The Project Gutenberg eBook ofArteriosclerosis and Hypertension, with Chapters on Blood PressureThis ebook is for the use of anyone anywhere in the United States and most other parts of the world at no cost and with almost no restrictions whatsoever. You may copy it, give it away or re-use it under the terms of the Project Gutenberg License included with this ebook or online atwww.gutenberg.org. If you are not located in the United States, you will have to check the laws of the country where you are located before using this eBook.Title: Arteriosclerosis and Hypertension, with Chapters on Blood PressureAuthor: Louis M. WarfieldRelease date: October 9, 2011 [eBook #37675]Language: EnglishCredits: Produced by Bryan Ness, Julia Neufeld and the OnlineDistributed Proofreading Team at http://www.pgdp.net (Thisfile was produced from images generously made availableby The Internet Archive/American Libraries.)*** START OF THE PROJECT GUTENBERG EBOOK ARTERIOSCLEROSIS AND HYPERTENSION, WITH CHAPTERS ON BLOOD PRESSURE ***
This ebook is for the use of anyone anywhere in the United States and most other parts of the world at no cost and with almost no restrictions whatsoever. You may copy it, give it away or re-use it under the terms of the Project Gutenberg License included with this ebook or online atwww.gutenberg.org. If you are not located in the United States, you will have to check the laws of the country where you are located before using this eBook.
Title: Arteriosclerosis and Hypertension, with Chapters on Blood PressureAuthor: Louis M. WarfieldRelease date: October 9, 2011 [eBook #37675]Language: EnglishCredits: Produced by Bryan Ness, Julia Neufeld and the OnlineDistributed Proofreading Team at http://www.pgdp.net (Thisfile was produced from images generously made availableby The Internet Archive/American Libraries.)
Title: Arteriosclerosis and Hypertension, with Chapters on Blood Pressure
Author: Louis M. Warfield
Author: Louis M. Warfield
Release date: October 9, 2011 [eBook #37675]
Language: English
Credits: Produced by Bryan Ness, Julia Neufeld and the OnlineDistributed Proofreading Team at http://www.pgdp.net (Thisfile was produced from images generously made availableby The Internet Archive/American Libraries.)
*** START OF THE PROJECT GUTENBERG EBOOK ARTERIOSCLEROSIS AND HYPERTENSION, WITH CHAPTERS ON BLOOD PRESSURE ***
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.
FORMERLY PROFESSOR OF CLINICAL MEDICINE, MARQUETTE UNIVERSITY MEDICALSCHOOL; CHIEF PHYSICIAN TO MILWAUKEE COUNTY HOSPITAL; ASSOCIATEMEMBER ASSOCIATION AMERICAN PHYSICIANS; MEMBER AMERICANASSOCIATION PATHOLOGISTS AND BACTERIOLOGISTS;AMERICAN MEDICAL ASSOCIATION, ETC., FELLOWAMERICAN COLLEGE OF PHYSICIANSTHIRD EDITIONST. LOUISC. V. MOSBY COMPANY1920
Copyright, 1912, 1920, by C. V. Mosby CompanyPress ofC. V. Mosby CompanySt. Louis
TOMY MOTHERTHIS VOLUME IS AFFECTIONATELYDEDICATED
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.
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 imperfectionsthan 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.
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.
pageCHAPTER I.Anatomy25Introduction, 25; Definition, 26; General Structure of the Arteries, 27; Arteries, 29; Veins, 30; Capillaries, 31.CHAPTER II.Pathology32Syphilitic Aortitis, 44; Experimental Arteriosclerosis, 50; Arteriosclerosis of the Pulmonary Arteries, 63; Sclerosis of the Veins, 64.CHAPTER III.Physiology of the Circulation65Blood 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 Arteriosclerosis13Auricular Flutter, 131; Auricular Fibrillation, 133; Ventricular Fibrillation, 138; Extrasystole, 138; Heart Block, 140.CHAPTER V.Blood Pressure in Its Clinical Applications147Blood 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.Etiology157Congenital 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 Arteries172Heart 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 Signs183General, 183; Hypertension, 185; The Heart, 188; Palpable Arteries, 189; Ocular Signs and Symptoms, 190; Nervous Symptoms, 191.CHAPTER IX.Symptoms and Physical Signs194Special, 194; Cardiac, 195; Renal, 199; Abdominal or Visceral, 201; Cerebral, 203; Spinal, 205; Local or Peripheral, 207; Pulmonary Artery, 209.CHAPTER X.Diagnosis210Early Diagnosis, 210; Differential Diagnosis, 215; Diseases in Which Arteriosclerosis is Commonly Found, 216.CHAPTER XI.Prognosis218CHAPTER XII.Prophylaxis224CHAPTER XIII.Treatment229Hygienic Treatment, 230; Balneotherapy, 233; Personal Habits, 234; Dietetic Treatment, 235; Medicinal, 238; Symptomatic Treatment, 245.CHAPTER XIV.Arteriosclerosis in Its Relation to Life Insurance249CHAPTER XV.Practical Suggestions256
page
Anatomy25
Introduction, 25; Definition, 26; General Structure of the Arteries, 27; Arteries, 29; Veins, 30; Capillaries, 31.
Pathology32
Syphilitic Aortitis, 44; Experimental Arteriosclerosis, 50; Arteriosclerosis of the Pulmonary Arteries, 63; Sclerosis of the Veins, 64.
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.
Important Cardiac Irregularities Associated With Arteriosclerosis13
Auricular Flutter, 131; Auricular Fibrillation, 133; Ventricular Fibrillation, 138; Extrasystole, 138; Heart Block, 140.
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.
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.
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.
Symptoms and Physical Signs183
General, 183; Hypertension, 185; The Heart, 188; Palpable Arteries, 189; Ocular Signs and Symptoms, 190; Nervous Symptoms, 191.
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.
Diagnosis210
Early Diagnosis, 210; Differential Diagnosis, 215; Diseases in Which Arteriosclerosis is Commonly Found, 216.
Prognosis218
Prophylaxis224
Treatment229
Hygienic Treatment, 230; Balneotherapy, 233; Personal Habits, 234; Dietetic Treatment, 235; Medicinal, 238; Symptomatic Treatment, 245.
Arteriosclerosis in Its Relation to Life Insurance249
Practical Suggestions256
FIG.page1. Cross section of a large artery282. Cross section of a coronary artery363. Arteriosclerosis of the thoracic and abdominal aorta394. Arteriosclerosis of the arch of the aorta405. Normal Aorta416. Radiogram showing calcification of both radial and ulnar arteries427. Syphilitic aortitis of long standing448. Diagrammatic representation of strain hypertrophy489. Strain hypertrophy4910. Cross section of small artery in the mesentery5611. Enormous hypertrophy of left ventricle5812. Aortic incompetence with hypertrophy and dilatation of left ventricle6113. Cooks modification of Riva-Roccis blood pressure instrument7214. Stanton's sphygmomanometer7315. The Erlanger sphygmomanometer with the Hirschfelder attachments7416. Desk model Baumanometer7517. Faught blood pressure instrument7618. Rogers' "Tycos" dial sphygmomanometer7719. Detail of the dial in the "Tycos" instrument7820. Faught dial instrument7921. Detail of the dial of the Faught instrument7922. The Sanborn instrument8023. Method of taking blood pressure with a patient in sitting position8124. Method of taking blood pressure with patient lying down8225. Observation by the auscultatory method and a mercury instrument8426. Observation by the auscultatory method and a dial instrument8527. Schema to illustrate decrease in pressure8628. Chart showing the normal limits of variation in systolic blood pressure8929. Tracing of auscultatory phenomena9430. Tracings of auscultatory phenomena9531. Clinical determination of diastolic pressure fast drum9632. Clinical determination of diastolic pressure slow drum9633. Venous blood pressure instrument12134. New venous pressure instrument12235. Events in the cardiac cycle12436. Simultaneous tracings of the jugular and carotid pulses12537. Jugular and carotid tracings12538. Right side of the heart showing distribution of the two vagus nerves12739. Normal electrocardiogram12840. Auricular flutter13241. Auricular fibrillation13442. Auricular fibrillation13443. Pulse deficit13544. Ventricular fibrillation13745. Auricular extrasystoles13946. Ventricular extrasystole13947. Delayed conduction14148. Partial heart block14149. Complete heart block14250. Alternating periods of sinus rhythm and auriculoventricular rhythm14451. Auriculoventricular or "nodal" rhythm14452. Influence of mechanical pressure on the right vagus nerve14453. Schematic distribution of right and left vagus14554. Blood pressure record from a normal reaction to ether14955. Chart showing the method of recording blood pressure during anoperation15056. Method of using blood pressure instrument during operation15157. Finger-tip palpation of the radial artery17858. Finger-tip palpation of the radial artery17859. Aneurysm of the heart wall19660. Large aneurysm of the aorta eroding the sternum198
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 diseasesui generis. It is bestviewed 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, beginningwith 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.
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 isusually 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.)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 lessthan 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.
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. Inthe 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.
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.
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.
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 muchon 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 arenow 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 onlya 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.)