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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
ANATOMY 25
Introduction, 25; Definition, 26; General Structure of
the Arteries, 27; Arteries, 29; Veins, 30; Capillaries, 31.
CHAPTER II
PATHOLOGY 32
Syphilitic Aortitis, 44; Experimental Arteriosclerosis, 50;
Arteriosclerosis of the Pulmonary Arteries, 63; Sclerosis
of the Veins, 64.
CHAPTER III
PHYSIOLOGY OF THE CIRCULATION 65
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 131
Auricular Flutter, 131; Auricular Fibrillation, 133;
Ventricular Fibrillation, 138; Extrasystole, 138;
Heart Block, 140.
CHAPTER V
BLOOD PRESSURE IN ITS CLINICAL APPLICATIONS 147
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
ETIOLOGY 157
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 ARTERIES 172
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 SIGNS 183
General, 183; Hypertension, 185; The Heart, 188; Palpable
Arteries, 189; Ocular Signs and Symptoms, 190; Nervous
Symptoms, 191.
CHAPTER IX
SYMPTOMS AND PHYSICAL SIGNS 194
Special, 194; Cardiac, 195; Renal, 199; Abdominal or
Visceral, 201; Cerebral, 203; Spinal, 205; Local or
Peripheral, 207; Pulmonary Artery, 209.
CHAPTER X
DIAGNOSIS 210
Early Diagnosis, 210; Differential Diagnosis, 215;
Diseases in Which Arteriosclerosis is Commonly Found, 216.
CHAPTER XI
PROGNOSIS 218
CHAPTER XII
PROPHYLAXIS 224
CHAPTER XIII
TREATMENT 229
Hygienic Treatment, 230; Balneotherapy, 233; Personal
Habits, 234; Dietetic Treatment, 235; Medicinal, 238;
Symptomatic Treatment, 245.
CHAPTER XIV
ARTERIOSCLEROSIS IN ITS RELATION TO LIFE INSURANCE 249
CHAPTER XV
PRACTICAL SUGGESTIONS 256
ILLUSTRATIONS
FIG. PAGE
1. Cross section of a large artery 28
2. Cross section of a coronary artery 36
3. Arteriosclerosis of the thoracic and abdominal aorta 39
4. Arteriosclerosis of the arch of the aorta 40
5. Normal aorta 41
6. Radiogram showing calcification of both radial and ulnar
arteries 42
7. Syphilitic aortitis of long standing 44
8. Diagrammatic representation of strain hypertrophy 48
9. Strain hypertrophy 49
10. Cross section of small artery in the mesentery 56
11. Enormous hypertrophy of left ventricle 58
12. Aortic incompetence with hypertrophy and dilatation of
left ventricle 61
13. Cook's modification of Riva-Rocci's blood pressure
instrument 72
14. Stanton's sphygmomanometer 73
15. The Erlanger sphygmomanometer with the Hirschfelder
attachments 74
16. Desk model Baumanometer 75
17. Faught blood pressure instrument 76
18. Rogers' "Tycos" dial sphygmomanometer 77
19. Detail of the dial in the "Tycos" instrument 78
20. Faught dial instrument 79
21. Detail of the dial of the Faught instrument 79
22. The Sanborn instrument 80
23. Method of taking blood pressure with a patient in sitting
position 81
24. Method of taking blood pressure with patient lying down 82
25. Observation by the auscultatory method and a mercury
instrument 84
26. Observation by the auscultatory method and a dial instrument 85
27. Schema to illustrate decrease in pressure 86
28. Chart showing the normal limits of variation in systolic
blood pressure 89
29. Tracing of auscultatory phenomena 94
30. Tracing of auscultatory phenomena 95
31. Clinical determination of diastolic pressure, fast drum 96
32. Clinical determination of diastolic pressure, slow drum 96
33. Venous blood pressure instrument 121
34. New venous pressure instrument 122
35. Events in the cardiac cycle 124
36. Simultaneous tracings of the jugular and carotid pulses 125
37. Jugular and carotid tracings 125
38. Right side of the heart showing distribution of the
two vagus nerves 127
39. Normal electrocardiogram 128
40. Auricular flutter 132
41. Auricular fibrillation 134
42. Auricular fibrillation 134
43. Pulse deficit 135
44. Ventricular fibrillation 137
45. Auricular extrasystoles 139
46. Ventricular extrasystole 139
47. Delayed conduction 141
48. Partial heart block 141
49. Complete heart block 142
50. Alternating periods of sinus rhythm and
auriculoventricular rhythm 144
51. Auriculoventricular or "nodal" rhythm 144
52. Influence of mechanical pressure on the right vagus nerve 144
53. Schematic distribution of right and left vagus 145
54. Blood pressure record from a normal reaction to ether 149
55. Chart showing the method of recording blood pressure
during an operation 150
56. Method of using blood pressure instrument during operation 151
57. Finger-tip palpation of the radial artery 178
58. Finger-tip palpation of the radial artery 178
59. Aneurysm of the heart wall 196
60. Large aneurysm of the aorta eroding the sternum 198
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.
[Illustration: 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.