early production of arteriosclerosis. The changes in the arteries occur for the most part, and always earlier, in the peripheral arteries, and the media is chiefly affected. Minute yellowish patches are found on the aorta, carotids, and coronaries. In persons who have passed through an attack of one of the fevers, and have later died from some other cause, regenerative changes are sometimes found to have taken place in the arteries, consisting of an ingrowth of elastic fibers from the intact adventitia to the diseased media.
That there are some other factors than the infectious disease which are concerned in the production of arterial changes seems evident from a study[14]made recently among a group of almshouse inmates ranging in age from 38 to 90 years. The study included 500 persons of both sexes. Careful histories were taken to determine the presence of antecedent infectious disease. The radial artery was palpated to determine the presence of sclerosis. Among the cases giving a history of one infectious disease the following table gives the results:
DISEASENO.++++++POSITIVENEGATIVEMeasles47106122819Infectious arthritis389641919Pneumonia305851812Typhoid276831710Scarlet fever1000446Smallpox1414059Miscellaneous122529317833373010078
A summary of the cases showed: 252 cases without sclerosis; 248 with sclerosis; 147 cases with infections but no sclerosis; 180 cases with infections and sclerosis.
This study failed to throw any positive light on the question. Infectious diseases undoubtedly play a certain rôle, particularly those continuing a long time and certain particular infectious diseases, as measles.
Syphilis is one of the most important of the etiologic factors in the production of arteriosclerosis. It has been shown that in 85 per cent of cases of aortic insufficiency in persons, usually males, over forty-five years, who did not have chronic infective endocarditis, the Wassermann reaction was positive. Acute aortitis affecting the ascending and transverse portions of the arch of the aorta is very commonly seen, and the irregular, scattered, slightly raised, yellowish-white patches of sclerosis in the arch which are found years after the syphilitic lesion, are considered by some to be very characteristic of syphilis. Mesaortitis is the primary lesion and acts as alocus minoris resistentiæwhere an aneurysm forms.
Hypertensive cardiovascular cases have been serologically studied, and a positive Wassermann reaction found in a large percentage of one series. In fifty cases, 90 per cent either gave a positive Wassermann reaction or luetin test, were known to have syphilis, or had children with hereditary syphilis. This suggests what might be called "familial cardiovascular syphilis."
Hypertensive disease is possibly one of the common so-called "late" 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 yearsof age are due to syphilitic aortitis. In the late stages of syphilis the arterial lesions may be of a diffuse character.
Lead, tobacco, and according to some, tea and coffee, are to be classed 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.Alcoholhas 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 quantities 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 bedifficult and is really not shown by my tabulations. There were cardiovascular changes, such as myocarditis, aortitis, valvular heart disease and arteriosclerosis in chronic alcoholics in 54.3 per cent of 461 cases, but this by no means constitutes a proof of the causal relationship 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 rôletobaccoplays 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.
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 repetition 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 wouldhave 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 rôle 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.
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 prone 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 class 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 timesufficient 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 is to be reckoned with as an etiologic factor. One sees it especially among the laboring class in both whites and negroes. Possibly other factors, as alcohol and coarse 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.
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 withblood 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 associated 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 associated 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 assurance 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 albumin 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.
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 résumé 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.
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 interspace 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 thelines 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 interspace, 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 interspaces, 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.
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 thelimits 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 assistance 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.
In auscultating the heart I prefer the binaural stethoscope of the Ford pattern. The recent substitution of an aluminum bell for the hard rubber bell is an improvement. Personally I do not favor the phonendoscope or any of the new patent non-roaring instruments now for sale by urgent instrument makers. The phonendoscope has its uses, for example in auscultating the back when a patient is lying in bed or in listening to the heart sounds when a patient is under an anesthetic; but for differentiating the murmurs and for heart diagnosis, I much prefer the regular bell stethoscope.
In arteriosclerosis the two places over which it is important to listen are the apex and the second right cartilage, the aortic area. Over the former, one gains data in regard to the strength of the heart as indicated by the first sound, over the latter point, one learns of the tension in the aorta by the character of the sound produced when the aortic valves close.
The hypertrophy of the heart in arteriosclerosis is invariably due to the enlargement and thickening of the left ventricle. From the nature of the position which the heart assumes in the thorax, this enlargement is downward and to the left. The apex beat will therefore be found in the fifth or sixth interspace, and definitely at an increased distance from the midsternal line. As stated above, it is most important that this distance be accurately measured and put down in the notes of the case for future reference. No satisfactory prognosis can be given unless this is done, for the gradual increase or the decrease under treatment in the size of the heart can thus be definitely known, and, knowing the other factors, a prognosis may be given which will be of some value to the patient.
It is exceedingly difficult at times to affirm definitely that an artery, the radial for example, is actually sclerosed. Much depends on the sensitiveness of the fingers of him who palpates, and much upon the relation of the palpated artery to the surrounding, chiefly underlying, structures. In the examination of arteries it is well to inspect the body for the pulsations caused by them. Frequently an exceedingly tortuous artery, such as the brachial, may be seen throughout its whole extent and yet the radial appear little, if any, thickened by palpation. Again the artery of a pulse of high tension which is small in size but full between the beats, may not be as sclerosed as one which collapses and feels much softer. It is difficult to obtain accurate data in regard to the tension in an artery by feeling it with the fingers of one hand. One should use both hands. With the middle finger of the right (left) hand the artery is compressed peripherally, that is, nearest the wrist. The blood is then pressed out of the artery with the middle finger of the left (right) hand, so as to obliterate completely the pulse wave and the two or three inches between the middle fingers are felt with the index fingers. By holding the finger firmly on the artery near the wrist so as to block any wave that may come through the palmar arch by anastomosis with the ulnar artery and by releasing pressure on the proximal middle finger, some idea may be had of the degree of pulse tension. However, no amount of practice can more than approximate the tension and when one is surest that he can tell how many millimeters of pressure there are, he is apt to be farthest wrong when he checks his guess with the sphygmomanometer.
Much may be learned from carefully palpating the peripheral arteries, and, as a rule, the sclerosis of these arteries means general arteriosclerosis, although there are many exceptions to this.
A more recent method, and one which in the author's hands has been found to be valuable, is that proposed by Wertheim-Salomonson who palpates the artery not with the ball of the finger but with the fingernail. The finger is held so that the nail is perpendicular to the surface of the skin and the artery is felt with the end of the nail. The sensation is perceived at the root and makes use of all the sensitive nerve endings there. In this way it is possible to feelthe arterial wall distinctly, and a little practice will enable one to determine whether or not the vessel wall is thickened. It is also possible to determine with a considerable degree of accuracy the diameter of the artery and the size of the wall when the current is cut off by pressure on the proximal side of the artery. It is best to have a firm background when this "fingernail" palpation is used. This may be obtained by palpating the radial artery against the lower end of the radius.
Probably the best method of palpating the arteries, especially the radial, to determine the degree of sclerosis and thickening, is to use the tip of the finger and roll it carefully over the artery. The tip of the finger is exceedingly sensitive and, moreover, it is a firmer palpating surface than the ball, thus enabling one to appreciate degrees of sclerosis which could not be differentiated by palpation with the soft yielding ball. This finger tip palpation is well illustrated in the figures here shown. (Figs. 57 and 58.)