Erratum
Page 75, Figure shown is not the Brown sphygmomanometer described in the text, but the Baumanometer manufactured by W. A. Baum Co., Inc., New York. It is claimed that the Baumanometer is made with particular care and hence the readings are said to be more accurate than other mercury instruments. It is apparently a good instrument. The author has had no personal experience with it.
ARTERIOSCLEROSIS
AND
HYPERTENSION
With Chapters on Blood Pressure
BY
LOUIS M. WARFIELD, A.B., M.D., (Johns Hopkins),
F.A.C.P.
FORMERLY PROFESSOR OF CLINICAL MEDICINE, MARQUETTE UNIVERSITY MEDICAL
SCHOOL; CHIEF PHYSICIAN TO MILWAUKEE COUNTY HOSPITAL; ASSOCIATE
MEMBER ASSOCIATION AMERICAN PHYSICIANS; MEMBER AMERICAN
ASSOCIATION PATHOLOGISTS AND BACTERIOLOGISTS;
AMERICAN MEDICAL ASSOCIATION, ETC., FELLOW
AMERICAN COLLEGE OF PHYSICIANS
THIRD EDITION
ST. LOUIS
C. V. MOSBY COMPANY
1920
Copyright, 1912, 1920, by C. V. Mosby Company
Press of
C. V. Mosby Company
St. Louis
TO
MY MOTHER
THIS VOLUME IS AFFECTIONATELY
DEDICATED
PREFACE TO THIRD EDITION
Several years have elapsed since the appearance of the second edition of this book. During this time there has been considerable experimentation and much writing on arteriosclerosis. The total of all work has not been to add very much to our knowledge of the etiology of arterial degeneration. Points of view and opinions change from time to time. It is so with arteriosclerosis. In this edition arteriosclerosis is not regarded as a disease with a definite etiologic factor. Rather it is looked upon as a degenerative process affecting the arteries following a variety of causes more or less ill defined. It is not considered a true disease. Possibly syphilitic arteritis may be viewed as an entity, the cause is known and the lesions are characteristic.
Much new material and many new figures have been added to this edition. Some rearranging has been done. The chapter on Blood Pressure has been much expanded and some original observations have been included. The literature has been selected rather than indiscriminately quoted. Much that is written on the subject is of little value.
It has always seemed to the author that there is not enough of the personal element in medical writings. At the risk of being severely criticized, he has attempted to make this book represent largely his own ideas, only here and there quoting from the literature.
New chapters on Cardiac Irregularities Associated with Arteriosclerosis, and Blood Pressure in Its Clinical Application have been added.
The fact that the book has passed through two editions is very gratifying and seems to show that it has met with favor. The author takes this opportunity of thanking those who have loaned him illustrations. Wherever figures are borrowed due credit is given.
It is hoped that the kind of reception accorded to the first and second editions will also not be withheld from this present edition.
Louis M. Warfield.
Milwaukee, Wisc.
PREFACE TO THE SECOND EDITION
In this second edition so many changes and additions have been made that the book is practically a new one. All the chapters which were in the previous edition have been carefully revised. Two chapters, "Pathology" and "Physiology," have been completely rewritten and brought up to date. It was thought best to add some references for those who had interest enough to pursue the subject further. These references have been selected on account of the readiness with which they may be procured in any library, public or private. Two new chapters have been added—one on "The Physical Examination of the Heart and Arteries," the other on "Arteriosclerosis in Its Relation to Life Insurance," and it is hoped that these will add to the practical value of the book.
Arteriosclerosis can scarcely be considered apart from blood pressure, and in the view expressed within, with which some may not concur, high tension is considered to be a large factor in the production of arteriosclerosis. As the data on blood pressure have increased, the importance of it has become more evident. The chapter on "Blood Pressure" has been wholly rewritten, expanded so as to give a comprehensive grasp of the essential features, and several illustrations have been added in order to elucidate the text more fully. The chief objects in view were to make clear to the physician the technique and the necessity for estimating both systolic and diastolic pressures.
The author is grateful for the kindly reception accorded the first edition. No one is more keenly aware of the imperfections than he. The necessity for a second edition is taken to mean that the book has found a place for itself and has been of use to some.
The author hopes that this new edition will fulfill adequately the purpose for which he prepared the book—namely, as a practical guide to the knowledge and appreciation of a most important and exceedingly common disease.
Louis M. Warfield.
Milwaukee, May, 1912.
PREFACE TO THE FIRST EDITION
It is hoped that this small volume may fill a want in the already crowded field of medical monographs. The author has endeavored to give to the general practitioner a readable, authoritative essay on a disease which is especially an outcome of modern civilization. To that end all the available literature has been freely consulted, and the newest results of experimental research and the recent ideas of leading clinicians have been summarized. The author has supplemented these with results from his own experience, but has thought it best not to burden the contents with case histories.
The stress and strain of our daily life has, as one of its consequences, early arterial degeneration. There can be no doubt that arterial disease in the comparatively young is more frequent than it was twenty-five years ago, and that the mortality from diseases directly dependent on arteriosclerotic changes is increasing. Fortunately, the almost universal habit of getting out of doors whenever possible, and the revival of interest in athletics for persons of all ages, have to some extent counteracted the tendency to early decay. Nevertheless, the actual average prolongation of life is more probably due to the very great reduction in infant mortality and in deaths from infectious and communicable diseases.
The wear and tear on the human organism in our modern way of living is excessive. Hard work, worry, and high living all predispose to degenerative changes in the arteries, and so bring on premature old age. The author has tried to emphasize this by laying stress on the prevention of arteriosclerosis rather than on the treatment of the fully developed disease.
No bibliography is given, as this is not intended as a reference book, but rather as a guide to a better appreciation and understanding of a most important subject. It has been difficult to keep from wandering off into full discussions of conditions incident to and accompanied by arteriosclerosis, but, in order to be clear in his statements and complete in his descriptions, the author has to invade the fields of heart disease, kidney disease, brain disease, etc. It is hoped, however, that these excursions will serve to show how intimately disease of the arteries is bound up with diseases of all the organs and tissues of the body.
Some authors have been named when their opinions have been given. Thanks are extended also to many others to whom the writer is indebted, but of whom no individual mention has been made.
The author also takes this opportunity of expressing his appreciation of the kindness of Dr. D. L. Harris, who took the microphotographs, and to the publishers for their unfailing courtesy and consideration.
Louis M. Warfield.
St. Louis, August, 1908.
CONTENTS
page
[CHAPTER I.]
Anatomy25
Introduction, 25; Definition, 26; General Structure of the Arteries, 27; Arteries, 29; Veins, 30; Capillaries, 31.
[CHAPTER II.]
Pathology32
Syphilitic Aortitis, 44; Experimental Arteriosclerosis, 50; Arteriosclerosis of the Pulmonary Arteries, 63; Sclerosis of the Veins, 64.
[CHAPTER III.]
Physiology of the Circulation65
Blood Pressure, 68; Blood Pressure Instruments, 70; Technic, 80; Arterial Pressure, 85; Normal Pressure Variations, 88; The Auscultatory Blood Pressure Phenomenon, 90; The Maximum and Minimum Pressures, 94; Relative Importance of the Systolic and Diastolic Pressures, 97; Pulse Pressure, 100; Blood Pressure Variations, 102; Hypertension, 106; Hypotension, 117; The Pulse, 123; The Venous Pulse, 123; The Electrocardiogram, 126.
[CHAPTER IV.]
Important Cardiac Irregularities Associated With Arteriosclerosis 13
Auricular Flutter, 131; Auricular Fibrillation, 133; Ventricular Fibrillation, 138; Extrasystole, 138; Heart Block, 140.
[CHAPTER V.]
Blood Pressure in Its Clinical Applications147
Blood Pressure in Surgery, 147; Head Injuries, 148; Shock and Hemorrhage, 148; Blood Pressure in Obstetrics, 152; Infectious Diseases, 153; Valvular Heart Disease, 155; Kidney Disease, 155; Other Diseases, Liver, Spleen, Abdomen, etc., 156.
[CHAPTER VI.]
Etiology157
Congenital Form, 157; Acquired Form, 159; Hypertension, 159; Age, Sex, Race, 161; Occupation, 162; Food Poisons, 163; Infectious Diseases, 163; Syphilis, 165; Chronic Drug Intoxications, 166; Overeating, 167; Mental Strain, 168; Muscular Overwork, 169; Renal Disease, 169; Ductless Glands, 171.
[CHAPTER VII.]
The Physical Examination of the Heart and Arteries172
Heart Boundaries, 172; Percussion, 174; Auscultation, 176; The Examination of the Arteries, 177; Estimation of Blood Pressure, 179; Palpation, 180; Precautions When Estimating Blood Pressure, 181; The Value of Blood Pressure, 181.
[CHAPTER VIII.]
Symptoms and Physical Signs183
General, 183; Hypertension, 185; The Heart, 188; Palpable Arteries, 189; Ocular Signs and Symptoms, 190; Nervous Symptoms, 191.
[CHAPTER IX.]
Symptoms and Physical Signs194
Special, 194; Cardiac, 195; Renal, 199; Abdominal or Visceral, 201; Cerebral, 203; Spinal, 205; Local or Peripheral, 207; Pulmonary Artery, 209.
[CHAPTER X.]
Diagnosis210
Early Diagnosis, 210; Differential Diagnosis, 215; Diseases in Which Arteriosclerosis is Commonly Found, 216.
[CHAPTER XI.]
Prognosis218
[CHAPTER XII.]
Prophylaxis224
[CHAPTER XIII.]
Treatment229
Hygienic Treatment, 230; Balneotherapy, 233; Personal Habits, 234; Dietetic Treatment, 235; Medicinal, 238; Symptomatic Treatment, 245.
[CHAPTER XIV.]
Arteriosclerosis in Its Relation to Life Insurance249
[CHAPTER XV.]
Practical Suggestions256
ILLUSTRATIONS
ARTERIOSCLEROSIS AND HYPERTENSION
CHAPTER I.
ANATOMY
With the increased complexity of our modern life comes increased wear and tear on the human organism. "A man is as old as his arteries" is an old dictum, and, like many proverbs, the application to mankind today is, if anything, more pertinent than it was when the saying was first uttered. Notwithstanding the fact that the average age of mankind at death has been materially lengthened—the increase in years amounting to fourteen in the past one hundred years of history—clinicians and pathologists are agreed that the arterial degeneration known as arteriosclerosis is present to an alarming extent in persons over forty years of age. Figures in all vital statistics have shown us that all affections of the circulatory and renal systems are definitely on the increase. "Arterial diseases of various kinds, atheroma, aneurysm, etc., caused 15,685 deaths in 1915, or 23.3 per 100,000. This rate, although somewhat lower than the corresponding ones for 1912 and 1913, is higher than that for 1914, and is very much higher than that for 1900, which was 6.1."
The great group of cases of which cardiac incompetence, aneurysm, cerebral apoplexy, chronic nephritis, emphysema, and chronic bronchitis are the most frequent and important appear as terminal events in which arteriosclerosis has probably played an important part.
Thus, in the sense in which we speak of tuberculosis or pneumonia as a distinct disease, we can not so designate the diseased condition of the arteries.
Arteriosclerosis is not a disease sui generis. It is best viewed as a degeneration of the coats of the arteries, both large and small resulting in several different more or less distinct types.
These types blend one into the other and in the same patient all types may be found. Thus the sclerosis of the arteries is the result of a variety of causes, none of which is definitely known in the sense of a bacterial disease. As we shall see later, one type of arteriosclerosis has a special pathology and etiology, the syphilitic arterial changes.
Bearing in mind that arteriosclerosis (called by some "arteriocapillary fibrosis," by others "atherosclerosis") is not a true disease, it may, for convenience be defined as a chronic disease of the arteries and arterioles, characterized anatomically by increase or decrease of the thickness of the walls of the blood vessels, the initial lesion being a weakening of the middle layer caused by various toxic or mechanical agencies. This weakness of the media leads to secondary effects, which include hypertrophy or atrophy of the inner layer—and not infrequently hypertrophy of the outer layer—connective tissue formation and calcification in the vessels, and the formation of minute aneurysms along them. The term arteriocapillary fibrosis has a broader meaning, but is a cumbersome phrase, and conveys the idea that the capillary changes are an essential feature of the process, whereas these are for the most part secondary to the changes in the arteries. The veins do not always escape in the general morbid process, and when these are affected the whole condition is sometimes called vascular sclerosis or angiosclerosis.
Upon the anatomical structure of the arteries depends, as a rule, the character and extent of the arteriosclerotic lesions. For the clear comprehension of the process, it is necessary to keep in mind the essential histological differences between the aorta and the larger and smaller branches of the arterial tree.
The vascular system is often likened to a central pump, from which emanates a closed system of tubes, beginning with one large distributing pipe, which gives rise to a series of tubes, whose number is constantly increasing at the same time that their caliber is decreasing in size. From the smallest of these tubes, larger and larger vessels collect the flowing blood, until, at the pump, two large trunks of approximately the same area as the one large distributing trunk empty the blood into the heart, thus completing the circle. This is but a rough illustration, and, while possibly useful, takes into account none of the vital forces which are constantly controlling every part of the distributing system.
General Structure of the Arteries
The aorta and its branches are highly elastic tubes, having a smooth, glistening inner surface. When the arteries are cut open, they present a yellowish appearance, due to the large quantity of elastic tissue contained in the walls. The elasticity is practically perfect, being both longitudinal and transverse. The essential portion of any blood vessel is the endothelial tube, composed of flat cells cemented together by intercellular substance and having no stomata between the cells. This tube is reinforced in different ways by connective tissue, smooth muscle fibers, and fibroelastic tissue. Although the gradations from the larger to the smaller arteries and from these to the capillaries and veins are almost insensible, yet particular arteries present structural characters sufficiently marked to admit of histological differentiation.
The whole vascular system, including the heart, has an endothelial lining, which may constitute a distinct inner coat, the tunica intima, or may be without coverings, as in the case of the capillaries. The intima (Fig. 1) consists typically of endothelium, reinforced by a variable amount of fibroelastic tissue, in which the elastic fibers predominate. The tunica media is composed of intermingled bundles of elastic tissue, smooth muscle fibers, and some fibrous tissue. The adventitia or outer coat is exceedingly tough. It is usually thinner than the media, and is composed of fibroelastic tissue. This division into three coats is, however, somewhat arbitrary, as in the larger arteries particularly it is difficult to discover any distinct separation into layers.
Fig. 1.—Cross section of a large artery showing the division into the three coats; intima, media, adventitia. The intima is a thin line composed of endothelial cells. The wavy elastic lamina is well seen. The thick middle coat is composed of muscle fibers and fibroelastic tissue. The loose tissue on the outer (lower portion of cut) side of the media is the adventitia. (Microphotograph, highly magnified.)
The muscular layer varies from single scattered cells, in the arterioles, to bands of fibers making up the body of the vessel in the medium-sized arteries and veins.
There is elastic tissue in all but the smallest arteries, and it is also found in some veins. It varies in amount from a loose network to dense membranes. In the intima of the larger arteries the elastic tissue occurs as sheets, which under the microscope appear perforated and pitted, the so-called fenestrated membrane of Henle.
The nutrient vessels of the arteries and veins, the vasa vasorum, are present in all the vessels except those less than one millimeter in diameter. The vasa vasorum course in the external coat and send capillaries into the media, supplying the outer portion of the coat and the externa with nutritive material. The nutrition of the intima and inner portion of the media is obtained from the blood circulating through the vessel. Lymphatics and nerves are also present in the middle and outer layers of the vessels.
Arteries
The structure of the arteries varies notably, depending upon the size of the vessel. A cross section of the thoracic aorta reveals a dense network of elastic fibers, occupying practically all of the space between the single layer of endothelial cells and the loose elastic and connective tissue network of the outer layer. Smooth muscle fibers are seen in the middle coat, but, in comparison with the mass of elastic tissue, they appear to have only a limited function.
In a cross section of the radial artery one sees a wavy outline of intima, caused by the endothelium following the corrugations of the elastica. The endothelium is seen as a delicate line, in which a few nuclei are visible. The media is comparatively thick, and is composed of muscle cells, arranged in flat bundles, and plates of elastic tissue. Between the media and the externa the elastic tissue is somewhat condensed to form the external elastic membrane. The adventitia varies much in thickness, being better developed in the medium-sized than in the large arteries. It is composed of fibrous tissue mixed with elastic fibers.
"Followed toward the capillaries, the coats of the artery gradually diminish in thickness, the endothelium resting directly upon the internal elastic membrane so long as the latter persists, and afterward on the rapidly attenuating media. The elastica becomes progressively reduced until it entirely disappears from the middle coat, which then becomes a purely muscular tunic, and, before the capillary is reached, is reduced to a single layer of muscle cells. In the precapillary arterioles the muscle no longer forms a continuous layer, but is represented by groups of fiber cells that partially wrap around the vessel, and at last are replaced by isolated elements. After the disappearance of the muscle cells the blood vessel has become a true capillary. The adventitia shares in the general reduction, and gradually diminishes in thickness until, in the smallest arteries, it consists of only a few fibroelastic strands outside the muscle cells." (Piersol's Anatomy.)
The large arteries differ from those of medium size mainly in the fact that there is no sharp line of demarcation between the intima and the media. There is also much more elastic tissue distributed in firm bundles throughout the media, and there are fewer muscle fibers, giving a more compact appearance to the artery as seen in cross section. The predominance of elastic tissue permits of great distention by the blood forced into the artery at every heartbeat, the caliber of the tube being less markedly under the control of the vasomotor nerves than is the case in the small arteries, where the muscle tissue is relatively more developed. The adventitia of the large arteries is strong and firm, and is made up of interlacing fibroelastic tissue, of which some of the bundles are arranged longitudinally.
Veins
The walls of the veins are thinner than those of the arteries; they contain much less elastic and muscular tissue, and are, therefore, more flaccid and less contractile. Many veins, particularly those of the extremities, are provided with cup-like valves opening toward the heart. These valves, when closed, prevent the return of the blood to the periphery and distribute the static pressure of the blood column. The bulgings caused by the valves may be seen in the superficial veins of the arm and leg. There are no valves in the veins of the neck, where there is no necessity for such a protective mechanism, gravity sufficing to drain the venous blood from the cranial cavity.
Capillaries
These are endothelial tubes in the substance of the organs, the tissue of the organ giving them the necessary support. They are the final subdivisions of the blood vessels, and the vast capillary area offers the greatest amount of resistance to the blood flow, thus serving to slow the blood stream and allowing time for nutritive substances or waste products to pass from and to the blood. Usually the capillaries are arranged in the form of a network, the channels in any one tissue being of nearly uniform size, and the closeness of the mesh depending upon the organ.
As far back as 1865, Stricker observed contraction of the capillaries. This observation was apparently forgotten until revived again by Krogh recently. The latter finds that the capillaries are formed of cells which are arranged in strands encircling the vessel. The capillaries are rarely longer than 1 mm., and, according to Krogh, are capable of enormous dilatation.
The rate of flow through any capillary area is very inconstant, and the usual explanation has been that the capillaries were endothelial tubes the blood flow of which was dependent upon the contraction or dilatation of the terminal arterioles. The actual fact that in an observed capillary area some capillaries are empty renders the above explanation untenable. The color of a tissue depends upon the state of filling of the capillaries with blood.
It would seem that all the evidence now leads us to believe that the capillaries themselves are contractile and it is even possible that they may be under vasomotor control. If the anatomic structure as stated above, is correct, it would take but a slight contraction of the encircling cell to shut off completely the capillary. When the enormous capillary bed is considered, it is not inconceivable that circulating poisons may act on large areas and produce a true capillary resistance to the onflow of blood which might express itself, if long continued, in actual hypertrophy of the heart.
CHAPTER II.
PATHOLOGY
The whole subject of the pathology of arteriosclerosis has been much enriched by the study of the experimental lesions produced by various drugs and microorganisms upon the aortas of rabbits. Simple atheroma must not be confused with the lesions of arteriosclerosis. The small whitish or yellowish plaques so frequently seen on the aorta and its main branches, may occur at any age, and have seemingly no great significance. Such plaques may grow to the size of a dime or larger, and even become eroded. They represent fatty degeneration of the intima which, at times, has no demonstrable cause; at times follows in the course of various diseases, and undoubtedly is due to disturbances of nutrition in the intima. Except for the remote danger of clot formation on the uneven or eroded spot, these places are of no special significance, and are not to be confused with the atheroma of nodular sclerosis.
The lesions of arteriosclerosis are of a different character. It has been customary to differentiate three types: (1) nodular; (2) diffuse; (3) senile. It must be understood that this is not a classification of distinct types. As a rule in advanced arteriosclerosis, lesions representing all types and all grades are found. The nodular type, however, may occur in the aorta alone, the branches remaining free. This is most often found in syphilitic sclerosis where the lesion is confined to the ascending portion of the arch of the aorta.
The retrogressive changes of advancing years can not be rightly termed disease, yet it becomes necessary to regard them as such, for the senile changes, as we shall see, may be but the advanced stages of true arteriosclerosis. Much depends on the nature of the arterial tissue and much on the factors at work tending to injure the tissue. A man of forty years may therefore have the calcified, pipe stem arteries of a man of eighty. Our parents determine, to great extent, the kind of tissue with which we start life. The arteries are elastic tubes capable of much stretching and abuse. In the aorta and large branches there is much elastic tissue and relatively little muscle. When the vessels have reached the organs, they are found to be structurally changed in that there is in them a relatively small amount of elastic tissue but a great deal of smooth muscle. This is a provision of nature to increase or decrease the supply of blood at any point or points.
The aorta and the large branches are distributing tubes only. It is after all in the arterioles and smaller arteries that the lesions of arteriosclerosis do the most damage. A point to be emphasized is that the whole arterial system is rarely, if ever, attacked uniformly. That is, there may be a marked degree of sclerosis in the aorta and coronary arteries with very little, if any, change in the radials. On the contrary, a few peripheral arteries only may be the seat of disease. A case in point was seen at autopsy in which the aorta in its entirety and all the large peripheral branches were absolutely smooth. In the brain, however, the arteries were tortuous, hard, and were studded with miliary aneurysms. It is not possible to judge accurately the state of the whole arterial system by the stage of the lesion in any one artery; but on the whole one may say that an undue thickening of the radial artery indicates analogous changes in the mesenteric arteries and in the aorta.
So far as the anatomical lesions in the aorta and branches are concerned, there is much uniformity even though the etiologic factors have been diverse. The only difference is one of extent. To Thoma we owe the first careful work on arteriosclerosis. He regarded the lesion in arteriosclerosis as one situated primarily in the media; there is a lack of resistance in this coat. His views are now chiefly of historical interest. As the author understands him, he considered a rupture in the media to be the cause of a local widening and consequently the blood could not be distributed evenly to the organ which was supplied by the diseased artery or arteries. Moreover, there was danger of a rupture at the weak spot unless this were strengthened. It was essential for the even distribution of blood that the lumen be restored to its former size. Nature's method of repair was a hypertrophy of the subintimal connective tissue and the formation of a nodule at that point. The thickening was compensatory, resulting in the establishment of the normal caliber of the vessel. Thoma showed that by injecting an aorta in the subject of such changes, with paraffin at a pressure of 160 mm. of mercury, these projections disappeared and the muscle bulged externally. He recognized the fact that the character of the artery changed as the years passed, and to this form he gave the name, primary arteriosclerosis. To the group of cases caused by various poisonous agents, or following high peripheral resistance and consequent high pressure, he gave the name, secondary arteriosclerosis. This is a useful but not essential division, as the changes which age and high tension produce may not be different from those produced in much younger persons by some circulating poison. And most important to bear in mind, octogenarians may have soft, elastic arteries.
As the body ages, certain changes usually take place in the arteries leading to thickening and inelasticity of their walls. This is a normal change, and in estimating the palpable thickening of an artery, such as the radial, the age of the individual must always be considered.
Thayer and Fabyan, in an examination of the radial artery from birth to old age, found that, in general, the artery strengthens itself, as more strain is thrown upon it, by new elastica in the intima and connective tissue in the media and adventitia. Up to the third decade there is only a strengthening of the media and adventitia. During the third and fourth decades there is also distinct connective tissue thickening in the intima. "In other words, the strain has begun to tell upon the vessel wall, and the yielding tube fortifies itself by the connective tissue thickening of the intima and to a lesser extent of the media." By the fifth decade the connective tissue deposits in the intima are marked, there is an increase of fibrous tissue upon the medial side of the intima and, in lesser degree, throughout the media. "Finally, in these sclerotic vessels degenerative changes set in, which are somewhat different from those seen in the larger arteries, consisting, as they do, of local areas of coagulation necrosis with calcification, especially marked in the deep layers of the connective tissue thickenings of the intima, and in the muscle fibers of the media, particularly opposite these points. These changes may ... go on to actual bone formation." The mesenteric artery differs in some respects from the radial, but in the main, the changes brought about by age are the same. Thayer and Fabyan note two striking points of difference: "(1) calcification is apparently much less frequent than in the radials; (2) in several cases plaques were seen with fatty softening of the deeper layers of the intima and superficial proliferation—a picture which we have never seen in the radial." (See Fig. 2.)
Fig. 2.—Cross section of a coronary artery, ×50, showing nodular sclerosis. Note the heaping up of cells in the intima, the fracture of the elastica, and the destruction of the media beneath the nodule. The primary lesion evidently was in the media. The thickened intima is the effort on the part of nature to heal the breach. At such places as shown here aneurysms may form. (Microphotograph.)
Aschoff's studies of the aorta show that, "in infancy the elastic laminæ of the media stand out sharply defined, well separated from each other by the muscle layers, which are well developed.... From childhood there is to be observed a slowly progressive increase in the elastic elements of the media. Not only do the individual lamellæ seen in cross-sections become thicker, but also they afford an increasing number of fine secondary filaments feathering off from these and crossing the muscle layer, so that now they are no longer sharply defined, but more ragged upon cross-section. This progressive increase attains its maximum at or about the age of thirty-five, and from now on for the next fifteen years the condition is relatively stationary. After fifty there is to be observed a slowly progressive atrophy of the elastica. The media becomes obviously thinner and presumably weaker." (Adami.) It has also been found (Klotz) that after the age of thirty-five, the muscle of the media begins to exhibit fatty degeneration which after fifty years is well marked. The fatty degeneration may then give place to a calcareous infiltration or the fibers may undergo complete absorption. It would appear that the thinning of the aortic media is due not so much to the atrophy of the elastic tissue as to that of the muscle tissue. The elastic tissue does lose its specific property and the artery thus becomes practically a connective tissue tube.
Scheel has made very careful measurements of the ascending, the thoracic, and the abdominal aorta, and the pulmonary artery. He found that from birth to sixty years, the aorta became progressively wider and lost its elasticity. The pulmonary changed little, if at all, after thirty to forty years, and where before it was wider than the aorta, it now was found to be smaller. In chronic nephritis both were widened. The continuous increase of width and length of the aorta stands in reverse relationship to the elasticity of its walls.
Although the division of the lesions into nodular, diffuse, and senile has been the usual one, it is better to separate three groups into (1) nodular, (2) diffuse or senile, and (3) syphilitic. There is more known about the histology of the syphilitic form and the lesions which consist of puckerings and scars seen on opening an aorta just above the valves, and on the ascending portion of the arch are characteristic. A macroscopic examination suffices in most cases for a definite diagnosis.
In the nodular form the lesions are found on the aorta and large branches particularly at or near the orifices of branching vessels. These nodules may increase in size, forming rather large, slightly raised plaques of yellowish-white color. They are, as a rule, irregularly scattered throughout the aorta and branches and tend to be more numerous and larger in the abdominal aorta. The initial lesion is in the media, consisting of an actual dissolution of this coat with rupture of the elastic fibers and infiltration with small round cells. There is thus a weak spot in the artery. Hypertrophy of the intimal cells takes place, layer upon layer being added in an attempt to strengthen the vessel at the injured place. Coincidently with this, there is thickening by a connective tissue growth in the adventitia. The process begins, at least in syphilis, around the terminals of the vasa vasorum. It will be recalled that the blood supply of the inner portion of the media comes from within the vessel itself. As the intimal growth increases, the blood supply is cut off. The inevitable result is softening of the portion farthest from the lumen of the vessel. As a rule there has been a sufficient growth of connective tissue in the media and adventitia to repair the damage done to the media. This softening and dissolution gives rise to a granular debris composed of degenerated cells and fat. This is the so-called atheromatous abscess. There are no leucocytes as in ordinary pus. These "abscesses" are frequent and in rupturing leave open ulcers with smooth bases, the atheromatous ulcer. A further change which often takes place is calcification of the bases of the ulcers and calcification of the softened spots before rupture takes place. This only occurs in advanced cases. (See Fig. 3.)
Fig. 3.—Arteriosclerosis of the thoracic and abdominal aorta, showing irregular nodules, atheromatous plaques, denudation of the intima, thin plates of bone scattered throughout with spicules extending into the lumen of the vessel. Note the contraction of the openings of the large branches, the rough appearance of the aorta and the greater degree of sclerosis of the upper two-thirds, i. e., of the aorta above the diaphragm. This aorta in the recent state was much thickened and almost inelastic.
Fig. 4.—Arteriosclerosis of the arch of the aorta. Numerous calcified plaques, thickening and curling of the aortic valves, giving rise to insufficiency of the aortic valves. The aortic ring is rigid and not much dilated. (Milwaukee County Hospital.)
Fig. 5.—Normal aorta. Compare with Fig. 3. Note the perfectly smooth, glossy appearance of the intima. The openings of all the intercostal arteries are distinctly seen. In the recent state this artery was highly elastic, capable of much stretching both transversely and longitudinally.
Rather contrary to what one would expect, there are no new capillaries advancing from the media to the intima in the nodular form of arteriosclerosis, consequently there is no granulation tissue to heal and leave scars. It must be borne in mind that these changes rarely, if ever, are the only ones found throughout the arterial system. Nevertheless, the manifold changes, as will be shown within, appear to be but stages of one primary process.
The character of the changes which are known as diffuse arteriosclerosis seems to have, at first sight, little in common with those of the nodular sclerosis. The aorta may or may not have plaques of nodular sclerosis, while the arteries, such as the radial or temporal, may be beaded or pipe stem in hardness. In spite of these far advanced peripheral lesions the aorta may appear smooth but it is markedly dilated, particularly the thoracic portion, it is noticeably thinned even on macroscopic examination, it has elongated as evidenced by its slight tortuosity, and it has lost the greater part of its elasticity. The abdominal aorta is not so extensively affected, although this, too, shows some elongation and slight thinning. This is considered by some pathologists to be the uncomplicated form of the so-called senile arteriosclerosis. It is more of the nature of a degenerative change, it is true, but, as will be shown later, it has its beginnings, at times, in comparatively young persons and its etiology is not simple. This type has been studied most carefully by Moenckeberg, who showed that on the large branches of the aorta there were depressions due to a degeneration of the middle coat. These depressions encircled the vessel to a greater or lesser extent, causing small bulgings at such places and giving to the vessel a beaded appearance. On viewing such an artery held to the light, the sacculated spots are seen to be much thinner than the contiguous normal artery. Associated with such changes in the aorta and large branches is marked sclerosis of the smaller arteries. Intimal fibrosis is common, together with hypertrophy and fibrosis of the middle coat. Not infrequently periarterial thickening is also seen. Calcification of the media is found and is said to be preceded by hypertrophy of the middle coat.
Pure cases of this, the so-called Moenckeberg type, are seen but seldom. Most commonly there are nodules and plaques in the aorta and large branches together with thinning and sacculation of other portions of the vessels' walls. While the two processes appear at a glance to be so different from each other, it is possible for them to have a common origin. The initial lesion is in the media but the resulting sclerotic changes depend upon the kind of vessel, the strength of the coats, the pressure in the vessel, and other causes.
Thus the sclerosis of the radials of such an extent that these arteries are easily palpable, appears to be a different process from that of the sclerosis in the aorta, yet fundamentally it is the same. The difference lies in the anatomic structure of the two vessels, and possibly also in the degree of stretching and strain to which the vessels are subjected at every heart beat. In the radial artery the media as usual is affected first. The muscle cells undergo degeneration and either marked thickening takes place or sacculation results, depending upon the severity of the exciting cause. Calcification of the media is common. This occasionally takes the form of rings encircling the vessel, and gives to the examining finger the sensation of feeling a string of fine beads. There may be calcification of the subintimal tissue without deposits of lime salts in the media, but this is more commonly found in the larger arteries. When the calcification occurs in plates through the media, the well known pipe stem vessel is produced. (Fig. 6.)
Fig. 6.—Radiogram of a man aged seventy-five, showing calcification of both radial and ulnar arteries.
The senile sclerosis found in old people is usually a combination of the Moenckeberg type in the large and medium-sized arteries, and the nodular type in the aorta, leading eventually to calcareous intimal deposits, and widened, elongated, inelastic aorta.
Syphilitic Aortitis
Fig. 7.—Syphilitic aortitis of long standing. The aortic valves are curled and thickened, the heart is enlarged and the cavity of the left ventricle is dilated. (Milwaukee County Hospital.)
The seat of election of the syphilitic poison is in the aorta just above the aortic valves, Fig. 7, and in the ascending portion of the arch. There are semitranslucent, hyaline-like plaques which have a tendency to form into groups and, instead of undergoing an atheromatous change as in the ordinary nodular form of arteriosclerosis, they are prone to scar formation with puckering, so that macroscopically the nature of the process may, as a rule, be readily diagnosed. Microscopically the process is found to be a subacute inflammation of the media, which has been called a mesaortitis. There is marked small celled infiltration around some of the branches of the vasa vasorum and there appears to be actual absorption of the tissue elements of the middle coat. This is accompanied by hypertrophy of the intimal tissue. There follows degeneration in the deeper portions of this new tissue and new capillaries are formed which have their origin in the inflammatory area in the media. As is everywhere the case throughout the body, granulation tissue in the process of healing contracts and forms scars. This explains the scar formation in the aorta. When the process is more acute, instead of there being a reparative attempt on the part of the intima, there is actual stretching of the wall at the weakened spot and there results an aneurysmal dilatation. Spirochetæ pallidæ have been found in the degenerated media and in small gummata which were situated beneath the intima. Within the past years it has been found that a large percentage of patients with cardiovascular disease give the Wassermann reaction. In cases of aortic insufficiency, the reaction is present in almost every case. This is in marked contrast to the cases of diffuse endocarditis where the reaction is rarely present.
According to Adami the effects of syphilis upon the aorta are the following: (1) the primary disturbance is a granulomatous, inflammatory degeneration of the media; (2) this leads to a local giving way of the aorta; (3) if this be moderate it results in a strain hypertrophy of the intima and of the adventitia, with the development of a nodose intimal sclerosis; (4) if it be extreme, there results, on the contrary, an overstrain atrophy of the intima and aneurysm formation; (5) the intimal nodosities are here not of an inflammatory type and are nonvascular, although, with the progressive laying down of layer upon layer of connective tissue on the more intimal aspect of the intima, the earlier and deeper-placed layers of new tissue gain less and less nourishment, and so are liable to exhibit fatty degeneration and necrosis; (6) these products of necrosis exert a chemotactic influence upon the nearby vessels of the medial granulation tissue, with, as a result, (a) a secondary and late entrance of new vessels into the early and deeply-placed atheromatous area, (b) absorption of the necrotic products, (c) replacement by granulation tissue, (d) contraction of the granulation tissue, and (e) depression and scarring of the sclerotic nodules so characteristic of syphilitic sclerosis.
In the smaller arteries and arterioles the arteriosclerotic process appears on superficial examination to be a different process from that in the aorta and large arteries, but the difference is only apparent. It will be recalled that there is relatively much more muscle tissue in the arterioles than in the large arteries. The size, of course, is much less. Large nodular plaques are not possible. The atheromatous degeneration is not marked. In the smaller muscular arteries is seen the intimal proliferation, the stretching of the Moenckeberg type, and the calcification of the media rather than the intima. The media is thinned beneath the marked intimal proliferation so that the artery exhibits translucent areas when held to the light. Again, there is seen degeneration of the muscle and replacement by connective tissue with or without hypertrophy of the intima. In the arterioles three kinds of changes occur: a muscular hypertrophy; a fibrosis of all the coats; or a marked proliferation of the intimal endothelium. The last two are probably the same process, the connective tissue having its origin in the proliferated endothelial cells. Such a deposition of layer upon layer of cells in an arteriole and the resulting fibrosis leads to the condition of disappearance of the lumen of the vessel, endarteritis obliterans. This obliterating endarteritis is not, of course, due alone to syphilis. Syphilis is only a type of poison which produces such changes as have been described above. It is in the organs such as the kidney, liver, spleen, and intestines that one sees the most perfect examples of this obliterating endarteritis. Endarteritis deformans is a term applied to the condition of the arteries as a result of irregular thickenings and deposits of lime salts in the walls. These changes give rise to marked tortuosity of the vessels.
Occasionally such an obliterating process takes place in a larger artery. A thrombus forms and by a process of central softening, new channels permeate the thrombus, thus restoring to some extent the function of the vessel.
That the same process leads at one time to thinning and at another time to thickening of the arterial walls has been noted above. Prof. Adami holds that the regular development of layer upon layer of new connective tissue is non-inflammatory. He calls it a "strain hypertrophy." It is analogous to the localized hypertrophy of bone where the muscle tendons are attached, as is so frequently seen in athletes. The increased tension on connective tissue, provided that it is not overstrained, leads to its overgrowth, but only when there is sufficient nourishment. Such conditions are adequately fulfilled in the arteries. When a local giving way under pressure occurs in the media, the intima is put on the stretch (see Fig. 8), and there results a hypertrophy of the intima until the volume of the new tissue and the resistance which this affords to the mean distending force, balances the loss sustained by the weakened media. When the balance is struck, the hypertrophy is arrested. The youngest tissue is thus found directly beneath the endothelium. Now should this local weakening of the media have an acute origin, instead of a stimulus to growth there is overstrain, and there is, in consequence, not hypertrophy but atrophy. The beginning process is here a mesaortitis, but the acuteness of the poison, and the pressure from within the artery so stretches the artery that there is no compensatory hypertrophy, but a thinning, and the ground is prepared for aneurysmal dilatation or pouching.
Fig. 8.—I, media weakened at M' with overgrowth of intima filling in the depression. II, with postmortem rigor and contraction of the muscles of the media and removal of the blood pressure from within, the stretched media at M'' contracts; the intimal thickening thus projects into the arterial lumen. (After Adami.)
Again, one not infrequently encounters intimal nodosities when the underlying media appears of normal thickness. The explanation of this apparent exception is that the media in the living aorta is actually thinned, but the layers of subintimal tissue deposited over the weak spot due to strain hypertrophy become bulged inward when the pressure is relieved, as at postmortem. The media has not lost all of its elasticity (see Fig. 9), hence it contracts and there is the appearance of a nodule on the intima beneath which is a media equal in thickness to that of the healthy surrounding media.
Fig. 9.—Schematic representation of the increased strain brought to bear upon the cells of the intima, Int., when the media, Med., undergoes a localized expansion through relative weakness. (After Adami.)
The essential lesion in arteriosclerosis of the aorta and large arteries is a degeneration in the middle coat. This may be brought about by a variety of poisons circulating in the body. In syphilis, for example, the initial lesion has been shown to be a mesaortitis. The media seems to be dissolved, the artery is consequently thinned, there is actual depression along the level of the vessel. The elastic fibers disappear and small-celled infiltration takes its place. The intima hypertrophies, layer upon layer being added in an attempt to restore the strength of the vessel. There is also, as a rule, rather pronounced hypertrophy of the adventitia.
Experimental Arteriosclerosis
Within the past few years many workers have attempted by various means, to produce arterial lesions in animals, chiefly rabbits and dogs. The present status is somewhat chaotic, some affirming and some denying that arterial changes follow the various methods employed. Following the injection of small, repeated doses of adrenalin over a certain period of time, changes occur in the arteries of rabbits which are arteriosclerotic in type, the essential lesion being a degeneration of the muscular and elastic tissue of the media with the consequent production of aneurysm in the vessel. This is said by some to be quite like the type of arteriosclerosis in man which has been so well described by Moenckeberg. The degenerations in the arteries following the experimental lesions are of the nature of a fatty metamorphosis, and later proceed to calcification. Barium chloride, digitalin, physostigmin, nicotin and other substances, as well as adrenalin, have been found to exert a selective toxic action on the muscle cells of the middle coat of the aorta. The infundibular portion of the pituitary body, the portion which is developed from the infundibulum of the brain, possesses an internal secretion, which, injected intravenously, causes a marked rise of blood pressure and slowing of the heart beat. So far as I know, this active principle of the gland has not been used in an attempt to produce experimentally the lesions of arteriosclerosis.
Wacker and Hueck succeeded in producing aortic disease in rabbits which they considered to be in many points quite like human arteriosclerosis. They injected the rabbits intravenously with cholesterin. They feel that this is of great importance in view of the fact that exercise (muscle metabolism) dyspnea, certain poisons, as well as adrenalin, and even adrenal extirpation occasion a high cholesterin content of the blood. Anitschow's experiments are confirmatory. He fed rabbits on large amounts of cholesterin-containing substances (yolk of egg, brain tissue) and pure cholesterin and found changes in the intima and inner portion of the media consisting of fatty infiltration between the muscle and elastic fibres, advent of small round cells and large phagocytic cells containing fat droplets of cholesterin esters. The elastic fibres were dissolved, broken up into fibrillæ and these seemed to be absorbed. The internal elastic lamina as such disappeared and the inner layer of the aorta fused with the middle coat. He considers these changes to be quite analogous to those found in human aortas.
Oswald Loeb produced changes in the arteries of rabbits by feeding them sodium lactate (lactic acid). His controls fed on other acids became cachectic, but showed no arterial changes. He further found that in 100 gm. of human blood there was normally from 15 to 30 mg. of lactic acid. After heavy work, he found as much as 150 gm. He considers that after adrenalin or nicotin injections, the function of the liver is so disturbed that lactic acid is not bound. The arteriosclerosis is actually due to the presence of free lactic acid in the circulation. He succeeded, also, in producing lesions of the intima in a dog fed for a long time on protein poor diet, plus lactic acid and sodium lactate.
Another investigator, Steinbiss, fed rabbits on animal proteins only, a diet totally foreign to their natural habits. He succeeded, however, in keeping some alive for three months. He also tried various substances and in the general conclusions says that no aortic changes could be produced in animals kept in natural living conditions by any mechanical means, increase of blood pressure, digital compression, hanging by hind legs, etc. In infectious diseases, especially septic, widespread sclerotic changes occurred in the aorta. A most suggestive conclusion in this "the most important result of feeding rabbits with animal proteins is, along with a constant glycosuria, disease of the aorta and peripheral arteries which is identical with changes in the aorta produced by injections of adrenalin. The degree of disease of the circulatory system increases with the duration of the experiment."
By a small addition of vegetable to the protein diet, the lives of the animals were prolonged at will. With this modification of the experiment, the findings in the vessel walls were noticeably altered. The changes affected chiefly the intima, to less degree the media, and histologically were very much like human intimal disease.
I have been unable to produce the slightest arterial lesions in rabbits by intravenous injections of lead. Frothingham had no success feeding animals with lead. In a study of autopsy material from persons up to 40 years, who died of infectious disease, he found changes in the arteries of those who had succumbed to infection with the pus cocci or to very severe infectious disease. These changes were, however, localized, and were not like those of the general diffuse arteriosclerosis.
Adler has recently reported experiments on dogs, to which he fed or injected intravenously various substances supposed to induce arteriosclerotic changes. He was unable to find any arterial lesions comparable to human arteriosclerosis.
The difficulty experienced by experimenters is not surprising when the character of the changes is considered. Arteriosclerosis is not an acute process. In its very nature, it is of months' or years' standing, the specific changes are of slow growth, and more in the nature of degeneration. It would seem that a very careful study of the histories of those with arteriosclerosis and a final examination upon the actual tissue might eventually give us data for the etiology.
The most frequent site of disease in these experimental lesions is the thoracic aorta, and it is there also that the most severe changes are seen. While the toxic action is felt in the vessels all over the body, the lesions are, as a rule, scattered and small. The thoracic aorta stands the brunt of the high pressure, and this combined with the poisonous action of the drug or drugs, results in the formation of a fusiform aneurysmal dilatation which stops at the diaphragmatic opening. The aortic opening in the diaphragm seems to act as a flood gate, allowing only a certain amount of blood to flow through, and thus the abdominal aorta is protected to a great extent from the deleterious effects of increased pressure. Focal degenerative lesions are, however, found in the abdominal aorta.
Changes somewhat analogous to those found in the human aorta as the result of intimal proliferations, are produced in animals by the toxins of the typhoid bacillus and the Streptococcus pyogenes. Clinically, Thayer and Brush have found that the arteries of those who have recovered from an attack of typhoid fever are more palpable than the arteries of average individuals of equal age who have never had the disease.
Experimentally, the changes caused by the toxins above noted are proliferations of cells in the intima and subintimal tissues, and a breaking up of the internal elastic laminæ into several parallel layers which stretch themselves among the proliferating cells. The diphtheria toxin, on the contrary, produces a lesion more like that caused by adrenalin. All pathologists are not agreed as to whether the experimental lesions produced by blood pressure raising drugs are similar to the arteriosclerotic changes in the arteries of man.
Some of the work on rabbits has been discredited for the reason that arteriosclerosis appears spontaneously in about fifteen per cent of all laboratory rabbits. Furthermore, comparatively young rabbits have been found with arteriosclerosis. O. Loeb, however, denies this. He has examined in the course of eight years 483 healthy rabbits and never found arterial changes. The spontaneous lesions can not be distinguished histologically from those due to adrenalin. They differ macroscopically in that the lesion is usually limited to a few foci near the origin of the aorta.
Lesions produced by the drugs enumerated above represent one type of experimental arteriosclerosis. More interesting and important are the experiments which seem to show that high tension alone is capable of producing lesions in arteries which in all respects correspond to Adami's strain hypertrophy and overstrain theory. It has been shown that when a portion of vein is placed under conditions of high arterial pressure, as in a transplantation of a portion of vein into a carotid artery, the vein undergoes marked connective tissue hypertrophy which includes all the coats. This is evidently strain hypertrophy. Again, it has been demonstrated that by suspending a previously healthy rabbit by the hind legs for three minutes daily over a period of three to four months, there results hypertrophy of the heart with thinning and dilatation of the arch and the upper part of the thoracic aorta. No change was found in the abdominal aorta. The carotids, however, were larger than normal and they showed typical intimal sclerosis with connective tissue thickening.
Neither I nor others have been able to confirm this experiment, so it is very doubtful whether mechanical pressure alone can produce true arteriosclerosis. Some evidence is adduced to bear on this point, however, in the fact that sclerosis of the pulmonary artery follows often upon mitral stenosis. Yet we do not know but that factors other than pressure alone produce the arteriosclerotic change in such cases, so we are forced back on our conclusion expressed above; viz., that experiments on animals fail to sustain the purely mechanical origin of arteriosclerosis.
The changes in the intima constitute the effort on the part of nature to repair a defect in the vessel wall which is to compensate for the weakened media and the widened lumen. This applies only to true arteriosclerosis, not to the condition produced experimentally by the toxin of the typhoid bacillus, for example.
When an artery loses its elasticity and begins to have connective tissue deposited in its walls, the pressure of the blood stretches the vessel which is now no longer capable of retracting when the pulse wave has passed, and, in consequence, the artery is actually lengthened. This necessarily causes a tortuosity of the vessel which can be easily seen in such arteries as the temporals, brachials, radials, and other arteries near the surface of the skin.
The exact mechanism of increase of blood pressure is not satisfactorily explained. The smaller arteries all over the body are supplied with vasoconstrictor and vasodilator nerve fibers from the sympathetic nervous system. Normally when an organ is actively functionating the vessels are widely dilated and the flow of blood is rapid. Among the many factors which influence blood pressure and blood supply must be reckoned the psychic.
We know that normally there is a certain resistance offered to the propulsion of blood through the arteries by the contraction of the heart. This tonus is essential to the maintenance of an equalized circulation. The muscular arterioles throughout the body by their tonus serve to keep up the normal blood pressure and to distribute the blood evenly to the various organs. Contraction of a large area of arterioles increases the blood pressure and, strangely enough, the arteries respond to increased arterial pressure, not by dilatation, but by contraction. It would appear that rise of blood pressure tends to throw increased work upon the musculature of the arterioles. This may be sufficient only to cause them to hypertrophy, but further strain may easily lead to exhaustion and to dilatation. "As a result strain hypertrophy of the intima shows itself with thickening, and it may also be of the adventitia, resulting in chronic periarteritis. And now with continued degeneration of the medial muscle in those muscular arteries, fibrosis of the media may also show itself. I would thus regard muscular hypertrophy of the arteries and fibrosis of the different coats as different stages in one and the same process. Whether these peripheral changes are the more marked, or the central, depends upon the relative resisting power of the elastic and muscular arteries of the individual respectively." (Adami.)
Fig. 10.—Cross-section of a small artery in the mesentery. Note that the vessel appears capable of being much widened. The internal elastic lamina is thrown into folds somewhat resembling the convolutions of the brain. Note also that the middle coat of the artery is composed almost entirely of muscle. The enormous number of such vessels in the mesentery and intestines explains the ability of the splanchnic area to accommodate the greater part of the blood in the body. Universal constriction of these vessels would naturally render the intestines anemic. The vasomotor control of these vessels plays an important rôle in the distribution of the blood. Small arteries in the skin and in other organs, possibly the brain, have a similar function. (Microphotograph, highly magnified.)
It is conceivable that in one section of the body the vessels may be markedly contracted, but if there is dilatation in some other part there will be no increased work on the part of the heart, and theoretically, there should be no rise of blood pressure. The vascular system, however, while likened to a system of rubber tubes, must be regarded as a very live system, every subsystem having the property of separate control.
For blood tension to be raised all over the body, conditions must favor the generalized contraction of a large area of arterioles. Some authors consider that the so-called viscosity of the blood also is a factor in the causation of increased tension. The usual cause for the high tension is probably the presence in the blood of some poisonous substance.
It is held by some authors that the great splanchnic area is capable of holding all the blood in the body and in respect of its liability to arteriosclerosis, it is second only to the aorta and coronary arteries. The enormous area of the skin vessels could probably contain most of the blood. The tone of the vasoconstrictor center controls the distribution of blood throughout the body. The fact that the vessels in the splanchnic area are frequently attacked by sclerotic changes means, as a rule, increase of work for the heart.[1] The resistance offered to the passage of the blood must be great and signifies that, for blood to travel at the same rate that it did before the resistance set in, more power must be expended in its propulsion. In other words, the heart must gradually become accustomed to the changed conditions, and, as a result of increased work, the muscle hypertrophies. (See Fig. 11.)
Fig. 11.—Enormous hypertrophy of left ventricle probably due to prolonged increased peripheral resistance. Note that the whole anterior surface of the heart is occupied by the left ventricle. The right ventricle does not appear to be much affected. × ⅔.
In diffuse arteriosclerosis accompanied by chronic nephritis the heart is always hypertrophied. This is a result, not a cause of the condition. In the pure type, there is hypertrophy only of the left ventricle without dilatation of the chamber. The muscle fibers are increased in number and in size, and there are frequently areas of fibrous myocarditis due to necrosis caused by insufficient nutrition of parts of the muscle. In these cases the coronary arteries share in the generalized arteriosclerotic process. The openings of the arteries behind the semilunar valves may be very small. There is often thickening and puckering of the aortic valves and of the anterior leaflet of the mitral valve leading, at times, to actual insufficiency of the orifice. Later, when the heart begins to weaken, there is dilatation of the chambers and loud murmurs result, caused by the inability of the nondistensible valves to close the dilated orifices. Until the compensation is established, it is impossible to say whether or not true insufficiency is present.
In senile arteriosclerosis there is the physiologic atrophy of the media to be reckoned with. This change has already been referred to. When such degeneration has taken place, the normal blood pressure may be sufficient to cause stretching of the already weakened media with or without hypertrophy of the intima. The arteries may be so lined with deposits of calcareous matter that they appear as pipe stems. More frequently there are rings of calcified material placed closely together or irregular beading, giving to the palpating finger the impression of feeling a string of very fine beads. The arteries are often tortuous, hard, and are absolutely nondistensible. At times no pulse wave can be felt.
The larger arteries such as the brachials and femorals are most affected. The walls become thinned and show cracks, and areas apparently, but not actually denuded of intima. Yellowish-white, irregular, raised plaques are scattered here and there. Interspersed among these areas are irregularly shaped clean-cut ulcers having as a rule a smooth base, and frequently on the base is a thin plate of calcified matter. The color of these denuded areas is usually brownish red or reddish brown. White thrombi may be deposited on these areas. The danger of an embolus plugging one of the smaller arteries is great and probably happens more often than we think. The collateral circulation is able to supply the thrombosed area. Should the thrombus be on the carotid arteries, hemiplegia may result from cerebral embolism. On microscopic examination of the arteries there is seen extreme degeneration of all the coats, the degeneration of the media leading almost to an obliteration of that coat. On seeing such arteries as these one wonders how the circulation could have been maintained and the organs nourished. Senile atrophy of the internal organs naturally goes hand in hand with such arterial changes.
There is, as a rule, no increase in arterial tension; on the contrary, the pressure is apt to be low. This is readily understood when the heart is seen. This organ is small, the muscle is much thinned, it is flabby and of a brownish tint, the so-called "brown atrophy." Microscopically, there is seen to be much fragmentation of the fibers with a marked increase of the brown pigment granules which surround the cell nuclei. Cases are seen, however, in which blood pressure increases as the patient grows older. The hearts in such cases are more or less hypertrophied and show extensive areas of fibroid myocarditis.
From what has been said, it follows that hypertension alone may be the cause of arteriosclerosis; that certain poisons in the blood which attack the media and cause it to degenerate and weaken cause arteriosclerosis without increased blood pressure; that the normal blood pressure may be, for the artery which is physiologically weakened in an individual over fifty, really hypertension, and arteriosclerosis may result. Our observations lead us to believe that the process is at bottom one and the same. The different types noted clinically depend upon the nature of the etiologic factors and the kind of arterial tissue with which the individual is endowed. This view at least brings some order out of previous chaos, and corresponds well with our present knowledge of the disease.
There are many cases of arteriosclerosis which lead to definite interference with the closure of the valves of the heart, particularly the aortic and the mitral. It has been said that puckerings of the valves frequently occur (Fig. 12). This arteriosclerotic endocarditis at times leads to very definite heart lesions, chiefly aortic or mitral insufficiency, or both with, at times, murmurs of a stenotic character at the base. There is rarely true aortic stenosis, however. The murmur is caused by the passage of the blood over the roughened valves and into the dilated aorta. Aortic stenosis is one of the rarest of the valvular lesions affecting the valves of the left heart, and should be diagnosed only when all factors, including the typical pulse tracings, are taken into consideration.
Fig. 12.—Aortic incompetence with hypertrophy and dilatation of left ventricle, the result of arteriosclerosis affecting the aortic valves. Note how the valves have been curled, thickened, and shortened, the edges of valves being a half inch below the upper points of attachment. The anterior coronary artery is shown, the lumen narrowed. (Reduced one-half.)
The kidneys, as a rule, show extensive sclerosis. They are small, firm, and contracted and not always to be differentiated from the contracted kidneys of chronic inflammation. The lesions of the arteriosclerotic kidney are due to narrowing and eventual obstruction of the afferent vessels. The organs are usually bright red or grayish red in color. At times there is marked fatty degeneration of cortex and medulla, giving to them a yellowish streaking. The capsule is here and there adherent, the cortex is much thinned and irregular. The surface presents a roughly granular appearance. The glomeruli stand out as whitish dots and the sclerosed arteries are easily recognized, as their walls are much thickened. The process does not, as a rule, affect the whole kidney equally, but rather affects those portions corresponding to the interlobular arteries. The replacement of the normal kidney tissue by connective tissue and the resulting contraction of this latter tissue leads to the formation of scars. As the process is not regular, the scarring is deeper in some places than in others, with the result that localized rather sharply depressed areas appear on the surface. The pelvis is relatively large and is filled with fat. The renal artery is often markedly sclerosed and the whole process may be due to localized thickening of the artery, or as part of a general arteriosclerosis. The latter is the more frequent. Microscopically, it is seen that the tubules are atrophied, the Bowman's capsules are, as a rule, thickened, and the glomeruli are shrunken or have been replaced by fibrous tissue. In places they have fallen out of the section. There is marked proliferation of connective tissue in cortex and medulla. The arterioles are thickened, the sclerosis being either of the intima or media or of both. There is even occlusion of many arterioles.
Changes in other organs as the result of arteriosclerosis of their afferent vessels occur, but are not so characteristic as in the kidney. In the brain the result of gradual thickening of the arterioles is a diminished blood supply, softening of the portion supplied by the artery, and later a connective tissue deposit. The occurrence of thrombi is favored and, now and again, a thrombus plugs an artery which supplies an important and even vital part of the brain. The arteries of the brain are end arteries, hence there is no chance for collateral circulation. It is therefore evident how serious a result may follow the disturbance in or actual deprivation of blood supply to any of the brain centers or to the internal capsule.
Arteriosclerosis of the Pulmonary Arteries
There have been a number of cases of sclerosis of the pulmonary arteries, either alone, or associated with general systemic arteriosclerosis.
A primary and a secondary form are recognized, the former in conjunction with congenital malformations of the heart, the latter as the result of severe infection or of mitral stenosis. These two causes seem to be the most important in the production of the arterial changes. The cases thus far described have revealed widespread thickening of the pulmonary arteries. If one may judge by the description of the pathologic changes, the condition is quite similar to that produced in a vein by transplantation along the course of an artery. The diffuse form with connective tissue thickening of all coats has been generally described. There is also obliterating endarteritis of the smaller vessels. In the etiology of the condition severe infection seems to play a prominent rôle. The constant presence of right ventricular hypertrophy is interesting, the heart dullness extends, as a rule, far to the right of the sternum. In some of the cases no demonstrable changes were observed in the bronchial arteries or in the pulmonary veins.
Sanders has described a case of primary pulmonary arteriosclerosis with hypertrophy of the right ventricle.
Recently Warthin[2] has reported a case of syphilitic sclerosis of the pulmonary artery which places the lesion in exactly the same category as that of syphilis in the systemic arteries. There was also aneurysm of the left upper division present and, to settle the etiologic nature of the process, Spirochete pallida were found in the wall of the aneurysm sac and in that of the pulmonary artery. The microscopic picture in the pulmonary artery could not be told from that in a syphilitic aorta.
Sclerosis of the Veins
Phlebosclerosis not infrequently occurs with arteriosclerosis. It is seen in those cases characterized by high blood pressure. Such increased pressure in the veins is due, for example, to cirrhosis of the liver which affects the portal circulation, or to mitral stenosis which affects the pulmonary veins. The affected vessels are usually dilated. The intima shows compensatory thickening especially where the media is thinned. As a rule all the coats are involved in the connective tissue thickening. Occasionally hyaline degeneration or calcification of the new-formed tissue is seen. "Without existing arteriosclerosis the peripheral veins may be sclerotic usually in conditions of debility, but not infrequently in young persons." (Osler.)
In many cases of arteriosclerosis, the pathologic changes are not confined to the arteries, but are found in the veins as well as in the capillaries. Such cases could be called angiosclerosis.
CHAPTER III.
PHYSIOLOGY OF THE CIRCULATION
No attempt will be made to cover the entire subject of the physiology of the circulation. Only in so far as it relates to arteriosclerosis and blood pressure and has a bearing on the probable explanation of blood pressure phenomena will it be discussed.
"The heart and the blood vessels form a closed vascular system, containing a certain amount of blood. This blood is kept in endless circulation mainly by the force of the muscular contractions of the heart; but the bed through which it flows varies greatly in width at different parts of the circuit, and the resistance offered to the moving blood is very much greater in the capillaries than in the large vessels. It follows, from the irregularities in size of the channels through which it flows, that the blood stream is not uniform in character throughout the entire circuit—indeed, just the opposite is true. From point to point in the branching system of vessels the blood varies in regard to its velocity, its head of pressure, etc. These variations are connected in part with the fixed structure of the system and in part are dependent upon the changing properties of the living matter of which the system is composed." (W. H. Howell.)
If the vascular system were composed of a central pump, projecting at every stroke a given amount of liquid into a series of rigid tubes, the aggregate cross sections of which were equal to the cross section of the main pipe, then the velocity at the openings would be the same as at the source (making allowances for friction). The problem would then be a simple one. In the circulation of the blood no such simple condition obtains. The capillary beds is an enormous area through which the blood flows slowly. From the time the blood is thrown into the aorta the velocity begins to diminish until it reaches its minimum in the capillaries. In no two persons is the initial velocity at the heart the same, nor in the same person is it the same at all times of day. The size of the heart, the actual strength of the muscle, the amount of blood ejected at every beat, and the size and elasticity of the aorta are some of the factors which determine the velocity of blood at the aortic orifice. When to these factors are added the differences in arterial tissue, the activity or resting stage of the various organs, etc., the question becomes exceedingly complicated. In spite of these many disturbing elements, attempts more or less successful have been made to estimate the velocity of the blood in animals. Thus, in the carotid of the horse the velocity was found to be 300 mm. per second (Volkman) and 297 mm. (Chauveau); in the carotid of the dog, 260 mm. (Vierordt). In the jugular vein of the dog Vierordt found the velocity to be 225 mm. per second. These figures do not represent the actual velocity of the blood in all horses or all dogs, but they do give us some general idea of the rate of flow of the blood. For man it has been calculated that the velocity in the aorta is about 320 mm. per second. The velocity is not uniform in the large arteries, where at every heart beat there is a sudden increase followed by a decrease as the heart goes into diastole. The farther away from the heart the measurements are made the more even is the flow.
Observations by W. H. Luedde with the Zeiss binocular corneal microscope on the rate of flow in the conjunctival capillaries must modify somewhat our former conceptions. He finds that "The rate varies in the different arteries, capillaries, and veins from a barely perceptible motion to a little more than 1 mm. per second. Further, some parts of the capillary network are ordinarily supplied with blood elements only occasionally. This is shown by the passage of a column of corpuscles along a certain line, followed after an interval of seconds, during which no corpuscles pass, by another column in the same line as before."
The vessels of the conjunctiva probably are quite like superficial vessels in the skin and mucous membranes. Therefore, we must be free to admit that the circulation in them is not absolutely steady. Luedde found further that in syphilitics there were tortuosities, irregularities, minute aneurysmal dilatations and even obliterations of capillaries. Some of the changes occurred as early as one month after infection.
The rate in the capillaries of man is estimated to be between 0.5 mm. and 0.9 mm. per second. As the blood is collected into the veins and the bed becomes smaller, the velocity increases until at the heart it is almost the same as in the aorta. That the velocity could not be exactly the same is evident from the fact that the cross section of the veins, which return the blood to the right auricle, is greater than is the cross section of the aorta.
The volume of the bed is subject to rapid and wide fluctuations, which are dependent on many causes, both physiologic and pathologic. The call of an actively functionating organ or group of organs causes a widening of a more or less extensive area, and the velocity necessarily varies. In states of great relaxation of the vessels there may be a capillary pulse. In order to force blood at the same rate through dilated vessels as through normal vessels, there must be more blood or there must be a more rapid contraction of the central pump. What actually happens, as a rule, is an increase in the rate of the heart beat. There are conditions—such, for example, as aortic insufficiency—where actually more blood is thrown into the circulation at every beat, so that the rate is not changed.
It has been calculated that the average amount of blood thrown into the aorta at every systole of the heart is from 50 to 100 c.c. This is forcibly ejected into a vessel already filled (apparently) with blood. In order to accommodate this sudden accession of fluid, the aorta must expand. The aortic valves close, and during diastole the blood is forced through the vascular system by the forcible, steady contraction of the highly elastic aorta. Other large vessels which branch from the aorta also have a part in this steady propulsion of blood. From seventy to eighty times a minute the aorta is normally forcibly expanded to accommodate the charge of the ventricle. It is not difficult to understand the great frequency of patches of sclerosis in the arch when these facts are borne in mind.
What relationship the viscosity of the blood has to the rate and volume of flow is not fully understood. As yet there is not much known about the subject, and no one has devised a satisfactory means of measuring the viscosity. It is thought by some that an increased viscosity assists in producing an increased amount of work for the heart.
Blood Pressure
Blood pressure is the expression used for a series of phenomena resulting from the action of the heart. As every heart beat is actual work done by the heart in overcoming resistance to the outflow of blood, this force is approximately measurable in a large artery such as the brachial. It has been determined that the pressure in the brachial artery is almost equal to the intraventricular pressure in the left ventricle. In animals it is easy to attach manometers to the carotid artery and to measure the blood pressure accurately. Formerly the method consisted in attaching a tube and allowing the blood to rise in the tube. The height to which the blood rose measured the maximum pressure. This is a crude method and has been replaced by the U-tube of mercury with connection made to the artery by saline or Ringer's solution. This apparatus is familiar to all physiologists.
In man the measurement is most conveniently made from the brachial artery. There is some difference in the pressure in the femoral and the brachial and some use both arteries. However, the difficulty of adjusting instruments to the upper leg, the great force which must be used to compress the femoral artery and the relative inaccessibility of the leg as compared to the arm, make the leg an inconvenient part for use in blood pressure determinations. It is not to be recommended.
Blood pressure is a valuable aid in diagnosis and of material help in many cases in prognosis, but it is not infallible neither can it be used alone to diagnose a case. Blood pressure is only one of many links in a chain of evidence leading to diagnosis. It has been badly used and much abused. It has been condemned unjustly when it did not furnish all the evidence. It has been made a fetish and worshipped by both doctors and patients. A sane conception of blood pressure must be widely disseminated lest we find it being discarded altogether.
Blood pressure consists of more than the estimation of the systolic pressure. The blood pressure picture consists of (1) the systolic pressure, (2) the diastolic pressure, (3) the pulse pressure which is the difference between the systolic and diastolic pressure, (4) the pulse rate. Expressed in the literature it should read thus: 120-80-40; 72. That tells the whole story in a brief, accurate form. This is recommended in history reporting. It must be ever kept in mind that a blood pressure reading represents the work of the heart at the moment when it was taken. Within a few minutes the pressure may vary up or down. There is no normal pressure as such, but an average pressure for any group of people of the same age living under similar conditions. The habit of speaking of any systolic figure as normal should be broken. A pressure picture may be normal but a systolic reading, whatever it may be, is not accurately designated as normal. This distinction is worth insisting upon.
Blood Pressure Instruments
There are several instruments which are in common use for the purpose of recording blood pressure in man.
Historically, the determination of blood pressure for man began with the attempt of K. Vierordt in 1855 to measure the blood pressure by placing weights on the radial pulse until this was obliterated. The first useful instrument, however, was devised by Marcy in 1876. He placed the hand in a closed vessel containing water connected by tubing with a bottle for raising the pressure and by another tube with a tambour and lever for recording the size of the pulse waves. He maintained that when pressure on the hand was made, the point where oscillations of the lever ceased was the maximal pressure, the point where the oscillations of the recording lever was largest, was the minimal pressure.
This pioneer work was practically forgotten for twenty-five years. It was not until 1887 that V. Basch devised an instrument which was used to some extent. This instrument recorded only maximum pressure. It consisted of a small rubber bulb filled with water communicating with a mercury manometer. The bulb was pressed on the radial artery until the pulse below it was obliterated and the pressure then read off on the column of mercury. V. Basch later substituted a spring manometer for the mercury column. Potain modified the apparatus by using air in the bulb with an aneroid barometer for recording the pressure. These instruments are necessarily grossly inaccurate. Moreover, they do not record the diastolic pressure.
In 1896 and 1897 further attempts were made to record blood pressure by the introduction of a flat rubber bag encased in some nonyielding material, which was placed around the upper arm. Riva-Rocci used silk, while Hill and Barnard used leather. The latter used a bulb or Davidson syringe to force air into the cuff around the arm and palpated the radial artery at the wrist, noting the point of return of the pulse after compression of the upper arm, and reading the pressure on a column of mercury in a tube.
Except that the width of the cuff has been increased from 5 cm. to 12 cm., this is the general principle upon which all the blood pressure instruments now in use are based. Most of the apparatuses make use of a column of mercury in a U-tube to record the millimeters of pressure. As the mercury is depressed in one arm to the same extent as it is raised in the other arm the scale where readings are made is .5 cm. and the divisions represent 2 mm. of mercury but are actually 1 mm. apart.
The cuff was made 12 cm. in diameter because it was shown (v. Recklinghausen) that with narrow cuffs much pressure was dissipated in squeezing the tissues. Janeway has shown that with the use of the 12 cm. cuff accurate values are obtained independently of the amount of muscle and fat around the brachial artery. In other words if an actual systolic blood pressure of 140 mm. is present in two individuals, the one with a thin arm, the other with a thick arm, the instrument will record these pressures the same where a 12 cm. arm band is used. We need have no fear of obtaining too high a reading when we are taking pressure in a stout or very muscular individual. Janeway also was the first to call attention to the fact that the diastolic or minimal pressure was at the point where the greatest oscillation of the mercury took place. This is difficult to estimate in many cases as the eye can not follow slight changes in the oscillation when the pressure in the cuff is gradually reduced. Practically this is the case in small pulses.
The Riva-Rocci instrument was modified by Cook. (See Fig. 13.) He used a glass bulb containing mercury into which a glass tube projected. The bulb was connected by outlet and tubing to the cuff and syringe. The glass tube was marked off in centimeters and millimeters and for convenience was jointed half way in its length. The instrument could be carried in a box of convenient size. This instrument is fragile and more cumbersome, although lighter in weight, than others and is very little used at present.
Fig. 13.—Cook's modification of Riva-Rocci's blood pressure instrument.
Stanton's instrument (Fig. 14) is practically Cook's made more rigid in every way but without the jointed tube. The cuff has a leather casing, the pressure bulb is of heavy rubber, the glass tube in which the mercury rises is fixed against a piece of flat metal and there are stopcocks in a metal chamber introduced between the bulb and mercury with which to regulate the in- and out-flow of air. The pressure can be gradually lowered conveniently without removing the pressure bulb.
Fig. 14.—Stanton's sphygmomanometer.
The most accurate mercury manometer is that of Erlanger. (Fig. 15.) The instrument is bulky and is not practicable for the physician in practice. The principle is that used by Riva-Rocci. There is an extra T-tube introduced between the manometer and air bulb connecting with a rubber bulb in a glass chamber. The oscillations of this are communicated to a Marey tambour and recorded on smoked paper revolving on a drum. There is a complicated valve which enables the operator to reduce the pressure with varying degrees of slowness. The mercury is placed in a U-tube with a scale alongside it. The instrument is expensive and not as easy to manipulate as its advocates would have us believe. Hirschfelder has added to the usefulness (as well as to the complexity) of the Erlanger instrument, by placing two recording tambours for the simultaneous registering of the carotid and venous pulses. In spite of its complexity and necessary bulkiness, very valuable data are obtained concerning the auricular contractions.
Fig. 15.—The Erlanger sphygmomanometer with the Hirschfelder attachments by means of which simultaneous tracings can be obtained from the brachial, carotid, and venous pulses.
One of the best of the mercury instruments is the Brown sphygmomanometer. In this (Fig. 16) the mercury is in a closed, all-glass tube so that it can not spill under any sort of manipulation. It is in this sense "fool-proof." The cuff, however, is poorly constructed. It is too short and there are strings to tie it around the arm. I have found that this causes undue pressure in a narrow circle and renders the reading inaccurate. In the clinic we use this mercury instrument with a long cuff like that provided by the Tycos instrument.
Fig. 16.—Desk model Baumanometer.
The Faught instrument (Fig. 17) is larger than the Brown, but is less easily broken and is not too cumbersome to carry around. The substitution of a metal air pump for the rubber makes the apparatus more durable.
Fig. 17.—The Faught blood pressure instrument. An excellent instrument which is quite easily carried about and is not easily broken.
The v. Recklinghausen instrument is not employed to any extent in this country. It is both expensive and cumbersome, and has no advantages over the other instruments.
Several other instruments have been devised and new ones are constantly being added to the already large list. With those employing mercury the principle is the same. The aim is to make an instrument which is easily carried, durable, and accurate.
In all the mercury instruments the diameter of the tube is 2 mm. One would suppose that there would be noticeable differences in the readings of the different mercury instruments depending upon the amount of mercury used in the tube. By actual weight there is from 35 to 45 gms. of mercury in the several instruments. After many trials, no noticeable differences in blood pressure readings can be made out between a column weighing 35 gm. and one weighing 45 gm.
There is, however, the inertia of the mercury to be overcome, friction between the tube and the mercury, and vapor tension. The mercury is therefore not as sensitive to rapid changes of pressure in the cuff as a lighter fluid would be. The mercury must be clean and the tube dry so that there is no more friction than what is inherent between the mercury and glass. In making readings on a rapid pulse the oscillations of the mercury column are apt to be irregular or to cease now and then, due to the fact that the downward oscillation coincides with a pulse wave, or an upward oscillation receives the impact of two pulse waves transmitted through the cuff. Instruments have been devised to obviate this difficulty, but they have not come into favor. They are usually too complicated and at present can not be recommended.
Fig. 18.—Rogers' "Tycos" dial sphygmomanometer.
An instrument devised by Dr. Rogers (the "Tycos") has met with considerable popularity. (Fig. 18.) This is not an instrument which operates with a spring and lever. The instrument is composed essentially of two metal discs carefully ground and attached at their circumferences to the metal casing below the dial. There is an air chamber between these discs through the center of which air is forced by the syringe bulb. When air is forced into the space between these two discs, they are forced apart to a very slight extent, with the highest pressures only 2-3 mm. of bulging occurs. From data gathered after extensive use for five years these discs were not found to have sprung. A lever attached to a cog which in turn is attached to the dial needle magnifies to an enormous extent the slightest expansion of the discs. Every dial is handmade and every division is actually determined by using a U. S. government mercury manometer of standard type. No two dials therefore are alike in the spacing of the divisions of the scale but every one is calibrated as an individual instrument. There is no doubt in the author's mind that for the general practitioner the instrument has some advantages over the mercury instruments. It reveals the slightest irregularity in force of the heart beat. The oscillation of the dial needle is more accurately followed by the eye than is that of the column of mercury. The needle passes directly over the divisions of the scale, while with usual mercury instruments the scale is an appreciable distance (sometimes .5 cm.) from the column of mercury at the side. (Fig. 19.) The diastolic pressure is more easily read on the "Tycos." It is where the maximum oscillation of the needle occurs as the pressure is slowly released from the cuff. Although it does not appear that this instrument, if properly made and standardized, could become inaccurate, nevertheless it is advisable to check it every few months against a known accurate mercury manometer instrument.
Fig. 19.—Detail of the dial in the "Tycos" instrument.
Fig. 20.—Faught dial instrument.
Fig. 21.—Detail of the dial of the Faught instrument.
Another perfectly satisfactory dial instrument is the Faught (Figs. 20 and 21). The general plan of this differs in some minor points from the "Tycos." I have compared the two and have found no difference in the readings. Both can be recommended.
Fig. 22.—The Sanborn instrument.
One or two other cheaper dial instruments are on the market. The Sanborn seems to be quite satisfactory. (Fig. 22.) It is cheaper than the other dial instruments. There is this much to be said, no instrument using a spring as resistance to measure pressure can be recommended.
Technic
The same technic applies to all the mercury instruments. The patient sits or lies down comfortably. The right or left arm is bared to the shoulder, the cuff is then slipped over the hand to the upper arm. (See Fig. 23.) At least an inch of bare arm should show between the lower end of the cuff and the bend of the elbow. The rubber is adjusted so that the actual pressure from the bag is against the inner side of the arm. The straps are tightened, care being taken not to compress the veins. The upper part of the cuff should fit more snugly than the lower part. The part of the instrument carrying the mercury column is now placed on a level surface; the two arms of the mercury in the tube must be even, and at 0 on the scale. With the fingers of one hand on the radial pulse, the bag is compressed until the pulse is no longer felt. (See Fig. 24.) One should raise the pressure from 10-12 mm. above this, and close the stopcock between the bulb and the mercury tube. In a good instrument the column should not fall. If it does there is a leak of air in the system of tubing and arm bag. Now with the finger on the pulse, or where the pulse was last felt, gradually allow air to escape by turning the stopcock so that the column of mercury falls about 2 mm. (one division on the scale) for every heart beat or two. One must not allow the column of mercury to descend too slowly as it is uncomfortable for the patient and introduces a psychic element of annoyance which affects the blood pressure. On the other hand, the pressure must not be released too rapidly, else one runs over the points of systolic and diastolic pressure and the readings are grossly inaccurate. It is impossible to say how rapidly the mercury must fall. Every operator must find that out for himself by practice. The first perceptible pulse wave felt beneath the palpating finger at the wrist, represents on the scale the systolic pressure. This can be seen to correspond to a sudden increase in the magnitude of the oscillation of the mercury column. The systolic pressure, thus obtained, is from 5-10 mm. lower than the real systolic pressure. The more sensitive the palpating finger, the more nearly does the systolic pressure reading approach that found by using such an instrument as Erlanger's, where the first pulse wave is magnified by the lever of the tambour.
Fig. 23.—Method of taking blood pressure with a patient in sitting position.
Fig. 24.—Method of taking blood pressure with patient lying down.
The pressure is now allowed to fall, until the palpating finger feels the largest possible pulse wave, which is coincident with the greatest oscillation of the mercury. This is the diastolic pressure. Beyond this point there is no oscillation of the mercury column. The difference between the two is the pulse pressure. Thus the pulse is felt after compression at 120 on the scale, and the maximum oscillation occurs at 80. The systolic pressure is 120 mm., the diastolic is 80 mm., and the pulse pressure is 40 mm.
With the "Tycos" or Faught the arm band is snugly wound around the arm, the bag next to the skin and the end tucked in, so that the whole band will not loosen when air is forced into the bag. The cuff is blown up until the pulse is no longer felt. One should raise the pressure not more than 10 mm. above the point of obliteration of the pulse. The valve is then carefully opened so that the needle gradually turns toward zero. At the first return of the pulse wave felt at the wrist, the needle is sure to give a sudden jump. This is the systolic pressure and is read off on the scale. The needle is now carefully watched until it shows the maximum oscillation. This is the diastolic pressure. The difference between the two is, as above, the pulse pressure.
In taking pressure one should take the average of several, three or four. Moreover, one must not take consecutive readings too quickly and one must be sure that between every two readings all the air is out of the cuff and that the mercury or dial is at zero. It has been repeatedly shown that in a cyanosed arm the systolic pressure is raised so that even slight cyanosis between readings must be carefully avoided.
The only accurate method of determining both the systolic and diastolic pressure, but especially the diastolic, is by the so-called auscultatory method. (See Fig. 25.) The cuff is adjusted in the usual way and one places the bell of a binaural stethoscope over the brachial artery from one to two centimeters below the lower edge of the cuff.[3] Care must be taken that the bell is not pressed too firmly against the arm and that the edge of the bell nearest the cuff is not pressed more firmly than the opposite end. For this purpose, one can not use the ordinary Bowles stethoscope or any of the other much lauded stethoscopes, because the surface of the bell is too large. The diameter of the bell must not be more than twenty-five millimeters, twenty is still better. It is advisable before beginning the observation to locate with the finger the pulse in the brachial artery just above the elbow, so that the stethoscope may be placed over the course of the artery. (Fig. 26.) The first wave which comes through is heard as a click, and occurs at a point on the manometer or dial scale from 5-10 mm. higher than can usually be palpated at the radial artery. This is the true systolic pressure. By keeping the bell of the stethoscope over the brachial artery while the pressure is falling, one comes to a point when all sound suddenly ceases. This is said to be the diastolic pressure. This is incorrect as will be shown later.
Fig. 25.—Observation by the auscultatory method and a mercury instrument. One hand regulates the stop cock which releases air gradually.
Fig. 26.—Observation by the auscultatory method and a dial instrument. The right hand holds the bulb and regulates the air valve.
Arterial Pressure
The arterial pressure in the large arteries undergoes extensive fluctuations with every heart beat. The maximum pressure produced by the systole of the left ventricle of the heart is known as the maximum or systolic pressure. It practically equals the intraventricular pressure. The minimum pressure in the artery, the pressure at the end of diastole, is called the diastolic pressure. The difference between the systolic and diastolic pressures is known as the pulse pressure. There is yet another term known as the mean pressure. For convenience, this may be said to be the arithmetical mean of the systolic and diastolic pressures. Actually, however, this can not be the case, owing to the form of the pulse wave, which is not a uniform rise and fall—the upstroke being a straight line, but the downstroke being broken usually by two notches. We do not make use of the mean pressure in recording results. It is of experimental interest and needs only to be mentioned here.
Fig. 27.—Schema to illustrate the gradual decrease in pressure from the heart to the vena cava: (a), arteries; (c), capillaries; (v), veins; (A), aorta, pressure 150 mm.; (B), brachial artery, pressure 130 mm.; (F), femoral vein, 20 mm.; (IVC), inferior vena cava, 3 mm. (Modified from Howell.)
It has been shown that the mean pressure is quite constant throughout the whole arterial system. The maximum pressure necessarily falls as the periphery of the vascular system is approached. In general it may be said that the minimal pressure is quite constant. Too little attention is paid to minimal and pulse pressure. The minimal pressure is important, for it gives us valuable data as to the actual propulsive force driving the blood forward to the periphery at the end of diastole.
It is readily understood how the maximum pressure falls as the periphery is approached, until in the arterioles the maximum and minimum pressures are about equal. The pressure then in these arterioles is practically the same as the diastolic pressure. Actually it is a few millimeters less. The diastolic blood pressure would, therefore, measure the peripheral resistance and, as the maximum for systolic pressure represents approximately the intraventricular pressure, the difference between the two, the pulse pressure, actually represents the force which is driving the blood onward from the heart to the periphery. It is hence very evident that the mere estimation of the systolic pressure gives us but a portion of the information we are seeking.
The pulse pressure is subject to wide fluctuations but as a rule for any one normal heart it remains fairly constant as the rate varies. In a rapidly beating heart the diastole is short and the diastolic pressure rises. If the systolic pressure does not also rise, as in a normal heart following exercise, we will say, the pulse pressure falls. We know that when the pulse rate is constant, vasodilatation causes a fall in diastolic pressure and a rise in pulse pressure. On the contrary, vasoconstriction causes a rise in diastolic pressure and a fall in pulse pressure.
It is very probably the case that with two individuals of equal age and equal pulse rate, and equal systolic pressure of 160 mm., the one with a diastolic pressure of 110 mm. and, therefore, a pulse pressure of 50 mm. is much worse off than the other with a diastolic pressure of 90 mm. and a pulse pressure of 70 mm. The latter may be normal for the age of the person especially when certain forms of fibrous arteriosclerosis accompanied by enlarged heart are present.
The former is not normal for any age. Low pulse pressure usually means a weak vasomotor control and is only found in failing circulation or in markedly run down states, such as after serious illness or in tuberculosis. Therefore, it is most important to estimate accurately the diastolic pressure as well as the systolic pressure, for only in this way can we obtain any data of value regarding the driving power of the heart and the condition of the vasomotor system. A high systolic pressure does not necessarily mean that a great deal of blood is forced into the capillaries. Actually it may mean that very little blood enters the periphery. The heart wastes its strength in dilating constricted vessels without actually carrying on the circulation adequately.
Normal Pressure Variations
The systolic pressure varies considerably under conditions which are by no means abnormal. Thus, the average for men at all ages is about 127 mm. Hg. (All measurements are taken from the brachial artery, with the individuals in the sitting posture.) For women the average is somewhat lower, 120 mm. Hg. The pressure is lowest in children. In children from 6-12 years the average systolic pressure is 112 mm. Normally, there is a gradual increase as age comes on, due, as will be shown in the succeeding chapter, to physiologic changes which take place in the arteries from birth to old age. In the chart here appended is graphically shown the normal variations in the blood pressure at different ages compiled from observations made on one thousand presumably normal persons. (Fig. 28.)
Fig. 28.—Chart showing the normal limits of variation in systolic blood pressure. (After Woley.)
The diastolic pressure has been estimated to be about 35 to 45 mm. Hg lower than the systolic pressure, and consequently these figures represent the pulse pressure in the brachial artery of man. This is equivalent to saying that every systole of the left ventricle distends this artery by a sudden increase in pressure equal to the weight of a column of mercury 2 mm. in diameter and 35 to 45 mm. high. Naturally, at the heart the pressure is highest. As the blood goes toward the capillary area the pressure gradually decreases until, at the openings of the great veins into the heart, the pressure is least. At the aorta (A) the pressure (systolic) is approximately 150 mm. Hg, at the brachial artery (B) it is 130 mm., in the capillary system (C) it is 30 mm., in the femoral vein (F) it is 20 mm., at the opening of the inferior vena cava (I) it is 3 mm.
Attention has been called to the normal systolic pressure at different ages. This is not the only cause for variations in the blood pressure. Normally, it is greater when in the erect position than when seated, and greater when seated than when lying down. During the day there are well-recognized changes. The pressure is lowest during the early morning hours, when the person is asleep. In women there are variations due to menstruation. Muscular exercise raises the blood pressure markedly. The effect of a full meal is to raise the blood pressure. The explanation is that during and following a meal there is dilatation of the abdominal vessels. This takes blood from other parts of the body, provided that the other factors in the circulation remain constant. A fall of pressure would necessarily occur in the aorta. To compensate for this, there is increased work on the part of the heart, which reveals itself as increased pressure and pulse pressure. It is well known that the interest in the process taken by an individual upon whom the blood pressure is estimated for the first time tends to increase the rate of the heart and to raise the blood pressure. For this reason the first few readings on the instrument must be discarded, and not until the patient looks upon the procedure calmly can the true blood pressure be obtained. As a corollary to this statement, mental excitement, of whatever kind, has a marked influence on the pressure. The patient must remain absolutely quiet. Raising the head or the free arm causes the pressure to rise. Another important physiologic variation is produced by concentrated mental activity. This tends to hurry the heart and increase the force of the beat. In short, it may be stated as a general rule that any active functioning of a part of the body which naturally requires a great excess of blood tends to elevate the blood pressure. At rest the pressure is constant. Variations caused by the factors mentioned act only transitorily, and the pressure shortly returns to normal.
The Auscultatory Blood Pressure Phenomenon
Since the first description of the auscultatory blood pressure sounds by Korotkov in 1905, this method has been more and more employed until today it is the standard, recognized method of determining the points in the blood pressure reading. When one applies the 12 cm. arm band over the brachial artery and listens with the bell of the stethoscope about one cm. below the cuff directly over the brachial artery near the bend of the elbow, one hears an interesting series of sounds when the air in the cuff is gradually reduced. The cuff is blown up above the maximum pressure. As the air pressure around the arm gradually is lowered, the series of sounds begins with a rather low-pitched, clear, clicking sound. This is the first phase. This only lasts through a few millimeters fall when a murmur is added and the tone becomes louder. This click and murmur phase is the second phase. A few millimeters more of drop in pressure and a clear, sharp, loud tone is audible. Usually this tone lasts through a greater drop than any of the other tones. This is the third phase. Rather suddenly the loud, clear tone gives place to a dull muffled tone. In general the transition is quite sharp and distinct. This is the fourth phase. The tone gradually or quickly ceases until no tone is heard. This is the fifth phase (Ettinger.)
The first phase is due to the sudden expansion of the collapsed portion of the artery below the cuff and to the rapidity of the blood flow. This causes the first sharp clicking sound which measures the systolic pressure.
The second, or murmur and sound phase, is due to the whorls in the blood stream as the pressure is further released and the part of the artery below the cuff begins to fill with blood.
The third tone phase is due to the greater expansion of the artery and to the lowered velocity in the artery. A loud tone may be produced by a stiff artery and a slow stream or by an elastic artery and a rapid stream. This tone is clear cut and in general is louder than the first phase.
The fourth phase is a transition from the third and becomes duller in sound as the artery approaches the normal size.
The fifth phase, no sound phase, occurs when the pressure in the cuff exerts no compression on the artery and the vessel is full throughout its length.
It is generally conceded that the sounds heard are produced in the artery itself and not at the heart.